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MEDICAL SURGICAL
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 bronchioles dilated to take more oxygen
4. RR increased
* Why GIT is not increased = GIT is not important! 5. Constipation & urinary retention
Increase blood flow to skeletal muscles, brain & heart.
I. Adrenergic Agents – Epinephrine (adrenaline)
SE: SNS effect
II. PNS: 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
SE:
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
ex CALCIBLOC or NEFEDIPINE
Peripheral nervous system: cholinergic/ vagal or sympatholitic response Effect of PNS: (cholinergic)
- Involved in fly or withdrawal response 1. Meiosis – contraction 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
S/E- of anti-hpn drugs:
1. orthostatic hpn
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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.
Types:
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
DEMYELLENATING DSE
1.)ALZHEIMER’S DISEASE– atrophy of brain tissue due to a deficiency of acetylcholine.
S&Sx:
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.
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
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1. Cerebrum – largest - Connects R & L cerebral hemisphere
- Corpus collusum
Rt cerebral hemisphere, Lt cerebral hemisphere
Function:
1. Sensory
2. Motor
3. Integrative
Lobes
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
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
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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 HR Increase HR CUSHINGS EFFECT
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.
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