NU 503- CIRCULATION EXAM QUESTIONS WITH CORRECT ANSWERS |LATEST UPDATE 100% SOLVED| GRADED A+

NU 503- CIRCULATION EXAM QUESTIONS WITH CORRECT ANSWERS |LATEST UPDATE 100%
SOLVED| GRADED A+




ANP and BNP mechanisms of action 1. kidneys = promote filtration and decreased Na
reabsorption

2. promote excretion of Na and H2O = decreased fluid volume

all d/t hypovolemia




Hypertension elevated vascular resistance




AHA HTN guidelines SBP >130

or

DBP >80




chronic HTN 1. stroke

2. CAD

3. LV hypertrophy

4. PAD

5. HF

6. CKD




Primary vs Secondary HTN Primary HTN- 90%- unknown etiology

,Secondary HTN- 10%- identifiable cause




Secondary HTN causes 1. CKD

2. Endocrine disorders




Chronic Kidney Disease in secondary HTN dysregulation of Na and H20 balance

chronically elevated RAAS activity




Endocrine disorders in secondary HTN 1. Cushing's disease

2. hyperthyroidism

3. pheochromocytoma




Cushing's disease increase renal reabsorption of sodium




hyperthyroidism increased adrenergic activity




pheochromocytoma increased epi and norepi excretion from an adrenal tumor




Chlorothiazides promote sodium excretion = HTN management




ACE inhibitors block effects of RAAS = HTN management

, Calcium channel blockers targets vascular smooth muscle calcium channels = HTN
management




beta-blockers decrease HR and contractility = HTN management




shock decreased peripheral resistance




shock progression 1. compensated shock

2. decompensated shock

3. irreversible shock and circulatory collapse




compensated shock increase HR, contractility

vasoconstriction

RAAS




compensated shock s/s tachycardia

decreased peripheral perfusion




decompensated shock tissue damage

severe hypoxia = anaerobic metabolism = lactic acidosis