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Nursing 3366 Pathologic Processes Implications for Nursing

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Nursing 3366 Pathologic Processes Implications for Nursing

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Nursing 3366 Pathologic Processes: Implications for Nursing
REQUIRED READING DOCUMENT #10
~~~~~~~~
Disorders of the Neurological System

Instructions:
1. Read this entire RRD (Required Reading Document) and other documents mentioned.
2. Work on Assignment #10 and submit by designated deadline.
Note about objectives /outcomes and studying for this course:
For ALL content in this course, the student will be able to DESCRIBE/DISCUSS/IDENTIFY correlations (links) between
pathophysiology of the disease and its clinical manifestations. In other words, #1: how does the pathophysiology of
a particular disease cause the signs and symptoms, and #2: if a patient presents the signs and symptoms of a
disease, be able to use critical thinking to figure out the disease process that is most likely in that context.

Objectives /outcomes for this subject:
1. The relationship between key aspects of normal neurological function and the pathophysiology involved in select
neurologically-related conditions, including:
• ophthalmic-related derangements/vocabulary
• alterations in homeostasis of the CNS, including:
o principles of CPP & ICP; effect of increased ICP (IICP) & cerebral edema
o meningitis
o seizures.
o brain attack—ischemic, hemorrhagic.
o migraines
o Parkinson’s
o Alzheimer’s
o multiple sclerosis
o alterations in homeostasis of the peripheral nervous system including myasthenia gravis
• Signs and symptoms and basic treatment modalities associated with above pathological conditions.
**********************************
Outline:
I. Disorders of the CNS II. Peripheral nervous system (PNS) disorders
A. Concepts of cerebral blood flow & alteration A. Overview
1. overview 1. main category--
2. CPP—cerebral perfusion pressure neuromuscular junction
3. ICP— intracranial pressure disorders
B. Brain attack (stroke) 2. normal A&P of
1. overview neuromuscular junction
2. ischemic brain attack 3. abnormalities
3. hemorrhagic brain attack B. Myasthenia gravis
4. S&S of brain attack 1. patho
5. bringing it all together 2. S&S
6. diagnosis & treatment 3. treatment
C. Degenerative diseases of the brain III. Ophthalmologic problems
1. Alzheimer’s disease A. General terminology & info related
2. Parkinson’s disease to eye / vision problems
3. multiple sclerosis 1. mydriasis
D. Miscellaneous CNS disorders 2. miosis
1. migraines 3. diplopia
2. seizures 4. nystagmus
3. meningitis 5 papilledema
B. Specific disease processes of the
eyes
Part III B not on test 1. cataracts
2. glaucoma
3. age-related macular
degeneration (AMD)

, 2
I. Disorders of the CNS: the brain

A. Concepts of cerebral blood flow & alteration

1. overview
a. cerebral blood flow is normally maintained at rate that matches metabolic needs of
brain → ensuring a constant supply of oxygen and glucose & waste removal (CO2)
b maintenance of effective cerebral blood flow dependent on keeping 2 forces in
balance: cerebral perfusion pressure (CPP--the pressure of blood going into brain)
and intracranial pressure (ICP—the pressure in the intracranial cavity)

2. CPP—cerebral perfusion pressure
a. pressure required to get oxygenated blood into the brain to perfuse the cells
of the brain
b. if EITHER too low (as happens in hypovolemia, hypotension, etc) OR too high (ex—
hypertension), the result is ineffective perfusion→ischemia to brain→
cellular hypoxia→ cell injury & death→ loss of cell membrane integrity→ water &
other cell contents are released→ results in cerebral edema and increased ICP →
further loss of effective perfusion.
c. summary: if CPP is either too high OR too low, can lead to cerebral edema and
increased ICP

3. ICP— intracranial pressure
a. ICP is the totality of pressures in the brain—arterial & venous pressures (blood) +
CSF pressure + Brain (tissue).
b. because the cranium is a bony structure, very little increase in pressure in the brain,
can be tolerated—“no place to go”—and some degree of pathologic alteration in
brain function (e.g., decreased LOC, impaired sensorimotor function, etc) can be
expected from even small amount of increased intracranial pressure (IICP).
