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Pharmacology > Renal Pharmacology > Flashcards

Renal Pharmacology Flashcards

1
Q

Acetazolamide

A

Diuretic

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2
Q

How does acetazolamide work

A

Inhibiting carbonic anhydride, halting the production of bicarbonate from water and CO2..leads to sodium bicarbonate diuretic, acidifying the blood and alkalyzing the urine

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3
Q

Indication for acetazolamideglaucoma,

A

altitude sickness, pseudotumor cerebri, CHF, metabolic alkalosis

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4
Q

Side effects acetazolamide

A

Hyperchloremic metabolic acidosis and paresthesias

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5
Q

Glaucoma and acetazolamide

A

Decreases aqueous humor , reducing intraocular pressure

Inhibits formation of bicarbonate int he eye, which draws in sodium, which is followed by water

Acetazolamide reduces bicarbonate, leading to decreased aqueous humor in the eye

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6
Q

Altitude sickness and acetazolamide

A

Decreasing bicarbonate stores, acidifying the blood pH. Facilitates the renal compensation for respiratory alkalosis, allowing ventilation to increase without having respiratory alkalosis

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7
Q

Acetazolamide and pseudotumor cerebri/idiopathic intracranial hypertension

A

Carbonic anhydride inhibitors may be able to reduce the rate of CSF production to lower pressure

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8
Q

Acetazolamide and DHF

A

Diuretic when treating CHF associated edema

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9
Q

Metabolic alkalosis and acetazolamide

A

Reduces total body stores of HCO3, i

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10
Q

MOA acetazolamide

A

Carbonic anhydride inhibitors (interfering its bicarbonate absorption into e kidneys so blood is acidified and urine is alkalyzed)
Sodium bicarbonate diuresis(reduces body stores of HCO3

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11
Q

Side effects of acetazolamide

A 
Metabolic acidosis (reduce HCO3)
Paresthesia
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12
Q

Mannitol

A

Osmotic diuretic which works to increase urine flow

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13
Q

Indications for mannitol

A

Acute treatment
Increased intracranial pressure
Glaucoma
Drug overdose

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14
Q

Mannitol is acute treatment

A

Intracranial hypertension, primary open angle glaucoma, drug overdose

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15
Q

Side effects mannitol

A

Use is dehydration, and patients should be monitored for this

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16
Q

Mannitol contradiction

A

Anuria and CHF

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17
Q

Indications mannitol

A

Increased intracranial pressure
Glaucoma
Drug overdose

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18
Q

Mannitol and increased intracranial pressure

A

Bolus0osmotic properties

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19
Q

Glaucoma and mannitol

A

Acute treatment of open angle
Until a more definitive treatment can be used
Decreased IOP by decreasing vitreous humor volume
Does not cross blood ocular barrier and thus exerts oncotic pressure which dehydrates the vitreous

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20
Q

Drug overdose and mannitol

A

Promote excretion of substances such as asprin and barbiturates

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21
Q

MOA mannitol

A

Osmotic diuretic, increased urine flow

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22
Q

How is mannitol and osmotic diuretic

A

Filtered by kidney glomeruli, but is incapable of being reabsorbed from the renal tubules. This results in water and Na reabsorption via its osmotic effect. Consequently mannitol increases water and Na excretion, thereby decreasing extracellular fluid volume

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23
Q

How does mannitol increase urine flow

A

Increases tubular fluid osmolarity which leads to increased Na and water flow through the collecting duct, resulting in increased urine flow

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24
Q

Side effects mannitol

A

Dehydration

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25
Q

Why no give mannitol to anuria

A

Is anuric is secondary to renal disease

Mannitol does not influence urine production, only enhances existing urine output. If there is no production (as in ARF) you would have hyperosmotic plasma due to mannitol since it would be trapped in that compartment (and thus be of no benefit and possible harm)

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26
Q

Why no mannitol in CHF

A

Causes retention of fluid in the plasma. It extracts water from the intracellular compartment and increases blood volume, which can worsen CHF and pulmonary edema

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27
Q

Loop diuretics

A

Class of diuretics that inhibit nak2cl symporter in the thick ascending limb or the loop of Henley

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28
Q

Most common loop diuretic

A

Furosemide (lasix)

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29
Q

Allergies to loop diuretics

A

Yea they are sulfa drugs, they contain a sulfonamide group and can cause allergic reactions in patients with sulfa allergies

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30
Q

Side effects loop diuretics

A

Electrolyte abnormalities (hypokalemia, hypokalemia)
Reduce irate excretion, leading to hyperuricemia, and gout
Ototoxicity

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31
Q

MOA loop diuretic

A

Inhibit NaK2CL at thick ascending loop (impermeable to water here-for diluting urine)
Prevent generation of a hypertonic renal medulla.
Prevents urine from being concentrated and leads to increased urine production, thus reducing intravascular volume

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32
Q

Why should we not give furosemide to patients with sulfa allergies

A

It is a sulfa drug

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33
Q

Gout and loop diuretics

A

High uric acid
Diuretics reduce rate of excretion by directly and indirectly increasing rate reabsorption and decreasing irate secretion.

