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Advanced Pathophysiology 530 - Exam 3: Graded Questions with Answers | Advanced Pathophysiology Exam 3 and NSG 530 Exam 3 Questions from the Best Institutions Across the Globe for Comprehensive Preparation$25.99
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Advanced Pathophysiology 530 - Exam 3: Graded Questions with Answers | Advanced Pathophysiology Exam 3 and NSG 530 Exam 3 Questions from the Best Institutions Across the Globe for Comprehensive Preparation
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Course
Advanced Pathophysiology 530
Institution
Advanced Pathophysiology 530
Advanced Pathophysiology 530 - Exam 3: Graded Questions with Answers | Advanced Pathophysiology Exam 3 and NSG 530 Exam 3 Questions from the Best Institutions Across the Globe for Comprehensive Preparation
Advanced Pathophysiology 530 - Exam 3, Advanced
Pathophysiology Exam 3, NSG 530 Exam 3 EXAMS
FROM THE BEST INSTITUTIONS ACROSS THE GLOBE
Graded questions with answers
how does collagen contribute to ECM remodeling - CORRECT ANSWER- --remodeling
results in the deposition of collagen btw myocytes, which can disrupt the integrity of the
muscle, decrease contractility, and make the ventricle more likely to dilate and fail
how does collagen contribute to fibrosis - CORRECT ANSWER- --fibroblast dysfunction
results in collagen imbalance
-matrix metalloproteinases - these become active and start degrading some of the proteins
in the ECM - change in shape and geometry
-causes slippage and over stretching
-excessive fibrosis (thickening of ventricular wall)
-seen post infarct
-small changes in volume accompanied by large change in pressure
vascular changes in HF - CORRECT ANSWER- --loss of ability to vasodilate (endothelial
dysfunction)
-imbalance in vasoconstrictors (endothelin) and vasodilators (nitric oxide)
-oxidative stress
-persistent vasoconstriciton
left ventricular remodeling - CORRECT ANSWER- -change in LV geometry, mass, and
volume that occurs over a period of time
,remodeling - CORRECT ANSWER- -muyocardium and vasculature-compensatory response
that results in structural and functional changes
long term clinical consequences with remodeling - CORRECT ANSWER- --return to fetal
proteins phenotype
-change in the number of pumps and receptors - HFrEF should be on a beta blocker
-loss of myocardial contractile force - poor CO and inotropic response to adrenergic stimuli
-contractile protein synthesis is not matched with increased mitochondrial synthesis - ATP
deficient
-myocardial energetics
activation of RAAS in HF - CORRECT ANSWER- -causes not only increases in preoload and
afterload, but also causes direct toxicity to the myocardium
angiotensin II in HF - CORRECT ANSWER- -mediates remodeling of the ventricular wall,
contributing to the sacromere death, loss of the normal collagen matrix, and interstitial
fibrosis
-leads to decreased contractility, changes in myocardial compliance, and ventricular
dilation
HFrEF
speak to the cascade and effects of RAAS in HF - CORRECT ANSWER- --triggered by a drop
in BP because of hypoperfusion and poor SV
-angiotensinogen
-renin converts to angiotensin
-then angiotensin I then II
-binds to AT I receptor triggering:
- vasoconstriction
, - oxidative stress
- cell growth (hypertrophy)
- proteinuria
- LV remodeling
- vascular remodeling
what does Angiotensin II do in HF - CORRECT ANSWER- --increased antidiuretic hormone
-vasoconstriction
-increased Na reabsorption
-increased aldosterone secretion
what does aldosterone lead to - CORRECT ANSWER- --sodium and water retention
-potassium and magnesium loss
-reduced baroreceptor reflex
-cardiac fibrosis
-ischemia
-sympathetic activation
pharmacological treatment of stage A HF - CORRECT ANSWER- -angiotensin converting
enzyme inhibitors (pril)
angiotensin II receptor blockers (sartan)
statins as appropriate
at risk for HF but without structural heart disease or symptoms of HF
pharmacological treatment of stage B HF - CORRECT ANSWER- -ACEI (pril)
ARBs (sartan)
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