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
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
