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Renal II Final > Kruse > Flashcards

Kruse Flashcards

1
Q 
A. What class of drugs can be used for acute mountain sickness? 
B. what is the prototypical drug? 
C. Where does it act?
A

A. Carbonic acid inhibitor
B. Acetazolamide
C. Proximal convoluted tubule

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2
Q

what is the mechanism of acetazolamide?

A

Inhibits the membrane-bound and cytoplasmic forms of carbonic anhydrase.

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3
Q 
As a result of acetazolamide indicate how the following is affected:
A. H+ production in PCT cells
B. action of Na/H antiport
C. Na and HCO3- in lumen
D. Diuresis
E. urine pH
F. body pH
A 
A. Decreased
B. Decreased 
C. Increased
D. Increased
E. Increased
F. decreased
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4
Q

A 60-year-old male presents to the emergency room with shortness of breath after waking up in the middle of the night with a “choking” sensation. The patient has a history of hypertension and MI. Physical examination reveals bibasilar inspiratory crackles and an S3 heart sound.

Which of the following drugs should be administered for rapid, significant relief of this patient’s symptoms?

  1. A drug that acts on the Na/Cl cotransporter in the distal convoluted tubule
  2. A drug that acts on the Na/K/Cl symporter in the thick ascending limb of the loop of Henle
  3. A drug that inhibits carbonic anhydrase
  4. A drug that competes for mineralocorticoid receptors in the collecting duct
  5. A drug that inhibits angiotensin converting enzyme
A
  1. A drug that acts on the Na/K/2Cl symporter in the TAL of the loop of Henle.

Loop diuretics, such as furosemide (Lasix), inhibit the Na/2Cl/K symporter in the ascending loop of Henle. Loop diuretics are the most potent diuretics and are first-line in the management of pulmonary edema associated with left heart failure.

Furosemide inhibits the absorption of sodium, potassium, and choride in the ascending limb of Henle, causing naturesis and diuresis as well as possible hypokalemia and hypomagnesemia. It may be given intravenously for swift management of pulmonary edema. This patient’s S3 and bibasilar inspiratory crackles are signs of left heart failure and volume overload, which require diuresis.

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5
Q

Loop diuretics act on which part of the nephron?

A

Thick ascending loop of Henle

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6
Q

On what transporter does Loop diuretics act on?

A

Na/K/2Cl cotransporter

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7
Q

What are the prototypical Loop diuretics?

A

Furosemide and ethacrynic acid

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8
Q 
Due to a loop diuretic, describe the effect of the following:
A. intracellular Na, K, Cl in TAL
B. Diffusion of K
C. Reabsorbption of Ca and Mg
D. Diuresis
A

A. Decrease
B. decrease diffusion of K and positive potential
C. Decrease
D. increase

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9
Q

Loop diuretics act on which side of the tubule, luminal or basolateral?

A

luminal side. that’s why diuretic activity is tied to secretion rates

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10
Q

What is the normal half life of a loop diuretic in a healthy pt? In an ESRD pt?

A

Healthy pt .5-2 hrs

ESRD pt 9hrs

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11
Q

What are the indications for a loop diuretics?

A
  • Edema
  • HF
  • HTN
  • ARF aka AKI
  • anion overdose
  • hypercalcemia
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12
Q

What are possible AE associated with the use of loop diuretics?

A
  • hypokalemia
  • alkalosis
  • hypocalcemia
  • hyperuricemia
  • ototoxicity
  • sulfonamide hypersensitivity (not all)
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13
Q

An 82-year-old male with osteoarthritis, hypertension and allergic rhinitis was diagnosed 3 months ago with congestive heart failure and resultant pulmonary edema. Until recently, the patient’s symptoms had been well controlled by furosemide therapy. Since beginning a new medication for a comorbid condition, he is more short of breath. Which of the following medications is likely responsible for these worsening symptoms?

  1. Spironolactone
  2. Naproxen
  3. Zileuton
  4. Montelukast
  5. Hydrochlorothiazide
A
  1. Naproxen

Concurrent administration of both NSAIDs (naproxen) and loop diuretics (furosemide) results in reduced efficacy of the diuretic.

Loop diuretics inhibit transport by the Na-K-2Cl symporter in the thick ascending limb of the loop of Henle, resulting in increased excretion of fluid and ions (diuretic effect). In addition to their diuretic action, loop diuretics also stimulate prostaglandin release. In turn, this vasodilatory prostaglandin release leads to elevated renal blood flow and, thus, increases in both GFR and renal tubule drug delivery. NSAIDS inhibit prostaglandin synthesis, minimizing the diuretic effect of loop diuretics.

