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Overview of the Structures & Functions of Nervous System

Central NS PNS ANS
Brain & spinal cord 31 spinal & cranial sympathetic NS
Parasypathatic NS

Somatic NS
C- 8
T- 12
L- 5
S- 5
C- 1
ANS (or adrenergic of parasympatholitic response)

SNS involved in fight or aggression response Effects of SNS (anti-cholinergic/adrenergic)

1. Dilate pupil – to aware of surroundings
Release of norepinephrine (adrenaline – cathecolamine) - medriasis
Adrenal medulla (potent vasoconstrictor) 2. Dry mouth
Increases body activities VS = Increase 3. BP & HR= increased
Except GIT – decrease GITmotility
4. RR increased- broncho dilation
* Why GIT is not increased = GIT is not important! 5. Constipation & urinary retention
Increase blood flow to skeletal muscles, brain & heart. 6. Nor/Epinephrine- neurotransmitter
7. Blood vessels-vasoconstriction
I. SNS: Adrenergic Agents – Epinephrine (adrenaline)
Anticholinergic , Sympathomimetic, Parasympatholytic
-Atropine sulfate

II. PNS: Cholinergics, Beta Adrenergic blockers, Sympatholitic, Parasympathomimetic

Beta adrenergic blocking agents (opposite of adrenergic agents) (all end in –‘lol’)
- Blocks release of norepinephrine.
- Decrease body activities except GIT (diarrhea)
Ex. Propanolol, Metopanolol

B – broncho spasm (bronchoconstriction)
E – elicits a decrease in myocardial contraction
T – treats HPN
A – AV conduction slows down

Given to angina & MI – beta-blockers to rest heart

Anti HPN agents:
1. Beta blockers (-lol)
2. Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL
3. Calcium antagonist

Peripheral nervous system: cholinergic/ vagal or sympatholitic response Effect of PNS: (cholinergic)
- Involved in fly or withdrawal response 1. Meiosis – constriction of pupils
- Release of acetylcholine (ACTH) 2. Increase salivation
- Decrease all bodily activities except GIT (diarrhea) 3. BP & HR decreased
4. RR decrease – broncho constriction
I Cholinergic agents 5. Diarrhea – increased GI motility
ex 1. Mestinon 6. Urinary frequency
Antidote – anti cholinergic agents Atropine Sulfate – S/E – SNS 7. Acetylcholine- neurotransmitter
8. Blood vessels- vasodilated
S/E- of anti-hpn drugs:
1. orthostatic hpn
2. transient headache & dizziness.-Mgt. Rise slowly. Assist in ambulation.

CNS (brain & spinal cord)

I. Cells – A. neurons
Properties and characteristics
a. Excitability – ability of neuron to be affected in external environment.
b. Conductivity – ability of neuron to transmit a wave of excitation from one cell to another
c. Permanent cells – once destroyed, cant regenerate (ex. heart, retina, brain, osteocytes)
Regenerative capacity
A. Labile – once destroyed cant regenerate
- Epidermal cells, GIT cells, resp (lung cells). GUT
B. Stable – capable of regeneration BUT limited time only ex salivary gland, pancreas cells cell of liver, kidney cells
C. Permanent cells – retina, brain, heart, osteocytes can’t regenerate.

3.) Neuroglia – attached to neurons. Supports neurons. Where brain tumors are found.
1. Astrocyte
2. Oligodendria

Astrocytoma – 90 – 95% brain tumor from astrocyte. Most brain tumors are found at astrocyte.
Astrocyte – maintains integrity of blood brain barrier (BBB).
BBB – semi permeable / selective
-Toxic substance that destroys astrocyte & destroy BBB.
Toxins that can pass in BBB:
1. Ammonia-liver cirrhosis.
2. 2. Carbon Monoxide – seizure & parkinsons.
3. 3. Bilirubin- jaundice, hepatitis, kernicterus/hyperbilirubenia.
4. 4. Ketones –DM.

OLIGODENDRIA – Produces myelin sheath – wraps around a neuron – acts as insulator facilitates rapid nerve impulse transmission.
No myelin sheath – degenerates neurons

Damage to myelin sheath – demyellenating disorders

1.)ALZHEIMER’S DISEASE– atrophy of brain tissue due to a deficiency of acetylcholine.

A – amnesia – loss of memory
A – apraxia – unable to determine function & purpose of object
A – agnosia – unable to recognize familiar object
A – aphasia –
- Expressive – brocca’s aphasia – unable to speak
- Receptive – wernickes aphasia – unable to understand spoken words
Common to Alzheimer – receptive aphasia
Drug of choice – ARICEPT (taken at bedtime) & COGNEX.
Mgt: Supportive & palliative.

Microglia – stationary cells, engulfs bacteria, engulfs cellular debris.

II. Compositions of Cord & Spinal cord

80% - brain mass
10% - CSF
10% - blood
MONROE KELLY HYPOTHESIS: The skull is a closed vault. Any increase in one component will increase ICP.

Normal ICP: 0-15mmHg
Brain mass

1. Cerebrum – largest - Connects R & L cerebral hemisphere

- Corpus collusum
Rt cerebral hemisphere, Lt cerebral hemisphere
1. Sensory
2. Motor
3. Integrative
1.) Frontal
a. Controls motor activity
b. Controls personality development
c. Where primitive reflexes are inhibited
d. Site of development of sense of umor
e. Brocca’s area – speech center
Damage - expressive aphasia
2.) Temporal –
a. Hearing
b. Short term memory
c. Wernickes area – gen interpretative or knowing Gnostic area
Damage – receptive aphasia
3.) Parietal lobe – appreciation & discrimation of sensory imp
- Pain, touch, pressure, heat & cold
4.) Occipital - vision
5.) Insula/island of reil/ Central lobe- controls visceral fx
Function: - activities of internal organ
6.) Rhinencephalon/ Limbec
- Smell, libido, long-term memory

Basal Ganglia – areas of gray matte located deep within a cerebral hemisphere
- Extra pyramidal tract
- Releases dopamine-
- Controls gross voluntary unit

Decrease dopamine – (Parkinson’s) pin rolling of extremiies & Huntington’s Dse.

Decrease acetylcholine – Myasthenia Gravis & Alzheimer’s
Increased neurotransmitter = psychiatric disorder Increase dopamine – schizo
Increase acetylcholine – bipolar

MID BRAIN – relay station for sight & hearing

Controls size & reaction of pupil 2 – 3 mm
Controls hearing acuity
CN 3 – 4
Isocoria – normal size (equal)
Anisocoria – uneven size – damage to mid brain
PERRLA – normal reaction

DIENCEPHALON- between brain

Thalamus – acts as a relay station for sensation
Hypothalamus – (thermoregulating center of temp, sleep & wakefulness, thirst, appetite/ satiety center, emotional responses,
controls pituitary function.

BRAIN STEM- a. Pons – or pneumotaxic center – controls respiration

Cranial 5 – 8 CNS

MEDULLA OBLONGATA- controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus
Vasomotor center, spinal decuissation termination, CN 9, 10, 11, 12

CEREBELLUM – lesser brain

- Controls posture, gait, balance, equilibrium
Cerebellar Tests:
a.) R – Romberg’s test- needs 2 RNs to assist
- Normal anatomical position 5 – 10 min
(+) Romberg’s test – (+) ataxia or unsteady gait or drunken like movement with loss of balance.
b.) Finger to nose test –
(+) To FTNT – dymetria – inability to stop a movement at a desired point
c.) Alternate pronation & supination
Palm up & down . (+) To alternate pronation & supination or damage to cerebellum – dymentrium

Composition of brain - based on Monroe Kellie Hypothesis

- Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP

Normal ICP – 0 – 15 mmHg

Foramen Magnum
C1 – atlas
C2 – axis

(+) Projectile vomiting = increase ICP

Observe for 24 - 48 hrs
CSF – cushions the brain, shock absorber
Obstruction of flow of CSF = increase ICP
Hydrocephalus – posteriorly due to closure of posterior fontanel
CVA – partial/ total obstruction of blood supply

INCREASED ICP – increase ICP is due to increase in 1 of the Intra Cranial components.
Predisposing factors:
1.) Head injury
2.) Tumor
3.) Localized abscess
4.) Hemorrhage (stroke)
5.) Cerebral edema
6.) Hydrocephalus
7.) Inflammatory conditions - Meningitis, encephalitis

B. S&Sx change in VS = always late symptoms

Earliest Sx:
a.) Change or decrease LOC – Restlessness to confusion Wide pulse pressure: Increased ICP
- Disorientation to lethargy Narrow pp: Cardiac disorder, shock
- Stupor to coma
Late sign – change in V/S
1. BP increase (systolic increase, diastole- same)
2. Widening pulse pressure
Normal adult BP 120/80 120 – 80 = 40 (normal pulse pressure)
Increase ICP = BP 140/80 = 140 – 80= 60 PP (wide)
3. RR is decreased (Cheyne-Stokes = bet period of apnea or hyperpnea with periods of apnea)
4. Temp increase
Increased ICP: Increase BP Shock – decrease BP –
Decrease RR Increase RR
Increase Temp Decrease temp
b.) Headache
Projectile vomiting
Papilledima (edema of optic disk – outer surface of retina)
Decorticate (abnormal flexion) = Damage to cortico spinal tract /
Decerebrate (abnormal extension) = Damage to upper brain stem-pons/

c.) Uncal herniation – unilateral dilation of pupil. (Bilateral dilation of pupil – tentorial herniation.)
d.) Possible seizure.

Nursing priority:
1.) Maintain patent a/w & adequate ventilation
a. Prevention of hypoxia – (decrease tissue oxygenation) & hypercarbia (increase in CO2 retention).

Hypoxia – cerebral edema - increase ICP

Hypoxia – inadequate tissue oxygenation
Late symptoms of hypoxia – B – bradycardia
E – extreme restlessness
D – dyspnea
C – cyanosis
Early symptoms – R – restlessness
A – agitation
T – tachycardia

Increase CO2 retention/ hypercarbia – cerebral vasodilatation = increase ICP

Most powerful respiratory stimulant increase in CO2
Hyperventilate decrease CO2 – excrete CO2

Respiratory Distress Syndrome (RDS) – decrease Oxygen

Suctioning – 10-15 seconds, max 15 seconds. Suction upon removal of suction cap.
Ambu bag – pump upon inspiration

c. Assist in mechanical ventilation

1. Maintain patent a/w
2. Monitor VS & I&O
3. Elevate head of bed 30 – 45 degrees angle neck in neutral position unless contra indicated to promote venous
4. Limit fluid intake 1,200 – 1,500 ml/day
(FORCE FLUID means:Increase fluid intake/day – 2,000 – 3,000 ml/day)- not for inc ICP.

5. Prevent complications of immobility

6. Prevent increase ICP by:
a. Maintain quiet & comfy environment
b. Avoid use of restraints – lead to fractures
c. Siderails up
d. Instruct patient to avoid the ff:
-Valsalva maneuver or bearing down, avoid straining of stool
(give laxatives/ stool softener Dulcolax/ Duphalac)
- Excessive cough – antitussive
-Excessive vomiting – anti emetic (Plasil – Phil only)/ Phenergan
- Lifting of heavy objects
- Bending & stooping
e. Avoid clustering of nursing activities
7. Administer meds as ordered:
1.) Osmotic diuretic – Mannitol./Osmitrol promotes cerebral diuresis by decompressing brain tissue

Nursing considerations: Mannitol

1. Monitor BP – SE of hypotension
2. Monitor I&O every hr. report if < 30cc out put
3. Administer via side drip
4. Regulate fast drip – to prevent formation of crystals or precipitate

2.) Loop diuretic - Lasix (Furosemide)

Nursing Mgt: Lasix
Same as Mannitol except
- Lasix is given via IV push (expect urine after 10-15mins) should be in the
morning. If given at 7am. Pt will urinate at 7:15
Immediate effect of Lasix within 15 minutes. Max effect – 6 hrs due (7am – 1pm)
S/E of Lasix
Hypokalemia (normal K-3.5 – 5.5 meg/L)
1. Weakness & fatigue
2. Constipation
3. (+) “U” wave in ECG tracing

Nursing Mgt:
1.) Administer K supplements – ex Kalium Durule, K chloride
Potassium Rich food:
ABC’s of K
Vegetables Fruits
A - asparagus A – apple
B – broccoli (highest) B – banana – green
C – carrots C – cantalope/ melon
O – orange (highest) –for digitalis toxicity also.
Vit A – squash, carrots yellow vegetables & fruits, spinach, chesa
Iron – raisins,
Food appropriate for toddler – spaghetti! Not milk – increase bronchial secretions
Don’t give grapes – may choke

S/E of Lasix:
1.) Hypokalemia
2.) Hypocalcemia (Normal level Ca = 8.5 – 11mg/100ml) or Tetany:
(+) Trousseau sign – pathognomonic – or carpopedal spasm. Put bp cuff on arm=hand spasm.
(+) Chevostek’s sign
Administer – Ca gluconate – IV slowly

Ca gluconate toxicity: Sx – seizure – administer Mg SO4

Mg SO4 toxcicity– administer Ca gluconate
B – BP decrease
U – urine output decrease
R – RR decrease
P – patellar reflexes absent

3.) Hyponatremia – Normal Na level = 135 – 145 meg/L

S/Sx – Hypotension
Signs of Dehydration: dry skin, poor skin turgor, gen body malaise.
Early signs – Adult: thirst and agitation / Child: tachycardia
Mgt: force fluid
Administer isotonic fluid sol

4.) Hyperglycemia – increase blood sugar level

P – polyuria
P – polyphagia
P – polydipsia

Nsg Mgt:
a. Monitor FBS (N=80 – 120 mg/dl)
5.) Hyperurecemia – increase serum uric acid. Tophi- urate crystals in joint.

Gou ty arthritis kidney stones- renal colic (pain)
Cool moist skin
Sx joint pain & swelling usually at great toe.

Nsg Mgt of Gouty Arthritis

a.) Cheese (not sardines, anchovies, organ meat)
(Not good if pt taking MAO)
b.) Force fluid
c.) Administer meds – Allopurinol/ Zyloprim – decrease uric acid production – drug of choice for gout
Colchicene – excretes uric acid. Acute gout drug of choice.
Kidney stones – renal colic (pain). Cool moist skin
1.) Force fluid
2.) Meds – narcotic analgesic
Morphine SO4

SE of Morphine SO4 toxicity

Respiratory depression (check RR 1st)
Antidote for morphine SO4 toxicity –Narcan (NALOXONE)
Naloxone toxicity – tremors

Increase ICP meds:

3.) Corticosteroids - Dexamethsone – decrease cerebral edema (Decadrone)
4.) Mild analgesic – codeine SO4. For headache.
5.) Anti consultants – Dilantin (Phenytoin)

Question: Increase ICP what is the immediate nsg action?

a. Administer Mannitol as ordered
b. Elevate head 30 – 45 degrees
c. Restrict fluid
d. Avoid use of restraints

Nsg Priority – ABC & safety

Pt suffering from epiglotitis. What is nsg priority?

a. Administer steroids – least priority
b. Assist in ET – temp, a/w
c. Assist in tracheotomy – permanent (Answer)
d. Apply warm moist pack? Least priority
Rationale: Wont need to pass larynx due to larynx is inflamed. ET can’t pass. Need tracheostomy only-

Magic 2’s of drug monitoring

Drug N range Toxicity Classification Indication

D – digoxin .5 – 1.5 meq/L 2 cardiac glycosides CHF
L - lithium .6 – 1.2 meq/L 2 antimanic bipolar
A – aminophylline 10 – 19 mg/100ml 20 bronchodilator COPD
D – Dilantin 10 -19 mg/100 ml 20 anticonvulsant seizures
A – acetaminophen 10 – 30 mg/100ml 200 narcotic analgesic osteoarthritis

Digitalis – increase cardiac contraction = increase CO

Nursing Mgt
1. Check PR, HR (if HR below 60bpm, don’t giveDigoxin)
Digitalis toxicity – antidote - Digivine
a. Anorexia -initial sx.
b. n/v GIT
c. Diarrhea
d. Confusion

e. Photophobia
f. Changes in color perception – yellow spots
(Ok to give to pts with renal failure. Digoxin is metabolized in liver not in kidney.)

L – lithium (lithane) decrease levels of norepinephrine, serotonine, acetylcholine

Antimanic agent
Lithium toxicity
S/Sx -
a.) Anorexia
b.) n/s
c.) Diarrhea
d.) Dehydration – force fluid, maintain Na intake 4 – 10g daily
e.) Hypothyroidism
(CRETINISM– the only endocrine disorder that can lead to mental retardation)

A – aminophyline (theophylline) – dilates bronchioles.

Take bp before giving aminophylline.
S/Sx : Aminophylline toxicity:
1. Tachycardia
2. Hyperactivity – restlessness, agitation, tremors

Question: Avoid giving food with Aminophylline

a. Cheese/butter– food rich in tyramine, avoided only if pt is given MAOI
b. Beer/ wine -
c. Hot chocolate & tea – caffeine – CNS stimulant tachycardia
d. Organ meat/ box cereals – anti parkinsonian

MAOI – antidepressant
m AR plan
n AR dil can lead to CVA or hypertensive crisis
p AR nate
3 – 4 weeks - before MAOI will take effect
Anti Parkinsonian agents – Vit B6 Pyridoxine reverses effect of Levodopa

D – dilatin (Phenytoin) – anti convulsant/seizure

Nursing Mgt:
1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate
- Do sandwich method
- Give NSS then Dilantin, then NSS!
2. Instruct the pt to avoid alcohol – bec alcohol + dilantin can lead to severe CNS depression

Dilantin toxicity:
G – gingival hyperplasia – swollen gums
i. Oral hygiene – soft toothbrush
ii. Massage gums
H – hairy tongue
A - ataxia
N – nystagmus – abnormal movement of eyeballs
A – acetaminophen/ Tylenol – non-opoid analgesic & antipyretic – febrile pts
Acetaminophen toxicity :
1. Hepato toxicity
2. Monitor liver enzymes
SGPT (ALT) – Serum Glutamic Piruvate Tyranase
SGOT- Serum Glutamic Acetate Tyranase
3. Monitor BUN (10 – 20)
Crea (.8-1)
Acetaminophen toxicity can lead to hypoglycemia

T – tremors, Tachycardia
I – irritability
R – restlessness
E – extreme fatigue
D – depression (nightmares) , Diaphoresis
Antidote for acetaminophen toxicity – Acetylcesteine = causes outporing of secretions. Suction.
Prepare suctioning apparatus.
Question: The following are symptoms of hypoglycemia except:
a. Nightmares
b. Extreme thirst – hyperglycemia symptoms
c. Weakness d. Diaphoresis

PARKINSONS DSE (parkinsonism) - chronic, progressive disease of CNS char by degeneration of dopamine
producing cells in substancia nigra at mid brain & basal ganglia
- Palliative, Supportive
Function of dopamine: controls gross voluntary motors.
Predisposing Factors:
1. Poisoning (lead & carbon monoxide). Antidote for lead = Calcium EDTA
2. Hypoxia
3. Arteriosclerosis
4. Encephalitis

High doses of the ff:

a. Reserpine (serpasil) anti HPN, SE – 1.) depression - suicidal 2.) breast cancer
b. Methyldopa (aldomet) - promote safety
c. Haloperidol (Haldol)- anti psychotic
d. Phenothiazide - anti psychotic

SE of anti psychotic drugs – Extra Pyramidal Symptom

Over meds of anti psychotic drugs – neuroleptic malignant syndrome char by tremors (severe)
S/Sx: Parkinsonism –
1. Pill rolling tremors of extremities – early sign
2. Bradykinesia – slow movement
3. Over fatigue
4. Rigidity (cogwheel type)
a. Stooped posture
b. Shuffling – most common
c. Propulsive gait
5. Mask like facial expression with decrease blinking eyes
6. Monotone speech
7. Difficulty rising from sitting position
8. Mood labilety – always depressed – suicide
Nsg priority: Promote safety
9. Increase salivation – drooling type
10. Autonomic signs:
- Increase sweating
- Increase lacrimation
- Seborrhea (increase sebaceous gland)
- Constipation
- Decrease sexual activity
Nsg Mgt
1.) Anti parkinsonian agents
- Levodopa (L-Dopa), Carbidopa (Sinemet), Amantadine Hcl (Symmetrel)
Mechanism of action
Increase levels of dopa – relieving tremors & bradykinesia
S/E of anti parkinsonian
- Anorexia
- n/v
- Confusion
- Orthostatic hypotension
- Hallucination
- Arrhythmia
1. Narrow angled closure glaucoma
2. Pt taking MAOI (Parnate, Marplan, Nardil)

Nsg Mgt when giving anti-parkinsonian

1. Take with meals – to decrease GIT irritation
2. Inform pt – urine/ stool may be darkened
3. Instruct pt- don’t take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg
- Cause B6 reverses therapeutic effects of levodopa
Give INH (Isoniazide-Isonicotene acid hydrazide.) SE-Peripheral neuritis.
2.) Anti cholinergic agents – relieves tremors
Artane mech – inhibits acetylcholine
Cogentin action , S/E - SNS

3.) Antihistamine – Diphenhydramine Hcl (Benadryl) – take at bedtime

S/E: adult– drowsiness,– avoid driving & operating heavy equipt. Take at bedtime.
Child – hyperactivity CNS excitement for kids.
4.) Dopamine agonist
Bromotriptine Hcl (Parlodel) – respiratory depression. Monitor RR.

