ANATOMY AND PHYSIOLOGY WITH INTEGRATED PATHOPHYSIOLOGY AND PHARMACOLOGY

NERVOUS SYSTEM

Neuron- basic structural unit

Basic Parts:
1. dendrites- root-like structures
-receiver of electrical signal from other neurons and organs
2. body- contains the nucleus; processes the electrical stimulation and initiate a response
3. axon- carries impulses away from the body; covered with myelin sheath (insulating material that
smoothen and accelerate the rate of impulse transmission)

Neuroglia- aka glial cells
-supporting structure of the nervous system
-capable of regeneration
-common origin of brain tumors

Types:
1. microglia- phagocytes; removes cellular debris and bacteria
2. astrocytes- contributes to the formation of blood brain barrier (BBB)
Clinical Significance:
BBB- maintain an optimal and stable environment for neurons
-prevents microorganism and harmful substances from entering the nervous system
-this also explains why some medications are not effective for nervous system pathologies
3. ependymal cells- lines the ventricles and choroid plexus; contribute in the production of cerebrospinal
fluid
4. oligodendrocyte- serves as the myelin sheath of central nervous system
5. schwann cell- forms the myelin sheath of the peripheral nervous system
Clinical Significance:
Multiple Sclerosis: destruction of myelin sheath (autoimmune, infection: epstain-Barr)>>>
inflammation>>> disruption of signal transmission>>> weakness and tingling sensation>>>
remyelination>>> scarring>>> remission>>> infection, stress, pregnancy>>>
exacerbation>>>optic neuritis (diplopia, blurring of vision and blindness), bowel and bladder
dysfunction (constipation and bladder contraction), muscle spasm
Diagnosis:
a. CSF analysis: presence of oligoclonal banding
b. electromyelography
c. MRI
Treatment:
a. steroid (methylprednisolone)- standard therapy; decreased inflammation and promote
immunosuppression
b. interferon- antiviral and immunoregulation
c. muscle relaxant (baclofen{lioresal}, dantrolene {dantrium}, diazepam {valium})
d. bethanechol and oxybutynin: bladder relaxant
Nursing diagnosis:
a. altered bowel elimination>>> fluid intake: 2000mL (400-500ml/meal; 200ml tid; limit after 6)
b. constipation: high fiber diet and fluid intake


c. fatigue: scheduling of activities with frequent rest periods
d. impaired physical mobility: range of motion exercises
source: Black and Hawks (pages 1909-1914)

Gullain-Barre Syndrome (Landrys paralysis): demyelination of PNS (autoimmune, infection:
campylobacter jejuni)>>> disruption of nerve impulse transmission>>> tingling sensation and
weakness>>> ascending paralysis>>> respiratory paralysis>>> remyelination>>> improvement is
descending
Treatment:
a. IV immunoglobulins- treatment of choice
b. Plasma exchange- removal of antibodies
source: Black and Hawks (pages 1915-1916)

Synapse- junction between 2 neurons or between a neuron and an effector organ (muscle and glands)

Parts:
1. Presynaptic terminal- contains neurotransmitter (chemicals the serves as communication medium)
2. synaptic cleft- space between the 2 neurons or effector organ; contains enzyme that degrades
neurotransmitter (acetylcholiesterase, monoamine oxidase)
3. Post synaptic terminal- has receptors where specific neurotransmitter can bind and initiate a
response

