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Flashcards in Hyperaldosteronim Deck (36):
1

Low BP is sensed in glomerulus trigger of _____ from JG cells

renin

2

catalyzes of cleavage of Ang I from angiotensinogen the to ang II via 

ACE

3

How does Ang II increase BP

causes vasoconstriction and increaes aldosterone release from the zona glomerulosa of adrenal cortex

4

Aldosterone works in dista tubule to affect Na and K balance.. Aldosterone will ______ Na+ thus get retnetion of Na in body. In response, K and Hyrogen will be _____ in the tuble

leads to overall:

Na resorbed

thus K and H will get secreated

end up with fluid retention and increased blood volume

5

drug to inhibit renin that works to decrease renin activity, but will see increased renin protein consentrtaions

Aliskiren

6

Adrenal glands (from adenoma or one adrenal or both adrenals w/ hyperplasia) secreate excessive aldosterone that is AUTONOMOUS and not being controlled by:

renin and ang II

should see negative feedback as aldosterone increases

7

What is a result of excessive aldosterone

increased urinary potassium loss and hypertension (d/t excessive Na+ and fluid retention) with clinical presentation of Hypertension and Hypokalemia

8

Hypertension and Hyperkalemia are often seen in 

hyperaldosteronism

9

pt comes in with Low K and high BP... what should we do?

consider test for primary hyperaldosteronism

also: resistant HTN, adrenal incidentaloma and HTN; onset of THN at young age <30 yr

10

We are thinking our patient has secondary hypertension, what kind of testing should we look into?

Morning blood sample in seated ambulant patient:

-Plasma aldosterone concentration (PAC)

Plasma renin activity (PRA) or plasma renin concentration

11

To make Dx of primary hyperaldosteronism, measure an incresaed ratio of:

Plasma Aldosterone : Plasma Renin (with potassium replete)

12

Aldosterone increasesd in pirmary hyperaldosteronism due to:

autonomous secreation from adrenal adenoma

13

Why is renin suppressed in pirmary hyperaldosteronism?

suppressed dt increaed blood pressure (baro reflex) and increased sodium (from increased reabsorption)

14

Pt has HTN and HYPOkalemia

see pt with resistant HTN

early onset HTN or very severe HTN

all signs of

Primary aldosteronism

15

What levels would we see to confirm primary aldosteronism:

PAC (plasma aldosterone concentration) and 

PRA (plasma renin activity)

see HIGH aldosterone and LOW renin

or

Aldosterone:Renin ratio > 20

16

Aldosterone secreating adrenocortical adenoma adn bilateral hyperplasia of Zona Glomerulosa can cause:

Primary Hyperaldosteronism

17

Renal ischemia, decreased intravascular volume, CHF, chrnoic diuretics, hypoproteinemic states, Na-wasting disorders and chronic renal fail can all cause:

Secondary Hyperaldosteronism

18

Renin ischeia increases renin secreation from:

JG cells

19

CHF increases renin secration via:

baroreflex

20

Diuretic/laxatives increase renin because of 

sodium and volume loss

21

ONce a dx of primary adlosteronism has been made you need to determine if this is from unilateral or bilateral adrenal source... what do we order?

CT scan of adrenal glands  or AVS or sampling of what the adrenal glands are draining

22

23

The result of excess aldosterone produciton in response to increased RAAS activity

secondary hyperaldosteornism

24

What do we use to distinguish difference between primary and secondary hyperaldosteronism 

Renin levels increase in secondary forms where as in primary renin decresaes

25

What needs to happen before we do a scan to determine cause of hyperaldosteronism?

need to have a biochemical confirmaiton

26

You get a CT or MRI of pt with hyperaldosteronism and it shows they ahve a unilateral adrenal tumor... what is the treamtement?

27

You get a CT or MRI of pt with hyperaldosteronism and it shows they ahve a bilateral adrenal abnormality... what is the next step?

Perform a selective venous catherteriszation for aldosterone and cortisol to see if you can identify source: if unilateral do adrenalectomy

if bilateral, you can't take out both adrenals, thus do medicla management

28

What medicaitons are used to mange pts with bilateral hyperaldosteronism?

need to block aldosterone at the level of the receptor:

spironolactone or eplereonone

29

MOA of spilarinone or eplereinone

Competitive receptor antagonists of aldosterone

result in decreasing Na dn water retention and increase serum potassium

30

Glycyrrhizic acid can decrease activity of what enZ?

11-HSD2 ; see hypertention and hypokalemia

31

caused by 11HSD2 impairment thus dont convert cortisol to cortisone and increase cortisol action on the mineralcorticoid receptor in the kidney (mimics aldosterone)

Apparent mineralcorticoid excess

32

AME causes what symptoms?

Hypertention and hypokalemia, metabolic alkasosis, low renin acitivty, normal plamsa cortisal levels

33

Pt is prsenting like they ahve primary hyperaldosteronism but lack high aldosteorne levels

 

Liddle syndrome

34

Cuase of Liddle syndrome

mutation in amiloride-sensitizing epithelial Na channel thus see increased activity of Na channel and increase Na reabsorption, K+ wasting, HTN and Hypokalemia

35

What do pts with Liddle sydrome have as far as renin and aldosterone levels?

Liddle

Low renin

Low aldosterone

36

What is our most importatn protector from hyperkalemia

aldosterone

as K increases, so does aldosterone to get rid of it