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Diuretics Flashcards

1
Q

How kidneys control ECF volume

A

Adjusting NaCl and H2O excretion

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2
Q

Diuretics

A

Increase urine volume and increase Na excretion and Cl excretion

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3
Q

Acetazolamide

A

Acts on PCT
CA inhibtor
Inhibits 85% of NaHCO3 reabsorption

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4
Q

Mannitol

A

Osmotic diuretic

Limits water reabsorption in water-permeable segments of nephron (PCT, thin descending limb, and CT with ADH)

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5
Q

Furosemide

A

Loop diuretic

Inhibits Na/K/2Cl cotransport in thick ascending limb

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6
Q

Thiazides

A

Inhibit NaCl co-transport in DCT

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7
Q

K sparing diuretics

A

Act on CT

Inhibition aldosterone actions or directly blocking Na channels

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8
Q

ADH antagonist

A

Prevent ADH-stimulated reabsorption of H2O in collecting tubulue

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9
Q

Diuretic Pharmacology

A

Primarily preventing Na entry into tubule cell
Diuretics enter tubule fluid, site of action determines which electrolyes will be affected
EXCEPT for spironolactone and some ADH antagonists, diuretics generally exert effects on luminal side of nephron

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10
Q

Entry into tubule

A

Mannitol: filtration at the glomerulus
Most other diuretics are tightly protein bound- get secreted across proximal tubulue (organic acid or base secretory pathway)

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11
Q

Tubule epithelial cells

A

Have Na/K ATPase on basolateral (blood) side
Pumps 3 Na out and 2 K in
Keeps Na concentration down so Na will leave lumen
Luminal side has pathways for passive movement of Na down its electrochemical gradient (Na/H exchangers)

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12
Q

Acetazolamide

MoA

A

Reversible inhibition of CA
Inhibits reabsorption of HCO3 in proximal tubule (more is peed out, less HCO3 in blood, blood more acidic)
Na accompanies HCO3 as it is excreted, and water goes with

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13
Q

Acetazolamide

Pharmacokinetics

A

Well absorbed PO
Effect begins within 30 minutes, max at 2 hours, duration 12 hours
Renally secreted via organic acid transporter

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14
Q

Acetazolamide

Adverse Effects

A

Metabolic acidosis
Hypokalemia
Ca phosphate stones
Drowsiness, paresthesia, hypersensitivity rxns

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15
Q

Acetazolamide

Contraindications

A

Cirrhosis (increased urine pH reduces NH3 secretion and increases serum NH3)
Tubular fluid is more alkaline (from the extra bicarb), NH3 is less likely to be protonated to NH4 and trapped/excreted. Goes back into blood

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16
Q

Acetazolamide

Clinical Indications

A

Weak diuretic agent, good as backup
Glaucoma
Urinary alkalinazation: drug overdose/stone removal
Acute mountain sickness: this drug can buy some time by acidifying the blood and reducing hemoglobin’s affinity to O2, releasing it to tissues. Also acidifying blood increases ventilation

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17
Q

Other CA inhibitors

A

Dichlorphenamide (30x more potent than acetazolamide)
Methazolamide (5x more potent)
Dorzolamide (topical for ocular use, reduces pressure)

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18
Q

Mannitol

MoA

A

Osmotic diuretic
Proximal tubulue and descending loop of Henle, collecting ducts (with ADH present)
IV causes expansion of IV volume
Powerful diuretic once it reaches the kideny

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19
Q

Mannitol

Pharmacokinetics

A

NOT ORALLY ABSORBED
Must be injected IV to reach kidney
1/2 life is 1.5 hours

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20
Q

Mannitol

Adverse Effects

A

If kidney filtration is impaired
More mannitol stays in blood, increases blood volume, capillary filtration, more fluid in ECS, hyponutremia, edema
Acute pulmonary edmea, dehydration, headache, nausea, vomiting