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14
Q

A 68-year-old male with congestive heart failure recently had his medication regiment adjusted to better control his hypertension. Three weeks later, laboratory analysis shows his serum calcium and magnesium levels have both decreased. The diuretic used in this patient acts predominantly on which nephron segment:

  1. Proximal tubule
  2. Descending loop of Henle
  3. Thick ascending loop of Henle
  4. Distal tubule
  5. Cortical collecting duct
A
  1. Thick ascending loop of Henle
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15
Q

A 67-year-old female is admitted to the hospital with enterococcus endocarditis and is treated with penicillin and gentamicin. During her admission, she develops worsening pulmonary edema secondary to valvular insufficiency and requires therapy with IV furosemide. This patient is most likely to experience which of the following adverse reactions to her current pharmacological treatment:

  1. Ringing in the ears and impaired hearing
  2. Hyperkalemia leading to possible cardiac arrhythmia
  3. Anemia and chronic fatigue
  4. Diffuse flushing and redness over body surface
  5. Pseudomembranous colitis and diarrhea
A
  1. Ringing in the ears and impaired hearing

Combination of both loop diuretics (furosemide) and aminoglycosides (gentamicin) increases the risk of ototoxicity. Both of these agents are individually associated with a risk of ototoxicity; their co-administration results in an additive effect, which manifests as tinnitus (ringing in the ears), vertigo, hearing impairment, or deafness.

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16
Q

If a patient is allergic to furosemide what other drugs can be given to have similar effects as furosemide?

A

Ethacrynic acid is the usual replacement for furosemide

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17
Q

What is the mechanism of action of Hydrochorothiazides?

A

Inhibition of Na/Cl cotransporter and block NaCl reabsorption in the DCT.

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18
Q

What is the site of action for HCTZ?

A

Early DCT

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19
Q

HCTZ enhances the reabsorption of particularly what ions in the DCT and PCT?

A

Calcium. possibly body’s reflex mechanism to reduce diuresis and restore ion balance

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20
Q

If you wanted the largest reduction in body’s Na which diuretic would be best?

A

HCTZ

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21
Q

What are HCTZ used for?

A
  • HTN
  • Mild HF
  • nephrogenic diabetes insipidus
  • Nephrolithiasis
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22
Q

Explain how HCTZ helps with nephrolithiasis.

A

Calcium stones (most common kidney stones) are formed in the lumen and so if you can reduce luminal Ca you can reduce the formation of or exacerbation of calcium stones. HCTZ helps to reabsorb Ca and thus reduces luminal Ca.

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23
Q

What are some AE associated with HCTZ?

A
  • Hypokalemia
  • alkalosis
  • hypercalcemia
  • hyperuricemia
  • hyperglycemia
  • hyperlipidemia
  • sulfonamide hypersensitivity
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24
Q

Which AE associated with HCTZ is not commonly seen as an AE with loop diuretics?

A

Hyperglycemia and hyperlipidemia. this is why it is used with caution in DM patients.

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25
Q

Where in the nephron does K sparing diuretics work?

A

Collecting ducts

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26
Q

On what receptors do K sparing diuretics work?

A
  1. Mineralocorticoid receptor (MR) (located inside the cell)
  2. Na channel (ENaC) inhibitors
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27
Q

K sparing diuretics is an agonist or antagonist of the minerlaocorticoid receptor?

A

Antagonist

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28
Q

Explain how K sparing diuretics work at the MR to spare K

A

Decreases the expression of Na channels by blocking the alodsterone receptor which would block the Na coming in.

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29
Q

What are the typical mineralocortiocid receptor antagonist K sparing diuretics?

A

Spironolactone and eplerenone

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30
Q

What are the typical Na channel inhibitors K sparing diuretics?

A

Amiloride and triamterene

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31
Q

What are some uses of Spironolactone?

A
  • Hyperaldosteronism
  • adjunct to K-wasting diuretics
  • antiandrogenic uses
  • Heart failure (reduces mortality)
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32
Q

What AE are associated with Spironolactone?

A
  • hyperkalemia,
  • acidosis,
  • antiandrogenic effects
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33
Q

What are some uses of amiloride?

A
  • adjunct to K wasting diuretics and lithium-induced nephrogenic diabetes insipidus
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34
Q

What AE are associated with amiloride?

A
  • hyperkalemia and acidosis
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35
Q 
Of the following which ones decrease body pH? 
A. Carbonic anhydrase inhibitors
B. Loop agents
C. Thiazides 
D. Loop agents plus thiazides 
E. K sparing agents
A

A and E decrease body pH. the other ones increase body pH

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36
Q

Which ACEI have the shortest half life?

A

Captopril. Has a high bioavailability (75%)

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37
Q

what is the bioavailability and half life of ramipril?