Nsg Mgt – Parkinson

1.) Maintain siderails
2.) Prevent complications of immobility
- Turn pt every 2h
Turn pt every 1 h – elderly
3.) Assist in passive ROM exercises to prevent contractures
4.) Maintain good nutrition
CHON – in am
CHON – in pm – to induce sleep – due Tryptopan – Amino Acid
5.) Increase fluid in take, high fiber diet to prevent constipation
6.) Assist in surgery – Sterotaxic Thalamotomy
Complications in sterotaxic thalmotomy- 1.) Subarachnoid hemorrhage 2.) aneurism 3.) encephalitis


Chronic intermittent disorder of CNS – white patches of demyelenation in brain & spinal cord.
- Remission & exacerbation
- Common – women, 15 – 35 yo cause – unknown
Predisposing factor:
1. Slow growing virus
2. Autoimmune – (supportive & palliative treatment only)
Normal Resident Antibodies:
Ig G – can pass placenta – passive immunity. Short acting.
Ig A – body secretions – saliva, tears, colostrums, sweat
Ig M – acute inflammation
Ig E – allergic reactions
IgD – chronic inflammation

S & Sx of MS: (everything down)

1. Visual disturbances
a. Blurring of vision
b. Diplopia/ double vision
c. Scotomas (blind spots) – initial sx
2. Impaired sensation to touch, pain, pressure, heat, cold
a. Numbness
b. Tingling
c. Paresthesia
3. Mood swings – euphoria (sense of elation )

4. Impaired motor function:
a. Weakness
b. Spasiticity –“ tigas”
c. Paralysis –major problem
5. Impaired cerebellar function

Triad Sx of MS
I – intentional tremors
N – nystagmus – abnormal rotation of eyes Charcots triad
A – Ataxia
& Scanning speech
6. Urinary retention or incontinence
7. Constipation
8. Decrease sexual ability
Dx – MS
1. CSF analysis thru lumbar puncture
- Reveals increase CHON & IgG
2. MRI – reveals site & extent of demyelination
3. Lhermitte’s response is (+). Introduce electricity at the back. Theres spasm & paralysis at spinal cord.
Nsg Mgt MS
- Supportive mgt
1.) Meds
a. Acute exacerbation
ACTH – adenocorticotopic
Steroids – to reduce edema at the site of demyelination to prevent paralysis
Spinal Cord Injury
Administer drug to prevent paralysis due to edema
a. Give ACTH – steroids
b. Baclopen (Lioresol) or Dantrolene Na (Dantrium)
To decrease muscle spasticity
c. Interferone – to alter immune response
d. Immunosuppresants
2. Maintain siderails
3. Assist passive ROMexercises – promote proper body alignment
4. Prevent complications of immobility
5. Encourage fluid intake & increase fiber diet – to prevent constipation
6. Provide catheterization due urinary retention
7. Give diuretics
Urinary incontinence – give Prophantheline bromide (probanthene)

Antispasmodic anti cholinergic

8. Give stress reducing activity. Deep breathing exercises, biofeedback, yoga techniques.
9. Provide acid-ash diet – to acidify urine & prevent bacteria multiplication
Grape, Cranberry, Orange juice, Vit C

MYASTHENIA GRAVIS (MG) – disturbance in transmission of impulses from nerve to muscle cell at neuro muscular
Common in Women, 20 – 40 yo, unknown cause or idiopathic
Autoimmune – release of cholenesterase – enzyme
Cholinesterase destroys ACH (acetylcholine) = Decrease acetylcholine
Descending muscle weakness
(Ascending muscle weakness – Guillain Barre Syndrome)
Nsg priority:
1) a/w
2) aspiration
3) immobility
S/ Sx:
1.) Ptosis – drooping of upper lid ( initial sign)
Check Palpebral fissure – opening of upper & lower lids = to know if (+) of MG.
2.) Diplopia – double vision
3.) Mask like facial expression
4.) Dysphagia – risk for aspiration!
5.) Weakening of laryngeal muscles – hoarseness of voice
6.) Resp muscle weakness – lead respiratory arrest. Prepare at bedside tracheostomy set
7.) Extreme muscle weakness during activity especially in the morning.

Dx test
1. Tensilon test (Edrophonium Hcl) – temporarily strengthens muscles for 5 – 10 mins. Short term- cholinergic. PNS effect.
Nsg Mgt
1. Maintain patent a/w & adequate vent by:
a.) Assist in mechanical vent – attach to ventilator
b.) Monitor pulmonary function test. Decrease vital lung capacity.
2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, 5/5, etc)
3. Siderails
4. Prevent complications of immobility. Adult-every 2 hrs. Elderly- every 1 hr.
5. NGT feeding
Administer meds –
a.) Cholinergics or anticholinesterase agents
Mestinon (Pyridostigmine)
Neostignine (prostigmin) – Long term
- Increase acetylcholine
s/e – PNS
b.) Corticosteroids – to suppress immune resp
Decadron (dexamethasone)

Monitor for 2 types of Crisis:

Myastinic crisis Cholinergic crisis
A cause – 1. Under medication Cause: 1 over meds
2. Stress S/Sx - PNS
3. Infection n/v, diarrhea, hypotension, meiosis, facial muscle twitching,
B S&Sx 1. Unable to see – Ptosis & abdominal cramps
2. Dysphagia- unable to swallow. Mgt. adm anti-cholinergic
3. Unable to breath - Atropine SO4
C Mgt – adm cholinergic agents - SNS – dry mouth
7. Assist in surgical proc – thymectomy. Removal of thymus gland. Thymus secretes auto immune antibody.
8. Assist in plasmaparesis – filter blood
9. Prevent complication – respiratory arrest
Prepare tracheostomy set at bedside.

GBS – Guillain Barre Syndrome

- Disorder of CNS
- Bilateral symmetrical polyneuritis
- Ascending paralysis
Cause – unknown, idiopathic
- Auto immune
- r/t antecedent viral infection
- Immunizations

Initial :
1. Clumsiness
2. Ascending muscle weakness – lead to paralysis
3. Dysphagia
4. Decrease or diminished DTR (deep tendon reflexes)
- Paralysis
5. Alternate HPN to hypotension – lead to arrhythmia - complication
6. Autonomic changes – increase sweating, increase salivation.
Increase lacrimation
Dx most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON (same with MS)

Nsg Mgt
1. Maintain patent a/w & adequate vent
a. Assist in mechanical vent
b. Monitor pulmonary function test
2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia
3. Siderails
4. Prevent compl – immobility
5. Assist in passive ROM exercises
6. Institute NGT feeding – due dysphagia

7. Adm meds (GBS) as ordered: – 1. Anti cholinergic – atropine SO4

2. Corticosteroids – to suppress immune response
3. Anti arrhythmic agents
a.) Lidocaine /Xylocaine –SE confusion = VTach
b.) Bretyllium
c.) Quinines/Quinidine – anti malarial agent. Give with meals.
- Toxic effect – cinchonism
Quinidine toxicity
S/E – anorexia, n/v, headache, vertigo, visual disturbances
8. Assist in plasmaparesis (MG. GBS)
9. Prevent comp – arrhythmias, respiratory arrest
Prepare tracheostomy set at bedside.


Meninges – 3-fold membrane – cover brain & spinal cord
Protection & support
Blood supply
3 layers
1. Duramater sub dural space
2. Arachmoid matter
3. Pia matter sub arachnoid space where CSF flows L3 & L4. Site for lumbar puncture.

MENINGITIS – inflammation of meningitis & spinal cord

Etiology – Meningococcus
Hemophilous influenza – child
Streptococcus – adult meningitis
MOT – direct transmission via droplet nuclei

- Stiff neck or nuchal rigidity (initial sign)
- Headache
- Projectile vomiting – due to increase ICP
- Photophobia
- Fever chills, anorexia
- Gen body malaise
- Wt loss
- Decorticate/decerebration – abnormal posturing
- Possible seizure

Sx of meningeal irritation – nuchal rigidity or stiffness
Opisthotonus- rigid arching of back

Pathognomonic sign – (+) Kernig’s & Brudzinski sign

Leg pain neck pain

1. Lumbar puncture – lumbar/ spinal tap – use of hallow spinal needle – sub arachnoid space L3 & L4 or L4 & L5
Aspirate CSF for lumbar puncture.
Nsg Mgt for lumbar puncture – invasive
1. Consent / explain procedure to pt
- RN – dx procedure (lab)
- MD – operation procedure
2. Empty bladder, bowel – promote comfort
3. Arch back – to clearly visualize L3, L4

Nsg Ngt post lumbar

1. Flat on bed – 12 – 24 h to prevent spinal headache & leak of CSF
2. Force fluid
3. Check punctured site for drainage, discoloration & leakage to tissue
4. Assess for movement & sensation of extremeties

1. CSF analysis: a. increase CHON & WBC Content of CSF: Chon, wbc, glucose
b. Decrease glucose
Confirms meningitis c. increase CSF opening pressure
N 50 – 160 mmHg
d. (+) Culture microorganism
2. Complete blood count CBC – reveals increase WBC
1. Adm meds
a.) Broad-spectrum antibiotic penicillin
1. GIT irritation – take with food
2. Hepatotoxicity, nephrotoxcicity
3. Allergic reaction
4. Super infection – alteration in normal bacterial flora
- N flora throat – streptococcus
- N flora intestine – e coli
Sx of superinfection of penicillin = diarrhea
b.) Antipyretic
c.) Mild analgesic
2. Strict resp isolation 24h after start of antibiotic therapy
A – Cushing’s synd – reverse isolation - due to increased corticosteroid in body.
B – Aplastic anemia – reverse isolation - due to bone marrow depression.
C – Cancer anytype – reverse isolation – immunocompromised.
D – Post liver transplant – reverse isolation – takes steroids lifetime.
E – Prolonged use steroids – reverse isolation
F – Meningitis – strict respiratory isolation – safe after 24h of antibiotic therapy
G – Asthma – not to be isolated

3. Comfy & dark room – due to photophobia & seizure

4. Prevent complications of immobility
5. Maintain F & E balance
6. Monitor vs, I&O , neuro check
7. Provide client health teaching & discharge plan
a. Nutrition – increase cal & CHO, CHON-for tissue repair. Small freq feeding
b. Prevent complication hydrocephalus, hearing loss or nerve deafness.
8. Prevent seizure.
Where to bring 2 yo post meningitis
- Audiologist due to damage to hearing- post repair myelomeningocele
- Urologist -Damage to sacral area – spina bifida – controls urination
9. Rehab for neurological deficit. Can lead to mental retardation or a delay in psychomotor development.

CEREBRO VASCULAR ACCIDENT – stroke, brain attack or cerebral thrombosis, apoplexy

- Partial or complete disruption in the brains blood supply
- 2 largest & common artery in stroke
Middle cerebral artery
Internal carotid artery
- Common to male – 2 – 3x high risk

Predisposing factor:
1. Thrombosis – clot (attached)
2. Embolism – dislodged clot – pulmo embolism
S/Sx: pulmo embolism
Sudden sharp chest pain
Unexplained dyspnea, SOB
Tachycardia, palpitations, diaphoresis & mild restlessness

S/Sx: cerebral embolism

Headache, disorientation, confusion & decrease in LOC

Femur fracture – complications: fat embolism – most feared complication w/in 24hrs
Yellow bone marrow – produces fat cells at meduallary cavity of long bone
Red bone marrow – provides WBC, platelets, RBC found at epiphisis
2.) Hemorrhage
3.) Compartment syndrome – compression of nerves/ arteries

Risk factors of CVA: HPN, DM, MI, artherosclerosis, valvular heart dse - Post heart surgery – mitral valve replacement

Lifestyle: 1. Smoking – nicotine – potent vasoconstrictor

2. Sedentary lifestyle
3. Hyperlipidemia – genetic
4. Prolonged use of oral contraceptives
- Macro pill – has large amt estrogen
- Mini pill – has large amt of progestin
- Promote lipolysis (breakdown of lipids/fats) – artherosclerosis – HPN - stroke
5. Type A personality
a. Deadline driven person
b. 2 – 5 things at the same time
c. Guilty when not dong anything
6. Diet – increase saturated fats
7. Emotional & physical stress
8. Obesity
S & Sx
1. TIA- warning signs of impending stroke attacks
- Headache (initial sx), dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or plegia (monoplegia – 1
Increase ICP
2. Stroke in evolution – progression of S & Sx of stroke
3. Complete stroke – resolution of stroke
a.) Headache
b.) Cheyne-Stokes Resp
c.) Anorexia, n/v
d.) Dysphagia

e.) Increase BP
f.) (+) Kernig’s & Brudzinski – sx of hemorrhagic stroke
g.) Focal & neurological deficit
1. Phlegia
2. Dysarthria – inability to vocalize, articulate words
3. Aphasia
4. Agraphia diff writing
5. Alesia – diff reading
6. Homoninous hemianopsia – loss of half of field of vision
Left sided hemianopsia – approach Right side of pt – the unaffected side

1. CT Scan – reveals brain lesion
2. Cerebral arteriography – site & extent of mal occlusion
- Invasive procedure due to inject dye
- Allergy test
All – graphy – invasive due to iodine dye
1.) Force fluid – to excrete dye is nephrotoxic
2.) Check peripheral pulses - distal

Nsg Mgt
1. Maintain patent a/w & adequate vent
- Assist mechanical ventilation
- Administer O2
2. Restrict fluids – prevent cerebral edema
3. Elevate head of bed 30-45 degrees angle. Avoid valsalva maneuver.
4. Monitor vs., I&O, neuro check
5. Prevent compl of immobility by:
a. Turn client q2h
Elderly q1h
- To prevent decubitus ulcer
- To prevent hypostatic pneumonia – after prolonged immobility.
b. Egg crate mattress or H2O bed
c. Sand bag or foot board- prevent foot drop
6. NGT feeding – if pt can’t swallow
7. Passive ROM exercise q4h
8. Alternative means of communication
- Non-verbal cues
- Magic slate. Not paper and pen. Tiring for pt.
- (+) To hemianopsia – approach on unaffected side
9. Meds
Osmotic diuretics – Mannitol
Loop diuretics – Lasix/ Furosemide
Corticosteroids – dextamethazone
Mild analgesic
Thrombolytic/ fibrolitic agents – tunaw clot. SE-Urticaria, pruritus-caused by foreign subs.
Tissue plasminogen activating
Monitor bleeding time
Anticoagulants – Heparin & Coumadin” sabay”
Coumadin will take effect after 3 days
Heparin – monitor PTT partial thromboplastin time if prolonged – bleeding give Protamine SO4- antidote.
Coumadin –Long term. monitor PT prothrombin time if prolonged- bleeding give Vit K – Aquamephyton- antidote.
Antiplatelet – PASA – aspirin paraanemo aspirin, don’t give to dengue, ulcer, and unknown headache.

Health Teaching
1. Avoidance modifiable lifestyle
- Diet, smoking
2. Dietary modification
- Avoid caffeine, decrease Na & saturated fats
Subarachnoid hemorrhage
Rehab for focal neurological deficit – physical therapy
1. Mental retardation
2. Delay in psychomotor development

CONVULSIVE Disorder (CONVULSIONS)- disorder of the CNS char. by paroxysmal seizures with or without loss of
consciousness, abnormal motor activity, alteration in sensation & perception & change in behavior.

Can you outgrow febrile seizure? Difference between: Seizure- 1st convulsive attack
Febrile seizure Normal if < 5 yo Epilepsy – 2nd and with history of seizure
Pathologic if > 5 yo

Predisposing Factor
Head injury due birth trauma
Toxicity of carbon monoxide
Brain tumor
Nutritional & metabolic deficit
Physical stress
Sudden withdrawal to anticonvulsants will bring about status epilepticus
Status epilepticus – drug of choice: Diazepam & glucose

S & Sx
I. Generalized Seizure –
a.) Grand mal / tonic clonic seizures
With or without aura – warning symptoms of impending seizure attack- Epigastric pain- associated with
olfactory, tactile, visual, auditory sensory experience
- Epileptic cry – fall
- Loss of consciousness 3 – 5 min
- Tonic clonic contractions
- Direct symmetrical extension of extremities-TONIC. Contractions-CLONIC
- Post ictal sleep -state of lethargy or drowsiness - unresponding sleep after tonic clonic
b.) Petimal seizure – (same as daydreaming!) or absent seizure.
- Blank stare
- Decrease blinking eye
- Twitching of mouth
- Loss of consciousness – 5 – 10 secs (quick & short)

II. Localized/partial seizure

a.) Jacksonian seizure or focal seizure – tingling/jerky movement of index finger/thumb & spreads to shoulder &
1 sideof the body with janksonian march
b.) Psychomotor/ focal motor - seizure
-Automatism – stereotype repetitive & non-purposive behavior
- Clouding of consciousness – not in control with environment
- Mild hallucinatory sensory experience

1. Auditory – schitzo – paranoid type
2. Visual – korsakoffs psychosis – chronic alcoholism
3. Tactile – addict – substance abuse

III. Status epilecticus – continuous, uninterrupted seizure activity, if untreated, lead to hyperprexia – coma – death
Seizure: inc electrical firing in brain=increased metabolic activity in brain=brain using glucose and O2=dec glucose, dec O2.
Tx:Diazepam (drug of choice), glucose

Dx-Convulsion- get health history!
1. CT scan – brain lesion
2. EEG electroencephalography
- Hyperactivity brain waves
Nsg Mgt
Priority – Airway & safety
1. Maintain patent a/w & promote safety
Before seizure:
1. Remove blunt/sharp objects
2. Loosen clothing
3. Avoid restraints
4. Maintain siderails
5. Turn head to side to prevent aspiration
6. Tongue guard or mouth piece to prevent biting of tongue-BEFORE SEIZURE ONLY! Can use spoon at home.
7. Avoid precipitating stimulus – bright glaring lights & noises
8. Administer meds
a. Dilantin (Phenytoin) –( toxicity level – 20 )

SE Ginguial hyperplasia
H-hairy tongue
A-acetaminophen- febrile pt
Mix with NSS
- Don’t give alcohol – lead to CNS depression
b. (Tegretol) Carbamasene- given also to Trigeminal Neuralgia. SE: arrythmia
c. Phenobarbital (Luminal)- SE: hallucinations

2. Institute seizure & safety precaution. Post seizure: Administer O2. Suction apparatus ready at bedside
3. Monitor onset & duration
- Type of seizure
- Duration of post ictal sleep. The longer the duration of post ictal sleep, the higher chance of having status
4. Assist in surgical procedure. Cortical resection
5. Complications: Subarachnoid hemorrhage and encephalitis

Question: 1 yo grand mal – immediate nursing action = a/w & safety

a. Mouthpiece – 1 yr old – little teeth only
b. Adm o2 inhalation – post!
c. Give pillow – safety (answer)
d. Prepare suction

Neurological assessment:
1. Comprehensive neuro exam
2. GCS - Glasgow coma scale – obj measurement of LOC or quick neuro check
3 components of ECS
M – motor 6
V – verbal resp 5
E – eye opening 4

15 – 14 – conscious
13 – 11 – lethargy
10 – 8 – stupor
7 – coma
3 – deep coma – lowest score

Survey of mental status & speech (Comprehensice Neuro Exam)

1.) LOC & test of memory

2.) Levels of orientation
3.) CN assessment
4.) Motor assessment
5.) Sensory assessment
6.) Cerebral test – Romhberg, finger to nose
7.) DTR
8.) Autonomics

Levels of consciousness (LOC) –

1. Conscious (conscious) – awake – levels of wakefulness
2. Lethargy (lethargic) – drowsy, sleepy, obtunded
3. Stupor (stuporous) – awakened by vigorous stimulation
Pt has gen body weakness, decrease body reflex
4. Coma (Comatose) light – (+) all forms of painful stimulations
Deep – (-) to painful stimulation
Question: Describe a conscious pt ?
a. Alert – not all pt are alert & oriented to time & place
b. Coherent
c. Awake- answer
d. Aware

Different types of pain stimulation

- Don’t prick
1. Deep sternal stimulation/ pressure 3x– fist knuckle
With response – light coma
Without response – deep coma
2. Pressure on great toe – 3x
3. Orbital pressure – pressure on orbits only – below eye
4. Corneal reflex/ blinking reflex
Wisp of cotton – used to illicit blinking reflex among conscious patients
Instill 1-drop saline solution – unconscious pt if (-) response pt is in deep coma
5. Test of memory – considered educational background
a.) Short term memory –
- What did you eat for breakfast?
Damage to temporal lobe – (+) antero grade amnesia
b.) Long term memory
(+) Retrograde amnesia – damage to limbic system
6. Levels of orientation
Time Place Person

Graphesthesia- can identify numbers or letters written on palm with a blunt object.
Agraphesthesia – cant identify numbers or letters written on palm with a blunt object.

CN assessment:
I– Olfactory s
II – Optic s
III – Oculomotor m
IV – Trocheal m smallest CN
V– Trigeminal b largest CN
VI – Abducens m
VII – Facial b
VIII – Acustic/auditory s
IX – Glassopharyngeal b
X– Vagus b longest CN
XI– Spinal accessory m
XII – Hypoglossal m

I. Olfactory – don’t use ammonia, alcohol, cologne irritating to mucosa – use coffee, bar soap, vinegar, cigarette tar
- Hyposmia – decrease sensitivity to smell
- Diposmia – distorted sense of smell

- Anosmia – absence of sense of smell
Either of 3 might indicate head injury – damage to cribriform plate of ethmoid bone where olfactory cells are located
or indicate inflammation condition – sinusitis

II optic- test of visual acuity – Snellens chart – central or distance vision

Snellens E chart – used for illiterate chart
N 20/20 vision distance by w/c person can see letters- 20 ft
Numerator – distance to snellens chart
Denominator – distance the person can see the letters
OD – Rt eye 20/20 20/200 – blindness – cant read E – biggest
OS – left eye 20/20
OU – both eye 20/20

2. Test of peripheral vision/ visual field

a. Superiority
b. Bitemporally
c. Inferiorly
d. Nasally

Common Disorders – see page 85-87 for more info on glaucoma, etc.
1. Glaucoma – Normal 12 – 21 mmHg pressure
- Increase IOP - Loss of peripheral vision – “tunnel vision”
2. Cataract – opacity of lens - Loss of central vision, “Blurring or hazy vision”
3. Retinal detachment – curtain veil – like vision & floaters
4. Macular degeneration – black spots

III, IV, VI – tested simultaneously

- Innervates the movementt of extrinsic ocular muscle
6 cardinal gaze EOM

Rt eye N left eye


3 – 4 EOM
IV – sup oblique
VI – lateral rectus
Normal response – PERRLA (isocoria – equal pupil)
Anisocoria – unequal pupil

1. Raising of eyelid – Ptosis
2. Controls pupil size 2 -3 cm or 1.5 – 2 mm

V – Trigeminal – Largest – consists of - ophthalmic, maxillary, mandibular

Sensory – controls sensation of the face, mucus membrane; teeth & cornea reflex

Unconscious – instill drop of saline solution

Motor – controls muscles of chewing/ muscles of mastication
Trigeminal neuralgia – diff chewing & swallowing – extreme food temp is not recommended

Question: Trigeminal neuralgia, RN should give

a. Hot milk, butter, raisins
b. Cereals
c. Gelatin, toast, potato – all correct but
d. Potato, salad, gelatin – salad easier to chew

VI Facial: Sensory – controls taste – ant 2/3 of tongue test cotton applicator put sugar.
-Put applicator with sugar to tip to tongue.
-Start of taste insensitivity: Age group – 40 yrs old
Motor- controls muscles of facial expression, smile frown, raise eyebrow
Damage – Bells palsy – facial paralysis
Cause – bells palsy pedia – R/T forcep delivery
Temporary only
Most evident clinical sign of facial symmetry: Nasolabial folds

VIII Acoustic/ vestibule cochlear (controls hearing) – controls balance (kenesthesia or position sense)
- Movement & orientation of body in space
- Organ of Corti – for hearing – true sense organ of hearing

Outer – tympanic membrane, pinna, oricle (impacted cerumen), cerumen

Middle – hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media
- Eustachean ear
Inner ear- meniere dse, sensory hearing loss (research parts! & dse)
Remove vestibule – meniere’s dse – disease inner ear

Archimedes law – buoyancy (pregnancy – fetus)

Daltons law – partial pressure of gases
Inertia – law of motion (dizziness, vertigo)

1.) Pt with multiple stab wound - chest

- Movement of air in & out of lungs is carried by what principle?
- Diffusion – Dalton’s law
2.) Pregnant – check up – ultrasound reveals fetus is carried by amniotic fluid
- Archimedes
3.) Severe vertigo due- Inertia

Test for acoustic nerve:

- Repeat words uttered

IX – Glossopharyngeal – controls taste – posterior 1/3 of tongue

X – Vagus – controls gag reflex

Test 9 – 10
Pt say ah – check uvula – should be midline
Damage cerebral hemisphere is L or R
Gag reflex – place tongue depression post part of tongue
 Don’t touch uvula

XI – Spinal Accessory - controls sternocleidomastoid (neck) & trapezius (shoulders and back)
- Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia
XII – Hypoglossal – controls movement of tongue – say “ah”. Assess tongue position=midline
L or R deviation
- Push tongue against cheek
- Short frenulum lingue –
Tongue tied – “bulol”


