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Medical Pharmacology Exam 2 > Diuretics > Flashcards

Diuretics Flashcards

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USMLE® Step 1 flashcards
1
Q

What ions are usually excreted when using a diuretic? (2) What ion may be spared?

A

Sodium, Chloride

Potassium

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2
Q

Where in the nephron is majority of water, potassium and sodium reabsorbed, and urine is isoosmotic with the blood?

A

The PCT

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3
Q

In what part of the nephron are organic acids actively secreted into the urine? What is the driving force for this secretion?

A

PCT

Sodium/K+ ATPase on basolateral surface

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4
Q

What 2 parts of the loop of henle are urea impermeable? What part is NaCl impermeable? What part is water impermeable?

A

Urea - Descending thin, ascending thick
NaCl - Descending thin
Water - Ascending thick

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5
Q

Where is the macula found? What is its function? What is the name for the phenomenon it is critical for?

A

End of thick ascending limb
Sense osmolality of urine
Tubuloglomerular feedback

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6
Q

What is actively transported out of the distal convoluted tubule? Describe fluid in the DCT relative to blood [hypo, hyper, iso-tonic]? What molecules are unable to pass through DCT? (2)

A

NaCl is actively transported out of DCT
Fluid is hypotonic
Urea and Water

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7
Q

The DCT is considered the [concentrating/diluting] segment of the nephron

A

Diluting

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8
Q

Under what circumstance is water able to leave the collecting ducts?

A

Only is vasopressin is present

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9
Q

What is the only area of the nephron that is permeable to urea?

A

The collecting ducts

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10
Q

What is the vasa recta? What two molecules escape the nephron and exit via the vasa recta to return to circulation?

A

Network of blood vessels surrounding the nephron

NaCl enter vasa recta, water follows

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11
Q

What is a diuretic?

A

increases solute excretion to increase the volume of urine

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12
Q

What is an aquaretic?

A

Increase water but not solute excretion

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13
Q

What is a natriuretic?

A

Increases excretion of sodium

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14
Q

What is a saluretic?

A

Increases the excretion of sodium and chloride

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15
Q

What is a kaliuretic?

A

Increases the excretion of potassium

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16
Q

What are 2 conditions that diuretics are used to treat?

A

Hypertension

Edema

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17
Q

What are the primary and secondary sites of action of carbonic anhydrase inhibitors?

A

Primary - PCT lumen

Secondary - distal collecting duct

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18
Q

What is the major effect of carbonic anhydrase inhibitors in the nephron?

A

Cause excretion of sodium bicarbonate. Usually sodium bicarb is reabsorbed to acidify urine, blocking carbonic anhydrase prevents that process

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19
Q

What is carbonic anhydrase inhibitors expected to cause? Metabolic acidosis / alkalosis?

A

They cause acidosis, so can be used to treat metabolic alkalosis

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20
Q

Carbonic anhydrase inhibitors affect the secretion of the following ions: Na, K, H, HCO3 and H2PO4. Which are increased and which are decreased?

A 
Na, K, HCO3 and H2PO4 increased. 
H decreased (can't acidify urine, stays in system)
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21
Q

What is the example of the carbonic anhydrase inhibitor provided? Why is it regarded as a potassium wasting drug?

A

Acetazolamide

A lot of Na+ reaches the distal nephron, K+ exchanged to absorb in. Exchanged K+ is excreted

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22
Q

What are 4 uses of acetazolamide?

A

Open angle glaucoma
Presurgical pressure reduction in glaucoma
Altitude sickness
Treating diuretic induced metabolic alkalosis

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23
Q

What are 4 side effects of acetazolamide?

A

Metabolic acidosis
Allergy
Kidney stones
Bone marrow depression, paresthesia, tingling

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24
Q

What patients should not use acetazolamide?

A

Liver cirrhosis - Renal ammonia returns to system, can worsen cirrhosis

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25
Q

What is the mechanism of osmotic diuretics? What is the effect on the medullary salt gradient? What is the primary site of action in the nephron?

A

Draws water from tissues into blood, increase renal blood flow
It washes out the gradient
Loop of Henle

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26
Q

What is the effect of osmotic diuretics on ADH activity?

A

Prevents the action of ADH (water reabsorption) because salt gradient is disrupted

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27
Q

Osmotic diuretics increase the excretion of essentially all ions. What is the exception?

A

Hydrogen (acid)

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28
Q

What are the 2 examples of osmotic diuretics provided?

A

Glycerin

Mannitol

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29
Q

What are 4 uses of osmotic diuretics?

