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20 Cards in this Set

  • Front
  • Back
most important behaviorald eterminants of bp
consumption of calories and salt; increases linearly w bmi
mcc secondary htn
chronic kidney disease
serum creatine levels needed to consider renal insufficiency
>1.2 women, > 1.4 men
Loud snoring, daytime somnolence, obesity, large neck
obstructive sleep apnea
headaches, paroxysmal htn, palpitations perspiration
Pheochromocytoma
Truncal obesity, wide and blanching purple striae, muscle weaknesss
Cushing syndrome
Hypokalemia, refractory htn
Primary aldosteronism
Arm pulses > leg pulses, arm BP > leg bp
`Coarctation of the aorta
New elevation in serum creatinine
Renovascular disease
Estimated GFR < 60mL/min/1.73 m
Renal parenchymal htn
Preeclampsia
may be 2 to impaired natriuresis or thickening of renal filtration barrier
pressure diuresis
as pressure increases, urinary volume increases

same w sodium (pressure naturesis)
septic shock + captopril
ACE inhibitor blocks RAAS so bp cant stay up
Goldblatt htn model
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
role of angiotensin in bp regulation
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
Infinite feedback gain
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
how to change the set arterial pressure level
1. change water and salt intake
2. change renal function
How do changes in TPR affect long term arterial pressure
it doesnt affect it, kidney compensates
autoregulation of arterial pressure
increased blood flow to tissues (by increasing CO) = vasoconstriction to decrease flow back to normal = increased pressure (diuresis)
salt intake and ECF volume
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