Anatomy and Physiology by Dennis Munoz2

 Anatomy and Physiology
 Prepared by
 DENNIS N. MUÑOZ, PT, RN,RM
 Organs of the Respiratory system
•Nose
•Pharynx
•Larynx
•Trachea
•Bronchi
•Lungs –
alveoli
Figure 13.1 SLIDE 13.1

 Functions of the Respiratory
System
Gas exchanges between blood and air (#1 = obtaining
oxygen & removing carbon dioxide)
Exchange place in the lungs in tiny air sacs, the alveoli
Passageways, purify, warm, and humidify air
filtering incoming air
Controlling the temperature & water content of incoming
air
Producing vocal sounds
Plays important roles in the sense of smell &
regulation of blood pH
–
SLIDE 13.2
 The Nose
•The only externally visible part of the respiratory

system
•Air enters the nose through the external nares
(nostrils)
•The interior is the nasal cavity
•divided by a nasal septum
Upper Respiratory Tract

Figure 13.2
SLIDE
13.3B
 Anatomy of the Nasal Cavity
•Olfactory receptors are located in the

olfactory epithelium
•The rest of the cavity is lined with
mucous membrane
•Moistens air
•Traps incoming foreign particles
SLIDE
13.4A

Olfactory epithelium
Figure 13.2
SLIDE
13.3B
•Lateral walls have projections called

conchae
•“turbinate” bones
•Increases surface area
•Increases air turbulence within the nasal
cavity
SLIDE
13.4B
•The nasal cavity is separated from the

oral cavity by the palate
•Anterior hard palate (bone)
•Posterior soft palate (muscle)
SLIDE
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
13.4B

Figure 13.2
SLIDE
13.3B
 Paranasal Sinuses
•Cavities within bones surrounding the

nasal cavity
•Frontal bone: 2
•Sphenoid bone: 1
•Ethmoid bone: 3
•Maxillary bones: 1 each
 Paranasal Sinuses
•Function of the sinuses

•Lighten the skull
•Act as resonance chambers for speech
•Produce mucus that drains into the nasal
cavity
SLIDE
13.5B
THE PARANASAL SINUSES
Anterior View Lateral View

Figure 7.11a, b
 Pharynx (Throat)
•Muscular passage from nasal cavity to
larynx
•Three regions
•Nasopharynx – superior, behind nasal
cavity
•Oropharynx – middle, behind mouth
•Laryngopharynx – inferior, attached to
larynx
SLIDE 13.6
Pharynx (Throat) SLIDE 13.6
•Nasopharynx is only
respiratory
•The oropharynx and
laryngopharynx
•Common
passageways for
air and food
•Part of two body
systems

 Structures of the Pharynx
•Auditory tubes enter the nasopharynx

•Tonsils
•Pharyngeal tonsil (adenoids) in
nasopharynx
•Palatine tonsils in oropharynx
•Lingual tonsils in oropharynx
SLIDE 13.7

Figure 13.2
SLIDE
13.3B
 Larynx (Voice Box)
•Routes air and food into proper channels

•Plays a role in speech
•Consists of 9 cartilage structures
SLIDE 13.8
ANATOMY OF THE LARYNX
Anterior View Lateral View
Figure 21.5a, b
 Structures of the Larynx
•Thyroid cartilage
•Largest hyaline cartilage
•Protrudes anteriorly (Adam’s apple)
•Epiglottis
•Superior opening of the larynx
•Protects larynx during swallowing
SLIDE
13.9A
 Structures of the Larynx
•False vocal cords

•Act as valves
•True vocal cords (vocal folds)
•Vibrate with expelled air to create sound
(speech)
•Glottis – opening between vocal cords
SLIDE
13.9B
MOVEMENTS OF THE VOCAL FOLDS
Figure 21.6
 Trachea (Windpipe)
•Connects larynx with bronchi

•Lined with ciliated mucous membrane
•Walls are reinforced
•C-shaped hyaline cartilage
•Keeps tube open
SLIDE
13.10
THE TRACHEA
Figure 21.7a
 Primary Bronchi
•Formed by division of the trachea

•Enter the lung at the hilus
•Right bronchus: wider, shorter,
and straighter than left
•Bronchi subdivide into smaller tubes
SLIDE
13.11
BRONCHIAL (RESPIRATORY) TREE
Figure 21.8a
 Lungs
•Occupy most of the thoracic cavity

•Apex is near the clavicle (superior)
•Base rests on the diaphragm (inferior)
•Each lung is divided into lobes by fissures
•Left lung – two lobes
•Right lung – three lobes
SLIDE
13.12A
STRUCTURE OF THE LUNGS
Figure 21.8a
 Coverings of the Lungs
•Visceral pleura covers the lung surface

•Parietal pleura lines the walls of the
thoracic cavity
•Pleural cavity contains serous fluid
SLIDE
13.13
 Pleural Membranes and Cavity
Figure 13.4b
SLIDE
13.12B
 Respiratory Tree Divisions
•Primary bronchi = 1 left = 1 right

•Secondary (lobar) bronchi = 3 left + 2
right
•Tertiary bronchi (segmental)= 10 left + 8
right
•Bronchioles
•Terminal bronchioles
SLIDE
13.14
BRONCHIAL (RESPIRATORY) TREE
Figure 21.8a
 Bronchioles
•Smallest
branches
of the
bronchi
Figure 13.5a
SLIDE
13.15A
 Bronchioles
•All but the
smallest
branches
have
reinforcing
cartilage
Figure 13.5a
SLIDE
13.15B
 Bronchioles
•Terminal
bronchioles
end in
alveoli
Figure 13.5a
SLIDE
13.15C
 Respiratory ZoneRegion of gas
exchange between
air and blood.
•Structures
•Respiratory
bronchioles
•Alveolar duct
•Alveoli
•The Site of gas
exchange
SLIDE
13.16
 Alveoli
•Structure of alveoli
•Alveolar duct
•Alveolar sac
•Alveolus
•Gas exchange:
•takes place in the alveoli
•across the respiratory membrane
ALVEOLI
 is 1 cell layer thick.
 Total air barrier is 2
cells across (2 µ m).

 2 types of cell Polyhedral in shape

and clustered like units of
honeycomb.

 ~ 300 million air sacs (alveoli).

 Large surface area (60–80
2
m ).
 Each alveolus s:
 Alveolar type I:
 Structural cells.
 Alveolar type II:
 Secrete surfactant.

SURFACTANT
Phospholipid produced by
alveolar type II cells.
Lowers surface tension.
 Reduces attractive forces

Insert fig. 16.12
of hydrogen bonding by
becoming interspersed
between H20 molecules.
 Surface tension in
alveoli is reduced.
As alveoli radius decreases,
surfactant’s ability to lower

surface tension increases.
Disorders:
 RDS.
 ARDS.
Respiratory Membrane

(Air-Blood Barrier)
•Simple squamous E.T. layer: lines

alveolar walls
•Pulmonary capillaries: cover external
surfaces of alveoli
SLIDE
13.18A
Respiratory Membrane

(Air-Blood Barrier)
Figure 13.6
SLIDE
13.18B
 Gas Exchange
•Gas crosses the respiratory membrane

by diffusion
•Oxygen enters blood
•Carbon dioxide enters alveoli
•Macrophages add protection
•Surfactant coats exposed alveolar
surfaces
SLIDE
13.19
 Events of
Respiration
•Pulmonary ventilation
– moving air in and
out of the lungs
•External respiration –
gas exchange
between pulmonary
blood and alveoli
 Events of Respiration
•Transport of oxygen and carbon dioxide

via the bloodstream
•Internal respiration – gas exchange
between blood in systemic capillaries
and tissue cells in body
SLIDE
13.20B
Mechanics of Breathing

(Pulmonary Ventilation)
Ventilation
•Completely mechanical
process
•Depends on volume
changes in the thoracic
cavity
•Volume changes lead to
pressure changes, which
lead to the flow of gases
to equalize pressure
Mechanics of

Breathing
(Pulmonary
Ventilation)
•Two phases
•Inspiration – flow of
air into lung
•Expiration – air
leaving lung

 Inspiration
•Diaphragm and
intercostal muscles
contract
•The size of the thoracic
cavity increases
•External air is pulled
into the lungs due to
an increase in
intrapulmonary
volume
QUIET INSPIRATION
Active process:

 Contraction of diaphragm,
increases thoracic volume
vertically.
Parasternal and external
intercostals contract, raising
the ribs; increasing thoracic
volume laterally.
Pressure changes:
 Alveolar changes from 0 to –

3 mm Hg.
 Intrapleural changes from –4
to –6 mm Hg.
 Transpulmonary pressure =
+3 mm Hg.
 Inspiration
Figure 13.7a
SLIDE
13.22B
 Expiration
•A passive process
•depends on natural lung elasticity
•As muscles relax, air is pushed out of the
lungs
•Forced expiration can occur by contracting
internal intercostal muscles
SLIDE
13.23A
Quiet expiration is a passive

process.
 After being stretched by
EXPIRATION
contractions of the diaphragm
and thoracic muscles; the
diaphragm, thoracic muscles,
thorax, and lungs recoil.
 Decrease in lung volume raises
the pressure within alveoli
above atmosphere, and
pushes air out.
Pressure changes:

 Intrapulmonary pressure
changes from –3 to +3 mm
Hg.
 Intrapleural pressure changes
from –6 to –3 mm Hg.
 Transpulmonary pressure = +6
mm Hg.

 Expiration
Figure 13.7b
SLIDE
13.23B
 Nonrespiratory Air Movements
•Can be caused by reflexes or voluntary
actions
•Examples
•Cough and sneeze – clear lungs of
debris
•Laughing
•Crying
•Yawn
•Hiccup
SLIDE
13.25
PULMONARY VENTILATION
Insert fig. 16.15

PULMONARY FUNCTION TESTS
• Assessed by spirometry.
• Subject breathes into a closed system in which
air is trapped within a bell floating in H20.
• The bell moves up when the subject exhales
and down when the subject inhales.
Terms Used to Describe Lung Volumes and Capacities
ANATOMICAL DEAD SPACE
Not all of the inspired air reached the alveoli.

As fresh air is inhaled it is mixed with air in
anatomical dead space.

 Conducting zone and alveoli where [02] is
lower than normal and [C02] is higher than
normal.
 Alveolar ventilation = F x (TV- DS).
 F = frequency (breaths/min.).
 TV = tidal volume.
 DS = dead space.
Respiratory Volumes and

Capacities
•Tidal volume [TV]:

•Normal breathing
•moves about 500 ml of air/breath
SLIDE
13.26

Capacities
•Inspiratory reserve volume (IRV)
•Amount of air that can be taken in
forcibly over the tidal volume
•Usually between 2100 and 3200 ml
SLIDE
13.27A

Capacities
•Expiratory reserve volume (ERV)
•Amount of air that can be forcibly
exhaled
•Approximately 1200 ml
SLIDE
13.27A

Capacities
•Residual volume
•Air remaining in lung after expiration
•About 1200 ml
SLIDE
13.27B

Capacities
•Vital capacity
•The total amount of exchangeable air
•Vital capacity = TV + IRV + ERV
•Dead air space or volume
•Air that remains in conducting zone
•Bronchi, bronchioles, ducts
•never reaches alveoli
•About 150 ml
SLIDE
Copyright © 2003 Pearson Education, Inc. publishing as Benjmin Cummings
13.28

Capacities
•Functional volume
•Air that actually reaches the respiratory
zone
•Usually about 350 ml
•Respiratory capacities are measured
with a spirometer

Capacities
•Factors that affect respiratory capacity
•Size
•Sex
•Age
•Physical condition
•
 Respiratory Capacities
Figure 13.9
 Gas Transport in the Blood
•Oxygen transport in the blood

•Inside red blood cells attached to
hemoglobin
•(oxyhemoglobin [HbO2])
•A small amount is carried dissolved in the
plasma
 Gas Transport in the Blood
•Carbon dioxide transport in the blood

•Most is transported in the plasma as
bicarbonate ion (HCO3–)
•A small amount is carried inside red
blood cells on hemoglobin-
carbaminohemoglobin
 Internal Respiration
Figure 13.11
SLIDE
13.34B
PARTIAL PRESSURES OF
GASES IN BLOOD
 When a liquid or gas (blood
and alveolar air) are at
equilibrium:
 The amount of gas
dissolved in fluid
reaches a maximum
value (Henry’s Law).
 Depends upon:
 Solubility of gas in the
fluid.
 Temperature of the fluid.
 Partial pressure of the gas.
 [Gas] dissolved in a fluid
depends directly on its
partial pressure in the gas
mixture.
SIGNIFICANCE OF BLOOD P0 AND 2
PC0 MEASUREMENTS
2
• At normal P0 2
arterial
blood is
about 100
mm Hg.
• P02 level in the
systemic
veins is
about 40
mm Hg.
nPC0 is 46 mm Hg in the systemic veins.

2
nProvides a good index of lung function.

PONS RESPIRATORY CENTERS
Activities of medullary rhythmicity center is

influenced by pons.
Apneustic center:
 Promotes inspiration by stimulating the I

neurons in the medulla.
 Pneumotaxic center:
 Antagonizes the apneustic center.
 Inhibits inspiration.
CHEMORECEPTORS
2 groups of chemo-
receptors that monitor
changes in blood PC0 , P0 , 2 2
and pH. Insert fig. 16.27

Central:
 Medulla.
Peripheral:

 Carotid and aortic bodies.

 Control breathing
indirectly via sensory
nerve fibers to the
medulla (X, IX).
EFFECTS OF BLOOD PC0 AND PH ON 2
VENTILATION
Chemoreceptor input modifies the rate


and depth of breathing.

 Oxygen content of blood decreases more
slowly because of the large “reservoir”
of oxygen attached to hemoglobin.
 Chemoreceptors are more sensitive to
changes in PC0 .
2
H20 + C02 H2C03 H+ + HC03-

Rate and depth of ventilation adjusted to
maintain arterial PC0 of 40 mm Hg.

2
CHEMORECEPTOR CONTROL
 Central chemoreceptors:
 More sensitive to changes in arterial PC0 . 2
 H20 + C02 H2C03 H+


H+ cannot cross the blood brain barrier.
C0
2 can cross the blood brain barrier and
will form H2C03.
 Lowers pH of CSF.
 Directly stimulates central chemoreceptors.

CHEMORECEPTOR CONTROL (CONTINUED)
CHEMORECEPTOR CONTROL OF
BREATHING
Factors Influencing Respiratory

Rate and Depth

•Physical factors
•Increased body temperature
•Exercise
•Talking
•Coughing
•Volition (conscious control)
•
Factors Influencing Respiratory

Rate and Depth

•Emotional factors
•Chemical factors
•Carbon dioxide levels
•Oxygen levels
•Chemoreceptors in aorta, carotid
arteries
•
Respiratory Rate Changes

Throughout Life
•Newborns: 40 to 80 respirations per
minute
•Infants: 30 respirations per minute
•Age 5: 25 respirations per minute
•Adults: 12 to 18 respirations per minute
•Rate often increases somewhat with old
age
SLIDE
13.49
Respiratory Rate Changes

Throughout Life
•Newborns: 40 to 80 respirations per
minute
•Infants: 30 respirations per minute
•Age 5: 25 respirations per minute
•Adults: 12 to 18 respirations per minute
•Rate often increases somewhat with old
age
SLIDE
13.49
Respiratory Disorders: Chronic

Obstructive Pulmonary Disease

(COPD): FYI
•Chronic bronchitis and emphysema

•Major causes of death and disability in
the United States
SLIDE
13.40A
 Emphysema: FYI
•Alveoli enlarge as adjacent chambers break

through
•Chronic inflammation promotes lung fibrosis
•Airways collapse during expiration
•Patients use a large amount of energy to
exhale
•Over-inflation of the lungs leads to a
permanently expanded barrel chest
•Cyanosis appears late in the disease
SLIDE
13.41
 Chronic Bronchitis: FYI
•Mucosa of the lower respiratory
passages becomes severely inflamed
•Mucus production increases
•Pooled mucus impairs ventilation and
gas exchange
•Risk of lung infection increases
•Pneumonia is common
•Hypoxia and cyanosis occur early
SLIDE
13.42
 Lung Cancer: FYI
•Accounts for 1/3 of all cancer deaths in

the United States: The #1 cause of death
from cancer
•Increased incidence associated with
smoking
•Three common types
•Squamous cell carcinoma
•Adenocarcinoma
•Small cell carcinoma
SLIDE
13.44
Sudden Infant Death syndrome

(SIDS): FYI
•Apparently healthy infant stops breathing

and dies during sleep
•Some cases are thought to be a problem
of the neural respiratory control center
•One third of cases appear to be due to
heart rhythm abnormalities
SLIDE
13.45
 Asthma: FYI
•Chronic inflamed hypersensitive

bronchiole passages
•May have allergic component
•May have emotional component
•More severe in cold weather
•Response to irritants with dyspnea,
coughing, and wheezing
SLIDE
13.46
Birth Defects of the Respiratory

System: FYI
•Important birth defects
•Cystic fibrosis
•Common genetic condition
•Over-secretion of thick mucus clogs
the respiratory system
•Cleft palate: developmental anomaly
SLIDE
13.47B
 Aging Effects: FYI
•Elasticity of lungs decreases
•Vital capacity decreases
•Blood oxygen levels decrease
•Stimulating effects of carbon dioxide
decreases
•More risks of respiratory tract infection
•New evidence that in estrogen may
be related to COPD
SLIDE
13.48
Pulmonary Physical
Examination and Health
Assessment
Prepared by
DENNIS NABOR MUÑOZ, R.N., R.M.

Common Symptoms
• Dyspnea
• Cough
• Sputum Production
• Hemoptysis
• Chest Pain
• Fever
• Pedal Edema
Assessment Skills
How to Perform a Patient Bedside

Assessment
The 2 Phases of Assessment
• Interviewing the Patient
– Taking a History
• Physical Examination
– Inspection
– Palpation
– Percussion
– Auscultation
Patient History
• History of Present Illness
• Past Health History
• Current Health Status
• Family History
• Social History
Common Symptoms of Lung
Problems
• Dyspnea- “How is your breathing today?”
(When are they S.O.B.?)
• Orthopnea- “Have you had to sit up to make
your breathing easier?”
• Cough- “What has your cough been like?”
– Is it productive? If so, how often? How much
sputum is coughed-out? What is its color?
(purulent?- mucoid?) Consistency?
Common Symptoms of Lung
Problems
• Does the patient have any of the following
complaints?
– Blood in the sputum - (hemoptysis)
– Chest pain - (during breathing?) pleuritis
– Fever
• Usually indicates an infection of some sort
Past Medical History
• Previous hospitalizations for similar
complaint?
• Relevant work history?
– Worked in dirty air environment
• Ever had asthma?
• Smoked? How many cigarettes/day for
how many years
– Pack years = #of pack/day x # of years
Inspecting the Patient
• General Appearance
– Wasted? Well-nourished? Obese?
Distressed? Relaxed? Disheveled? Well-
cared-for? Diaphoretic? Pale? Cyanotic?
• Level of consciousness
– Oriented to person, time & place (x3)
– Obtunded? Lethargic? Confused?
• Vital Signs
– Temperature - Febrile? Hypothermic?
– Pulse - Tachycardia? Irregular? Faint?
Pulsus paradoxicus? Pulsus alterans
– Respiration- Tachypnea? Shallow?
Deep?
– Blood pressure- Hypotensive?
Hypertensive? Syncope?
• Examination of Head
– Nasal Flaring
– Cyanosis
– Pursed lip breathing
– Look of anxiety
• Examination of Neck
– Trachea: midline?
– Jugular veins distended?

Examination of the Thorax & Lungs
• Thoracic configuration:
• Barrel chest?
• Kyphosis
• Scoliosis?
• Kyphoscoliosis?
• Pectus excavatum
• Breathing Pattern & Effort
• Retractions? intercostal; supraclavicular
Breathing Pattern & Effort continued
• Synchrony of diaphragm & upper chest?
– Diaphragm & upper chest should work
together
– Abdominal paradox - upper chest rises
while diaphragm falls
• This indicates fatigue of the diaphragm
• Is a excellent predictor of impending
“respiratory failure”
Palpation
• The art of touching the chest wall to
evaluate underlying structures
Aspects of Palpation
• Skin & subcutaneous tissues
– evidence of subcutaneous emphysema?
• Aka - crepitus
– pain associated with bruising &/or rib
fractures?
• Vocal fremitus
• Thoracic expansion
Percussion of the Chest
• Act of tapping on the chest wall (rib
interspaces) to evaluate underlying
structures
– Percussion Sounds:
• Dull - indicates fluid or increased tissue
density
• Hyperressonant (hollow sound) - indicates
increased air- (heard above a
pneumothorax)
Auscultation of the Lungs
• Listening to body sounds with stethescope
Auscultation
• Listening to breath sounds
– Stethoscope
• Bell - for low pitched sounds (heart
sounds)
• Diaphragm - for higher pitched sounds
(breath sounds)
– Technique
• Patient breathes through their mouth
• Ideally, sounds on one side of the chest
should be compared to the opposite side
• May be necessary to have patient roll patient
side-to-side
Normal Breath Sounds
• Vesicular sounds
– Soft “rustling” sounds heard over most lung tissue
• Bronchovesicular sounds
– Has characteristics of above two
– Heard only over major airways
• Tracheal sounds
– Hollow tubular sounds
–

Abnormal (Adventitious) Breath
Sounds
• Crackles (rales)
– discontinuous ”pop-like” sounds
• generally heard on inspiration but can be
heard on exhalation also
• Wheezes
– high-pitched continuous musical sounds
• can be heard on both inspiration or
exhalation
•
Abnormal Breath Sounds Continued
• Rhonchi
– low-pitched snoring sound that is
continuous
• can be heard on inspiration or exhalation
• Bronchial Breath Sounds
– same as Tracheal Sounds except heard
over lung parenchyma
• Stridor - high pitched raspy sound
– is heard at it’s loudest over the trachea
–
– indicates upper airway narrowing
– heard in such conditions as;
• post extubation stenosis
• croup in young children
• Pleural Friction Rub
• Egophony - e to a changes
– first section heard is the normal e sound
– second sound heard is the example of
egophony: letter “e” heard as “a”

Crackles can indicate
• Atelectasis
• Bronchitis
• Pneumonia
• Pulmonary edema
• Pulmonary fibrosis (dry crackles)
Ronchi indicates
• Secretions in larger airways
– frequently clear with a cough
– seen in any condition that creates lung
mucus
– in COPD ronchi may occur because of
airflow obstruction unrelated to
secretions
Other “Less Common” Sounds
• Pleural friction rub
– occurs when pleural surfaces rub together
– seen in some pneumonias effecting pleural
surfaces
• Stridor
– High pitched rasping sound heard mainly
on inspiration
– Indicative of upper airway obstruction
Breathing Patterns
• Cheyne-Stokes Breathing
– Irregular patterns of deep breathing followed by
periods of shallow breathing; usually ending with
a period of apnea
• Biot’s Breathing
– Irregular patterns of breathing; usually very
disorganzied. May be periods of apnea
• Kussmaul’s Breathing
– Rapid & deep breathing
More Breathing Patterns
• Apneustic Pattern
– Prolonged inspirations; serial inspirations w/o
exhalation after each followed by “summative”
exhalation
• Asthmatic Pattern
– Excessively long expiratory periods
• Paradoxical Breathing
– Is present when a portion of chest wall moves in
the opposite direction as it should during the
breathing cycle
Voice Sounds
• Egophony
 1. Place stethoscope over lung area
 2. Ask patient to say the letter “e”
 3. If you actually hear the hard “a” sound;
 4. The area has a fluid or consolidation
• Bronchophony
– An increase in intensity and clarity of
vocal sounds.
Cardiac Sounds
• Lub - Dub
• S1, S2
• PMI (Point of Maximal Impulse)
– Fifth intercostal, mid clavicular, left side
• PVC’s are common
• Heaves, gallops, murmurs, bruits
Abdominal Examination
• Is the abdomen distended?
• Is the abdomen hard when palpating it?
• Increased abdominal pressure can put increased
pressure on the diaphragm making breathing
more difficult. Causes
– Hepatomegaly
– Intra-abdominal bleeding
Examination of the Extremities
• Look for evidence of
– Cyanosis
• hands, feet, mucous membranes
– Pedal edema (pitting edema)
• +1 to +5 scale used
– Clubbing of fingers
• seen in a variety of inflammatory diseases
– Capillary refill
– Peripheral skin temperature
Clubbing illustrated
Respiratory Assessment
• Thoracic cage bony conical shape with

narrow at top
• Defined by sternum, 12 pairs ribs and 12
thoracic vertebrae
• Rib 1-7 attached to sternum via costal
cartilages
• Rib 8,9,10 attached to costal cartilage
• Rib 11,12 “floating” with free palpable tips
•
• Anterior thoracic Landmarks;
– Suprasternal notch, “U” shaped
 Sternum-”breastbone” has three parts:
 The body
 The xiphoid
 The Manubrium
 Manubriosternal Angle- “Angle of Louis”-

is articulation of the manubrium and the
body of the sternum; continuous with the
2ed rib; marks site of the tracheal
bifurcation into the R & L bronchi
 Costal Angle- R & L costal margins form
angle where meet at xiphoid process
• Posterior thoracic Landmarks
– Vertebra Prominens
– Spinous Processes
– Interior Boarder of Scapula
– 12th Rib

• Anterior Chest
• Midsternal Line
• Midclavicular Line- bisects the center of
each clavicle at point halfway between
the palpated sternoclavicular and
acromioclavicular joint, near nipple
line
• Posterior Chest
• vertebral Line- midspinal
• Scapular line- extends through inferior
angle of scapula
• Lateral Chest- Lift arms 90* & divide by 3
lines
• Anterior axillary- down from anterior
axillary fold to where the pectoralis
major muscle inserts
• Posterior anillary down from posterior
axillary fold to where latissimus dorsi
muscle inserts
• Midaxillary line-down from apex of
axilla, lies between and parallel to
other two
• Thoracic cavity
– Mediastinum- middle section of thoracic
cavity contains esophagus, trachea,
heart and great vessels; and the Left
& Right pleural cavities
– Lung Borders- anterior
• Apex 9 highest point of lungs 3-4
cm above inner 3rd of clavicles
• Base- lower border, rest on
diaphragm about 6th rib in
midclavicular line
•
– Lungs Border- posterior

• C7-Apex of lung tissue
• Lungs- 2 pair
• Anterior
– Right lung shorter because of
underlying liver; has 3 lobes
• Anterior Right Upper Lobe (RUL)
• Right Middle Lobe (RML)
• Right Lower Lobe (RLL)
 - Left Lung- narrower because heart
bulges
 to left; has 2 lobes

-
–
–
• Anterior Left Upper Lobe (LUL)
• Anterior Left Lower Lobe (LLL)
• Posterior
– Right Upper Lobe (RUL) and Left Upper
Lobe (LUL)- from apices at T1 down to
T3
– Right Lower Lobe (RLL) and Left Lower
Lobe (LLL)- from the above border to
T10 on expiration and to T12 on
inspiration.
•
• Pleurae- thin slippery which forms an
envelope between lungs and chest wall.
• Visceral Pleura- lines outside of lungs down
into fissures
• Parietal Pleura- lining inside the chest
wall and diaphragm.

• Trachea- lies anterior to esophagus; is

10– 11 cm long in adult; starts at
cricoid cartilage bifurcates below
sternal angle into R and L bronchi;
posterior bifurcates at T4 or T5;
 R bronchus shorter wider;
 L bronchus vertical than L main
• Function of Trachea and bronchi- transport
gases between environment and lung
parenchyma.
– Bronchial tree- protect alveoli from small
particulate matter in the inhaled air
– Bronchi lined- goblet cells which secrete
mucus that entraps particles
– Bronchi line with cilia- which sweeps
particles upward swallowed or
expelled
– Acinus- functional respiratory unit
consist of bronchioles, alveolar ducts,
alveolar sac and alveoli
• Alveolar duct & Alveolar-gaseous
exchange takes place
•
• Major function of Respiratory System-
1.Supply oxygen to body for energy
production
2.Remove CO 2 as waste product for
energy reaction
3.Maintaining homeostasis (acid-base
balance) of arterial blood
4.Maintaining heat exchange (less
important to humans)
• Control of Respirations
– Involuntary control mediated in
respiratory center in brain stem (pons
& medulla)
– Change in carbon dioxide and oxygen
levels in blood
– Hypercapnia- Increase of carbon
dioxide-stimulus to breathe
– Hypoxemia ) decrease in oxygen in
blood can cause increase in
respirations but less effective
– Hypoventilation – slow, shallow
breathing causes carbon dioxide to
build in blood
 -With age less surface area available for
gas exchange
 Increases older person risk for
postoperative pulmonary complications
due to decreased ability to cough
–
• Assessment ( need to note normal from
abnormal)
A. Subjective Data: questions to ask-what
client tells you
1.Cough - cold in particular to children;
how frequent, when, time of day,
contributing factors; what kind of
cough (hacking, dry, with blood),
what makes it worse or better
2.SOB- older adults on exercise
3.Chest pain with breathing
4.History of respiratory infections- chronic
 allergies, history of asthma, TB.
 Pulmonary disease in older adults
 5. Environmental exposure- where did

you or do you work, do you smoke, do
you live or work near pollutants
 6. Self care behavior- chest x-ray, TB
testing, etc.
7.Allergies in family- particularly in
children


 Objective
A.Inspection (what you see)
1.Shape and Configuration of chest
wall.
a.Thorax symmetric, elliptical
shape with downward
sloping ribs
b.Any signs tumors, lumps,
bruising on chest
–Check shape for:
»Scoliosis (“s” shape)
»Kyphosis (humpback)
»Barrel chest
»
 Skin color and condition
»Person’s position
»Level of consciousness
(LOC)
B. Palpation

a.Symmetric expansion- place hands of

posterolateral chest wall with thumbs
at level of T9 or T10; Slide hands
medially to pinch up a small fold of
skin between thumb; have person take
a deep breath
 your thumbs should move apart symmetrically
b.Tactile Fremitus- palpable vibrations- with
palmar base ( the ball) of fingers or ulna edge
of one hand touch person’s chest and have
then repeat “ninety-nine” or “blue moon”
should feel vibration; varies among people
but symmetry most important

 Affecting normal intensity of Tactile

Fremitus:

 -Relative location of bronchi to chest wall

 - Thickness of chest wall

 - Pitch and intensity
 Check for:
 Decreased fremitus
 Increased fremitus
 Rhonchal fremitus
 Pleural friction fremitus
 Crepitus

C Percuss

• Tapping on client’s skin with short sharp

strokes to assess underlying structure
• Strokes yield palpable vibrations and
characteristics sounds that depict
location, size, density of underlying organ
pg.163
• Two methods-
– Direct- striking hand direct contact with
body wall. Used in infant’s thorax
and adult sinus areas
– Indirect- use both hands. Striking hand
 contacts stationary hand fixed on
client’s skin
–
 Avoid striking client’s ribs & scapulae,
always a dull sound & yields no data

 Lung Field
• Start at apices at top of both
shoulders
• Percuss interspaces comparing
side to side going down lung
region
–Hyperresonance- too much
air present
–Resonance-voice heard
through stethoscope; is
muffled nondistinct
 -Dull- abnormal density in lung

 c. Diaphragmatic Excursion- mapping

out lower lung border at expiration &
inspiration; somewhat higher due to liver
 C. Auscultation-with the diaphragm of

stethoscope from apex to base, from side to
side.


 a. Evaluate the presence and quality of

normal breath sounds.
 b. With flat diaphragm of stethoscope listen
at least one full respiration in each location
 c. Compare side to side and top to bottom
( Go from left to right and then down or from right
to left and then down
 d. analyze breath sounds
 e. detect any abnormal sounds
 f. examine sounds produced by spoken word
 g. pulse oximeter-noninvasive method of
assessing arterial oxygen saturation (SpO2)



 h Listening to own breathing
 Stethoscope tubing bumping
 Patient shivering
 Patient has hairy chest
 Rustling of paper gown
 Music or talking in background
 i. Normal breathing Sounds- for adults
a.Bronchial (tracheal) –loud, high
pitched, over trachea and larynx
b.Bronchovesicular-moderate,
moderate pitch, over major bronchi
posterior between scapular
especially right anterior upper
sternum at 1st and 2ed intercostal
spaces
c.

 c. Vesicular- Soft, low pitch, rustling sound of wind
through trees; over peripheral lung field
I. Decreased Sounds
• Obstruction- by secretion, mucus
 plug or foreign body
• Loss of Elasticity- in lung fiber &
 decreased force of inspired air
• Something obstructs transmission
 of sound between lung and
 stethoscope
 2. No breath sounds- no air moving;
ominous sign
I.
I.
 3. Increased breath sounds-
bronchial
 sounds are abnormal when
heard
 over abnormal location
i. Adventitious Sounds- sounds not
normally heard in the lungs; if
present are superimposed on breath
sounds

