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Pharm block 4 hemostasis and cardiac > diuretics > Flashcards

diuretics Flashcards

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1
Q

define diuretic

A

A substance or drug that tends to increase the discharge of urine.

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2
Q

Carbonic Anhydrase Inhibitors MOA

A

Acetazolamide, dorzolamide,
methazolamide, and dichlorphenamide inhibit CA in luminal membrane of proximal tubule, reducing proximal HCO3- reabsorption.

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3
Q

Osmotic Diuretics MOA

A

Freely filterable, non-reabsorbable osmotic agents like mannitol, glycerol, and urea act primarily on the proximal tubule to reduce the reabsorption of H2O and solutes including NaCl.

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4
Q

loop diuretics MOA

A

Furosemide, bumetanide, torsemide, and ethacrynic acid inhibit the Na+/ K+/2Cl- cotransport system in the thick
ascending limb of Henle’s loop (ALH).

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5
Q

Thiazide MOA

A

Chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide inhibit NaCl cotransport in
early distal convoluted tubule (DCT).

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6
Q

K+ sparing diuretics MOA

A

Spironolactone & eplerenone competitively block the actions of aldosterone on the collecting tubules.

Amiloride and triamterene reduce Na+ entry across the luminal membrane of the principal cells of the collecting
tubules.

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7
Q

ADH antagonist MOA

A

Doxycycline, lithium, tolvaptan, conivaptan, mozavaptan, etc. prevent ADH induced water reabsorption in the
principal cells of the collecting tubule

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8
Q

what are the 6 classes of diuretics?

A 
Carbonic Anhydrase Inhibitors
Osmostic Diuretics
Loop Diuretics
Thiazide
K+ sparing Diuretics
ADH antagonists
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9
Q

acetazolamide is what type of diuretic and where does it primarily work

A

acts primarily in the PCT as a prototypical CA inhibitor. At its maximal effect, it can inhibit 85% of NaHCO3 reabsorption.

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10
Q

mannitol is what type of diuretic and where does it work

A

Mannitol is a prototypical osmotic diuretic, which limits water reabsorption in the water-permeable segments of the nephron (PCT, thin descending limb, and CT (with ADH)).

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11
Q

Furosemide is what type of diuretic and where does it work

A

Furosemide is a prototypical loop diuretic, which inhibits Na+/K+/2Cl- cotransport in the thick ascending limb of Henle’s loop.

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12
Q

where do thiazide diuretics work

A

inhibit NaCl co-transport in the DCT.

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13
Q

where do K+ sparing diuretics work

A

K+-sparing diuretics act on the CT by inhibition of aldosterone actions or directly blocking Na+ channels.

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14
Q

where do ADH antagonist work

A

ADH antagonists prevent the ADH-stimulated reabsorption of H2O in the CT.

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15
Q

what is the primary therapeutic goal of diuretic use

A

reduce edema (must have NaCl output greater than intake)

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16
Q

Most diuretics exert their effects from which side of the lumen? what are the exceptions?

A

Mostly from the luminal side of the nephron.

Exceptions are spironolactone and some ADH antagonist

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17
Q

how do diuretics enter the nephron and what is the consequence of this

A

Most are secreted across the proximal tubule via the organic acid/base secretory pathway
exception is Mannitol which is filtered

therefore decreased renal blood flow or renal failure reduces diuretic effectiveness as well as drugs that compete for the secretory pump

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18
Q

Na+ reabsorption is primarily driven by

A

the Na+/K+ ATPase on the basolateral (blood side) of the epithelial cells

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19
Q

where is bicarbonate reabsorbed

A

proximal convoluted tubule

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20
Q

ACETAZOLAMIDE belongs to which class and what is the mechanism of action?

