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renal - drugs Flashcards

1
Q

nephron anatomy (and cortex vs medulla)

A

glomerulus (cortex) –> proximal convoluted tubule (cortex and medulla) –> descending limb loop of Henle (medulla) –> loop of henle (medulla) –> ascending limb of henle (medulla and cortex) distal convoluted tubule (cortex) –> collecting duct

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2
Q

diuretics - group of drugs

A
  1. mannitol
  2. Acetazolamide
  3. loop diuretics
  4. thuazide
  5. K+ sparing diuretics
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3
Q

mannitol - mechanism of action

A

acts on proximal convoluted tubule and on descending loop of Henle

  1. osmotic dieuretic: increases tubular fluid osmolarity –> increased urine flow
  2. decreased intracranial/intraocular pressure
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4
Q

mannitol - clinical use

A
  1. drug overdose

2. elevated intracranial/intraocular pressure

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5
Q

mannitol - adverse effects

A
  1. pulmonary edema
  2. dehydration
    CONTRAINIDCATED IN ANURIA, HF, CEREBRAL HEMORRHAGE
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6
Q

mannitol - contraindicated in

A
  1. anuria
  2. HF
    3, Cerebral hemorrhage
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7
Q

acetazolamide - mechanism of action

A

carbonic anhydrase inhibitor in PCT –> self limited NaHCO3 diuresis and low total body HCO3- stores

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8
Q

acetazolamide - location of action

A
  1. PCT (cytoplasm and brush border)

2. other tissues (eye, brain)

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9
Q

acetazolamide - clinical use

A
  1. Glaucoma
  2. urinary alkalinization
  3. metabolic alkalosis
  4. pseudotumor cerebri
  5. altitude sickness
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10
Q

altitude sickness?

A

illness caused by ascent to high altitude, characterized by hyperventilation, nausea, and exhaustion resulting from shortage of oxygen

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11
Q

acetazolamide - adverse effects

A
  1. proximal renal tubular acidosis
  2. Paresthesias
  3. NH3 toxicity
  4. sulfa allergy
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12
Q

Loop diuretics are divided to (and drugs)

A

Sulfonamide loop diuretic –> a. Furosemide b. bumetanide c. torsemide
Nonsulfonamide loop diuretics –> ethacrynic acid

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13
Q

Sulfonamide loop diuretics - drugs

A

a. Furosemide
b. bumetanide
c. torsemide

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14
Q

Sulfonamide loop diuretics - mechanism of action

A
  1. inhibit contrasport system (Na+/K+/2CL-) of thick ascending limb of loop of Henle –> Abolish hypertonicity of medulla, preventing concentration of urine, increase Ca2+ and Mg2+ excretion
  2. stimulates PGE release (vasodilatory effect on afferent arteriole)
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15
Q

Sulfonamide loop diuretics - clinical use

A
  1. edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edem)
  2. hypertension
  3. hypercalcemia
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16
Q

Sulfonamide loop diuretics - adverse effects

A
  1. ototoxiicty
  2. Hypokalemia
  3. Dehydration
  4. Allergy (sulfa)
  5. metabolic alkalosis
  6. interstitial nephritis
  7. gout
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17
Q

Nonsulfonamide loop diuretics - drugs

A

ethacrynic acid

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18
Q

Nonsulfonamide loop diuretics (ethacrinic acid) - mechanism of action

A

inhibit contrasport system (Na+/K+/2CL-) of thick ascending limb of loop of Henle

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19
Q

Nonsulfonamide loop diuretics (ethacrinic acid) - clinical use

A

diuresis in patient with allergic to sulfa drug

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20
Q

Nonsulfonamide loop diuretics (ethacrinic acid) - side effects

A

similar to Sulfonamide loop diuretics but more OTOTOXIC and no sulfa): 1. ototoxiicty 2. Hypokalemia

  1. Dehydration 4. metabolic alkalosis
  2. interstitial nephritis 6. gout
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21
Q

Nonsulfonamide loop diuretics (ethacrinic acid) - side effects are similar to Sulfonamide loop diuretics but more