1. Crackles- rales
 2. Wheeze – rhonchi
 3. Atelectatic crackles-short,
popping, crackling sounds like fine
crackles
j. Voice Sounds-Vocal Resonance ; soft
muffled indistinct, heard through
stethoscope
 1. Bronchophony-repeat “99”-
soft,muffled, indistinct heard through
stethescope cannot distinguish.
2.Egophony- auscultate chest
person phonates long “ee-ee-ee-
ee-” through stethoscope
 3. Whispered pectoriloquy-
perslecton whispers phrase “one-
two-three”; response faint, muffled
and almost inaudible


• Normal Adult Respiration Patterns
– Rate- 10 to 20 breaths/minute
– Depth- 500 ml to 800 mo
– Pattern- even
– Ratio to Respiration- fairly constant 4:1
– Depth- air moving in & out each respiration
– Sigh- occasional normal pattern;
purposeful to expand alveoli
–
• Respiration Patterns:
• Tachypnea- rapid shallow breathing;
increased to >24
•
–
– Bradypnea- Slow breathing decrease but
regular; < 10/minute
– Cheyne-Stokes- breathing periods last 30
to 45 seconds, with periods of apnea (20
seconds); alternating the cycle
– Hyperventilation- Increase both in rate
and depth
– Hypoventilation- irregular shallow pattern
– Biot’s Respiration- similar to Cheyne-
Stokes except pattern is irregular
– Orthopnea- difficulty breathing when
supine
– Paroxysmal nocturnal dyspnea-is
awakening from sleep with SOB & needs
to be upright to achieve comfort
- Hyperventilation- rapid, deep breathing
causes carbon dioxide to be blown off
• Chest size changes-
– Inspiration- lung size increases;
diaphragm descends and flattens;
negative pressure air rushes in
– Expiration- chest size recoils;
diaphragm decreases in chest size
and relaxes; positive pressure air
flows out
•
• Abnormal Tactile Fremitus
– Increased tactile Fremitus-increased
density of lung tissue, thereby making a
better conducting medium for vibration
– Decreased Tactile Fremitus- anything
obstructs transmission of vibration.
– Rhonchal Fremitus- vibration felt when
inhaled air passes through thick
secretions in larger bronchi
– Pleural Friction Fremitus- inflammation of
the parietal or visceral pleura causes a
decrease
 in normal lubricating fluid
• Adventitious Lung Sounds:
• Discontinuous Sounds- are discrete crackling
sounds
– Crackles-fine; formerly called rales, high-
pitched, short crackling, popping sounds
heard during inspiration cannot be
cleared by coughing
– Crackles-coarse; loud, low-pitched,
bubbling & gurgling sounds that start in
early inspiration and may be present in
expiration; sound like Velcro fastener
opening
– Atelectatic crackles; sound like fine
crackles, but do not last and are not
pathologic
– Pleural friction rub- is coarse & low pitch has,
Sounds is inspiratory and expiratory
• Continuous Sounds are musical sounds
– Wheeze- high pitched- musical sound that
sound polyphonic; predominately in
expiration but may occur in inspiration &
expiration
– Wheeze- low pitched- rhonchi; monophonic
single note; musical snoring; moaning
sound; more prominent on expiration; may
be cleared by coughing
– Stridor- high pitched- monophonic, crowing
sound, heard on inspiration

• Common Respiratory Conditions:
– Atelectasis-collapsed shrunken section
of alveoli or entire lung due to:
• Airway obstruction, Compression
on lung, Lack of surfactant
• Pt. exhibits-cough, increased pulse
& respiration, possible cyanosis
• None if bronchus obstructed;
occasional fine crackles is
bronchus patent
– Lobar Pneumonia- Consolidation;
• alveoli consolidated with fluid,
bacteria, RBC’s & WBC’s
• Crackles, fine to medium
•
– Bronchitis-proliferation of mucous glands in
passageway
• Bronchial inflammation and copious
secretions
• Deflated alveoli beyond obstruction
• Crackle over deflated area; may have
wheeze
• Pt. exhibits hacking rasping productive
cough
– Emphysema-destruction of pulmonary
connective tissue
• Over distended alveoli with destruction
of
• septa; permanent enlargement of
air sacs distal to terminal
bronchioles
• Pt. exhibits barrel chest, uses
accessory muscles to aid
respiration, SOB, tachy-pnea,
• Adventitious Sounds- usually
none; occasionally wheeze
– Asthma- allergic hypersensitivity to
certain inhaled allergens
• Bronchospasm
• Edema of bronchial mucosa
• Thick mucus
• Pt exhibit-SOB with audible
wheeze, retraction of intercostal
spaces, use of accessory
muscles,cyanosis
– Pleural Effusion- excess fluid in the
intrapleural space with compression of
overlying lung tissue
• Effusion maybe; Transudative
(watery capillary fluid),
Exudatative ( protein),
 Empyemic (purulent matter)

 Hemothorax (blood),Chylothorax
(Milky lymphatic fluid)
• Presence of fluid subdues lung
sounds
• No adventitious sounds
• Pt. exhibits-increased respirations,
dyspnea
 dry cough, abdominal distention,
cyanosis
– Heart Failure- pump failure increasing
pressure of cardiac overload causes
pulmonary congestion
• Bronchial mucosa may be swollen
• Dependent airways deflated
• Adventitious Sounds-crackles at
lung base
• SOB, increased respiratory rate,
PND, nocturia, ankle edema
•
– Tuberculosis (TB) Tuberculosis-inhale
tubercle bacilli into alveolar wall
• Initial complex is acute
inflammatory
• Rust colored sputum
• Night sweats
• Low grade afternoon fever
• High incidence of Asian immigrant
•
– Initial complex is acute
inflammatory
• Scar tissue forms, lesion calcifies
• Reactivation of previously healed
lesion
• Extensive destruction as lesion
erodes into bronchus
• Adventitious sounds, crackles over
upper lobes, persist following full
expiration and cough
– Pneumocystis carinii Pneumonia
• Virulent form of pneumonia
associated with AIDS
• Cysts containing organism &
macrophages form in
alveolar space; alveolar walls
thicken
• Adventitious sounds-crackles may
be present but often absent
•
– Pulmonary Embolism-undissolved
material originating in legs or pelvis,
detach
 and travels and lodges to occlude
pulmonary vessels
• Sometimes occluded medium
pulmonary branches
• Client exhibits chest pain, worse on
inspiration, dyspnea, anxious,
apprehensive, Crackles and
wheezes
• Adventitious Sounds- Crackles,
Wheezes
– Acute Respiratory Distress Syndrome
(ARDS)
• Acute pulmonary insult, damages
alveolar capillary membrane,
increased permeability of pulmonary
capillaries, alveolar epithelium, to
pulmonary edema
• Adventitious Sounds- crackles, rhonchi
• Pt. exhibit-acute dyspnea,
apprehension, shallow rapid
breathing, thin frothy
sputum,retraction of intercostal
spaces
•
• Measurement of Pulmonary Function Status-
– Forced expiratory time-number of seconds it
– Pulse Oximeter- noninvasive method to
assess arterial oxygen saturation
(Spo2) Sensor attaches to client’s
finger detector measures amount of
light absorbed by oxyhemoglobin
(HbO2) and unoxygenated (reduced)
hemoglobin (Hb); ratio of light emitted
to light absorbed con converts to % of
oxygen saturation; Healthy person no
lung disease or anemia has a Spo2 of
97% to 98 %.
– 12 minute distance (12MD) walk, clinical
measure of functional status of clients
with COPD; used as outcome
measure for

people in pulmonary rehabilitation

• Infants and children
• Inspect and then listen to lung sounds of
infants sleeping, can concentrate on
breath sounds
• May sit in parents lap and play with
stethoscope reduces fear
• Older children like to listen to their own
lungs
A. Inspection
• Infants has rounded thorax with equal

anteroposterior-to-transverse chest
diameter
•
• Infants and Children
• Respiratory system develops in utero
• Respiratory system doesn’t function till
birth
• At birth when cord cut blood
gushes to pulmonary circulation,
the foramen oval in heart closes,
the ductus arteriosus contracts
and closes some hrs. later and
the pulmonary circulation
functions
• In childhood-respiratory
development continues,
increases in diameter and length
in size and number of alveoli
• Chest wall thin with little musculature; ribs
& xiphoid are prominent; thoracic cage
soft & flexible
• Newborn first respiratory assessment is
part of Apgar scoring system to measure
successful transition to extrauterine
lifescored at 1 minute and at 5 minutes
after birth; 1 minute score of 7 to 10 very
good condition, needs only suction of
nose and mouth
• Age 6 thorax ratio is 1:2 (anteroposterior-
to-transverse diameter) pg 464; Count
respiratory rate for 1 full minute; normal
rate is 30 to 40 breaths/minute; may go
to 60/minute; get count when infant
asleep
•
– Breathe through nose rather than mouth
– Intercostal muscles not well developed
– Abdominal bulges with each inspiration
but see little thoracic expansion
–
B. Other observations
 Evidence of Infection, Cough, Wheezes,

 Cyanosis, Chest Pain, Sputum, Bad
 breath
–
 C. Palpation
 encircle infant’s thorax with both
hands; should be no lumps, masses
or crepitus; may feel costochondral
junctions.
D. Percussion-limited, fingers of adult too
large
 in relation to tiny chest.; note hypper-
 resonance occurs normally in infants
 and young child due to thin chest wall
E. Auscultation-normally bronchovesicular
 breath sounds in infants up to 5-6 year
 old; breath sounds are louder and
 harsher
 -fine crackles commonly heard
immediate

 in newborns
 -Cackles in upper lung field occur with
cystic fibrosis
 -Expiratory wheezing occurs in lower
airway obstruction e.g., asthma,
bronchiolitis
 -Stridor- high pitched inspiratory
crowing with upper arway
obstruction, e.g., croup, foreign body
aspiration, acute epiglottitis


– Depth of respirations-
• Hyperpnea- too deep
• Hypopnea- too shallow
– -Retraction- sinking in of soft tissue
relative to the cartilaginous and bony
thorax; in severe airway obstruction-
retraction extreme.
– Nasal flaring- sign of respiratory distress
– Head bobbing- in sleeping or exhausted
infant sign of dyspnea
– Noisy breathing- “snoring” obstruction,
polyps or foreign body in nasal
passages
– Grunting- sign of chest pain- acute
pneumonia/ pleural involvement
– Chest pain-older children maybe
pulmonary and or nonpulmonary
– Clubbing- proliferation of tissue about
the terminal phalanges, associated
with chronic hypoxia, chronic
pulmonary disease or primarily cardiac
defect
– Cough- maybe associated with
respiratory disease; is protective
mechanism

F. Tests-
– Pulse oximetry- similar to adults
however can position around foot, toe,
earlobe
– Transcutaneous Oxygen Monitor –Tc
Po2
 measures O2 diffusion across skin
G. Oxygen Therapy
– Delivered by mask, nasal cannula, tent,

hood, face tent, or ventilator
– Oxygen mask- various sizes, delivers
higher O2 concentration than cannula;
can cause skin irritation
– Nasal Cannula-low-moderate O2
– concentration; can talk ad eat; must
have patent nasal passages
• Oxygen Tent-lower O2
concentrations; can increase
concentration while eating; fit
around bed to prevent leakage;
cool & wet environment; poor
access to child
• Oxygen hood, face tent- high O2
concen-tration; free access to
child’s chest; high humidity; need
to be removed for feeding & care;
humidified O2 not blown directly
on infants/child face
• Pregnancy
– Thoracic cage wider; costal angle feels
wider; respirations deeper; although
this can be quantified only with
pulmonary function test
– Pregnancy induces small degree of
hyperventilation as tidal volume
increases steadily throughout
pregnancy
– Diaphragm elevated and subcostal
angle increased due to enlarging
uterus
– Lung disease maybe aggravated by
pregnancy
• Pregnancy
– As uterus increases elevates diaphragm
which decreases the vertical diameter
of thoracic cage but is compensated
by increase in horizontal diameter.
– As fetus grows there is increase in
oxygen demand on mother’s body;
increasing tidal volume( deep
breathing)
–

• Aging Adults
– Costal cartilages calcifies, less mobile
thorax
– Respiratory muscles strength declines
after 50 and continues to do so till 70
– Decrease in elastic properties of lungs,
becomes harder to inflate
– Decrease in Vital Capacity- maximum
amount of air that a person can expel
from lungs after first filling lungs to
maximum

– Increase in Residual Volume- amount of
air remaining in lungs even after most
forceful expiration
– With age less surface area available for
gas exchange
 -Chest cage increases anteroposterior
diameter; looks barrel shape and
outward
 curvature of thoracic spine;
compensates holding head extended
and tilted back
 -Chest expansion decreases though still
symmetric
 -cartilages becomes calcified

-Older adults fatigue easily, make sure do not
hyperventilate and become dizzy
-Allow brief periods of rest
-If feeling faint, holding breath for few seconds
will restore equipibrium
THE CARDIOVASCULAR SYSTEM,
HEMATOLOGY AND IMMUNOLOGY PREPARED BY
DENNIS NABOR MUÑOZ, PT, RN,RM

The Cardiovascular System
•A closed system: heart and blood

vessels
•The heart pumps blood
•Blood vessels allow blood to
circulate
•A double system:
•Pulmonary circuit
•Systemic circuit
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 11.1
The Cardiovascular System
•Functions:
•Delivery system for everything!
•Remove carbon dioxide and other
waste products
The Heart
•Location
•Thoracic cavity, between the lungs
•In mediastinum
•Pointed apex directed toward left hip
•2/3 to left of median plane
•Size: About the same as your fist
•
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 11.2a
Location and Orientation within the Thorax
Figure 18.2
The Heart: Did You Know…
•A blue whale’s heart may weight 1000

pounds (454,000 grams)
•It’s the size of a VW beetle!
•An elephant heart may weigh 75 pounds
•Heart rate about 10 bpm
•A mouse’s heart weighs ~ 10 grams
•Heart rate about 250 bpm
•
The Heart: Coverings
•Pericardium – a double serous

membrane
•Visceral pericardium
•On the surface of the heart
•Parietal pericardium
•Lines pericardial cavity
•Pericardial cavity: between layers

•Serous fluid fills the space
•Fluid required for lubrication
•Heart moves!!
Structure of the Heart –
Coverings
Figure 18.3
The Heart Wall
•Three layers
•Epicardium
•Outside layer
•This layer is the visceral pericardium
•Connective tissue layer
•Thin, shiny, slick
Fig. 12.12
Structure of the
Heart Wall
Epicardium
= visceral
pericardium
Figure 18.3
The Heart: Heart Wall
•Myocardium
•Middle layer
•Mostly cardiac muscle
•Very thick
•Endocardium
•Inner layer
•Endothelium (Simple squamous E.T)
•Slick, shiny
Structure of the Heart Wall
Fig. 12.12
Myocardium
Endocardium
Figure 18.3
The Heart: Chambers
•Right and left side are separate systems

•Four chambers
•Atria
•Thin walled upper chambers
•Receiving chambers
•Right atrium (-O2 blood)
•Left atrium (+O2 blood)
External Heart Anatomy
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 11.2a Slide 11.5
The Heart: Chambers
•Ventricles
•Thick walled, lower chambers
•Pumping chambers
•Right ventricle:
•to pulmonary circuit (-O2
blood)
•Left ventricle
•To systemic circuit (+O2
blood)
External Heart Anatomy
The Heart: Valves
•Function: to direct blood flow

•Two pairs
•Atrioventricular valves – between atria and
ventricles
•Bicuspid (Mitral) valve (left)
•Tricuspid valve (right)
•“Active”: function with cardiac muscle
•
Heart Valves and Major Blood Vessels
Superior Aorta
Vena cava
Pulmonary Arteries
Semilunar Pulmonary Veins
valve LA
RA
Bicuspid (mitral)
Tricuspid Valve
Valve LV
Inferior RV
Vena cava
Heart Valves
Figure 18.5c
The Heart: Valves
•
•Semilunar valves between ventricle and
artery
•“Passive”: depend on blood pressure
•Pulmonary semilunar valve
•RV to pulmonary trunk
•Aortic semilunar valve
•LV to aorta
Heart Valves
Figure 18.5c
The Heart: Valves
•Valves open as blood is pumped through

•AV valves held in place by chordae
tendineae (“heart strings”)
•Close to prevent backflow
Heart Valves
Fig. 12.7
Figure 18.5c
Operation of Heart Valves
Fig. 12.9
Figure 11.4
The Heart: Associated Great Vessels
•Great Arteries
•Aorta
•Leaves left ventricle
•Supplies systemic circuit
•Pulmonary trunk (artery)
•Leaves right ventricle
•Supplies pulmonary circuit
Great Arteries
The Heart: Associated Great Vessels
•Great Veins
•Venae cavae (superior, inferior)
•Enter right atrium
•Drain systemic circuit
•Pulmonary veins (four)
•Enter left atrium
•Drain pulmonary circuit
Great Vessels
Figure 18.5c
Coronary Circulation
•The heart muscle has its own blood

supply
•Part of systemic circuit
•Coronary arteries (+O2 blood)
•Cardiac veins (-O2 blood)
•Blood returns to the right atrium via the
coronary sinus (-O2 blood)
•
Coronary Circuit, Anterior View
Coronary Circuit, Posterior View
The Heart: Conduction System
•Intrinsic conduction system

(nodal system)
•Heart muscle cells contract without nerve
impulses
•Heart has an intrinsic rhythm (“built in”)
The Heart: Conduction System
•Specialized cardiac muscle tissue

•Sinoatrial (SA) node
•Pacemaker
•Atrioventricular (AV) node
•Atrioventricular bundle (of His)
•Bundle branches (R and L)
•Purkinje fibers
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 11.13b
The Heart: conduction system
Fig. 12.15
Figure 11.5

Heart Contractions
•Contraction is initiated by the sinoatrial
node: “pacemaker”
•Sends information to all muscle cells of
both atria
•Atria contract simultaneously
The Heart: conduction
system
Fig. 12.15
Figure 11.5

Heart Contractions
•Impulse transmission
•AV Node serves as “booster station”
•Sends impulse through AV
bundle, along bundle branches
•Finally to Purkinje fibers
•Ventricle muscles contract
simultaneously
•
Heart: conduction system
Figure 11.5
Artificial Pacemakers
•implantable
•computer programmable
•sense heart rate and stimulate
as appropriate (e.g. during complete
heart block; next lecture)
lithium batteries
hybrid circuit
Pulse Generator
left atria
left ventricle
right atria
right ventricle
Sense and Stimulate

•implantable
V V V V V V
normal ecg
A A A A A A
•implantable
A A A A A A A A A
V V V V V
ECG during third degree heart block Ectopic Pacemakers

Blood Flow Regulation
To Individual Organs
Arteriole Venule
•Smooth Muscle
Local control of
blood flow
The Heart: Cardiac Cycle
•Atria contract simultaneously

•Atria relax, then ventricles contract
•Systole = contraction of ventricles
•Diastole = relaxation of ventricles
The Cardiac Cycle
Fig. 12.17
Figure 11.6
Fig. 12.16
ECG
P wave:
Atrial depolarization.
QRS complex:
Ventricular
depolarization.
Atrial repolarization.
T wave:
Ventricular
repolarization.
electrocardiograph = a machine
that measures & records these
electrical signals
electrocardiogram = the reading produced
by this machine
the ECG is an important tool used to
diagnose abnormal heart rhythms &
patterns
heartbeat regulation
Heart Sounds
“Lubb-dupp” – sound of valves closing

First sound “lubb” – the AV valves closing
Second sound “dupp” – the semilunar
valves closing
The Heart: Cardiac Output
•Cardiac output (CO)

•Amount of blood pumped by each side of
the heart in one minute
•CO = (heart rate) x (stroke volume)
•Stroke volume
•Volume of blood pumped by each
ventricle in one contraction
Cardiac Output Regulation
Figure 11.7
Overview of Stroke Volume Regulation
Blood Vessels
and
Circulation Slide 2.1

The Heart: Regulation of Heart Rate
•Increased heart rate

•Sympathetic nervous system
•Hormones
•Epinephrine
•Thyroxine
•Exercise
•Decreased blood volume
The Heart: Regulation of Heart Rate
•Decreased heart rate

•Parasympathetic nervous system
•Vagus Xth Cranial nerve
•High blood pressure or blood volume
•Decreased venous return
Blood Vessels: The Vascular System
•Circulate blood throughout the body

•Arteries
•Arterioles
•Capillaries
•Venules
•Veins
The Vascular System
Figure 11.8b
Blood Vessels: Anatomy
•Three layers (tunics)

•Tunic intima (interna)
•Endothelium
•Thinnest, slick
•Tunic media
•thickest
•Smooth muscle
Tunics of Elastic and Muscular Arteries
Fig. 13.1a
Figure 11.8b
Blood Vessels: Anatomy
•Tunic externa
•Mostly fibrous connective tissue
•Provides support
•Prevents over-expansion of vessels
The Vascular System
Figure 11.8b
Differences Between Blood Vessel Types
•Walls of arteries are thickest

•Especially tunica media
•More smooth muscle
•More elastic tissue
•Lumens of veins are larger
The Anatomy of Veins
Figure 11.8b
Differences Between Blood Vessel Types
•Walls of veins are thin

•May have valves
•Usually in veins below heart
•Prevent backflow
•Valves assisted by skeletal muscle
Movement of Blood Through Vessels
•Arterial blood is
pumped by the heart
•Veins use the milking
action of muscles to
help move blood
Figure 11.9
Vessels: Anatomy of a Capillary
•Capillaries
Fig. 13.3
•Form vast,
complex Slide 11.26
networks
•Walls one cell
layer thick
•Thin, leaky
•Allow for
exchange of
materials

Capillary Beds
•Capillary beds:
networks
•Vascular shunt: directly
connects an arteriole
to a venule
•
•
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 11.10 Slide 11.28a
Capillary Beds
•Exchange
vessels
•Oxygen and
nutrients
exit blood
•Carbon
dioxide and
waste
products
enter blood
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 11.10 Slide 11.28b
Blood Vessels: Did you know….
•Humans have about 60,000 miles of

vessels
•Vessels reach every millimeter of tissue
•We have at least two veins for every
artery in our extremities
•We have 200 miles of vessels in every
pound of adipose tissue
Capillary Exchange
•Substances exchanged due to

concentration gradients (diffusion!)
•Oxygen and nutrients leave the blood,
enter cells
•Carbon dioxide and other wastes leave
the cells, enter blood
Diffusion at Capillary Beds
Figure 11.20
Special Circuits: Cerebral Arterial Circle
Fig. 13.10
Figure 11.13
Special Circuits: Hepatic Portal System
Fig. 13.19
Figure 11.14
Special Circuits: Fetal Circulation
Figure 11.15
Pulse
•Pulse: pressure
wave of blood
•Caused by
contraction
of heart
•Monitored at
superficial
“pressure
points”
Figure 11.16
Pulse
•Pulse – should
match heart
rate
•Averages 60-80
beats/minute
Figure 11.16
Blood Pressure
•Measurements are made on the

pressure in large arteries
•Commonly use brachial artery
•Systolic – pressure at the peak of
ventricular contraction
•Diastolic – pressure when ventricles
relax
•
•Pressure in blood
vessels
•decreases
with distance
from the
heart
•Is lowest in
Slide 11.36
venous
system
Blood Pressure

Measuring Arterial Blood Pressure
Figure 11.18
Factors Determining Blood Pressure
Figure 11.19
Variations in Blood Pressure
•Human normal range is variable

•Normal
•140–110 mm Hg systolic
•80–75 mm Hg diastolic
•120/80 is “ideal” B.P.
Variations in Blood Pressure
•
•Hypotension
•Low systolic (below 110 mm Hg)
•May be associated with illness
•Hypertension
•High systolic (above 140 mm Hg)
•High diastolic (above 90 mm Hg)
•Can be dangerous:
•stroke, heart attack, blindness
Slide 2.1
BLOOD

Blood: General Information
•The only fluid tissue in the human body

•Classified as a connective tissue
•Living components = “formed elements”
•Some are not true cells
•Non-living matrix = plasma
Blood
Figure 10.1
Blood: Functions
•Transportation system
•Temperature regulation
•Acid-base balance (blood buffers)
•Protection
•Clotting
•Antibody production
•
•
Physical Characteristics of Blood
•Color is due to Oxygen carrying pigment:

hemoglobin
•Oxygen-rich blood is scarlet red
•Contains oxyhemoglobin
•Oxygen-poor blood is bluish
•Contains deoxyhemoglobin
Physical Characteristics of Blood
•Average volume: 4.5-5.5 liters

•pH must remain between 7.35–7.45
•Is this acidic or alkaline??
•Blood temperature is slightly higher than
body temperature
Blood Plasma
•Approximately 90% water

•Transports dissolved substances
•Nutrients
•Salts (electrolytes, ions)
•Respiratory gases
•Hormones
•Proteins
•Waste products
Blood
Figure 10.1
Plasma Proteins
•Albumin – regulates osmotic pressure

•Clotting proteins – active in clot
formation
•Antibodies – help protect the body from
illness and infection
Formed Elements
•Erythrocytes = red blood cells (RBCs)

•Leukocytes = white blood cells (WBCs)
•Platelets = cell fragments (thrombocytes)
Erythrocytes (Red Blood Cells)
•The main function is to carry oxygen

•Anatomy of erythrocytes
•Biconcave disks
•Essentially bags of hemoglobin
•Anucleate (no nucleus)
•Contain few organelles
make up 44% of the total volume of
blood
produced in the red bone marrow of the
ribs, humerus, femur, sternum, and
other long bones only have a nucleus in
the early stages of development
active about 120 days, then broken
down in the spleen & liver by
macrophages via phagocytosis
contain hemoglobin, an iron-rich protein
molecule that binds to O2
oxygenated RBC’s carry oxygen from
carbon dioxide in the blood:
70% of the CO2 combines with

water in plasma to form
bicarbonate
30% is attached to hemoglobin
or dissolved in plasma
An Erythrocyte
Figure 17.3
Erythrocytes: Levels in Blood
•Live only four (4) months or ~120 days

•Average RBC count:
•Males: 5.4 million/mm3
•Females: 4.8 million/mm3
•Outnumber white blood cells 1000:1
Fate of Erythrocytes
•Unable to divide, grow, or synthesize

proteins
•Wear out in 100 to 120 days
•Removed by phagocytes in the spleen or
liver
•New RBCs made by stem cells in bone
marrow
Did you know…
•About 2 million RBCs are destroyed each

second
•About 2 million RBCs are producedeach
second (by what process??)
•Humans have over a trillion RBCs
•Blue Whales have 7,000 GALLONS of
blood
•Blood is thicker than water (4x)
Erythrocytes: Disorders
•Anemias:
•Hemorrhagic: due to blood
loss
•Aplastic: RBCs not made
•Hemolytic: RBCs destroyed
•Polycythemia: too many RBCs
•
•
Hemoglobin
•Iron-containing protein
•Binds reversibly to oxygen
•Each molecule has four oxygen binding
sites
•Each erythrocyte can carry 250 million
hemoglobin molecules
Leukocytes (White Blood Cells)
•Play a role in immune response

•Typical cells with nucleus, organelles
•Able to move into and out of blood
vessels by…
•Diapedesis: Gr. “leaping through”
white blood cells (WBC’s): leukocytes
infection fighters
play a major role in protecting
you from foreign substances,
and from invading bacteria
make up 1% of total blood
volume
they are larger than RBC’s &
they have a nucleus
Types of Leukocytes
L to R: lymphocyte, basophil, monocyte,

neutrophil, eosinophil
Leukocytes (White Blood Cells)
•Move by ameboid motion

•Respond to chemicals released by
damaged tissues
•“chemotaxis” – chemical attraction
•Allows for immune response
Leukocyte Levels in the Blood
•Normal levels are between 4,000 and

11,000 cells per mm3
•Abnormal leukocyte levels
•Leukocytosis
•Above 11,000 leukocytes/ml
•Generally indicates an infection
Leukocyte Levels in the Blood
•Leukopenia
•Abnormally low leukocyte level
•<4000/mm3
•May be caused by certain drugs
•
•Leukemia: cancer of WBCs
•myeloid
•lymphoid
Types of Leukocytes
•Granulocytes
•Granules in
their cytoplasm
can be stained
•Include
neutrophils,
eosinophils,
and basophils
Figure 10.4
Granulocytes
•Neutrophils: Slide 10.11a
•Multilobed nucleus
with
•Fine, pale purple
granules in cytoplasm
•Act as phagocytes
•Most numerous in
blood
•

Types of Leukocytes
•
•
•Neutrophils
Figure 10.4
Granulocytes
•
Slide 10.11a
•Eosinophils:
•Large brick-red
cytoplasmic granules
•Respond to allergies
and parasites
•Rare in blood

Types of Leukocytes
•
•
•Eosinophils
Figure 10.4
Granulocytes
•Basophils: Slide 10.11b
•Have dark blue/black granules

•Granules contain histamine,
serotonin, heparin
•Initiate inflammation
•Rarest in blood
•Most live in respiratory
tract
•

Types of Leukocytes
•
•
•Basophils
Figure 10.4
Agranulocytes
•Lymphocytes:
•Nucleus fills most of
Slide 10.12
the cell
•Major role in immunity
•“B” lymphocytes
•make antibodies
•plasma cells
•“T” lymphocytes:
mediate function of B
cells

Types of Leukocytes
Slide 10.10a
•Lymphocytes
Figure 10.4

Agranulocytes
Slide 10.12
•Monocytes:
•Largest of the white
blood cells
•Function as phagocytes
•Called
macrophages in
tissues
•Fight chronic infection

Types of Leukocytes
•
•
•Monocytes
Figure 10.4
Platelets
•Cytoplasmic fragments of marrow cells

(megakaryocytes)
•Needed for the clotting process
•Normal platelet count = 300,000/mm3
•Replaced in 24 hours
•(apheresis…)
Types of Leukocytes
•
•
•Platelets
Figure 10.4
Hematopoiesis
•Blood cell formation

•Occurs in red bone marrow
•All blood cells are derived from a common
stem cell
•Hemocytoblast
Hematopoiesis
•
•
Figure 10.4
•Stoppage of blood
flow
•Result of a break in a
blood vessel
•Hemostasis involves Slide 10.18
three phases
•Platelet plug
formation
•Vascular spasms
•Coagulation
Hemostasis: Blood
Clotting
Platelet Plug Formation
•Collagen fibers are exposed by injury to

vessel
•Platelets become “sticky” and cling to
fibers
•Platelets release chemicals to attract
more platelets
•Platelets pile up to form a platelet plug
Hemostasis, con’t…
Slide 10.19
Fig. 11.8
•Platelet plug
formation
•

Vascular Spasms
•Anchored platelets release serotonin

•Serotonin causes blood vessel muscles
to spasm
•Spasms narrow the blood vessel,
decreasing blood loss
Coagulation
•Injured tissues release thromboplastin
•Thromboplastin, clotting factors, and
calcium ions interact to trigger a clotting
“cascade”
•Prothrombin activator converts
prothrombin to thrombin (an enzyme)
Coagulation
Fig. 11.9
Slide 10.21a
•“Cascade” of reactions in clot formation

Coagulation
•Process requires Vit. K

•Thrombin converts fibrinogen proteins
into hair-like fibrin
•Fibrin forms a meshwork: traps RBCs
(the basis for a clot)
Clot Retraction
•After clot is formed, shrinkage occurs

•Squeezes out serum
•A clear yellow fluid
•Plasma minus clotting proteins
Blood Clotting
•Blood should clot in 3 to 6 minutes

•The clot remains till endothelium
regenerates
•The clot is broken down after tissue
repair
Undesirable Clotting
•Thrombus
•A clot in an unbroken blood vessel
•Can be deadly
•Coronary thrombosis
•DVT: deep vein thrombosis
Thrombus in Artery
Undesirable Clotting
•Embolus
•Clot moving through a vessel
•Can be deadly in areas like the brain,
lung
•Pulmonary embolism
•Cerebral embolism
Bleeding Disorders
•Thrombocytopenia
•Platelet deficiency
•Causes bleeding from small blood vessels
•Can result from chemo, radiation
•May be age-related
Bleeding Disorders
•
•Hemophilia
•Hereditary bleeding disorder
•Normal clotting factors are missing
•Many types, depending on clotting factor
•A gene mutation: Queen Victoria
Blood Groups and Transfusions
•Large losses of blood have serious

consequences
•Loss of 15 to 30 percent causes
weakness
•Loss of over 30 percent causes shock,
which can be fatal
Blood Groups and Transfusions
•Transfusions are the only way to replace

blood quickly
•Transfused blood must be of the same
blood group
•Wrong group: dead patient
•First done: William Harvey, England
(1600’s?)
Human Blood Groups
•RBCs carry genetically determined

proteins
•Called antigens (Ag)
•Proteins embedded in cell
membrane
•A foreign protein (Ag) may be attacked
by the immune system
Human Blood Groups
•How blood is “typed”:

•Uses antibodies (Ab)
•Made by body against foreign
proteins
•cause “different” blood to clump
(agglutination)
Blood Typing
Blood antigens
Type A
Type B
Agglutininins (Ab)
Act in blood typing
Antigen-antibody reaction
Human Blood Groups
•There are over 30 red blood cell antigens

•Two groups cause serious transfusion
reactions
•ABO group antigens
•Rh group antigens
ABO Blood Groups
•Based on the presence

or absence of two
antigens
•Type A
•Type B
•
•The lack of both these
antigens is called
type O

blood plasma contains
antibodies that are shaped to
correspond with the different
blood surface antigens
the antibodies react with the
matching antigen if they are
brought together, resulting in
clumped blood
you don’t have

antibodies for your
own antigen type
type A blood has A antigens and anti-B
antibodies
type B blood has B antigens and anti-A
antibodies
ABO Blood Groups
•The presence of A is called type A

•The presence B is called type B
•The presence of both A and B is called
type AB
•
Blood Types and their
corresponding Abs
Type A, anti-B
Type B, Anti-A
Type AB, neither
Blood Groups
Type O, both
Rh Blood Groups
•Depends on presence or absence of Rh

antigens (agglutinogen D)
•Most Americans are Rh+ (85%)
•Rest are Rh-
•Problems can occur in mixing Rh+ blood
into a body with Rh– blood
Rh factor = Rhesus factor:
another antigen which may be
present (Rh+) or absent (Rh-)
Rh factor is an inherited
characteristic
only 15% of the U.S. population is
Rh-
Rh Dangers During
Pregnancy
•Called hemolytic disease of
the newborn or
Erythroblostosis fetalis
•Danger is only when
•the mother is Rh–
•the father is Rh+
•the child inherits the
Rh+ factor

Rh Dangers During Pregnancy
•Problem in an Rh– mother carrying

an Rh+ baby:
•The first pregnancy usually
proceeds without problems
•At birth, mother may receive
some of baby’s RBCs
•
•Mom’s immune system is sensitized

•Makes antibodies against Rh
•In a subsequent pregnancy:
•Mother’s blood carries antibodies
•Anti-Rh antibodies cross placenta
•Attack the Rh+ blood in the fetus
prevention: mom is treated with a
substance to prevent the production of
antibodies in her blood at 28 weeks & again
shortly after the birth of the first baby
•Erythroblostos
is fetalis, or
•Hemolytic
Slide 10.29b
Fig. 11.13
disease of the
newborn
•

Blood Typing
•Blood samples are mixed with anti-serum

•anti-A: “against” A antigens
•anti-B: “against” B antigens
•Presence/absence of agglutination
determines blood type
Blood Typing
Blood Typing
•Typing for Rh factors is done in the same

manner
•Cross matching
•testing for agglutination of donor
RBCs by the recipient’s serum
•testing for agglutination of recipient
RBCs by the donor’s serum
Lymphatic
System and
Immunity
The Lymphatic System
•Consists of two components

•Lymphatic vessels
•Lymphoid tissues and organs
•Functions
•Transport fluids back to the blood
•Body’s defense against disease
Lymphatic Characteristics
•Lymph
•Tissue fluid in lymphatic vessels
•Body produces ~3L/day (how much
blood do we have???)
•Properties of lymphatic vessels
•One way system toward the heart
•No pump
•Assisted by skeletal muscle
Lymphatic Vessels
•Lymph Capillaries
•“Blind tubes”
•Walls have valves
•Fluid leaks into lymph capillaries
•Higher pressure inside closes valves
Lymphatic Vessels
Figure 12.1
Lymphatic Vessels
•Collect lymph
from lymph
capillaries
•Carry lymph to
nodes
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 12.2 Slide 12.4a
Lymphatic Vessels
(continued)
•Returns fluid to
subclavian veins
•Right
lymphatic
duct
•Thoracic
duct
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 12.2 Slide 12.4b
Lymph
•Materials returned to the blood

•Water
•Blood cells
•Proteins
Lymph
•Harmful materials that enter lymph vessels

•Bacteria
•Viruses
•Cancer cells
•Cell debris
Lymph Nodes
•Filter lymph before it is returned to the

blood
•Nodes house immune WBCs
•Macrophages
•Lymphocytes
Lymph Nodes
Figure 12.3
Lymph Node Structure
•Bean shaped, less than 1” long

•Cortex
•Contains collections of lymphocytes
•Medulla
•Contains macrophages
Lymph Node Structure
Figure 12.4
Other Lymphoid Organs
•
•Spleen
•Thymus
•Tonsils
•Peyer’s
patches
Figure 12.5
The Spleen
•Located on the left side of the abdomen

•Filters blood
•Destroys worn out blood cells
•Forms blood cells in the fetus
•Acts as a blood reservoir
The Thymus
•Located deep to sternum

•Functions mostly during childhood
•Produces hormones
•Thymosin, thymopoietin
•Program T-lymphocytes
•
Lymphoid Organs
Thymus:
atrophies
with age
Spleen: can
live without
this
Figure 20.8
Tonsils
•Masses of lymphoid tissue surrounding

pharynx
•Trap and remove bacteria and other
foreign materials
•Tonsillitis: caused by infection with
bacteria
Peyer’s Patches
•Found in the wall of the small intestine

•Collections of lymphocytes
•Capture and destroy bacteria in the
intestine
Fig. 14.3
Lymphoid Organs
Tonsils: 3
sets
Peyer’spatche
s: part of
GALT
Figure 20.8
Body Defenses
•The body is constantly assaulted by

micro-organisms
•We have two forms of defense
•Nonspecific or Innate defenses
•Protect against a variety of invaders
•Responds immediately
•Includes granulocytes and
monocytes
Body Defenses, con’t…
Slide 12.15b
•Specific or
F ig. 14.15
Acquired
defense system:
Cell Mediated
response
•Specific
defense is
required for
each type of Cell mediated
invader response
•T-cells:
viruses, fungi,
cancer cells
Acquired Defenses, con’t…
Fig. 14.11
Slide 12.15b
•Humoral
Immunity
•T-cells
influence B-
cells
•B-cells:
Bacteria
•B-cells make
antibodies
(Ab) Humoral Immunity: Ab
•Ab circulate in production
blood
Nonspecific Body Defenses
•Body surface coverings

•Intact skin
•Mucous membranes
•Specialized WBCs
•Chemicals produced by the body
Defensive Cells
•Phagocytes
•Neutrophils
•Monocyte/
Macrophages
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 12.6b Slide 12.18a
Defensive Cells
•Natural killer cells

•A lymphocyte
•Can kill cancer
cells
•Can destroy
virus- infected
cells
•How: surface Ag
change
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 12.6b Slide 12.18b
Inflammatory Response is the
Second Line of Defense: FYI
•Triggered by injury
•Produces four signs
•Redness
•Heat
•Swelling
•Pain
Functions of the Inflammatory Response:
FYI
•Prevents spread of damaging agents

•Disposes of cell debris and pathogens
•Sets the stage for repair
Steps in the Inflammatory Response: FYI
Figure 12.7
Antimicrobial Chemicals: FYI
•Complement
•Protein cascade
•Kills invaders
•Interferon
•Proteins secreted by virus-infected cells
•Inhibit virus binding to healthy cells
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 12.22c
Fever: FYI
•Abnormally high body temperature

•Inhibits the release of substances
needed by bacteria
•Increases the speed of tissue repair
Lymphatic
System and
Immunity
Specific Defense: The Immune Response
•Characteristics:
•Antigen specific: for a particular
foreign substance
•Systemic: affects entire body
•Has memory: protects against
future infection
Types of Immunity
•Humoral immunity
•Targets bacteria
•B-lymphocytes
•Cell-mediated immunity
•Targets virus infected cells, cancer
•T-lymphocytes
Antigens (Non-self)
•Any substance capable of:

•exciting the immune system
•provoking an immune response
•Any “foreign” protein
•Anything that is not “you”
Cells of the Immune Response
•Lymphocytes
•B lymphocytes mature in the bone marrow
•Make plasma cells that make
antibodies
•T lymphocytes mature in the thymus
•Memory Cells: from B or T cells
•Macrophages
•Arise from monocytes
•Most live in lymphoid organs
Cells of the Immune Response
Slide 12.29
Fig. 14.17b

Allergies: FYI
•Some molecules are not antigenic, but

link up with our proteins
•The immune system may recognize
these as “foreign”
•The immune response is harmful in this
instance
•because it attacks our own cells
Activation of Lymphocytes; FYI
Figure 12.9
Vaccinations and Booster Shots: FYI
•Memory cells are

long-lived
•First response: Ab
production
•Secondary
response: more
Ab production
•Stronger
Figure 12.11
Antibody Structure: for Lab…
•Four peptides
linked by
covalent bonds
•Two heavy
chains
•Two light chains
•Recombinant
DNA!
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 12.13b Slide 12.38a
Organ Transplants and Rejection: FYI
•Major types of grafts

•Autografts – “self graft”, i.e., skin graft
•Isografts – tissue grafts from an identical
twin
•Allografts – tissue taken from an
unrelated person
•Xenografts – tissue taken from a different
animal species
Organ Transplants and Rejection: FYI
•Autografts and isografts are ideal donors

•Xenografts are never successful
•Allografts are more successful with a
closer tissue match
Disorders of Immunity:
Immunodeficiencies (FYI)
•Production or function of immune cells or

complement is abnormal
•May be congenital or acquired
•Includes AIDS – Acquired Immune
Deficiency Syndrome
Autoimmune Diseases (FYI)
•The immune system does not distinguish

between self and non-self
•The body produces antibodies and
sensitized T-lymphocytes that attack its
own tissues
Autoimmune Diseases: FYI
•Examples:
•Multiple sclerosis
•Myasthenia gravis
•Type I diabetes
•Rheumatoid arthritis
•Systemic lupus erythematosus (SLE)
•Glomerulonephritis
Neurological ANATOMY &
PHYSIOLOGY
WITH
Health Assessment
DENNIS N. MUÑOZ, PT, RN, RM

Review of Anatomy &
Physiology
 The function of the nervous system is to
control all motor, sensory & autonomic
functions of the body.
 Divided Into:
 Central Nervous System (CNS)
 Consisting of the brain and spinal cord. e
Peripheral Nervous
System (PNS)
Cranial nerves (12) and spinal
nerves (31)
Autonomic Nervous System
Sympathetic Division:
“fight or flight” response
Parasympathetic
Division: “rest & digest”
respons
Cells of the Nervous System
 The Neuron
 Functional unit of the nervous system; transmits
impulses
 Cell Body: Controls metabolic activity
 Dendrite: Transmits impulses to the cell body
 Axon: Transmits impulse away from the cell body
 Many myelinated (white matter)
 Insulation; speeds transmission of impulses
 Some non-myelinated (gray matter)
Neuroglial Cells
Provide support, nourishment, & protection to the
neuron
Four Types:
Astroglia,
oligodendroglia,
ependyma &
microglia
The Neuron: Cellular Impulses
Action Potentials

 Based on ion shifts, which create electrical

charges
See Smeltzer & Bare pp . 1822 ; Table

Synapses
Connects the neuron to another neuron or target tissue (muscle, organ or
gland)
Neurotransmitters
Chemical substances that enhance or inhibit nerve impulses across
synapses.
i.e. Acetylcholine and Dopamine
CNS: The Brain
The brain controls, initiates and integrates all

body functions.
 Composed of both gray matter and white matter.
Protective Mechanisms:
Skull (cranium): Bony container surrounding the brain
Meninges: Three additional layers of protection
Dura mater, arachnoid mater & pia mater
Potential & Actual Spaces
Epidural Space
Subdural Space
Subarachnoid Space
Cerebrum
Divided into two hemispheres:

 Right Hemisphere
 The right side of the brain controls & receives
information from the left side of the
body.
 Left Hemisphere
 The left side of the brain controls & receives
information from the right side of the body.
 Dominant hemisphere in most people
Lobes of the Cerebrum
Frontal Lobe

 Primary motor area

 Broca’s area for motor speech
 Memory, abstraction, affect,
judgment, personality & inhibitions.
Parietal Lobe

 Primary sensory area

 i.e. Interpretation of pain, touch, temperature &
pressure
 Awareness of body parts and body part position
sense
Lobes of the Cerebrum Cont.,
Temporal Lobe
 Wernicke’s area for interpretative speech
 Auditory Center
Limbic Lobe
 Anatomically part of the temporal lobe
 Moods, behaviors, emotions and visceral
processes needed for
survival
 Interpretation of smell
 Learning and memory
Occipital Lobe
 Primary visual area
The Diencephalon &
Cerebellum
Diencephalon

 Thalamus: “Relay Station”

 Hypothalamus: Regulates ANS, appetite,
temperature, fluid balance & emotions
 Pituitary Gland: “Master gland” controlling
numerous hormonal functions (i.e. posterior
pituitary releases ADH)
Cerebellum

 Coordinates smooth muscle

movements; posture, equilibrium,
muscle tone &
position sense.
The Brainstem
Brainstem:

 Reticular Activating System (RAS)

 Controls level of consciousness (awareness &
alertness)
 Cranial Nerves
Structures of the Brainstem

 Midbrain:
 Aqueduct of Sylvius
 Pons:
 Cardiac & Respiratory Centers (rate & length)
 Medulla Oblongata:
 Auditory, Cardiac & Respiratory Center (basic
rhythm)
Cerebral Circulation
Arterial Circulation:

 Internal carotid arteries → anterior cerebral

artery (ACA) & middle cerebral artery
(MCA) = anterior cerebral circulation.

 Posterior vertebral arteries → basilar artery

→ two posterior cerebral arteries (PCA) =
posterior cerebral circulation.
Cerebral Circulation Cont.,
Arterial Circulation Cont.,

 Circle of Willis
 Internal carotid, basilar artery & the anterior,
middle & posterior arteries join together via
small communicating arteries to form a ring
at the base of the brain.
Venous Circulation:

 Cerebral veins → dural venous sinuses →

internal jugular veins → superior vena cava
= back to right atrium.
Central Nervous System:
Other Considerations
 Blood-Brain Barrier (BBB)
 Selective Permeability:
 Substances that can pass include oxygen, glucose,
carbon dioxide, alcohol, anesthetics & water
 Substances that can not pass include medications
such as many antibiotics & systemic
chemotherapy agents.
 Cerebrospinal Fluid (CSF)
 Ventricular system: CSF-filled core of the brain
 Two lateral, third & fourth ventricles
 Subarachnoid Space
 CSF surrounds the brain & spinal cord
 Protective Role: “Shock absorber”

The Spinal Cord
Controls body movement; regulates visceral
function; processes sensory information &
transmits information to and from the brain.
A continuation of the brain stem.
 Exits the skull through the foramen magnum, an

opening in the base of the skull.
 Spinal cord itself ends at L1 or L2, yet the vertebral
column continues to the coccyx.
Protection

 Vertebral Column
 Intervertebral Disks
 Meninges
Peripheral Nervous System (PNS)
Spinal Nerves (31 pairs)
 Mixed Nerve Fibers: Exiting the spinal cord to
receive information and to transmit
information to the cord → brain.
 Posterior Root = Sensory
 Anterior Root = Motor
 Reflex Arc
 Interneurons connecting sensory & motor fibers.
 Dermatomes
 Sensory depiction of the corresponding spinal
nerves
*See Smeltzer & Bare pp. 1829; Figure 6
PNS: Cranial Nerves
There are 12 pair of cranial nerves.

 Sensory: CN I, II & VIII

 Motor: CN III, IV, VI, XI & XII
 Mixed: CN V, VII, IX & X

See: Handout & Smeltzer & Bare pp. 1837 Table 60

REVIEW!!! CNS - Brain
Lobes of the Cerebrum
CNS – Spinal Cord
Spinal Roots
Peripheral Nervous System (PNS)
Spinal Nerves
Reflex
Dermatome
• Area of skin that is
innervated by
cutaneous
branches of a
single spinal nerve.
• Useful in identifying
neurological
lesions.
Autonomic Nervous System (ANS)
Assessment
Mental Status
Neuro Assessment
Neuro Assessment
Neuro Assessment
Mental Status
Speech and Language
Language
Neuro Assessment
Language & Speech: assessed together; located in

the dominant hemisphere (left in most, including

lefties) LEFT:
written & spoken language, reasoning, number
skills, scientific knowledge, right hand control
RIGHT: insight, 3-D forms, art
awareness, imagination, music
awareness , left hand control
Neuro Assessment
Note: speech patterns, fluency, word

usage ability to follow 1 or 2

commands (must cross the midline)
ability to name common objects
and their use
Neuro Assessment
Neuro Assessment

Broca’s Aphasia: (motor,
expressive) unable to convert
thoughts to words; speech
limited to “yes/no”, name or 5
words or less; difficulty in
finding correct word; difficulty
repeating words & writing;
understands; profanity and
ability to carry a tune well
preserved

Wernicke’s Aphasia:
(sensory, receptive)
fluent speech; lacks content &
meaning;
does not understand spoken or
written word; substitutes
other words or uses non-words;
perseverates; not aware of
speaking errors
Neuro Assessment
 Example: A patient with Broca’s might say “where is
book”? and a patient with Wernicke’s might say “where
is the paper of the cover”?

Global Aphasia:both motor and receptive; non-fluent
speech with poor comprehension and repetitive ability
Dysarthria:loss of
articulation, phonation d/t muscle weakness or loss of
breath control
Thought Processes and Perception
Cognitive Abilities and Mentation
Cranial Nerves I-VI (p. 661)
Cranial Nerves VII - XII
Neuro Assessment
Neuro Assessment
Neuro Assessment
Neuro
Assessment
Cranial Nerves:

CN V Trigeminal:3

branches;
sensation to the face,
cornea and scalp;
opens jaw against
resistance
CN VII
Facial: moves the
face; taste
Neuro
Assessment

Cranial Nerves
CN VIII
Acoustic: 2
branches, acoustic (hearing)
and
vestibular (balance)
CN IX
Glossopharyngeal:
moves the
pharynx (swallow,
speech & gag)
CN X
Vagus:
voice quality
Neuro Assessment
Neuro Assessment

Cranial Nerves

Test gag, swallow and


speech together ( IX,

X, XII)
CN Tips: observe for
nystagmus with EOMS (2-3
beats normal with lateral
gaze)
diplopia (double vision):
cover one eye, should clear
if sixth nerve palsy (offer
eye patch over good eye)
Motor System
Motor System (Cerebellum)
Gait Abnormalities (Table 23-5)
Motor System
Tremors
Tremors continued
Neuro Assessment
Neuro Assessment
Neuro Assessment
Neuro Assessment
Neuro Assessment
Neuro Assessment

Sensory: Best assessed with the cooperative patient but
can be assessed by using pain; observe for symmetry of
grimace or withdrawal with pain. * Eyes closed
* Use cheekbone, forearm & lower leg
* Patient identifies which area and which or both
sides; note amount Of grimace/withdrawal if using pain

* Test enough times to ascertain validity of
responses
Sensory Assessment
Light Touch
• Client sitting
• Eyes closed
• “Say where you are
touched.”
• Compare bilaterally,
and distally to
proximally.
•
Vibratory Sensation
• Close eyes
• Strike fork & start on
most distal bony
prominence & work
medially with
neuropathy
• Ask when do you feel
the vibration start
and when do you
feel the vibration
stop.
Stereognosis
• Close eyes
• Place object in hand
• “Identify object.”
• Test bilaterally with
different objects.
• Note speed and
accuracy
• Astereognosis –
unable to identify
object
Graphesthesia (Parietal Lobe)
• Close eyes
• Draw letter or
number on hand
• “Identify figure.”
• Test bilaterally
• Note speed and
accuracy
• Agraphesthesia –
inability to identify
figure
Reflexes
Reflex Charting

• 4+ - Hyperactive,
commonly with
clonus
• Clonus – continued
movement after
stimulations removed
DTR Testing
Abnormal Reflexes
Biceps Reflex
• Support the client’s
forearm
• Client’s arm flexed at
45-90 degree angle
• Hold arm loosely
• Strike tendon with a
brisk wrist motion
on top of your
thumb
Brachioradialis Reflex
Triceps Reflex
• Relaxed arm
required.
• extension of the
forearm.
Patellar Reflex
• Sit on edge of table
with leg hanging
free.
• Place hand over
quadriceps muscle
• Strike patellar tendon
just below the
patella – blunt end of
hammer
Achilles Reflex
• Loosely support foot
in hand.
• Briskly strike Achilles
tendon.
• Plantar flexion of the
foot.
Abdominal Reflex
Plantar Reflex
• Stroke up the lateral
side of the sole &
across the ball of
the foot to just
below the great toe.
• Plantar flexion of the
toes, normal
response.
• Negative Babinski
sign.
Meningeal Irritation
Neurosurgery Considerations
Newborn Considerations
Newborn Reflexes
Plantar
Moro Reflex
Tonic Neck
Babinski
• Positive Babinski
reflex – normal with
infant
• Abduction of the toes
with dorsiflexion of
the great toe
Placing & Stepping Reflex
Gerontological Variations
Normal Findings after 65
Brain Teaser
QUESTIONS
Question 1
Question 2
Question 3
Neurological Disorders
DENNIS N. MUÑOZ, R.N., R.M.
Neurological Assessment
Health History
General Signs & Symptoms
Physical Examination Considerations
 Level of Consciousness
 Motor Function
 Pupillary Function / Eye Movements
 Vital Signs
 Respiratory Patterns
Laboratory & Diagnostic Testing

Neurological Health History
 Explore Presenting Compliant (s) → “OLD
CART”
 Precipitating Events
 Traumatic Event Data
 Type of force and direction of force
 + / - loss of consciousness (if + duration
too).
 Progression of signs / symptoms
 Client Information
 Allergies
 Past Medical & Surgical History
 Medications
 Habits / Lifestyle Changes
 Familial History of Neurologic Disorders
General Signs / Symptoms
• Memory Loss • Headache / Pain

• Disorientation • Weakness
• Changes in level of • Loss of Coordination
consciousness
• Tremors
• Seizures
• Speech or • Numbness / Tingling
Swallowing • Paralysis
Difficulties • Nausea / Vomiting
• Vision & Pupillary • Bowel or Bladder
Changes
Difficulties
• Dizziness
Physical Examination
Considerations
Level of Consciousness

 Most important aspect of neurologic examination

 Level of consciousness first to deteriorate; changes
often subtle, therefore requiring careful
monitoring.
Consciousness:

 Composed of Two Components:

 Arousal (Alertness)
 Awareness (Content)
 Assessment: Orientation vs. Disorientation
 Person, Place & Time
 Varying sequence of questions is important !!
Categories of Consciousness
Alert:

 Responds immediately to minimal external (visual,

tactile or auditory) stimuli.
Lethargic:

 A state of drowsiness; client needs increased

external stimuli to be awakened but, remains
easily arousable; verbal, mental & motor
responses are slow or sluggish.
Obtunded:

 Very drowsy, when not stimulated, but can follow

simple commands when stimulated (i.e. shaking
or shouting) ; verbal responses include one or
two words, but will drift back to sleep without
Categories of Consciousness
Stuporous:

 Awakens only to vigorous and continuous

noxious (painful) stimulation; minimal
spontaneous movement; motor responses to
pain are appropriate but, verbal responses are
minimal and incomprehensible (i.e. moaning).
Comatose:

 Vigorous external stimulation fails to produce

any verbal response; both arousal and
awareness are lacking; no spontaneous
movements but, motor responses to noxious
stimuli maybe be purposeful (light coma) or
non-purposeful or absent (deep coma).
Thalen : Table 24 - 1
pp . 647
LOC: Assessment Tools
Glasgow Coma Scale (GCS)

 Three Categories:
 Eye opening
 Best motor response
 Best verbal response
 Scoring
 Highest or best possible score 15
 A score of < 8 indicates coma
 Lowest or worst possible score 3
 Not appropriate for use in:
 Children, intoxicated clients or spinal cord injuries
Motor Assessment Techniques
Steps of Examination:
 Observe for spontaneous movement
 Elicit motor movement in response to stimuli
Types of Stimuli:
 Verbal
 Simple and direct statements; no visual or tactile
stimuli
 Reduce environmental stimuli or distractions
 Noxious (painful)
 When no response to verbal stimuli
 Acceptable methods: nail bed pressure, trapezius
pinch & supraorbital pressure (not used with
head injury).
Motor Responses
Abnormal Motor Responses

 In the unconscious client noxious stimuli

may elicit abnormal posturing:
 Decorticate (abnormal flexion)
 Decerebrate (abnormal extension)
 Flaccidity
↑ Decorticate
↑ Decerebrate
Motor Assessment Cont.,
Motor Movements & Strength

 Evaluate each extremity and compare with

opposite side; record each extremity
separately.
 Graded: 0 to 5
 (O = Paralysis → 3 = ROM / Gravity → 5 = ROM /
Full Resistance)
Deep Tendon Reflexes (DTR)

 Tap appropriate tendon with percussion or

reflex hammer
 Achilles, quadriceps, brachioradialis, biceps and
triceps
 Graded: 0 to +4
 ( 0= Absent→ +2 = Normal → +4= Hyperactive)
Motor Assessment Cont.,
Superficial Reflexes

 Normal Adult Reflexes

 Corneal
 Gag
 Swallowing
 Abnormal Adult Reflexes
 Babinski
Ocular Responses
Evaluate both pupils for equality:

 Size (mm)
 Shape
 Reactivity to Light
 Extraocular Movements (EOM)
 CN III, CN IV and CN VI
Ocular Responses Cont.,
Ocular Reflexes (unconscious client)

 Oculocephalic (Doll’s Eye) Reflex

 While the eyes are held open the head is
briskly turned from side-to-side.
 Oculovestibular (Cold Caloric) Reflex
 With HOB elevated 30 degrees; 20-100 ml of
iced water is injected into the external
auditory canal.

Vital Signs: Abnormal
Respiratory Patterns
Cheyne-Stokes

 Rhythmic; crescendo & decrescendo rate and depth

of respiration; brief periods of apnea
Central Neurogenic Hyperventilation

 Very deep, very rapid respirations; no apnea

Apneustic

 2-3 second inspiratory and / or expiratory pause

Cluster Breathing

 Groupings of irregular, gasping respirations separated

by long periods of apnea
Ataxic Respirations

 Irregular, random pattern; deep and shallow

respirations with periods of apnea (irregular too).
Diagnostic Testing
Imaging Studies of the Skull & Spine

 X-rays
 MRI
 CT Scans
 Position Emissions Tomography (PET) Scans
 A radioactive substance is either inhaled or
injected to provide images of the brain’s
function.
 Used to assess blood flow, tissue composition &
brain metabolism, therefore it indirectly
measures brain function.

Diagnostic Testing
Cerebral Angiography

 Involves artery access (usually femoral),

then a contrast medium is injected to
visualize cerebral circulation.
 Used to detect aneurysms, traumatic
injuries, vascular occlusions, tumors or
arteriovenous malformations.
 Nursing Considerations
 Prior to the procedure
 Maintain NPO status
 Assess for allergies to iodine, shellfish or IV
dye
Diagnostic Testing
Cerebral Angiography

 Nursing Considerations Cont.,

 Procedural Education
 Requires the client to remain still and lie a
hard, cold table.
 Injection of contrast medium may cause a
burning or flushing sensation
 Post Procedure
 Maintain bedrest with HOB elevated < 30
degrees and the puncture site extremity
straight as prescribed
 Neurovascular & puncture site assessments
regularly

Diagnostic Testing
Lumbar Puncture (Spinal Tap)

 A needle is inserted into the subarachnoid

space between the third and fifth lumbar
vertebrae.
 Used to obtain CSF, measure CSF fluid or
pressure or to inject a contrast medium or a
medication.
 Contraindicated with increased intracranial
pressure !!
 Nursing Considerations:
 Post Procedure
 Activity as prescribed; often bedrest with lying flat
 Encourage fluids (if not contraindicated)
 Complications
 Spinal headache
Diagnostic Testing
Myelography

 Allows for visualization of the vertebral

column, intervertebral disks, spinal nerve
roots & blood vessels.
 Requires a lumbar puncture to inject the
contrast medium into the subarachnoid
space of the spine.
 Assess for allergies to iodine, shellfish or IV
dye
 Post-Procedure
 Maintain the head of bed elevated 15-30
degrees
 Encourage fluids (if not contraindicated)
Diagnostic Testing
Electroencephalogram (EEG)

 Records the electrical activity of the brain through

a series of electrodes on the scalp.
 Used to diagnose and evaluate seizures
disorders, identify tumors, brain abscesses or
infections and to confirm of brain death.
Evoked Potentials (EPs)

 A series of electrodes on the scalp and an

external stimulus is applied to the peripheral
sensory receptors to elicit change in brain
waves.
 Stimulus maybe be visual, auditory or electrical.
Laboratory Testing
Cerebrospinal Fluid (CSF) Analyses

 Normal Findings:
 pH 7.35-7.45
 Specific Gravity: 1.007
 Appearance: Clear, colorless and odorless
 Cells: minimal number of WBCs and no RBCs
 Positive Protein
 Positive Glucose (2/3 blood sugar value)

Intracranial Pressures (ICP)
Brain contained within the skull (closed

container)
 Intracranial space is occupied by three
components:
 Blood (10%)
 Cerebral Spinal Fluid (CSF) (10%)
 Brain Tissue (80%)
 Normal physiologic conditions ICP < 10 mmHg
 An ICP value of 20 mmHg (sustained) requires
Intracranial Pressures (ICP)
Cont.,
Monro-Kellie Hypothesis:

 Increase in one intracranial component must

be compensated by a decrease in one or
more of the other components.
 The body has a limited ability to compensate
in response to increases in ICP.
 Displacing CSF
 Increasing Absorption of CSF
 Decreasing Cerebral Blood Volume
Increased Intracranial
Pressures
Compensatory mechanisms will eventually
be exhausted and clinical manifestations
of increased ICP will occur.
Causes of Increased ICP:
 Traumatic Brain Injuries

 Brain Tumors
 Other Causes:
 Meningitis or Encephalitis
 Brain Abscesses
 Hydrocephalus
Cerebral Perfusion Pressure
Cerebral perfusion pressure (CPP) represents the

pressure gradient driving cerebral blood flow (CBF) and

hence oxygen and metabolite delivery :

CPP = MAP - ICP
 CPP Normal Limits: 80-100mmHg
 CPP of 80 mmHg is needed to ensure adequate blood
supply to the brain

 CPP < 30 mmHg (sustained) will result in irreversible
neurologic damage.
 Clinically - CPP is maintained by either increasing
MAP or decreasing ICP.
Clinical Manifestations:
Stages of Increased ICP
Stage I: (Full Compensatory)

 Alert & Orientated

 History of head injury
 Vital signs / pupillary responses normal
 May complain of a headache
Stage II: (Partial Compensatory)

 Mental Status Changes

 Confusion and restlessness
 Decreased Level of Consciousness
 Lethargy
 Vital signs / pupillary responses normal
Stage III (Beginning Decompensation)

 Further decrease in level of consciousness

 Obtunded → Stupor
 Cushing’s Triad:
 Systolic HTN (widening pulse pressure)
 Bradypnea
 Bradycardia (bounding, slow pulse)
 Small pupils (< 3mm); sluggish responses to
light
 Vomiting (maybe projectile)
Stage IV (Herniation)

 Comatose
 Pupillary dilation & fixation (ipsilateral →
bilateral)
 Abnormal Posturing:
 Decorticate → Decerebrate → Flaccidity
 Cushing’s Triad Progresses To:
 Narrowing pulse pressure
 Weak, thready pulse
 Respirations: Cheyne-Stokes → Ataxic
Respirations
Stage V (Death)

ICP Monitoring
Four Methods of ICP Monitoring:


 Intraventricular
 A small catheter is placed within the ventricular
system (ventriculostomy); allows for CSF
drainage.
 Subarachnoid
 Hollow bolt or screw into the subarachnoid space
 Epidural
 Small fiberoptic sensor into epidural space
(between skull & dura)
 Intraparechymal
 Small fiberoptic catheter into the white matter of
brain tissue (parenchyma)
Increased ICP: Medical Management
Control of Cerebral Edema


 Osmotic Diuretics (i.e. Mannitol)

 Monitor urinary output carefully !!
 Cortiocsteriods (i.e. dexamethasone)
 Monitor blood glucose levels carefully
 Often accompanied by a proton-pump inhibitor or
H2 blocker
Control of Intracranial Volume

