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diuretics 51/52 Flashcards

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1
Q

Acetazolamide (Diamox)

A

Carbonic Anhydrase Inhibitor
sulfonamide derivatives

inhib NaHCO3 reabsorption via CA @ the proximal tubule (organic acid secretory system) site of secretion and action

limited effectiveness: enhanced Na reabsorption (in the form of NaCl) by all the remaining tubule segments

not very effective diuretics; places further down in the tubule where Na+ (NaCl) can be reabsorbed

“amides”

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2
Q

Mannitol (Osmitrol)

A

Osmotic Diuretic

in EC space but doesn’t cross BBB

filtered by the glomeruli (no tubular secretion), with minimal tubular reabsorption

increase in the osmotic pressure of the glomerular filtrate, which leads to decreased reabsorption of water (and its solutes) in nephron segments that are freely permeable to water
Na+ follows the water- unique!

proximal tubule and descending limb of loop of Henle

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3
Q

Furosemide (Lasix)

A

Loop Diuretic/High ceiling Diuretic (Inhibitors of apical Na+‐K+‐2Cl‐ symport)

sulfonamide derivatives

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4
Q

Ethacrynic Acid (Edecrin)

A

Loop Diuretic/High ceiling Diuretic (Inhibitors of apical Na+‐K+‐2Cl‐ symport)

phenoxyacetic acid derivative

no sulfa like rxn!
but worse ototoxicity

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5
Q

Hydrochlorothiazide (Microzide)

A

Thiazide and thiazide‐like diuretic (Inhibitor of apical Na+‐Cl‐symport

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6
Q

Chlorothiazide (Diuril)

A

Thiazide and thiazide‐like diuretic (Inhibitor of apical Na+‐Cl‐symport

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7
Q

Chlorthalidone (Thalitone)

A

Thiazide and thiazide‐like diuretic (Inhibitor of apical Na+‐Cl‐symport

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8
Q

Indapamide

A

Thiazide and thiazide‐like diuretic (Inhibitor of apical Na+‐Cl‐symport

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9
Q

Triamterene (Dyrenium)

A

K+ sparing Diuretic (Inhibitor of renal Na+ Channels)

poorly soluble and may precipitate kidney stones

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10
Q

Amiloride

A

K+ sparing Diuretic (Inhibitor of renal Na+ Channels)

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11
Q

Spironolactone (Aldactone)

A

K+ sparing Diuretic (Aldosterone antagonist)

“-one”

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12
Q

Eplerenone (Inspra)

A

K+ sparing Diuretic (Aldosterone antagonists)

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13
Q

Drospirenone + ethinyl estradiol (Yasmin)

A

K+ sparing Diuretic (Aldosterone antagonists)

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14
Q 
Desmopressin acetate (1‐Deamino‐8‐D‐Arginine Vasopressin) (DDAVP,
Stimate)
A

Anti‐diuretic drug

similar in structure to arginine vasopressin (the antidiuretic hormone; ADH)

increases water reabsorption by the collecting duct system in the kidney, increase in the insertion of water channels in the apical membrane

greater antidiuretic activity than vasopressin itself but has less cardiovascular vasopressor activity

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15
Q

skip pgs

A

7,8,9, table pg 10

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16
Q

Most diuretics have in common the ability to ???

A

inhibit sodium reabsorption and thus promote sodium excretion–>promote water excretion

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17
Q

keep in mind the nephron segment where the diuretic acts and the capabilities of distal and proximal nephron segments

A

drugs acting proximal of the collecting duct increase the delivery of Na+ to the collecting duct and increase K+ excretion which causes hypokalemia

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18
Q

edema

A

in the interstitial space

generalized (ANASARCA = severe generalized edema)
OR
localized to a specific part of the body (e.g. hydrothorax, hydropericardium, ascites).