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21
Q

Mannitol

Contraindications

A

Congestive heart failure
Renal failure
Pulmonary edema

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22
Q

Mannitol

Clinical Indications

A 
Maintain or increase urine volume
Used in acute renal failure
May promote renal excretion of toxic substances (dyes, drugs)
Reduce intracranial pressure
Reduce intraocular pressure
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23
Q

Thick Ascending Limb of Loop of Henle

A

Impermeable to H2O
Na/K/2Cl cotransporter
Na gradient from Na/K ATPase drives the gradient
Influx of K from both sides raises the intracellular [K]
K diffuses back into the lumen creating a (+) charge in lumen
(+) charge in lumen causes Mg2+ and Ca2+ to leave lumen via paracellular diffusion

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24
Q

Loop Diuretics

MoA

A

Big one: Furosemide (LASIX)
Block Na/K/2Cl transporter in apical membrane
More Na and K in lumen, urine is more diluted (more fluid stays in lumen)
Increases excretion of Na, K, Ca, Mg, and water
MOST EFFECTIVE CLASS
Also, something with prostaglandin production, causes renal venodilation

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25
Loop Diuretics | Pharmacokinetics
Rapid oral absorption Short half life Renally secreted via organic acid transporter
26
Loop Diuretics - Furosemide | Adverse Effects
``` Lasix Hyponatremia, hypokalemia, hypomagnesemia Dehydration metabolic alkalosis Mild hyperglycemia Ototoxicity Hypersensitivity rxns ```
27
Loop Diuretics - Furosemide | Clinical Indications
Acute pulmonary edema, CHF edema, acute hypercalcemia, acute hyperkalemia, hypertension
28
Additional Loop Diuretics | Bumetanide
40x more potent Shorter half-life 50% metabolized by the liver
29
Additional Loop Diuretics | Torsemide
Longer half life than lasix Longer duration of action Better oral absorption 80% metabolized by the liver
30
Additional Loop Diuretics | Ethacrynic Acid
Last resort, only used when hypersensitive to others No CA inhibition Nephrotoxic and ototoxic Worse side effects
31
Distal Convoluted Tubule
Na/Cl contransporter Na gradient drives this Ca reabsorption is controlled by PTH (regulates production of Ca channels in luminal border) Basolateral Na/Ca pump (Ca pumped into blood)
32
Thiazide Diuretics - Hydrochlorothiazide | MoA
Inhibits apical Na/Cl cotransporter (into cell) in distal tubule Produces mild diuresis Results in increased Ca reabsorption
33
Thiazide Diuretics - Hydrochlorothiazide | Pharmacokinetics
Good oral absorption and renal elimination | Half life of 2.5
34
Thiazide Diuretics - Hydrocholorothiazide | Hypercalcemic Effects of Thiazide Diuretics
Inhibition of apical Na/Cl cotransporter decreases intracellular Ca Na/Ca pump will compensate by increases Na pumped into cell and Ca pumped out of cell into blood
35
Thiazide Diuretics - Hydrochlorothiazide | Adverse Effects
Hyponatremia and ***hypokalemia Dehydration ***Metabolic alkalosis Hyperuricemia (competes with organic acid transporter that also transports uric acid) Hyperglycemia (thought to be secondary to hyperkalemia) Hyperlipidemia (increased LDL) Weakness, fatigue, parathesias and hypersensitivity
36
Thiazide Diuretics - Hydrochlorothiazide | Clinical Indications
Hypertension Congestive heart failure Reduce Ca excretion to prevent kidney stones
37
Collecting Tubule | Principal Cells
Na and K Channels Na gradient in lumen drives Na back into cell K effluxes out of cells into lumen More Na in than K out, (-) lumen, drives paracellular K secretion Aldosterone regulates expression of basolateral Na/K ATPase and channels ADH regulates water channels and water absorption (segment is usually impermeable to water until ADH acts on it)