Fx of endocrine – ductless gland

Main gland – Pituitary gland – located at base of brain of Stella Turcica
Master gland of body
Master clock of body

Anterior pituitary gland – adenohypophysis
Posterior pituitary gland – neurohypophysis

Posterior pituitary:
1.) Oxytocin – a.) Promotes uterine contraction preventing bleeding/ hemorrhage.
- Give after placental delivery to prevent uterine atony.
b.) Milk letdown reflex with help of prolactin.
2.) ADH – antidiuretic hormone – (vasopressin) -Prevents urination – conserve H2O

A. DIABETIS INSIPIDUS (DI- dalas ihi) – hyposecretion of ADH

Cause: idiopathic/ unknown
Predisposing factor:
1. Pituitary surgery
2. Trauma/ head injury
3. Tumor
4. Inflammation

* alcohol inhibits release of ADH

S & Sx:
1. Polyuria
2. Sx of dehydration (1st sx of dehydration in children-tachycardia)
- Excessive thirst (adult)
- Agitation
- Poor skin turgor
- Dry mucus membrane
3. Weakness & fatigue
4. Hypotension – if left untreated -
5. Hypovolemic shock
Anuria – late sign hypovolemic shock

Dx Proc:
1. Decrease urine specific gravity- concentrated urine
N= 1.015 – 1.035
2. Serum Na = increase (N=135 -145 meq/L) Hypernatremia
1. Force fluid 2,000 – 3,000ml/day
2. Administer IV fluid replacement as ordered
3. Monitor VS, I&O
4. Administer meds as ordered
a.) Pitresin (vasopressin) IM
5. Prevent complications
Most feared complication – Hypovolemic shock

B.) SIADH - Syndrome of Inappropriate Anti-Diuretic Hormone

- Increase ADH
- Idiopathic/ unknown

Predisposing factor
1. Head injury
2. Related to Bronchogenic cancer or lung caner-
Early Sign of Lung Ca - Cough –1. non productive 2. productive
3. Hyperplasia of Pit gland
Increase size of organ

1. Fluid retention
2. Increase BP – HPN
3. Edema
4. Wt gain
5. Danger of H2O intoxication –Complications: 1. cerebral edema – increase ICP – 2. seizure

Dx Proc:
1. Urine specific gravity increase – diluted urine
2. Hyponatremia – Decreased Na

Nsg Mgt:
1. Restrict fluid
2. Administer meds as ordered eg. Diuretics: Loop and Osmotic
3. Monitorstrictly V/S, I&O, neuro check – increase ICP
4. Weigh daily
5. Assess for presence edema
6. Provide meticulous skin care
7. Prevent complications – increase ICP & seizures activity

Anterior Pituitary Gland – adeno

1. Growth hormone (GH) (Somatotropic hormone)
Fx: Elongation of long bones
Decrease GH – dwarfism children
Increase GH – gigantism
Increase GH – acromegaly – adult
Puberty 9 yo – 21 yo
Epiphyseal plate closes at 21 yo

Square face
Square jaw

Drug of choice in acromegaly: Ocreotide (Sandostatin) SE dizziness

- Somatostatin Hormone – antagonizes the release of of GH
2. Melanocytes stimulating hormone - MSH
- Skin pigmentation
3. Prolactin/luteotrpic hormone/ lactogenic hormone - Promotes development of mammary gland
(Oxytocin-Initiates milk letdown reflex)
4. Adrenocorticotropic hormone – ACTH - Development & maturation of adrenal cortex
5. Luteinizing hormone – produces progesterone.
6. FSH- produces estrogen

1. Secretes Melatonin – inhibits lutenizing hormone (LH) secretion


Question: Normal physical finding on TG:
a. With tenderness – thyroid never tender
b. With nodular consistency- answer
c. Marked asymmetry – only 1 TG
d. Palpable upon swallowing - Normal TG never palpable unless with goiter

TG hormones:
T3 T4 Thyrocalcitonin
- Triodothyronine -Tetraiodothyronine/ Tyroxine FX – antagonizes effects of parathormone

- 3 molecules of iodine - 4 molecules of iodine

Metabolic hormone

Increase metabolism brain –inc cerebration, inc v/s all v/s down, constipation

Hypo T3 T4 - lethargy & memory impairment –

Hyper T3 T4 - agitation, restlessness, and hallucination
7. Increase VS, increase motility

HYPOTHYROIDISM – all decreased except wt & menstruation, loss of appetite but with wt gain
menorrhagia – increase in mens
HYPERTHYROIDISM - Increase appetite – wt loss, amenorrhea
SIMPLE GOITER – enlarged thyroid gland - iodine deficiency
Predisposing factors
1. Goiter belt area - Place far from sea – no iodine. Seafood’s rich in iodine
2. Mountainous area – increase intake of goitrogenic foods (US: Midwest, NE, Salt Lake)
Cabbage – has progoitrin – an anti thyroid agent with no iodine
Example: Turnips (singkamas), radish, peas, strawberries, potato, beans, kamote, cassava (root crops), all nuts.
3. Goitrogenic drugs:
Anti thyroid agents :(PTU) prephyl thiupil
Lithium carbonate, Aspirin PASA
Cobalt, Phenyl butasone
Endemic goiter – cause # 1
Sporadic goiter – caused by #2 & 3

S & Sx – enlarged TG
Mild restlessness
Mild dysphagia

Dx Proc.
1. Thyroid scan – reveals enlarged TG
2. Serum TSH – increase (confirmatory)
3. Serum T3, T4 – N or below N

Nsg Mgt:
1. Administer meds
a.) Iodine solution – Logol’s solution or saturated sol of K iodide SSKI

Nsg Mgt Lugol’s sol – violet color

1. use straw – prevent staining teeth
2. Prophylaxis 2 -3 drops Treatment – 5 to 6 drops
Use straw – to prevernt staining of teeth
1. Lugol’s sol., 2. tetracycline 3. nitrofurantin (macrodantin)-urinary anticeptic-pyelonephritis. 4. Iron solution.

B. Thyroid h / Agents
1. Levothyroxine (Synthroid)
2. Liothyronine (cytomel)
3. Thyroid extract

Nsg Mgt: for TH/agents

1. Monitor vs. – HR due tachycardia & palpitation
2. Take it early AM – SE insomnia
3. Monitor s/e
Tachycardia, palpitations
Signs of insomnia
Hyperthyroidism restlessness agitation
Heat intolerance

3. Encourage increase intake iodine – iodine is extracted from seaweeds (!)

Seafood- highest iodine content oysters, clams, crabs, lobster
Lowest iodine – shrimps
Iodized salt –easily destroyed by heat take it raw not cooked

4. Assist surgery- Sub total thyroidectomy-

Complication: 1. Tetany 2. laryngeal nerve damage 3.Hemorrhage-feeling of fullness at incision site.Check nape for
wet blood. 4.Laryngeal spasm – DOB, SOB – trache set ready at bedside.

2.) HYPOTHYROIDISM – decrease secretion of T3, T4 – can lead to MI / Atherosclerosis

Adult – myxedema
Child- cretinism – only endocrine dis lead to mental retardation
Predisposing factor:
1. `Iatrogenic causes – caused by surgery
2. Atrophy of TG due to:
a. Irradiation
b. Trauma
c. Tumor, inflammation
3. Iodine def
4. Autoimmune – Hashimoto disease

S&Sx everything decreased except wt gain & mens increase)

Early signs – weakness and fatigue
Loss of appetite – increased lypolysis – breakdown of fats causing atherosclerosis = MI
Wt gain
Cold intolerance – myxedema - coma
Late Sx – brittle hair/ nails
Non pitting edema due increase accumulation of mucopolysacharide in SQ tissue -Myxedema
Horseness voice
Decrease libido
Decrease VS – hypotension bradycardia, bradypnea, and hypothermia
Memory impairment leading to psychosis-forgetfulness

1. Serum T3 T4 decrease
2. Serum cholesterol increase – can lead to MI
3. RA IU – radio iodine uptake – decrease

Nsg Mgt:
1. Monitor strictly V/S. I&O – to determine presence of myxedema coma!
Myxedema Coma - Severe form of hypothyroidism
Hypotension, hypoventilation, bradycardia, bradypnea, hyponatremia, hypoglycemia, hypothermia
Might lead to progressive stupor & coma
Impt mgt for Myxedema coma
1. Assist mech vent – priority a/w
2. Adm thyroid hormone
3. Adm IVF replacement – force fluid

Mgt myxedema coma
1. Monitor VS, I&O
2. Provide dietary intake low in calories – due to wt gain
3. Skin care due to dry skin
4. Comfortable & warm environment due to cold intolerance
5. Administer IVF replacements
6. Force fluid
7. Administer meds – take AM – SE insomia. Monitor HR.
Thyroid hormones
Levothyroxine(Synthroid), Liothyronine (cytomel)
Thyroid extracts
8. Health teaching & discharge plan
a. Avoidance precipitating factors leading to myxedema coma:
1. Exposure to cold environment
2. Stress 3. Infection
4. Use of sedative, narcotics, anesthetics not allowed – CNS depressants V/S already down

9. Hypovolemic shock, myxedema coma
10. Hormonal replacement therapy - lifetime
11. Importance of follow up care

HYPERTHYROIDISM - Graves dse or thyrotoxicosis ( everything up except wt and mens)

-Increased T3 & T4
Predisposing factors:
1. Autoimmune disease – release of long acting thyroid stimulator (LATS)
Enopthalmos – severe dehydration depressed eye
2. Excessive iodine intake
3. Hyperplasia of TG

1. Increase in appetite – hyperphagia – wt loss due to increase metabolism
2. Skin is moist - perspiration
3. Heat intolerance
4. Diarrhea – increase motility
5. All VS increase = HPN, tachycardia, tachypnea, hyperthermia
6. CNS changes
8. Irritability & agitation, restlessness, tremors, insomnia, hallucinations
7. Goiter
8. Exopthalmos – pathognomonic sx
9. Amenorrhea

1. Serum T3 & T4 - increased
2. Radio iodine uptake – increase
3. Thyroid scan – reveals enlarged TG

Nsg Mgt:
1. Monitor VS & I & O – determine presence of thyroid storm or most feared complication: Thyrotoxicosis
2. Administer meds
a. Antithyroid agents
1. Prophylthiuracil (PTU)
2. Methymazole (Tapazole)
Most toxic s/e agranulocytosis- fever, sore throat, leukocytosis=inc wbc: check cbc and throat swab culture
Most feared complication : Thrombosis – stroke CVS

3. Diet – increase calorie – to correct wt loss

4. Skin care –
5. Comfy & cool environment
6. Maintain siderails- due agitation/restlessness
7. Provide bilateral eye patch – to prevent drying of eyes- exopthalmos
8. Assist in surgery – subtotal thyroidectomy

Nsg Mgt: pre-op

Adm Lugol’s solution (SSKI) K iodide
9. To decrease vascularity of TG
10. To prevent bleeding & hemorrhage
Mgt post op:
Complication: 1. Watch out for signs of thyroid storm or thyrotoxicosis

Triad signs of thyroidstorm;

a. Tachycardia /palpitation
b. Hyperthermia
c. Agitation

Nsg Mgt Thyroid Storm:

1. Monitor VS & neuro check
Agitated might decrease LOC
2. Antipyretic – fever
Tachycardia - β blockers (-lol)
3. Siderails – agitated

Comp 2. Watch for inadvertent (accidental) removal of parathyroid gland

Secretes Para hormone

If removed, hypocalcemia - classic sign tetany – 1. .(+) Trousseau sign/ 2. Chvosteck’s sign
Nsg Mgt:
Adm calcium gluconate slowly – to prevent arrhythmia
Ca gluconate toxicity – antidote – MgSO4
3. Laryngeal (voice box) nerve damage (accidental)
Sx: hoarseness of voice
***Encourage pt to talk or speak post operatively asap to determine laryngeal nerve damage
Notify physician!

4. Signs of bleeding post subtotal thyroidectomy

- “Feeling of fullness” at incision site
Nsg mgt:
Check soiled dressing at nape area

5. Signs of laryngeal spasm

a. DOB
b. SOB
Prepare at bedside tracheostomy

6. Hormonal replacement therapy - lifetime

7. Importance of follow up care
(Liver cirrhosis – bedside scissor – if pt complaints of DOB)

(Cut cystachean tube to deflate balloon)

Parathyroid gland – pair of small nodules located behind the TG

11. Secrets parathyroid hormone – promotes Ca reabsorption

Thyrocalcitonin – antagonises secretion of parathyroid hormone

1. Hypoparthroidism – decrease of parathyroid hormone
2. Hyperparathroidsm

HYPOPARATHYROIDISM – decreased parathormone

Hypocalcemia Hyperphosphatemia
(Or tetany)

[If Ca decreases, phosphate increases]

A. Predisposing, factors:
1. Following subtotal thyroidectomy
2. Atrophy of parathyroid gland due to
a. Irradiation
b. Trauma

1. Acute tetany
a. Tingling sensation
b. Paresthesia
c. Dysphagia
d. Laryngospasm
e. Bronchospasm

Pathognomonic Sign of tetany:

a. (+) Trousseau’s or carpopedial spasm
b. (+) Chvosteck’s sign

f. Seizure most feared complication

g. Arrhythmia

2. Chronic tetany
a. Loss of tooth enamel
b. Photophobia & cataract formation
c. GIT changes – anorexia, n/v, general body malaise
d. CNS changes – memory impairment, irritability

1. Serum calcium – decrease (N 8.5 – 11 mg/100ml)
2. Serum phosphate increase (N 2.5 – 4.5 mg/100ml)
3. X-ray of long bone – decrease bone density
4. CT Scan – reveals degeneration of basal ganglia

Nsg Mgt:
1. Administration of meds:
a.) Acute tetany –
Ca gluconate – IV, slowly
b.) Chronic tetany
1. Oral Ca supplements
Ex. Ca gluconate
Ca carbonate
Ca lactate

Vit D (Cholecalceferol)

Drug diet sunlight

Cholecalceferol calcidiol calcitriol 7am – 9am

2. Phosphate binder
Alumminum DH gel (ampho gel)
SE constipation
Aluminum containing acids Mg containing antacids
Ex. Milk or magnesia
Aluminum OH gel Diarrhea

Constipation Maalox – magnesium & aluminum - Less s/e

2. Avoid precipitating stimulus such as bright lights & noise: photophobia leading to seizure
3. Diet – increase Ca & decrease phosphorus
- Don’t give milk – due to increase phosphorus
Good = anchovies – increase Ca, decrease phosphorus + inc uric acid. Tuna & green turnips- Inc Ca.
4. Bedside – tracheostomy set –due to laryngospasm
5. Encourage to breath with paper bag in order to produce mild respiratory acidosis – to promote increase ionized Ca levels
6. Most feared complication : Seizure & arrhythmia
7. Hormonal replacement therapy - lifetime
8. Important fallow up care

HYPERPARATHYROIDISM - increase parathormone. Complication: Renal failure

Hypercalcemia can lead to Hypophosphatemia

Bone dse - kidney stones


Leading to bone fracture

Ca – 99% bones
1% serum blood

Predisposing Factors:
1. Hyperplasia parathyroid gland (PTG)
2. Over compensation of PTG due to Vit D deficiency
Children – Rickets Vit D
Adults – Osteomalacia deficiency

Sippy’s diet – Vit D diet – not good for pt with ulcer

2 -4 cups of milk & butter
Karrel’s diet – Vit D diet – not good for pt with ulcer
6 cups of milk & whole cream

Food rich in CHON – eggnog – combination of egg & milk

Bone fracture
1. Bone pain (especially at back), bone fracture
2. Kidney stone –
a. Renal colic
b. Cool moist skin
3. GIT changes – anorexia, n/v, ulcerations
4. CNS involvement– irritability, memory impairment

Dx Proc:
1. Serum Ca increase
2. Serum phosphorus decreases
3. X-ray long bones – reveals bone demineralization

Nsg Mgt: Kidney Stone

1. Force fluids – 2,000 – 3,000/day or 2-3L/day

2. Isotonic solution
3. Warm sitz bath – for comfort
4. Strain all urine with gauze pad
5. Acid ash diet – cranberry, plum, grapefruit, vit C, calamansi – to acidify urine
6. Adm meds
a. Narcotic analgesic – Morphine SO4, Demerol (Meperidine Hcl)
S/E – resp depression. Monitor RR)
Narcan/ Naloxone – antidote
Naloxone toxicity – tremors
7. Siderails
8. Assist in ambulation
9. Diet – low in Ca, increase phosphorus lean meat
10. Prevent complication
Most feared – renal failure
11. Assist surgical procedure – parathyroidectomy
12. Impt ff up care
13. Hormonal replacement- lifetime
12. Atop of @ kidney
13. 2 parts
Adrenal cortex – outermost layer
Adrenal medulla - innermost layer
14. Secrets cathecolamines
a.) Epinephrine / Norephinephrine – potent vasoconstrictor – adrenaline=Increase BP

Adrenal Medulla’s only disease:

PHEOCHROMOCYTOMA- presence of tumor at adrenal medulla
-increase nor/epinephrine. HPN with pounding headache.
-with HPN and resistant to drugs
-drug of choice: beta blockers
-complication: HPN crisis = lead to stroke
-no valsalva maneuver. Son’t smoke. No caffeine.

Adrenal Cortex –
1. Zona fasiculata – secrets glucocorticoids. Ex. Cortisol - Controls glucose metabolism (SUGAR)
2. Zona reticularis – secrets traces of glucocorticoids & androgenic hormones
M – testosterone
F – estrogen & progesterone
Fx – promotes development of secondary sexual characteristics
3. Zona glomerulosa - secretes mineralcortisone. Ex. Aldosterone Fx: promotes Na & H2O reabsorption & excretion of
potassium (SALT)

ADDISON’S DISEASE – Steroids-lifetime

Decreased adrenocortical hormones leading to:
a.) Metabolic disturbances (sugar)
b.) F&E imbalances- Na, H2O, K
c.) Deficiency of neuromuscular function (salt & sex)

Predisposing Factors:
1. Atrophy of adrenal gland
2. Fungal infections
3. Tubercular infections

1. Decrease sugar – Hypoglycemia – Decreased glucocorticoids - cortisol
T – tremors, tachycardia
I - irritability
R - restlessness
E – extreme fatigue
D – diaphoresis, depression

2. Decrease plasma cortisol

Decrease tolerance to stress – lead to Addisonian’s crisis

3. Decrease salt – Hyponatermia – Decreased mineralocorticoids - Aldosterone

a.) Hypotension
b.) Signs of dehydration – extreme thirst, agitation
c.) Wt loss
4. Hyperkalemia
a.) Irritability
b.) Diarrhea
c.) Arrhythmia
5. Decrease sexual urge or libido- Decreased Androgen
6. Loss of pubic and axillary hair

To Prevent STD Local – practice monogamous relationship

CGFNS/NCLEX – condom
7. Pathognomonic sign– bronze like skin pigmentation due to decrease cortisol will stimulate pituitary gland to release
melanocyte stimulating hormone.

Dx Proc:
1. FBS – decrease FBS (N 80 – 120 mg/dL)
2. Plasma cortisol – decreased
Serum Na – decreased (N 135 – 145 meg/L)
3. Serum K – increased (N 3.5 – 5.5 meg/L)

Nsg Mgt:
1. Monitor VS, I&O – to determine presence of Addisonian crisis
15. Complication of Addison’s dse : Addisonian crisis
16. Results the acute exacerbation of Addison’s dse characterized by :
Hypotension, hypovolemia, hyponatremia, wt loss, arrhythmia
17. Lead to progressive stupor & coma

Nsg Mgt Addisonian Crisis (Coma)

1. Assist in mechanical ventilation
2. Adm steroids
3. Force fluids

2. Administer meds
a.) Corticosteroids - (Decadron) or Dexamethazone
- Hydrocortisone (cortisone)- Prednisone

Nsg Mgt with Steroids

1. Adm 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm.

2. Taper the dose (w/draw, gradually from drug) – sudden withdrawal can lead to addisonian crisis
3. Monitor S/E (Cushing’s syndrome S/Sx)
a.) HPN
b.) Hirsutism
c.) Edema
d.) Moon face & buffalo hump
e.) Increase susceptibility to infection sue to steroids- reverse isolation

b.) Mineralocorticoids ex. Flourocortisone

3. Diet – increase calorie or CHO

Increase Na, Increase CHON, Decrease K
4. Force fluid
5. Administer isotonic fluid as ordered
6. Meticulous skin care – due to bronze like
7. HT & discharge planning
a) Avoid precipitating factors leading to Addisonian crisis
1. Sudden withdrawal crisis
2. Stress
3. Infection
b) Prevent complications
Addisonian crisis & Hypovolemic shock
8. Hormonal replacement therapy – lifetime
9. Important: follow up care

CUSHING’S SYNDROME – increase secretion of adrenocortical hormone

Predisposing Factors:
1. Hyperplasia of adrenal gland
2. Tubercular infection – milliary TB
1. Increase sugar – Hyperglycemia
3 P’s
1. Polyuria
2. Polydipsia – increase thirst
3. Polyphagia – increase appetite
Classic Sx of DM – 3 P’s & glycosuria + wt loss
2. Increase susceptibility to infection – due to increased corticosteroid
3. Hypernatrermia
a. HPN
b. Edema
c. Wt gain
d. Moon face
Buffalo hump
Obese trunk classic signs
Pendulous abdomen
Thin extremities
4. Hypokalemia
a. Weakness & fatigue
b. Constipation
c. ECG – (+) “U” wave
5. Hirsutism – increase sex
6. Acne & striae
7. Increase muscularity of female
1. FBS – increase↑ (N: 80-120mg/dL)
2. Plasma cortisol increase

3. Na – increase (135-145 meq/L)
4. K- decrease (3.5-5.5 meq/L)
Nsg Mgt:
1. Monitor VS, I&O
2. Administer meds
a. K- sparing diuretics (Aldactone) Spironolactone
- promotes excretion of NA while conserving potassium

Not lasix due to S/E hypoK & Hyperglycemia!

3. Restrict Na
4. Provide Dietary intake – low in CHO, low in Na & fats
High in CHON & K
5. Weigh pt daily & assess presence of edema- measure abdominal girth- notify doc.
6. Reverse isolation
7. Skin care – due acne & striae
8. Prevent complication
- Most feared – arrhythmia & DM
(Endocrine disorder lead to MI – Hypothyroidism & DM)
9. Surgical bilateral Adrenolectomy
10. Hormonal replacement therapy – lifetime due to adrenal gland removal- no more corticosteroid!