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19
Q

Edema is caused by

A

increased movement of fluid from the capillary intravascular space into the interstitial space

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20
Q

main factors influencing fluid movement in and out of the capillary

A

Capillary intravascular hydrostatic pressure (pushes out)

and plasma colloid osmotic pressure (pulls back in)- via plasma proteins

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21
Q

Factors that increase transudation (oozing like movement of fluid through a membrane or between cells) into the interstitium and cause edema:

A

Increase in capillary intravascular hydrostatic pressure

Decrease in capillary intravascular colloid osmotic pressure

Impaired lymphatic drainage of interstitial

Renal retention of salt and water

Increased capillary permeability

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22
Q

Increase in capillary intravascular hydrostatic pressure

A

*arteriolar dilation

venular constriction

increased venous pressure as in CHF

*venous obstruction

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23
Q

Decrease in capillary intravascular colloid osmotic pressure

A
  • decreased production of plasma proteins
  • increased loss of plasma proteins

accumulation of osmotically active substances in the interstitial
space

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24
Q

Impaired lymphatic drainage of interstitial (can’t tx with meds)

A

Obstruction, e.g. neoplastic blockage and Filariasis (elephantiasis)

Radical Mastectomy (destruction of lymphatics)

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25
Renal retention of salt and water due to
(1) Kidney disease (2) Liver disease (3) Heart disease
26
Increased capillary permeability due to
``` inflammatory substances (histamines, kinins) i.e. anaphylactic shock ```
27
CHF ??
ventricular pumping is inadequate CO is low renal perfusion is decreased-->RAAS activated both ventricles, so systemic (R) and pulmonary (L) edema
28
Edema associated with liver disease (Cirrhosis)
Decreased synthesis of plasma proteins (albumin) and thus lowered colloid osmotic pressure. b. Decreased liver metabolism of sodium and water retaining hormones (e.g. aldosterone and vasopressin) c. Scarring of liver tissue in cirrhosis increases hydrostatic pressure in the portal capillaries, the result is transudation of fluid into the peritoneum and the development of ascites. d. decreased renal blood flow due to sequestration of fluid in the liver leads to compensatory renal retention of sodium and water.
29
Edema associated with renal disease
Nephrotic syndrome (aluminuria/hypoproteinemia-->dec. osmotic pressue-->edema) Acute renal failure, prevent progression to irreversible failure
30
non-edematous uses of diuretics
HTN Nephrolithiasis (kidney stones) Hypercalcemia (Furosemide increases renal excretion of calcium) Nephrogenic Diabetes Insipidus Glaucoma therapy and Ocular surgery Acute Mountain sickness Urinary excretion of toxins, overdose treatment, prevention of renal toxicity NOT for edema of pregnancy
31
Many kidney stones are caused by
too much renal leak of calcium. Thiazide diuretics enhance calcium reabsorption in the distal convoluted tubule and thus (by decreasing Ca++ excretion) are useful in patients with kidney stones (suggested that dietary NaCl be reduced)
32
Nephrogenic Diabetes Insipidus
paradoxical antidiuretic action of thiazide diuretics dec. plasma volume,  dec. glomerular filtration rate,  inc. proximal reabsorption of NaCl and water, and  dec. delivery of fluid to the diluting segments.
33
Mountain sickness is associated with
respiratory alkalosis, which leads to headache, irritability, anorexia, vomiting. Carbonic anhydrase inhibitors are useful due to induction of metabolic acidosis, and decreasing production of cerebral spinal fluid (CSF).
34
Acetazolamide (Diamox) SEs