38
Collecting Tubule | Intercalated Cells
Luminal: proton pumps transport H into lumen, the H ATPase is regulated by aldosterone Basolateral: HCO3/Cl is passive countertransporter
39
Hypokalemia | CA inhibitors
Acetazolamide Proximally increases HCO3 (in proximal convoluted tubule) Increase in luminal HCO3 increases (-) charge of lumen More K is effluxed into lumen to counteract the (-) charge Less K in the blood
40
Hypokalemia | Loop and Thiazide Diuretics
Inhibition of apical Na/Cl cotransporter in distal convoluted tubule decreases Na/Cl going into cell, more hangs out in the lumen, lumen is more (-) More (-) lumen encourages more K effluxed from cell into lumen. Less K in blood.
41
Metabolic Alkalosis | Loop and Thiazide Diuretics
Increased Na and Cl from inhibition of cotransporter in distal convoluted tubule makes lumen more (-) More H will be pumped from intercalated cells into lumen Concurrently HCO3 will go into the blood, blood is alkalotic
42
K Sparing Diuretics
Given to avoid hypokalemia NEVER BE GIVEN IN HYPERKALEMIA or if pts are on drugs/have disease states that can cause hyperkalemia: Diabetes mellitus, multiple myeloma, tubulointerstitial renal disease, and renal insufficiency K supplements and ACEi
43
Spironolactone | MoA
Competetive inhibition of aldosterone receptor Anti-androgenic effects (decrease testosterone synthesis, competitive inhibition of DHT receptor) Mild diuresis from decreased Na reabsorption (secondary to aldosterone inhibition) "Sparing" of K and H also secondary
44
Spironolactone | Pharmacokinetics
Slow onset of action, takes DAYS | Liver metabolism to several active metabolites
45
Spironolactone | Adverse Effects
Hyperkalemia Metabolic acidosis Gynecomastia, amenorrhea, impotence, decreased libido Gi upset, peptic ulcers CNS effects: headache, fatigue, confusion, etc
46
Eplerenone
More expensive than spironolactone Competitive antagonist of aldosterone binding to MR Does not inhibit testosterone binding Does not induce gynecomastia or other anti-androgenic side effects
47
Spironolactone
Primary hyperaldosteronism Secondary hyperaldosteronism (renin-angiotensin system activated) Liver cirrhosis Hypertesion
48
Amiloride | MoA
Blocks Na channels in principal cells | Blocking Na influx decreases the driving force for K efflux so K IS SPARED
49
Amiloride | Pharmacokinetics
1/2 life of 21 hours Secreted into tubule via organic base transporter Excreted unchanged by the kidney
50
Amiloride | Adverse Effects
Hyperkalemia (NSAIDs can exacerbate this) GI upset: nausea, vomiting, diarrhea Muscle cramps CNS effects: headache, dizziness, etc
51
Amiloride | Clinical Indications
Edema Hypertension Usually used in combination with other diuretics to reduce K loss Not very efficacious by themselves
52
Triamterene | MoA
Blocks Na channels in principal cells | Blocking Na influx decreases driving force for K efflux so K is "spared"
53
Traimteren | Pharmacokinetics
1/2 life of 4 hours 10X less potent than AMILORIDE Liver metabolizes the drug to it active form Active metabolite secreted into proximal tubule using the organic base transporter
54
ADH Antagonists
Antagonize ADH, decrease water channel insertion, decreases water reabsorption in collecting tubule
55
ADH Antagonists | Demeclocycline
Tetracycline antibiotic | Nephrotoxic
56
ADH Antagonists | Litium
Psych drug used for mania | Nephrotoxic
57
ADH Antagonists | Tolvaptan
Selective antagonist of vasopressin V2 receptor Induces increased, dose-dependent production of dilute urine Does not alter serum electrolyte balance Orally available 1/2 life 6 hours