A

CA inhibitor, reversible inhibition of CA (inhibiting reabsorption of HCO3- in the proximal tubule

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21
Q

Acetazolamide adverse effects

A

Metabolic acidosis
Hypokalemia
Calcium phosphate stones
Drowsiness, paresthesias & hypersensitivity rxns (sulfa drug)

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22
Q

Acetazolamide contraindicaitons

A

Cirrhosis (increased urine pH reduces NH3 secretion and thereby increases serum NH3)

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23
Q

Dichlorphenamide is what kind of drug

A

CA inhibitor - 30x more potent than acetazolamide

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24
Q

Methazolamide is what kind of drug

A

CA inhibitor - 5x more potent than acetazolamide

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25
Dorzolamide is what kind of drug
CA inhibitor - topical preparation for ocular use (avoids systemic effects)
26
ACETAZOLAMIDE clinic uses
Diuretic agent: weak, but ok as backup Glaucoma: reduction of intraocular pressure Urinary alkalinization: drug overdose/some stones Acute mountain sickness: buy’s some time only
27
Mannitol MOA
Osmotic diuretic Major osmotic effects in proximal tubule and descending limb of the loop of Henle; collecting ducts too, if ADH is present
28
Can mannitol be given orally
No - not absorbed must be given via IV to reach the kidneys
29
how does Mannitol enter the nephron
via filtration in the glomerulous- adverse effects predominiate if filtration is impaired
30
Mannitol adverse effects
``` Adverse effects • Major toxicity due to increased plasma osmolality. With reduced glomerular filtration rate (CHF or renal failure) mannitol is retained in ECF. This moves water out of cells into ECF potentially worsening heart failure. In addition, Na+ follows water movement out of cells leading to hyponatremia. • Acute pulmonary edema • Dehydration • Headache, nausea & vomiting ```
31
Mannitol contraindications
Congestive heart failure Renal failure Pulmonary edema
32
Mannitol clinical indications
Maintain or increase urine volume may be useful to treat or prevent acute renal failure may promote renal excretion of toxic substances (eg., contrast dye or myoglobinemia) Reduce intracranial pressure Reduce intraocular pressure (glaucoma)
33
Does mannitol cross the BBB
NO- therefore it can draw fluid out of the intracranial compartment
34
Is the thick ascending limb permeable to water
NO
35
what is the most effective diuretic class
Loop diuretics - can cause excretion of up to 20% of the filtered Na+
36
how do loop diuretics work
* Act primarily by blocking the Na+/K+/2Cl- co-transporter in the apical membrane of the thick ascending limb of Henle's loop. * Reduce ability to concentrate ECF and to dilute lumenal fluid. * Increase urinary water, Na+, K+, Ca2+, and Mg2+ excretion. Most efficacious diuretic class; can cause excretion of up to 20% of the filtered Na+. * *Also cause dilation of the venous system and renal vasodilation -- effects that may be mediated by prostaglandins. (unique to loop diuretics)
37
FUROSEMIDE (Lasix® ) is what kind of diuretic
Loop diuretic - Reduces reabsorption of Na+, K+, Cl- as expected, but also Ca2+ & Mg2+ due to loss of (+) luminal charge Renal vasodilation improves renal blood flow
38
Furosemide pharmacokinetics
Oral absorption is rapid but variable for each patient *Half-life is short (1-1.5 hrs) so duration is only 2-3 hrs Renal secretion mechanism; organic acid transporter
39
ferosemide adverse effects
mainly due to over diuresises of a pt bc they are so powerful ``` Hyponatremia, hypokalemia, hypomagnesemia Dehydration Metabolic alkalosis Mild hyperglycemia Ototoxicity Hypersensitivity rxns ```
40
clinical indications for ferosemide
``` Acute pulmonary edema Edema associated with congestive heart failure Acute hypercalcemia Acute hyperkalemia Hypertension ```