SJS: sulfa hypersn. rxn Hyperchloremic metabolic acidosis ‐ Bicarbonate wasting without much significant chloride excretion Urinary alkalinization can lead to precipitation of calcium phosphate, which may lead to kidney stones. Some hypokalemia because of  K+ excretion Contraindicated in hepatic cirrhosis
35
Acetazolamide (Diamox) uses: Glaucoma
Glaucoma ‐ Inhibition of CA decreases intraocular pressure by decreasing aqueous humor formation topical
36
Acetazolamide uses: mountain sickness
provide relief from the respiratory alkalosis and cerebral edema due to induction of metabolic (non-respiratory) acidosis and decreased production of CSF
37
Acetazolamide uses: epilepsy
again due to the induction of metabolic acidosis and CNS actions
38
Acetazolamide uses: Urinary alkalinization
can enhance renal excretion of weak acids (uric acid, aspirin)
39
Acetazolamide uses: correct metabolic alkalosis
cause metabolic acidosis *if too great may cause kidney stones
40
mannitol uses
oliguric acute renal failure reduction of intraocular and intracranial pressure (increasing plasma osmotic pressure) Urinary excretion of toxins/overdose treatment/prevention of renal toxicity mono or combo for peripheral edemas of nephrotic, cirrhotic and cardiac origins
41
mannitol SEs
extract too much water from peripheral intracellular stores and this increases the extracellular fluid volume: CHF pt: more pulmonary edema hyponatriemia CI in severe renal disease, cranial bleeding hyperglycemia (Glycerin metabolism)
42
loop diuretics: Furosemide (Lasix) Ethacrynic Acid (Edecrin)
secreted by the *proximal tubule via organic acid secretion mechanism* -uric acid will buildup from competition, bad for gout pts** act in *thick ascending limb of Henle’s loop* where they block the Na+‐K+‐2Cl‐ symporter in the luminal (apical) membrane (incr. excretion of these 3 ions) high‐ceiling diuretics because of the high reabsorptive capacity of the thick ascending limb (25%) The diuresis results in enhanced excretion of not only Na+ and Cl‐, but also K+, H+, Ca++, Mg++, ammonium and possibly phosphate
43
loop diuretic uses
``` CHF acute pulmonary edema HTN (thiazides better, longer half lives) hypercalcemia (inc. excretion) Edema of nephrotic syndrome Edema with liver cirrhosis OD hyponatremia ```
44
loop diuretics SEs
PROFOUND e-lyte and fluid loss: hypotension, hypovolemia, hyponatremia inc. K+/H+ excretion: hypochloremic metabolic alkalosis and hypokalemia metabolic: hyperglycemia and increased plasma levels of LDL and triglyceride gout exacerbation ototoxicity (more common w/ ethacrynic acid, also with amino glycoside abx tx (i.e. Gentamicin) sulfa-like rxns Hypomagnesemia lithium toxicity dec. effects by NSAIDS
45
thiazides get into kidney via
filtered by the glomerulus and also sec. by organic acid secretory mech in *proximal tubule* -->competition for uric acid-->gouty -bound heavily to plasma proteins
46
where/how thiazides inhibit Na reabsorb
inhibit the Na+‐Cl‐ symporter in the *luminal (apical) membrane of the *early distal convoluted tubule* (cortical diluting segment) promoting NaCl excretion and water diuresis. Diuretic action is independent of patient acid‐base balance
47
thiazide uses
mild-moderate edema of heart failure (loop diuretice for more severe, esp. if GFR drops below 30 ‐ 40 ml/min) HTN kidney stones (nephrolithiasis), osteoporosis Nephrogenic diabetes insipidus ascites due to liver cirrhosis
48
Nephrogenic diabetes insipidus
Paradoxical antidiuretic effect ‐ reduce urine volume up to 50% due to plasma volume contraction leading to fall in GFR with associated increased proximal tubular reabsorption.
49
kidney stones (nephrolithiasis), osteoporosis thiazide mechanism
indirectly inc. reabsorption (dec. excretion) of Ca2+ from urine in distal convoluted tubule -dependent on steeper Na+ gradient (Na+ reab. inhibitited, so pumped into cell, Ca2+ pumped out into blood)
50
thiazide SEs