A

Acute renal failure
Acute tubular necrosis
Dialysis disequilibrium (too much solute removal)
Mannitol - Reduce brain swelling before neurosurgery

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30
Q

What are 3 adverse effects associated with osmotic diuretics?

A

Hyponatremia
Hyponatremia and dehydration
Hyperglycemia (Glycerin metabolism)

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31
Q

What are 3 populations that should be cautious about using osmotic diuretics?

A

Pulmonary congestion - Can become pulmonary edema
Patients with Anuria
Patients with intracranial bleeding (Mannitol)

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32
Q

What is the primary site of action of the loop diuretics? How do they enter the urine?

A

Thick ascending limb of loop of Henle

Organic ion transporters in proximal tubules

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33
Q

What is the specific transporter inhibited by the loop diuretics? What is its effect on the medullary ion gradient? What is its effect on urine volume and concentration?

A

Na, K, Cl Symporter
Diminishes the ion gradient
Increases urine volume, Increased concentration

34
Q

What is the effect of loop diuretics on ion excretion? Which are spared?

A

All ion excretion is increased. None are spared

35
Q

What are the 4 examples of loop diuretics provided? Which is uniquely metabolized in the kidney (glucuronidation)?

A

Furosemide (Glucuronidation in kidney)
Bumetanide
Ethacrynic acid
Torsemide

36
Q

Among the loop diuretics, which is also a weak carbonic anhydrase inhibitor and can increase venous capacitance? Being able to increase venous capacitance makes this drug useful for what 2 conditions?

A

Furosemide

Heart failure, pulmonary edema

37
Q

How do loop diuretics circumvent limits of salt excretion i.e. referred to as high ceiling diuretics?

A

Prevent salt transport into the macula, therefore no tubuloglomerular feed back to alter excretion rates

38
Q

What are 4 uses of loop diuretics?

A

Acute pulmonary edema
Congestive heart failure
Nephrotic Syndrome
Edema and ascites from cirrhosis

39
Q

What class of diuretic is likely to cause hyponatremia, hypokalemia, volume depletion and metabolic alkalosis?

A

Loop diuretics

40
Q

Regarding mechanism, how thiazide diuretics work?

A

They block the sodium chloride symporter. No effect on potassium symport

41
Q

How do the thiazide diuretics get to the urine? What part of the nephron do they act on?

A

Enter urine via organic ion transporters in proximal tubule

Act in distal convoluted tubule

42
Q

What is the difference between the symporters targeted by loop diuretics and thiazide diuretics?

A

Loop - Na, Cl, K symporter

Thiazide - Na, Cl symporter

43
Q

What is the source of energy for the NaCl symporter?

A

basolateral Na+/K+ antiporter

44
Q

What is the one ion whose excretion is decreased during use of thiazide diuretics? Why?

A

Calcium excretion is decreased

Activity of the Na-Ca antiporter

45
Q

Why are thiazide diuretics not limited by tubuloglomerular feedback? What can happen to plasma calcium with prolonged use of thiazide diuretics?

A

They act distal to the macula

Plasma calcium can go up

46
Q

What are the two examples of thiazide diuretics provided? What is the example of thiazide like provided (1)?

A

Thiazide - Hydrochlorothiazide and Chlorothiazide

Thiazide like - Metolazone

47
Q

How does half life influence the use of thiazide and thiazide like diuretics?

A

Long half like (metolazone) - Hypertension

Short half life (Hydrochlorothiazide and Chlorothiazide) - acute diuresis

48
Q

What are 4 uses of thiazide diuretics?

A

Hypertension
Edema from CHF
Nephrogenic diabetes
Calcium nephrolithiasis

49
Q

Hypotension, hypokalemia, hyponatremia, metabolic alkalosis, hypercalcemia and hyperuricemia. These are all potential side effects of _

A

Thiazide diuretics

50
Q

What patient population should not use thiazide diuretics? What drug class decreases diuretic response? What drug increases the effective dose?

A

People with sulfonamide sensitivity
NSAIDs
Probenecid

51
Q

What are the 2 examples of inhibitors of renal sodium channels provided? Where do the function? What is their net effect?

A

Amiloride and Triamterene
Distal convoluted tubule, collecting duct
Slight increase in sodium excretion, Potassium SPARING

52
Q

Renal sodium channel blockers are diuretics that decrease the secretion of most ions. What are the 2 exceptions i.e. what 2 ions are secreted more with sodium channel blockers?

A

Sodium and chloride

53
Q

Where is triamterene metabolized?

A

Liver

54
Q

What is the effect of amiloride and triamterene on potassium reabsorption?

A

Strongly increases K+ reabsorption

55
Q

How can the effects of the renal sodium channel blockers be enhanced?

