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
what is the primary clinical application for aliskiren
hypertension (especially those with renal insufficiency)
26
what are the major adverse effects of aliskiren
hypotension, acute renal failure, angioedema, rash, diarrhea, cough
27
what are the contraindications for aliskiren
pregnancy, hyperkalemia, cyclosporine therapy
28
how can aliskiren effect protein aria in chronic kidney disease
may reduce it
29
what do the ACE inhibitors end with
-pril
30
what are the clinical applications of ACE inhibitors
HTN, heart failure, diabetic nephropathy, MI
31
what are the common adverse effects with ACE inhibitors
cough, edema, hypotension, rash, hyperkalemia, altered taste
32
what are the contraindications for ACE inhibitor use
bilateral renal artery stenosis, renal failure, pregnancy
33
what pattern of metabolism does captopril have
administered as active drug and processed as active metabolite
34
what pattern of metabolism does enalapril and ramipril have
ester prodrugs converted to active metabolites in plasma
35
what pattern of metabolism does lisinopril have
administered as active drug and excreted unchanged
36
what is the cough and angioedema side effects of ACE inhibitors caused by
bradykinin action
37
what can co-administration of ACE inhibitors and allopurinol may predispose for
hypersensitivity reactions including stevens-johnson syndrome and anaphylaxis
38
what do the angiotensin II receptor antagonists end in
-artan
39
why do angiotensin II receptor antagonists not cause dry cough, as the ACE inhibitors do
because they have no effect on bradykinin
40
what are the clinical applications of angiotensin II receptor antagonists
HTN, diabetic nephropathy, heart failure, MI, prevention of stroke
41
what are the common adverse effects of angiotensin II receptor antagonists
rhabdomyolysis, Hypotension, diarrhea, asthenia, dizziness
42
what are the contraindications for angiotensin II receptor antagonists
bilateral renal artery stenosis, pregnancy
43
what grade of contraindication are angiotensin II receptor antagonists
category C in first trimester; category D in 2nd and 3rd
44
what is the mechanism of action of B-type natriuretic peptide (BNP)
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
what is the clinical application of BNPs
acutely decompensated heart failure
46
what is nesiritide no effect if given orally
because it is a peptide
47
what are the major adverse effects of BNPs
hypotension, headache, confusion, tremor, pruritis
48
what are the contraindications for BNPs
cariogenic shock, systolic pressure less than 90
49
how does nesiritide effect capillary wedge pressure
decreases it
50
what drug, administered in co-administration with nesiritide, cause increase risk of hypotension
ACE inhibitors
51
what hormones in the body does nesiritide lower the plasma levels of
aldosterone and endothelin-1
52
what are the vasopressin receptor 2 antagonists
conivaptan and tonivaptan
53
how is conivaptan administered
IV
54
how is tolvaptan administered
orally
55
what are the contraindications for V2 antagonists
concurrent use of potent CYP 3A4 inhibitors, hypovolemic hyponatremia
56
what are the clinical applications of conivaptan and tolvaptan
SIADH, euvolemia hyponatremia, heart failure, cirrhotic ascites, autosomal dominant polycystic kidney disease
57
what are common side effects of conivaptan and tolvaptan
atrial fibrillation, orthostatic hypotension, HTN, dyspepsia
58
what tetracycline analogue can treat SIADH
demeclocycline
59
what is the clinical application of acetazolamide
high altitude sickness, glaucoma, heart failure, epilepsy
60
what are common side effects of acetazolamide
metabolic acidosis, diarrhea, weight and appetite loss
61
what are the contraindications for acetazolamide
adrenal gland failure, cirrhosis, hyperchloremic acidosis, hyponatremia/hypokalemia
62
what volume regulating drug can be used for treatment of acute mountain sickness
acetazolamide
63
how does aspirin effect acetazolamide
increases its plasma concentration, potential leading to CNS toxicity
64
what is the mechanism of action of mannitol
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
what are the clinical applications of mannitol
cerebral edema, increased intraocular pressure, prophylaxis of oliguria in acute renal failure
66
what are the contraindications of mannitol
anuria, severe dehydration, heart failure
67
why does mannitol require careful monitoring of volume status
because it promotes vigorous natriuresis
68
what co-transporter do loop diuretics inhibit
NKCC2
69
what are the loop diuretics
furosemide, bumetanide, torsemide, ethacrynic acid
70
what are the clinical applications for loop diuretics
hypercalcemia, hyperkalemia, HTN
71
what does coadministration of sulfonamides with loop diuretics increase
ototoxicity and nephrotoxicity
72
what loop diuretic can be given to individuals who are allergic to sulfonamides
ethacrynic acid
73
what loop diuretic is most ototoxic
ethacrynic acid
74
what part of the kidney do thiazide diuretics effect
distal convoluted tubule cells
75
what do thiazide diuretics promote the reabsorption of
transcellular calcium reabsorption
76
what are the contraindications for thiazide diuretic use
anuria, hypersensitivity to sulfonamides, co-adminsitration with agents that prolong QT interval
77
what volume regulating drug can be used to decrease urinary calcium wasting in osteoporosis
thiazide diuretics
78
what is hydrochlorothiazide's effect on glucose
decreases glucose tolerance and amy unmask diabetes in patients at risk for impaired glucose metabolism
79
what effect can thiazide diuretics have on patients with nephrotic diabetes insipidus
paradoxically produces a modest decrease in urine flow
80
what is the mechanism of action of spironolactone and eplerenone
inhibit aldosterone action by binding to and prevent nuclear translocation of the mineralocorticoid receptor
81
what is the mechanism of action of amiloride and triamterene
competitive inhibitors of the principal cell apical membrane ENaC sodium channel
82
what are the clinical applications of spironolactone and eplerenone
HTN, CHF, hypokalemia, primary aldosteronism
83
what volume regulator can be used to treat acne vulgaris
spironolactone
84
what volume regulator can be used to treat female hirsutism
spironolactone
85
what are the common side effects of spironolactone and eplerenone
hyperkalemia metabolic acidosis, GI hemorrhage, breast cancer, gynecomastia, abnormal menstruation
86
what are the contraindications for spironolactone and eplerenone
anuria, hyperkalemia, acute renal insufficiency
87
what are the clinical applications for amiloride and tramterene
HTN, liddle's syndrome
88
what are the side effects of amiloride and triamterene
diseases of hematopoietic stem, nephrotoxicity (tramterene), hyperkalemia metabolic acidosis
89
what is effected in liddle's syndrome
ENaC sodium channel