PANCREAS – behind the stomach, mixed gland – both endocrine and exocrine gland
Acinar cells (exocrine gland) Islets of Langerhans (endocrine gland ductless)

Secrete pancreatic juices at pancreatic ducts. α cells

Aids in digestion (in stomach) secrets glucagon

Fxn: hyperglycemia (high glucose)

β Cells

Secrets insulin

Fxn: hypoglycemia

Delta Cells

Secrets somatostatin

Fxn: antagonizes growth hormone

3 disorders of the Pancreas

1. DM
2. Pancreatic Cancer
3. Pancreatitis

Overview only:

PANCREATITIS (check page 72)– acute inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to
Autodigestion – self-digestion
Cause: unknown/idiopathic
18. Or alcoholism

Pathognomonic sign- (+) Cullen’s sign - Ecchymosis of umbilicus (bluish color)- pasa
(+) Grey turner’s sign – ecchymosis of flank area

Both sx means hemorrhage


Predisposing factors - unknown
Risk factor:
1. History of hepatobiliary disorder
2. Alcohol
3. Drugs – thiazide diuretics, oral contraceptives, aspirin, penthan
4. Obesity
5. Hyperlipidemia
6. Hyperthyroidism
7. High intake of fatty food – saturated fats

DIABETES MELLITUS - metabolic disorder characterized by non utilization of CHO, CHON,& fat metabolism
I. Type I DM (IDDM) – “Juvenile “ onset, common in children, non-obese “brittle dse”
-Insulin dependent diabetes mellitus
Incidence rate
1.) 10% of population with DM have Type I
Predisposing Factor:
1. 90% hereditary – total destruction of pancreatic dells
2. Virus
3. Toxicity to carbon tetrachloride
4. Drugs – Steroids both cause hyperglycemia
Lasix - loop diuretics

3 P’S + G
1.) Polyuria
2.) Poydipsia
3.) Polyphagia
4.) Glycosuria
5.) Weight loss
6.) Anorexia
7.) N/V
8.) Blurring of vision
9.) Increase susceptibility to infection
10.) Delayed/ poor wound healing

1. Insulin Therapy

Complications – Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA) – due to increase fat catabolism or breakdown of fats

DKA –(+) fruity or acetone breath odor
Kassmaul’s respiration – rapid, shallow breathing

Diabetic coma (needs oxygen)

II. Type II DM – (NIDDM)

Adult/ maturity onset type – age 40 & above, obese
Incidence Rate
1. 90% of pop with DM have Type II
Mid 1980’s marked increase in type II because of increase proliferation of fast food chains!

Predisposing Factor:
1. Obesity – obese people lack insulin receptors binding site
2. Hereditary

1. Asymptomatic
2. 3 P’s and 1G
1. Oral Hypoglycemic Agents (OHA)
2. Diet
3. Exercise

Complication: HONKC
H – hyper
O – osmolar
N – non
K – ketotic
C – coma

III. GESTATIONAL DM – occurs during pregnancy & terminates upon delivery of child

Predisposing Factors:
1. Unknown/ idiopathic
2. Influence of maternal hormones
S/Sx :
Same as type II –
1. Asymptomatic
2. 3 P’s & 1G

Type of delivery – CS – due to large baby

Sx of hypoglycemia on infant
1. High pitched shrill cry
2. Poor sucking reflex
a.) Pancreatic tumor
b.) Cancer
c.) Cushing’s syndrome


Anabolism Catabolism
1. CHON glucose glycogen
2. CHON amino acids nitrogen
3. Fats fatty acids free fatty acids (FFA) – Cholesterol & Ketones

Pancreas → glucose → ATP (Main fuel/energy of cell )

Reserve glucose – glycogen

Liver will undergo – glucogenesis – synthesis of glucagons
& Glycogenolysis – breakdown of glucagons
& Gluconeogenesis – formation of glucose form CHO sources – CHON & fats

Hyperglycemia – pancreas will not release insulin. Glucose can’t go to cell, stays at circulation causing hyperglycemia.
increase osmotic diuresis – glycosuria
Lead to cellular starvation

Lead to wt loss stimulates the appetite/ satiety center polyuria

Cellular dehydration
Stimulates thirst center (hypothalamus)


Increased CHON catabolism

Lead to (-) nitrogen balance

Tissue wasting (cachexia)

Increase fat catabolism

Free fatty acids

Cholesterol ketones DKA

Atherosclerosis coma

HPN death

MI stroke


- Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Coma.
- Ketones- a CNS depressant

Predisposing factor:
1. Stress – between stress and infection, stress causes DKA more.
2. Hyperglycemia
3. Infection

S/Sx: 3 P’s & 1G

1. Polyuria
2. Polydipsia
3. Polyphagia
4. Glycosuria
5. Wt loss
6. Anorexia, N/V
7. (+) Acetone breath odor- fruity odor pathognomonic DKA
8. Kussmaul's resp-rapid shallow respiration
9. CNS depression
10. Coma

Dx Proc:
1. FBS increase, Hct – increase (compensate due to dehydration)
N =BUN – 10 -20 mg/100ml --increased due to severe dehydration
Crea - .8 – 1 mg/100ml

Hct 42% (should be 3x high)-nto hgb

Nsg Mgt:
1. Can lead to coma – assist mechanical ventilation
2. Administer .9NaCl – isotonic solution
Followed by .45NaCl hypotonic solution
To counteract dehydration.
3. Monitor VS, I&O, blood sugar levels
4. Administer meds as ordered:
a.) Insulin therapy – IV push
Regular Acting Insulin – clear (2-4hrs, peak action)
b.) To counteract acidosis – Na HCO3
c.) Antibiotic to prevent infection
Insulin Therapy
A. Sources:
1. Animal source – beef/ pork-rarely used. Causes severe allergic reaction.
2. Human – has less antigenecity property
Cause less allergic reaction. Humulin

If kid is allergic to chicken – don’t give measles vaccine due it comes from chicken embryo.
3. Artificially compound

B. Types of Insulin
1. Rapid Acting Insulin - Ex. Regular acting I
2. Intermediate acting I - Ex. NPH (non-protamine Hagedorn I)
3. Long acting I - Ex. Ultra lente
Types of Insulin color & consistency onset peak duration
1. Rapid clear - 2-4h -
2. Intermediate cloudy - 6-12h -
3. Long acting cloudy - 12-24h -

Ex. 5am Hemoglucose test (HGT)

250 mg/dl
Adm 5 units of RA I
Peak 7-9am – monitor hypoglycemic reaction at this time- TIRED

Nsg Mgt: upon injection of insulin:

1.Administer insulin at room temp! – To prevent lipodystrophy = atrophy/ hypertrophy of SQ tissues
2. Insulin is only refrigerated once opened!
3. Gently roll vial bet palms. Avoid shaking to prevent formation of bubbles.
4. Use gauge 25 – 26needle – tuberculin syringe
5. Administer insulin at either 45(for skinny pt) or 90° (taba pt)depending on the client tissue deposit.
6. Don’t aspirate after injection
7. Rotate injection site to prevent lipodystrophy
8. Most accessible site – abdomen
9. When mixing 2 types of insulin, aspirate
1st regular/ clear – before cloudy to prevent contaminating clear insulin & to promote accurate calibration.
10. Monitor signs of complications:
a. Allergic reactions – lipodystrophy

b. Somogyi’s phenomenon – hypoglycemia followed by periods of hyperglycemia or rebound effect of insulin.
11. 1ml or cc of tuberculin = 100 units of insulin

- - 1 cc = 100 units

- - .5cc = 50 units

- - .1 cc = 10 units

6 units RA

Most Feared Complication of Type II DM

Hyper ↑ osmolarity = severe dehydration
Non - absence of lipolysis
Ketotic - no ketone formation
Coma – S/Sx: headache, restlessness, seizure, decrease LOC = coma

Nsg Mgt; - same as DKA except don’t give NaHCO3!

1.Can lead to coma – assist mechanical ventilation

2. Administer .9NaCl – isotonic solution
Followed by .45NaCl hypotonic solution
To counteract dehydration.
3.Monitor VS, I&O, blood sugar levels
4.Administer meds
a.) Insulin therapy – IV
b.) Antibiotic to prevent infection

O ral
H ypoglycemic
A gents
19. Stimulates pancreas to secrete insulin

Classifications of OHA
1. First generation Sulfonylurear
a. Chlorpropamide (diabenase)
b. Tolbutamide (orinase)
c. Tolazamide (tolinase)

2. 2nd generation sulfonylurear

a. Diabeta (Micronase)
b. Glipside (Glucotrol)

Nsg Mgt or OHA

1. Administer with meals – to lessen GIT irritation & prevent hypoglycemia
2. Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction=CNS depression=coma) Antabuse-Disufram
Dx for DM
1. FBS – N 80 – 120 mg/dl = Increased for 3 consecutive times =confirms DM!!
+ 3 P’s & 1G
2. Oral glucose tolerance (OGTT) - Most sensitive test
3. Random blood sugar – increased
4. Alpha Glucosylated Hgb – elevated

Nsg Mgt;
1. Monitor for PEAK action of OHA & insulin
Notify Doc
2. Monitor VS, I&O, neurocheck, blood sugar levels.
3. Administer insulin & OHA therapy as ordered.
4. Monitor signs of hyper & hypoglycemia.

Pt DM –“ hinimatay”
20. You don’t know if hypo or hyperglycemia.
Give simple sugar
(Brain can tolerate high sugar, but brain can’t tolerate low sugar!)
Cold, clammy skin – hypo – Orange Juice or simple sugar / warm to touch – hyper – adm insulin
5. Provide nutritional intake of diabetic diet:
CHO – 50%
CHON – 30%
Fats – 20%
-Or offer alternative food products or beverage.
-Glass of orange juice.
6. Exercise – after meals when blood glucose is rising.
7. Monitor complications of DM
a. Atherosclerosis – HPN, MI, CVA
b. Microangiopathy – small blood vessels
Eyes – diabetic retinopathy , premature cataract & blindness
Kidneys – recurrent pyelonephritis & Renal Failure
(2 common causes of Renal Failure : DM & HPN)
c. Gangrene formation
d. Peripheral neuropathy
1. Diarrhea/ constipation
2. Sexual impotence
e. Shock due to cellular dehydration
8. Foot care mgt
a. Avoid waking barefooted
b. Cut toe nails straight
c. Apply lanolin lotion – prevent skin breakdown
d. Avoid wearing constrictive garments

9. Annual eye & kidney exam

10. Monitor urinalysis for presence of ketones
Blood or serum – more accurate
11. Assist in surgical wound debridement
12. Monitor signs or DKA & HONKC
13. Assist surgical procedure
BKA or above knee amputation


I Blood
55% Plasma, 45% cellular/ formed elements
II Blood vessels
III Blood forming organs
1. Thymus – removed myasthenia gravis
2. Liver – largest gland
3. Lymph nodes
4. Lymphoid organs – payers patch
5. Bone marrow
6. Spleen – destroys RBC
Blood vessels
1. Veins –SVC, IVC, Jugular vein – blood towards the heart
2. Artery – carries blood away from the
21. Aorta, carotid
3. Capillaries

Blood 45% formed elements – 55% plasma – fluid portion of vlood. Yellow color.

Serum Plasma CHON’s (Produced in Liver)

1. Albumin- largest, most abundant plasma
Maintains osmotic pressure preventing edema
FXN: promotes skin integrity
2. Globulins – alpha – transports steroids Hormones & bilirubin
β - Transports iron & copper

Gamma – transport immunoglobulins or antibodies (Acute or Chronic)

3. Prothrombin and Fibrinogen – clotting factor to prevent bleeding
Cellular Elements:
1. RBC (erythrocytes) Spleen life span = 120 days
(N) 3 – 6 M/mm3
- Anucleated
- Biconcave discs
- Has molecules of Hgb (red cell pigment)
Transports & carries O2

SICKLE CELL ANEMIA –sickle shaped RBC. Should be round. Impaired circulation of RBC.
-immature cells=hemolysis of RBC=decreased hgb
3 Nsg priority
1. AIRWAY (priority) – avoid deoxygenating activities
- High altitude is bad
2. Fluid deficit – promote hydration
3. Pain & comfort

Hgb ( hemoglobin)- red cell pigment which transport O2

F= 12 – 14 gms %
M = 14-16 gms %
Hct – 3x hgb 12 x 3 = 36
(hamatocrit) F 36 – 42% 14 x 3 = 42 *Hematocrit is the red cell pigment in whole blood
M 42 – 48% *Erythropoietin- stimulate bone marrow to produce RBC
Average 42%
- Red cell percentage in whole red

Substances needed for maturation of RBC

a.) Folic acid
b.) Iron
c.) Vit C
d.) Vit B12 (cyanocobalamin)
e.) Vit B6 (Pyridoxine)
f.) Intrinsic factor

Pregnant: 1st trimester- Folic acid – prevent neural tube deficit

3rd tri – iron
Life span of rbc – 80 – 120 days. Destroyed at spleen.

WBC – leukocytes 5,000 – 10,000/mm3

1. Polymorphonuclearneutrophils 1. Monocytes (macrophage) - largest WBC
Most abundant 60-70% WBC - involved in long term phagocytes
- fx – short term phagocytosis - For chronic inflammation
For acute inflammation - Other name macrophage

2. PM Basophils Macrophage in CNS- microglia

Macrophage in skin – Histiocytes
-Involved in Parasitic infection Macrophage in lungs – alveolar macrophage
- Release of chemical mediators for inflammation -- Macrophage in Kidneys – Kupffer cells
Serotonin, histamine, prostaglandin, bradykinins
2. Lymphocytes
3. PM Eosinophils B Cell – L – bone marrow or bursa dependent immunity
- Allergic reactions T cell – dev’t of immunity- target site for HIV
NK cell – natural killer cell
Have both antiviral & anti-tumor properties

3.Platelets (thrombocytes)
N- 150,000 – 450, 000/ mm3
it promotes hemostasis – prevention of blood loss by activating
- Consists of immature or baby platelets known as megakaryocytes
– target of virus – dengue
- Normal lifespan 9 – 12 days

Drug of choice for HIV Zidovudine (AZT) or Ritonavir or Retrovir

Standard precaution for HIV gloves, gown, goggles & mask

Malaria – night biting mosquito

Dengue – day biting mosquito

Signs of platelet dys function:

a.) Petechiae Hemophilia
b.) Ecchymoses/ bruises DIC
c.) Oozing or blood ON venipuncture site

Iron deficiency Anemia – chronic normocytic, hypochromic (pale), microcytic anemia due to inadequate absorption of iron leading to
hypoxemic tissue injury.

Incidence rate:
1. Common – developed country – due to high cereal intake
Third leading cause of death in the US due to accidents
2. Common – tropical countries – blood sucking parasites
3. Women – 15 – 35yo – reproductive yrs
4. Common among the poor – poor nutritional intake

Suicide - common in teenagers
Poisoning – common in children (aspirin)
Aspiration – common in infant
Accidents – common in adults
Choking – common in toddler
SIDS – common in infant in US
22. Common in tropical zone – Phil due blood sucks
Predisposing factors:
1. Chronic blood loss
a. Trauma
b. Mens
c. GIT bleeding:
i. Hematemesis-
ii. Melena – upper GIT – duodenal cancer
iii. Hematochezia – lower GIT – large intestine – fresh blood from rectum
2. Inadequate intake of food rich in iron
A. Eggs
B. Organ meats, eggs, oatmeals, dried fruits, legumes, raisins
3. Inadequate absorption of iron – due to :
a. Chronic diarrhea
b. Malabsorption syndrome –celiac disease-gluten free diet. Food for celiac pts- sardines
c. High cereal intake with low animal CHON ingestion
d. Subtotal gastrectomy- partial removal of the stomach
4. Improper cooking of food

1. Usually asymptomatic
2. Weakness and Fatigue
3. Headache, dizziness, dyspnea, palpitations, cold sensitivity, gen body malaise, pallor
4. Brittle hair, spoon shaped nails (KOILONYCHIA)=Dec O2=hypoxia=atrophy of epidermal cells
5. Atropic glossitis, dysphagia, stomatitis
6. Pica – abnormal craving for non edible food (caused by hypoxia=dec tissue perfusion=psychotic behavior)

Brittle hair, spoon shaped nail – atrophy of epidermal cells

N = capillary refill time < 2 secs
N = shape nails – biconcave shape, 180°
Atrophy of cells “Plummer Vinsons Syndrome” due to cerebral hypoxia
1. Atropic glossiti s– inflammation of tongue due to atrophy of pharyngeal and tongue cells
2. Stomatitis – mouth sores
3. Dysphagia

Dx Proc:
1. RBC
2. Hgb
3. Reticulocyte
4. Hct
5. Iron
6. Ferritin

Nsg Mgt
1. Monitor signs of bleeding of all hema test including urine & stool, GIT
2. Complete bed rest – don’t overtire pt =weakness and fatigue=activity intolerance
3. Encourage – iron rich food
23.Raisins, legumes, egg yolk
4. Instruct the pt to avoid taking tea - impairs iron absorption
5. Administer meds
a.) Oral iron preparation
Ferrous SO4
Fe gluconate
Fe Fumarate
Nsg Mgt oral iron meds:
1. Administer with meals – to lessen GIT irritation
2. If diluting in iron liquid prep –adm with straw
1. Lugol’s
2. Tetracycline
3. Oral iron
4. Macrodantine

3. Give Orange juice – for iron absorption

4. Monitor & inform pts S/E
a. Anorexia
b. n/v
c. Abdominal pain
d. Diarrhea or constipation
e. Melena

If pt can’t tolerate oral iron prep – administer parenteral iron prep example:
1. Iron dextran (IV, IM)
2. Sorbitex (IM)

Nsg Mgt parenteral iron prep

1. Administer of use Z tract method to prevent discomfort, discoloration leakage to tissues.
2. Don’t massage injection site. Ambulate to facilitate absorption.
3. Monitor S/E:
a.) Pain at injury site
b.) Localized abscess (“nana”/ pus formation)
c.) Lymphadenopathy
d.) Fever/ chills
e.) Urticaria – itchiness
f.) Hypotension – anaphylactic shock

Anaphylactic shock – give epinephrine

PERNICIOUS ANEMIA - megaloblastic, chronic anemia due to deficiency of intrinsic factor leading to
Hypochlorhydria – decrease Hcl acid secretion. Lifetime B12 injections. With CNS involvement.

Predisposing factor
1. Subtotal gastrectomy –partial removal stomach
2. Hereditary
3. Inflammatory dse of ileum
4. Autoimmune
5. Strict vegetable diet


Parietal or argentaffin Oxyntic cells

Fxn – produce intrinsic factor Fxn – secrets Hcl acid

For reabsorption of B12 Fx aids in digestion

For maturation of RBC

6. Diet high caloric or CHO to correct wt loss

1. Headache dizziness, dyspnea, palpitations, cold sensitivity, gen body malaise, pallor
GIT changes
a. Red – beefy tongue – PATHOGNOMONIC – mouth sores
b. Dyspepsia – indigestion
c. Wt loss
d. Jaundice
3. CNS –
Most dangerous anemia: pernicious due to neuroglogic involvement.
a. Tingling sensation
b. Paresthesia
c. (+) Romberg’s test (Ataxia)
d. Psychosis
Dx: Schilling’s test—measures reabsorption of Vit B12
Confirmatory: absence of intrinsic factor

Nsg Mgt – Pernicious anemia

1. Enforce CBR
2. Administer B12 injections at monthly intervals for lifetime as ordered. IM- dorsogluteal or ventrogluteal. Not given oral –
due pt might develop resistance to drug
Does not develop toxicity because of it is water soluble therefore it is easily excreted
3. Diet – high calorie or CHO. Increase CHON, iron & Vit C
4. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encouraged. Provide oral care
5. Avoid applying electric heating pads or any heat application – can lead to burns

APLASTIC ANEMIA – stem cell disorder due to bone marrow depression leading to pancytopenia – all RBC are decreased

Decrease RBC decrease WBC decrease platelets

Anemia leukopenia thrombocytopenia
Increase WBC leukocytocystosis
Increase RBC polycythemia vera – complication stroke, CVA, thrombosis

Predisposing factors leading to Aplastic Anemia

1. Chemicals – Banzene & its derivatives
2. radiation
3. Immunologic injury
4. Drugs – cause bone marrow depression
a. Broad spectrum antibiotic - Chloramphenicol
- Sulfonamides – bactrim
b. Chemo therapeutic agents
Methotrexate – alkylating agents
Nitrogen mustard – anti metabolic
Vincristine – plant alkaloid

1. Anemia:
a. Weakness & fatigue
b. Headache, dizziness, dyspnea
c. cold sensitivity, pallor
d. palpitations
2. Leukopenia – increase susceptibility to infection
3. Thrombocytopenia –
a. Petecchiae
b. Oozing of blood from venipuncture site
c. ecchymoses
1. CBC – pancytopenia
2. Bone marrow biopsy/ aspiration at post iliac crest – reveals fatty streaks in bone marrow
Nsg Mgt:
1. Removal of underlying cause
2. Blood transfusion as ordered
3. Complete bed rest
4. O2 inhalation
5. Reverse isolation due leukopenia
6. Monitor signs of infection
7. Avoid SQ, IM or any venipuncture site = HEPLOCK
8. Use electric razor when shaving to prevent bleeding
9. Administer meds
Immunological injury: give steroids
Immunosuppresants: Anti lymphocyte globulin (Alg) given via central venous catheter, 6 days – 3 weeks to achieve max
therapeutic effect of drug.

1. To replace circulating blood volume
2. To increase O2 carrying capacity of blood
3. To combat infection if there’s decrease WBC
4. To prevent bleeding if there’s platelet deficiency

Nsg Mgt & principles in Blood Transfusion

1. Proper refrigeration
2. Proper typing & crossmatching
Type O – universal donor
AB – universal recipient
85% of people are RH (+)
3. Asceptically assemble all materials needed:
a.) Filter set
b.) Isotonic or PNSS or .9NaCl to prevent Hemolysis
Hypotonic sol – swell or burst
Hypertonic sol – will shrink or crenate
c.) Needle gauge 18 - 19 or large bore needle to prevent hemolysis.
d.) Instruct another RN to recheck the following .
Pts name, blood typing & cross typing, expiration date, serial number.
e.) Check blood unit for presence of bubbles, cloudiness, dark in color & sediments – indicates bacterial contamination.
Don’t dispose. Return to blood bank.
f.) Never warm blood products – may destroy vital factors in blood.
- Warming is done if with warming device – only in EMERGENCY! For multiple BT.
- Within 30 mins room temp only!
g.) Blood transfusion should be completed < 4hrs because blood that is exposed at room temp for > 2h causes blood
deterioration may cause bacterial contamination.
h.) Avoid mixing or administering drug at BT line – leads to hemolysis
i.) Regulate BT 15-20 gtts/min KVO or 100cc/hr to prevent circulatory overload
j.) Monitor VS before, during & after BT especially q15 mins(local board) for 1st hour. NCLEX-q5min for 1st 15min.
- Majority of BT reaction occurs within 1h.