c. the main culprit in causing IICP & the loss of balance between ICP & CPP is
cerebral edema; ex: ischemia from a blockage (plaque or stricture) of an artery in
brain or going into brain (ex—carotid) → cells become hypoxic→ swell, increased
vascular permeability→ edema→ increased ICP→ decreased CPP→ further brain
ischemia
d. same “scenario” can be applied to many situations: brain tumors, injuries,
aneurysms, irritants like infections & acidosis, direct hypoxia→ all ultimately lead to
cerebral edema & IICP (these two almost always go “hand in hand”).

FYI: Some numbers to give you perspective: Normal ICP: 10–15 mmHg (this is usually measured by an ICP
monitoring device that is placed in the ventricles of the brain). Normal CPP: 60 – 150 mmHg. CPP is the pressure
needed to adequately get blood into brain—depends on BP & ICP; formula for CPP: mean arterial pressure (MAP)
– ICP. Ex: MAP: a BP of 120/80 = a MAP of ~93mm Hg, so someone with a 93 MAP & an ICP of 15 would have a
CPP of 78mmHg (93mm Hg -15mm Hg), which is normal. Clinical application: if someone was in ICU with a head
injury or stroke or other cause of increased cerebral edema and !CP, we would monitor these numbers and make
treatment adjustments to keep them in the ranges that are most effective in getting perfusion to the brain.

, 3

cerebral perfusion pressure intracranial pressure
(CPP--the pressure of blood going into brain) (ICP—the pressure in the intracranial cavity)

HTN Head injury Brain tumor Brain attack
(stroke)
balanc
Hypotension
e Infections, acid/base imbalance,
Blockage of arterial flow into brain
hypoxemia from respiratory
disorders, meningitis→ all can
cause inflammation of brain tissue


Any disturbance of this balance (examples are seen in above mini-concept map) can lead to increased ICP and consequent cerebral edema,
with potential negative sequelae. S&S that are seen depend on site of brain affected & extensiveness of the edema in the brain.


B. Brain attack
1. overview
a. definition of brain attack --the process of any interruption of the normal blood
FYI: brain supply to a part of the brain or the entire brain, resulting in damaged brain tissue.
attacks are b. brain attacks were more commonly called “strokes” or “CVAs” (cerebrovascular
3rd leading
cause of
accidents) but in recent years, “brain attack” is favored as best terminology to
death & convey to lay people that they need to seek help as quickly as if having a heart
disability in attack.
US c. most common underlying etiologies of brain attack (BA) are:
1) atherosclerosis of cerebral arteries (within the brain) and/or of incoming
arteries (carotids & vertebral arteries).
2) HTN
3) “other”— brain aneurysms, heart problems → which can lead to ↓ cardiac
output → ↓ blood to brain.
d. thus the risk factors for BA are same for all atherosclerotic disorders & include:
1) preexisting hx of atherosclerosis in any part of body
2) preexisting hx of HTN
3) older age (most strokes occur in pts over 65, though 28% occur in younger)
4) family history
5) diabetes (pts w/ DM are 3 times more likely to have strokes)
6) lifestyle choices such as smoking (increases risk by 50%) and high-fat diets
e. the two main, broad categories of BA are based on underlying mechanism--
ischemic cause and hemorrhagic cause (more on these below). Some important
general points:
1) no matter what mechanism (ischemic or hemorrhagic), ultimately the actual
negative effects of a stroke are still cerebral edema & IICP
2) S&S don’t depend on whether a stroke is ischemic or hemorrhagic, but
treatment does depend on knowing which kind is occurring; this is usually
determined by CAT scan or MRI of brain.

2. ischemic brain attack (~80% of all brain attacks)
a. cause is usually the narrowing or blockage of arteries supplying brain (carotid or
vertebral arteries) or intracranial arteries themselves
1) usually related to atherosclerosis and other processes that damage arterial
walls, resulting in same process as plaque formation in coronary arteries

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