The Neuro-mascular Junction
-major neutransmitter: acetylcholine
-in order for a muscle to contract, nerve implulses in the presynaptic terminal will stimulate the release
of Ach in the synaptic cleft>>> bind to its receptor on the post synaptic cleft>>> initiate sodium-
potassium pump>>> contraction
-post stimulation ACH can be re-uptaken (recycle) or degraded by acetylcholinesterase
Clinical Significance:
Myasthenia gravis: destruction of Ach receptors (autoimmune)>>> inability of Ach to bind to its
receptor>>> muscle weakness>>> increases with activity and at the end of the day>>> ptosis,
diplopia, dysphagia, dysphonia, snarling smile, respiratory paralysis
Diagnosis:
a. tensilon test- administration of acetylcholinesterase inhibitor such as edrophonium (block the
effect of Achase>>> allow the Ach to bind on its receptor>>> improves muscle contraction>>>
alleviation of muscle weakness
how it is done: a test dose of 2mg is initially given>>> no muscle weakness or changes in VS>>>
8 mg is injected>>> (+) if there is improvement in muscle weakness
Treatment:
a. acetylcholinesterase inhibitor (pyridostigmine (mestinon) and neostigmine (prostigmin)-
block the effect of Achase>>> allow the Ach to bind on its receptor>>> improves muscle
contraction (cholinergic effect); given BEFORE MEALS TO PROMOTE MUSCLE STRENGTH
PREVENTING ASPIRATION
complications:
>cholinergic crisis- overmedication; antidote: atropine sulfate
Manifestations include abdominal cramps, diarrhea, excessive pulmonary secretions, salivation,
paradoxical increase muscle weakness, bronchial spasm and later on resp. failure
>myasthenic crisis-undermedication; increased dose of medication


Manifestations include respiratory distress, marked increased in BP and tachycardia due to
hypoxia, restlessness
b. corticosteroid such as prednisone to promote immunosuppression
c. azathioprine (immuran) and cyclosporine (sandimmune)- promote immunosuppression
d. plasmapharesis- separates the plasma from the formed elements and remove antibodies
e. surgery: thymectomy- prevents the production of Ach receptor antibodies
Nursing Diagnosis:
a. ineffective airway clearance: deep breathing and coughing exercises
b. impaired swallowing: upright when eating, tilt head forward, do not speak while eating
c. fatigue: pacing of activities and frequent rest period
Source: Black and Hawks (pages 1916-1918)

Magnesium sulphate as neuromascular blocking agent- prevent the binding of Ach to its
receptor; given to client with pre-eclampsia to prevent convulsion
Nursing management:
a. assess RR and DTR before administration
b. inject deep IM using Z track technique, do not massage the area post injection

The junction between 2 neurons
-neurotransmitter: serotonin, norepinephrine and dopamine
-post stimulation the neurotransmitters can be re-uptaken or degraded by monoamine oxidase
Clinical Significance:
Antidepressants- effect is after 2-4 weeks, initiate suicide precaution
-one etiology of depression is decreased in the neurotransmitter norepi and serotonin
a. selective serotonin re-uptake inhibitors (SSRIs)- prevent the re-uptake of serotonin>>>
increase availability of serotonin; drug of choice
b. tricyclic antidepressant (TCAs)- prevent the re-uptake of norepi
c. mono amine oxidase inhibitors (MAOIs)- prevent the degradation of neurotransmitter
Strategy: SONG
Para matandaan mga SSRi na yan
Eto ang dapat niyong malaman
Fluoxetine, Paroxetine, Flovoxamine, Sertraline
At kung TCA mga PRAMINE iyan
TRYPTYLINE AT AMOXAPINE
At kung MAOI naman, PANAMA iyan
Parnate, Nardil at Marplan

Hypertensive crisis: prevent degradation of tyramine (precursor of cathecholamine)





Structural Division of the Nervous System
Nervous system

Central Nervous System Peripheral Nervous System



Brain Spinal Cord Sensory Motor

Autonomic Somatic

Sympathetic Parasympathetic

A. Central Nervous System (neuronal bodies and dendrites)
1. Brain
Parts:
a. Cerebrum-largest part of the brain; divided by the longitudinal fissure into 2 hemisphere: the logical
and analytical left hemisphere and the creative/ spatial right hemisphere

