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20 Cards in this Set
- Front
- Back
most important behaviorald eterminants of bp
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consumption of calories and salt; increases linearly w bmi
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mcc secondary htn
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chronic kidney disease
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serum creatine levels needed to consider renal insufficiency
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>1.2 women, > 1.4 men
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Loud snoring, daytime somnolence, obesity, large neck
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obstructive sleep apnea
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headaches, paroxysmal htn, palpitations perspiration
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Pheochromocytoma
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Truncal obesity, wide and blanching purple striae, muscle weaknesss
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Cushing syndrome
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Hypokalemia, refractory htn
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Primary aldosteronism
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Arm pulses > leg pulses, arm BP > leg bp
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`Coarctation of the aorta
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New elevation in serum creatinine
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Renovascular disease
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Estimated GFR < 60mL/min/1.73 m
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Renal parenchymal htn
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Preeclampsia
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may be 2 to impaired natriuresis or thickening of renal filtration barrier
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pressure diuresis
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as pressure increases, urinary volume increases
same w sodium (pressure naturesis) |
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septic shock + captopril
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ACE inhibitor blocks RAAS so bp cant stay up
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Goldblatt htn model
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one kidney clamped, bp increases rapidly but decreases over the next several months (other kidney compensates)
vs one kidney clamped and other removed = bp increases rapidly and stays elevated |
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role of angiotensin in bp regulation
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immediate vasoconstriction and increases TPR
rapid Na reabsorb in prox tubule and thick ascending limb slower -> stim aldosterone release from adrenal gland = increased sodium retention from principal cell = retention of water/blood volume |
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Infinite feedback gain
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When arterial pressure increases above salt/water intake, renal output of water and salt increases to return it to normal
when below water/salt intake, renal output is decreased until it returns to normal arterial pressure wil lalways return to normal to match water/salt intake |
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how to change the set arterial pressure level
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1. change water and salt intake
2. change renal function |
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How do changes in TPR affect long term arterial pressure
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it doesnt affect it, kidney compensates
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autoregulation of arterial pressure
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increased blood flow to tissues (by increasing CO) = vasoconstriction to decrease flow back to normal = increased pressure (diuresis)
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salt intake and ECF volume
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increased salt intake
1. osmolality of fluid increases = stim thirst center = drink more water to get its conc back to normal 2. increased ADH secretion by hypothalamic posterior pituitary gland to bring conc back to normal thus increased salt intake = increased arterial pressure |