 Draining CSF (i.e. ventriculostomy)

 Must be done slowly to prevent collapse of the
ventricles.
 Controlled Hyperventilation
 PaCO2 low end of normal current trend (35
mmHg)
Control of Metabolic Demand


 Sedatives
 Benzodiazepines i.e. lorazepam (Ativan)
 Neuromuscular Blockade / Paralyzing Agents
 i.e. vecuronium (Norcuron)
 Must still provide sedation and / or pain management !!
 Barbiturate Therapy (Induced Coma)
 i.e. pentobarbital or thiopental; used when conventional
medical interventions fail to reduce ICP; controversial.
Other Medical Interventions:

 Temperature Regulation
 Prevent Hyperthermia (i.e. antipyretics, ice packs &
cooling blankets)
 Blood Pressure Regulation
 Delicate balance in the client with increased ICP; often
maintained on the high end of normal to ensure
adequate cerebral perfusion!!
 Sedatives often enough, if not antihypertensive agents
used
 Seizure Control / Prevention
 Antiseizure Agents i.e. phenytoin (Dilantin)
Increased ICP: Nursing
Considerations
Nursing Assessment / Monitoring


Frequent Vital Signs & Neurological Exams
 Trends in signs and symptoms are paramount !!
 Report deterioration of neurologic status promptly
 Maintain ICP monitoring device
 Document amount & appearance of CSF drainage
 Aseptic technique with dressing changes
 Strict I & O and Daily Weights
 Laboratory Values
 i.e. CBC, SMA 7, Electrolytes & ABG’s
Considerations
Nursing Activities

 HOB elevated to 30 degrees

 Trendelenburg, prone positions should be avoided /
limited
 Head should be maintained neutral position (midline)
 Avoid extreme neck angulation and hip flexion
 Identify daily care activities that increase ICP
 Provide rest periods
 Avoid Valsalva Maneuver; turning or straining with BM
 Reduce noxious environmental stimuli
 Manage pain with alternative and pharmacologic
Considerations
Nursing Activities Cont.,

 Respiratory / Ventilator Considerations

 Deep Suctioning
 Hyperoxygenate with each pass
 Limit the number of passes & < 10 seconds each pass
 Ensure tracheostomy ties are not too tight
 Limit / avoid unnecessary coughing or gagging
 Prevention of Infection:
 Ensure aseptic techniques with invasive line care
 Prevention of Injury
 Maintain seizure precautions (i.e. padded side-rails)
Considerations
Nursing Activities Cont.,

 Administer medications as prescribed

 Maintain Nutritional Support
 High-protein & high-fiber diet
 Total Parenteral Nutrition (TPN)
 Dietary Supplements
 Maintain Therapeutic Environment
 Encourage contact from significant others
 Provide emotional support and education
Increased ICP: Surgical
Management
Craniotomy

 Involves opening the skull to gain access to

intracranial structures.
 Indicated for relief of Increased ICP by tumor
removal, hematoma or abscess evacuation or
controlling hemorrhage.
 Surgical Approaches:
 Transcranial
 Transsphenoidal
Craniotomy Considerations
Preoperative Nursing Care

 Assessment
 Frequent vital signs and neurological exams
 Documentation of neurological baseline
 Diagnostic / Laboratory Tests
 Blood tests / blood type and cross match
 Chest x-ray and 12 lead EKG
 Education
 Avoid activities known to increase ICP
 Surgery specific instructions
 Provide Emotional Support
Postoperative Nursing Management

 Frequent Monitoring of Neurologic Status & Vital

Signs
 Maintain ICP Monitoring Device
 Prevent Increased ICP
 Client positioning
 Prompt management of vomiting, fever & pain
 Administer anti-seizure medications as ordered
 Maintain Fluid / Electrolyte Balances
 I&O’s and daily weights
 Prevent / Monitor for Infection
 Aseptic technique for dressings & ICP monitoring device

Postoperative Nursing Management Cont.,

 Prevent Injury
 Seizure / Falls Precautions
 Eye Care / Skin Care
 Providing Emotional Support
 Patient Education
 Signs & symptoms of increased ICP
 Signs & symptoms of infection
 Incisional care
 Medications
 Neurologic Rehabilitation
 Stress importance; PT / OT consults helpful .
Complications

 Increased ICP
 Surgical Hemorrhage
 Fluid / Electrolyte Imbalance
 CSF Leak
 DVT
 Gastric Ulcers
 Pneumonia
 Seizures
Complications of Increased ICP
• Diabetes Insipidus
• SIADH (Syndrome of Inappropriate Antidiuretic
Hormone)
• Herniation
• Brain Death
Diabetes Insipidus
Decreased secretion of antidiuretic hormone

(ADH)
 Clinical Manifestations:
 Hypernatremia (serum)
 Excessive water losses via urine (↑ UO)
Client may experience volume depletion !!
 Management:
 Fluid Volume Replacements
 Encourage oral intake of fluids (if possible)
 I.V. fluids; careful monitoring: laboratory results and
BP
 Electrolyte Replacements
 Vasopressin therapy:
 Pitressin or Desmopression DDAVP
SIADH
Increased secretion of antidiuretic hormone
(ADH)
Clinical Manifestations:
 Hyponatremia (serum)
 Decreased water losses via urine (↓ UO)

Volume overload (i.e. weight gain)
Management:

 Fluid restriction usually sufficient


Herniation & Brain Death
Herniation

 Result of excessive ICP downward displacement

of brain tissue resulting in the cessation of CBF.
 Leads to irreversible brain anoxia and brain
death
Brain Death

 Complete, irreversible cessation of function of the

entire brain and brain stem.
 Mechanical support sustaining life
 Emotional support to significant others
 Organ donation
Neurological Disorders
Exploring Causes of Increased
ICP
Head Injury
Broad term to classify sudden trauma to
head, which includes injuries sustained
to the scalp, skull or brain.
Most common causes:
 MVA: motor vehicle collisions (50%)

 Falls (21%)
 Violence (12%)
 Sports related-injuries (10%)
The most serious type of head injury is

traumatic brain injury (TBI)

TBI: Pathophysiology
Primary Injury

 Initial damage to the brain that results from

the traumatic event.
Secondary Injury

 Additional damage to the brain tissue

occurring minutes to hours after the initial
traumatic event.
 As a result of the cellular changes that
occur with cerebral edema, ischemia and
hemorrhage.
TBI: Clinical Manifestations
Neurological Deficits • Headache
Altered Level of • Dizziness
Consciousness • Impaired Hearing
Confusion or Vision
Pupillary Abnormalities • Sensory or Motor
Vital sign Changes Dysfunction
Altered Reflexes • Seizures
 Gag •
 Corneal
TBI: Mechanisms of Injury
Penetrating / Missile Injuries

 Object forcefully enters the cranial vault causing

damage to the meningeal layers, blood vessels &
the brain tissue.
 Associated with an increase risk of infection
 Communication of intracranial contents with
external environment; Dura mater no longer intact
!!
 Causes:
 Gunshot Wounds (most common)

Stab Wounds
Cont.,
Blunt, Non-Missile Injuries

 Deformation Injuries
 Occurs when an object strikes the head
 Often resulting in skull fractures, concussion,
contusion or intracranial hemorrhage.
 Causes: baseball bat or bottle

Cont.,
Blunt, Non-Missile Injuries

 Acceleration-Deceleration Injuries
 Also, called Coup-Contrecoup Injuries
 When the brain rapidly accelerates
and decelerates within the skull.
 Two areas of brain injury:
 Site of impact

Opposite side of the brain
 Often resulting in contusions & intracranial
hemorrhage
 Cause: Motor vehicle collision (MVC)
Scalp Injuries
• Isolated scalp injuries usually classified as
minor head injuries.
• The scalp is highly vascular with poor
constrictive abilities; bleeding is often
profuse
• Infection is a major concern, which must be
prevented!!
Skull Fractures
Actual break in continuity of skull

 Cause can be blunt force trauma or penetrating injury

 Brain injury may or may not occur
 Skull fractures considered closed if dura mater is intact;
open if dura mater is torn.
Types of Skull Fractures:

 Linear:
 Non-displaced fracture of the skull
 Depressed:
 Fracture involving the downward depression of bone into
brain tissue
 Comminuted:
 Fragmentation and downward displacement of bone into brain
tissue
 Basilar:
Skull Fractures Cont.,
Basilar Skull Fractures

 Fracture at base of skull; usually temporal or frontal

areas
 Often an open head injury
 Bleeding from nose, pharynx, ears or into
conjunctiva
 Bruising:
 Battle’s sign: ecchymosis over mastoid
 Raccoon (eyes) sign: bilateral periorbital ecchymosis
 Monitor For A CSF Leak !!
 Observe nose or ears
 Halo Sign
 Prevent Infection !!
Cerebral Concussion
Head injury with temporary loss of neurological

function with no structural damage.

 Cause: jarring of the brain results in temporary
disruption of synaptic activity; often occurs with
acceleration-deceleration injuries.

 Loss of consciousness; usually brief

 Amnesia regarding events immediately prior to injury
Postconcussion Syndrome

 Usually occurs within 24 to 48 hours after injury and

may present up to several months later, but will
subside in time.
 S/Sx: HA, lethargy, irritability, memory deficits, dizziness &
Cerebral Contusion
Bruising of the brain tissue; actual structural

damage visible on diagnostic testing (i.e. CT

scan).
 Often caused by deformation or acceleration-
deceleration injuries (often two focal areas of
bruising)
Clinical Manifestations

 Loss of consciousness (more than brief)

 Vary depending on the location & size of
contusion
Secondary injury is possible (i.e. hemorrhage or

Diffuse Axonal Injury (DAI)
Wide spread brain injury causing direct damage

to the axons or disruption of axonal

processes.
 Caused by high-velocity shearing, rotational and
acceleration-deceleration forces.
 Microscopic hemorrhaging throughout the brain
tissue; not usually visible on diagnostic testing,
unless severe them small hemorrhages maybe
seen.
Clinical Manifestations

 Most present in a comatose state

and often require long-term care.
Intracranial Hemorrhage (ICH)
Trauma can cause bleeding within the brain

tissue or within the spaces surrounding the

brain.
 The result is hematomas or collections of blood
within cranial vault; most serious of brain injuries
Classified according to location:

 Epidural hematoma
 Subdural hematoma
 Intracerebral hematoma
Epidural Hematoma (EDH)
Blood collects between the dura mater & the

skull
 Most often arise from arterial hemorrhage
 Cause usually is injury of middle meningeal artery;
resulting in rapid accumulation of blood.
 Clinical Manifestations:
 + LOC after initial trauma; usually at the location of
injury
 Lucid interval (30-50% experience)
 Rapid deterioration in neurologic status; S/Sx of ↑ ICP
 Management
 Medical emergency requiring immediate medical and
Subdural Hematoma (SDH)
Blood collects between the dura mater & the

arachnoid mater
 Often originating from venous hemorrhage
 Cause is usually injury to bridging veins; venous blood
tends to accumulate more slowly than arterial blood,
therefore signs/symptoms of ↑ ICP tend not occur as
quickly.
 Two Main Types of SDH
 Acute (less than 48 hours after injury)
 Requires immediate medical and /or surgical intervention
 Chronic (over 2 weeks after injury)
 Often forget actual injury; common in elderly
 S/Sx of ↑ ICP fluctuate or “come and go”
 Management: Burr hole clot evacuation or craniotomy
Intracerebral Hematoma (ICH)
Blood collects within the brain tissue

(parenchyma)
 Bleeding causes displacement of brain tissue; even
small bleeds can cause significant neurological
alterations.
 Destroys brain tissue
 Causes cerebral edema
 Increases ICP
 S/Sx of ↑ ICP maybe be immediate or develop
overtime
 Management:
 Depends on location of the bleed and size of the
bleed
TBI: Management
Considerations
Medical / Surgical Management

 Supportive Interventions
 Prevention or Management of Increased ICP
 Airway
 Ventilation
 Nutrition
 Pain and anxiety management
 Prevention of seizures & agitation
 See previous discussion of medical / surgical
management of increased ICP
TBI: Management
Considerations
Nursing Considerations

 Frequent neurologic assessments / vital signs

 Fluid and electrolyte balances
 I & O and daily weights
 Increased ICP (see previous discussion)
 Client positioning & Care
 Nursing Activities
 Maintain skin integrity
 Protection from injury
 Prevent infection
 Provide rest
 Provide support & education to client and/or significant
others
Brain Tumors
Space-occupying intracranial lesions

 Benign or malignant.
Clinical manifestations differ according to area of
lesion and rate of growth
Common Signs / Symptoms:
 Alterations in consciousness
 Neurologic deficits
 Motor & Visual Disturbances
 Headaches
 Seizures
 Vomiting (maybe sudden and projectile)
Types of Brain Tumors
Brain tumors within the brain tissue

 Gliomas: Most common type of brain tumor

 Astrocytomas
 Most common type of Glioma
 Slow growing; benign but may become malignant
 Invasive (difficult to surgically remove entire tumor)
 Glioblastomas Mulitforme
 Is a advanced stage of Astrocytomas
 Rapid growing; malignant; invasive
 Poorest prognosis
Types of Brain Tumors Cont.,
Brain tumors arising from supporting structures

 Meningiomas
 Encapsulated, non-invasive; usually benign
 Slow growing; well defined
 Compresses rather than invades
 Acoustic Neuromas
 Non- malignant ; slow growing
 CN VIII affected: HA, tinnitus, hearing loss, impaired
balance, unsteady gait & facial pain / numbness on the
side of tumor
Developmental Tumors

 Angiomas
 A benign mass of abnormal blood vessels with thin
walls; prone to rupture
Brain Tumor: Management
Considerations
Increased Intracranial Pressure

 Pharmacologic Agents
 Corticosteroids (dexamethasone and prednisone)
 H2 blocker or proton pump inhibiter must accompany
 Osmotic Diuretics
 Antiseizure, antiemetic & analgesic medications
 See previous discussion of ↑ ICP management
& nursing considerations
Tumor Removal / Destruction

 Surgical Interventions
 Craniotomy
 ICP monitoring
Considerations
Tumor Removal / Destruction Cont.,

 Medical Interventions
 Chemotherapy (often a combination of agents
utilized)
 Routes of Administration
 Intrathecal Route
 Intracranial Route
 Disk-shaped drug wafers (Gliadel wafers) maybe
implanted for some tumors (i.e. glioblastomas
multiforme or recurrent tumors) during a craniotomy.
 Systemic / Venous Route
 Most agents poorly penetrate the blood-brain barrier
 Temodar (temozolomide) can penetrate; widely used
Considerations
Radiation Therapy

 External radiation therapy

 Gamma Knife (stereotactic radiosurgery)
 Single dose of high ionized radiation
to selectively destroy the tumor.
 Requires the use of a helmet device;
therapy usually takes about a
hour
 The client usually will stay over-night
at the hospital for observation.
 Internal radiation therapy (Brachytherapy)
 A catheter is inserted in or just next to a tumor to deliver
radiation by means of radioactive capsules “seeds”
 The radioactive source will then be left in place from several
hours to several days to kill the tumor cells; Client
Increased ICP Nursing
Diagnoses
• Ineffective cerebral tissue perfusion related to
increased ICP and decreased CPP.
•
• Potential for impaired skin integrity related to

bedrest or immobility.
•
• Knowledge deficit related to increased ICP or its

treatments.
•
• Decreased sensory perception related to

neurological impairment.
•
• Risk for injury related to altered level of

consciousness or seizures.
Increased ICP Nursing Diagnoses
• Ineffective airway clearance related to diminished

protective reflexes (i.e. cough or gag).
•
• Interrupted family processes related to health crisis.

•
• Risk for infection related to ICP monitoring device.

•
• Fluid volume deficit related to decreased level of

consciousness or hormonal imbalance (DI).
• Imbalanced nutrition, less then body requirements
related to inadequate intake.
• Potential for sleep disturbances related to frequent
neurological status monitoring.
 Essentials of Anatomy and Physiology
Digestive System
 The Digestive System
•Second system to function in embryo

•A “tube within a tube”
•Material is not “inside” body
•Humans are omnivores
•Diet tempered by culture, situation
FUNCTIONS OF THE DIGESTIVE
SYSTEM
1. ingestion = taking food in

2. propulsion via peristalsis (wave-like
muscular contractions)
3. mechanical digestion = physically
breaking food into smaller pieces

SYSTEM
4. chemical digestion = breaking food down into


its building blocks using enzymes

 proteins –>amino acids
 lipids –> fatty acids & glycerol
 carbohydrates –> monosaccharides
 nucleic acids –> nucleotides
5. absorption of nutrients + water

 Molecules enter body
 Via transport into blood
SYSTEM
6. defecation = to eliminate wastes in the


form of feces

 Technically, food in the digestive tract is

outside the body because the tube is open
at both ends

Review!!!!
Functions of Digestive system

Motility
• The digestive tract is surrounded by layers
of smooth muscle
• These muscles enable mixing and
propulsive movement to be carried out
by the digestive tract
Secretion
• Digestion requires that enzymes be
secreted by the pancreas and other
organs
• Mucous secretions protect the digestive
tract
• Acid is secreted in the stomach
• There are other secretions of importance
DIGESTION
• Breaking down complex foodstuffs into

absorbable units by enzymes produced
in the digestive system
• Involves the breakdown of carbohydrates,
proteins fats, and other foods
Absorption
• All other functions support this one
•
• This is how we obtain the necessary fuel
for our cells
Regulation of the GI Tract
Extrinsic innervation:

 Parasympathetic nervous system:
 Vagus and spinal nerves:

 Stimulate motility and GI secretions.
 Sympathetic nervous system:

 Postganglionic sympathetic fibers that pass
through submucosal and myenteric plexuses
and innervate GI tract:
 Reduce peristalsis and secretory activity.
Regulation of the GI Tract (continued)
Enteric nervous system:


 Sites where parasympathetic fibers synapse with

postganglionic neurons that innervate smooth
muscle.
Submucosal and myenteric plexuses:

 Local regulation of the GI tract.

Paracrine secretion:

 Molecules acting locally.

Hormonal secretion:

 Secreted by the mucosa.

Organs of the Digestive System
Figure 14.1
Slide
14.2b
 Organs of the Digestive System
•Two components
•Alimentary canal – continuous coiled
hollow tube
•Accessory digestive organs –
everything else
Slide
14.2a
 Organs of the Alimentary Canal
•Mouth
•Pharynx
•Esophagus
•Stomach
•Small intestine
•Large intestine
•Anus
Figure 14.1
Slide
14.2b
 Mouth (Oral Cavity) Anatomy
•Lips (labia)
•Cheeks
•Hard palate
•Soft palate
•Uvula
Figure 14.2a
MOUTH oral cavity
• mechanical digestion =
biting & chewing food
(mastication)
• chemical digestion =
breaking starches
(polysaccharides) into
disaccharides using the
enzyme amylase
MOUTH oral cavity
different teeth do

different jobs: 32
total
 incisors cut /
bite
 canines or
cuspids tear
& shred
 premolars &
molars
MOUTH
• the tongue is made of skeletal muscle & it

moves food around the mouth and it aids in
swallowing + it’s covered with taste buds
• chewed food + saliva = bolus
• Umami is the 5th taste of savory and comes
from amino acids, especially glutamate, such
as MSG, also in nucleotides. The foods
containing these constituents are meats,
cheeses, soy sauce, mushrooms, anchovies,
MOUTH oral cavity
• the uvula is a fingerlike projection of the
soft palate
• the tonsils are part of the body’s defense
system
THE SALIVARY GLANDS
Functions of saliva:

 cleanses the mouth

 dissolves food chemicals so that they can be
tasted
 moistens food & aids in bolus formation
 begins chemical digestion of starchy foods
THE SALIVARY GLANDS
3 main salivary glands:


 Parotid – near ear

 Submandibular – under the jaw
 Sublingual – under the tongue
mumps = a viral infection that causes

swollen parotid glands, spread in saliva

from person to person
PHARYNX
• located at the intersection of the food and
breathing passageways
• connects the mouth to the esophagus & to the
trachea
• the epiglottis covers the opening to the
respiratory tract when you swallow
• the esophageal sphincter is contracted when
you’re not swallowing
• if food accidentally “goes down the wrong pipe”
it triggers a coughing reflex designed to clear
the airways
ESOPHAGUS gullet
• runs from the pharynx through the
diaphragm to the stomach
• about 10 inches long, conducts peristalsis
to move food along
• heartburn or acid reflux disease result
when gastric juices backflow into the
esophagus
•
•Vestibule
•Oral cavity: space
•Tongue:
•attached to bone
•lingual frenulum
Figure 14.2a
•Tonsils
•Palatine
tonsils
•Lingual tonsil
Figure 14.2a
 Digestive Functions of the Mouth
•Mastication (chewing) of food

•Mixing food with saliva
•Initiation of swallowing
•by the tongue
•Taste receptors
 Digestive Functions of the Mouth
•Mechanical digestion
•Food broken down by chewing
•Chemical digestion
•Food mixed with saliva
•Starch digestion begins
Slide
14.48
 Pharynx Anatomy
•Nasopharynx
•Oropharynx: posterior
to oral cavity
•Laryngopharynx:
•posterior to
larynx
•Connects to
esophagus
Figure 14.2a
ESOPHAGUS gullet
• runs from the pharynx through the
diaphragm to the stomach
• about 10 inches long, conducts peristalsis
to move food along
• heartburn or acid reflux disease result
when gastric juices backflow into the
esophagus
 Pharynx Function
•Passageway for air and food

•Moves food to esophagus by muscle
contraction
•Longitudinal inner layer
•Circular outer layer
•Peristalsis: wave-like
contractions
 Esophagus
•Extends from pharynx to stomach

•passes through the diaphragm
•Conducts food by peristalsis
•Passageway for food only
Slide
14.10
Activities of the Pharynx and

Esophagus
•These organs have no digestive function

•Serve as passageways to the stomach
Slide
14.49
 Deglutition (Swallowing)
Figure 14.13
Slide
14.52
Swallowing
• A programmed all-or-none reflex
• Chewing and moving the bolus of food back is manly
voluntary (striated muscle)
• Pressure of bolus on pharynx triggers involuntary reflex
(smooth muscle)
• Tongue prevents food from moving back
• Uvula elevated, sealing nasal passage
• Larynx elevates and closure of glottis
• Respiration briefly inhibited
• Pharyngeal muscles force bolus back
• Peristaltic waves move bolus through esophagus
•
PERISTALSIS
Ringlike
contraction
sweeps down
the esophagus
 Layers of Organs in Alimentary
Canal
•Mucosa
•Innermost layer
•Simple columnar E.T.
•Lots of Goblet cells
•Protects, secretes, absorbs
Slide
14.11a
Layers of Alimentary Canal Organs
Figure 14.3
Slide
14.13
 Layers of Alimentary Canal Organs
•Submucosa
•Deep to mucosa
•Loose connective tissue
•blood vessels
•nerve endings
•lymphatics
Slide
14.11b
Figure 14.3
Slide
14.13
 Layers of Alimentary Canal Organs
•Muscularis: smooth muscle

•Inner circular layer
•Outer longitudinal layer
•Serosa
•Outermost layer = visceral peritoneum
•Serous membrane
Slide
14.12
Figure 14.3
Slide
14.13
Review!!!!!!!!!
Mucosa
Lines the lumen of GI tract.


 Consists of simple columnar epithelium.

Lamina propria:

 Thin layer of connective tissue containing lymph

nodules.
Muscularis mucosae:

 Thin layer of smooth muscle responsible for the

folds.
 Folds increase surface area for absorption.
Goblet cells:

 Secrete mucus.
Submucosa
Thick, highly vascular layer of connective

tissue.
Absorbed molecules enter the blood and
lymphatic vessels.
Submucosal plexus (Meissner’s plexus):
 Provide autonomic nerve supply to the

muscularis mucosae.
Muscularis
Responsible for segmental contractions and


peristaltic movement through the GI tract.

 Inner circular layer of smooth muscle.
 Outer longitudinal layer of smooth muscle.
Contractions of these layers move food through
the tract; pulverize and mix the food.
Myenteric plexus located between the 2 muscle
layers.
 Major nerve supply to GI tract.
 Fibers and ganglia from both sympathetic

and parasympathetic nervous systems.
Serosa
• Binding and protective outer layer.

• Consists of areolar connective tissue covered
with simple squamous epithelium.
STOMACH
• C-shaped, on the left side, about 10
inches long, holds 1/2 – 1 gallon or so
• When empty, the stomach folds into rugae
• the cardiac sphincter opens, allowing food
into the stomach
• mechanical digestion continues here, as
the stomach churns
STOMACH
chemical digestion also continues here, as the


food is mixed with gastric juices:

 pepsin breaks down proteins into
peptides
 hydrochloric acid (HCl) lowers the pH to 2
where pepsin works best

the stomach lining is protected by a mucus
layer
hormones insure that gastric juices are
secreted only when the stomach has food in

it
rapid cell division allows the replacement of
the lining every 1-3 days

gastric ulcers can form if the stomach lining is
eroded by gastric juice

 mostly caused by bacteria (not stress) & treated
with antibiotics
STOMACH
• food remains here 2-4
hours & reaches the
consistency of tomato
soup (now called
chyme)
• the pyloric sphincter
opens, allowing
chyme into the small
intestine
 Stomach Anatomy
•“J” shaped flat bag

•Located in epigastric, left hypochondriac
regions
•Food enters through gastroesophageal
(cardiac) sphincter
Slide
14.15a
 Stomach Anatomy
Figure 14.4a
Slide
14.17
 Stomach Anatomy
•Regions of the stomach

•Cardiac region
•Fundus
•Body
•Pylorus – terminal end
•Food empties into the small intestine at
the pyloric sphincter
Slide
14.15b
 Stomach Anatomy
•Rugae – internal folds of the mucosa

•External regions
•Lesser curvature
•Greater curvature
Slide
14.16a
 Stomach Anatomy
•Layers of peritoneum attached to the

stomach
•Lesser omentum
•Greater omentum
•Contains fat to insulate, cushion,
and protect abdominal organs
Slide
14.16b
 Stomach Anatomy
Figure 14.4a
Slide
14.17
 Stomach Functions
•Acts as a storage site for food

•Chemical digestion of protein begins
•Delivers chyme (processed food) to the
small intestine
Slide
14.18
 Specialized Mucosa of the
Stomach
•Simple columnar epithelium
•Gastric glands – secrete gastric juice
•Chief cells – produce pepsinogens
•Parietal cells – produce hydrochloric acid
•Endocrine cells – produce gastrin
Slide
14.19
 Structure of the Stomach Mucosa
•Gastric pits
•formed by folded mucosa
•Glands and specialized cells
•are deeper in the gastric gland region
Slide
14.20a
 Structure of the Stomach Mucosa
Figure 14.4b, c
Slide
14.20b
FACTORS INFLUENCING
GASTRIC MOTILITY
• Distension of stomach: increases
• Feedback from the small intestine:
decreases
• Control from CNS
• Gastrin: increases
FACTORS CONTROLLING
STOMAC EMPTYING
• Gastric Motility
• Enterogastric reflex: Via intrinsic and
autonomic nerves
• Enterogastrones: secretin, cholecystokinin
(CCK), gastric inhibitory peptide
•
FACTORS IN SMALL INTESTINE CONTROLLING
STOMAC EMPTYING
• Fat
• Acid
• Hypertonicity
• Distension
 Small
Intestine
•Site of nutrient absorption

•Muscular tube ~20’ long
•extends from pyloric sphincter to
ileocecal valve
•Suspended from the posterior abdominal
wall by mesentery

Subdivisions of

the Small
Intestine
•Duodenum
•Attached to the stomach
•Curves around the head of the pancreas
•Jejunum
•Second portion, ~8’
•Ileum
•Longest portion, ~10’

Chemical Digestion in the Small
Intestine
•Enzymes mix with chyme. Come from:

•Intestinal cells
•Pancreas (also adds HCO3-)
•Bile enters from the gall bladder
Slide
14.23a
Chemical Digestion in the Small
Intestine
Figure 14.6
Slide
14.23b
 Villi of the Small Intestine
•Fingerlike
structures formed
by the mucosa
•Provide more
surface area
Figure 14.7a
Slide
14.24
Structures Involved in Absorption

of Nutrients
•Absorptive cells
•Blood capillaries
•Lacteals (specialized
lymphatic capillaries)
Figure 14.7b
Slide
14.26
 Folds of the Small Intestine
•Called circular folds or plicae circulares

•Submucosal specialization
•has Peyer’s patches
•collections of lymphatic tissue
Slide
14.27
SMALL INTESTINE
 uses pancreatic amylase to turn
starch into disaccharides
 uses trypsin to turn proteins into
peptides
 uses pancreatic lipase to turn fats
into fatty acids & glycerol
 uses nucleases to turn nucleic
acids into nucleotides
SMALL INTESTINE
the small intestine makes several enzymes to


chemically digest food

 maltase turns maltose into a
monosaccharide
 sucrase turns sucrose into a
monosaccharide
 lactase turns lactose into a monosaccharide

SMALL INTESTINE
 peptidase turns peptides into amino acids

 nuclease turns nucleotides into sugar and
nitrogen bases
 Digestion is complete by the time the food
reaches the end of the duodenum
 The jejunum & the ileum are specialized for
nutrient absorption
SMALL INTESTINE
 food molecules are absorbed into the
cells of villi (fingerlike projections) and
enter into the bloodstream
 villi covered with microvilli greatly
increase the surface area of the small
intestine to aid absorption of food
 spread out it would cover a tennis court!
SMALL INTESTINE
 liquid food stays in the small intestine
3-5 hours & is moved along via
peristalsis toward the large intestine
 passes through the ileocecal valve into
the large intestine
 Large Intestine
•Larger in diameter, but shorter than the
small intestine
•~6’ long
•Has subdivisions
•Named for direction of food
movement
•
Slide
14.28
 Large Intestine
Figure 14.8
Slide
14.28
LARGE INTESTINE “colon”
• anaerobic bacteria synthesize vitamins B
and K
• major divisions: cecum, appendix, colon,
rectum, anal canal
• the appendix hangs from the 1st section
on the right side and may
become inflamed = appendicitis
• the colon’s main regions are the
ascending colon, the transverse colon,
the descending colon, and the sigmoid
colon
• after 18-24 hours, the indigestible

material reaches the rectum
• now called feces, it is eliminated
through the anus via the anal
sphincter in a process called
defecation
• The colon can be removed to treat colon

cancer in a procedure called an
ileostomy where the ileum is brought out
to the abdominal wall & fecal matter is
caught in a bag
 Functions of the Large Intestine
•Absorption of water
•Eliminates indigestible food as feces
•Does not participate in digestion
•Goblet cells produce mucus for
lubrication
Slide
14.29
 Functions of the Large Intestine
•Contains many bacteria (mostly E. coli)

•Bacteria digest our wastes
•Produce vitamins, amino acids
•Vits. B, K
•We absorb their “wastes”
Slide
14.29
 Structures of the Large Intestine
•Cecum – saclike first part

•Appendix
•Accumulation of lymphatic tissue
that may become inflamed
(appendicitis)
•Hangs from the cecum
Slide
14.30a
 Structures of the Large Intestine
•Colon
•Ascending
•Transverse
•Descending
•Sigmoid (S-shaped)
•Rectum
•Anus – external body opening
Slide
14.30b
 Large Intestine
Figure 14.8
Slide
14.28
Modifications to the Longitudinal

Layer of Muscle
•Smooth muscle reduced to three bands

(taeniae coli)
•Muscle bands are shorter than colon
•Walls are formed into pouches called
haustra
Slide
14.31
 Accessory Digestive Organs
•Salivary glands
•Teeth
•Pancreas
•Liver
•Gall bladder
Slide
14.32
Figure 14.1
Slide
14.2b
 Salivary Glands
•Salivary glands: 3 pairs

•Parotid glands – located anterior to ears
•Submandibular glands
•Sublingual glands
Slide
14.33
 Saliva
•Mixture of mucus and serous fluids
•Helps to form food into a bolus
•Contains salivary amylase
•starch digestion
•Dissolves chemicals for taste buds
•We produce ~1 liter/day
Slide
14.34
 Teeth
•Function to masticate (chew) food