A

ototoxic

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22
Q

chronic loop diuretic use may mimic

A

Bartter syndrome

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23
Q

Thiazide diuretics - drugs

A
  1. Hydrochlorothiazide
  2. chlorthalidone
  3. metolazone
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24
Q

Thiazide diuretics - mechanism of action

A

Inhibit NaCL reabsorption in early DCT –> low diluting capacity of nephron and low Ca2+ excretion

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25
Q

Thiazide diuretics - clinical use

A
  1. hypertension
  2. HF
  3. Idiopathic hypercalciuria
  4. Nephrogenic diabetes insibitus
  5. osteoporosis
  6. chronic calcium stone formation
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26
Q

Thiazide - adverse effects

A
  1. Hypokalemic metabolic acidosis
  2. hyponatremia
  3. Hyperglycemia
  4. Hyperlipidemia
  5. hyperurichemia
  6. hypercalcemia
  7. sulfa allergy
27
Q

Potassium-sparing diuretics - drugs

A
  1. Spironolactone
  2. eplerone
  3. Triampterene
  4. Amiloride
28
Q

Potassium-sparing diuretics - mechanism of action

A
  • Spironolactone and eplerone are competitive aldosterone receptor antagonistis in cortical collecting tubule
  • triamterene and amiloride act at the same part of the tubule by blocking Na+ channe;s in the cortical collecting tubule
29
Q

Potassium-sparing diuretics - clinical use

A
  1. hyperaldosterinism
  2. K+ depletion
  3. HF
  4. hepatic ascites (spironolactone)
  5. nephrogenic DI (amiloride)
  6. Liddle syndrome (amiloride)
30
Q

Potassium-sparing diuretics - side effects

A
  1. Hyperkalemia (–> arrhythmia)

2. endocrine effects with spironolactone gynecomastia, antiandrogen effects)

31
Q

Liddle syndrome - treatment

32
Q

Diuretics - electrolyte changes - urine NaCL

A

increased with ALL diuretics (strength varies based on potency of diuretic effect) –> serum NaCL decreased as a result

33
Q

Diuretics - electrolyte changes - urine K+

A
  • increased esp with loop and thiazide diuretics (and maybe acetazolamide) –> decreased serum K+
  • decreased in K+ sparing diuretics –> hyperkalemia
34
Q

Diuretics - electrolyte changes - Urine Ca2+ (and mechanism)

A

increased with loop diuretics (decrease paracellular Ca2+ reabsorption)–> hypocalcemia
decreased with thiazide (enhanced Ca2+ reabsorption)
–> hypercalcemia

35
Q

diuretics that affect blood pH

A
  1. acidemia: a. carbonic anhydrase inhibitors b. K+ sparing diuretics
  2. alkalemia: a. loop diuretics b. alkalosis
36
Q

carbonic anhydrase inhibitors causes acidemia - mechanism

A

decrease HCO3- reabsorption

37
Q

K+ sparing diuretics causes acidemia - mechanism

A
  1. aldosterone blockage prevents K+ secretion and H+ secretion
  2. Hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells
38
Q

Loop diuretics and thiazides causes alkalemia - mechanism

A
  1. K+ loss lead to K+ exiting all cells (via Na+/K+ exchanger) in exchange for H+ entering cells
  2. Volume contraction –> AT II –> Na/H+ exchange in PCT –> high HCO3 reabsortion (contraction alkalosis)
  3. In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule –> alkalosis and paradoxical aciduria)
39
Q

Angiotensin II action

A
  1. acts at angiotensin II receptor (type 1-AT1) on vascular SMC –> vasoconstriction –> increases BP
  2. constricts EFFERENT arteriole of glomerus –> increases Filtration fraction to preserve GFR in low volumes states (eg. when low RBF)
  3. Aldosterone secretion (adrenal gland) –> a. increases Na channel and Na/K pump in principal cells b. enchance K+ and H+ exretion by way of prinicipal cell K channels and α-intercalated cells H+ ATPase –> creats favorable Na+ gradient for Na and H20 reabsorption
  4. ADH posterior pituitary –> increases aquaporin insertion in principal cells –> H2O reabsorption
  5. increases PCT Na/H+ exchanger activity –> Na+, HCO3- and H2O reabsorption –> permit contraction alkalosis
  6. Stimulates hypothalamus –> thirst
40
Q