Hypokalemia and metabolic alkalosis due to  excretion of K+ and H+ in the late distal tubule and cortical collecting duct Gout ‐ decreased excretion of uric acid sulfonamide hypersensitivity hyperglycemia inc. plasma LDL cholesterol, total cholesterol, and total triglycerides (not: Indapamide) hyperglycemia (dec. insulin secretion)
51
How do K+ wasting diuretics waste K+? | Goodman+Gilman theory
diuretics which increase delivery of Na+ to the collecting duct system are K+ wasting because they: inc. Na+ conductance (movement) through a luminal (apical) channel leading to a lumen negative transepithelial voltage which indirectly promotes inc. K+ secretion -also pulls H+, causes alkalosis in blood theory failure: not nec. inc. in NET Na+
52
How do K+ wasting diuretics waste K+? | Peuler's theory
increase delivery of both Na+ AND Cl‐ to the collecting duct system where Na+ uptake via the cellular luminal (apical) Na+ channels occurs at a disportionately faster rate than Cl‐ uptake via the paracellular route. Obviously, this leaves the urine remaining here in the lumen more negatively charged thus attracting more secretion (and therefore excretion) of positively‐charged K+ (and H+) at this site.
53
loop and thiazide diuretics: | one more thing that contributes to K+ wasting
Compensatory increase in activity of the renin‐angiotensin‐aldosterone system (RAAS), if it occurs, can also contribute to K+ wasting here due to the known actions of aldosterone: facilitates Na+/K+ ATPase
54
K+ sparing diuretics: Triamterene (Dyrenium) Amiloride
get into kidney via organic BASE secretory mech in the *proximal tubule* (don't worry about uric acid buildup) Both amiloride and thriamterene act on the *principal cells in the *collecting duct system* where they inhibit luminal (apical) Na+ channels , which obviously inhibits Na+ reabsorption secretion by making the urine in the lumen but also indirectly inhibits K+ secretion by making the urine in the lumen more positively charged less H+ secretion by the intercalated cells of the collecting duct system.
55
K+ sparing diuretics: Triamterene | Amiloride uses
not powerful diuretics since collecting duct system reabsorbs only 3% of the filtered load of Na+ and Cl‐ (this may or may not be true for aldosterone receptor antagonists) Thus, because of limited diuretic capacity, these agents are mostly used in combination with other diuretics (thiazide, loop diuretic) to treat edema (CHF, hepatic cirrhosis, hyperaldosteronism), and hypertension used to counterbalance the hypokalemia caused by thiazide and loop diuretics.
56
other K+ sparing diuretics (Triamterene, | Amiloride) uses
CF | Liddle's syndrome
57
Liddle's syndrome
defect in the collecting duct system such that these cells respond as if they are exposed to high levels of aldosterone ( Na+ reabsorption,  K+ secretion,  H+ secretion) ‐ The result is hypokalemic metabolic alkalosis and hypertension. (pseudohyperaldosteronism) Amiloride and Triamterene are useful in offsetting this condition by blocking sodium channels.
58
amiloride and triamterene SEs
life‐threatening hyperkalemia: (cardiac arrhythmias, muscle weakness) and thus also contraindicated in hyperkalemic patients and with the use of K+ supplements. ``` N/V kidney stones (triamterene) ```
59
amiloride and triamterene should not be administered with ?? due to risk of life‐ threatening hyperkalemia
aldosterone receptor blockers (e.g. spironolactone)
60
K+‐sparing diuretics should be used with caution with blockers of the ?? due to risk of hyperkalemia.
renin‐angiotensin‐aldosterone system (RAAS)
61
K+ sparing Diuretics (Aldosterone receptor blockers) ‐ Spironolacatone (Aldactone) and Eplerenone (Inspra), Drospirenone
antagonists (blockers) at mineralocorticoid receptors (aldosterone receptors). Binding to the receptor prevents aldosterone‐induced gene transcription clinical efficacy of these drugs is dependent on the levels of endogenous aldosterone
62
K+ sparing Diuretics (Aldosterone receptor blockers) block aldosterone effects:
main effects of the hormone aldosterone in the collecting duct system are  Na+ conductance out of the lumen to inside of cells via more Na channel activity and  basolateral Na+/K+‐ATPase activity, and thus indirectly  secretion of K+ and H+ (due to increased lumen electronegativity as well as the increased basolateral Na+/K+ exchange). Accordingly, aldosterone receptor blockers block these effects.
63
spironolactone and eplerenone usually administered with a loop diuretic or thiazide diuretic to treat edema and hypertension. Helps by ?? also effective in treating ??
reducing edema fluid and preventing hypokalemia. hyperaldosteronism (primary or secondary)
64
spironolactone and eplerenone diuretics of choice for
CHF, hepatic cirrhosis (edema)
65
Toxicity, adverse reactions, and contraindications: spironolactone and eplerenone
If used alone (except perhaps in high aldo states) can induce life‐ threatening hyperkalemia (cardiac arrhythmias, muscle weakness) and thus also contraindicated in hyperkalemic patients and with the use of K+ supplements Use with another K+ sparing diuretic (amiloride, triamterene) is obviously also contraindicated. Antiandrogen effects (Spironoloactone more so than >Eplerenone (more selective)) Use with caution with drugs that block RAAS (e.g. ACE inhibitors) due to increased risk of hyperkalemia
66
``` ?? is considered a more selective antagonist at just mineralcorticoid (aldosterone) receptors, and unlike spironolactone it appears not to interact with androgen receptors, glucocorticoid receptors and progesterone receptors. ```
Eplerenone
67
desmopressin uses
Nocturnal enuresis, due to neurogenic, Central (pituitary) Diabetes insipidus (i.e. lack of vasopressin secretion; DDAVP is drug of choice).
68
desmopressin SEs
Water intoxication, use with caution in patients with angina, hypertension and heart failure
69
diuretic SE case study (pg. 26, important!***) muscle cramps, painful toe, prescribed hydrochlorothiazide -high uric acid -low K+ why musc. cramps and constipation?
hypokalemia: destabilize muscle cell membranes -dangerous, can lead to heart failure can also have problem with hyperkalemia warning sign to cardiac failure due to hypokalemia (could also have this situation with HYPERkalemia)
70
why hypokalemia from thiazide secondary explanation for hypokalemia (thiazide-induced) correct by ??
increasing Na+ delivery to collecting duct system, increasing Na+/K+ exchange later in tubule, increasing K+ wasting in urine reduction in BV can BP can activate compensatory RAAS and inc. aldosterone inc. K+ secretion correct by eat bananas, potatoes, etc. K+ supplements or K+ sparing diuretics
71
gout brought on by
thiazides inc. uric acid: inhibit uric acid secretion in proximal tubule (organic acid secretory mechanism) diuretic-induced hypovolemia
72
summary: Carbonic Anhydrase Inhibitor: Acetazolamide works where ?? does what ??
Proximal Tubule and distal tubule Inhibit carbonic anhydrase  decrease Na+‐H+ exchange increase NaHCO3 diuresis
73
summary: Osmotic Diuretic: Mannitol works where ?? does what ??
Proximal Tubule and Loop of Henle increase osmotic Pressure decrease reabsorption of water and solutes
74
summary: Loop Diuretics: Furosemide, Ethacrynic Acid work where ?? do what ??
Loop of Henle (thick ascending limb) Inhibit Na+‐K+‐2Cl‐ symporter
75
summary: Thiazide and Thiazide‐like diuretics: Hydrochlorothiazide Chlorthalidone work where ?? do what ??
Distal Convoluted Tubule Inhibit Na+‐Cl‐ symporter
76
summary: K+ sparing Diuretics: Triamterene and Amiloride work where ?? do what ??
Late distal tubule and collecting Duct Block Na+ channels decrease secretion of K+ and H+
77
summary: K+ sparing Diuretics: Spironolactone and Eplerenone work where ?? do what ??
Late distal tubule and collecting Duct Aldosterone Antagonist  decrease Na+ conductance decrease Na+/K+‐ATPase activity decrease secretion of K+ and H+

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