41
BUMETANIDE advantages/disadvantages over ferosemide
About 40X more potent than furosemide Shorter half-life than furosemide: ~ 1 hr 50% metabolized by the liver
42
TORSEMIDE advantages/disadvantages over ferosemide
Longer half-life than furosemide: ~ 3 hrs Longer duration of action, too: ~ 5-6 hrs Better oral absorption than furosemide 80% metabolized by the liver
43
ETHACRYNIC ACID advantages/disadvantages over ferosemide
Last resort; used only when others exhibit hypersensitivity No CA inhibition Nephrotoxic and ototoxic
44
Thiazide diuretics MOA
Inhibition of Na+/Cl- cotransporter in distal tubule Produces relatively mild diuresis **Results in increased Ca2+ reabsorption (opposite loop diuretics)
45
Hydochlorothiazide pharmacokinetics
Good oral absorption and renal elimination | Half-life of 2.5 hrs
46
HYDROCHLOROTHIAZIDE adverse effects
``` Adverse Effects Hyponatremia & **hypokalemia Dehydration *Metabolic alkalosis Hyperuricemia **Hyperglycemia **Hyperlipidemia (increased LDL) Weakness, fatigue, paresthesias & hypersensitivity ```
47
HYDROCHLOROTHIAZIDE clinical uses
Hypertension* main use Congestive heart failure Reduce Ca2+ excretion to prevent kidney stones
48
CHLOROTHIAZIDE compared to hydrochlorothiazide
1/10th the potency of Hydrochlorothiazide | Half-life of 1.5 hrs (shorter)
49
Metolazone compared to hydrochlorothiazide
10X more potent than Hydrochlorothiazide Half-life of 4-5 hrs (longer) not a sulfa drug
50
Indapamide compared to hydrochlorothiazide
20X more potent than Hydrochlorothiazide | *Half-life of 10-22 hrs; metabolized extensively by the liver
51
Chlorthalidone compared to hydrochlorothiazide
Same potency as Hydrochlorothiazide | Half-life of 44 hrs** (much much longer)
52
how do CA inhibitors cause hypokalemia?
K+ moves with its concentration gradient in the collecting tubule (principal cells). The CA inhibitors increase the amount of HCO3- in the lumen increasing its negative potential which increases the efflux of K+ out of the cells.
53
how do thiazide and loop diuretics cause hypokalemia?
thiazide and loop diuretics increase the amount of Cl- in the lumen which makes the lumenal potential more negative. This increases K+ efflux in the collecting ducts.
54
how do thiazide and loop diuretics cause metabolic ALKalosis
by increasing the luminal negative potential (higher concentrations of Na+ and Cl-) more H+ is secreted from the intercalculated cells of the collecting ducts
55
how are potassium sparing diuretics used
These agents are often given to avoid the hypokalemia that accompanies the agents previously described.
56
when should you NEVER give a K+ sparing diuretic
They should never be given in the setting of hyperkalemia or in patients on drugs or with disease states likely to cause hyperkalemia. These include diabetes mellitus, multiple myeloma, tubulointerstitial renal disease, and renal insufficiency. or with drugs that can cause hyperkalemia potassium supplements and ACE inhibitors are common.
57
SPIRONOLACTONE MOA
Competitive inhibition of the aldosterone receptor Anti-androgenic effects - Decrease testosterone synthesis - Competitive inhibition of DHT receptor
58
SPIRONOLACTONE effects
Mild diuresis due to decreased Na+ reabsorption secondary to aldosterone inhibition “Sparing” of K+ & H+ also secondary to aldosterone inhibition
59
Spironolactone pharmacodynamics
Slow onset of action; days to take effect Liver metabolism to several active metabolites
60
spironolactone adverse effects
Hyperkalemia Metabolic acidosis Gynecomastia, amenorrhea, impotence, decreased libido (due to also binding the mineralocorticoid receptor) GI upset, including association with peptic ulcers CNS effects: headache, fatigue, confusion, etc.
61
EPLERENONE MOA and advantages