Angiotensin converting enzyme inhibitors (ACE inhibitors) - drugs

A
  • PRIL
    1. captopril
    2. enalapril
    3. lisinopril
    4. ramapril
41
Q

Angiotensin converting enzyme inhibitors - mechanism of action

A

inhibit ACE –>
A. low AT II –>
1. low GFR by preventing constriction of efferent arteriooles
2. high renin due to loss of negative feedbacK
B. Inhibiton of ACE also preent inactivation of bradykinin, a potent vasodilator

42
Q

Angiotensin converting enzyme inhibitors - clinical use

A
  1. hypertension
  2. HF (decrease mortality)
  3. proteinurua
  4. diabetic nephropathy
  5. Prevent unfavourable heart remodeling as a results of chronic hypertension
  6. ADPKD
43
Q

Angiotensin converting enzyme inhibitors action in diabetic nephropathy

A

decrease intraglomerular pressure –> slowing GBM thickening

44
Q

Angiotensin converting enzyme inhibitors - adverse effects

A
  1. cough
  2. angioedema (due to increase bradykinin–> contraindicated in C1 esterase inhibitor deficiency
  3. teratogen (fetal renal malformations)
  4. increased creatinine (decrease GFR)
  5. Hyperkalemia
  6. Hypotension
45
Q

Angiotensin converting enzyme inhibitors - renin levels

46
Q

Angiotensin converting enzyme inhibitors - used with caution in …. (why)

A

bilateral artery stenosis, because ACE inhibitors will further decrease GFR –> renal failure

47
Q

Angiotensin converting enzyme inhibitors - teratogenesis

A

fetal renal malformations

48
Q

Angiotensin II receptor inhibitors - drugs

A
  • SARTAN
    1. losartan
    2. Candesartan
    3. Valsartan
49
Q

Angiotensin II receptor inhibitors - mechanism of action

A

selectively block binding of angotenisn II to AT1 receptor –> effects similar to ACE inhibitors but ARBs do not incrrease Bradykinin

50
Q

Angiotensin II receptor inhibitors - clinical use

A
  1. hypertension
  2. HF
  3. proteinuria
  4. diabetic neuropathy
  5. ADPKD
    when intolerance with ACE inhibitors (eg. cough, angioedema)
51
Q

Angiotensin II receptor inhibitors - adverse effects

A
  1. hyperkalemia
  2. decreased GFR (in cation with bilateral artery stenosis)
  3. teratogen
  4. hypotension
52
Q

Aliskiren - mechanism of action

A

direct renin inhibitor –> block conversion of angiotenisongen to angiotensin I

53
Q

direct renin inhibitor - drug

54
Q

Aliskiren - clinical use

A

hypertension

55
Q

Aliskiren - adverse effects

A
  1. Hperkalemia
  2. low GFR
  3. Hypotension
    RELATIVELY CONTRAINDICATED IN PATIENS ALREADY TAKING ACE inhibitors or ARBs
56
Q

Aliskiren - contraindications

A

relatively contraindicated in patients taking already ACE inhibitors or ARBs

57
Q

Ammonia Toxicity - symptoms

A
  1. Rhinorrhea
  2. Scratchy throat
  3. Chest tightness
  4. Cough
  5. Dyspnea
  6. Eye irritation
58
Q

Lifelong thizide diuretics mimics

A

Gitelman syndrome

59
Q

Thiazide diuretics - drugs

A
  1. Hydrochlorothiazide
  2. chlorthalidone
  3. metolazone
60
Q

diuretics for nephrogenic DI

A
  1. amiloride

2. thiazide

61
Q

Diuretics with sulfa allergy

A
  1. acetazolamide
  2. sulfonamide loop diuretics
  3. Thuazide diuretics
62
Q

1 extra thiazide

A

indapamide

63
Q

ACE inhibitors causes dry cough due to increase in (except bradykinin)

A
  1. sub P

2. prostagladins

Renal (15 decks)

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