•Humans have two sets
•Deciduous (baby or milk) teeth
•20 teeth are fully formed by age two
Slide
14.35a
 Teeth
•Permanent teeth
•Replace deciduous teeth beginning ~6
years of age
•A full adult set is 32 teeth
•some people do not have wisdom
teeth
Slide
14.35b
Classificatio
n of Teeth
•Incisors (2)
•Canines (1)
•Premolars (2)
•Molars (3)
•Same number and type of teeth in each
“quadrant” so….
•“Dental Formula”: 2-1-2-3

different teeth do different jobs: 32
n
total
uincisorscut / bite
ucanines or cuspids tear &
shred
upremolars & molars crush /
grind
 Classification of Teeth
Figure 14.9
Slide
14.36b
 liver: weighs 3 pounds
 produces bile to emulsify fats
(mechanical digestion)
 bile travels from the liver to the
hepatic duct to the gall bladder to

the bile duct & into the duodenum
 high cholesterol can cause gall
stoneswhich consist of crystallized

bile salts. They can block the bile
duct
Liver disease:
• hepatitis is inflammation of the
liver, often due to viral
infection (A, B, C, D, E, F)
• Cirrhosis = progressive &
chronic inflammation of the
liver due to alcoholism or
severe hepatitis
 Liver
•Largest gland in the body
•Located in right hypochondriac region
•Four lobes
•Suspended by the falciform ligament
•Connected to gall bladder via common
hepatic duct
Slide
14.39
 Primary Function of Liver
•Produces bile for fat emulsification

•Composition: water, plus…
•Bile salts
•Bile pigment (mostly bilirubin)
•Cholesterol
•Phospholipids
•Electrolytes
Slide
14.40
 Role of the Liver in Metabolism
•Final metabolism of most food

•Detoxifies drugs and alcohol
•Degrades hormones
•Produces cholesterol, blood proteins
•Regulates distribution of nutrients
Slide
14.77
 Gall Bladder
ugall
bladder:
«stores bile
produced by the
liver
«may be surgically
removed, but that
decreases a
person’s ability to
digest fats
efficiently
•Sac attached to inferior surface of liver
•Stores, concentrates bile
•Bile enters duodenum in the presence of fatty food
•Requires hormonal signals, autonomic innervation
•Gallstones can cause blockages

 pancreas:
 a soft, flattened
gland
 secretes digestive
enzymes and
hormones
 Pancreatic juice (pH
8) is bicarbonate
rich & it neutralizes
the acidic chyme as
it leaves the
stomach
 Pancreas
•Exocrine function: Produces digestive enzymes
•Enzymes: secreted into duodenum
•Bicarbonate ions: neutralize acidic chyme
•Endocrine products of pancreas
•Insulin
•Glucagon
Slide
14.38
Processes of the Digestive System
Figure 14.11
Slide
14.46
 Control of Digestive Activity
•Mostly by reflexes via the

parasympathetic division
•Chemical and mechanical receptors
trigger reflexes
Slide
14.47a
•Stimuli include:
•Stretch of the organ
•pH of the contents
•Presence of breakdown products
Slide
14.47b
•
•Reflexes include:
•Activation or inhibition of glandular
secretions
•Smooth muscle activity
Slide
14.47b
Digestion and Absorption in the

Stomach
•Proteases act on:

•Pepsin –protein digestion
•Rennin –milk protein digestion
•Absorption of:
•Water, alcohol and aspirin
Slide
14.55
 Digestion in the Small Intestine
•Pancreatic enzymes provide…

•Complete digestion of starch
•Amylase
•Other carbohydrases
•About half protein digestion (trypsin, etc.)
Slide
14.57a
 Digestion in the Small Intestine
•Pancreatic enzymes, cont…

•Fat digestion (lipase)
•Nucleic acid digestion (nucleases)
•Alkaline content neutralizes acidic chyme
Slide
14.57b
Stimulation of the Release of

Pancreatic Juice
•Vagus nerve
•Local hormones
•Secretin
•Cholecystokini
n
Figure 14.15
Slide
14.58
 Absorption in the Small Intestine
•Water
•Products of digestion
•Most molecules absorbed by active
transport
•Lipids absorbed by diffusion
•Nutrients transported to the liver
Slide
14.59
 Nutrition
•Nutrient – substance used by the body
for growth, maintenance, and repair
•Categories of nutrients
•Carbohydrates
•Lipids
•Proteins
•Vitamins
•Mineral
•Water
Slide
14.63
 Cellular Metabolism
•“All the chemical reactions necessary to

maintain life”
•Anabolism: a constructive process
during which larger molecules are built
from smaller ones
•Usually involves condensation
•AKA dehydration synthesis
•
Slide
14.67
 Cellular Metabolism, con’t…
•Carbohydrates
•Monosaccharides = simple sugars
•Glucose, fructose
•Disaccharides = Combinations of
monosaccharides, removal of water
•Sucrose, lactose, maltose
•Polysaccharides: usually
polymers of glucose
•Starch, cellulose, chitin
•
Slide
14.67
•Lipids
•1 glycerol + 3 fatty acids
neutral fat + 3 H2O
•These are triglycerides
•Further modifications
produce:
•Phospholipids (cell
membrane)
•glycolipids (cell
membrane)
Slide
•Lipoproteins (cell 14.67
•Proteins
•Two amino acids a dipeptide
+ H2O
•Covalent bond formed is a
peptide bond
•Unique to proteins
•Polypeptides: 2-100 amino
acids
•Protein: >100 amino acids
•Require additional
Slide
modification to become 14.67
•Proteins
•Modification occurs on four levels
•Primary: string of amino
acids
•Secondary: helix or “pleat”
structures
•Tertiary: 3-D folding
•Quarternary: two or more 3-
D proteins that act as a
functional unit
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings •i.e., hemoglobin, Slide
14.67
•Proteins
•Recall from Chemistry: 

•Proteins each have a unique
3-D shape
•Shape determines function
•Loss of shape leads to loss
of function
•“denaturing” proteins
with heat, pH changes
Slide
14.67
•Proteins
•May be structural or functional
•Structural:
•Play a role in cellular
architecture
•Collagen, fibrin, actin,
myosin, etc.
•Functional:
•Play a role in cell
metabolism
Slide
•Enzymes, neurotransmitters,
14.67
•Enzymes:
•Biological catalysts
•Highly specific for a substrate
•Substrate: substance upon
which an enzyme acts
•i.e., peptidases act
only on peptide bonds
in small polypeptides
•Produced only in presence of
substrate
Slide
14.67
•Enzymes:
•Huge protein molecules
•Alter shape to conform to
shape of substrate (“wrap
around” effect)
•Average 1500/cell (>5000 in liver
cells)
•Most require co-enzymes
Slide
14.67
•Enzymes:
•Recognize substrate by
shape of binding site
•Serve to lower energy
required for reaction to occur
(activation energy)
•therefore speed up reactions
•Not changed or used up during
reaction
Slide
14.67
•Co-Enzymes:
•Required to activate enzymes
•Facilitate enzymatic reactions
•May be a metal ion (Zn++ , Cu++ ,
Fe++ )
•May be a vitamin
•Vitamins are co-enzymes
•Only function if “their”
enzyme is available
• Slide
14.67
Cellular Metabolism
• Catabolism: substances are broken
down into molecules
• “destructive” process
• Large molecules broken down into
smaller molecules
• Usually by hydrolysis
• “splitting with water”
• Adds H2O back into molecule
• Breaks covalent bonds

Cellular Metabolism
• Catabolism
• Energy is released when bonds
break
• Reverse of dehydration synthesis
(condensation)
• Hydrolysis = chemical digestion
• Occurs simultaneously (and
continuously) with anabolism
• Processes controlled by enzymes
•

Cellular Energy
• Cellular energy is chemical energy
• Derived from breaking chemical
bonds
• ~ ½ Energy is stored as ATP
• ~ ½ Energy is released as heat
• Helps maintain body
temperature
• Enzymes control in the process

Cellular Energy
 All nutrient molecules are ultimately
degraded or converted to glucose
 Only glucose can be used to make
ATP
 Oxidation: cellular process of
chemically breaking apart a
glucose molecule to release
energy
Cellular Energy
 Glucose oxidation occurs in 2
phases
 Anerobic metabolism
 Occurs in cytoplasm
 Without oxygen
 AKA glycolysis
 Splits glucose into two 3-Carbon
molecules: pyruvate
Cellular Energy
 Glycolysis
 Process also produces 2 ATPs
 In yeast, plant cells:
 Pyruvate can undergo alcoholic
fermentation
 In bacteria, animal cells:
 Pyruvate can produce lactic acid
Cellular Energy
 Aerobic metabolism
 Uses oxygen
 AKA Kreb’s Cycle or Citric Acid
cycle or Tricarboxylic Acid (TCA)
Cycle
 Occurs in mitochondria
 Makes more ATP than anerobic
processes
Cellular Energy
 CO2 and H2O are waste products
 CO2:
 Diffuses out of cells
 Dissolves in plasma
 Produces HCO3- in blood
 Exhaled from lungs
Cellular Energy
 H2O:
 “metabolic” water
 Exhaled from lungs
 Final products of glucose oxidation:
 CO2, H2O, ATP
Cellular Energy
 For each molecule of glucose:
 2 ATP formed in glycolysis
 36 ATP formed in TCA cycle
 Energy stored in phosphate bonds
 A reversible reaction
Metabolic Pathways
 “A particular sequence of enzymatic
reactions”
 Such as glycolysis, TCA cycle
 Carbohydrate pathways
 Carbos should comprise most of
our diet (~ 50% complex carbs)
 Used as a primary energy source
 Produce 4kcal/gm
Metabolic Pathways
 Carbohydrate pathways
 Excess carbs converted to energy
storage forms
 Glycogen (muscle, liver)
 Adipose tissue (hips)
 Process is anabolism
Metabolic Pathways
 Lipid pathways
 Metabolism controlled by liver
 Should comprise <30% of calories
in diet
 Get 9 kcal/gm (more ATP!)
 Must be degraded into glycerol,
fatty acids, then pyruvate
 A reversible catabolic process

Metabolic Pathways
 Protein pathways
 Proteins should comprise ~30% of
diet
 Get 4 kcal/gm
 Catabolism is more complex
 Proteins contain nitrogen
Metabolic Pathways
 Deamination: removal of nitrogen
from amino acids
 Occurs in liver
 Nitrogen is converted to urea
 A nitrogenous waste product
 Sent to kidneys for excretion
Metabolic Pathways
 After deamination:
 amino acid “skeleton” is processed
 in TCA cycle
 May produce CO2, H2O, ATP
 May form glucose or fat
Metabolic Pathways
 Glucose formed from amino acid
skeletons may be re-converted to
amino acids
 “Essential” amino acids:
 Body cannot make these
 Must obtain in the diet
Regulation of Metabolic
Pathways
 Enzyme “saturation”
 Too much substrate for number of
enzyme molecules
 Reaction rate cannot increase
 A single enzyme can control an
entire metabolic pathway
 “rate limiting” enzyme

 Digestive System: Disorders
•Ulcers: bacterial infection with H. pylori

•Vomiting: controlled by center in medulla
oblongata
•Activity of tract slows in old age
•Fewer digestive juices
•Peristalsis slows
•Diverticulosis and cancer more common
Slide
14.92b
 Digestive System: Disorders
•IBS: irritable bowel syndrome

•Crohn’s disease (autoimmune)
•Constipation
•Diarrhea
•Colitis
•Colon polyps/cancers
Slide
14.92b
Review !!!!!
Activation of Pepsin
Chief PEPSIN-OGEN PEPSIN

Cell
HCl
Digests
Parietal Protein
Cell
STIMULATION OF GASTRIC
SECRETION: Cephalic Phase
Seeing, Vagus Intrinsic Nerves Parietal
Smelling, & Chief
Tasting Pyloric Area Cells
Food
Increased
Gastrin Gastric
Secretion
STIMULATION OF GASTRIC
SECRETION: Gastric Phase
Stimuli Intrinsic Nerves Parietal
in Stomach: Vagus & Chief
protein, Pyloric Area Cells
distension,
caffeine,
alcohol
Increased
Gastrin Gastric
Secretion
THE GASTRIC MUCOSAL
BARRIER
• Protects the cells from contents of
stomach
• Luminal membranes of cells are
impermeable to protons
• Cells are tightly adjoined
• Rapid turnover
• If broken, peptic ulcer may result: positive
feedback involving histamine
Gastrin secretion inhibition
• Acid in antrum
•
• removal of protein as stomach empties
PANCREATIC AND BILLIARY
SECRETIONS
• THE PANCREAS IS BOTH ENDOCRINE AND
EXOCRINE
• THE EXOCRINE PANCREAS SECRETES DIGESTIVE
ENZYMES AND AN AQUEOUS ALKALINE FLUID
• PANCREATIC SECRETION IS HORMONALLY
REGULATED
• PANCREATIC SECRETIONS REACH THE SMALL
INTESTINE VIA THE COMMON BILE DUCT
THE EXOCRINE PANCREAS
SECRETES DIGESTIVE ENZYMES
• PROTEOLYTIC ENZYMES
• PANCREATIC AMYLASE
• PANCREATIC LIPASE
HORMONAL CONTROL OF
PANCREATIC SECRETION
• ACID IN DUODENAL LUMEN >SECRETIN:
STIMULATES PANCREATIC DUCT CELLS
TO PRODUCE SIGNIFICANT QUANTITES
OF AQUEOUS ALKALINE SECRETION
• FAT AND PROTEIN IN DUODENAL
LUMEN>CHOLECYSTOKININ
(CCK):STIMULATES PANCREATIC ACINAR
CELLS TO SECRETE DIGESTIVE ENZYMES
FUNCTIONS OF THE LIVER
• METABILIC PROCESSING OF ABSORBED
FOOD
• DETOXIFICATION2
• SYNTHESIS OF PLASMA PROTEINS
• STORAGE OF GLYCOGEN AND FAT, ETC.
• REMOVAL OF BACTERIA AND WORN-OUT
RBC
• EXCRETION OF CHOLESTEROL AND
BILIRUBIN
•
BILE SECRETION, STORAGE,
AND CIRCULATION
• SECRETED BY THE LIVER
• RECYCLED THROUGH
ENTEROHEPATIC CIRCULATION
• STORED IN GALL BLADDER
LIVER BLOOD FLOW
INFERIOR
VENA CAVA AORTA
HEART
HEPATIC HEPATIC
VEIN ARTERY
LIVER
HEPATIC
PORTAL ARTERIES TO
VEIN DIGESTIVE TRACT
STOMACH
AND
SMALL
INTESTINE
BILE SALT CIRCULATION
LIVER
GALL BLADDER
SPHINCTER
OF ODDI
DUODENUM
S.I. MOTILITY
• SEGMENTATION CONTRACTIONS
•
• PACEMAKER CELLS
•
• MIXING AND PROPULSION
SEGMENTATION
CONTRACTIONS
• INITIATED BY PACEMAKER CELLS

• MIXING ACTION
• MOVES CHYME DOWNWARD
• ILEOCECAL VALVE
S.I. SECRETIONS
• MANLY MUCOUS
•
• NO DIGESTIVE ENZYMES
DIGESTION
• MAINLY IN THE SMALL INTESTINE
•
• PANCREATIC ENZYMES
•
• BRUSH BORDER ENZYMES
ABSORPTION
• LARGE SURFACE AREA
• ACTIVE SODIUM TRANSPORT
• FLUID AND ELECTROLYTES
• SUGARS AND AA BY SECONDARY
ACTIVE TRANSPORT
• FAT
• VITAMINS AND MINERALS
•
LARGE SURFACE AREA
• LONG TUBE
• CIRCULAR FOLDS
• VILLI
• MICROVILLI
• SIZE OF TENIS COURT
FLUID AND ELECTROLYTES
• SODIUM IS ACTIVELY TRANSPORTED ALONG
CELL’S BASOLATERAL MEMBRANE
• CHLORIDE FOLLOWS FOR ELECTRONEUTRALITY
• WATER FOLLOWS FOR OSMOTIC BALANCE
• POTASSIUM AND OTHER ELECTROLYTES ARE
MAINLY ABSORBED BY PASSIVE DIFFUSION
Absorption is a Function of the Epithelial Cells
Making up the Intestinal Wall
Lumen
Cells
Plasma
Sodium Absorption
PUMP: Na/K ATPase
Lumen Sodium
Cells
Potassium
Plasma
Chloride
Water
AVERAGE DAILY INTAKE OF IRON
(NORTH AMERICA AND EUROPE)
• BETWEEN 10 AND 30 mg
• ABOUT 5 TO 7 mg PER 1000 CALORIES
• IF ON A 1000 TO 1500 CALORIE DIET,
ONLY 6-9 mg
• INFLUENCED BY COOKING UTENSILS
• DEPENDS ON BEVERAGE
CONSUMPTION
THE LARGE INTESTINE
• PRIMARILY A DRYING AND STORAGE
ORGAN
• HAUSTRAL CONTRACTIONS
• MASS MOVEMENTS
• PROTECTIVE SECRETIONS
• FORMATION OF FECES
THE DEFICATION REFLEX
• DISTENTION OF RECTUM STIMULATES
• INTERNAL ANAL SPHINCTER (SMOOTH
MUSCLE) RELAXES
• EXTERNAL ANAL SPHINCTER
(SKELETAL MUSCLE) UNDER
VOLUNTARY CONTROL
GASTROINTESTINAL
HORMONES
• GASTRIN
• SECRETIN
• CHOLECYSTOKININ
GASTRIN
• ENDOCRINE CELLS IN PYLORIC STOMACH
• STIMULATED BY PROTEIN IN STOMACH
• STIMULATES SECRETION BY PARIETAL AND
CHIEF CELLS
• STIMULATES ILEAL MOTILITY
• RELAXES ILEOCECAL SPHINCTER
• INDUCES COLONIC MASS MOVEMENTS
SECRETIN
• ENDOCRINE CELLS IN DUODENAL MUCOSA
• ACID IN DUODENAL LUMEN
• INHIBITS GASTRIC EMPTYING
• INHIBITS GASTRIC SECRETION
• STIMULATES AQUEOUS BICARBONATE SECRETION
BY PANCREAS
• STIMULATES BICARBONATE RICH BILE SECRETION
BYLIVER
•
CHOLECYSTOKININ
• ENDOCRINE CELLS IN DUODENAL MUCOSA
• FAT AND PROTEIN IN DUODENAL LUMEN
• INHIBITS GASTRIC EMPTYING
• INHIBITS GASTRIC SECRETION
• CAUSES GALL BLADDER CONTRACTION
• CAUSES RELAXATION OF THE SPHINCTER OF ODDI
• CONTRIBUTES TO SATIETY
TOTAL BODY IRON IN
HUMANS
• WEIGHT
• SEX
• SIZE OF STORAGE COMPARTMENT
• HEMOGLOBIN CONCENTRATION
• HISTORY
ABSORPTION OF IRON FROM
FOODS
FOOD DOSE (mg) % ABSORBED
RICE 2 1
SPINACH 2 2-3
LETTUCE 17 3-5
WHEAT 2-4 5
VEAL 3 10-18
LIVER
FISH 1-2 10-15

VEAL 3-4 20
MUSCLE
HEMOGLOBIN 3-4 10-15

SOME DISEASES LINKED WITH DIET
• CANCER
• HEART DISEASE
• HIGH BLOOD PRESSURE
• OBESITY
• DIVERTICULITIS
FOOD INGREDIENTS AND DISEASE
• REFINED SUGAR
• FAT
• SALT
• LOW IN FIBER
CANCER AND DIET: PHYTOCHEMICALS
• FOUND ONLY IN PLANTS

• IMMUNE FUNCTION
• HORMONE BALANCE
• DETOXIFICATION
•
CANCER AND DIET N.R.C.RECOMMENDATIONS
• EAT LESS FAT (30% OR LESS 0F TOTAL

CALORIES)
• EAT FRUITS, VEGITABLES, AND WHOLE-
GRAIN CEREAL FOODS EVERY DAY
(ESPECIALLY THOSE HIGH IN VITAMINS A
AND C)
• AVOID HIGH DOSE SUPPLIMENTS OF
VITAMINS OR OTHER NUTRIENTS
• ALCOHOL ONLY IN MODERATION
PROTEIN SOURCES-EXCEPTIONS
• SOYBEANS
•
• QUINONA
•
• SPINACH
•
• HAVE THE SAME QUALITY AS MILK
INCOMPLETE PROTEINS NEEDED TO MEET
REQUIREMENTS
• 2 2/3 CUPS COOKED WHEAT

• 3 CUPS COOKED RICE
• 5 3/4 SLICES BASIC BREAD
• 3 CUPS DICED POTATOES
• 1/3 CUP SOY SPREAD
• 1/2 CUP WHEAT GERM
• 2 3/4 CUPS RICE WITH 1/3 CUP COOKED
PEAS
SOME WAYS TO CUT DOWN ON FAT
• EAT MORE VEGETARIAN MEALS

• EAT MORE FRESH FRUIT OR YOGURT
INSTEAD OF DESSERTS
• USE YOGURT AS DRESSING INSTEAD
OF OIL
• USE FRESH HERBS INSTEAD OF
BUTTER (AND INSTEAD OF SALT)
•
FIBER
• ROUGHLY SPEAKING, EVERYTHING IN
PLANT FOODS OUR DIGESTIVE ENZYMES
CAN NOT BREAK DOWN
• NURTURES AEROBIC BACTERIA IN GUT
• SOLUABLE FIBER REDUCES INSULIN NEED
IN DIABETICS
• CHELATORS-INCREASE NEED FOR
MINERALS
TYPES OF FIBER
• PECTINS: IN CELL WALL OF FRUITS, BIND BILE
SALTS
• GUMS: STICKY SUBSTANCES EXUDED BY PLANTS,
LOWER CHOLESTEROL UPTAKE AND SLOW
SUGAR ABSORPTION
• CELLULOSE: PLANT CELL WALLS, BULK AND TOXIN
ELIMINATION
• HEMICELLULOSES: PLANT CELL WALLS, BULK
• LIGNIN: ROOT VEGETABLES, BULK
EFFECT ON MICROFLORA
• LOWER TOTAL ANAEROBIC, IN
PARTICULAR, CLOSTRIDIUM
• DIET CAN ALTER THE METABOLIC
ACTIVITY OF THE FLORA
• MEAT AND UNREFINED SUGAR
INCREASES UNWANTED BACTERIA
• VEGETARIAN DIET LOWERS RISKS OF
BOWEL CANCER
RECOMMENDED FIBER INTAKE
• 20 - 25 g/day WITH AN UPPER LIMIT OF
35 g/day
•
• FAMILY HISTORY OF DIET-IMPLICATED
CANCER 35-40 g/day
•
• DIABETICS UP TO 50 g/day
SOURCES OF FIBER
• LEGUMES (ALSO PROTEIN SOURCE)
•
• FRUITS AND VEGETABLES
•
• WHOLE GRAIN CEREALS AND FLOURS
SOLUABLE AND INSOLUABLE DIETARY FIBER
• SOLUABLE • INSOLUABLE
• SOME • LIGNIN
HEMICELLULOSE • CELLULOSE
• PECTIN • SOME
• GUM HEMICELLULOSE
• MUCILAGES
CHELATORS LOWER MINERAL ABSORPTION
• PHYTATES
•
• OXALATES
SUPPLIMENTS FROM PLANTS
• ECHINACEA: IMMUNE BOOSTING AND ANTIBIOTIC
• PSYLLIUM SEEDS: SOURCE OF FIBER
• CHAMOMILE: MILD SEDATIVE
• ALOE VERA: PROMOTES HEALING
• SAW PALMETTO EXTRACT: PROSTATE PROBLEMS
• GREEN TEA: ANTI CANCER , ANTIOXIDENT
• GARLIC: ANTIBACTERIAL, ANTIVIRAL, LOWERS
CHOLESTEROL
Chapter 18
The Digestive
System
Functions of the GI Tract
§ Motility:
 Movement of of food through the GI tract.
 Ingestion:
 Taking food into the mouth.
 Mastication:
 Chewing the food and mixing it with saliva.
 Deglutition:
 Swallowing the food.
 Peristalsis:
 Rhythmic wave-like contractions that move food
through GI tract.
Functions of the GI Tract (continued)
Secretion:

 Includes both exocrine and endocrine

secretions.
 Exocrine:
 HCl, H20, HC03-, bile, lipase, pepsin, amylase,
trypsin, elastase, and histamine are secreted into
the lumen of the GI tract.
 Endocrine:
 Stomach and small intestine secrete hormones to
help regulate the GI system.
 Gastrin, secretin, CCK, GIP, GLP-1, guanylin, VIP,
and somatostatin.
Functions of the GI Tract (continued)
 Digestion:
 Breakdown of food particles into subunits
(chemical structure change).
 Absorption:
 Process of the passage of digestion
(chemical subunits) into the blood or
lymph.
 Storage and elimination:
 Temporary storage and elimination of
indigestible food.
Digestive System (GI)
GI tract divided

Insert fig. 18.2
into:
 Alimentary
canal.
 Accessory
digestive
organs.
GI tract is 30 ft

long and
extends from
mouth to anus.
Layers of GI Tract
Composed of 4

tunics:
 Mucosa.
 Submucosa.
nMuscularis.
nSerosa.
Mucosa
Lines the lumen of GI tract.


 Consists of simple columnar epithelium.

Lamina propria:

 Thin layer of connective tissue containing lymph

nodules.
Muscularis mucosae:

 Thin layer of smooth muscle responsible for the

folds.
 Folds increase surface area for absorption.
Goblet cells:

 Secrete mucus.
Submucosa
Thick, highly vascular layer of connective

tissue.
Absorbed molecules enter the blood and
lymphatic vessels.
Submucosal plexus (Meissner’s plexus):
 Provide autonomic nerve supply to the

muscularis mucosae.
Muscularis
Responsible for segmental contractions and


peristaltic movement through the GI tract.

 Inner circular layer of smooth muscle.
 Outer longitudinal layer of smooth muscle.
Contractions of these layers move food through
the tract; pulverize and mix the food.
Myenteric plexus located between the 2 muscle
layers.
 Major nerve supply to GI tract.
 Fibers and ganglia from both sympathetic

and parasympathetic nervous systems.
Serosa
• Binding and protective outer layer.

• Consists of areolar connective tissue covered
with simple squamous epithelium.
Regulation of the GI Tract
Extrinsic innervation:

 Parasympathetic nervous system:
 Vagus and spinal nerves:

 Stimulate motility and GI secretions.
 Sympathetic nervous system:

 Postganglionic sympathetic fibers that pass
through submucosal and myenteric
plexuses and innervate GI tract:
 Reduce peristalsis and secretory
activity.
Regulation of the GI Tract (continued)
Enteric nervous system:


 Sites where parasympathetic fibers synapse with

postganglionic neurons that innervate smooth
muscle.
Submucosal and myenteric plexuses:

 Local regulation of the GI tract.

Paracrine secretion:

 Molecules acting locally.

Hormonal secretion:

 Secreted by the mucosa.

From Mouth to Stomach
Mastication (chewing):

 Mixes food with saliva which contains salivary

amylase.
 Enzyme that can catalyze the partial digestion of
starch.
Deglutition (swallowing):

 Begins as a voluntary activity.

 Involves 3 phases:
 Oral phase is voluntary.
 Pharyngeal and esophageal phases are involuntary.
 Cannot be stopped.
 Larynx is raised.
 Epiglottis covers the entrance to respiratory tract.
From Mouth to Stomach (continued)
Involuntary muscular contractions and

relaxations in the mouth, pharynx, larynx, and
esophagus are coordinated by the swallowing
center in the medulla.
Esophagus:
 Connects pharynx to the stomach.

 Upper third contains skeletal muscle.
 Middle third contains a mixture of skeletal and
smooth muscle.
 Terminal portion contains only smooth muscle.

Esophagus
Peristalsis:

 Produced by a series of Insert 18.4a

localized reflexes in
response to distention
of wall by bolus.
Wave-like muscular

contractions:
 Circular smooth
muscle contract
behind, relaxes in
front of the bolus.
 Followed by
longitudinal
contraction
(shortening) of
smooth muscle.
 Rate of 2-4 cm/sec.
Stomach
Most distensible part of GI tract.


 Empties into the duodenum.

Functions of the stomach:

 Stores food.
 Initiates digestion of proteins.
 Kills bacteria.
 Moves food (chyme) into intestine.

Stomach (continued)
Contractions of

the stomach
churn chyme. Insert fig. 18.5
 Mix
chyme
with
gastric
secretio
ns.
 Push food
into
intestin
e.
Stomach (continued)
• Gastric mucosa
has gastric Insert fig. 18.7
pits in the
folds.
• Cells that line
the folds
deeper in the
mucosa, are
gastric
glands.
Gastric Glands
Secrete gastric juice:


 Goblet cells: mucus.

 Parietal cells: HCl and intrinsic factor.
 Chief cells: pepsinogen.
 Enterochromaffin-like cells (ECL):
histamine and serotonin.
 G cells: gastrin.
 D cells: somatostatin.
 Stomach: ghrelin.
HCl Production
• Parietal cells
secrete H+ into
gastric lumen
by primary Insert fig. 18.8
active
transport,
through H+/ K+
ATPase pump.
• Parietal cell’s
basolateral
membrane
takes in Cl-
against its
electrochemica
l gradient, by
coupling its
transport with
HC03-.
HCl Production (continued)
HCl production is stimulated:


 Indirectly by gastrin.
 Indirectly by ACh.
ACh and gastrin stimulate release of

histamine.
 Histamine:
 Stimulates parietal cells to secrete HCl.
HCl Functions
Makes gastric juice


very acidic. Insert fig. 18.9

 Denatures
ingested
proteins
(alter tertiary
structure) so
become
more
digestible.
Activates

pepsinogen to
pepsin.
 Pepsin is more
active at pH
of 2.0.
Digestion and Absorption in the
Stomach
• Proteins partially digested by pepsin.

• Carbohydrate digestion by salivary
amylase is soon inactivated by acidity.
• Alcohol and aspirin are the only
commonly ingested substances
absorbed.
Gastric and Peptic Ulcers
Peptic ulcers:

 Erosions of the mucous membranes of the stomach or

duodenum produced by action of HCl.
Zollinger-Ellison syndrome:

 Ulcers of the duodenum are produced by excessive

gastric acid secretions.
Helicobacter pylori:

 Bacterium that resides in GI tract that may produce

ulcers.
Acute gastritis:

 Histamine released by tissue damage and

inflammation stimulate further acid secretion.
Protective Mechanisms of Stomach
• Parietal and chief cells impermeable to

HCl.
• Alkaline mucus contains HC03-.
• Tight junctions between adjacent
epithelial cells.
• Rapid rate of cell division (entire
epithelium replaced in 3 days).
• Prostaglandins inhibit gastric secretions.
Small Intestine
• Each villus is a fold in

the mucosa. Insert fig. 18.12
• Covered with columnar
epithelial cells
interspersed with
goblet cells.
• Epithelial cells at the tips
of villi are exfoliated
and replaced by
mitosis in crypt of
Lieberkuhn.
• Lamina propria contain
lymphocytes,
capillaries, and
Absorption in Small Intestine
Duodenum and jejunum:


 Carbohydrates, amino acids, lipids, iron, and

Ca2+ .
Ileum:

 Bile salts, vitamin B12 , electrolytes, and H20.

Intestinal Enzymes
 Microvilli contain brush border enzymes that
are not secreted into the lumen.
 Brush border enzymes remain attached to the
cell membrane with their active sites exposed
to the chyme.
 Absorption requires both brush border
enzymes and pancreatic enzymes.
Intestinal Contractions and Motility
2 major types of

contractions occur in the

small intestine: Insert fig. 18.14
 Peristalsis:
 Slow movement.
 Pressure at the pyloric
end of small intestine
is greater than at the
distal end.
 Segmentation:
 Major contractile
activity of the small
intestine.
 Contraction of circular
smooth muscle.
 Mix chyme.
Contractions of Intestinal Smooth
Muscles
Occur automatically in
response to Insert fig. 18.15
endogenous
pacemaker activity.
Rhythm of contractions is
paced by graded
depolarizations called
slow waves.
 Slow waves
produced by
interstitial cells of
Cajal.
 Slow waves spread
from 1 smooth
muscle cell to
Contractions of Intestinal Smooth
Muscles
 When slow waves above threshold, it triggers

APs by opening of VG Ca2+ channels.

Inward flow of Ca2+ :
 Produces the upward depolarization phase.
 Stimulates contraction of smooth muscle.
 Repolarization:
 VG K+ channels open.
 Slow waves decrease in amplitude as they are
conducted.
 May stimulate contraction in proportion to the
magnitude of depolarization.
Cells and Electrical Events in the
Muscularis
Insert fig. 18.16

Large Intestine
Outer surface bulges outward to form haustra.

Little absorptive function.
 Absorbs H20, electrolytes, several vitamin B complexes,

vitamin K, and folic acid.
 Intestinal microbiota produce significant amounts of folic acid
and vitamin K.
 Bacteria ferment indigestible molecules to produce short-
chain fatty acids.
 Does not contain villi.
Secretes H20, via active transport of NaCl into intestinal

lumen.
 Guanylin stimulates secretion of Cl- and H20, and
inhibits absorption of Na+ (minor pathway).