BT reactions S/Sx Hemolytic reaction:

H – hemolytic Reaction 1. Headache, dizziness, dyspnea, palpitation, lumbar/ sterna/ flank pain,
A – allergic Reaction hypotension, flushed skin , (red) port wine urine.
P – pyrogenic Reaction
C – circulatory overload
A – air embolism
T - thrombocytopenia
C – citrate intoxication – expired blood =hyperkalemia
H – hyperkalemia
Nsg Mgt: Hemolytic Reaction:
1. Stop BT
2. Notify Doc
3. Flush with plain NSS
4. Administer isotonic fluid sol – to prevent acute tubular necrosis & conteract shock
5. Send blood unit to blood bank for reexamination
6. Obtain urine & blood samples of pt & send to lab for reexamination
7. Monitor VS & Allergic Rxn

Allergic Reaction:
1. Fever/ chills
2. Urticaria/ pruritus
3. Dyspnea
4. Laryngospasm/ bronchospasm
5. Bronchial wheezing

Nsg Mgt:
1. Stop BT
2. Notify Doc
3. Flush with PNSS
4. Administer antihistamine – diphenhydramine Hcl (Benadryl). Give bedtime.SE-Adult-drowsiness. Child-hyperactive
If (+) Hypotension – anaphylactic shock administer – epinephrine
5. Send blood unit to blood bank
6. Obtain urine & blood samples – send to lab
7. Monitor VS & IO
8. Adm antipyretic & antibiotic for pyrogenic Rxn & TSB

Pyrogenic Reaction:

a.) Fever/ chills d. tachycardia
b.) Headache e. palpitations
c.) Dyspnea f. diaphoresis

Nsg Mgt:
1. Stop BT
2. Notify Doc
3. Flush with PNSS
4. Administer antipyretics, antibiotics
5. Send blood unit to blood bank
6. Obtain urine & blood samples – send to lab
7. Monitor VS & IO
8. Tepid sponge bath – offer hypothermic blanket

Circulatory Overload:
a. Dyspnea
b. Orthopnea
c. Rales or crackles
d. Exertional discomfort

Nsg Mgt:
1. Stop BT
2. Notify Doc. Don’t flush due pt has circulatory overload.
3. Administer diuretics –Loop (Furosemide)
Priority cases:
Hemolytic Rxn – 1st due to hypotension – 1st priority – attend to destruction of Hgb – O2 brain damage
Allergic 3rd
Pyrogenic 4th
Circulatory 2nd

Hemolytic 2nd
Anaphylitic 1st priority

24. Acute hemorrhagic syndrome char by wide spread bleeding & thrombosis due to a defiency of clotting factors (Prothrombin
& Fibrinogen).

Predisposing factor:
1. Rapid BT
2. Massive trauma
3. Massive burns
4. Septicemia
5. Hemolytic reaction
6. Anaphylaxis
7. Neoplasia – growth of new tissue
8. Pregnancy


1. Petechiae – widespread & systemic (lungs, lower & 4. Hemoptysis – cough blood
upper trunk) 5. Hemorrhage
2. Ecchymoses – widespread 6. Oliguria – late sx
3. Oozing of blood from venipunctured site

Dx Proc–
1. CBC – reveals decrease platelets
2. Stool for occult blood (+)
Specimen – stool
3. Opthalmoscopic exam – sub retinal hemorrhage
4. ABG analysis – metabolic acidosis

R pH PCO2 respiratory alkalosis

O ph PCO2 respiratory acidosis

M ph HCO3 metabolic alkalosis

E ph HCO3 metabolic acidosis

Diarrhea – met acidosis

Vomitting – met alk
Pyloric stenosis – met alkalosis – vomiting
Ileostomy or intestinal tubing – met acidosis
Cushing’s – met alk
DM met acid
Chronic bronchitis – resp acid – with hypoxemia, cyanosis

Nsg Mgt DIC

1. Monitor signs of bleeding – hema test + urine, stool, GIT
2. Administer isotonic fluid solution to prevent shock.
3. Administer O2 inhalation
4. Administer meds
a. Vit K aquamephyton
b. Pitressin or vasopressin – to conserve water
5. NGT – lavage
- Use iced saline lavage- for decompensation, iced saline is used
6. Monitor NGT output
7. Provide heplock
8. Prevent complication: hypovolemic shock
Late signs of hypovolemic shock: anuria
Oncologic Nsg:
Oncology – study of neoplasia –new growth

Benign (tumor) Malignancy (cancer)

Diff - well differentiated poorly or undifferentiated

Encapulation – (+) (-)
Metastasis – (-) (+)
Prognosis – good poor
Therapeutic modality surgery 1. Chemotherapy plenty S/E
2. Radiation
3. Surgery most preferred treatment
4. Bone marrow transplant - Leukemia only
Predisposing factors: (carcinogenesis)
G – genetic factors
I – immunologic factors
V – viral factors
a. Human papiloma virus – causing warts
b. Epstein barr virus
E – environmental Factors 90%
a. Physical – irradiation, UV rays, nuclear explosion, chronic irritation, direct trauma
b. Chemical factors –
- Food additives (nitrates
- Hydrocarbon vesicants, alkalies
- Drugs (stillbestrol)
- Uraehane
- Hormones
- Smoking
3.) Prostate cancer - common 40 & above (middle age & above)
BPH – 50 & above
1.) Lung cancer
2.) Liver cancer

1. Breast cancer – 40 yrs old & up – mammography 15 – 20 mins (SBE – 7 days after mens)
2. Cervical cancer – 90% multi sexual partners
5% early pregnancy
3. Ovarian cancer

Classes of cancer
Tissue typing
1. Carcinoma – arises from surface epithelium & glandular tissues
2. Sarcoma- from connective tissue or bones
3. Multiple myeloma – from bone marrow
Pathological fracture of ribs & back pain
4. Lymphoma – from lymph glands
5. Leukemia – from blood

Warning / Danger Sx of CA
C – change in bowel /bladder habits
A – a sore that doesn’t heal
U – unusual bleeding/ Discharge
T – thickening of lump – breast or elsewhere
I – indigestion? Dysphagia
O – obvious change in wart/ mole
N – nagging cough/ hoarseness
U – unexplained anemia A - anemia
S – sudden wt loss L – loss of wt

Therapeutic Modality:
1. Chemotherapy – use various chemotherapeutic agents that kills cancer cells & kills normal rapidly producing cells – GIT,
bone marrow, and hair follicle.

a.) Alkylating agents –
b.) Plant alkaloids – vincristine
c.) Anti metabolites – nitrogen mustard
d.) Hormones – DES
e.) Antineoplastic antibiotics

S/E & mgt

GIT - -Nausea & vomiting
Nsg Mgt:
1. Administer anti emetic 4 – 6h before start of chemo
2. Withhold food/ fluid before start of chemo
3. Provide bland diet post chemo
25. Non irritating / non spicy

- Diarrhea
1. Administer anti diarrheal 4 – 6h before start of chemo
2. Monitor urine, I&O qh
- Stomatitis/ mouth sores
1. Oral care – offer ice chips/ popsickles
2. Inform pt – hair loss – temporary alopecia
Hair will grow back after 4 – 6 months post chemo.
-Bone marrow depression – anemia
1. Enforce CBR
2. O2 inhalation
3. Reverse isolation
4. Monitor signs of bleeding
Repro organ – sterility
1. Do sperm banking before start of chemo
Renal system – increase uric acid
1. Administer allopurinol/ xyloprin (gout)
26. Inhibits uric acid
27. Acute gout – colchicines
28. Increase secretion of uric acid
Neurological changes – peristalsis – paralytic ileus
Most feared complication ff any abdominal surgery
Vincristine – plant alkaloid causes peripheral neuropathy

2. Radiation therapy – involves use of ionizing radiation that kills cancer cells & inhibit their growth & kill N rapidly producing

Types of energy emitted

1. Alpha rays – rarely used – doesn’t penetrate skin tissues
2. Beta rays – internal radiation – more penetration
3. Gamma ray – external radiation – penetrates deeper underlying tissues

Methods of delivery
1. External radiation- involves electro magnetic waves
Ex. cobalt therapy
2. Internal radiation – injection/ implantation of radioisotopes proximal to CA site for a specific period of time.
2 types:
a.) Sealed implant – radioisotope with a container & doesn’t contaminate body fluid.
b.) Unsealed implant – radioisotope without a container & contaminates body fluid.
Ex. Phosphorus 32

3 Factors affecting exposure:

A.) Half life – time period required for half of radioisotopes to decay.
- At end of half life – less exposure
B.) Distance – the farther the distance – lesser exposure
C. ) Time – the shorter the time, the lesser exposure
D.) Shielding – rays can be shielded or blocked by using rubber gloves – α & β gamma – use thick lead on concrete.

S/E & Mgt:

a.) Skin errythema, redness, sloughing
1. Assist in battling pt
2. Force fluid – 2,000 – 3,000 ml/day
3. Avoid lotion or talcum powder – skin irritation
4. Apply cornstarch or olive oil
b.) GIT –nausea / vomiting -
1. Administer antiemetic 4 – 6h before start of chemo - Plasil
2 Withhold food/ fluid before start of chemo
3. Provide bland diet post chemo
Non irritating / non spicy
Dysglusia – decrease taste sensitivity
-When atrophy papilla (taste buds) – 40 yo
c.) Bone marrow depression
1. Enforce CBR
2. O2 inhalation
3. Reverse isolation
4. Monitor signs of bleeding

Overview of function & structure of the heart

- Muscular, pumping organ of the body
- Left mediastinum
- Weigh 300 – 400 grams
- Resembles a closed fist
- Covered by serous membrane – pericardium

Parietal layer Pericardial Visceral layer

(outer) Fluid – to prevent (inner)
Friction rub (10-20 cc)

1. Epicardium – outermost
2. Myocardium – inner – responsible for pumping action/ most dangerous layer - cardiogenic shock
- may lead to myocarditis, which may lead to RHD
3. Endocardium – innermost layer

1. Upper – collecting/ receiving chamber - Atria
2. Lower – pumping/ contracting chamber - Ventricles
1. Atrioventricular valves - Tricuspid & mitral valve
Closure of AV valves – gives rise to 1st heart sound or S1 or “lub”
2. Semi lunar valve
a.) Pulmonic
b.) Aortic
Closure of semilunar valve – gives rise to 2nd heart sound or S2 or “dub”
Extra heart Sound
S3 – ventricular Gallop – CHF
S4 – atrial gallop – MI, HPN

Coronary Arteries- arise from base of the aorta

Right main coronary artery Supply the
Left main coronary artery myocardium

Heart conduction system

1. Sino atrial node (SA node) (or Keith-Flock node)
Loc – junction of SVC & Rt atrium
Fx- primary pace maker of heart
-Initiates electric impulse of 60 – 100 bpm
2. Atrioventicular node (AV node or Tawara node)
Loc – inter atrial septum
Delay of electric impulse to allow ventricular filling (for about ,08millisecond)
3. Bundle of His – location interventricular septum
Rt main Bundle Branch
Lt main Bundle Branch
4. Purkinje Fibers
Loc- walls of ventricles leading to Ventricular contractions

SA node


Purkenjie Fibers
Bundle of His

Complete heart block or the bundle block – insertion of pacemaker at Bundle Branch is needed
Metal – Pace Maker – change q3 – 5 yo

Prolonged PR – atrial fib T wave inversion – MI

ST segment depression – angina widening QRS – arrhythmia
ST – elev – MI

CAD – coronary artery dse or Ischemic Heart Dse (IHD) ==Nsg Mgt: decrease myocardial workload

1. Atherosclerosis – Myocrdial injury
2. Angina Pectoris – Myocardial ischemia
3. MI- myocardial necrosis

- Narrowing of artery due to fat - Hardening or artery due to calcium & CHON
- lipid deposits at tunica intima. deposits at tunica media.

Artery – tunica adventitia – outer

- Tunica intima – innermost
- Tunica media – middle

Predisposing Factor
1. Sex – male
2. Black race
3. Hyperlipidemia, increase in saturated fats
4. Smoking
5. HPN
6. DM
7. Oral contraceptive- prolonged use
8. Sedentary lifestyle
9. Obesity
10. Hypothyroidism
11. Stress

Signs & Symptoms

1. Chest pain
2. Dyspnea
3. Tachycardia
4. Palpitations
5. Diaphoresis
P – percutaneous
T – tansluminar For single occluded vessels
C – coronary
A – angioplasty
1. To revascularize the myocardium
2. To prevent angina
3. Increase survival rate

PTCA – done to pt with single occluded vessel .

Multiple occluded vessels
C – coronary
A – arterial for 2 or more occluded vessels
B – bypass
A –and
G – graft surgery

Nsg Mgt Before CABAG

1. Deep breathing cough exercises
2. Use of incentive spirometer
3. Leg exercises

ANGINA PECTORIS- A clinical syndrome characterized by paroxysmal chest pain usually relieved by REST or NGT
nitroglycerin, resulting fr temp myocardial ischemia.
Predisposing Factor: (same with CAD)
1. sex – male
2. black race
3. hyperlipidemia
4. smoking
5. HPN
6. DM
7. oral contraceptive prolonged
8. sedentary lifestyle
9. obesity
10. hypothyroidism
Precipitating factors
4 E’s
1. Excessive physical exertion
2. Exposure to cold environment - Vasoconstriction
3. Extreme emotional response
4. Excessive intake of food – saturated fats

Signs & Symptoms

1. Initial symptoms – Levine’s sign – hand clutching of chest
2. Chest pain – sharp, stabbing excruciating pain.
Location – substernal
-radiates back, shoulders, axilla, arms & jaw muscles
-relieve by rest or NGT
3. Dyspnea
4. Tachycardia
5. Palpitation
6. diaphoresis
1. History taking & PE
2. ECG – ST segment depression
3. Stress test – treadmill = abnormal ECG
4. Serum cholesterol & uric acid - increase
Nursing Management
1.) Enforce CBR
2.) Administer meds as ordered
NTG – small doses – venodilator
Large dose – vasodilator

1st dose NTG – give 3 – 5 min

2nd dose NTG – 3 – 5 min
3rd & last dose – 3 – 5 min
Still painful after 3rd dose – notify doc. MI!

55 yrs old with chest pain:

1st question to ask pt: what did you do before you had chest pain.
2nd question: does pain radiate?
If chest pain radiates – heart in nature. If not radiate – pulmonary origin (PTB, Pneumonia, Emphysema)

Nitroglycerin- act as Venodilator (if given in small doses)– dilate veins of lower ext – increase venous pooling lead to
decrease venous return.
Large doses- vasodilators

A. NTG- Nsg Mgt:
1. Keep in a dry place.
2. Avoid moisture & heat, sunlight may inactivate the drug.
3. Monitor S/E:
orthostatic hypotension – dec bp
transient headache
4. Rise slowly from sitting position
5. Assist in ambulation.
6. If giving NTG via patch:
i. avoid placing it near hairy areas-will dec drug absorption (SHAVE AREA)
ii. avoid rotating transdermal patches- will dec drug absorption
iii. avoid placing near microwave oven or during defibrillation-will burn pt due aluminum foil in patch

B. Beta blockers – PROPANOLOL (inderal)

C. ACE inhibitors – CAPTOPRIL
D. Ca antagonist - NIFEDIPINE
3.) Administer O2 inhalation
4.) Semi-fowler
5.) Diet- Decrease Na and saturated fats, caffeine
6.) Monitor VS, I&O, ECG
7.) HT: Discharge planning:
a. Avoid precipitating factors – 4 E’s
b. Prevent complications – MI
c. Take meds before physical exertion-to achieve maximum therapeutic effect of drug
d. Importance of follow-up care.

MI – MYOCARDIAL INFARCTION – heart attack – terminal stage of CVD characterized by malocclusion leading to
necrosis and scarring

A. According to Location

1. Trasmural MI – most dangerous MI – Mal-occlusion of both R&L coronary artery

2. Sub-endocardial MI – mal-occlusion of either R & L coronary artery

Most critical period upon dx of MI – 48 to 72h—most dangerous hours: first 6-8 hours (majority of arrythmias occur, PVCs)
- Majority of pt suffers from PVC premature ventricular contraction.

B. According to mortality
Killip I – 15-20% chance of mortality (75-80% survival)
Killip II – 30-35% mortality
Killip III- 45-50% mortality
Killip IV- 65-70% mortality—spiritual support is needed, pt chronically ill characterized by cardiogenic shock

Predisposing factors Signs & symptoms Diagnostic Exam

1. sex – male 1. chest pain – excruciating, visceral pain located 1. cardiac enzymes
2. black raise substernal or precodial area (rare) a.) CPK – MB – Creatinine Phosphokinase (12-
3. hyperlipidemia - radiates back, arm, shoulders, axilla, jaw & abd 24H)--increased
4. smoking muscles (abdominal ischemia). b.) LDH – lactic acid dehydrogenase--increased
5. HPN - not usually relived by rest or NTG c.) SGPT – (ALT) – Serum Glutanic Pyruvate
6. DM 2. dyspnea Transaminase- increased
7. oral contraceptive 3. Hyperthermia d.) SGOT (AST) – Serum Glutamic Oxalo-
prolonged 4. initial increase in BP acetic - increased
8. sedentary lifestyle 5. mild restlessness & apprehensions 2. Troponin test – increase
9. obesity 6. cool, moist ashen skin 3. ECG tracing – ST segment
10. hypothyroidism increase/elevation, T wave inversion,
7. occasional findings widening or QRS complexes – means
a.) split S1 & S2 arrhythmia in MI indicating PVC
b.) pericordial friction rub 4. serum cholesterol & uric acid - increase
c.) rales /crackles 5. CBC – increase WBC
d.) S4 (atrial gallop) –(MI and Hypertension)

Nursing Management
1. Narcotic analgesics – Morphine SO4 – to induce vasodilation & decrease levels of anxiety.
2. Administer O2 inhalation – low inflow (CHF-increase inflow)—2-3L/min (high inflow may lead to respiratory arrest)
3. Enforce CBR without BRP
a.) use Bedside commode
4. Avoid Valsalva maneuver (give laxatives)
5. Semi fowler
6. Provide a general liquid to soft diet that is low in saturated fats, Na, caffeine
7. Monitor VS, I&O & ECG tracings
8. Take 20 – 30 ml/week – wine, brandy, or whisky to induce vasodilation.
9. Assist in surgical; CABAG
Complications: 1. Pneumonia
2. Thrombophlebitis
3. Infarction
10. Provide pt HT
a.) Avoid modifiable risk factors (diet, lifestyle)
b.) Prevent complications:
1. Arrhythmias – PVC
2. Shock – cardiogenic shock. Late signs of cardiogenic shock in MI – oliguria
3. Thrombophlebitis - deep vein thrombosis
4. CHF – left sided
5. Dressler’s syndrome – post MI syndrome
-Resistant to medications
-Administer 150,000 – 450,000 units of streptokinase
c.) Strict compliance to meds
- Vasodilators
1. NTG
- Antiarrythmic
1. Lydocaine blocks release of norepinephrine
2. Bretylium
- Beta-blockers – “lol”
1. PROPANOLOL (Inderal)
- ACE inhibitors - pril
1. CAPTOPRIL– (Enalapril)
- Ca – antagonist
- Thrombolytics or fibrinolytics– to dissolve clots/ thrombus

S/E allergic reactions/ uticaria

1. Streptokinase—S/E: allergic reaction (urticaria or pruritus)—bec Streptokinase is a foreign protein substance
2. Urokinase
3. Tissue plasminogen activating factor—S/E: chest pain

Monitor for bleeding:

- Anticoagulants
1. Heparin (short acting) 2. Coumadin (Warfarin) – delayed reaction takes 2 – 3 days to take effect


If prolonged bleeding prolonged bleeding

Antidote antidote Vit K

Protamine sulfate
- Anti platelet PASA (aspirin)—anti-thrombotic properties
C/I: Dengue, vasoconstrictors, unknown cause of headache

d.) Resume ADL – sex/ activity – 4 to 6 weeks

Post-cardiac rehab
1.)Sex as an appetizer rather then dessert –
Before meals not after, due after meals increase metabolism – heart is pumping hard after meals.
2.) Position – non-weight bearing position.
When to resume sex/ act: When pt can already use staircase, then he can resume sex.
e.) Diet – decrease Na, Saturated fats, and caffeine
f.) Teach importance of follow up care.

CHF – CONGESTIVE HEART FAILURE - Inability of heart to pump blood towards systemic circulation.
- Backflow
1.) Left sided heart failure:

Predisposing factors:
1.) 90% mitral valve stenosis – due RHD, aging
RHD affects mitral valve – streptococcal infection
Dx: - Aso titer – anti streptolysine O > 300 total units
Drugs given - Steroids
- Penicillin
- Aspirin
Complication: RS-CHF
Aging – degeneration / calcification of mitral valve
Ischemic heart disease
HPN, MI, Aortic stenosis

Pulmonary congestion/ Edema
1. Dyspnea
2. Orthopnea (Diff of breathing- put patient on sitting pos – platypnea)—2-3 pillows or high fowlers
3. Paroxysmal nocturnal dysnea – PNO- nalulunod (DOB at night)
4. Productive cough with blood tinged sputum
5. Frothy saliva (from lungs)
6. Cyanosis
7. Rales/ crackles – due to fluid
8. Bronchial wheezing
9. PMI – displaced lateral – due cardiomegaly
10. Pulsus alternons – weak- pulse followed by alternating strong bounding pulse
11. Anorexia & general body malaise
12. S3 – ventricular gallop

1. CXR – cardiomegaly
2. PAP – Pulmonary Arterial Pressure
PCWP – Pulmonary CapillaryWedge Pressure

PAP – measures pressure of R ventricle. Indicates cardiac status.

PCWP – measures end systolic/ diastolic pressure
Swan – Ganz catheterization – cardiac catheterization is done at bedside at ICU
Operating room: laryngeal/throat cancer- tracheostomy set
(Trachesostomy – bedside) - Done 5 – 20 mins – scalpel & trachesostomy set

CVP – indicates fluid or hydration status (N: 4-10cm of H2O)

Increase CVP – decrease flow rate of IV
Decrease CVP – increase flow rate of IV
3. Echocardiography – reveals enlarged heart chamber or cardiomyopathy

4. ABG – PCO2 increase, PO2 decrease = = hypoxemia = resp acidosis

2.) Right sided HF

Predisposing factor
1. 90% - tricuspid stenosis
3. Pulmonary embolism
4. Pulmonic stenosis
5. Left sided heart failure

Venous congestion
- Neck or jugular vein distension
- Pitting edema
- Ascites
- Wt gain
- Hepatomegalo/ splenomegaly
- Jaundice
- Pruritus
- Esophageal varies
- Anorexia, gen body malaise

1. CXR – cardiomegaly
2. CVP – measures the pressure at R atrium
Normal: 4 to 10 cm of water
Increase CVP > 10 – hypervolemia – give loop diuretics
Decrease CVP < 4 – hypovolemia (fluid challenge by inc IVF rate)
Flat on bed – post of pt when giving CVP
Position during CVP insertion – Trendelenburg to prevent pulmonary embolism & promote ventricular

3. Echocardiography – enlarged heart chamber / cardiomyopathy

4.Liver enzyme elevation

Nsg mgt: Increase force of myocardial contraction = increase cardiac output

3 – 6L of CO enforce CBR
1. Administer meds:
Tx for LSHF: M – morphine SO4 to induce vasodilatation
A – aminophylline & decrease anxiety
D – digitalis (digoxin)
D - diuretics
O - oxygen
G - gases

a.) Cardiac glycosides

Increase myocardial = increase CO
Digoxin (Lanoxin). Antidote: digivine
Digitoxin: metabolizes in liver not in kidneys not given if with kidney failure.
b.) Loop diuretics: Lasix – effect with in 10-15 min. Max = 6 hrs
c.) Bronchodilators: Aminophyline (Theophyline). Avoid giving caffeine
d.) Narcotic analgesic: Morphine SO4 - induces vasodilaton & decrease anxiety
e.) Vasodilators – NTG
f.) Anti-arrythmics – Lidocaine
Ethacrynic acid- Thiazide diuretics

2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula

3. High fowlers
4. Restrict Na!
5. Provide meticulous skin care
6. Weigh pt daily. Assess for pitting edema.
Measure abdominal girth daily & notify MD
7. Monitor V/S, I&O, breath sounds, EKG tracings
8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous
9. Diet – decrease salt, fats & caffeine
10. HT:
a) Complications :shock
Cor Pulmonale – RT ventricular hypertrophy
b.) Dietary modifications
c.) Adherence to meds


Arterial ulcers venous ulcer

1. Thromboangitis Obliterans (Buergers)– male/ feet 1. Varicose veins
2. Reynauds – female/ hands 2. Thrombophlebitis

1.) Thromboangitis obliterates/ BUERGERS DISEASE- Acute inflammatory disorder affecting small to medium sized
arteries & veins of lower extremities. Male/ feet

Predisposing factors:
- Males greater than 30yo (high risk group)
- Smokers

1. Intermittent claudication – leg pain upon walking - Relieved by rest
2. Cold sensitivity & skin color changes

White bluish red

Pallor cyanosis rubor

3. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis

4. Trophic changes
5. Ulcerations
6. Gangrene formation

1. Oscillometry – decrease peripheral pulse volume.
2. Doppler UTZ – decrease blood flow to affected extremities.
3. Angiography – reveals site & extent of malocculsion.