competitive antagonist of aldosterone binding to mineralocorticoid receptor. Eplerenone is considerably more expensive than spironolactone, but it does not inhibit testosterone binding and therefore it does not induce gynecomastia or other related anti-androgenic side effects.
62
How does Spironolactone cause metabolic acidosis
Decreased lumen negative potential Reduced driving force for H+ Decreased expression of H+ pumps therefore less H+ is excreted and more is left in the blood
63
Spironolactone clinical uses
Primary hyperaldosteronism Secondary hyperaldosteronism Liver cirrhosis* (drug of choice for edema w/liver cirrhosis) Hypertension
64
Amiloride MOA and class
K+ sparing diuretic Mechanism of Action Blocks Na+ channels in the principal cell Blocking Na+ influx decreases the driving force for K+ efflux so K+ is “spared” (less negative outside the cell)
65
amiloride adverse effects
Hyperkalemia (NSAIDs can exacerbate this) GI upset: nausea, vomiting, diarrhea Muscle cramps CNS effects: headache, dizziness, etc.
66
how does amiloride's cause hyperkalemia
by blocking the Na+ channel in the principle cells there is more Na+ in the lumen which makes the lumenal potential more positive therefore decreasing the force driving K+ out of the principal cells
67
AMILORIDE clinical indications
Edema Hypertension Usually used in combination with other diuretics to reduce K+ loss
68
Triamterene MOA and pharmacodynamics
Blocks Na+ channels in the principal cells Pharmacodynamics Blocking Na+ influx decreases the driving force for K+ efflux so K+ is “spared” Active form can precipitate in the tubules and obstruct flow
69
which is more potent amiloride or triamterene
amiloride (triamterene is 10x less potent)
70
ADH antagonists that are no longer used
Demeclocycline and lithium both are nephrotoxic
71
TOLVAPTAN MOA
is a selective antagonist of the vasopressin V2 receptor. Induces increased, dose-dependent production of dilute urine. Does not alter serum electrolyte balance. Tolvaptan is orally available and has a half-life of 6 to 8 hours.
72
what are the V2 receptor antagonists
tolvaptan, moxavaptan, and lixivaptan
73
what are the V1a and V2 antagonists
conivaptan
74
adverse affects of ADH receptor antagonists
hypernatremia, thirst, dry mouth, hypotension, dizziness.
75
indications for use of ADH receptors antagonist
SIADH, euvolemic or hypervolemic hyponatremia; congestive heart failure.
76
which ADH receptor antagonist can be used for euvolemic hyponatremia
conivaptam
77
with CA inhibitors what is the main electrolytes in the urine
NaHCO3
78
with thiazide diuretics what is the main electrolyte in the urine
NaCl
79
with loop diuretics what is the main electrolyte in the urine
NaCl
80
how does diabetic nephropathy affect potassium balance and which diuretics should be used
often associated with hyperkalemia- can use thiazide or loop diuretics
81
best drug for HEPATIC CIRRHOSIS
Spironolactone - resistant to loop diuretics
82
drug use for heart failure
Loop diuretics (IV for acute left sided failure, oral for chronic right sided)
83
Tolvaptan is what kind of drug and is useful in what disease process
vasopressin antagonist and is shown to be useful in pts with CHF in addition to standard therapy including diuretics
84
symptoms of hyponatriemia
``` Headache/disorientation Fatigue Hallucinations Respiratory arrest Seizures Coma Death ```
85
what drug should be used for uncomplicated hypertension
thiazide diurteic either alone or with another drug
86
what is the effect of using a thiazide diuretic in pts with diabetes insipidus
reduced polyuria and increase urine osmolarity (the opposit of what was though)
87
how are thiazide diuretics helpful to pts with kidney stones
decreases Ca concentrations in the urine
88
what kind of diuretic may be helpful to pts with hypercalcemia
loop diuretics - increase Ca excretion (avoid thiazide diuretics)

Pharm block 4 hemostasis and cardiac (12 decks)

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