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LECOM pharmacology notecards > chapter 20- pharm of volume regulation > Flashcards

chapter 20- pharm of volume regulation Flashcards

1
Q

where are low pressure volume sensors located

A

atria and pulmonary vasculature

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2
Q

where are high pressure volume sensors located

A

specialized baroreceptors in the aortic arch, carotid sinus, JG apparatus

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3
Q

what is the result of renin

A

vasoconstriction and sodium retention

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4
Q

what cells in the cortical thick ascending limb respond to increased luminal NaCl

A

macula densa cells

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5
Q

what is type A natriuretic peptides released by

A

atria

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6
Q

what is type B natriuretic peptides released by

A

ventricles

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7
Q

what is type C natriuretic peptides released by

A

vascular endothelial cells

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8
Q

what is uroguanylin released by

A

enterocytes

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9
Q

what is uroguanylin (UGN) released in response to

A

dietary ingestion of salt

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10
Q

what do ANP and BNP bind with high affinity to

A

NRP-A

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11
Q

what binds to NRP-B

A

CNP

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12
Q

what is the role of ADH

A

constricts the peripheral vasculature and promotes water reabsorption in the renal collecting duct

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13
Q

what do V1 ADH receptors do

A

stimulate vasoconstriction through Gq-mediated mechanism

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14
Q

where are V1 ADH receptors located

A

in vascular smooth muscle cells

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15
Q

where are V2 ADH receptors located

A

collecting duct principal cells

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16
Q

what do V2 ADH receptors do

A

stimulates water reabsorption by Gs-mediated mechanism

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17
Q

what is the first reabsorptive site in the nephron

A

proximal tubule

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18
Q

where does paracellular reabsorption of luminal Ca++ and Mg++ ions across cation-selective channels occur

A

thick ascending limb of loop of hence

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19
Q

what does right heart failure lead initially to

A

peripheral edema

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20
Q

what does left heart failure lea initially to

A

pulmonary edema

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21
Q

what is nephrotic syndrome characterized by

A

proteinuria, edema, hypoalbuminemia, and often hypercholesterolemia

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22
Q

what is the primary cause of nephrotic syndrome

A

glomerular dysfunction

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23
Q

what does the massive proteinuria in nephrotic syndrome lead to

A

decreased plasma oncotic pressure

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24
Q

what is the mechanism of action of aliskiren

A

inhibits renin, leading to decreased conversion of angiotensinogen 2 to angiotensin 1, thereby reducing the substrate for ACE and decreasing arteriolar vasoconstriction, aldosterone synthesis, renal proximal tubule NaCl reabsorption, and ADH release

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25
Q

what is the primary clinical application for aliskiren

A

hypertension (especially those with renal insufficiency)

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26
Q

what are the major adverse effects of aliskiren

A

hypotension, acute renal failure, angioedema, rash, diarrhea, cough

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27
Q

what are the contraindications for aliskiren

A

pregnancy, hyperkalemia, cyclosporine therapy

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28
Q

how can aliskiren effect protein aria in chronic kidney disease

A

may reduce it

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29
Q

what do the ACE inhibitors end with

A

-pril

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30
Q

what are the clinical applications of ACE inhibitors

A

HTN, heart failure, diabetic nephropathy, MI

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31
Q

what are the common adverse effects with ACE inhibitors

A

cough, edema, hypotension, rash, hyperkalemia, altered taste

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32
Q

what are the contraindications for ACE inhibitor use

A

bilateral renal artery stenosis, renal failure, pregnancy

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33
Q

what pattern of metabolism does captopril have

A

administered as active drug and processed as active metabolite

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34
Q

what pattern of metabolism does enalapril and ramipril have

A

ester prodrugs converted to active metabolites in plasma

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35
Q

what pattern of metabolism does lisinopril have

A

administered as active drug and excreted unchanged

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36
Q

what is the cough and angioedema side effects of ACE inhibitors caused by

A

bradykinin action

37
Q

what can co-administration of ACE inhibitors and allopurinol may predispose for

A

hypersensitivity reactions including stevens-johnson syndrome and anaphylaxis

38
Q

what do the angiotensin II receptor antagonists end in

A

-artan

39
Q

why do angiotensin II receptor antagonists not cause dry cough, as the ACE inhibitors do

A

because they have no effect on bradykinin

40
Q

what are the clinical applications of angiotensin II receptor antagonists

A

HTN, diabetic nephropathy, heart failure, MI, prevention of stroke

41
Q

what are the common adverse effects of angiotensin II receptor antagonists

A

rhabdomyolysis, Hypotension, diarrhea, asthenia, dizziness

42
Q

what are the contraindications for angiotensin II receptor antagonists

A

bilateral renal artery stenosis, pregnancy

43
Q

what grade of contraindication are angiotensin II receptor antagonists

A

category C in first trimester; category D in 2nd and 3rd

44
Q

what is the mechanism of action of B-type natriuretic peptide (BNP)

A

increase intracellular concentrations of cGMP by binding to the particulate guanylyl cyclase receptor NPR-A of vascular smooth muscle and endothelial cells, resulting in school muscle relaxation