A

Co-admin with loop or thiazide diuretics. This also reduces the loss of potassium

56
Q

In what sub-population are the renal sodium channels particularly effective? Why? What syndrome is it used to treat? How can it be used in cystic fibrosis

A

5% African Americans
They have a mutation in ENaC beta subunit
Liddle syndrome
Used to clear mucus in CF patients (aerosol)

57
Q

What are 2 serious side effects of renal sodium channel blockers? What class of drug may reduce their diuretic efficiency?

A

Hyperkalemia (can lead to cardiac arrhythmia/death)
Megaloblastic anemia (triamterene)
NSAIDs

58
Q

What are the 2 examples of mineralocorticoid antagonists provided? How do they work? Where do they work?

A

Spironolactone and Eplerenone
They antagonize the mineralocorticoid receptor (Aldosterone)
Distal convoluted tubule and collecting duct

59
Q

What is they function of aldosterone? How does it work? What is a major trigger for its signalling?

A

Salt and water retention, increased secretion of K+ and protons
Induces transcription of proteins that activate silent sodium channels to increase sodium retention
Dehydration

60
Q

In addition to the renal sodium channel blockers, what other group of drugs are potassium sparing?

A

Mineralocorticoid receptor antagonists

61
Q

Mineralocorticoid receptor blockers are diuretics that decrease the secretion of most ions. What are the 2 exceptions i.e. what 2 ions are secreted more with mineralocorticoid receptor blockers?

A

Sodium and chloride

62
Q

To mitigate the great increase in potassium secretion by loop and thiazide diuretics, what is usually coadministered with these drug?

A

Mineralocorticoid antagonists

Renal sodium channel blockers

63
Q

What are 3 uses for spironolactone?

A 
Primary hyperaldosteronism
Secondary hyperaldosteronism (heart failure, cirrhosis, ascites, nephrotic syndrome)
Ascites and edema
64
Q

What is the major side effect associated with the use of mineralcorticoid antagonists? What is a second concern regarding other hormones?

A

Hyperkalemia

Can cross react with other steroid receptors (feminization, menstrual irregularities)

65
Q

What class of drug decrease the diretic effect of mineralocorticoid receptor blockers

A

NSAIDs (same effect on renal sodium channel blockers)

66
Q

Because of its ability to cause diarrhea, gastritis, gastric bleeding, for what group of patients is mineralocorticoid receptor blockers contra-indicated?

A

Patients with peptic ulcers

67
Q

What is a draw back from the prolonged use of spironolactone?

A

Development of malignancies

68
Q

What are the 2 examples of antidiuretic drugs provided? How are they related?

A

Vasopressin (ADH) and Desmopressin (DDAVP)

DDAVP is synthetic analog of vasopressin

69
Q

What receptor subtypes do vasopressin and desmopressin bind?

A

Vasopressin - V1 and V2

Desmopressin - V2 mainly

70
Q

What is arginine vasopressin?

A

Synthetic intranasal or subQ form of vasopressin

71
Q

What is the effect of activating the V1 subtype of the vasopressin receptor?

A

Reduced medullary blood flow, increased medullary salt gradient and more water reabsorption

72
Q

What is the effect of activating the V2 subtype of the vasopressin receptor? (3)

A
  • More aquaporins in membrane
  • More urea permeability (distal duct)
  • Increased Na, K and Cl symporter activity (thick ascending limb)
73
Q

What is vasopressin used for?

A

Diabetes insipidus

74
Q

What are 2 side effects of vasopressin?

A

Coronary artery constriction

Water intoxication

75
Q

What is the effect of chlorpropamide?

A

Increases the secretion of ADH

76
Q

Beyond its use as a diuretic, what is another use for amiloride?

A

Used to treat lithium induced diabetes insipidus, blocks sodium channel uptake of lithium

77
Q

What causes the pain associated with gout? What are 3 drugs that can be used to treat it?

A

Presence of urate crystals in tissues and joints

Probenecid, allopurinol, colchicine

78
Q

What is the mechanism of action of allopurinol?

A

Blocks conversion of xanthine to uric acid by inhibiting xanthine oxidase

79
Q

What is the effect of colchicine?

A

Blocks neutrophil activity

80
Q

What is the biphasic effect of uricosuric agents?

A

First - decrease uric acid secretion

Second - In lumen, block uric acid reabsorption, increased excretion rate

81
Q

What are 2 major considerations / side effects of probenecid?

A

Increased risk of kidney stones

Interferes with renal excretion of several drugs (e.g. thiazide diuretics)

Medical Pharmacology Exam 2 (16 decks)

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