Layers:
>basal ganglia- inner layer; contain a structure known as substantia nigra that produces dopamine
-dopamine is a neurotransmitter that helps to produce smooth and coordinated voluntary movement
Clinical Significance:
Parkinsons disease: degeneration of the subtantia nigra>>> decreased production of
dopamine>>> imbalance between dopamine and Ach>>> disruption in voluntary movement>>>
muscle rigidity and tremors (mask like facies, stoop posture, bradykinesia, pill rolling, resting
tremors: initially on one side, shuffling or festinating gait, dysarthria, micographia, monotonous
voice)
Treatment:
a. dopamine precursors: levodopa combined with carbidopa (sinemet) to prevent the
degradation of the medication at the periphery
b. dopaminergics (bromocriptine {parlodel}): increases the production of dopamine of remaining
cells
c. MAOIs- prevent degradation of dopamine
d. anticholinergics (ABBCTA: akineton/biperiden, benztropine/congentin,
trihexiphenidal/artane)- relieves muscle rigidity
e. alternative treatment: Coenzyme q10 (1200mg/day)
Nursing Diagnosis:
a. risk for injury: remove loose carpeting, install hand grab, elevate toilet seat, use of assistive
devices
b. impaired physical mobility: ROM, use firm mattress, avoid using pillow, periodic prone
position, to assist in initiating a movement>>> rock oneself front and back, toss a paper; to
manage hand tremors>>> squeeze a coin of hand ball, frequent rest periods
c. risk for aspiration: eat in upright, take small bites and chew slowly
d. constipation: fluid intake and fiber
Black and Hawks (pages 1902-1906)

> cerebral cortex- outer layer that is mainly made up of gray matter (neuronal body and dendrites)
Subdivisions:
a. frontal lobe- memory, attention, concentration, primary motor center (controls voluntary movement),
contains the brocas area
b. temporal lobe- hearing cortex and contains the wernickes area
c. parietal lobe- primary sensory cortex: pain, touch, pressure, temperature
d. occipital lobe- visual cortex
Clinical Significance:


Alzheimers disease: atrophy of the cerebrum, most common form of dementia (loss of
memory, judgment, reasoning and language)
Incidence: common among 60 y/o
Pathophysiology:
>presence of plaque (deposit of amyloid protein that are insoluble)
>neurofibrillary tangles-destruction in the microtubules that help tha neurons in
communication
>decreased Ach
manifestations:
a. amnesia (initially short term memory loss or anterograde amnesia)
b. aphasia- can be motor (inability to express oneself using spoken words), sensory (inability to
understand written and spoken words or both also known as global aphasia
c. apraxia- inability to perform previously learned motor skills
d. agnosia- inability to use object correctly
stages:
1. mild: confusion, disorientation, agitation or restlessness, difficulty of problem solving and
short term memory loss
2. moderate: language disturbance (difficulty in finding words, circumlocution), hyperorality,
palilalia, apraxia, wandering, delusions and depression
3. severe: inability to communicate, loss of long term memory, lack of movement, incontinence
Treatment:
a. acetylcholinesterase inhibitor (ACER: Aricept/donepezil; cognex/tacrine; Exelon/rivastigmine;
reminyl/galanthamine
b. alternative medications: omega 3 from fish decrease possibility of AD by 60%, 2000IU of
vitamin E slow the progression of AD
Nursing Diagnosis:
a. impaired memory: re-orient the client, place calendar and clock on visible area, allow the
client to reminisce
b. risk for injury: remove clutters, provide a structured environment,
c. disturbed thought process: provide simple, repetitive instructions, divide task into simple
steps
Source: Black and Hawks (pages 1893-1902)

Miscellaneous Disorder:
Amyotrophic Lateral Sclerosis (ALS) aka Lou Gehrigs disease or charcots disease
-degenaeration of the anterior horn (spinal cord) and corticospinal tract>>> carries motor impulses
(action/response) from brain to spinal cord
-muscle weakness, cramps , spasticity and fascilutions initially on upper extremities, neck and throat>>>
dyaphagia and dysarthria
-treatment: rilutek>>> neuroprotective;
-nursing management: promote rest, pacing of activities, small, frequent, high calorie feeding, maintain
upright position during eating, avoid talking while eating, papase>>> thins the saliva, have suction
machine at the bedside

b. brainstem- connects the cerebrum to the spinal cord; contains CN except 1 and 2; contains asceding
and descending tracts
parts:
1. midbrain: motor coordination; visual and hearing relay center; CN 3 and 4