Nsg Mgt:
1. Encourage a slow progression of physical activity
a.) Walk 3 -4 x / day
b.) Out of bed 2 – 3 x a / day
2. Meds
a.) Analgesic
b.) Vasodilator
c.) Anticoagulant
3. Foot care mgt like DM –
a.) Avoid walking barefoot
b.) Cut toe nails straight
c.) Apply lanolin lotion – prevent skin breakdown
d.) Avoid wearing constrictive garments
4. Avoid smoking & exposure to cold environment
5. Assist patient in surgery: BKA (Below the knee amputation)

2.)REYNAUD’S PHENOMENON – acute episodes of arterial spasm affecting digits of hands & fingers
Predisposing factors:

1. Female, 40 yrs
2. Smoking
3. Collagen dse
a.) SLE – pathognomonic sign – butterfly rash on face
Chipmunk face – bulimia nervosa
Cherry red skin – carbon monoxide poisoning
Spider angioma – liver cirrhosis
Caput medusae – leg & trunk umbilicus- Liver cirrhosis
Lion face – leprosy

b.) Rheumatoid arthritis –

4. Direct hand trauma – piano playing, excessive typing, operating chainsaw
1. Intermittent claudication - leg pain upon walking - Relieved by rest
2. Cold sensitivity

Nsg Mgt:
a. Analgesics
b. Vasodilators
c. Encourage to wear gloves especially when opening a refrigerator.
d. Avoid smoking & exposure to cold environment

1. VARICOSITIES / Varicose veins - Abnormal dilation of veins – lower ext & trunk
- Due to:
a.) Incompetent valves leading to
b.) Increase venous pooling & stasis leading to
c.) Decrease venous return

Predisposing factors:
a. Hereditary
b. Congenital weakness of veins
c. Thrombophlebitis
d. Heart dse
e. Pregnancy
f. Obesity
g. Prolonged immobility - Prolonged standing
1. Pain especially after prolonged standing
2. Dilated tortuous skin veins
3. Warm to touch
4. Heaviness in legs

1. Venography
2. Trendelenberg’s test – vein distend quickly < 35 secs

Nsg Mgt:
1. Elevate legs above heart level – to promote venous return – 1 to 2 pillows
2. Measure circumference of leg muscles to determine if swollen.
3. Wear anti embolic or knee high stockings. Women – panty hose
4. Meds: Analgesics
5. Surgery: vein sweeping & ligation
Sclerotherapy – spider web varicosities
S/E thrombosis

THROMBOPHLEBITIS (deep vein thrombosis) - Inflammation of veins with thrombus formation

Predisposing factors:
1. Smoking
2. Obesity
2. Hyperlipedemia
4. Prolonged use of oral contraceptives
5. Chronic anemia
6. DM
7. MI
8. CHF
9. Postop complications
10. Post cannulation – insertion of various cardiac catheters
1. Pain at affected extremities
2. Cyanosis
3. (+) Homan’s sign - Pain at leg muscles upon dorsiflexion of foot.
1. Angiography
2. Doppler UTZ
Nsg Mgt:
1. Elevate legs above heart level.
2. Apply warm, moist packs to decrease lymphatic congestion.
3. Measure circumference of leg muscles to detect if swollen.
4. Use anti embolic stockings.
5. Meds: Analgesics.
Anticoagulant: Heparin
6. Complication:

Pulmonary Embolism:
- Sudden sharp chest pain
- Dyspnea
- Tachycardia
- Palpitation
- Diaphoresis
- Mild restlessness


I. Upper respiratory tract:
1. Filtering of air
2. Warming & moistening
3. Humidification
a. Nose – cartilage
- Parts: Rt nostril separated by septum
Lt nostril

- Consists of anastomosis of capillaries –

Liessel – Bach Plexus – site of epistaxis
b. Pharynx (throat) – muscular passageway for air& food
1. Oropharynx
2. Nasopharynx
3. Layngopharynx

c. Larynx – voice box

1. For phonation- voice or speech production
2. Cough reflex
Made up of framework:
a. epiglottis
b. hyoid bone
c. thyroid & crichoid cartilage

Glottis – opening of larynx

Opens to allow passage of air
Closes to allow passage of food
-Inability to cough, complete obstruction of airway

II. Lower Respiratory tract – Fx for gas exchange

d. Trachea – windpipe
- has cartillagenous rings
- site for permanent/ artificial a/w – tracheostomy
b. Bronchus – R & L main bronchus
c. Lungs – R – 3 lobes = 10 segments
L – 2 lobes – 8 segments

Post pneumonectomy - position affected side to promote expansion of lungs==Semi Fowlers

Post segmental lobectomy – position unaffected side to promote drainage

Serous membrane
Parietal Visceral

Pleural Fluid

Pleural Friction Rub ches pain- pain upon inspiration


Pleural Effusion
Lungs – covered by pleural cavity, parietal lobe & visceral lobe
Alveoli – acinar cells
- site of gas exchange (O2 & CO2)-diffusion
- diffusion: Daltons law of partial pressure of gases
- basic living units
Powerful stimulating stimulant—increase CO2
COPD – decrease O2 stimulant
Ventilation – movement of air in & out of lungs
Respiration – movement of air into cells

Type II cells of alveoli – secretes surfactant, lipoprotein in nature

Surfactant - decrease surface tension of alveoli—prevents collapse of lungs also known as atelectasis

Lecithin & spinogomyelin

L/S ratio 2:1 – indicator of lung maturity

If 1:2 – adm O2 - < 40% Concentration to prevent atelectasis & retinopathy or blindness.

Retrolental Fibroplasia-retinopathy/blindness in prematurity

I. PNEUMONIA – inflammation of lung parenchyma leading to pulmonary consolidation as alveoli is filled with exudates.

Etiologic agents:
1. Streptococcus pneumoniae (pnemococcal pneumonia)
2. Haemophilus pneumoniae(Bronchopneumonia) in children
3. Escherichia coli
4. Klebsiella P.
5. Diplococcus P.

High risk: elderly & children below 5 yo bec of low resistance

Predisposing factors:
1. Smoking
2. Air pollution
3. Immuno-compromised patients
b. Bronchogenic CA - Non-productive to productive cough-- CXR
4. Prolonged immobility – CVA- hypostatic pneumonia
5. Aspiration of food
6. Over fatigue

1. Productive cough – pathognomonic: greenish to rusty sputum
2. Dyspnea with prolonged respiratory grunt
3. Fever, chills, anorexia, gen body malaise
4. Wt loss
5. Pleuritic friction rub
6. Rales/ crackles
7. Cyanosis
8. Abdominal distension leading to paralytic ileus (absence of peristalsis)

Sputum exam – could confirm presence of TB & pneumonia

1. Sputum GSCS- gram staining & culture sensitivity - Reveals (+) culture microorganism.
2. CXR – pulmonary consolidation
3. CBC – increase WBC and inc Erythrocyte sedimentation rate
4. ABG – PO2 decrease, hypoxemia

Nsg Mgt:
1. Enforce CBR
2. Strict respiratory isolation
3. Meds:
a.) Broad spectrum antibiotics
Penicillin or tetracycline
Macrolides – ex azythromycin (zythromax)
b.) Anti pyretics
c.) Mucolytics or expectorants
4. Force fluids – 2 to 3 L/day
5. Institute pulmonary toilet-
a.) Deep breathing exercise
b.) Coughing exercise

c.) Chest physiotherapy – cupping
d.) Turning & reposition - Promote expectoration of secretions
6. Semi-fowler
7. Nebulize & suction as necessary, O2 inhalation
8. Comfy & humid environment
9. Diet: increase CHO or calories, CHON & Vit C
10. Postural drainage - To drain secretions using gravity

Mgt for postural drainage:

a.) Best done before meals (breakfast) or 2 – 4 hrs after meals to prevent Gastroesophageal Reflux
b.) Monitor VS & breath sounds
Normal breath sound – bronchovesicular
c.) Deep breathing exercises
d.) Adm bronchodilators 15 – 30 min before procedure
e.) Stop if pt can’t tolerate procedure
f.) Provide oral care – it may alter taste sensation
g.) C/I – pt with unstable VS & hemoptysis, increase ICP, increase IOP (glaucoma)
Normal IOP – 12 – 21 mmHg
11. HT:
a.) Avoidance of precipitating factors (smoking)
b.) Complication: Atelectacies & meningitis
c.) Compliance to meds

PULMONARY TUBERCULOSIS (KOCH’S DSE) - Inflammation of lung tissue caused by invasion of mycobacterium TB
or tubercle bacilli or acid fast bacilli – gram (+) aerobic, motile & easily destroyed by heat or sunlight.

Predisposing factors:
1. Malnutrition
2. Overcrowding
3. Alcoholism
4. Ingestion of infected cattle (mycobacterium BOVIS)
5. Virulence
6. Over fatigue or stress
1. Productive cough – yellowish
2. Low grade afternoon fever
3. Night sweats
4. Dyspnea
5. Anorexia, generalized body malaise, wt loss
6. Chest/ back pain
7. Hempotysis
==Airborne transmission, droplet nuclei infection

1. Skin test – Mantoux test – infection of Purified Protein Derivative PPD
DOH – 8-10 mm induration
WHO – 10-14 mm induration
Result within 48 – 72h
(+) Mantoux test – previous exposure to tubercle bacilli

Mode of transmission – droplet infection

2. Sputum AFB – (+) to cultured microorganism
3. CXR – pulmonary infiltrate caseous necrosis
4. CBC – increase WBC

Nursing Mgt:
1. CBR
2. Strict resp isolation
3. O2 inhalation
4. Semi fowler
5. Force fluid to liquefy secretions
6. Deep breathing and cough exercises
7. Nebulize & suction if necessary
8. Provide comfortable & humid environment
9. Diet – increase CHO & calories, CHON, Vit, minerals
10. Short course chemotherapy:

Intensive phase

1. INH – isoniazid - both given before meals for absorption

2. Rifampicin - both given within 4 months, given simultaneously to prevent resistance
-S/E: peripheral neutitis – vit B6 (cereals, green leafy vegetables, organ meat)
Rifampicin -All body secretions turn to red orange color urine, stool, saliva, sweat & tears.

3. PZA – Pyrazinamide – given 2 mos/ after meals. S/E: allergic rxn, nephrotoxicity & hepatoxicity

PZA may be replaced by ETHAMBUTOL (S/E: optic neuritis)
Standard regimen
1. Injection of streptomycin – Aminoglycosides
Ex. Kanamycin, gentamycin, neomycin
a.) Ototoxicity – damage CN # 8 – tinnitus (ringing in the ears), dizziness, vertigo
b.) Nephrotoxicicity – monitor BUN (10-20) & Creatinine (.8-1)
a.) Avoid predisposing factors like alcoholism, crowded places
b.) Provide the dietary intake of increased CHO,calories, CHONm and Vitamin C
c.) Avoid complications:
1.) Atelectasis
2.) Miliary TB – spread of Tb to other system
b.) Strict compliance to meds (if one misses a dose, continue taking the meds)
- Religiously take meds
e) Know the importance of follow up care

HISTOPLASMOSIS- acute fungal infection caused by inhalation of contaminated dust with Histoplasma Capsulatum
transmitted from bird’s manure.
S/Sx: Same as pneumonia & PTB – like
1. Productive cough
2. Dyspnea
3. Chest & joint pains
4. Cyanosis
5. Anorexia, gen body malaise, wt loss
6. Hemoptysis
7. Fever and chills

1. Histoplasmin skin test = (+) Histoplasma Capsulatum
2. ABG – pO2 decrease

Nsg Mgt:
1. CBR
2. Meds:
a.) Antifungal agents
Amphotericin B (Fungizone)
a.) Nephrotoxcicity check BUN and Creatinine
b.) Hypokalemia
c.) Mucolytic/ or Expectorants
3. Administer O2, force fluids
4. Encourage deep breathing and coughing exercises
5. Nebulize, suction
6. Complications:
a.) Atelectasis
b.) Bronchiectasis COPD
7. Prevent spread of histoplasmosis:
a.) Spray breading places or kill the bird.

COPD – Chronic Obstructive Pulmonary Disease

1. Chronic bronchitis
2. Bronchial asthma
3. Bronchiectasis
4. Pulmonary emphysema – terminal stage

CHRONIC BRONCHITIS - called BLUE BLOATERS inflammation of bronchus due to hypertrophy or hyperplasia of goblet
mucus producing cells leading to narrowing of smaller airways.

Predisposing factors:
1. Smoking – all COPD types
2. Air pollution
1. Productive cough
2. Dyspnea on exertion
3. Prolonged expiratory grunt
4. Scattered rales/ rhonchi
5. Cyanosis
6. Pulmonary HPN – a.) Leading to peripheral edema
b.) Cor pulmonale – right ventricular hypertrophy --respiratory in origin
7. Anorexia, gen body malaise

1. ABG
PO2 PCO2 Resp acidosis

Hypoxemia – causing cyanosis - Complications: Emphysema and Pleurisy

Nsg Mgt:
(Same as emphysema)

2.) BRONCHIAL ASTHMA- reversible inflammation lung condition due to hyerpsensitivity to allergens leading to narrowing
of smaller airways.
Predisposing factor:
1. Extrinsic Asthma – called Atopic/ allergic asthma
a.) Pollen
b.) Dust
c.) Gases
d.) Smoke/fumes
e.) Dander
f.) Lints
g.) Viral infection

2. Intrinsic Asthma- called Non-Atopic, non-allergic asthma

Drugs – aspirin, penicillin, β blockers (beta blockers are bronchoconstrictors)
Food additives – nitrites
Foods – seafood, chicken, eggs, chocolates, milk
Physical/ emotional stress
Sudden change of temp, humidity &air pressure
3. mixed type: combination of both extrinsic & intrinsic Asthma
90% cause of asthma
1. C – cough – non productive to productive
2. D – dyspnea
3. W – wheezing on expiration
4. Cyanosis
5. Mild apprehension & restlessness
6. Tachycardia & palpitation
7. Diaphoresis
1. Pulmo function test – decrease vital lung capacity
2. ABG – PO2 decrease, PCO2 increase- hypoxemia, Ph decreased
Respiratory Acidosis

Nsg Mgt:
1. CBR – all COPD
2. Meds-
a.) Bronchodilator through inhalation or metered dose inhaled / pump. Given 1st before corticosteroids to facilitate
b.) Corticosteroids – due inflammatory. Given 10 min after adm bronchodilator
c.) Mucolytic/ expectorant
d.) Mucomist (Acetylcysteine) – at bedside put suction machine.
e.) Antihistamine
2. Force fluids
3. Institute pulmonary toilet
4. O2 – all COPD low inflow to prevent resp distress
5. Nebulize & suction client PRN
6. Diet: increase CHO, CHON
7. Semifowler – all COPD except emphysema due late stage
8. HT
a.) Avoid predisposing factors (dust, pollen, etc), provide a comfortable environment
b.) Complications:
• Status astmaticus- give epinephrine & bronchodilators
- Emphysema
c.) Adherence to meds to prevent status asmaticus
d.) Teach the importance of follow up care

BRONCHIECTASIS – abnormal permanent dilation of bronchus resulting to destruction of muscular & elastic tissues of alveoli.
Predisposing factors:
1. Recurrent upper & lower respiratory tract infections
2. Congenital anomalies
3. Lung Tumors
4. Chest Trauma
1. Productive cough
2. Dyspnea
3. Anorexia, generalized body malaise- all energy are used to increase respiration.
4. Cyanosis
5. Hemoptisis

1. ABG – PO2 decrease
2. Bronchoscopy – direct visualization of bronchus using fiberscope.
3. Chest xray
Nsg Mgt: before bronchoscopy
1. Consent, explain procedure – MD/ lab explain RN
2. NPO
3. Monitor VS
Nsg Mgt after bronchoscopy
1. Feeding after return of gag reflex
2. Instruct client to avoid talking, smoking or coughing
3. Monitor signs of frank or gross bleeding
4. Monitor of laryngeal spasm
- Prepare at bedside tracheostomy set

Mgt: same as emphysema except Surgery

Pneumonectomy – removal of affected lung – lie on affected side
Segmental lobectomy – position of pt – unaffected side to promote drainage

PULMONARY EMPHYSEMA – irreversible terminal stage of COPD

- Characterized by inelasticity of alveolar walls leading to air trapping, leading to maldistribution of gases.
- Body will compensate over distension of thoracic cavity
- Barrel chest
Predisposing factor:
1. Smoking
2. Allergy
3. Air pollution
4. High risk – elderly (above 65yo)
5. Hereditary - α 1 anti trypsin to release elastase for recoil of alveoli.
1. Consistent productive cough
2. Dyspnea at rest with prolonged expiratory grunt – due terminal
3. Anorexia & generalized body malaise
4. Barrel chest
5. Rales/ rhonchi
6. Bronchial wheezing
7. Decrease tactile fremitus (should have vibration) – palpation – “99”. Decreased - with air or fluid
8. Resonance to hyperresonance – percussion
9. Decreased or diminished breath sounds on affected lungs
10. Pathognomonic: barrel chest – increase post/ anterior diameter of chest
11. Pursed lip breathing – to eliminated CO2
12. Flaring of alai nares/ ala nasi

1. Pulmonary function test – decrease vital lung capacity
2. ABG –
a.) Panlobular / centri lobular emphysema
pCO2 increase
pO2 decrease – hypoxema resp acidosis Blue bloaters – Chronic bronchitis
b.) Panacinar/ Centriacinar
pCO2 decrease
pO2 increase – hyperaxemia resp alkalosis Pink puffers
Nursing Mgt:
1. CBR
2. Meds –
a.) Bronchodilators
b.) Corticosteroids- prone to infection
c.) Antimicrobial agents
d.) Mucolytics/ expectorants
e.) Antipyretics PRN
--Patient is prone to develop an infection

3. O2 – Low inflow – to avoid rsp arrest

4. Force fluids
5. High fowlers
6. Nebilize & suction
7. Institute
P – posture
E – end
E – expiratory to prevent collapse of alveoli
P – pressure
8. HT
a.) Avoid smoking
b.) Prevent complications
1.) Cor pulmonale – R ventricular hypertrophy
2.) CO2 narcosis – lead to coma
3.) Atelectasis
4.) Pneumothorax – air in pleural space
9. Adherence to meds
10. Encourage deep breathing and coughing exercises
11. Diet: increase CHO, DHON, vitamins and minerals
12. Importance of follow up care


PNEUMOTHORAX – partial / or complete collapse of lungs due to entry or air in pleural space.
1. Spontaneous pneumothorax – entry of air in pleural space without obvious cause.
eg. Rupture of bleb (alveoli filled sacs) in pt with inflammed lung conditions
2. Open pneumothorax – air enters pleural space through an opening in chest wall
-Stab/ gun shot wound
3. Tension Pneumothorax – air enters plural space with @ inspiration & can’t escape leading to over distension of thoracic
cavity resulting to shifting of mediastinum content to unaffected side.
Eg. Flail chest – “paradoxical breathing pattern”

Predisposing factors:
1. Chest trauma
2. Inflammatory lung conditions
3. Tumor
1. Sudden sharp chest pain
2. unexplained Dyspnea or SOB
3. Cyanosis
4. Diminished or decreased breath sound of affected lung
5. Cool moist skin- initial sign of shock
6. Mild restlessness/ apprehension, anxiety
7. Resonance to hyperresonance
8. decreased tactile fremitus
1. ABG – pO2 decrease –
2. CXR – confirms pneumothorax/ collapse of lung
Nursing Mgt:
1. Assist in endotracheal intubation
2. Assist in thoracenthesis
3. Administer meds – Morphine SO4 – due to pain
- Anti microbial agents- due to bacteria
4. Assist in test tube thoracotomy attached to H2O sealed drainage system
Purpose of H2O sealed drainage
1. Restablish (-) pressure in the lungs- lung 6-12mm Hg
2. Promote reexpansion of the lungs
3. Drain fluid, blood and air
4. To prevent reflux of blood fluid and air

Nursing Mgt if pt is on CPT attached to H2O drainage

1. Maintain strict aseptic technique
2. DBE
3. At bedside
a.) Petroleum gauze pad if dislodged Hemostat
b.) If with air leakage – clamp
c.) Extra bottle
4. Meds – Morphine SO4
5. Monitor & assess for oscillation fluctuations or bubbling
a.) If (+) to intermittent bubbling means normal or intact
- H2O rises upon inspiration
- H2o goes down upon expiration
b.) If (+) to continuous, remittent bubbling
1. Check for air leakage
2. Clamp towards chest tube
3. Notify MD
c.) If (-) to bubbling
1. Check for loop, clots, and kink
2. Milk towards H2O seal
3. Indicates re-expansion of lungs
4. Auscultate for breath sounds, Xrays
5. Removal of CTT
When will MD remove chest tube?
1. If (-) fluctuations
2. (+) Breath sounds
3. CXR – full expansion of lungs

Nursing Mgt of removal of chest tube

1. Encourage DBE
2. Instruct to perform Valsalva maneuver for easy removal, to prevent entry of air in pleural space.
3. Apply vaselinated air occlusive dressing
- Maintain dressing dry & intact
4. Prepare: Extra bottle, excellent clamp, petroleum gauze

I. Upper alimentary canal - function for digestion
a. Mouth
b. Pharynx (throat)
c. Esophagus
d. Stomach- site of digestion
e. 1st half of duodenum
II. Middle Alimentary canal – Function: for absorption
- Complete absorption – large intestine
a. 2nd half of duodenum for absorption
b. Jejunum
c. Ileum
d. 1st half of ascending colon
III. Lower Alimentary Canal – Function: elimination
a. 2nd half of ascending colon for elimination
b. Transverse for complete absorption— L I
c. Descending colon
d. Sigmoid
e. Rectum
IV. Accessory Organ
a. Salivary gland
b. Verniform appendix
c. Liver
d. Pancreas – auto digestion
e. Gallbladder – storage of bile
I. Salivary Glands
1. Parotid – below & front of ear
2. Sublingual
3. Submaxillary

- Produces saliva – for mechanical digestion

- 1,200 -1,500 ml/day - saliva produced
Lacrimal gland- depression on the frontal bone
Lacrimal duct- outer canthus

PAROTITIS – “mumps” – inflammation of parotid gland


1. Fever, chills anorexia, generalized body malaise
2. enlarged parotid gland
3. Swelling of parotid gland
4. Dysphagia
5. Earache – otalgia

Mode of transmission: Direct transmission & droplet nuclei

Incubation period: 14 – 21 days
Period of communicability – 1 week before swelling & immediately when swelling begins.

