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Maryville 611 Patho Exam 4 questions with correct answers.
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- Maryville University Of St. Louis
Maryville 611 Patho Exam 4 questions with correct answers.
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Maryville 611 Patho Exam 4 questions with correctanswers
Define diffuse cortical dysfunction. Correct Answer-Disease processes
(encephalitis) may produce diffuse bilateral cortical dysfunction. Results
from the effects of head rotation-the brain experiences shearing stresses
resulting in axonal damage ranging from concussion to a severe diffuse
axonal injury (DAI) state. Several categories of diffuse brain injury
exist, mild concussion, classic concussion, mild DAI, moderate DAI,
and severe DAI. Severity of the diffuse injury correlates with the
direction and velocity of rotation, how much shearing force was applied
to the brainstem. Supratentorial disorders produce a decreased level of
arousal by one of three mechanisms: 1) Diffuse bilateral cortical
dysfunction, 2) bilateral subcortical dysfunction, 3) localized
hemispheric dysfunction. Disease processes may produce diffuse
bilateral cortical dysfunction (encephalitis, extracerebral disorders,
neoplasms, closed head injury, dementia, and Alzheimer's). May occur
in either the cerebral cortex or the underlying white matter. There may
be CNS involvement, focal pathologic findings, and obstructive
hydrocephalus (CVA, brainstem trauma).
Identify populations at risk for neurological pathophysiology Correct
Answer-Adolescents and young adults 15-35 year old, greater than 70.
Men 1.5x as likely to sustain a TBI, persons living in high crime area,
military, professional sports players, order of spinal cord trauma (MVA,
falls, acts of violence (GSW, recreational sports).
Define the types of cerebral edema. Correct Answer-Vasogenic edema is
caused by the increased permeability of the capillary endothelium of the
brain after injury to the vascular structure. Cytotoxic edema, toxic
,factors directly affect the cellular elements of the brain parenchyma,
causing failure of the active transport system.
Subarachnoid hemorrhage causes hydrocephalus by what mechanism?
Correct Answer-Hydrocephalus from impaired absorption outside the
ventricles is called communicating (extraventricular) hydrocephalus.
SAH occurs when blood escapes from defective or injured vasculature
into the subarachnoid space. When a vessel tears, blood under pressure
is pumped into the subarachnoid space. The blood produces an
inflammatory reaction in these tissues. Clinical manifestations of an
SAH include HA, AMS, transient motor weakness, and numbness and
tingling. Vasospasm and delayed cerebral ischemia are serious
complications. Treatment of vasospasm includes use of CCB to prevent
or reverse vasospasm and augmentation cerebral perfusion by volume
expansion and hemodilution.
List the sequence of events that lead to hyperreflexia induced
bradycardia. Correct Answer-The intact ANS reflexively responds with
an arteriolar spasm that increases BP. Baroreceptors in the cerebral
vessels, the carotid sinus, and the aorta sense the HTN and stimulate the
PNS. The HR decreases, but the visceral and peripheral vessels don't
dilate because efferent impulses cannot pass through the cord.
Stimulation of the carotid sinus to the vagus nerve to the SA node. The
intact ANS reflexively responds with an arteriolar spasm that increases
BP. Baroreceptors in the cerebral vessels, the carotid sinus, and the aorta
sense the HTN and stimulate the PNS. The HR decreases, but the
visceral and peripheral vessels don't dilate because efferent impulses
cannot pass through the cord. Sudden dangerous increase in BP. Occurs
anytime after spinal shock resolves. Massive, uncompensated
cardiovascular response to stimulation of SNS. Individuals most at risk
have lesions T6 or higher. Characterized by paroxysmal HTN up to 300,
, HA, blurred vision, sweating above level of the lesion with flushing of
skin, nasal congestion, piloerection and bradycardia often in
combination with distended bladder or rectum. The ANS reflexively
responds with an arterial spasm that increases BP. Baroreceptors in the
cerebral vessels, carotid sinus, and the aorta sense the HTN and
stimulate the PNS.
Differentiate the types of headaches: migraine, cluster, and tension.
Correct Answer-Migraine: is defined as repeated, episodic HA lasting 4-
72 hours. Symptoms are unilateral head pain, worsening with
movement, accompanied by photophobia or phonophobia, and presence
of any one of the following throbbing quality, moderate to severe nausea
or vomiting. Familial episodic disorder/HA, with or w/o an aura,
precipitated by triggering event (lack of sleep, overexertion, weather,
skipping meals). More prevalent in women. Classic photophobia,
triggers, need cool room, sleep, n/v common. With and w/o aura, often
genetic. Cortical spreading depression. Neurotransmitters: substance P,
calcitonin. Over activity of trigeminovascular system of the brain.
Dysfunction of brainstem pathways. Abnormal sensory modulation. The
clinical phases of a migraine attack are the premonitory phase, the
migraine aura, the HA phase and the recovery phase. Exact mechanism
is not known. Trigeminal nerve- brain stem, pain impulses to thalamus
to sensory cortex. Activity worsens pain. Goal is to eliminate
nocioception to trigeminal nucleus. Monitor diet, decreases stress,
improves lifestyle. Migraine HA likely involves: serotonergic and other
neurotransmitter alterations.
Cluster: The HA attack usually begins w/o warning and is characterized
by severe, unilateral, tearing, burning, periorbital, and retrobulbar or
temporal pain lasting 30 minutes to 2 hours. Acute and chronic occurs in
episodes several times daily for period of days. Unilateral pain, intense
tearing and burning. s/s: ptosis, lacrimation, eye redness, and nausea.
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