A

half life 13-17hrs. Bioavailability is 50-60%

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38
Q

what is the half life, bioavailability and active metabolite of enalapril?

A

Half life:

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39
Q

What does ACEI do to TPR and diastolic and systolic BP?

A

Lowers TPR

  • diastolic
  • systolic BP
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40
Q

How does ACEI affect cardiac function of uncomplicated hypertension patients?

A

Little change in cardiac function. Stroke volume and cardiac output may increase slightly with sustained treatment.

41
Q

what adverse effects are associated with acetazolamide

A

Acetazolamide and other CA inhibitors leads to acidosis, hypokalemia, renal stones, paresthesias with high dose, sulfonamide hypersensitivity.

42
Q

what is the MOA of ACEI?

A

inhibit the conversion of Ang I to ang II; prevent bradykinin breakdown and other vasodilator peptides

43
Q

what are the clinical indication for ACEI?

A
  • HTN
  • HF
  • LVD
  • prophylaxis of four CV events (e.g. MI, CAD, stroke) and nephropathy (+/- diabetes)
44
Q

what AE are associated with ACEI?

A
  • hypotension
  • cough
  • angioedema
  • hyperkalemia
  • ARF
  • contraindicated in pregnancy
45
Q

what drug interactions are associated with ACEI?

A
  • antacids
  • capsaisin,
  • NSAIDs
  • Kspring
  • digoxin
  • Lithium
  • Allopurinol
46
Q

ARB works at what receptors?

A

G-protein coupled receptors

47
Q

ARB works at which receptor type?

A

AT 1 and 2

48
Q

If ARB work at AT1, what signaling pathway does it take?

A

Gq–> PLC –> IP3—> DAG –> smooth muscle contraction

49
Q

what effects does ARB have at AT2?

A

activation cause production of NO and bradykinin and thus smooth muscle dilation.

50
Q

What is the MOA of losartan and valsartan?

A

Blocks AT 1 and causes decreased contraction of vascular smooth muscle, ALD secretion, pressor responses and cardiac cellular hypertrophy and hyperplasia.

51
Q

what are the indication for ARB’s?

A
  • HTN
  • diabetic nephrophaty,
  • HF
  • HF or LV dysfunction after AMI
  • prophylaxis of CV events
52
Q

what AEs are associated with ARB?

A
  • hypotension
  • hyperkalemia
  • ARF
  • contraindicated in pregnancy

Notice it’s similar to AE of ACEI but no cough and angioedema. Still contraindicated for pregnancy.

53
Q 
Which of these is not a vasodilator? 
A. Amlodipine
B. Nifedipine
C. Diltiazem
D. Verapamil
E. Hydralazine
F. Nitroprusside
G. None of the above
H. All of the above
A

H. All of the above are vasodilators. Have different MOA.

54
Q

What is the prototypical Calcium channel blockers?

A

Amlodipine
Nifedipine
Diltiazam
Verapamil

55
Q 
Which of these is not a Non-Dihydropyridines? 
A. Diltiazem
B. Verapamil
C. Nicardipine
D. Minoxidil
E. A and B
F. C and D
A

F. C and D. Both A and B are Non-DHP.

56
Q 
which of these is not a Dihydropyridines CCB
A. Amlodipine
B. Nifedipine
C. Felodipine
D. Verapamil
A

D. Verapamil is not a DHP.

57
Q

All CBBs bind to what channel?

A

L-type Channels

58
Q

which group DHP or NON-DHP have predominantly arteriolar vasodilation?

A

DHP

59
Q

which group of CBB have prominent cardiac effects, but also act at vascular tissues?

A

Non-hydropyridines

60
Q

which CCB would be useful in resetting the chronicity of the heart?

A

NON-DHT such as diltiazam and verapamil.

61
Q

Which CCBB has a stronger effect overall: vasodilation, suppression of cardiac contractility, Supression of SA and Av nodes?

A

Verapamil

62
Q

which CCB would you wanna use if you do not want to interrupt SA and AV?

A

DHP. they only work on vasodilation and cardiac muscle contractility.

63
Q

what AE’s are associated with CBBs?

A

dizziness, hypotension, headaches, flusing, nausea

- Constipation (esp verapamil), peripheral edema, coughing, wheezing, pulmonary edema

64
Q

Which CCB are contraindicated with betablockers?

A

non-dhp: verapamil and diltiazem

65
Q

what are the clinical indications for CCbs?

A
  1. HTN. most useful when combined with other agents to counteract reflex tachy
  2. HTN emergencies via IV
  3. Angina: reduction of O2 demand
66
Q

What is the MOA of potassium channel opener?