2. pons: respiratory center>>> pneumataxic center; CN 5 , 6, 7 (a neural center in the upper part of the
pons that provides inhibitory impulses on inspiration and thereby prevents overdistension of the lungs
and helps to maintain alternately recurrent inspiration and expiration)
3. medulla oblongata: vital center (RR, CR); vasomotor center and vomiting center; CN 8-12
(inspiratory and expiratory center)
*reticular activating center-structures scattered on the brainstem that regulates sleep-wake cycle

c. diencephalon
1. thalamus: relay sensory impulses to the cerebral cortex
2. hypothalamus: regulation of autonomic response; satiety center, thirst center, thermoregulatory
center

d. cerebellum: balance, posture, coordination and fine motor movement

2. Spinal cord: extends from the foramen magnum to 2
nd
lumbar vertebra
Clinical Significance: this is the reason why the needle in lumbar puncture is inserted between l3 and l4
or L4 and L5
-seat of reflex
Assessment:
0-absent
+-hypoactive/dimished
++-normal
+++-active than normal
++++-hyperactive

B. Peripheral Nervous System (PNS)
-made up of nerves and ganglia
a. cervical nerves-receives impulses from the periphery and transmit it towards the spinal cord for
interpretation
subdivisions:
8 cervical nerves
12 thoracic nerves
5 lumbar nerves
5 sacral nerves
1 coccygeal nerves

Plexus: group of nerves
Cervical plexus- C1-C4: innervates the neck
Brachial plexus-C5-T1: innervates the shoulder, axilla, arm and forearm
Lumbo-sacral Plexus- L1-S4: innervates the perineum and lower extremities
Clinical Significance:
Spinal cord injuries:
a. cervical nerve: above C4: respiratory difficulty and quadriplegia
b. thoracic: paralysis of chest, trunk, legs, bowel and bladder
c. lumb0-sacral: paraplegia, neurogenic bladder (bladder contraction but without emptying),
injury above S2 will allow erection but not ejaculation, injury between s2 and s4 prevent
erection and ejaculation
Emergency Management:


Immobilize the client; maintain an extended position; place the head in neutral position; place
hands on the side of the client head; logroll the client
Spinal/neurogenic shock- depression of reflex below the level of spinal cord injury
Manifestations: areflexia, hypotension, bradycardia, paralytic ileus
Autonomic dysreflexia/ hyperreflexia- usually preceded by autonomic shock, occurs in injury
above T6, commonly caused by distended bladder, visceral distention and impacted stool,
manifestations include: severe hypertention, throbbing headache, flushing above the level of
injury while paleness below the injury, pupil dilation, sweating, piloerection
Mgt: Position: high fowler, monitor V/s especially BP q 15 minutes, urinary catheterization

Autonomic Nervous System
Sympathetic: fight or flight response
Parasympathetic: vegetative/ resting response

Adrenergic Receptors:
a1: blood vessel, iris, urinary bladder>>> vasoconstrcition
a2:nerve membranes; prevents the further release o epi/nor epi
b1: heart>>> increased heart rate
b2: lungs>>>> bronchodilation
SYMPATHETIC PARASYMPATHETIC
Adrenaline (epi/nor epi) Neurotransmitter acetylcholine
Adrenergic response Other name Cholinergic response
Body activity increase except
GIT/GUT
Response All decrease except GIT and GUT
Midriasis, bronchodilation,
hypertension, tachycardia,
tachypnea, vasoconstriction

Decreased salivation,
constipation, urinary retention