warfarin, atrial fibrillation, stroke Flashcards

1
Q

what are two types of strokes?

A
  1. Ischemic: more common; a clot blocks blood flow to an area of the brain
  2. Hemorrhagic: bleeding occurs inside or around brain tissue
    a. Intracerebral: a blood vessel within the brain bursts, allowing blood to leak inside the brain
    b. Subarachnoid: a blood vessel just outside the brain ruptures. The area of the skull just around the brain (the subarachnoid space) rapidly fills with blood.
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2
Q

What is a stroke? why does it occur?

A

stroke is caused by the interruption of blood supply and oxygen to the brain as a result of ischemia or hemor- rhage. The most common type is ischemic stroke induced by thrombosis (in 60% to 80% of cases) of a cerebral vessel. Ischemic stroke also can result from occlusion of a cerebral blood vessel by distant emboli. Hemorrhage causes about 15% of all strokes and carries a 1-year mortality rate greater than 60%.12,13

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3
Q

what is the primary factor associated with stroke? and what increases the risk of stroke?

A

Cerebrovascular disease is the primary factor associ- ated with stroke. Atherosclerosis and cardiac pathosis (myocardial infarction, atrial brillation) increase the risk of thrombolic and embolic strokes, whereas hyper- tension is the most important risk factor for intracerebral hemorrhagic stroke.12,13 Approximately 10% of persons who have had a myocardial infarction will have a stroke within 6 years.12,13 Additional factors that increase the risk for stroke include the occurrence of transient isch- emic attacks, a previous stroke, high dietary fat, obesity and elevated blood lipid levels, physical inactivity, uncon- trolled hypertension, cardiac abnormalities, diabetes mellitus, elevated homocysteine levels, elevated hemato- crit, elevated antiphospholipid antibodies, heavy tobacco smoking, increasing age (risk doubles each decade after the age of 65 years), and periodontal disease.12,13 Increased risk for hemorrhagic stroke also occurs with use of phenylpropanolamine, an α-adrenergic agonist.12,13

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4
Q

what are pathologic changes associated with stroke result from?

A

Pathologic changes associated with stroke result from infarction, intracerebral hemorrhage, or subarachnoid hemorrhage. Cerebral infarctions most commonly are caused by atherosclerotic thrombi or emboli of cardiac origin. The extent of an infarction is determined by a number of factors, including site of the occlusion, size of the occluded vessel, duration of the occlusion, and col- lateral circulation. The production and circulation of proin ammatory cytokines, the occurrence of clotting factors, and arterial in ammation contribute to platelet aggregation. Neurologic abnormalities result from excitotoxicity, free radical accumulation, in ammation, mitochondrial and DNA damage, and apoptosis of the region supplied by the damaged artery.12,13

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5
Q

what is the most ocmmon cause of intracerebral hemorrhage?

A

The most common cause of intracerebral hemorrhage is hypertensive atherosclerosis, which results in microan- eurysms of the arterioles (Figure 27-4). Vessels within the circle of Willis often are affected (Figure 27-5). Rupture of these microaneurysms within brain tissue leads to extravasation of blood, which displaces brain tissue, causing increase in intracranial volume until resul- tant tissue compression halts bleeding. Hemorrhagic strokes also may be caused by subarachnoid hemor- rhage.

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6
Q

what is the most serious outocme of stroke?

A

The most serious outcome of stroke is death, which occurs in 8% of those who experience ischemic strokes and 38% to 47% of those with hemorrhagic strokes within a month of the event. Overall, about 23% of patients die within 1 year.15-17 Mortality rates are directly related to type of stroke, with 80% of patients dying after an intracerebral hemorrhage, 50% after a subarachnoid hemorrhage, and 30% after occlusion of a major vessel by a thrombus. Death from stroke may not be immediate (sudden death) but rather may occur hours, days, or even weeks after the initial stroke episode.15-17

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7
Q

what does the residual deficit that results from stroke depend on?

A

The type of residual de cit that results from a stroke is directly dependent on the size and location of the infarct or hemorrhage. De cits include unilateral paraly- sis, numbness, sensory impairment, dysphasia, blindness, diplopia, dizziness, and dysarthria. Return of function is unpredictable and usually takes place slowly, over several months. Even with improvement, patients frequently are left with some permanent residual problem, such as dif- culty in walking, using the hands, performing skilled acts, or speaking. Dementia also may be an outcome of stroke.15-19

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8
Q

what are risk factors for stroke?

A
hypertension
congestive heart failure
diabetes mellitus
history of TIAs or previous CVA
Age >75 years
hypercholersterolemia
coronary atherosclerosis
smoking tobacco
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9
Q

what is the Chads Vasc score?

A

. Chads Vasc Score: estimates risk of embolization in patients with atrial fibrillation.

Congestive heart failure +1
hypertension +1
Age 75 years or older +2
Diabetes Mellitus +1
Stroke, TIA (transient ischemic attach or ministroke), or TE +2
Vascular disease
Age 65to 74 years +1
Sex Category (female) +1

score of 0 = low risk, score of 1 = moderate risk, score of >1 = high risk

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10
Q

what is coumarin?

A

Warfarin (Coumadin), the most widely used coumarin in the United States, is an oral anticoagulant that inhibits the biosynthesis of vitamin K–dependent coagulation proteins (factors VII, IX, and X and pro- thrombin). Warfarin is named after the patent holder, Wisconsin Alumni Research Foundation. Warfarin is bound to albumin, metabolized through hydroxylation by the liver, and excreted in the urine. PT is used to monitor warfarin therapy because it measures three of the vitamin K–dependent coagulation proteins: factors VII and X and prothrombin. PT is particularly sensitive to factor VII deficiency. Therapeutic anticoagulation with warfarin takes 4 to 5 days.34,37,38

PT has been shown to be imprecise and variable. Little comparability has been seen of PT values obtained from different laboratories. These differences are caused by the source of thromboplastin (human brain, rabbit brain), the brand of thromboplastin, and the type of instrumentation used. This has caused problems with bleeding that results from a high degree of anticoagulation based on an arti - cially low PTT. INR is now used to monitor patients on warfarin therapy. Reliance on the INR (INR = [PTR]ISI; PTR = prothrombin time ratio; ISI = international sensi- tivity index for the thromboplastin used) allows better comparison of PT values among different laboratories and minimizes the risk of bleeding due to artificially low PT values.33,36,37 The recommended INR goal for a patient on low-intensity warfarin therapy is 2.5, with a range of 2.0 to 3.0. With a patient on high-intensity anticoagula- tion therapy, the INR goal is 3.0, with a range of 2.5 to 3.5. Table 24-3 shows the conditions for which warfarin therapy is recommended and the recommended INR.33,36,37 Figure 24-14 shows a patient with deep venous thrombo- sis, which is one of the conditions for which warfarin treatment is required. Table 24-4 summarizes the antico- agulants now in use and in later stages of clinical trials.

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