A

Increase K permeability which stabilizes smooth muscle cell membranes at resting potential, reducing the probability of conraction

67
Q

What the two prototypical K channel opner?

A

Diazoxide and Minoxidil

68
Q

Diazoxide is a 1 that which work by _ 2_. These drugs have diminishing use in hypertensive emergencies due to AE such as _

A
  1. Vasodilator
  2. increase K permeability and thus reduce muscle contraction
  3. Excessive hypotension –> stroke and MI; and hyperglycemia.

Avoid in renal disease

69
Q

what are the clinical use of minoxidil?

A
  • severe HTN and baldness
70
Q

What are the AE’s of minoxidil?

A
  • HA, sweating
  • hypertrichosis
  • Reflex tachychardia and edema
  • must be used with beta-blocker and diuretic to avoid these effects.
71
Q

What receptor does Fenoldopma work on?

A

D1. receptor agonists

72
Q

which receptor agonist is good at increasing renal blood flow.

A

Fenoldopam cuz it has D1 receptors on afferent arteries

73
Q

What is fenoldopam used for?

A
  • hypertensive emergencies pre and post operatively
74
Q

what AE is associated with fenoldopam?

A

Tachycardia, HA, flushing.

75
Q

Feloldopam is an contraindication what which comorbidity?

A

glaucoma due to increased intraocular pressure

76
Q

what is the MOA of hydralazine?

A

release NO from endothelium thus dilate arterioles but NOT veins

77
Q

Hydralazine is a first line therapy in which patients?

A

Hypertension in pregnancy with methyldopa.

78
Q

Combination of hydralazine with what other drug is effect in patients with HF?

A

nitrates

79
Q

What AE are associated with hydralazine

A

fluid and Na retension

  • HA, nausea, anorexia, sweating, flushing, palpations
  • reflex tachy
  • lupus like syndromes
80
Q

Which NO donor is associated with reflex tachycardia that can provoke angina in patients with ischemic heart disease?

A

hydralazine

81
Q

what is the MOA of Nitroprusside?

A

metabolism release NO –> increase cGMP. Powerful dilation of arterial and venous vessels, reduce peripheral vascular resistance, and venous return

82
Q

In the absence of HF, how does nitroprusside affect CO?

A

does not affect CO.

83
Q

what is the indication for nitroprusside?

A

HTN emergencies; acute decompensated HF.

84
Q

What are the AE associated with Nitroprusside?

A
  • excessive hypotension

- Cyanide thiocyanate metabolism

85
Q

what is the MOA of nitroglycerin?

A

release NO via enzymatic metabolism and preferentially dilates veins and has no effect on cardiac or skeletal muscle.

86
Q

what is the contraindication for nitroglycerin?

A

intracranial pressure

87
Q

what is the AE associated with nitroglycrin?

A

orthostatic hypotension, syncope, throbbing headache.

88
Q

what drug drug interaction are associated with nitroglycerin

A

phosphodiesterase type 5.

89
Q

what is the indication for nitroglycerin?

A

HTN emergencies, angina, and HF

90
Q

what receptors do carvedilol and labetalol block?

A

they’re nonselective for alpha 1 and beta 1 and 2.

91
Q

what is the prototype of the non selective beta blockers that which is used for preventing reflex tachy and reduce mortality after MI; and in patients with heart failure?

A

Propranolol. decrease blood pressure by dereasing CO.

92
Q

what are some common contraindication/side effects of beta blockers?

A
    1. Asthama/COPD
      diabetes (cuz glycogenolysis is partially inhibited after beta blocker)
  2. bradycardia, fatigue, sexual dysfunction and depression may occur.
93
Q

what is the prototype of the a1 blocker that which is areversible antagonist at a1 receptors and works by preventing vasoconstriction of both arteries and veins,

A

Prazosin

94
Q

what is prazosin commonly used in combo with and with what other unrelated condition?

A

used in men with concurrent hypertention and BPH and in combo with a beta blocker and a diuretic.

95
Q

what is the MOA of clonidine and methyldopa?

A

A2 agonist. reduce sympathetic outflow from vasomotor centers in the brainstem but allow these centers to retain or even increase their sensitivity to baroreceptor control.

96
Q

what AE is associated with clonidine?

A

sedation, dry mouth, depression, sexual dysfunction. abrupt withdrawal –> life threatening hypertensive crisis.

97
Q

what is clonidine used for?

A

decrease blood pressure and peripheral vascular resistance.

98
Q

what is the indication for methyldopa?

A

hypertension during pregnancy

99
Q

what is the MOA of methyldopa?

A

analog of L dopa thats converted to methylnorepinephrhrine. works to lower BP by reducing peripheral vascular resistance

Renal II Final (4 decks)

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