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renal - drugs Flashcards

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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
Thiazide diuretics - clinical use
1. hypertension 2. HF 3. Idiopathic hypercalciuria 4. Nephrogenic diabetes insibitus 5. osteoporosis 6. chronic calcium stone formation
26
Thiazide - adverse effects
1. Hypokalemic metabolic acidosis 2. hyponatremia 3. Hyperglycemia 4. Hyperlipidemia 5. hyperurichemia 6. hypercalcemia 7. sulfa allergy
27
Potassium-sparing diuretics - drugs
1. Spironolactone 2. eplerone 3. Triampterene 4. Amiloride
28
Potassium-sparing diuretics - mechanism of action
- 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
Potassium-sparing diuretics - clinical use
1. hyperaldosterinism 2. K+ depletion 3. HF 4. hepatic ascites (spironolactone) 5. nephrogenic DI (amiloride) 6. Liddle syndrome (amiloride)
30
Potassium-sparing diuretics - side effects
1. Hyperkalemia (--> arrhythmia) | 2. endocrine effects with spironolactone gynecomastia, antiandrogen effects)
31
Liddle syndrome - treatment
amiloride
32
Diuretics - electrolyte changes - urine NaCL
increased with ALL diuretics (strength varies based on potency of diuretic effect) --> serum NaCL decreased as a result
33
Diuretics - electrolyte changes - urine K+
- increased esp with loop and thiazide diuretics (and maybe acetazolamide) --> decreased serum K+ - decreased in K+ sparing diuretics --> hyperkalemia
34
Diuretics - electrolyte changes - Urine Ca2+ (and mechanism)
increased with loop diuretics (decrease paracellular Ca2+ reabsorption)--> hypocalcemia decreased with thiazide (enhanced Ca2+ reabsorption) --> hypercalcemia
35
diuretics that affect blood pH
1. acidemia: a. carbonic anhydrase inhibitors b. K+ sparing diuretics 2. alkalemia: a. loop diuretics b. alkalosis
36
carbonic anhydrase inhibitors causes acidemia - mechanism
decrease HCO3- reabsorption
37
K+ sparing diuretics causes acidemia - mechanism
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
Loop diuretics and thiazides causes alkalemia - mechanism
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
Angiotensin II action
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
Angiotensin converting enzyme inhibitors (ACE inhibitors) - drugs
- PRIL 1. captopril 2. enalapril 3. lisinopril 4. ramapril
41
Angiotensin converting enzyme inhibitors - mechanism of action
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
Angiotensin converting enzyme inhibitors - clinical use
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
Angiotensin converting enzyme inhibitors action in diabetic nephropathy
decrease intraglomerular pressure --> slowing GBM thickening
44
Angiotensin converting enzyme inhibitors - adverse effects
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
Angiotensin converting enzyme inhibitors - renin levels
increased
46
Angiotensin converting enzyme inhibitors - used with caution in .... (why)
bilateral artery stenosis, because ACE inhibitors will further decrease GFR --> renal failure
47
Angiotensin converting enzyme inhibitors - teratogenesis
fetal renal malformations
48
Angiotensin II receptor inhibitors - drugs
- SARTAN 1. losartan 2. Candesartan 3. Valsartan
49
Angiotensin II receptor inhibitors - mechanism of action
selectively block binding of angotenisn II to AT1 receptor --> effects similar to ACE inhibitors but ARBs do not incrrease Bradykinin
50
Angiotensin II receptor inhibitors - clinical use
1. hypertension 2. HF 3. proteinuria 4. diabetic neuropathy 5. ADPKD when intolerance with ACE inhibitors (eg. cough, angioedema)
51
Angiotensin II receptor inhibitors - adverse effects
1. hyperkalemia 2. decreased GFR (in cation with bilateral artery stenosis) 3. teratogen 4. hypotension
52
Aliskiren - mechanism of action
direct renin inhibitor --> block conversion of angiotenisongen to angiotensin I
53
direct renin inhibitor - drug
Aliskiren
54
Aliskiren - clinical use
hypertension
55
Aliskiren - adverse effects
1. Hperkalemia 2. low GFR 3. Hypotension RELATIVELY CONTRAINDICATED IN PATIENS ALREADY TAKING ACE inhibitors or ARBs
56
Aliskiren - contraindications
relatively contraindicated in patients taking already ACE inhibitors or ARBs
57
Ammonia Toxicity - symptoms
1. Rhinorrhea 2. Scratchy throat 3. Chest tightness 4. Cough 5. Dyspnea 6. Eye irritation
58
Lifelong thizide diuretics mimics
Gitelman syndrome
59
Thiazide diuretics - drugs
1. Hydrochlorothiazide 2. chlorthalidone 3. metolazone
60
diuretics for nephrogenic DI
1. amiloride | 2. thiazide
61
Diuretics with sulfa allergy
1. acetazolamide 2. sulfonamide loop diuretics 3. Thuazide diuretics
62
1 extra thiazide
indapamide
63
ACE inhibitors causes dry cough due to increase in (except bradykinin)
1. sub P | 2. prostagladins

Renal (15 decks)

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