Membrane contains Na+/K+ pumps.
 Minor pathway.
Fluid and Electrolyte Absorption in
the Intestine
Small intestine:

 Most of the fluid and electrolytes are absorbed by

small intestine.
 Absorbs about 90% of the remaining volume.
 Absorption of H20 occurs passively as a result of
the osmotic gradient created by active transport.
 Aldosterone stimulates NaCl and H20 absorption in the
ileum.
Large intestine:

 Absorbs about 90% of the remaining volume.

 Absorption of H20 occurs passively as a result of the osmotic
gradient created by active transport of Na+ and Cl-.

Defecation
Waste material passes to the rectum.
Occurs when rectal pressure rises and
external anal sphincter relaxes.

Defecation reflex:
 Longitudinal rectal muscles contract to

increase rectal pressure.
 Relaxation of internal anal sphincter.
 Excretion is aided by contractions of
abdominal and pelvic skeletal muscles.
 Push feces from the rectum.
Structure of Liver
Liver largest internal organ.


 Hepatocytes form hepatic plates that are 1–2 cells

thick.
 Arranged into functional units called lobules.
Plates separated by sinusoids.

 More permeable than other capillaries.

Contains phagocytic Kupffer cells.
Secretes bile into bile canaliculi, which are drained
by bile ducts.
Structure of Liver (continued)
Insert fig. 18.20

Hepatic Portal System
Products of digestion that are absorbed are
delivered to the liver.
Capillaries drain into the hepatic portal vein,
which carries blood to liver.

 ¾ blood is deoxygenated.
 Hepatic vein drains liver.
Enterohepatic Circulation
Compounds that

recirculate between
liver and intestine.
 Many compounds Insert fig. 18.22
can be absorbed
through small
intestine and
enter hepatic
portal blood.
 Variety of
exogenous
compounds are
secreted by the
liver into the bile
ducts.
Can excrete these

Major Categories of Liver Function
Bile Production and Secretion
The liver produces and secretes 250–1500 ml of

bile/day.
Bile pigment (bilirubin) is produced in spleen, bone
marrow, and liver.

 Derivative of the heme groups (without iron) from
hemoglobin.
Free bilirubin combines with glucuronic acid and forms

conjugated bilirubin.
 Secreted into bile.
Converted by bacteria in intestine to urobilinogen.

 Urobilogen is absorbed by intestine and enters the

hepatic vein.
 Recycled, or filtered by kidneys and excreted in urine.
Metabolism of Heme and Bilirubin
Insert fig. 18.23

Bile Production and Secretion (continued)
Bile acids are derivatives of


cholesterol.
 Major pathway of Insert fig. 18.25
cholesterol
breakdown in the
body.
Principal bile acids are:

 Cholic acid.
 Chenodeoxycholic
acid.
 Combine with glycine
or taurine to form
bile salts.
 Bile salts
aggregate as
micelles.
Detoxification of the Blood
Liver can remove hormones, drugs, and other


biologically active molecules from the blood

by:
 Excretion into the bile.
 Phagocytosis by Kupffer cells.
 Chemical alteration of the molecules.
 Ammonia is produced by deamination of amino acids
in the liver.
 Liver converts it into urea.
 Excreted in urine.
Detoxification of the Blood (continued)
Inactivation of steroid hormones and


drugs.
 Conjugation of steroid hormones and
xenobiotics make them anionic.
 Can be transported into bile by multispecific
organic anion transport carriers.
 Steroid and xenobiotic receptors stimulate
production of cytochrome P450
enzymes.
Secretion of Glucose, Triglycerides
and Ketones
Liver helps regulate blood glucose

concentration by:
 Glycogenesis and lipogenesis.
 Glycogenolysis and gluconeogenesis.
Contains enzymes required to convert free

fatty acids into ketone bodies.

Production of Plasma Proteins
Albumin and most of the plasma globulins

(except immunoglobulins) are produced by
the liver.
Albumin:
 Constitutes 70% of the total plasma protein.

 Contributes most to the colloid osmotic pressure
in the blood.
 Globulins:
 Transport cholesterol and hormones.
 Inhibit trypsin.
 Produce blood clotting factors I, II, III, V, VII,
IX, XI.
Gallbladder
Sac-like organ attached to the inferior surface of
the liver.
Stores and concentrates bile.
When gallbladder fills with bile, it expands.
 Contraction of the muscularis layer of the

gallbladder, ejects bile into the common bile duct
into duodenum.
When small intestine is empty, sphincter of Oddi

closes.
 Bile is forced up to the cystic duct to gallbladder.
Pancreas
Exocrine:

Insert fig. 18.26
 Acini:
 Secrete
pancre
atic
juice.
Endocrine:

 Islets of
Langerha
ns:
 Secrete
insulin
and
glucag
on.
Pancreatic Juice
• Contains H20, HC03- and digestive enzymes.

•
Pancreatic Juice
 Complete digestion of food

requires action of both
pancreatic and brush
border enzymes.
 Most pancreatic Fig. 18.29
enzymes are
produced as
zymogens.
 Trypsin (when
activated by
enterokinase)
triggers the
activation of other
pancreatic
enzymes.
 Pancreatic trypsin inhibitor
attaches to trypsin.
 Inhibits its activity in
the pancreas.
Neural and Endocrine Regulation
• Neural and endocrine mechanisms modify

the activity of the GI system.
• GI tract is both an endocrine gland, and a
target for the action of hormones.
Regulation of Gastric Function
Gastric motility and secretion are automatic.

Waves of contraction are initiated
spontaneously by pacesetter cells.

Extrinsic control of gastric function is divided
into 3 phases:
 Cephalic phase.
 Gastric phase.
 Intestinal phase.
Cephalic Phase
Stimulated by sight, smell, and taste of food.
Activation of vagus:
 Stimulates chief cells to secrete
pepsinogen.
 Directly stimulates G cells to secrete
gastrin.
 Directly stimulates ECL cells to secrete
histamine.
 Indirectly stimulates parietal cells to
secrete HCl.

Continues into the 1st 30 min. of a meal.
Gastric Phase
Arrival of food in stomach stimulates the gastric phase.
Gastric secretion stimulated by:
 Distension.
 Chemical nature of chyme (amino acids and short
polypeptides).
 Stimulates G cells to secrete gastrin.
 Stimulates chief cells to secrete pepsinogen.
 Stimulates ECL cells to secrete histamine.
 Histamine stimulates secretin of HCl.
 Positive feedback effect.
 As more HCl and pepsinogen are secreted, more
polypeptides and amino acids are released.

Gastric Phase (continued)
Secretion of HCl is also


regulated by a
negative feedback
effect:
Insert. Fig. 18.30
 HCl secretion
decreases if pH
< 2.5.
 At pH of 1.0,
gastrin secretion
ceases.
 D cells
stimulate
secretion of
somatostatin
.
 Paracrin
e
Intestinal Phase
Inhibits gastric activity when chyme enters the
small intestine.
Arrival of chyme increases osmolality and
distension.
 Activates sensory neurons of vagus and produces
an inhibitory neural reflex:
 Inhibits gastric motility and secretion.
 In the presence of fat, enterogasterone inhibits gastric
motility and secretion.
Hormone secretion:

 Inhibit gastric activity:

 Somatostatin, CCK, and GLP-1.

Enteric Nervous System
• Submucosal and myenteric plexuses

contain 100 million neurons.
• Include preganglionic parasympathetic
axons, ganglion cell bodies,
postganglionic sympathetic axons;
and afferent intrinsic and extrinsic
sensory neurons.
Enteric Nervous System (continued)
• Peristalsis:
• ACh and
substance P Insert fig. 18.31
stimulate
smooth
muscle
contraction
above the
bolus.
• NO, VIP, and
ATP stimulate
smooth
muscle
relaxation
Paracrine Regulators of the Intestine
Serotonin (5-HT):

 Stimulates intrinsic afferents, which send impulses

into intrinsic nervous system; and activates motor
neurons.
Motilin:

 Stimulates contraction of the duodenum and stomach

antrum.
Guanylin:

 Activates guanylate cyclase, stimulating the

production of cGMP.
 cGMP stimulates the intestinal cells to secrete Cl- and H20.
 Inhibits the absorption of Na+.
Uroguanylin:

 May stimulate kidneys to secrete salt in urine.

Intestinal Reflexes
Intrinsic and extrinsic regulation controlled by

intrinsic and paracrine regulators.
Gastroileal reflex:
 Increased gastric activity causes increased motility

of ileum and movement of chyme through
ileocecal sphincter.
Ileogastric reflex:

 Distension of ileum, decreases gastric motility.

Intestino-intestinal reflex:

 Overdistension in 1 segment, causes relaxation

throughout the rest of intestine.
Secretion of Pancreatic Juice
Secretion of pancreatic juice and bile is stimulated by:

Secretin:
 Occurs in response to duodenal pH < 4.5.
 Stimulates production of HC0 - by pancreas.

3
 Stimulates the liver to secrete HC0 - into the bile.
3
CCK:

 Occurs in response to fat and protein content of

chyme in duodenum.
 Stimulates the production of pancreatic enzymes.
 Enhances secretin.
 Stimulates contraction of the sphincter of Oddi.
Digestion and Absorption of
Carbohydrates
Salivary amylase:

Begins starch
Insert fig. 18.32

digestion.
Pancreatic amylase:

 Digests starch to
oligosaccharides.
 Oligosaccharides
hydrolyzed by
brush border
enzymes.
Glucose is transported

by secondary active
transport with Na+ into
the capillaries.
Digestion and Absorption of Protein
Digestion begins in the stomach when pepsin

digests proteins to form polypeptides.
In the duodenum and jejunum:
 Endopeptidases cleave peptide bonds in the

interior of the polypeptide:
 Trypsin.
 Chymotrypsin.
 Elastase.
 Exopeptidases cleave peptide bonds from the

ends of the polypeptide:
 Carboxypeptidase.
 Aminopeptidase.
Digestion and Absorption of Protein
(continued)
• Free amino acids

absorbed by
cotransport
with Na+.
• Dipeptides and
tripeptides
transported by
Insert fig. 18.33
secondary
active transport
using a H+
gradient to
transport them
into the
cytoplasm.
• Hydrolyzed into
free amino
Digestion and Absorption of Lipids
Arrival of lipids in the duodenum serves as a

stimulus for secretion of bile.
Emulsification:
 Bile salt micelles are secreted into duodenum to

break up fat droplets.
Pancreatic lipase and colipase hydrolyze

triglycerides to free fatty acids and

monglycerides.
 Colipase coats the emulsification droplets and
anchors the lipase enzyme to them.
 Form micelles and move to brush border.
Digestion and Absorption of Lipids
(continued)
Free fatty acids, monoglycerides, and


lysolecithin leave micelles and enter into

epithelial cells.
 Resynthesize triglycerides and phospholipids
within cell.
 Combine with a protein to form chylomicrons.
Secreted into central lacteals.

Transport of Lipids
In blood, lipoprotein lipase hydrolyzes

triglycerides to free fatty acids and glycerol for
use in cells.
Remnants containing cholesterol are taken to
the liver.
 Form VLDLs which take triglycerides to cells.
 Once triglycerides are removed, VLDLs are
converted to LDLs.
 LDLs transport cholesterol to organs and blood
vessels.
 HDLs transport excess cholesterol back to liver.
Absorption of Fat
Insert fig. 18.36

The Classical Endocrine
System
• Pineal gland
• Hypothalamus / Pituitary
• Thyroid
• Parathyroid
• Thymus
• Adrenal glands
• Pancreas
• Gonads
Other Endocrine Organs
• Stomach - releases gastrin from G-cells

•
• Duodenum – CCK, secretin

•
• Heart – ANP
•
• Kidney – renin, erythropoietin

•
• Placenta - hCG
Endocrine
System
Function
• Maintenance of homeostasis
through negative feedback
loops
Endocrine System Function
 Communication between organ systems

within the body (like nervous system)

 Differs from the nervous system:

 changes take longer to occur
 and changes persist longer as well.

Endocrine System Function
• Hormones are utilized as chemical

messengers
•
• Messages are received by target cells

Hormone
s
 Recall the distinction between exocrine
and endocrine glands

 Exocrine: through a duct


 Endocrine: into the blood

Hormone
s
 Endocrine hormones are transmitted in the
bloodstream to all parts of the body

 Hormones only have an effect on those cells

that have a hormone receptor embedded in
the cell membrane (target cells)

 2 types of endocrine hormones:

 steroid & non-steroid
Hormones
Steroid Non-steroid
Derived from

Derived from an amino

cholesterol (lipid)

acid

- Lipid soluble –passes Hormone is 1st

through cell messenger
membrane to directly - Membrane receptor

cause a change in DNA alters protein inside

within the nucleus the cell, which serves
(activates a gene) as the 2nd messenger
to alter metabolism of
Hormones
Steroid Hormones
• Slower, longer lasting effect than non-
steroid hormones
•
• Derived form cholesterol

•
• Lipid soluble, need to be transported in

the
 bloodstream combined with a
transport protein


Steroid Hormones
 Mainly from the adrenal cortex and/or
gonads

 Mineralocoritcoid → aldosterone
 Glucocorticoids → cortisol, cortisone
 Sex steroids → progestin, estrogens,
androgens
Non-steroid Hormones
• Water soluble – most are transported

freely in the blood
•
• Cascade of reactions within the cell

“amplifies” the signal
•
• This type of hormone causes a more rapid

onset and shorter duration of the effect
than steroid hormones
•
Non-steroid Hormones
 Types of Non-steroid hormones

 Protein (polypeptide) – insulin, growth

hormone, FSH

 Glycoprotein – LH, TSH


 Oligopeptide – ADH, oxytocin


 Amine –norepinephrine, epinephrine,

dopamine (neurotransmitters)
Paracrine Hormones
• Do not enter the general circulation

•
• Communication from cell to cell within

a specific tissue
•
• Very low levels in the blood

•
• Have little or no effect in distant tissue

•
• Example: prostaglandins
•
Pituitary
• Interacts with many (not all) endocrine

glands as part of a feedback loop
between the hypothalamus and the
respective gland.
Pituitary
• The pituitary serves as a link between

the CNS (hypothalamus) and the rest
of the endocrine system
•
Pituitary
• The pituitary is suspended from a stalk

(infundibulum) attached to the
hypothalamus and enclosed within the
sella turcica (sphenoid bone)
Pituitary
• Actually 2 separate glands: anterior

pituitary & posterior pituitary
•
• No blood brain barrier in the

hypothalamus
Anterior
Pituitary
• The releasing hormone is secreted into a

portal system
•
• Cells in the anterior pituitary are stimulated

to secrete another hormone
•
Posterior Pituitary
• Neurons from the hypothalamus enter
the posterior pituitary and stimulate
cells to secrete hormones
•
•
Anterior Pituitary
hypothalamus GHRH PRF TRH CRH GnRH
(releasing
hormones)
pituitary GH PRL TSH ACTH FSH/LH

(tropic
hormones)
end organ muscle,bone mammary thyroid adrenal ovary &

adipose gl. cortex testes
Note:
1.GH is also called somatotropin
2.There are also inhibitory factors from the hypothalamus for G
Posterior Pituitary
ADH anti-diuretic hormone, causes kidney to

Oxytocin retain waterof smooth muscle
contraction
(uterus/childbirth & mammary gland ducts)
* failure of the posterior pituitary to secrete ADH

results in Diabetes Insipidus (DI)……if no ADH is
produced the result is production of LARGE volumes of
dilute urine
Growth Hormone
• GHRH/somatostatin  GH or
somatotropin  cells related to body
growth
•
• Produced in the ant. Pituitary

•
• Secretion declines gradually with age

•
• Many more GH producing cells in ant.

pituitary than any other type
Growth Hormone
• Increased cell division (mitosis) &

increased cell growth & differentiation
• The main effects are on cartilage,
muscle, bone, fat
• Promotes protein synthesis
(transcription/translation)
• Anti-insulin effect - elevates blood
sugar
Growth Hormone
 Catabolism of fat for energy
instead of glucose

 Muscle & bone are effected

indirectly through Insulin
like Growth Factor (IGF-1)

 increased muscle mass,

bone lengthening and
decreased fat tissue

Growth Hormone
• Continued secretion of high levels after
epiphysial plate closure is called acromegaly
•
• Bones continue to thicken even after
epiphysial plate closure
•
Growth Hormone
• Acromegaly is usually
related to a pituitary
tumor
Prolactin
• More PRF/and less PIF from the

hypothalamus
•
• Causes PRL secretion from the ant.

Pituitary
•
• Effects the mammary gland in
women/testes in men
Prolactin
 In women
 increased levels during pregnancy
 after delivery causes mammary glands to
produce milk

 In men
 increases sensitivity to LH and indirectly
enhances testosterone production
Thyroid
Gland
• TRH (hypothalamus) → TSH (pituitary) →

Thyroid hormone (Thyroid gland)
Thyroid Gland
• 2 lobes, on either
side of the
trachea,
connected by
an isthmus
Microscopic
Thyroid Gland

anatomy

• Thyroid follicles,
lined by secretory
epithelium
(follicular cells)
•
• Filled with
thyroglobulin
(transport protein)
•
• Parafollicular cells
between the
follicles
Thyroid
Function
• Secretes two
hormones
(both require
iodine as a
precursor)
•
•Thyroxine (T4) & Triiodothyronine (T3)

Thyroid Function
• (T4): 90% of all
Thyroid
hormone
•
• Less active
•
• Converted to T3 in
the cell
•
• Most remains in
the bloodstream
as reservoir of
thyroid hormone
Thyroid Function
• (T3): 5 times more

metabolically
active, but only
10% of total
hormone that is
produced
Thyroid Function
•Binds to three
sites in the cell
1.Mitochondria: increased cellular respiration

2.Ribosomes: increased protein synthesis
3.Chromatin: increased transcription DNA to
mRNA
Hyperthyroidism
 Thyroid hormones promote cellular respiration

 Cellular respiration requires oxygen, therefore

heart rate & respiratory rate are increased
 Produces heat; causes sweating

 Higher metabolic rate requires more calories,

which is a stimulus for hunger
• The most common Graves
form of
hyperthyroidism Disease
(autoimmune)
•
• Signs and symptoms

may include heat
intolerance, 
Exophthalmos may be due
appetite, weight
to an autoimmune,
loss, warm moist
inflammatory reaction in
skin, nervousness,
the soft tissue that is
tremor,  BP,
confined within the boney
tachycardia, goiter,
orbit
exophthalmos

 A goiter is an enlarged thyroid Endemic

gland Goiter

 Endemic goiter is due to lack of

iodine in the diet

 No thyroid hormone is produced so

there is no negative feedback

 The thyroid gland hypertrophies as

it “tries” to make more thyroid
hormone
Hypothyroidism
In children (cretinism)

 permanent mental retardation due to

inadequate nervous system development

In adults

 common cause of fatigue

 other symptoms are related to low BMR
 cold intolerance, weight gain,  CNS function
(mentation), BP, dry skin
Adrenal
Glands
• Each gland is
actually 2
separate
glands: the
cortex &
medulla
Adrenal Functions
Adrenal Medulla
Secretes Catecholamines

 (Epinephrine & Norepinephrine)

Derived from SNS neurons (Chromaffin

cells) that lack dendrites & axons

Adrenal Medulla
• Innervated by SNS
•
• Secretes SNS neurotransmitters mostly

Epinephrine (Adrenalin)
•
• The presence of these neurotransmitters in

the circulation lowers the threshold for
transmission of an impulse in the SNS for
about 30 min.
Epinephrine
 Elevates blood sugar – glucose sparing
effects to preserve glucose for the CNS

 glycogenolysis
 gluconeogenesis
Adrenal Cortex
3

layer
s
Adrenal Cortex
Zona mineralocorticoidsAldosterone:
Glomerulosa renal Na+ & water
Zona gluccorticoids reabsorption
Cortisol
Fasciculata
Zona sex steroids Androgen,

Reticularis Estrogen
Adrenal Cortex: Z. Glomerulosa
 Aldosterone – Na+ retention/ K+ secretion

 Water follows Sodium, so fluid volume

and BP increase too

 Recall that aldosterone secretion can be

promoted by:
1.ACTH
2.Angiotensin II
3.Low Na+
4.High K+

Adrenal Cortex: Z. Fasciculata
 Secretes Cortisol (hydrocortisone)


 Corticosterone and cortisone are two other

similar hormones that are secreted
 Steroid medication can suppress adrenal
function

1.
Adrenal Cortex: Z. Fasciculata
Two basic effects of Cortisol:



1.Glucose sparing effects: increased glucose

synthesis & protein/lipid catabolism
(gluconeogenesis)
2.Anti-inflammatory effects: inhibits WBC
function, decreased phagocytosis,
decreased chemotaxis, decreased mast
cell degranulation
1.
Adrenal Cortex: Z. Reticularis
 Sex steroids – small amount of estrogens &
weak androgens (DHEA), which is a
precursor of testosterone

 Testosterone is required in men & women –

pubic & axillary hair, libido, apocrine sweat
glands
 most testosterone is produced in testes in
men
 50% produced by the adrenal gland in
women
 Hyperfunction of the Adrenal Cushing’s
glands

Disease
 Disrupts normal
carbohydrate & protein
metabolism (Cortisol)
 characteristic lipid deposits
in the face

 Potential electrolyte
imbalance (Aldosterone)

 Mood changes
(Testosterone)

Gonads
 Ovaries  Testes
 
• Secrete estrogen & • FSH promotes

progesterone spermatogenesis
during the • LH causes interstitial
menstrual cycle cells to secrete
• FSH from the testosterone
pituitary causes • Testosterone from
maturation of the adrenal gland is
follicle & egg also present in
• LH causes women, but at much
ovulation (rupture lower levels
of the follicle – • Produces secondary
release of the sexual
egg) characteristics in
men
Parathyroid
Glands
• Not linked to the hypothalamic-pituitary

axis
•
• 4 small nodules of tissue in the thyroid

gland
Parathyroid Glands
 PTHis secreted in response to low serum
Ca++ (hypocalcemia)

1.Promotes synthesis of calcitrol (active

metabolite of vitamin D), which ↑ GI
absorption of Ca++
2.
3.Limits Ca++ secretion by the kidney

4.
5.Stimulates osteoclasts to reabsorb bone

1.
 PTH is opposed by the Parathyroid
action of calcitonin

Glands
 Secreted in response to
elevated Ca++
(hypercalcemia) by
parafollicular (C-cells)
of the thyroid gland

 Little effect in adults


 Stimulates mineral
deposition in bone by
osteoblasts
Pancreas
• Not linked to hypothalamic
pituitary axis
• Both exocrine & endocrine
functions
Pancreas
• Endocrine hormones: insulin & glucagon
secreted by cells in the islets of
Langerhans
•
Glucagon
 Alpha cells secrete glucagon

 Glucagon is secreted in response to low blood
sugar, causing glycogen to be converted to
glucose (glycogenolysis)
Beta cells secrete insulin

Insulin
 insulin is secreted in response to ↑ blood
sugar, causes ↑ permeability of cell
membranes throughout the body to glucose

•Except
CNS...does not
require insulin
to take up
glucose
Diabetes Mellitus
• Elevated blood sugar
•
• Normal fasting blood sugar is 70 – 100

mg/dL
•
• 100 – 125 mg/dL is “prediabetic”

•
• Higher than 125 mg/dL is either Type I or

Type II diabetes
Type I Diabetes Mellitus
 A failure of beta cells to produce insulin

 Also called IDDM (Insulin Dependent DM)

 complete loss of insulin means that
replacement is required

 Usually onset is in childhood (juvenile onset)

 Abrupt onset of symptoms

 DKA (diabetic ketoacidosis)

 No glucose is available to cells
 They utilize lipids instead
 This produces ketoacids (lower the pH)

 Polydipsia (thirst)

 Polyphagia (hunger)

 Polyuria (osmotic diuresis)

 The renal threshold for glucose resorption is
exceeded resulting in glycosuria

 Poorly controlled DM is a disease of small

blood vessels
 diabetic nephropathy
 diabetic retinopathy
 diabetic neuropathy
 changes in coronary & peripheral vessels
increase the risk of vascular disease
Diabetes Mellitus type II
An insensitivity of an insulin receptor in cell

membranes to insulin
 NIDDM (Non Insulin Dependent DM)
 usually does not require insulin (oral
hypoglycemics)
 Usually onset is as an adult
 Onset is insidious
 Usually no ketoacidosis
Diabetes Mellitus
• Long term monitoring of blood sugar
levels (months)
•
• Hgb A1C (glycosylated hemoglobin)

•
• A type of hgb that incorporates a sugar

molecule
•
• More Hgb A1C is made when blood

sugar levels are high
Pineal gland
• The main hormone is
melatonin
• The precursor is a
CNS
neurotransmitter,
serotonin
Pineal
gland
• Production and secretion of melatonin is

stimulated by darkness
•
• Information about light levels is provided

through the retina in mammals
•
 Circadian rhythm Pineal gland

 Regulates sleep / wake cycle


 Undergoes involution during childhood,

which may bring about the onset of
puberty

 Near the skin in non-mammal vertebrates

 Light levels are perceived directly

 Regulates seasonal behavior in other

animals
 Migratory patterns in birds
 Breeding cycles in animals with seasonal
Thymus
• Posterior to the
sternum
•
• Larger in
adolescence
•
• Regresses at
puberty
•
• Secretes thymosin
•
Thymus
cortex
medulla
• Thymosin causes undifferentiated

lymphocytes to become T cells
•
• Blood – thymus barrier in the cortex

•
• Only T cells that are “self tolerant” are

released to the medulla and into the rest of
the body
Stress
• A stressor is a stimulus to promote a
response to a threatening situation
physical stress - an psychological stress
actual physical change

post surgical 
originates in the

hot/cold cerebral cortex

trauma 
abstraction about a

malnutrition potentially harmful

hemorrhage situation

anger, grief, depression,
anxiety, guilt
Stress
 3 phases of the stress response

1.The alarm phase

2.Resistance phase: occurs as glycogen
is consumed
3.Exhaustion phase: chronic stress
occurs over a period of weeks
Stress: The Alarm Phase
• An immediate response
•
• Increased sympathetic output (fight or flight)

•
• The adrenal medulla secretes

catecholamines like adrenalin (SNS
neurotransmitter)
•
Stress: The Alarm Phase
 SNS input to the kidney initiates the RAA
cascade which leads to :

 Increased BP to supply large skeletal muscles


 Increased fluid retention to compensate for

potential fluid loss through sweat or
hemorrhage

 Glycogen stores are consumed in a few hours

Stress:
The Resistance
Phase
Occurs as glycogen is

consumed:
 Hypothalamus → CRH
→ ACTH → Cortisol
Stress: The Resistance Phase
• Cortisol decreases glucose use

peripherally (glucose sparing for the
CNS)
•
• Promotes the breakdown of protein & fatty

acids, which are converted to glucose in
the liver (gluconeogenesis)
•
Stress and Blood Sugar
• Both Adrenaline (alarm phase) and
Cortisol (resistance phase) elevate
blood sugar
•
•
Stress: The Exhaustion Phase
Chronic stress occurs over a period of

weeks:
Less protein is available for immune
system function (gluconeogenesis)


 ↓ ability to make antibodies (protein)

 ↑ susceptibility to infections
 ↓ protein available for wound healing
Paracrine Secretions
• Paracrine
hormones exert
a local effect
•
• Eicosanoids are
paracrine
secretions
•
• They are
produced by the
Arachidonic
acid pathway
Arachidonic Acid Pathway
• Arachidonic acid
(a fatty acid) is
produced from
phospholipids
in the cell
membrane
•
• This reaction is
catalyzed by
phospholipase
A2
 Arachidonic acid is
then subjected to
either of two
metabolic
pathways

1.lipoxygenase –
leads to the
production of
leukotrienes,
chemical
mediators of
inflammation
2.cyclooxygenase
– leads to the
production of
prostaglandin
s,
thromboxane,
and
prostacyclin
 Thromboxane is secreted by platelets to
enhance platelet aggregation

 Prostaglandins have many effects depending

upon the specific metabolite
 fever
 pain
 etc.
• Steroid medication
(e.g.
cortisol/predniso
ne) blocks the
production of
arachidonic acid
(phosphlipase)
•
• •*Non-steroidal anti-inflammatories (NSAID’s)
like aspirin and Ibuprofen block the
cyclooxygenase pathway to reduce
inflammation & fever
 ANATOMY AND
PHYSIOLOGY

 Dennis N. Muñoz,
Muñoz PT, RN,RM

Urinary System
 General Information
•Waste products of metabolism are
toxic (CO2 , ammonia, etc.)
•Removal from tissues:
•by blood and lymph
•Removal from blood by:
•Respiratory system
•Urinary system
 Functions of the Urinary
System
•Elimination of waste products

•Nitrogenous wastes
•Toxins
•Drugs
 Functions of the Urinary
System
•Regulate homeostasis
•Water balance
•Electrolytes
•Acid-base balance in the blood
•Blood pressure
•Red blood cell production
 Organs of the Urinary system
•Kidneys
•Ureters
•Urinary bladder
•Urethra
Figure 15.1a
 Location of the Kidneys
•Retroperitoneally
•Lateral to vertebral column
•The right kidney is slightly lower
than the left
•Atop each kidney is an adrenal gland
 Organs of the Urinary system
•Kidneys
•
Figure 15.1a
Structure of the Kidney
Outer cortex:

 Contains
many
capillaries.
Medulla:

 Renal
pyramids
separated
by renal
columns.
 Pyramid
contains
n minor
Major calyces form renal pelvis.
calyces
n Renal pelvis collects urine.
which
n Transports urine to ureters.
unite to
 Coverings of the Kidneys
•Renal capsule
•Surrounds each kidney
•Adipose capsule
•Surrounds the kidneys
•Provides protection to the kidneys
•Helps hold kidneys in place
 Regions of the Kidney
•Renal cortex:
outer region
•Renal medulla:
pyramids and
columns
•Renal pelvis:
collecting system
Figure 15.2b
 Kidney Structures
•Medullary pyramids – triangular
regions of tissue
•Renal columns– cortical material
between pyramids
•Calyces (sing. Calyx)
•cup-shaped structures
•collect urine
Structures involved in Urine

•Vascular
Formation Components
•Afferent arteriole
•Glomerulus
•Efferent arteriole
•Peritubular capillaries
•Tubular Components
•Bowman’s capsule
•Proximal convoluted tubule
•Loop of Henle
•Distal convoluted tubule
•
 Blood Flow
in/to the
Kidneys
•Is extensive!!!
Figure 15.2c
Renal Blood Vessels (continued)
Insert fig. 17.5

Renal Blood Vessels
Afferent arteriole:

 Delivers blood into the glomeruli.

Glomeruli:

 Capillary network that produces filtrate

that enters the urinary tubules.
Efferent arteriole:

 Delivers blood from glomeruli to

peritubular capillaries.
Peritubular capillaries:

 Deliver blood to vasa recta.

Nephron
Functional unit
of the kidney.
Consists of:
 Blood
vessels:
 Vasa recta.
 Peritubular
capillaries.
 Urinary
tubules:
 PCT.
 LH.
 DCT.
Type of Nephrons
Cortical nephron:

 Originates in
outer 2/3 of
cortex. Insert fig. 17.6
 Osmolarity of
300 mOsm/l.
 Involved in
solute
reabsorption.
Juxtamedullary

nephron:
 Originates in
inner 1/3
cortex.

