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Urinary Exam 2 > ANP, Renal Prostaglandins, ADH > Flashcards

ANP, Renal Prostaglandins, ADH Flashcards

1
Q

What are the three forms of natriuretic peptides?

A

ANP
BNP
CNP

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2
Q

When are the natriuretic peptides released?

A

Under control of stretch receptors in the right atrium and ventricles

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3
Q

What are the potency of natriuretic peptides from greatest to least?

A

ANP > BNP > CNP

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4
Q

Which natriuretic peptides are better vasodilators?

A

CNP

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5
Q

Which natriuretic peptides are more effective natriuretics?

A

ANP

BNP

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6
Q

What cleaves ANP, BNP, CNP in the plasma?

A

Neprilysin (neutral endopeptidases/metalloprotease)

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7
Q

What does ANP C receptor do?

A

Binds the natriuretic peptides and internalizes them into the cell

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8
Q

What does inhibition of neprilysin cause?

A

Natriuresis

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9
Q

What is Sacubitril?

A

A prodrug converted by esterases to an inhibitor of metalloproteases

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10
Q

What are metalloproteases?

A

Neutral endopeptidases

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11
Q

What do neutral endopeptidases do?

A

Breaksdown endothelin, A2, ANP

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12
Q

What does Sacubitril do?

A

Inhibits neutral endopeptidases/metalloproteases

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13
Q

What is Sacubitril used to treat?

A

In combination with valsartan (A2 antagonist) for CHF

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14
Q

What are the three natriuretic peptide receptors?

A

A B and C

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15
Q

What do A and B natriuretic peptide receptors do?

A

Have physiological actions

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16
Q

What does natriuretic C peptide receptor do?

A

Gets rid of ANP, internalizes receptor with peptide bound to it

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17
Q

What is a marker for heart failure/LV dysfunction?

A

BNP levels (higher levels is worse)

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18
Q

Where is BNP released from?

A

Left ventricle

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19
Q

What drug is essentially BNP in a bottle?

A

Neseritide

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20
Q

What is Neseritide used for?

A

Patients on the maximum amount of diuretic that still need help via natriuresis

21
Q

What is a potential side effect of Neseritide?

A

Depletion of patients plasma sodium

22
Q

Which endothelin has pathological involvement in pulmonary HTN?

A

ET-1

23
Q

What causes release of endothelin?

A

Low shear stress on vascular endothelium

24
Q

Three ET receptors and what each do?

A

ETa: vascular smooth muscle contraction
ETb: vascular smooth muscle contraction
ETb: endothelium vasodilation via NO and prostacyclin release

25
Q

What is Bosentan?

A

Non-selective (ETa, ETb, ETc) antagonist

26
Q

What is Ambrisentan?

A

Selective ETa receptor antagonist

27
Q

When would you give Ambrisentan?

A

For blocking ETa in pulmonary hypertension

28
Q

Where is vasopressin made?

A

Supraoptic and paraventricular nuclei

29
Q

Where is vasopressin released from?

A

Posterior pituitary

30
Q

What triggers release of vasopressin?

A

In response to changes in plasma hyperosmolality (controlled by drugs too)

31
Q

V2 vasopressin receptor:

A

Gs: adenylate cyclase to form cAMP causing increased permeability

32
Q

V1/V3 vasopressin receptor:

A

Gq: DAG and IP3 to activate Ca2+ release causing vasoconstriction

33
Q

What does vasopressin cause in the uterus?

A

Oxytocin receptor stimulation

34
Q

What does vasopressin work on?

A

DCT

CD

35
Q

What are V2 receptor sensitizers used for?

A

Used for patients with V2 receptor or porin channel genetic defects

36
Q

What do V2 receptor sensitizers do?

A

Makes V2 receptor more sensitive to ADH/Vasopressin

37
Q

What drug is a V2 sensitizer?

A

Chlorpropamide

38
Q

What drug is a V2 receptor antagonist?

A

Demeclocycline (tetracycline antibiotic)

39
Q

What are ADH peptide substitutes?

A

Lypressin

Desmopressin (drug of choice)

40
Q

What two drugs are non-peptide V1, V2 antagonists?

A

Conivaptan (IV only)

Tolvaptan (oral)

41
Q

What do mesangial cells produce?

A

Vasodilatory prostaglandins

42
Q

What triggers mesangial cells to produce prostaglandins?

A

Increased BP
Increased bradykinin
Increased A-II
Increased endothelin

43
Q

What affect do PGI2 and PGE2 have?

A

Decrease BP
Decrease afferent arteriolar resistance
Decreased glomerular filtration pressure
Decreased albuminuria

44
Q

What affect do prostacyclins have on the nephron?

A

Decreased Na+ reabsorption in ascending loop of Henle

Reduced ADH efficacy in CD

45
Q

What is Bartter’s Syndrome?

A

NKCC2 deficiency

46
Q

Bartter’s Syndrome treatment?

A

NSAIDs + ACE inhibitors

47
Q

What is Gitelman’s Syndrome?

A

NCC deficiency

48
Q

Final results of Bartter syndrome?

A

Severe dehydration
Severe hypokalemia
Polyuria

49
Q

Final results of Gitelman syndrome?

A

Dehydration
Hypokalemia
Polyuria

Urinary Exam 2 (16 decks)

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