58
V2 receptor antagonists
Tolvaptan Mozavaptan Lixivaptan
59
V1 and V2 receptor antagonist
Conivaptan
60
Diuretics and Edema
Diuretics tend to decrease capillary hydrostatic pressure and increase plasma oncotic pressure Favor absorption over filtration
61
Kidney Diseases
Most cause retention of Na and H2O Renal insufficiency reduces efficacy of most diuretics (reduced glomerular filtration) Diabetic nephropathy (associated with hyperkalemia) can be treated with THIAZIDES or LOOP DIURETICS
62
Hepatic Cirrhosis
Portal hypertension, hypoalbuminemia Reduction in plasma volume Activates renin-angiotensin-aldosterone system Secondary hyperaldosteronism results in Na retention in kidney Associated with edema and acites RESISTANT to loop diuretics Spironolactone is effective
63
Diuretics and Congestive Heart Failure
Renin-angiotensin-aldosterone system activated, Na retention and edema Thiazide or loop diuretics can cause K loss if aldosterone is high Hypokalemia can lead to coronary events/stroke/death Spironolactone may be effective adjunct/alternative to prevent hypokalemia-induced cardiac dysfunction ACEi may be combined with thiazide or loop diuretics, but NOT WITH SPIRONOLACTONE
64
RHF (chronic)
ECFV redistributes from arterial to venous circulation Venous, hepatic, splenic congestion Peripheral tissue edema ORAL LOOP DIURETICS
65
LHF (acute)
Increased hydrostatic pressure in lung capillaries Pulmonary edema Life-threatening, need rapid, aggressive therapy I.V. LOOP DIURETIC
66
Hyponatremia
Serum Na below 136 mEq/L Symptoms: Headache, fatigue, hallucinations, respiratory arrest, seizures, coma, death Associated with hypovolemia, euvolemia, hypervolemia ADH receptor antagonists can increase serum [Na] Tolvaptan, mozavaptan, lixivaptan, conivaptan
67
Uncomplicated Hypertension
THIAZIDE diuretic
68
Patients with BP that is more than 20 over systolic goal or 10 diastolic goal
Use two agents | Usually one is a THIAZIDE diuretic
69
Nephrogenic Diabetes Insipidus
Loss of ADH effects ADH binds to V2 vasopressin receptors on principal cells AC -> cAMP -> PKA -> Aquaporin 2 channels and H2O reabsorption In insipidus this does not work, we cannot concentrate the urine and end up peeing a ton THIAZIDE use, don't know MoA
70
Kidney stones
Contain Ca, usually occur in hypercalciuria | THIAZIDE diuretics decrease [Ca] in urine by promoting Ca reabsorption in distal convoluted tubule
71
Hypercalcemia
Serum calcium > 14 mg/dL Nausea, vomiting, AMS, abdominal pain, constipation, lethargy, depression, weakness and vague muscle/joint aches, polyuria, headache, coma LOOP DIURETIC Avoid thiazides because they INCREASE reabsorption of Ca
72
Diuretic Resistance | NSAIDs
NSAIDs increase expression of Na/K/2Cl | Compete for organic acid transporter
73
Diuretic Resistance | CHF or Renal failure
Decreases delivery of diuretics to tubule | Also build-up of organic acids competes for secretory transport into tubule
74
Diuretic Resistance | Nephrotic Syndrome
Protein in tubule bind to diuretic drugs and limits their actions
75
Diuretic Resistance | Hepatic Cirrhosis
Decreased GFR causes increased PCT absorption of Na Decreased delivery of Na to distal nephron decreases effect of drugs that target Na transporters or channels in these segments
76
Combination Therapy | Loop + Thiazide Diuretics
Only in patients refractory to one or the other | May be too robust -> K wasting
77
Combination Therapy | K sparing + Loop or Thiazide
Prevents hypokalemia | Avoid in renal insufficiency

Pharmacology (44 decks)

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