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NURS 6501 Advanced Pathophysiology Final Exam & Review

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NURS 6501 Advanced Pathophysiology Final Exam & ReviewNURS 6501 Advanced Pathophysiology Final Exam & ReviewNURS 6501 Advanced Pathophysiology Final Exam & Review NURS 6501 Advanced Pathophysiology Final Exam & ReviewNURS 6501 Advanced Pathophysiology Final Exam & ReviewNURS 6501 Advanced Pathophysiology Final Exam & ReviewNURS 6501 Advanced Pathophysiology Final Exam & ReviewV

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Hochgeladen auf
9. märz 2022
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24
geschrieben in
2021/2022
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NURS 6501 Final Exam Review Guide (Weeks 7-11)


• Structure and Function of the Cardiovascular and Lymphatic Systems
• Pathophysiological changes related to Pain, Temperature Regulation, Sleep,
and Sensory Function
• How does patient characteristics such as racial and ethnic variables impact
altered physiology?
• How does the pathophysiology of spinal injuries impact patients?
• What is the impact of patient characteristics on disorders and altered
physiology.

Common Neurological and MS disorders and the pathophysiological nature of
these issues in adults and children:

Concepts of Neurological and Musculoskeletal Disorders

Stroke
 Cerebrovascular disease is the most frequently occurring neurologic
disorder. Any abnormality of the blood vessels of the brain is referred to as
cerebrovascular disease includes vessel wall abnormalities and vascular
malformations, thrombotic or embolic occlusion, and increased blood
viscosity or clotting.
 Cerebrovascular disease causes
o ischemia with or without infarction and hemorrhage.
o The common clinical manifestation is a cerebrovascular accident
(CVA) or stroke syndrome.
o Hypertension is the greatest risk factor followed by other
preventable risks.
 CVAs are classified according to the pathophysiology and include
ischemic (thrombotic, embolic, and hypoperfusion), lacunar (small vessel
disease), and hemorrhagic strokes.
 Ischemic strokes result from interruption in brain-blood flow with a core
of irreversible ischemia and necrosis or infarction that appears pale (white
infarct).
o The zone around the infarction has reversible ischemia, is called
the ischemic penumbra, and can regain neurologic function,
particularly with thrombolytic treatment.
o Leaking blood vessels can develop in the infarcted area, resulting
in a hemorrhagic transformation (a red infarct) that can be
exacerbated by thrombolytic therapy.
o Reperfusion injury can occur with ischemic stroke.
 Intracerebral hemorrhagic stroke is primarily associated with vessel
disease related to hypertension.
 Subarachnoid hemorrhage is associated with ruptured aneurysms,
arteriovenous malformations (AVMs), or cavernous angioma.

, o Subarachnoid hemorrhage is bleeding into the subarachnoid space
commonly associated with intracranial aneurysms, AVM, and
hypertension. The expanding hematoma increases ICP,
compresses brain tissue, reduces cerebral perfusion, disrupts the
bloodbrain barrier, and causes inflammation and neuronal death.
Secondary brain injury follows. Seizures and hydrocephalus can
accompany neurologic deficits.

Multiple sclerosis
 MS is a chronic inflammatory disease involving degeneration of CNS
myelin in genetically susceptible individuals.
 The cause is unknown and autoreactive T and B cells recognize myelin
autoantigens and produce myelin-specific antibodies triggering
inflammatory demyelination with loss of oligodendrocytes and plaque
formation leading to disruption of nerve conduction.
 The clinical manifestations of MS involve different types: relapsing-
remitting, primary progressive, secondary progressive, and progressive-
relapsing.

Transient Ischemic Attack
 A transient ischemic attack is a transient episode of neurologic dysfunction
resulting from focal cerebral ischemia with risk for progressing to stroke.

Myasthenia gravis
 Myasthenia gravis results from a defect in nerve impulse transmission at
the neuromuscular junction with generalized, ocular, or neonatal subtypes.
Autoantibodies, complement deposits, and membrane attack complex
destroy the acetylcholine receptor (AChR) sites, causing decreased
transmission of nerve impulses, leading to muscle weakness, including
ocular and systemic muscles. There can be childhood and adult onset.

Headache
 Migraine is an episodic disorder whose marker is headache lasting 4 to
72 hours.
o Migraine is classified as a headache with and without aura and
chronic migraine (migraines 15 days in a month for more than 3
months).
o Migraine may be precipitated by a triggering event.
o The aura is associated with cortical spreading depression, which
initiates the release of neurotransmitters, particularly CGRP, that
stimulate vasodilation in the trigeminal vascular system,
inflammation, and sensitization of pain receptors. Glutamate is
increased and serotonin is decreased.
 Cluster headaches (trigeminal autonomic cephalalgia) occur in
episodes several times during a day for a period of days at different times
of the year, primarily in men.

, o The pain is unilateral, intense, tearing, and burning and associated
with ptosis, lacrimation, reddening of the eye, and nausea. The
cause of trigeminal activation is unknown.
o There is sympathetic nervous system underactivity and
parasympathetic overactivity with trigger events similar to migraine.
The two forms are acute and chronic
o Chronic paroxysmal hemicranias are a cluster-type headache that
occurs 4 to 12 times per day for 20 to 120 minutes in both men and
women.
o There is sympathetic activity different from that in cluster headache,
as it is relieved with indomethacin. 40.
 Tension-type headache (TTH) is the most common type of headache.
o Both central and peripheral pain mechanisms are associated with
the etiology.
o The headache is bilateral, with the sensation of a tight band around
the head. The pain may last for hours or days.
o There are acute and chronic forms.

Seizure disorders
 Seizures represent abnormal, excessive hypersynchronous discharges of
cerebral neurons with transient alterations in brain function.
 Seizures may be focal or generalized.
 The categories of seizures include genetic, structural, metabolic, immune,
infectious, and unknown.

Head injury
 Traumatic brain injury (TBI) is an alteration in brain function or other
evidence of brain pathology caused by an external force.
 Primary brain injury is caused by an impact and can be focal or diffuse
with open- or closed-head injury.
o Severity of TBI is graded using the Glasgow Coma Score.
 Focal brain injury includes coup and contrecoup, contusion
(bruising of the brain), laceration (tearing of brain tissue),
extradural hematoma (accumulation of blood above the dura
mater), subdural hematoma (blood between the dura mater
and arachnoid membrane), intracerebral hematoma
(bleeding into the brain), and open-head trauma.
o Open-head injury involves a skull fracture with exposure of the
cranial vault to the environment.
 The types of skull fracture include compound fracture or
perforated fracture and linear, comminuted, and basilar skull
fracture.
o Closed-head injuries occur in a precise location, and most are
mild. More severe damage includes contusions and epidural,
subdural, subarachnoid, and intracerebral hemorrhage.

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