 Nephrons Review !!!!
•The structural and functional units
of the kidneys
•Responsible for forming urine
•Components of the nephrons
•Renal corpuscle
•Glomerulus and Bowman’s capsule
•Renal tubules
Glomerular Capsule
Bowman’s

capsule:
 Surrounds
Insert fig. 17.6
the
glomerulu
s.
 Location
where
glomerul
ar
filtration
occurs.
Proximal Convoluted Tubule
Loop of Henle
Distal Convoluted Tubule
 Glomerulus (“a ball of yarn”)
•A specialized
capillary bed
•Attached to
arterioles on both
sides
•Wide afferent
arteriole
•Narrow efferent
arteriole
Figure 15.3c
 Glomerulus
•Covered by
glomerular
capsule
•first part of
the renal
tubule
•AKA Bowman’s
capsule
Figure 15.3c
 Renal Tubule
•Bowman’s
capsule
•Proximal
convoluted
tubule
•(PCT)
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 15.3b Slide 15.10
 Renal Tubule
•Loop of Henle
•Distal
convoluted
tubule
•DCT
 Peritubular Capillaries
•Arise from efferent arteriole

•Attached to a venule distally
•Surround renal tubule
•Reabsorb substances from tubules
into blood
 Renal Tubule
•Peritubular
capillaries
Glomerular Filtration Membrane
Glomerular Filtration Membrane (continued)
 Filtrate must pass through the

basement membrane:
 Thin glycoprotein layer.
 Negatively charged.
 Podocytes:
 Foot pedicels form small filtration
slits.
 Passageway through which filtered
molecules must pass.
Glomerular Filtration Membrane (continued)
Insert fig. 17.8

Glomerular Ultrafiltrate
Regulation of GFR
 Vasoconstriction or dilation of the

afferent arterioles affects the rate of
blood flow to the glomerulus.
 Affects GFR.
 Mechanisms to regulate GFR:
 Sympathetic nervous system.
 Autoregulation.
 Changes in diameter result from
extrinsic and intrinsic mechanisms.
Sympathetic Regulation of GFR
Stimulates

vasoconstriction of
afferent arterioles. Insert fig. 17.11
 Preserves blood
volume to muscles
and heart.
Cardiovascular

shock:
 Decreases
glomerular
capillary
hydrostatic
Renal Autoregulation of GFR
 Ability of kidney to maintain a constant GFR
under systemic changes.
 Achieved through effects of locally produced
chemicals on the afferent arterioles.
When MAP drops to 70 mm Hg, afferent
arteriole dilates.
When MAP increases, vasoconstrict afferent
arterioles.
Tubuloglomerular feedback:
 Increased flow of filtrate sensed by macula densa

cells in thick ascending LH.
 Signals afferent arterioles to constrict.
 Urine Formation Processes
•Filtration
•Reabsorption
•Secretion
Figure 15.4
 Filtration
•Nonselective passive process
•Depends on hydrostatic pressure
•Stops if B.P. falls too low
•Water and some solutes (no proteins)
•forced through capillary walls
•Taken out of blood
 Filtration
•Blood cells cannot pass
•Filtrate is collected in the
glomerular capsule
•This will become urine
•Leaves capsule through the renal
tubule
•Alterations to filtrate occur in
tubule
 Reabsorption
•Moving reusable material back into the
blood
•The peritubular capillaries reabsorb
several materials
•Some water
•Glucose
•Amino acids
•Ions
Reabsorption, con’t…
•Some is passive, most is active

•65% of reabsorption occurs in the PCT
•Glucose, Na+ , Ca++ , Cl- , HCO3 -
•Water (by osmosis)
•Amino acids (by pinocytosis)
Reabsorption, con’t…
•Loop of Henle
•15% more filtrate reabsorbed
•Descending limb:
•Water, by osmosis
•Ascending limb:
•Cl- by active transport
•Na+ by diffusion
•
REMEMBER!!!!
Reabsorption of Salt and H20
Return of most of the molecules and


H20 from the urine filtrate back into the

peritubular capillaries.
 About 180 L/day of ultrafiltrate produced;
however, only 1–2 L of urine excreted/24
hours.
 Urine volume varies according to the needs of
the body.
Minimum of 400 ml/day urine necessary

to excrete metabolic wastes (obligatory

water loss).
 Materials Not Reabsorbed
•Nitrogenous waste products

•Urea
•Uric acid
•Creatinine
•Excess water
Reabsorption in Proximal Tubule
Insert fig. 17.13

PCT
PCT (continued)

Na+/K+ ATPase pump located in basal
and lateral sides of cell membrane,
creates gradient for diffusion of Na+
across the apical membrane.
Na+/K+ ATPase pump extrudes Na+.
 Creates potential difference across the wall

of the tubule, with lumen as –pole.
Electrical gradient causes Cl-movement

towards higher [Na+].

 H20 follows by osmosis.
Salt and Water Reabsorption in Proximal Tubule
Insert fig. 17.14

Significance of PCT Reabsorption
Countercurrent Multiplier
In order for H20 to be reabsorbed,
interstitial fluid must be hypertonic.
Osmotic pressure of the interstitial tissue
fluid is 4 x that of plasma.

 Results partly from the fact that the tubule
bends permitting interaction between the
descending and ascending limbs.
Ascending Limb LH
• NaCl is actively
extruded Insert fig. 17.15
from the
ascending
limb into
surrounding
interstitial
fluid.
• Na+ diffuses
into tubular
cell with the
secondary
active
Ascending Limb LH (continued)
• Na+ actively
transported
across the Insert fig. 17.15
basolateral
membrane by
Na+/ K+
ATPase
pump.
• Cl- passively
follows Na+
down
electrical
gradient.
Descending Limb LH
• Deeper regions of
medulla reach 1400 Insert fig. 17.16
mOsm/L.
• Impermeable to
passive diffusion of
NaCl.
• Permeable to H20.
• Hypertonic interstitial
fluid causes H20
movement out of
the descending limb
via osmosis, and
Countercurrent Multiplier System
Multiplies the
[interstitial fluid] Insert fig. 17.16
and [descending
limb fluid].
Flow in opposite
directions in the
ascending and
descending
limbs.
Close proximity of
the 2 limbs:
 Allows
Vasa Recta
Countercurrent
exchange.
Recycles NaCl in Insert fig. 17.17
medulla.
Transports H 0 from
2
interstitial fluid.
Descending limb:
 Urea transporters.
 Aquaporin proteins
(H20 channels).
Ascending limb:

 Fenestrated
Vasa Recta (continued)
• Vasa recta maintains hypertonicity by

countercurrent exchange.
• NaCl and urea diffuse into descending
limb and diffuse back into medullary
tissue fluid.
• At each level of the medulla, [solute] is
higher in the ascending limb than in the
interstitial fluid; and higher in the
interstitial fluid than in descending
vessels.
• Walls are permeable to H20, NaCl and
Osmolality of Different Regions of the Kidney
Insert fig. 17.19

Urea
Contributes to
total osmolality
of interstitial
fluid. Insert fig. 17.18
Ascending limb
LH and terminal
CD are
permeable to
urea.
 Terminal CD
has urea
transporters.
Collecting Duct
Medullary area impermeable to high [NaCl]

that surrounds it.

 The walls of the CD are permeable to H20.
H20 is drawn out of the CD by osmosis.

 Rate of osmotic movement is determined

by the # of aquaporins in the cell
membrane.
Permeable to H20 depends upon the

presence of ADH.
 When ADH binds to its membrane
receptors on CD, it acts via cAMP.
 Stimulates fusion of vesicles with plasma membrane.
 Incorporates water channels into plasma membrane.
Secretion: Reabsorption in

Reverse
•Some materials move from peritubular
capillaries into renal tubules
•Hydrogen and potassium ions
•Creatinine
•Most secretion occurs in DCT
Secretion: Reabsorption in

Reverse
•What’s left?? Urine!
•Moving urine out of kidneys:
tubules 
 collecting duct
 minor calyces
 major calyces
 renal pelvis
 ureter
Secretion
 Secretion of substances from the peritubular
capillaries into interstitial fluid.
 Then transported into lumen of tubule, and into
the urine.
 Allows the kidneys to rapidly eliminate certain
potential toxins.
Proximal Tubule
Insert fig. 17.13
Secretion
Transport Process Affecting Renal Clearance
Ability of the kidneys to remove
molecules from plasma and excrete
those molecules in the urine.
If a substance is not reabsorbed or
secreted, then the amount excreted =

amount filtered.
 Quantity excreted = V x U
 Quantity excreted = mg/min.
 V = rate of urine formation.
 U = inulin concentration in urine.
Measurement of GFR
If a substance is neither reabsorbed nor

secreted by tubule:
 The amount excreted in urine/min. will be
equal to the amount filtered out of the
glomeruli/min.
Rate at which a substance is filtered by
the glomeruli can be calculated:
 Quantity filtered = GFR x P
 P = inulin concentration in plasma.
Amount filtered = amount excreted
 GFR = V x U
Renal Clearance of Inulin
Insert fig. 17.22

Renal Plasma Clearance
Volume of plasma from which a
substance is completely removed in 1
min. by excretion in the urine.
Substance is filtered, but not reabsorbed:
 All filtered will be excreted.

Substance filtered, but also secreted and

excreted will be:

 > GFR (GFR = 120 ml/ min.).
Renal Plasma Clearance
 Renal plasma clearance = V x U
P
 V = urine volume per min.
 U = concentration of substance in urine
 P = concentration of substance in plasma
 Compare renal “handling” of various
substances in terms of reabsorption or
secretion.

Clearance of Urea
Urea is secreted into blood and filtered
into glomerular capsule.
Urea clearance is 75 ml/min., compared to
clearance of inulin (120 ml/min.).

 40-60% of filtered urea is always
reabsorbed.
 Passive process because of the presence
of carriers for facilitative diffusion of urea.
Measurement of Renal Blood Flow
 Not all blood delivered to glomeruli is
filtered in the glomerular capsules.
 Most of glomerular blood passes to the
efferent arterioles.
 20% renal plasma flow filtered.
 Substances are returned back to blood.
 Substances in unfiltered blood must be
secreted into tubules to be cleared by
active transport (PAH).
 PAH can be used to measure renal plasma
flow.
Measurement of Renal Blood Flow (continued)
 Filtration and secretion clear only the

molecules dissolved in plasma.
 PAH clearance actually measures renal
plasma flow.
 To convert to total renal blood flow, the
amount of blood occupied by
erythrocytes must be taken into account.
 Averages 625 ml/min.
Total Renal Blood Flow
• 45% blood
is RBCs
Insert fig. 17.23
• 55%
plasma
• Total renal
blood
flow =
PAH
clearance
 0.55
Glucose and Amino Acid Reabsorption
 Filtered glucose and amino acids are
normally reabsorbed by the nephrons.
 In PCT occurs by secondary active
transport with membrane carriers.
 Carrier mediated transport displays:
 Saturation.
 Tm.
 [Transported molecules] needed to saturate carriers
and achieve maximum transport rate.
 Renal transport threshold:
 Minimum plasma [substance] that results in
excretion of that substance in the urine.
 Renal plasma threshold for glucose = 180-200
mg/dl.
Electrolyte Balance
Kidneys regulate Na+, K+, H+, Cl-, HC03-,
and PO4-3 .
Control of plasma Na+ is important in
regulation of blood volume and pressure.

Control of plasma of K+ important in
proper function of cardiac and skeletal

muscles.
 Match ingestion with urinary excretion.
Na+ Reabsorption
• 90% filtered
Na+
reabsorbed in Insert fig. 17.26
PCT.
• In the absence
of
aldosterone,
80% of the
remaining Na+
is reabsorbed
in DCT.
• Final [Na+]
controlled in
Rennin-Angiotensin-Aldosterone System
DIURETICS
K+ Secretion

90% filtered K+ is reabsorbed in early part of
the nephron.

Secretion of K+ occurs in CD.

Amount of K+ secreted depends upon:

Amount of Na+ delivered to the region.
 Amount of aldosterone secreted.

As Na+is reabsorbed, lumen of tubule becomes
–charged.

Potential difference drives secretion of K+ into tubule.

Transport carriers for Na+ separate from transporters for
K+.

DUAL CONTROL OF ALDOSTERONE
SECRETION
Fall in sodium
Increased ECF Volume
Plasma
Potassium Blood Pressure
Increased Aldosterone secretion
Increased Tubular Increased Tubular

Potassium Secretion Sodium Reabsorption
Increased Urinary
Potassium Secretion Fall in Urinary
Sodium Excretion
K+ Secretion (continued)
Final [K+]

controlled in
CD by Insert fig. 17.24
aldosterone.
 When
aldosterone
is absent,
no K+ is
excreted in
the urine.
High [K+] or low

[Na+]
stimulates the
secretion of
Juxtaglomerular Apparatus
Region in each nephron where the

afferent arteriole comes in contact with
the thick ascending limb LH.
Granular cells within afferent arteriole
secrete renin:
 Converts angiotensinogen to angiotensin I.
 Initiates the renin-angiotensin-aldosterone system.
 Negative feedback.
 Macula densa:
 Region where ascending limb is in contact with
afferent arteriole.
 Inhibits renin secretion when blood [Na+] in blood
Juxtaglomerular Apparatus (continued)
Insert fig. 17.25

ANP
Na+, K+, and H+ Relationship
• Na+reabsorption
in CD creates
electrical
gradient for K+
secretion. Insert fig. 17.27
• Plasma [K+]
indirectly
+
affects
[H ].
• When
extracellular
[H++] increases,
H moves into
the
+
cell, causing
K to diffuse
into the ECF.
• In severe
acidosis, H+ is
secreted at the
expense of K+.
Renal Acid-Base Regulation
Kidneys help regulate blood pH by
excreting H+ and reabsorbing HC03-.
Most of the H+ secretion occurs across
the walls of the PCT in exchange for

Na+.
 Antiport mechanism.

Moves Na+ and H+ in opposite directions.
Normal urine normally is slightly acidic

because the kidneys reabsorb almost

all HC03- and excrete H+.
 Returns blood pH back to normal range.
Reabsorption of HCO3-
 Apical membranes of tubule cells are
impermeable to HCO3-.
 Reabsorption is indirect.
 When urine is acidic, HCO3- combines
with H+ to form H2C03-, which is
catalyzed by ca located in the apical cell
membrane of PCT.
 As [C02] increases in the filtrate, C02
diffuses into tubule cell and forms H2C03.
 H2C03 dissociates to HCO3- and H+.
 -
 Formation of Urine
Figure 15.5
Acidification of Urine
Insert fig. 17.28

Urinary Buffers
Diuretics
 Increase urine volume excreted.
 Increase the proportion of glomerular filtrate that is
excreted as urine.
 Loop diuretics:
 Inhibit NaCl transport out of the ascending limb of the
LH.
 Thiazide diuretics:

Inhibit NaCl reabsorption in the 1st segment of the DCT.
 Ca inhibitors:
 Prevent H20 reabsorption in PCT when HC0s- is
reabsorbed.
Clinical Diuretics Sites of Action
Insert fig. 17.29

Kidney Diseases
Kidney Diseases (continued)
 Normal components of Urine
•Straw colored (pale yellow)

•Sterile
•Slightly aromatic 
•Normal pH of around 6
•Specific gravity of 1.001 to 1.035
 Normal volume of Urine
•0.6 – 2.5 liters/day. Depends on:
•Adequate B.P.
•Fluid intake
•Temperature, humidity
•Activity levels
•<30cc/hour output = kidney
failure
•Average is 115-125 ml/hr
 Abnormal components of Urine
•Glucose
•Ketones
•Hemoglobin/blood cells
•Proteins
•pH <4 or >8
 Ureters
•Tubes attaching kidney to urinary
bladder
•Continuous with the renal pelvis
•Enter the posterior aspect of the
bladder
•Retroperitoneal
•Peristalsis, gravity move urine
Essentials of Anatomy and
Physiology
Fifth edition
 Seeley, Stephens and Tate

Chapter 18: Urinary System
 Urinary Bladder
•Smooth, collapsible, muscular sac
•Temporarily stores urine
Figure 15.6
 Urinary Bladder
•Trigone – three openings
•Two from the ureters
•One to the urethra
Figure 15.6
 Urinary Bladder Wall
•Three layers of smooth muscle
(detrusor muscle)
•Mucosa made of transitional
epithelium
•Walls are thick and folded
•If bladder is empty
•Bladder can expand significantly
 Urethra
•Thin-walled tube that
•carries to the outside of the
body
•by peristalsis
•Release of urine is controlled by:
•Internal urethral sphincter
(involuntary)
•External urethral sphincter
(voluntary)
Urethra
• Release of urine
is controlled by:
• Internal
urethral
sphincter
(involuntar
y)
• External
urethral
sphincter
(voluntary)
 Urethra: Gender Differences
•Length
•Females – 3–4 cm (1 inch)
•Males – 20 cm (8 inches)
•Location
•Females – anterior to the vagina
•Males – through the prostate and
penis
 Urethra: Gender Differences
•Function
•Females – only carries urine
•Males – carries urine and semen
 Micturition (Voiding)
•Both sphincter muscles must open

•The internal urethral sphincter
relaxes when bladder stretches
•Activation is from pelvic nerves
•The external urethral sphincter must
be voluntarily relaxed
Micturition Reflex
 Actions of the internal urethral sphincter and the
external urethral sphincter are regulated by
reflex control center located in the spinal cord.

 Filling of the urinary bladder activates the stretch

receptors, that send impulses to the micturition
center.
 Activates parasympathetic neurons, causing rhythmic
contraction of the detrusor muscle and relaxation of the
internal urethral sphincter.
 Voluntary control over the external urethral
sphincter.

 When urination occurs, descending motor tracts

to the micturition center inhibit somatic motor
fibers of the external urethral sphincter.
 Maintaining Water Balance
•Normal amount of water in the human
body
•Young adult females – 50%
•Young adult males – 60%
•Babies – 75%
•Old age – 45%
•Water levels must be maintained
 Distribution of Body Fluid
•Intracellular
fluid (inside
cells)
•Extracellular
fluid (outside
cells)
•Interstitial
fluid
•Blood plasma
Figure 15.7
 The Link Between Water and
Salt
•Changes in electrolyte balance
causes water to move from one
compartment to another
•Alters blood volume and blood
pressure
•Can impair the activity of cells
•Water intake must equal water output
•Intake
•Ingested foods and fluids
•Water produced from metabolic processes
•Output
•Lungs
•Perspiration
•Feces
•Urine production
•More urine is produced if water

intake is excessive
•Less urine (concentrated) is produced
if large amounts of water are lost
•Electrolyte concentrations must be
maintained
Regulation of Water and

Electrolyte Reabsorption
•Regulation is primarily by hormones
•Antidiuretic hormone (ADH) prevents
excessive water loss in urine
•Aldosterone regulates sodium ion
content of extracellular fluid
•Cells in the kidneys and hypothalamus
are active monitors
Regulation of Water and

Electrolyte Balance
•Primarily by hormones
•Antidiuretic hormone (ADH): prevents
excessive water loss
•Aldosterone: regulates sodium ion
content ECF
•Monitored by cells in kidneys and
hypothalamus
Maintaining Acid-Base Balance
in Blood
•Most acid-base balance is maintained

by the kidneys
•Other acid-base controlling systems
•Blood buffers
•Respiration
Renal Mechanisms of Acid-

Base Balance
•Excrete bicarbonate ions if needed

•Conserve or generate new bicarbonate
ions if needed
•Urine pH varies from 4.5 to 8.0
 Effects of Aging on the Urinary
System: FYI
•There is a progressive decline in
urinary function
•Output decreases ~1cc/yr >50
•The bladder shrinks with aging
•Urinary retention is common in males
Disorders of the Urinary System:
FYI
•Nephritis: inflammation of nephrons
•Protein appears in urine
•Kidney stones
•More common in males
•Glucosuria
•Sugar in urine: diet or diabetes??
Disorders of the Urinary System:

FYI
•Cystitis
•Bacterial infection of urinary
bladder
•Gout
•Genetic. Uric acid crystals
ppct in joints
•Non-gonococcal urethritis (NGU)
•A sexually transmitted infection
Renal Failure
THE URINARY BLADDER STORES THE
URINE
Reflex and Voluntary Control of
Micturition
• Bladder filling • Stretch receptors

reflexively in bladder send
contracts the inhibitory
bladder impulses to
• Internal Sphincter external sphincter
mechanically • Voluntary signals
opens from cortex can
override the
reflex or allow it
to take place
REGULATION OF
FLUID AND
ELECTROLYTE
BALANCE
DENNIS N. MUÑOZ, P.T., R.N., R.M.

1051
FLUIDS AND ELECTROLYTE 05/24/2010
05/24/2010
•Body Fluids and Fluid

Compartments
•Body Fluid and Electrolyte
Balance – fluid and electrolyte
homeostasis
Why do we care about this?
üECF volume
üOsmolarity
1052
05/24/2010
The Body as an Open System

● “Open System”. The body exchanges
material and energy with its
surroundings.
1053
WATER STEADY STATE 05/24/2010
• Amount Ingested = Amount Eliminated
• Pathological losses
üvascular bleeding (H20,
Na+)
üvomiting (H20, H+)
üdiarrhea (H20, HCO3-).
1054
05/24/2010
ELECTROLYTE (NA+, K+, CA++ ) STEADY

STATE
• Amount Ingested = Amount Excreted.

• Normal entry: Mainly ingestion in food.
• Clinical entry: Can include parenteral
administration.
1055
05/24/2010
ELECTROLYTE LOSSES
1056
05/24/2010
FLUIDS and ELECTROLYTES
BODY FLUIDS
Functions of Fluids
qBody fluids:
üFacilitate in the transport
[nutrients, hormones, proteins,
& others…]
üAid in removal of cellular
metabolic wastes
üProvide medium for cellular
metabolism
üRegulate body temperature
üProvide lubrication of
musculoskeletal jts. 1057
05/24/2010
REVIEW OF FUNCTIONS OF
WATER IN THE BODY
• Transporting nutrients to cells and wastes from cells
• Transporting hormones, enzymes, blood platelets, and
red and white blood cells
• Facilitating cellular metabolism and proper cellular
chemical functioning
• Acting as a solvent for electrolytes and nonelectrolytes
• Helping maintain normal body temperature
• Facilitating digestion and promoting elimination
• Acting as a tissue lubricant
1058
BODY WATER DISTRIBUTION
•Individual variability (lean body mass)
–55 - 60% of body weight in adult males Input
–50 - 55% of body weight in adult female
–~42 L For a 70 Kg man.
RBC PLASMA WATER

5% 3 L ECF
20 % 14 L
CELL WATER INTERSTITIAL
FLUID
40 % 28 L COMPARTMENT
15 % 10 L
TRANSCELLULAR WATER
05/24/2010 1% 1 L 1059
05/24/2010
ELECTROCHEMICAL EQUIVALENCE
 Equivalent (Eq/L) = moles x valence


Monovalent Ions (Na+, K+, Cl-):
 1 milliequivalent (mEq/L) = 1 millimole

Divalent Ions (Ca++ , Mg++ , and
HPO42- )
 1 milliequivalent = 0.5 millimole
1060
05/24/2010
TWO COMPARTMENTS OF FLUID IN

THE BODY
Intracellular fluid (ICF)—fluid within cells
(70%)
Extracellular fluid (ECF)—fluid outside cells
(30%)
 Includes intravascular and interstitial fluids
1061
05/24/2010
VARIATIONS IN FLUID CONTENT

Healthy person—total body water is 50% to
60% of body weight
An infant has considerably more body fluid
and ECF than an adult

 More prone to fluid volume deficits
Sex and amount of fat cells affect body

water
 Women and obese people have less body
water
1062
05/24/2010
TOTAL BODY FLUID REPRESENTING 50%–

60% OF BODY WEIGHT OF NORMAL
ADULT
1063
05/24/2010
TRANSPORTING BODY FLUIDS

• Osmosis—water passes from area of lesser solute
concentration to greater concentration until equilibrium
is established
• Diffusion—tendency of solutes to move freely throughout
a solvent (“downhill”)
• Active transport—requires energy for movement of
substances through cell membrane from lesser solute
concentration to higher solute concentration
• Filtration—passage of fluid through permeable
membrane from area of higher to lower pressure
1064
05/24/2010
OSMOLARITY OF A SOLUTION
• Isotonic—same concentration of particles

as plasma
• Hypertonic—greater concentration of
particles than plasma
• Hypotonic—lesser concentration of
particles than plasma
1065
05/24/2010
FILTRATION
• Colloid osmotic pressure
• Hydrostatic pressure
1066
05/24/2010
SOURCE OF FLUIDS FOR THE BODY

• Ingested liquids
• Food
• Metabolism
1067
05/24/2010
WATER INTAKE AND OUTPUT
Figure 26.4
1068
05/24/2010
FLUID LOSSES
• Kidneys — urine
• Intestinal tract — feces
• Skin — perspiration
• Insensible water loss
1069
05/24/2010
FLUID INTAKE AND LOSSES: ABOUT

EQUAL IN HEALTH
1070
05/24/2010
PRIMARY ORGANS OF
HOMEOSTASIS
Kidneys normally filter 170 L plasma, excrete 15
L urine
Cardiovascular system pumps and carries
nutrients and water in body
Lungs regulate oxygen and carbon dioxide
levels of blood
Adrenal glands help body conserve sodium,
save chloride and water, and excrete
potassium
Thyroid gland increases blood flow in body and
increases renal circulation
1071
05/24/2010
PRIMARY ORGANS OF
HOMEOSTASIS (CONT.)
• Parathyroid glands regulate the level of
calcium in ECF
• GI tract absorbs water and nutrients that
enter body though this route
• Nervous system is a switchboard to inhibit
and stimulate fluid balance (thirst center
and ADH storage)

1072
05/24/2010
QUESTION
 Tell whether the following statement is

true or false.
 A hypertonic solution has a greater
osmolarity, causing water to move out of
the cells and to be drawn into the
intravascular compartment, causing the
cell to shrink.
 A. True
 B. False
1073
05/24/2010
ANSWER
 Answer: A. True
 A hypertonic solution has a greater
osmolarity, causing water to move out of
the cells and to be drawn into the
intravascular compartment, causing the
cell to shrink.

1074
05/24/2010
BODY FLUIDS
Distribution of Body Fluids – 50-70% of total body weight;

infant [70-80%], elderly [45-50%]
ICF ECF
60-kg man
TBW = 0.6 x 60 kg
= 3.6 L
ICF = 0.4 x ECF

P IS 60 kg = 12
= 24 L L
3 9
L L
40 % TBW 20 % TBW
1075
05/24/2010
BODY FLUIDS
Factors that Dictate Body Water Requirement
1)Amount needed to give the proper osmotic

concentration
2)Amount needed to replace water lost excretion
Normal Routes of water gain and loss
INTAKE ml/day OUTPUT ml/day
Fluid intake 1 , 200 Insensible loss 700

Food 1 , 000 Sweat 100
Metabolic water 300 Feces 200
Urine 1 , 500
TOTAL 2 , 500 TOTAL 2 , 500
1076
05/24/2010
FLUID EXCHANGE BETWEEN BODY FLUID

COMPARTMENTS
ICF ECF
Osmotic Pressure Gradient
Oncotic P (Colloid osmotic P)
Capillary P (Hydrostatic P)
P ISF
1077
05/24/2010
Control of Osmotic Pressure, Volume &

Electrolyte Concentration
OBLIGATORY Reabsorption
qoccurs in the proximal tubules
q178 L/day of glomerular filtrate (80%
reabsorbed)
q2 to solute reabsorption
qindependent of the water requirement
FACULTATIVE Reabsorption
qoccurs in the distal & collecting tubules
qindependent of the active solute
transport
qdependent of body’s need of water 1078
05/24/2010
REGULATION OF WATER INTAKE
1079
05/24/2010
REGULATION OF WATER INTAKE
1080
05/24/2010
REGULATION OF WATER INTAKE: THIRST MECHANISM
Figure 26.5
1081
05/24/2010
REGULATION OF WATER OUTPUT
1082
05/24/2010
INFLUENCE AND REGULATION OF ADH
1083
05/24/2010
MECHANISMS AND CONSEQUENCES OF

ADH RELEASE
Figure 26.6
1084
05/24/2010
DISTURBANCES IN FLUID BALANCE
EDEMA (Dropsy)
Ø in the interstitial fluid volume of about 2 L or

more due to increase transudation of fluid
from capillaries 2° to:
qIncreased HP [pregnancy, CHF]

qDecreased OP [malnutrition, end-stage
liver dse, nephrotic syndrome]
1085
05/24/2010
FLUID VOLUME SHIFTS
1086
05/24/2010
CAUSES OF THIRD-SPACING
1087
05/24/2010
ASSESSMENT OF THIRD-SPACING
1088
05/24/2010
PHASES OF THIRD-SPACING
1089
05/24/2010
TREATMENT
1090
05/24/2010
EVALUATION
1091
05/24/2010
FLUID VOLUME DEFICIT
1092
05/24/2010
DISORDERS OF WATER BALANCE:

DEHYDRATION
1 Excessive loss of H2O from 2 ECF osmotic 3 Cells lose H2O

ECF pressure rises to ECF by
osmosis; cells
shrink
(a) Mechanism of dehydration
Figure 26.7a
1093
05/24/2010
FLUID VOLUME DEFICIT
1094
05/24/2010
SIGNS AND SYMPTOMS
1095
05/24/2010
SIGNIFICANT POINTS
1096
05/24/2010
SIGNIFICANT POINTS
1097
05/24/2010
LABS
1098
05/24/2010
INTERVENTIONS
1099
05/24/2010
FLUID VOLUME EXCESS (FVE)
1100
05/24/2010
DISORDERS OF WATER BALANCE:

HYPOTONIC HYDRATION
1 Excessive H2O enters 2 ECF osmotic 3 H2O moves into

the ECF pressure falls cells by osmosis;
cells swell
(b) Mechanism of hypotonic hydration
Figure 26.7b
1101
05/24/2010
CAUSES
1102
05/24/2010
SIGNS/SYMPTOMS
1103
05/24/2010
SIGNS / SYMPTOMS
1104
05/24/2010
SIGNS / SYMPOTMS
1105
05/24/2010
INTERVENTIONS
1106
05/24/2010
SOURCES OF WATER
1107
05/24/2010
“NORMAL” WATER LOSS
1108
05/24/2010
OTHER CAUSES OF WATER LOSS
1109
05/24/2010
OTHER CAUSES OF WATER LOSS
1110
05/24/2010
IV FLUID REPLACEMENT
1111
05/24/2010
IV FLUID REPLACEMENT
1112
05/24/2010
Volume Disorders 2° Alteration in Sodium Balance

Volume ECF ICF Water
Conditions
Disorder Vol . Vol . Shift
Expansion
Isotonic Inc N No net change
Isotonic fluid
ingestion
Hypertonic Inc Dec ICF  ECF Sea
water
ingestion
Hypotonic Inc Inc ECF  ICF
Hypotonic IVF
Contraction
Isotonic Dec N No net change
Diarrhea
Hypertonic Dec Dec ICF  ECF
Diabetes insipidus
Hypotonic Dec Inc ECF  ICF
Addison ’ s dse
1113
05/24/2010
ELECTROCHEMICAL EQUIVALENCE
 Equivalent (Eq/L) = moles x valence


Monovalent Ions (Na+, K+, Cl-):
 1 milliequivalent (mEq/L) = 1 millimole

Divalent Ions (Ca++ , Mg++ , and
HPO42- )
 1 milliequivalent = 0.5 millimole
1114
05/24/2010
SOLUTE OVERVIEW:
INTRACELLULAR VS. EXTRACELLULAR
• Ionic composition very different

• Total ionic concentration very similar
• Total osmotic concentrations virtually
identical
1115
05/24/2010
SUMMARY OF IONIC COMPOSITION
Protein
Organic Phos.
400 Inorganic Phos
Bicarbonate
300 Chloride
Magnesium
200 Calcium
Potassium
100 Sodium
0 Plasma InterstitialCell
H2O H2O H 2O
1116
05/24/2010
NET OSMOTIC FORCE DEVELOPMENT
1117
05/24/2010
OSMOTIC PRESSURE ( )
= p
S S S
S
S S S
S S S
S S S
1118
05/24/2010
GLUCOSE EXAMPLE
Initial Gl Gl Gl Gl
10 L 10 L
Final Gl Gl Gl Gl
15 L 5 L
1119
05/24/2010
OSMOTIC CONCENTRATION
Proportional to the number of osmotic particles

formed: Osm/L = moles x n (n, # of particles in
solution) e.g. 1 M NaCl = 2 M Glu in
Assuming complete dissociation: Osm/L
 1mole of NaCl forms a 2 osmolar solution
in 1L
 1mole of CaCl forms a 3 osmolar solution
2
in 1L
Physiological concentrations:
 milliOsmolar units most appropriate

1 mOSM = 10-3 osmoles/L
1120
05/24/2010
PRINCIPLES OF BODY WATER

DISTRIBUTION
1121
05/24/2010
INTRA-ECF WATER REDISTRIBUTION

PLASMA VS. INTERSTITIUM
 Balance of Starling Forces acting across

the capillary membrane
 osmotic forces
 hydrostatic forces
1122
05/24/2010
INTRACELLULAR FLUID VOLUME
ICFV altered by: changes in extracellular

fluid osmolarity.
ICFV NOT altered by: iso-osmotic
changes in extracellular fluid volume.