Nursing Mgt:
1. CBR
2. Institute a strict respiratory isolation
3. Meds: analgesic
Antibiotics – to prevent 2° complications
4. Alternate warm & cold compress at affected part (vinegar promotes cooling)
5. General liquid to soft diet
6. Complications
Women – cervicitis, vaginitis, oophoritis
Both sexes – meningitis & encephalitis/ reason why antibiotics is needed
Men – orchitis might lead to sterility if it occurs during / after puberty.

VERNIFORM APPENDIX – Rt iliac or Rt inguinal area
- Function – lymphatic organ – produces WBC during fetal life - ceases to function upon birth of baby

APENDICITIS – inflamation of verniform appendix

Predisposing factor:
1. Microbial infection
2. Feacalith – undigested food particles – tomato seeds, guava seeds
3. Intestinal obstruction

1. Pathognomonic sign: (+) rebound tenderness
2. Low grade fever, anorexia, n/v
3. Diarrhea &/ or constipation
4. Pain at Rt iliac region-- MCBURNEY’S point – site of surgical incision
5. Late sign due pain – tachycardia

1. CBC – mild leukocytosis – increase WBC
2. PE – (+) rebound tenderness (flex Rt leg, palpate Rt iliac area – rebound)
3. Urinalysis—(+) acetone in urine

Treatment: - appendectomy 24 – 45°

Nursing Mgt:
1. Secure consent
2. Routinary nursing measures:
a.) Skin prep
b.) NPO
c.) Avoid enema – lead to rupture of appendix
3. Meds:
*Don’t give analgesic – will mask pain
- Presence of pain means appendix has not ruptured.
4. Avoid heat application – will rupture appendix.
5. Monitor VS, I&O bowel sound
6. Maintain a patent IV line

Peritonitis, Septicemia

Nursing Mgt: post op

1. If (+) to Penrose drain – indicates rupture of appendix
Position- affected side to drain
2. Meds: analgesic due post op pain
Antibiotics, Antipyretics PRN
3. Monitor VS, I&O, bowel sound- N- borborygmy sound
4. Maintain patent IV line
5. Complications- peritonitis, septicemia

Liver – largest gland

- Occupies most of right hypochondriac region
- Color: scarlet red, brown shiny and transparent
- Covered by a fibrous capsule – Glisson’s capsule
- Functional unit – liver lobules

1. Produces bile
Bile – emulsifies fats—H2O and bile salts= cholesterol
Right sided pain: Cholelithiasis- easy bruising
Left sided pain: Pancreatitis
- Composed of H2O & bile salts
-Gives color to urine – urobilin
Stool color – stechobilin
2. Detoxifies drugs
3. Promotes synthesis of vit A, D, E, K - fat soluble vitamins (needs fat for absorption)

Hypervitaminosis – vit D & K

Vit A – retinol
Def Vit A – night blindness
Vit D – cholecalciferon
- Helps calcium
- Rickets, osteoarthritis

4. It destroys excess estrogen hormone

5. for metabolism
A. CHO –
1. Glycogenesis – synthesis of glycogens
2. Glycogenolysis – breakdown of glycogen
3. Gluconeogenesis – formation of glucose from CHO sources
1. Promotes synthesis of albumin & globulin
Liver Cirrhosis – decrease albumin; ascites and edema
Albumin – maintains osmotic pressure, prevents edema
2. Promotes synthesis of prothrombin & fibrinogen
3. Promotes conversion of ammonia to urea.
Ammonia like breath – fetor hepaticus
C. FATS – promotes synthesis of cholesterol to neutral fats – called triglycerides

LIVER CIRRHOSIS - lost of architectural design of liver leading to fat necrosis & scarring
Laennac Cirrhosis- loss of architectural design of the liver leading to fat necrosis and scarring

Early sign – hepatic encephalopathy

1. Asterixis – flapping hand tremors
Late signs – headache, restlessness, disorientation, decrease LOC – hepatic coma.
Nursing priority – assist in mechanical ventilation

Predisposing factor:
Decrease Laennac’s cirrhosis – caused by alcoholism
1. Chronic alcoholism- major cause
2. Malnutrition – decreaseVit B, thiamin - primary cause
3. Virus –
4. Toxicity- eg. Carbon tetrachloride (CCL4)
5. Use of hepatotoxic agents
Early signs:
a.) Weakness, fatigue
b.) Anorexia, n/v
c.) Stomatitis
d.) Urine – tea color
Stool – clay color
e.) Amenorrhea
f.) Decrease sexual urge
g.) Loss of pubic, axilla hair
h.) Hepatomegaly
i.) Jaundice
j.) Pruritus or urticaria
k.) Decrease bowel sounds

2. Late signs
a.) Hematological changes – all blood cells decrease
Leukopenia- decrease
Thrombocytopenia- bleeding tendencies
Anemia- decrease
b.) Endocrine changes
Spider angiomas, Gynecomastia
Caput medusae, Palmar errythema, loss of tortousity of the umbilicus

c.) GIT changes

Ascites, bleeding esophageal varices – due to portal HPN
d.) Neurological changes:
hepatic encephalopathy

Hepatic encephalopathy - ammonia (cerebral toxin)

Late signs: Early signs:
Headache and dizziness asterexis
Fetor hepaticus (flapping hand tremors)
Decrease LOC

Hepatic coma

1. Liver enzymes- increase

2. Serum cholesterol & ammonia increase
3. Indirect or conjugated bilirubin increase
4. CBC - pancytopenia
5. PTT – prolonged bleeding
6. Hepatic ultrasonogram – fat necrosis of liver globules

Nursing Mgt
1. CBR
2. Restrict Na!
3. Monitor VS, I&O
4. Weigh pt daily & assess pitting edema
5. Measure abdominal girth daily – notify MD
6. Meticulous skin care
7. Diet – increase CHO, vit & minerals. Moderate fats. Decrease CHON
Well balanced diet
8. Complications of liver cirrhosis:
a.) Ascites – fluid in peritoneal cavity
Nursing Mgt:
1. Meds: Loop diuretics – 10 – 15 min effect
2. Assist in abdominal paracentesis - aspiration of fluid
- Void before paracentesis to prevent accidental puncture of bladder as trochar is inserted

b.) Bleeding esophageal varices

- Dilation of esophageal veins
1. Meds: Vit K
Pitressin or Vasopressin (IM)
2. NGT decompression- lavage
- Give before lavage – ice or cold saline solution
- Monitor NGT output
3. Assist in mechanical decompression
- Insertion of Sengstaken-Blackemore tube- to decompress veins of esophagus-to prevent esophageal
- 3 lumen typed catheter
- Scissors at bedside to deflate/decompress balloon. Prep scissors when pt complains of DOB
c.) Hepatic encephalopathy –
1. Assist in mechanical ventilation – due coma
2. Monitor VS, neuro check
3. Siderails – due restless
4. Meds – Laxatives – to excrete ammonia (Lactulose)

HEPATITIS- jaundice (icteric sclera)


Kernicterus/ hyperbilirubinia

Irreversible brain damage

Pancreas – mixed gland (exocrine & endocrine gland); found behind the stomach

PANCREATITIS – acute or chronic inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto
digestion (self-digestion).
Bleeding of pancreas - Cullen’s sign on umbilical area

Predisposing factors:
1. Chronic alcoholism
2. Hepatobilary disease
3. Obesity
4. Hyperlipidemia
5. Hyperparathyroidism
6. Drugs – Thiazide diuretics,aspirin, pills, Pentamidine HCL (Pentam) for clients with AIDS,
7. Diet – increase saturated fats
1. Severe Lt epigastric pain – radiates from back &flank area (left upper quadrant)
- Aggravated by eating, accompanied by DOB
2. N/V
3. Tachycardia
4. Palpitation due to pain
5. Dyspepsia /indigestion
6. Decrease bowel sounds
7. (+) Cullen’s sign - ecchymosis of umbilicus hemorrhage
8. (+) Grey Turner’s spots – ecchymosis of flank area
9. Hypocalcemia
1. Serum amylase & lipase – increase
2. Urine lipase – increase
3. Serum Ca – decrease
Nursing Mgt:
1. Meds
a.) Narcotic analgesic - Meperidine Hcl (Demerol)
Don’t give Morphine SO4 –will cause spasm of sphincter.
b.) Smooth muscle relaxant/ anti cholinergic
- Ex. Papavarine Hcl
Prophantheline Bromide (Profanthene)
c.) Vasodilator – NTG
d.) Antacid – Maalox
e.) H2 receptor antagonist - Ranitidin (Zantac) to decrease pancreatic stimulation
f.) Ca – gluconate

2. Withold food & fluid – aggravates pain

3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation
Complications of TPN
1. Infection—maintain a strict aseptic technique
2. Pulmonary Embolism—check all connection to system
3. Hyperglycemia
4. Hyperkalemia
4. Institute stress mgt tech
a.) DBE
b.) Biofeedback
5. Comfy position - Knee chest or fetal lie position
6. If pt can tolerate food, give increase CHO, decrease fats, and moderate CHON
7. Complications: Chronic hemorrhagic pancreatitis, Peritonitis, Septicemia, Shock

GALLBLADDER – storage of bile – made up of cholesterol.

CHOLECYSTITIS/ CHOLELITHIASIS – inflammation of gallbladder with gallstone formation.
Predisposing factor:
1. High risk – women 40 years old
2. Post menopausal women – undergoing estrogen therapy
3. Obesity
4. Sedentary lifestyle, prolonged immobility
5. Hyperlipidemia
6. Neoplasm
7. Obstruction
1. Severe Right abdominal pain (after eating fatty food). Occurring especially at night
= epigastric or right abdominal quadrant after eating a heavy meal
2. Fat intolerance
3. Anorexia, n/v, feeling of fullness
4. Jaundice
5. Pruritus
6. Easy bruising
7. Tea colored urine
8. Steatorrhea

1. Oral cholecystogram (or gallbladder series)- confirms presence of gall stones
2. Increased indirect bilirubin
3. Increased alkaline phosphatase
4. increased serum and amylase
Nursing Mgt:
1. Meds – a.) Narcotic analgesic - Meperdipine Hcl – Demerol
b.) Anti cholinergic/Anti-spasmodic - Atropine SO4
c.) Anti emetic
Phenergan – Phenothiazide with anti emetic properties
d) Broad spectrum antibiotics
2. Diet – increase CHO, moderate CHON, decrease fats
3. Meticulous skin care
4. Surgery: Cholecystectomy
Nursing Mgt post cholecystectomy
-Maintain patency of T-tube intact & prevent infection

Stomach – widest section of alimentary canal

- J shaped structures
1. Anthrum
2. Pylorus
3. Fundus
Valves – prevent GERD
1. 1.cardiac sphincter valve
2. Pyloric sphincter valve- stomach and first half of duodenum
1. Chief/ Zymogenic cells – secrets
a.) Gastric amylase - digest CHO/ sugars
b.) Gastric lipase – digest fats
c.) Pepsin – CHON
d.) Rennin – digests milk products
2. Parietal / Argentaffin / oxyntic cells
a.) Produces intrinsic factor – promotes reabsorption of vit B12 cyanocobalamin – promotes maturation of RBC
b.) Secrets Hcl acid – aids in digestion
3. Endocrine cells - Secretes gastrin – increase Hcl acid secretion

Function of the stomach

1.Mechanical digestion
3.Storage of food
-CHO, CHON- stored 1 -2 hrs. Fats – stored 2 – 3 hrs

PEPTIC ULCER DISEASE – (PUD) – excoriation / erosion of submucosa & mucosal lining due to:
a.) Hypercecretion of acid – pepsin
b.) Decrease resistance to mucosal barrier

Incidence Rate:
1. Men – 40 – 55 yrs old
2. Aggressive persons/ type A personality
3. Hereditary
4. Emotional Stress
Predisposing factors:
1. Hereditary
2. Emotional
3. Smoking – vasoconstriction – GIT ischemia
4. Alcoholism – stimulates release of histamine = Parietal cell release Hcl acid = ulceration
5. Caffeine – tea, soda, chocolate
6. Irregular diet
7. Rapid eating
8. Ulcerogenic drugs – NSAIDS, aspirin, steroids, indomethacin, ibuprofen
Indomethacin - S/E corneal cloudiness. Needs annual eye check up.
NSAID and steroids= gastropathy

9. Gastrin producing tumor or gastrinoma – Zollinger Ellisons syndrome

10. Microbial invasion – helicobacter pylori. Metronidazole (Flagyl)
Types of ulcers
Ascending to severity
1. Acute – affects submucosal lining
2. Chronic – affects underlying tissues – heals & forms a scar, deeper

According to location
1. Stress ulcer
2. Gastric ulcer
3. Duodenal ulcer – most common

Stress ulcers – common among eritically ill clients

2 types
1. Curling’s ulcer – cause: trauma & Burns


GIT schemia

Decrease resistance of mucosal barriers to Hcl acid


2. Cushing’s ulcer – cause – stroke/CVA/ head injury

Increase vagal stimulation


Treatment: Vagotomy- done to prevent hemorrhage and shock prior to surgery on the stomach


SITE Antrum or lesser curvature Duodenal bulb
PAIN -30 min – 1 hr after eating -2-3 hrs after eating
- epigastrium - mid epigastrium

- gaseous & burning - cramping & burning pain
- not usually relieved by food & - usually relieved by food & antacid
antacid - 12 MN – 3am pain
HYPERSECRETION Normal gastric acid secretion Increased gastric acid secretion
VOMITING common Not common
HEMORRHAGE hematemesis Melena
WT Wt loss Wt gain
COMPLICATIONS a. stomach cancer a. perforation
b. hemorrhage
HIGH RISK 60 years old and above 20 years old and above
90-95% are cases ofduodenal ulcers- less bicarbonate ions, decrease so increase incidence
1. Endoscopic exam
2. Stool from occult blood (+)
3. Gastric analysis – Gastric Ulcer: normal gastric acid secretion
Duodenal: increased gastric acid secretion
4. GI series – confirms presence of ulceration
Nursing Mgt:
1. Diet – bland, non irritating, non spicy
2. Avoid caffeine & milk/ milk products

Increase gastric acid secretion

3. Administer meds
a.) Antacids

Aluminum containing antacids Magnesium containing antacids
Ex. aluminum hydroxide gel ex. milk of magnesia
(Amphogel) S/E diarrhea
S/E constipation

Maalox (fever S/E)

b.) H2 receptor antagonist

1. Ranitidine (Zantac) SE: fever
2. Cimetidine (Tagamet)—hastens the effect of oral anticoagulants
3. Famotidine (Pepcid) SE: fever
- Avoid smoking – decrease effectiveness of drug

Nursing Mgt:
1. Administer antacid & H2 receptor antagonist (Cimetidine) – 1hr apart
-Cemetidine decrease antacid absorption & vise versa
c.) Cytoprotective agents
1. Sucralfate (Carafate) - Provides a paste like subs that coats mucosal lining of stomach
2. Misoprostol (Cytotec) –SE: menstrual spotting
d.) Sedatives/ Tranquilizers - Valium, lithium
e.)Anticholinergics / Antispasmodic
1. Atropine SO4
2. Prophantheline Bromide (Profanthene)

(Pt has history of hpn crisis with peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na.

3. Surgery: subtotal gastrectomy - Partial removal of stomach

Billroth I (Gastroduodenostomy) Billroth II (Gastrojejunostomy)

-Removal of ½ of stomach & anastomoses of gastric stump - Removal of ½ -3/4 of stomach & duodenal bulb & anastomostoses of
to the duodenum. gastric stump to jejunum.

Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first.

Nursing Mgt:
1. Monitor NGT output or drainage immediately post op- bright red
a.) Immediately post op should be bright red
b.) Within 36- 48h – output is yellow green
c.) After 48h – output is dark red due to HCl acid
2. Administer meds:
a.) Analgesic
b.) Antibiotic
c.) Antiemetics
3. Maintain patent IV line
4. VS, I&O & bowel sounds
5. Complications:
a.) Hemorrhage – hypovolemic shock
Late signs – anuria
b.) Peritonitis
c.) Paralytic ileus – most feared
d.) Hypokalemia
e.) Thromobphlebitis
f.) Pernicious anemia
g.) Septicemia
7.)Dumping syndrome – common complication – rapid gastric emptying of hypertonic food solutions – CHYME leading to
Sx of Dumping syndrome:
1. Dizziness
2. Diaphoresis
3. Diarrhea
4. Palpitations

Nursing mgt:
1. Avoid fluids in chilled solutions, sweets (fluids must be taken after meals)
2. Small frequent feedings-6 equally divided feedings
3. Diet – decrease CHO, moderate fats & CHON
4. Flat on bed 15 -30 minutes after q feeding

1. Diverticulum- an outpouching of the intestinal mucosa particularly the sigmoid colon
2. Diverticulosis- multiple diverticulum
3. Diverticulitis- inflammation of diverticula
A. Predisposing Factors
1. High Risk Groups- men (40-45yo)
2. Congenital weakness of muscle fibers of the intestine.
3. low roughage and fiber in the diet
1. Intermittent lower left abdominal quadrant pain, particularly in the rectosigmoid area
2. tenderness
3. alternating bouts of constipation or diarrhea with blood or mucous
1. Barium enema—reveals inflammatory process
2. CBC reveals: decreased hematocrit and hemoglobin
Nsg Mgt:
1. Administer meds as ordered:
a. antibiotics
b. bulk laxatives
c. stool softeners
d. anti spasmodic agents
2. Instruct clients to take foods high in fiber if there is diverticulosis
3. Monitor for signs of infection
Feared complications: Peritonitis
4. Assists in surgical procedure
Resection of the diseased bowel and creation of a colostomy

BURNS – direct tissue injury caused by thermal, electric, chemical & smoke inhaled (TECS)
Nursing Priority – infection (all kinds of burns)
Head burn-priority- a/w
2nd priority for 1st & 2nd ° - pain
2nd priority for 3rd ° - F&E

Thermal- direct contact – flames, hot grease, sunburn.

Electric, – wires
Chem. – direct contact – corrosive materials acids
Smoke – gas / fume inhalation

1. Emergent phase – Removal of pt from cause of burn. Determine source or loc or burn
2. Shock phase – 48 - 72°. Characterized by shifting of fluids from intravascular to interstitial space

- BP decrease
- Urine output
- HR increase
- Hct increase
- Serum Na decrease
- Serum K increase
- Met acidosis

3. Diuretic/ Fluid remobilization phase - 3 to 5 days. Return of fluid from interstitial to intravascular space
4. Recovery/ convalescent phase – complete diuresis. Wound healing starts immediately after tissue injury.

I. Partial Burn
1. 1st degree – superficial burns
- Affects epidermis
- Cause: thermal burn
- Painful
- Redness (erythema) & blanching upon pressure with no fluid filled vesicles
2. 2nd degree – deep burns
- Affects epidermis & dermis
- Cause –chem. burns
- very painful
- Erythema & fluid filled vesicles (blisters)
II Full thickness Burns
1. Third & 4th degrees burn
- Affects all layers of skin, muscles, bones
- Cause – electrical
- Less painful
- Dry, thick, leathery wound surface – known as ESCHAR – devitalized or necrotic tissue.
Assessment findings
Rule of nines
Head & neck = 9%
Ant chest = 18%
Post chest = 18%
@ Arm 9+9 = 18%
@ leg 18+18 = 18%
Genitalia/ perineum= 1%
Total 100%

Nursing Mgt
1. Meds
a.) Tetanus toxoid- burn surface area is source of anaerobic growth – Claustridium tetany


Tetanolysin tetanospasmin

Hemolysis muscle spasm

b.) Morphine SO4

c.) Systemic antibiotics
1. Ampicillin
2. Cephalosporin
3. Tetracyclin
4. Topical antibiotic :
1. Silver Sulfadiazene (silvadene)
2. Sulfamylon
3. Silver nitrate
4. Povidone iodine (betadine)
2. Administer isotonic fluid sol & CHON replacements
3. Strict aseptic technique
4. Diet – increase CHO, increase CHON, increase Vit C, and increase K- orange
5. If (+) to burns on head, neck, face - Assist in intubation
6. Assist in hydrotherapy
7. Assist in surgical wound debridement. Administer analgesic 15 – 30 minutes before debridement
8. Complications:
a.) Infection
b.) Shock
c.) Paralytic ileus - due to hypovolemia & hypokalemia
d.) Curling’s ulcer – H2 receptor antagonist
e.) Septicemia blood poisoning
f.) Surgery: skin grafting

GUT – genito-urinary tract

1. Promote excretion of nitrogenous waste products
2. Maintain F&E & acid base balance

1. Kidneys – pair of bean shaped organ

- Located retroperitonially (back of peritoneum) on either side of vertebral column. Encased in Bowmans’s capsule.
1. Renal pelvis – pyelonephritis – inflammation of the renal pelvis
2. Cortex
3. Medulla

Nephrons – basic living unit of the kidneys consisting of glomerulus

Glomerulus – filters blood going to kidneys

Function of kidneys:
1. Urine formation

2. Regulation of BP

Urine formation – 25% of total CO (Cardiac Output) is received by kidneys (3,000-6,000 ml.)
125ml/ min filtered by the glomerulus > Glomerular filtration rate
1. Filtration
2. Tubular Reabsorption—124ml of ultra filtered are reabsorbed in the blood
3. Tubular Secretion- 1 ml is excreted in the urine
Filtration – Normal GFR/ min is 125 ml of blood
Tubular reabsorption – 124ml of ultra infiltrates (H2O & electrolytes is for reabsorption)
Tubular secretion – 1 ml is excreted in urine

Causes of CRF:
1. HPN
2. DM

Regulation of BP:
Predisposing factor:
Ex CS – hypovolemia – decrease BP going to kidneys
Activation of RAAS

Release of Renin (hydrolytic enzyme) at juxtaglomerular apparatus

Angiotensin I mild vasoconstrictor

Angiotensin II vasoconstrictor

Adrenal cortex increase CO increase PR

Increase BP
Increase Na &
H2O reabsorption


Ureters – 25 – 35 cm long, passageway of urine to bladder

Bladder – loc behind symphisis pubis. Muscular & elastic tissue that is distensible
- Function – reservoir of urine
1200 – 1800 ml – Normal adult can hold
200 – 500 ml – needed to initiate micturition reflex

Color – amber
Odor – aromatic
Consistency – clear or slightly turbid
pH – 4.5 – 8
Specific gravity – 1.015 – 1.030
WBC/ RBC – (-)
Albumin – (-)
E coli – (-)
Mucus thread – few
Amorphous urate (-)

Urethra – extends to external surface of body. Passage of urine, seminal & vaginal fluids.
- Women 3 – 5 cm or 1 to 1 ½ “
- Male – 20cm or 8”

CYSTITIS – inflammation of bladder
Predisposing factors:
1. Microbial invasion – E. coli
2. High risk – women
3. Obstruction
4. Urinary retention
5. Increase estrogen levels
6. Sexual intercourse
1. Pain – flank area
2. Urinary frequency & urgency
3. Burning upon urination
4. Dysuria & hematuria
5. Fever, chills, anorexia, gen body malaise
6. Nocturia

