HTN and the Kidney Gosmanova

Question 1

ENaC mutation

Answer 1

Liddle’s disease - monogenic HTN

Question 2

Genetic mutation of aldosterone synthase that’s active to ACTH

Answer 2

glucocoricoid remediable aldosteronism

Question 3

inactivating mutations in 11B-HSD-2 gene

Answer 3

apparent mineralocorticoid excess

Question 4

MAP =

Answer 4

MAP = CO x SVR = DBP +1/3(SBP-DBP)

Question 5

Does increased cardiac output in HTN persist?

Answer 5

no

Question 6

Effect of transplanting kidney from hypertensive patient to normotensive pt?

Answer 6

recipient gets HTN (& visa versa)

Question 7

Goyton’s theory of pressure natriuresis

Answer 7

increased BP leads to increase Na excretion, which leads to decreased BP

Question 8

Ouabain

Answer 8

reduces Na/K ATPase –> endothelin and sympathetic nervous system increase arterial tone -> BP up.

Question 9

Brenner’s hypothesis of essential HTN

Answer 9

low nephron mass –> htn

Question 10

Role of dietary salt in HTN

Answer 10

no salt = no htn, even with aging.

salt -> volume up -> CO up -> HTN

Question 11

beta1-Rc activation in granular or JG cells?

Answer 11

increased renin

Question 12

adenosin2-RC activation

Answer 12

decreased renin

Question 13

prostaglandin receptor activation effect on renin

Answer 13

increased renin

Question 14

increased salt to macula densa cells

Answer 14

adenosine

Question 15

decreased NaCl to macula densa cells

Answer 15

NO and prostaglandins

Question 16

Is renin elevated in everyone with HTN?

Answer 16

No.

20% high renin
30% low renin

50% normal renin

Question 17

unilateral renal artery stenosis Tx

Answer 17

ACE inhibitors reduce BP

Question 18

bilateral renal artery stenosis Tx

Answer 18

ACE inhibitor refractory

Question 19

Aldosterone excess result

Answer 19

upregulation of ENaC in collecting duct

-> sodium retention, BP up

Question 20

Cushing’s syndrome effect on kindey

Answer 20

glucocorticoid excess - behaves like aldosterone.

overcomes 11Beta-HSD2 (hydroxysteroiddehydrogenase)

Question 21

pseudohypoaldosteronism

Answer 21

Deficiency in 11Beta-HSD2

Can be inhibited by licorice ingestion (candies & chew)

Question 22

Liddle’s syndrome

Answer 22

Autosomal dominant constitutive activation of ENaC in distal tubule

Tx: triamterene or amiloride

Question 23

Why hypokalemia and metabolic alkalosis in phseudohypoaldosteronism?

Answer 23

Na in = K out.

increased MC activation leads to H pump upregulation, so H+ excreted

Question 24

Gordon Syndrome

Answer 24

Salt-sensitive hypertension, hyperkalemia metabolic acidosis

constitutive activation of NaCl channels in DCT (Na in, K out)