45
Q

what is the clinical application of BNPs

A

acutely decompensated heart failure

46
Q

what is nesiritide no effect if given orally

A

because it is a peptide

47
Q

what are the major adverse effects of BNPs

A

hypotension, headache, confusion, tremor, pruritis

48
Q

what are the contraindications for BNPs

A

cariogenic shock, systolic pressure less than 90

49
Q

how does nesiritide effect capillary wedge pressure

A

decreases it

50
Q

what drug, administered in co-administration with nesiritide, cause increase risk of hypotension

A

ACE inhibitors

51
Q

what hormones in the body does nesiritide lower the plasma levels of

A

aldosterone and endothelin-1

52
Q

what are the vasopressin receptor 2 antagonists

A

conivaptan and tonivaptan

53
Q

how is conivaptan administered

A

IV

54
Q

how is tolvaptan administered

A

orally

55
Q

what are the contraindications for V2 antagonists

A

concurrent use of potent CYP 3A4 inhibitors, hypovolemic hyponatremia

56
Q

what are the clinical applications of conivaptan and tolvaptan

A

SIADH, euvolemia hyponatremia, heart failure, cirrhotic ascites, autosomal dominant polycystic kidney disease

57
Q

what are common side effects of conivaptan and tolvaptan

A

atrial fibrillation, orthostatic hypotension, HTN, dyspepsia

58
Q

what tetracycline analogue can treat SIADH

A

demeclocycline

59
Q

what is the clinical application of acetazolamide

A

high altitude sickness, glaucoma, heart failure, epilepsy

60
Q

what are common side effects of acetazolamide

A

metabolic acidosis, diarrhea, weight and appetite loss

61
Q

what are the contraindications for acetazolamide

A

adrenal gland failure, cirrhosis, hyperchloremic acidosis, hyponatremia/hypokalemia

62
Q

what volume regulating drug can be used for treatment of acute mountain sickness

A

acetazolamide

63
Q

how does aspirin effect acetazolamide

A

increases its plasma concentration, potential leading to CNS toxicity

64
Q

what is the mechanism of action of mannitol

A

acts as ormolu, filtered at the glomerulus but not subsequently reabsorbed in the nephron; exert an intraluminal osmotic force and limit reabsorption of water across water-permeable nephron segments

65
Q

what are the clinical applications of mannitol

A

cerebral edema, increased intraocular pressure, prophylaxis of oliguria in acute renal failure

66
Q

what are the contraindications of mannitol

A

anuria, severe dehydration, heart failure

67
Q

why does mannitol require careful monitoring of volume status

A

because it promotes vigorous natriuresis

68
Q

what co-transporter do loop diuretics inhibit

A

NKCC2

69
Q

what are the loop diuretics

A

furosemide, bumetanide, torsemide, ethacrynic acid

70
Q

what are the clinical applications for loop diuretics

A

hypercalcemia, hyperkalemia, HTN

71
Q

what does coadministration of sulfonamides with loop diuretics increase

A

ototoxicity and nephrotoxicity

72
Q

what loop diuretic can be given to individuals who are allergic to sulfonamides

A

ethacrynic acid

73
Q

what loop diuretic is most ototoxic

A

ethacrynic acid

74
Q

what part of the kidney do thiazide diuretics effect

A

distal convoluted tubule cells

75
Q

what do thiazide diuretics promote the reabsorption of

A

transcellular calcium reabsorption

76
Q

what are the contraindications for thiazide diuretic use

A

anuria, hypersensitivity to sulfonamides, co-adminsitration with agents that prolong QT interval

77
Q

what volume regulating drug can be used to decrease urinary calcium wasting in osteoporosis

A

thiazide diuretics

78
Q

what is hydrochlorothiazide’s effect on glucose

A

decreases glucose tolerance and amy unmask diabetes in patients at risk for impaired glucose metabolism

79
Q

what effect can thiazide diuretics have on patients with nephrotic diabetes insipidus

A

paradoxically produces a modest decrease in urine flow

80
Q

what is the mechanism of action of spironolactone and eplerenone

A

inhibit aldosterone action by binding to and prevent nuclear translocation of the mineralocorticoid receptor

81
Q

what is the mechanism of action of amiloride and triamterene

A

competitive inhibitors of the principal cell apical membrane ENaC sodium channel

82
Q

what are the clinical applications of spironolactone and eplerenone

A

HTN, CHF, hypokalemia, primary aldosteronism

83
Q

what volume regulator can be used to treat acne vulgaris

A

spironolactone

84
Q

what volume regulator can be used to treat female hirsutism

A

spironolactone

85
Q

what are the common side effects of spironolactone and eplerenone

A

hyperkalemia metabolic acidosis, GI hemorrhage, breast cancer, gynecomastia, abnormal menstruation

86
Q

what are the contraindications for spironolactone and eplerenone

A

anuria, hyperkalemia, acute renal insufficiency

87
Q

what are the clinical applications for amiloride and tramterene

A

HTN, liddle’s syndrome

88
Q

what are the side effects of amiloride and triamterene

A

diseases of hematopoietic stem, nephrotoxicity (tramterene), hyperkalemia metabolic acidosis

89
Q

what is effected in liddle’s syndrome

A

ENaC sodium channel

LECOM pharmacology notecards (22 decks)

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