ECF undergoes proportional changes in:
 Interstitial water volume

 Plasma water volume
1123
05/24/2010
PRIMARY DISTURBANCE:
INCREASED ECF OSMOLARITY
 Water moves out of cells

 ICF Volume decreases (Cells shrink)
 ICF Osmolarity increases
 Total body osmolarity remains higher
than normal
1124
05/24/2010
PRIMARY DISTURBANCE:
DECREASED ECF OSMOLARITY
 Water moves into the cells

 ICF Volume increases (Cells swell)
 ICF Osmolarity decreases
 Total body osmolarity remains lower than
normal.
1125
05/24/2010
PLASMA OSMOLARITY MEASURES

ECF OSMOLARITY
1126
05/24/2010
SOLUTIONS USED CLINICALLY FOR

VOLUME REPLACEMENT THERAPY
• Isotonic Solutions --> n.c. ICF

• Hypertonic Solutions --> Decrease
ICF
• Hypotonic --> Increase ICF
1127
05/24/2010
TYPE OF SOLUTIONS
 Saline solutions
Come in a variety of concentrations:
hypotonic (eg., 0.2%), isotonic (0.9%), and
hypertonic (eg. 5%).
 Dextrose in Saline
Glucose is rapidly metabolized to CO2 +
H2O
The volume therefore is distributed
intracellularly as well as extracellularly
Again available in various concentrations
Used for simultaneous volume replacement
and caloric supplement
 Dextran, a long chain polysaccharide
Solutions are confined to the vascular
compartment and preferentially expand
this portion of the ECF

1128
05/24/2010
Body Fluid and Electrolyte

Balance
• Water input and output
üThe role of the kidneys in
maintaining balance of water and
electrolytes
üThe regulation of body water
balance
−thirst sensation
−control of renal water excretion by
ADH
ü 1129
05/24/2010
1130
05/24/2010
1131
05/24/2010
ü Thirst centers in the hypothalamus

−relay information to the cerebral cortex
where thirst becomes a conscious sensation
−controls the release of ADH
ü Stimuli for thirst sensation
−Baroreceptors and stretch receptors as
detectors
−impulses sent to the thirst control centers
in the hypothalamus
ü Effect of ADH (vasopressin)
1132
05/24/2010
Factors
affecting ADH
release 1133
05/24/2010
1134
05/24/2010
1135
05/24/2010
•Sodium balance
ü The kidneys - the major site
of control of sodium output
ü Influence of dietary input on
appropriate changes in sodium
excretion by the kidneys
ü Effector mechanisms include
changes in:
-glomerular filtration rate
-plasma aldosterone levels
-peritubular capillary Starling
forces
1136
05/24/2010
1137
05/24/2010
1138
05/24/2010
-renal sympathetic nerve activity

-intrarenal blood flow distribution
-plasma atrial natriuretic factor (ANF
ü Effects of aldosterone
ü The renin-angiotensin system
−release of renin
−action of renin on the formation of
angiotensin II
−effects of angiotensin II: a.blood
pressure; b. synthesis and release of
aldosterone; c. stimulation of the
hypothalamic thirst centers; d. release
of ADH
1139
05/24/2010
Pathway of
RAAS
1140
05/24/2010
Principal cells & aldosterone
1141
05/24/2010
üNet reabsorption of salt and water by the

proximal convoluted tubule
−peritubular capillary hydrostatic forces
−colloid osmotic pressure
üDecrease in renal sodium excretion by
stimulation of renal sympathetic nerves
üRelease of Atrial natriuretic peptide (ANP)
−in response to an increase in blood volume
−increase sodium excretion by increasing GFR and
inhibiting sodium reabsorption
1142
05/24/2010
•Atrial natriuretic
peptide
•Decreased blood pressure

stimulates renin
secretion
1143
05/24/2010
üThe regulated variable affecting sodium

excretion - effective arterial blood
volume
üChanges in effective arterial blood
volume can elicit the appropriate renal
response by three possible mechanisms
−a change in blood volume  glomerular blood
flow and capillary pressure  GFR
−a change in blood volume detected by an
intrarenal baroreceptor  release of renin
−a change in blood volume could change
peritubular capillary Starling forces
−
1144
05/24/2010
üOther factors affecting sodium excretion

include:
− glucocorticoids
− estrogen
− osmotic diuretics
− poorly reabsorbed anions
− diuretic drugs
1145
Homeostas is : severe
dehydrati on
05/24/2010
1146
05/24/2010
• Potassium balance
ü Potassium plays a number of
important roles in the body
−electrical excitability of cells
−major osmotically active solute in
cells
−acid-base balance
−cell metabolism
ü The kidneys are the major site in
control of potassium balance
1147
05/24/2010
ü Factors affecting the distribution of

potassium between cells and extracellular
fluid include:
− activity of the sodium-potassium pump
− acid-base status of body fluids
− availability of insulin
− cellular breakdown due to trauma,
infection, ischemia, and heavy exercise
ü The regulation of plasma potassium by
hormones
− insulin
− epinephrine
− aldosterone,
1148
05/24/2010
ü Factors affecting potassium excretion

include:
− intracellular potassium concentration
− aldosterone
− excretion of anions
− urine flow rate
1149
05/24/2010
ELECTROLYTES
Ions

 Cations—positive charge
 Anions—negative charge
Homeostasis—total cations equal to total

anions
1150
05/24/2010
FLUID BALANCE
• Solvents—liquids that hold a substance in
solution (water)
• Solutes—substances dissolved in a
solution (electrolytes and non-
electrolytes)
1151
05/24/2010
MAJOR ELECTROLYTES/CHIEF
FUNCTION
• Sodium—controls and regulates volume of body
fluids
• Potassium—chief regulator of cellular enzyme
activity and water content
• Calcium—nerve impulse, blood clotting, muscle
contraction, B12 absorption
• Magnesium—metabolism of carbohydrates and
proteins, vital actions involving enzymes
• Chloride—maintains osmotic pressure in blood,
produces hydrochloric acid
• Bicarbonate—body’s primary buffer system
• Phosphate—involved in important chemical reactions
in body, cell division, and hereditary traits
1152
05/24/2010
QUESTION

true or false.
 Molecules in the body’s chemical
compounds that remain intact are called
electrolytes.
 A. True
 B. False
1153
05/24/2010
ANSWER
 Answer: B. False
 Molecules in the body’s chemical
compounds that remain intact are called
nonelectrolytes.
1154
05/24/2010
ELECTROLYTES
Ø
Ø salts or minerals in extracellular or
intracellular body fluids
q Sodium – major cation of ECF

q
q Potassium – major cation of ICF
q
q Chloride- major anion of ICF
q
q Protein – in ICF > ISF
1155
05/24/2010
ELECTROLYTE Composition
Electrolyte Conc Plasma ( mEq / L ) ISF
ICF
Sodium, Na+ 142 141 10
Potassium, K+ 5 4.1 150
Calcium, Ca++ 5 4.1 -
Magnesium, Mg++ 3 3 40
( 155 )
Chloride, Cl- 103 115 15
Bicarbonate, HCO3- 27 29 10
Biphosphate, HPO4- 2 2 100
Sulfate, SO4-2 1 1 20
Protein 16 1 60
Organic foods 6 3.4 -
( 155 )
1156
05/24/2010
ELECTROLYTES
Functions of Electrolytes
qContribute most of the osmotically

active particles in body fluids
qProvide buffer systems for pH

regulation
qProvide the proper ionic environment for

normal neuromuscular irritability &
tissue function
1157
05/24/2010
ELECTROLYTES
Hyponatremia [Na+ < 135 mEq/L; Normal = 135-145 mEq/L]
qCauses
ü Na+ intake
ü Na+ excretion [diaphoresis, GI
suctioning]
üAdrenal insufficiency
qAssessment
üN & V, abdominal cramps, weight
loss
üCold, clammy skin,  skin turgor
üApprehension, HA, convulsions,
focal neurologic deficit, coma 1158
05/24/2010
ELECTROLYTES
Hyponatremia [Na+ < 135 mEq/L; Normal = 135-145 mEq/L]
qManagement
üProvide foods high in sodium
üAdminister NSS IV
üAssess blood pressure frequently
[measure lying down, sitting & standing]
1159
05/24/2010
ELECTROLYTES
Hypernatremia [Na+ >145 mEq/L; Normal = 135-145 mEq/L]
qCauses
üExcessive, rapid IV adm’n of NSS
üInadequate water intake
üKidney disease
qAssessment
üDry, sticky mucus membranes
üFlushed skin
üRough dry tongue, firm skin turgor
üIntense thirst
üEdema, oliguria to anuria
üRestlessness, irritability [cerebral 1160
05/24/2010
ELECTROLYTES
Hypernatremia [Na+ >145 mEq/L; Normal = 135-145 mEq/L]
qNursing Intervention
üWeigh daily
üAssess degree of edema
frequently
üMeasure I & O
üAssess skin frequently & institute
nursing measures to prevent
breakdown
üEncourage sodium-restricted diet
1161
05/24/2010
ELECTROLYTES
Hyperkalemia [K+ > 5.5 mEq/L; Normal = 3.5-5.5 mEq/L]
qCauses
üRenal insufficiency
üAdrenocortical insufficiency
üCellulose damage [burns]
üInfection
üAcidotic states
üRapid infusion of IV sol’n w/
potassium-conserving diuretics
1162
05/24/2010
ELECTROLYTES
qAssessment
üThready, slow pulse
üShallow breathing
üN & V, diarrhea, intestinal colic
üIrritability
üMuscle weakness, flaccid paralysis
üNumbness, tingling
üDifficulty w/ phonation,
respiration
1163
05/24/2010
ELECTROLYTES
qNursing Interventions
üAdminister kayexalate as ordered
üAdminister/monitor IV infusion of
glucose & insulin
üControl infection
üProvide adequate calories &
carbohydrates
üDiscontinue IV or oral sources of
K+
1164
05/24/2010
ELECTROLYTES
Hypokalemia [K+ < 3.5 mEq/L; Normal = 3.5-5.5 mEq/L]
qCauses
üRenal insufficiency
üAdrenocortical insufficiency
üCellulose damage [burns]
üInfection
üAcidotic states
üRapid infusion of IV sol’n w/
potassium-conserving diuretics
1165
05/24/2010
ELECTROLYTES
qAssessment
üThready, rapid, weak pulse
üFaint heart sounds
ü BP
üSkeletal muscle weakness
ü or absent reflexes
üShallow respirations
üMalaise, apathy, lethargy
üLoss of orientation
üAnorexia, vomiting, weight loss
üGaseous intestinal distention
1166
05/24/2010
ELECTROLYTES
üAdminister K+ supplements to
replace losses
üBe cautious in administering
drugs that are not potassium-
sparing
üMonitor acid-base balance
üMonitor pulse, BP and ECG
1167
05/24/2010
ELECTROLYTES
Hypercalcemia [Ca > 5.8 mEq/L; Normal = 4.5-5.8 mEq/L]
qCauses
üHyperparathyroidism
üImmobility
üIncreased vitamin D intake
üOsteoporosis & osteomalacia
[early stages]
qAssessment
üN & V, anorexia, constipation
üHeadache, confusion
üLethargy, stupor
1168
üDecreased muscle tone
05/24/2010
ELECTROLYTES
Hypercalcemia [Ca > 5.8 mEq/L; Normal = 4.5-5.8 mEq/L]
üEncourage mobilization
üLimit vitamin D intake
üLimit calcium intake
üNormal saline
üAdminister diuretics
üCalcitonin
1169
05/24/2010
ELECTROLYTES
Hypocalcemia [Ca < 4.5 mEq/L; Normal = 4.5-5.8 mEq/L]
qCauses
üAcute pancreatitis
üDiarrhea
üHypoparathyroidism
üLack of vitamin D I the diet
üLong-term steroid therapy
qAssessment
üPainful tonic muscle & facial
spasms
üFatigue, dyspnea
1170
üLaryngospasm, convulsions
05/24/2010
ELECTROLYTES
Hypocalcemia [Ca < 4.5 mEq/L; Normal = 4.5-5.8 mEq/L]
üAdminister oral Ca lactate or
IV CaCl2 or gluconate
üProviding safety by padding
side rails
üAdminister dietary sources of
calcium
üVitamin D
üProvide quiet environment
1171
05/24/2010
ELECTROLYTES
Hyermagnesemia [Mg > 3.0 mEq/L; Normal = 1.5-3.0 mEq/L]
qCauses
üRenal insufficiency, dehydration
üExcessive use of Mg-containing
antacids or laxatives
qAssessment
üLethargy, somnolence, confusion
üN & V
üMuscle weakness, depressed
reflexes
ü pulse and respirations
1172
üWithhold Mg-cont’g drugs/foods;
05/24/2010
ELECTROLYTES
Hypomagnesemia [Mg < 1.50 mEq/L; Normal = 1.5-3.0 mEq/L]
qCauses
üLow intake of Mg in the diet
üProlonged diarrhea
üMassive diuresis
üHypoparathyroidism
qAssessment
üParesthesias, muscle spasm
üConfusion, hallucination, convulsions
üAtaxia, tremors, hyperactive deep
reflexes
üFlushing of the face, diaphoresis
1173
ELECTROLYTE DISORDERS
SUMMARY
SIGNS AND SYMPTOMS
Electrolyte Excess Deficit
Sodium (Na) Hypernatremia Hyponatremia
Thirst CNS deterioration
CNS deterioration
Increased interstitial fluid
Potassium (K) Hyperkalemia Hypokalemia

Ventricular fibrillation Bradycardia
ECG changes ECG changes
CNS changes CNS changes
05/24/2010 1174
ELECTROLYTE DISORDERS
SIGNS AND SYMPTOMS
Electrolyte Excess Deficit
Calcium (Ca) Hypernatremia Hypocalcemia
Thirst Tetany
CNS deterioration Chvostek’s, Trousseau’s
Increased interstitial fluid Muscle twitching
CNS changes
EKG changes
Magnesium (Mg) Hypermagnesemia Hypomagnesemia
Loss of deep tendon reflexes Hyperactive deep tendon
(DTRs) reflexes
Depression of CNS CNS changes
Depression of neuromuscular EKG changes
function
05/24/2010 1175
05/24/2010
PROTEIN IMBALANCES
1176
05/24/2010
HYPOPROTEINEMIA
1177
05/24/2010
HYPOPROTEINEMIA
• Poor absorption d/t GI malabsorptive

diseases
•
• Inflammation → protein can shift out of
intravascular space
•
• Hemorrhage
•
• 1178
05/24/2010
HYPOPROTEINEMIA:
CLINICAL MANIFESTATIONS
1179
05/24/2010
HYPOPROTEINEMIA
1180
05/24/2010
EXTRACELLULAR FLUID VOLUME

IMBALANCES
1181
05/24/2010
EXTRACELLULAR FLUID VOLUME

IMBALANCES
1182
05/24/2010
NURSING DIAGNOSES: HYPERVOLEMIA
1183
05/24/2010
NURSING DIAGNOSES: HYPOVOLEMIA
1184
05/24/2010
NURSING IMPLEMENTATION FOR

VOLUME IMBALANCES
1185
NURSING IMPLEMENTATION FOR
05/24/2010
VOLUME IMBALANCES
 Neurologic function

 LOC
 PERLA
 Voluntary movement of extremities
 Muscle strength
 Reflexes
1186
05/24/2010
IV FLUIDS
1187
05/24/2010
SOLUTION TYPES
1188
05/24/2010
SOLUTION TYPES
1189
05/24/2010
SOLUTION TYPES
1190
05/24/2010
D5W
1191
05/24/2010
D5W
1192
05/24/2010
NORMAL SALINE (NS; 0.9% NACL)
1193
05/24/2010
NORMAL SALINE (NS; 0.9% NACL)
1194
05/24/2010
LACTATED RINGER’S
1195
05/24/2010
D5 ½ NS
1196
05/24/2010
D5 ½ NS (HYPERTONIC)
1197
05/24/2010
PLASMA EXPANDERS (HYPERTONIC)
1198
05/24/2010
IV FLUID REPLACEMENT THERAPY
Indications
qReplacement of abnormal fluid &

electrolyte losses [surgery, trauma,
burns, GI bleeding]
q
qMaintenance of daily fluid & electrolyte
needs
q
qCorrection of fluid disorders
q
qCorrection of electrolyte disorders
1199
05/24/2010
IV FLUID REPLACEMENT THERAPY
Types of Solutions
qIsotonic
ü0.9% sodium chloride (NSS)
üLactated Ringer’s sol’n
qHypotonic
ü5% dextrose and water (D5W)
ü0.45% sodium chloride
ü0.33% sodium chloride
qHypertonic
ü3% NaCl
üProtein sol’ns
qColloids
1200
üSalt pour albumin Plasmanate,
05/24/2010
FLUID IMBALANCES REVIEW!!!
• Involve either volume or distribution of

water or electrolytes
• Hypovolemia—deficiency in amount of
water and electrolytes in ECF with near
normal water/electrolyte proportions
• Dehydration—decreased volume of water
and electrolyte change
• Third-space fluid shift—distributional shift
of body fluids into potential body spaces
1201
05/24/2010
FLUID VOLUME EXCESS

• Hypervolemia—excessive retention of
water and sodium in ECF
• Overhydration—above normal amounts of
water in extracellular spaces
• Edema—excessive ECF accumulates in
tissue spaces
• Interstitial-to-plasma shift—movement of
fluid from space surrounding cells to
blood
1202
05/24/2010
ELECTROLYTE IMBALANCES
• Hyponatremia and hypernatremia
• Hypokalemia and hyperkalemia
• Hypocalcemia and hypercalcemia
• Hypomagnesemia and hypermagnesemia
• Hypophosphatemia and
hyperphosphatemia
1203
05/24/2010
QUESTION
 Which one of the following electrolyte

imbalances occurs due to a sodium deficit
in ECF caused by a loss of sodium or gain
of water?
 A. Hyponatremia
 B. Hypernatremia
 C. Hypokalemia
 D. Hyperkalemia
1204
05/24/2010
ANSWER
 Answer: A. Hyponatremia
 Rationale:
 Hyponatremia refers to a sodium deficit in ECF
caused by a loss of sodium or gain of water.
 Hypernatremia refers to a surplus of sodium in ECF.
 Hypokalemia refers to a potassium deficit in ECF.
 Hyperkalemia refers to an excess of potassium in
ECF.

1205
05/24/2010
BURNS
BURNS
Øwounds caused by excessive exposure to the
following agents or causes:
Causes of Burns:
qThermal [moist or dry heat]

qElectrical
qChemical [strong acids and strong alkali
qRadiation [UV, x-rays, radium, sunburns]
1206
05/24/2010
BURNS
CLASSIFICATION OF BURNS
qSuperficial Partial thickness (1st degree)

üOuter layer of dermis
üErythema, pain up to 48 hrs
üHealing 1-2 wks [sunburn]
qDeep Partial thickness (2nd degree)
üEpidermis & dermis
üBlisters & edema, frequently quite
painful
üHealing 14-21 days
qFull thickness (3rd degree)
üEpidermis, dermis, subcutaneous
fat
üDry, pearly white or charred in 1207
05/24/2010
BURNS
STAGES OF BURNS
1st : Shock/Fluid Accumulation Phase
q1st 48 hrs
qIVC  ISC
qGeneralized DHN [fluid shifting]
qHypovolemia [plasma loss],  BP,  C.O.
qHemoconcentration,  Hct [liquid blood
component  ISC]
qOliguria [ renal perfusion], ADH release
& aldosterone
qHyperK, hypoNa
qMetabolic acidosis
1208
05/24/2010
BURNS
STAGES OF BURNS
2nd : Diuretic/Fluid Remobilization Phase
qAfter 48 hrs
qISC  IVC
qHypervolemia,
qHemodilution,  Hct
qDiuresis [ renal perfusion],  ADH &
aldosterone secretion
qHypoK, hypoNa [K moves back into the
cells, Na+ still trapped in the edema
fluids
qMetabolic acidosis
1209
05/24/2010
BURNS
STAGES OF BURNS
3rd : Recovery Phase
q5th day onwards

qHypocalcemia
§Ca is lost on the exudates
§Ca is utilized in the granulation
tissue formation
qNegative nitrogen balance
§Due to stress response
§ protein catabolism
§Protein intake is lesser than the
demand
qHypoK 1210
05/24/2010
BURNS
ASSESSMENT
1.Assess extent of body surface burned

qGreater morbidity & mortality for burns
affecting face, hands & perineum
qAssess for dyspnea, stridor, hoarseness
1.Assess extent of burn injury

qRule of nine – immediate appraisal
qLund-Browder chart – more accurate
qBerkow’s method – based on client’s age &
changes that occur in proportion of
head & legs to the rest of the body as
one grows
1211
05/24/2010
BURNS
ASSESSMENT
9%
Front=18 %
9% Back=18 % 9%
1%
Burn Evaluation
18 % 18 %
Chart
1212
05/24/2010
BURNS
ASSESSMENT
3. Assess depth of burn

qMajor burns – 2nd degree over 30% of
body
qHospitalization - eyes, face, neck, hands,
perineum, genitalia
4. Assess unique contributing factors

qAge of client
qHealth history
üDiabetes, preexisting ulcers
üTetanus immunization
1213
05/24/2010
BURNS
EMERGENCY MANAGEMENT
Stop the burning process

qRemove patient from source of injury
qAdvise client to roll on the ground if
clothing is in flame [STOP-DROP-ROLL]
qThrow a blanket over the client to
smother the flame
qRemove clothing only if hot or for scald
burn
qImmerse affected part in cold water [10
min]
qIrrigate copiuosly w/ large amount of
running water w/ chemical burns
[except w/ phosphorus] 1214
05/24/2010
BURNS
MANAGEMENT
qMaintenance of adequate airway
qPromoting comfort: relieve pain
qPromoting fluid-electrolyte, acid-base

balance
qPreventing infection
qMaintaining adequate nutrition
qWound care
1215
05/24/2010
BURNS
METHODS OF TREATING BURNS
qOpen method or Exposure method

üFace, neck, perineum, trunk
üAllowing exudate to dry in 3 days
ü
qOcclusive
üLess pain, absorption of secretion,
comfort, transportability,
accelerated debridement
üAesthetic considerations
qSemi-open method
üCovering of wound w/ topical
antimicrobials: 1216
05/24/2010
BURNS
BIOLOGIC DRESSING (Skin Graft)
qAllograft
üSkin taken from other person
[cadaver]
ü
qAutograft
üSame person
qHeterograft
üDifferent species
üXenograft [segment of skin from
animal such as pig or dog]
1217
05/24/2010
BURNS
FLUID REPLACEMENT
Types of fluids:
qColloids
üBlood
üPlasma & plasma expanders
qElectrolytes
üLactated Ringers
qNon-electrolyte
üD5W
1218
05/24/2010
BURNS
FLUID REPLACEMENT
EVAN’S Formula:
qC– 1ml x % burns x kgBW

qE- 1ml x % burns x kgBW
qGlucose 5% for insensible loss – 2,000ml
D5W
vAdminister sol’n 1st 24 hrs – ½ [1st 8hrs], ½

[16hrs]
BROOKE Formula: [Administer as in Evan’s]
qC– 0.5ml x % burn x kgBW 1219

05/24/2010
BURNS
FLUID REPLACEMENT
MOORES BURN BUDGET:
q75 ml of plasma, 75 ml of electrolyte-

cont’g fluid for q 1%TBSA plus 2000
D5W
HYPERTONIC RESUSCITATION Formula:
qHypertonic salt containing 300mEq of

Na+, 100mEq of Cl-, 200mEq lactate
qAdministered to maintain urinary output
of 30-40 ml/hr
1220
05/24/2010
REGULATION OF CALCIUM AND

PHOSPHATE
1221
05/24/2010
REGULATION OF CALCIUM AND

PHOSPHATE
Filtered phosphate is actively reabsorbed in

the proximal tubules
In the absence of PTH, phosphate
reabsorption is regulated by its transport

maximum and excesses are excreted in
urine
High or normal ECF calcium levels inhibit PTH
secretion
 Release of calcium from bone is inhibited
 Larger amounts of calcium are lost in feces and
urine
 More phosphate is retained
1222
05/24/2010
INFLUENCE OF CALCITONIN
• Released in response to rising blood

calcium levels
• Calcitonin is a PTH antagonist, but its
contribution to calcium and phosphate
homeostasis is minor to negligible
1223
05/24/2010
REGULATION OF ANIONS
1224
05/24/2010
ACID-BASE BALANCE
1225
05/24/2010
SOURCES OF HYDROGEN IONS
1226
05/24/2010
HYDROGEN ION REGULATION
1227
05/24/2010
CHEMICAL BUFFER SYSTEMS
1228
05/24/2010
CHEMICAL BUFFER SYSTEMS
1229
05/24/2010
BICARBONATE BUFFER SYSTEM
1230
05/24/2010
BICARBONATE BUFFER SYSTEM
1231
05/24/2010
PHOSPHATE BUFFER SYSTEM
1232
05/24/2010
PROTEIN BUFFER SYSTEM
1233
05/24/2010
PHYSIOLOGICAL BUFFER SYSTEMS
1234
05/24/2010
PHYSIOLOGICAL BUFFER SYSTEMS
1235
05/24/2010
RENAL MECHANISMS OF ACID-BASE

BALANCE
1236
05/24/2010

BALANCE
1237
05/24/2010

BALANCE
1238
05/24/2010
REABSORPTION OF BICARBONATE
1239
05/24/2010
REABSORPTION
• Carbonic acid OF BICARBONATE
formed in
filtrate
dissociates to
release carbon
dioxide and
water
• Carbon dioxide
then diffuses
into tubule
cells, where it
acts to trigger
further
hydrogen ion
1240
Figure 26.12
05/24/2010
GENERATING NEW BICARBONATE IONS
1241
05/24/2010
HYDROGEN ION EXCRETION
Dietary hydrogen ions must be counteracted by

generating new bicarbonate
The excreted hydrogen ions must bind to
buffers in the urine (phosphate buffer system)

Intercalated cells actively secrete hydrogen
ions into urine, which is buffered and excreted

Bicarbonate generated is:
 Moved into the interstitial space via a cotransport

system
 Passively moved into the peritubular capillary
blood
1242
05/24/2010
HYDROGEN ION EXCRETION

In response to
acidosis:
 Kidneys
generate
bicarbonate
ions and add
them to the
blood
 An equal
amount of
hydrogen ions
are added to
the urine
1243
Figure 26.13
05/24/2010
AMMONIUM ION EXCRETION
1244
05/24/2010
AMMONIUM ION
EXCRETION
Figure 26.14
1245
05/24/2010
BICARBONATE ION SECRETION
1246
05/24/2010
Blood Gas Interpretation
Respiratory Metabolic
Acidosis Alkalosis
26 45
HCO3 Normal Ranges PaCO2
22 35
Metabolic Respiratory
Acidosis Alkalosis
7 . 35
pH
7 . 45
1247
05/24/2010
RESPIRATORY ACIDOSIS AND ALKALOSIS
1248
05/24/2010
RESPIRATORY ACIDOSIS AND ALKALOSIS
1249
05/24/2010
METABOLIC ACIDOSIS
1250
05/24/2010
METABOLIC ALKALOSIS
1251
05/24/2010
RESPIRATORY AND RENAL

COMPENSATIONS
1252
05/24/2010
RESPIRATORY COMPENSATION
1253
05/24/2010
RESPIRATORY COMPENSATION
1254
05/24/2010
RENAL COMPENSATION
1255
05/24/2010
RENAL COMPENSATION
Alkalosis has Low PCO2 and high pH


 The kidneys eliminate bicarbonate from the

body by failing to reclaim it or by actively
secreting it
1256
05/24/2010
DEVELOPMENTAL ASPECTS
1257
05/24/2010
PROBLEMS WITH FLUID, ELECTROLYTE,

AND ACID-BASE BALANCE
Occur in the young, reflecting:


 Low residual lung volume

 High rate of fluid intake and output
 High metabolic rate yielding more metabolic
wastes
 High rate of insensible water loss
 Inefficiency of kidneys in infants
1258
05/24/2010
ACID–BASE IMBALANCES
Occur when carbonic acid or bicarbonate


levels become disproportionate

 Respiratory acidosis—primary excess of
carbonic acid in ECF
 Respiratory alkalosis—primary deficit of
carbonic acid in ECF
 Metabolic acidosis—proportionate deficit of
bicarbonate in ECF
 Metabolic alkalosis—primary excess of
bicarbonate in ECF
1259
05/24/2010
NURSING ASSESSMENTS
• Identify patients at risk for imbalances
• Determine a specific imbalance is present
and its severity, etiology, and
characteristics
• Determine effectiveness of plan of care
1260
05/24/2010
PARAMETERS OF ASSESSMENT
• Nursing history and physical assessment
• Fluid intake and output
• Daily weights
• Laboratory studies
1261
05/24/2010
LAB STUDIES TO ASSESS FOR

IMBALANCES
• Complete blood count
• Serum electrolytes
• Urine pH and specific gravity
• Arterial blood gases
1262
05/24/2010
RISK FACTORS FOR IMBALANCES

• Pathophysiology underlying acute and
chronic illnesses
• Abnormal losses of body fluids
• Burns
• Trauma
• Therapies that disrupt fluid and electrolyte
balance
1263
05/24/2010
NURSING DIAGNOSES RELATED TO

IMBALANCES
• Excess fluid volume
• Deficient fluid volume
• Risk for imbalanced fluid volume
1264
05/24/2010
EXPECTED OUTCOMES
• Maintain approximate fluid intake and
output balance (2500 mL intake and
output over 3 days)
• Maintain urine specific gravity within
normal range (1010 to 1025)
• Practice self-care behaviors to promote
balance
1265
05/24/2010
IMPLEMENTING
• Dietary modifications
• Modifications of fluid intake
• Medication administration
• IV therapy
• Blood and blood products replacement
• TPN
1266
05/24/2010
ADMINISTERING MEDICATIONS
• Mineral-electrolyte preparations
• Diuretics
• Intravenous therapy
1267
05/24/2010
INTRAVENOUS THERAPY
• Vascular access devices
• Peripheral venous catheters
• Midline peripheral catheter
• Central venous access devices
• Implanted ports
1268
05/24/2010
QUESTION

true or false.
 Central venous access devices provide
access for a variety of IV fluids,
medications, blood products, and TPN
solutions and allow a means for
hemodynamic monitoring and blood
sampling.
 A. True
 B. False
1269
05/24/2010
ANSWER
 Answer: A. True
 Central venous access devices provide
access for a variety of IV fluids,
medications, blood products, and TPN
solutions and allow a means for
hemodynamic monitoring and blood
sampling.
•
1270
05/24/2010
VEIN SITE SELECTION

• Accessibility of a vein
• Condition of vein
• Type of fluid to be infused
• Anticipated duration of infusion
1271
05/24/2010
PLACEMENT OF PERIPHERALLY
INSERTED CENTRAL CATHETER
(PICC)
1272
05/24/2010
ADMINISTERING BLOOD AND

BLOOD PRODUCTS
• Typing and cross-matching
• A, B, AB, and O type blood
• Rh factor
• Selecting blood donors
• Initiating transfusion
• Transfusion reactions
1273

Anatomy and Physiology by Dennis Munoz2

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 Anatomy and Physiology

Figure 13.1 SLIDE 13.1

•The only externally visible part of the respiratory

•Olfactory receptors are located in the

•Lateral walls have projections called

•The nasal cavity is separated from the

•Cavities within bones surrounding the

•Function of the sinuses

Anterior View Lateral View

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

•Auditory tubes enter the nasopharynx

•Routes air and food into proper channels

Anterior View Lateral View

•False vocal cords

•Connects larynx with bronchi

•Formed by division of the trachea

•Occupy most of the thoracic cavity

•Visceral pleura covers the lung surface

•Primary bronchi = 1 left = 1 right

 2 types of cell Polyhedral in shape

 ~ 300 million air sacs (alveoli).

 Reduces attractive forces

surfactant’s ability to lower

•Simple squamous E.T. layer: lines

•Gas crosses the respiratory membrane

•Transport of oxygen and carbon dioxide

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings

 Alveolar changes from 0 to –

Insert fig. 16.15

Not all of the inspired air reached the alveoli.

anatomical dead space.

•Tidal volume [TV]:

•Oxygen transport in the blood

•Carbon dioxide transport in the blood

nPC0 is 46 mm Hg in the systemic veins.

nProvides a good index of lung function.

Activities of medullary rhythmicity center is

 Promotes inspiration by stimulating the I

and pH. Insert fig. 16.27

 Carotid and aortic bodies.

Chemoreceptor input modifies the rate

and depth of breathing.

H20 + C02 H2C03 H+ + HC03-

maintain arterial PC0 of 40 mm Hg.

 H20 + C02 H2C03 H+

Rate and Depth

Rate and Depth

Obstructive Pulmonary Disease

•Chronic bronchitis and emphysema

•Alveoli enlarge as adjacent chambers break

•Accounts for 1/3 of all cancer deaths in

•Apparently healthy infant stops breathing

•Chronic inflamed hypersensitive

DENNIS NABOR MUÑOZ, R.N., R.M.

How to Perform a Patient Bedside

• Thoracic cage bony conical shape with

 Manubriosternal Angle- “Angle of Louis”-

– Lungs Border- posterior

• Trachea- lies anterior to esophagus; is

 5. Environmental exposure- where did

a.Symmetric expansion- place hands of

 Affecting normal intensity of Tactile

 -Relative location of bronchi to chest wall