Diagnosis: Urine culture & sensitivity - 80% of the cases are (+) to E. coli
Nursing Mgt:
1. Force fluid – 2000 ml= to prevent bacterial multiplication
2. Warm sitz bath – to promote comfort
3. Monitor & assess for gross hematuria
4. Monitor and assess urine for color, odor, and bleeding N pH: 4.8
5. Acid ash diet – cranberry, vit C -OJ to acidify urine & prevent bacterial multiplication
6. Meds: systemic antibiotics
Sulfonamides – cotrimoxazole (Bactrim)
- Gantrism (ganthanol)
Aminoglycosides: Gentamycin
Urinary antiseptics – Nitrofurantoin (Macrodantin)
Urinary analgesic- Pyridum
6. Ht
a.) Importance of Hydration
b.) Void after sex (male and female)
c.) Female – avoids cleaning back & front
Bubble bath, Tissue paper, Powder, perfume
d.) Complications:

PYELONEPHRITIS – acute/ chronic infl of 1 or 2 renal pelvis of kidneys leading to tubular destruction, interstitial abscess
- Lead to Renal Failure

Predisposing factor:
1. Microbial invasion (Bacterial)
a.) E. Coli
b.) Streptococcus
2. Urinary retention /obstruction
3. Pregnancy
4. DM
5. Exposure to renal toxins or nephrotoxic agents
Acute pyelonephritis
a.) Costovertibral angle pain, tenderness
b.) Fever, anorexia, gen body malaise
c.) Urinary frequency, urgency
d.) Nocturia, dysuria, hematuria
e.) Burning upon urination
Chronic Pyelonephritis
a.) Fatigue, wt loss, weakness
b.) Polyuria, polydypsia
c.) HPN

1. Urine culture & sensitivity – (+) E. coli & streptococcus
2. Urinalysis
(+) WBC, (+)RBC, (+) Pus cells
3. Cystoscopic exam – urinary obstruction

Nursing Mgt:
1. Provide CBR – especially during acute phase
2. Force fluid
3. Acid ash diet
4. Provide a warm sitz bath for comfort

5. Meds:
a.) Urinary antiseptic – nitrofurantoin (macrodantin)
SE: peripheral neuropathy
GI irritation
Hemolytic anemia
Staining of teeth
b.) Urinary analgesic – Pyridium
2. Complication- Renal Failure

NEPHROLITHIASIS/ UROLITHIASIS- formation of stones at urinary tract

- calcium , oxalate, uric acid

milk cabbage anchovies
cranberries organ meat
nuts tea nuts
chocolates sardines

Predisposing factors:
1. Diet – increase Ca & oxalate
2. Hereditary – gout
3. Obesity
4. Sedentary lifestyle
5. Hyperparathyroidism

1. Renal colic
2. Cool moist skin (shock)
3. Burning upon urination
4. Hematuria
5. Anorexia, n/v
1. IVP – intravenous pyelography. Reveals location of stone
2. KUB – reveals location of stone
3. Cytoscopic exam- urinary obstruction
4. Stone analysis – composition & type of stone
5. Urinalysis – increase EBC, increase CHON
Nursing Mgt:
1.Force fluid
2.Strain urine using gauze pad
3.Warm sitz bath – for comfort
4.Alternate warm compress at flank area
5. a.) Narcotic analgesic- Morphine SO4
b.) Allopurinol (Zyeoprim)
c.) Patent IV line
d.) Diet – if + Ca stones – acid ash diet
If + oxalate stone – alkaline ash diet - (Ex milk/ milk products)
If + uric acid stones – decrease organ meat / anchovies sardines
6. Surgery
a.) Nephectomy – removal of affected kidney
Litholapoxy – removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones
b.) Extracorporeal shock wave lithotripsy
- Non - invasive
- Dissolve stones by shock wave
7. Complications: Renal Failure

BENIGN PROSTATIC HYPERTROPHY - enlarged prostate gland leading to

a.) Hydro ureters – dilation of ureters
b.) Hydronephrosis – dilation of renal pelvis
c.) Kidney stones Stone formation-- Renal failure
d.) Renal failure
 encircles the neck of the bladder
 decreased form of urinary stream
 Caurse is unknown

Predisposing factor:
1. High risk – 50 years old & above
60 – 70 – (3 to 4 x at risk)
Prostate cancer: 40 years old & above
2. Influence of male hormone
1.Decrease force of and amount of urinary stream
4.Burning upon urination
5.Terminal dribbling—early sign of BPH
8. Hesitancy
1. Digital rectal exam – enlarged prostate gland
2. KUB – urinary obstruction
3. Cystoscopic exam – obstruction
4. Urinalysis – increase WBC, CHON, RBC
Nursing Mgt:
1. Prostatic message – promotes evacuation of prostatic fluid
2. Limit fluid intake
3. Provide catheterization
4. Provide a warm sitz bath for comfort
5. Meds:

a. Terazozine (hytrin) - Relaxes bladder sphincter, relaxes the smooth muscle of urinary sphincter
S/E: HA, hypotension
b. Fenasteride (Proscar) - Atrophy of Prostate Gland (given after meals)
S/E: N&V, Anorexia
5. Surgery: Prostatectomy – TURP- Transurethral resection of Prostate- No incision
Without incision: for debilitated clients
-Assist in cystoclysis or continuous bladder irrigation.
1. Hemorrhage
2. Urinary obstruction
3. Penile dysfunction

Nursing mgt:
c. Monitor signs and symptoms of infection
d. Monitor symptoms gross/ frank bleeding. Normal bleeding within 24h.
3. Maintain irrigation or tube patent to flush out clots - to prevent bladder spasm & distention

ACUTE RENAL FAILURE – sudden immobility of kidneys to excrete nitrogenous waste products & maintain F&E balance
due to a decrease in GFR. (N 125 ml/min)

Predisposing factors:
Pre renal cause- decrease blood flow
1. Septic shock
2. Hypovolemia
3. Hypotension decrease flow to kidneys
4. CHF
5. Hemorrhage
6. Dehydration (chronic diarrhea)
Intra-renal cause – involves renal pathology= kidney problem
1. Acute tubular necrosis 3. HPN
2. Pyelonephritis 4. Acute Glumerulonephritis

Post renal cause – involves mechanical obstruction

1. Urinary strictures
2. Urolithiasis
3. BPH
4. Presence of tumors
**I. OLIGURIC STAGE (1-2 weeks)
- involves passage of urine < 400ml/day
- S/S:
a. Hyperkalemia- arrhythmia
b. Hypernatremia
c. Hyperphosphatemia
d. Hypocalcemia
e. High BUN 10-20 and creatinine .8-1
f. Metabolic acidosis 1-2wks
--increased amount of urine
a. Hypokalemia
b. Hyponatremia
c. Metabolic Acidosis
d. Increased Creatinine and BUN

CHRONIC RF – irreversible loss of kidney function

Predisposing factors:
1. DM
2. HPN
3. Recurrent UTI/ nephritis/ pyelonephritis
4. Exposure to renal toxins

Stages of CRF
1. Diminished Reserve Volume – asymptomatic
Normal BUN & Crea, GFR < 10 – 30%
2. Renal Insufficiency
3. End Stage Renal disease

1.) Urinary System 2.) Metabolic disturbances
a.) polyuria a.) azotemia (increase BUN & Crea)

b.) nocturia b.) hyperglycemia
c.) hematuria c.) hyperinulinemia
d.) Dysuria
e.) oliguria
3.) CNS 4.) GIT
a.) headache a.) n/v
b.) lethargy b.) stomatitis
c.) disorientation c.) uremic breath
d.) restlessness d.) diarrhea/ constipation
e.) memory impairment
5.) Respiratory 6.) hematological
a.) Kassmaul’s resp a.) Normocytic anemia
b.) decrease cough bleeding tendencies
7.) Fluid & Electrolytes 8.) Integumentary
a.) hyperkalemia a.) itchiness/ pruritus
b.) hypernatermia b.) uremic frost
c.) hypermagnesemia 9.) Cardiovascular changes
d.) hyperposphatemia a. HPN
e.) hypocalcemia b. CHF
f.) met acidosis c. Pericarditis
Nursing Mgt:
1. Enforce CBR, reverse isolation
2. Monitor strictly VS, I&O, neurocheck, monitor for signs of hypocalcemia
3. Meticulous skin care. Uremic frost – assist in bathing pt
4. Meds:
a.) Na HCO3 – due Hyperkalemia
b.) Kayexelate enema
c.) Anti HPN – Hydralazine (Apresoline)
d.) Vit & minerals (Multivitamins)
e.) Phosphate binder
(Amphogel) Al OH gel - S/E constipation
f.) Decrease Ca – Ca gluconate
5. Assist in hemodialysis
1.) Consent/ explain procedure
2.) Weigh patient
3.) Obtain baseline data & monitor VS before and during q30mins, I&O, wt, blood exam
4.) Encourage patient to void
5.) Strict aseptic technique
6.) Monitor for signs of complications:
B – bleeding (due to heparin)
E – embolism
D – disequilibrium syndrome
S – septicemia
S – shock – decrease in tissue perfusion
Disequilibrium syndrome – from rapid removal of urea & nitrogenous waste prod leading to:
a.) n/v
b.) HPN
c.) Leg cramps
d.) Disorientation
e.) Paresthesia

2. Avoid BP taking, blood extraction, IV, at side of shunt or fistula. Can lead to compression of fistula.
3. Maintain patency of shunt by:
i. Palpate for thrills & auscultate for bruits if (+) patent shunt!
ii. Bedside- bulldog clip
- If with accidental removal of fistula to prevent embolism.
- Infersole (diastole) – common dialisate used
7. Complication
- Peritonitis (most feared)
- Shock
Inflow time: 10-20mins
Indwelling time: 30-45 mins

8. Assist in surgery:
Renal transplantation : Complication – rejection (feared complication). Reverse isolation
Rejection time in Acute—6mos to 1 year
Rejection time in Chronic—5-10 years

External parts
1. Orbital cavity – made up of connective tissue protects eye form trauma.
2. EOM – extrinsic ocular muscles – involuntary muscles of eye needed for gazing movement.
3. Eyelashes/ eyebrows – esthetic purposes
4. Eyelids – palpebral fissure – opening upper & lower lid. Protects eye from direct sunlight
Meibomean gland – secrets a lubricating fluid inside eyelid
b.) Stye/ sty or Hordeolum- inflamed Meibomean gland
5. Conjunctiva
6. Lacrimal apparatus – tears

Process of grieving
a. Denial
b. Anger
c. Bargaining
d. Depression
e. Acceptance
2. Intrinsic coat
I. sclerotic coat – outer most
a.) Sclera – white. Occupies ¾ post of eye. Refracts light rays
b.) Canal of schlera – site of aqueous humor drainage
c.) Cornea – transparent structure of eye

II/ Uveal tract – nutritive care

Uveitis – infl of uveal tract
Consist of:
a.) Iris – colored muscular ring of eye
2 muscles of iris:
1. Circular smooth muscle fiber - Constricts the pupil
2.radial smooth muscle fiber - Dilates the pupil

2 chambers of the eye

1. Anterior
a.) Vitereous Humor – maintains spherical shape of the eye
b.) Aqueous Humor – maintains intrinsic ocular pressure
Normal IOP= 12-21 mmHg

II. Retina (innermost layer)

i. Optic discs or blind spot – nerve fibers only

No auto receptors

cones (daylight/ colored vision) rods – night twilight vision

phototopic vision “scotopic vision” = vit A deficiency – rods insufficient

ii. Maculla lutea – yellow spot center of retina

iii. Fovea centralis – area with highest visual acuity oracute vision

Physiology of vision
4 Physiological processes for vision to occur:
1. Refraction of light rays – bending of light rays
2. Accommodation of lens
3. Constriction & dilation of pupils
4. Convergence of eyes

Unit of measurements of refraction – diopters

Normal eye refraction – emmetropia

ERROR of refraction
1. Myopia – near sightedness – Treatment: biconcave lens
2. Hyperopia/ or farsightedness – Treatment: biconvex lens
3. Astigmatisim – distorted vision – Treatment: cylindrical
4. Prebyopia – “old slight” – inelasticity of lens due to aging – Treatment: bifocal lens or double vista
Accommodation of lenses – based on thelmholtz theory of accommodation

Near vision = far vision=

Ciliary muscle contracts= ciliary muscle dilates / relaxes=
Lens bulges lens is flat

Convergence of the eye:

1. Exotropia – 1 eye normal
2. Esophoria – corrected by corrective eye surgery
3. Strabismus- squint eye
4. Amblyopia – prolong squinting

GLAUCOMA – increase IOP – if untreated, atrophy of optic nerve disc – blindness

Predisposing factors:
1. High risk group – 40 & above
2. HPN
3. DM
4. Hereditary
5. Obesity
6. Recent eye trauma, infl, surgery

1. Chronic – (open angle G.) – most common type
Obstruct in flow of aqueous humor at trabecular meshwork of canal of schlema
2. Acute (close angle G.) – Most dangerous type
Forward displacement of iris to cornea leading to blindness.
3. Chronic (closed – angle) - Precipitated by acute attack

1. Loss of peripheral vision – tunnel vision
2. Halos around lights
3. Headache
4. n/v
5. Steamy cornea
6. Eye discomfort
7. If untreated – gradual loss of central vision – blindness

1. Tonometry – increase IOP >12- 21 mmHg
2. Perimetry – decrease peripheral vision
3. Gonioscopy – abstruction in anterior chamber

Nursing mgt:
1. Enforce CBR
2. Maintain siderails
3. Administer meds
a.) Miotics – lifetime - contracts ciliary muscles & constricts pupil. Ex Pilocarpine Na (Carbachol)
b.) Epinephrine eye drops – decrease secretion of aqueous humor
c.) Carbonic anhydrase inhibitors. Ex. acetapolamide (Diamox)
- Promotes increase out flow of aquaeous humor
d.) Temoptics (Timolol maleate)- Increase outflow of aquaous humor
2. Surgery:
a.) Trabeculectomy – eyetrephining – removal of trabelar meshwork of canal or schlera to drain aqueous humor
b.) Peripheral Iridectomy – portion of iris is excised to drain aqueous humor

Trabeculoctomy (eye laser surgery)

Nursing Mgt pre op- all types surgery

1. Apply eye patch on unaffected eye to force weaker eye to become stronger.

Nursing Mgt post op – all types of surgery

1. Position unaffected/ unoperated side - to prevent tension on suture line.
2. Avoid valsalva maneuver
3. Monitor symptoms of IOP
a.) Headache
b.) n/v
c.) Eye discomfort
d.) Tachycardia
2. Eye patch – both eyes - post op

CATARACT – partial/ complete opacity of lens

Predisposing factor:
1. 90-95% - aging (degenerative/ senile cataract)
2. Congenital
3. Prolonged exposure to UV rays
4. DM-

1. Loss of central vision - “Hazy or blurring of vision”
2. Painless
3. Milky white appearance at center of pupil
4. Decrease perception of colors

Diagnosis: Opthalmoscopic exam – (+) opacity of lens

Nsg Mgt:
1. Reorient pt to environment – due opacity
2. Siderails
3. Meds – a.) Mydriatics – dilate pupil – not lifetime
Ex. Mydriacyl
c.) Cyslopegics – paralyzes ciliary muscle. Ex. Cyclogye

4. Surgery

E – extra
C - capsular
C – cataract partial removal of lens
L - lens
E – extraction

I - intra
C - capsular
C – cataract total removal of lens & surrounding capsules
L - lens
E – extraction

Nursing Mgt:

1.Position unaffected/ unoperated side - to prevent tension on suture line.

2.Avoid valsalva maneuver

3.Monitor symptoms of IOP

a.) Headache
b.) n/v
c.) Eye discomfort
d.) Tachycardia
4.Eye patch – both eyes - post op

RETINAL DETACHMENT- separation of 2 layers of retina

Predisposing factors:
1. Severe myopia – nearsightedness
2. Diabetic Retinopathy
3. Trauma
4. Following lens extraction
5. HPN

1. “Curtain –veil” like vision
2. Flashes of lights
3. Floaters
4. Gradual decrease in central vision
5. Headache

Diagnosis- opthaloscopic exam

Nursing Mgt:
1. Siderails (all visual disease)
2. Surgery:
a.) Cryosurgery
b.) Scleral buckling

1. Hearing
2. Balance (Kinesthesia or position sense)

1. Outer-
a.) Pinna/ auricle – protects ear from direct trauma
b.) Ext. auditory meatus – has ceruminous gland. Cerumen
c.) Tympanic membrane – transmits sound waves to middle ear

Disorders of outer ear

Entry of insects – put flashlight to give route of exit
Foreign objects – beans (bring to MD)
H2O - drain
2. Middle ear
a.) Ear osssicle

1. Hammer -malleus
2. Anvil -Incus for bone conduction disorder conductive hearing loss
3. Stirrups -stapes

b. Eustachian tube - Opens to allow equalization of pressure on both ears
- Yawn, chew, and swallow
Children – straight, wide, short
c.) Otitis media
Adult – long, narrow & slanted

c. Muscles
1. Stapedius
2. Tensor tympani
3. Inner ear
a. Bony labyrinth – for balance, vestibule

Utricle & succule

Otolithe or ear stone – has Ca carbonate

Movement of head = Righting reflex = Kinesthesia

b. Membranous Labyrinth
1. Cochlea – ( function for hearing) has organ of corti
2. Endolymph & perilymph – for static equilibrium
3. Mastoid air cells – air filled spaces in temporal bone in skull

Complications of Mastoditis – meningitis

Types of hearing loss:

1. Conductive hearing loss – transmission hearing loss
a.) Impacted cerumen – tinnitus & conduction hearing loss- assist in ear irrigaton
b.) Immobility of stapes – OTOSCLEROSIS
d.) Middle ear disease char by formation of spongy bone in the inner ear causing fixation or immobility of stapes
e.) Stapes can’t transmit sound waves

Stapedectomy – removal of stapes, spongy bone & implantation of graft/ ear prosthesis

Predisposing factor:
1. Familiar tendency
2. Ear trauma & surgery

1. Tinnitus
2. Conductive hearing loss

1. Audiometry – various sound stimulates (+) conductive hearing loss
2. Weber’s test – Normal AC> BC
result BC > AC

Nursing Mgt post op
1. Position pt unaffected side
2. DBE
No coughing & blowing of nose
- Night lead to removal of graft
3. Meds:
a.) Analgesic
b.) Antiemetic
c.) Antimotion sickness agent. Ex. meclesine Hcl (Bonamine)
4. Assess – motor function – facial nerve - (Smile, frown, raise eyebrow)
5. Avoid shampoo hair for 1 to 2 weeks. Use shower cap


1. Tumor on cocheal
2. Loud noises (gun shot)
3. Presbycusis – bilateral progressive hearing loss especially at high frequencies – elderly
Face elderly to promote lip reading
4. Meniere’s disease – endolymphatic hydrops
f.) Inner ear disease char by dilation of endo – lympathic system leading to increase volume of endolin

Predisposing factor of MENIERE’S DISEASE

30 years old
Obesity – (+) chosesteatoma

Ear trauma & infection

1. TRIAD symptoms of Meniere’s disease
a.) Tinnitus
b.) Vertigo
c.) Sensory neural hearing loss
2. Nystagmus
3. n/v
4. Mild apprehension, anxiety
5. Tachycardia
6. Palpitations
7. Diaphoresis

1. Audiometry – (+) sensory hearing loss

Nursing mgt:
1. Comfy & darkened environment
2. Siderails
3. Emetic basin
4. Meds:
a.) Diuretics –to remove endolymph
b.) Vasodilator
c.) Antihistamine
d.) Antiemetic
e.) Antimotion sickness agent
f.) Sedatives/ tranquilizers

5. Restrict Na
6. Limit fluid intake
7. Avoid smoking
8. Surgery – endolymphatic sac decompression- Shunt
Clindamycin, KCl===NOT for IV push—it may cause arrhythmia
Chloramphenicol===NOT for IM
Procaine, Penicillin, Benzatine, Pen G, Vancomycin HCl, Acyclovir (Zovirax) ===NOT for IV

Opened bottles must be used in 8 hours

Hep Lock- flush with NSS

KCl < 80meq/L

Epinephrine 1:10,000
Lidocaine- 4 mg /ml (1g/250ml)


Phenytoin COMPATIBLE WITH D5W ONLY Nitroprusside
Vit K Epinephrine NaHCO3
Vit B6 Norepinephrine
Vit C Ephedrine


Not to be diluted in LR
Penicillin G

PRBC—to be infused within 2-4hours

FFP—1-1.5 hours
Platelet concentrate—infuse immediately and quickly

Pathognomonic sign:
Pernicious Anemia- red beefy tongue
Carbon monoxide poisoning- cherry red face
Addison’s Disease- bronze pigmentation of skin
Cushing’s syndrome- buffalo hump
Bulimia Nervosa- chipmunk face
Liver Cirrhosis- spider angioma & Caput medusae
Leprosy- lion face
SLE- butterfly rash on face
Emphysema- barrel chest
Parkinson’s – pill rolling tremors
Myasthenia Gravis- ptosis & Descending paralysis

GBS- Ascending paralysis- clumsiness
Meningitis- nuchal rigidity. Kernig’s & Brudzinskis sign
Hypoparathyroidism- Trousseau sign & Chvosteck sign
Pancreatitis- Cullen’s sign & Grey Turner’s sign
DKA- Acetone breath odor & Kussmaul’s respiration
Angina Pectoris- Levine’s sign
Pneumonia- rusty sputum
Chronic bronchitis- Blue bloaters
Asthma- Pink puffers
Appendicitis- rebound tenderness
Glaucoma-loss of peripheral vision- Tunnel vision
Cataract- Loss of central vision
Retinal detachment-Curtain-veil like vision

Decreased dopamine- Parkinson’s disease

Increased dopamine- Schizophrenia
Decreased acetylcholine- Myasthenia Gravis / Alzheimer
Increased acetylcholine- Bipolar

Autoimmune diseases
Multiple Sclerosis Hypothyroidism Acute Glomerulonephritis
Myasthenia Gravis Hyperthyroidism
GBS Pernicious Anemia

Apparatus needed at bedside:

Acetaminophen toxicity- Acetylcisteine. Prepare suction apparatus-acetylcysteine causes outpouring of secretions.
Myasthenia Gravis- tracheostomy set. For respiratory arrest.
Hemodyalisis- bulldog clip
Senkstaken tube- scissors to deflate balloon.
Guillain Barre Syndrome- tracheostomy set. For respiratory arrest.
Convulsion- suction apparatus. Increased secretions.
Hyperthyroidism- tracheostomy set. For laryngeal spasm post subtotal thyroidectomy complication.
Goiter- tracheostomy set. For laryngeal spasm post subtotal thyroidectomy complication.
Hypoparathyroidism- tracheostomy set. For laryngeal spasm.

Isolation precautions:
Cushing’s synd – reverse isolation - due to increased corticosteroid in body.
Aplastic anemia – reverse isolation - due to bone marrow depression.
Cancer any type – reverse isolation – immunocompromised.
Post liver transplant – reverse isolation – takes steroids lifetime.
Prolonged use steroids – reverse isolation
Meningitis – strict respiratory isolation – safe after 24h of antibiotic therapy
TB- strict respiratory isolation