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34
Q

Ototixicity of loop diuretics

A

Vertigo, tinnitus

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35
Q

Hypocalcemia and loop diuretics

A

Inhibit calcium reabsorption in the kidney and can lead to hypocalcemia. Occurs bc calcium reabsorption in the thick ascending limb is dependent on an electrochemical potential difference which is normally maintained by nak2cl symporter. When this symporter is inhibited there is decreased calcium resorption

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36
Q

Hypokalemia and loop diuretics

A

Prevent reabsorption of na and cl in loop of Henley, increased sodium and water passes through collecting tubules in the kidney. Increases distal tubular sodium concentration stimulates the aldosterone sensitive sodium pump to increase sodium reabsorption in exchange for k and h Ions which are lost to the urine. Also volume depletion due to increased urine output causes further increased secretion of aldosterone which further increases the secretion of k into the collecting duct and into the urine. It

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37
Q

Ethacrynic acid

A

Phenoxyacetic acid derivative and is not a sulfonamide. Loop diuretic, and works to decrease blood volume, treating hypertension and edema

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38
Q

MOA ethacrynic acid

A

Loop diuretic

Inhibits nak2cl

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39
Q

Side effects ethacrynic acid

A

Hypokalemia, ototoxicity, and gout

Large doses lead to hepatotoxicity

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40
Q

MOA erthacrynic acid

A

Non sulfa drug (can give to people with sulfa allergies)
Is a phenoxyacetic acid derivative and is composed of a ketone group and methylene group
Loop diuretic
Inhibits nak2cl

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41
Q

Indications for ethacrynic acid

A

Diuresis

Decreasing blood volume (hypertension or edema)

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42
Q

Side effects ethacrynic acid

A

Hypokalemia
Ototoxicity
Gout

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43
Q

Thiazides diuretics

A

First line treatments for hypertensionsulfa drugs (allergic)

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44
Q

Thiazides diuretics MOA

A

Inhibit NaCL reabsorption by blocking the NaCl cotransporter int he early distal tubule. Increased sodium excretion can lead to hyponatremia and increased delivery of sodium to the collecting ducts can lead to hypokalemia metabolic alkalosis

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45
Q

Side effects thiazides diuretics

A 
Hyperglycemia
Hyperlipidemia
Hypercalcemia
Hyperuricemia
Hyponatremia
Hypokalemia metabolic alkalosis
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46
Q

Thiazides and hyperglycemia

A

Decrease insulin

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47
Q

Hyperlipidemia and thiazides

A

Decrease insulin

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48
Q

Hypercalcemia and thiazides

A

Inhibit nacl transport, na concentration in the cell drops , causing increased activity of the basolateral na ca exchanged which brings na from the blood into the cell, while extruding ca into the blood, leading to hypercalcemia
Also induce hypovolemia which increases na and water absorption in the proximal tubula, which passively increases ca reabsorption as well

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49
Q

Hyperuricemia and thiazide

A

Reduce irate excretion by directly and indirectly increasing irate reabsorption and decreasing irate secretion. May lead to gout

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50
Q

Hyponatremia and thiazide

A

Block reabsorption of na in the distal convoluted tubule

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51
Q

Thiazide and hypokalemic metabolic alkalosis

A

Increased delivery of na to the collecting ducts causes increased cellular uptake of na from the lumen by apical. Epithelial na channels which causes the basolateral na k exchanger to more actively exchange na for k, resulting in k loss. The increased delivery of k to the collecting ducts also facilitates the exchange of k for h by the h/k exchanger on the intercalated alpha cells resulting in loss of h causing a metabolic alkalosis. Further loss of k is also stimulated by activation of renin-angiotensin-aldosterone system

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52
Q

Hydrochlorothiazide (HCTZ0

A

Most commonly used thiazide diuretic due to its function int reating high bp and fluid retention

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53
Q

Indications for HCTZ

A

Essential hypertension, edema, diabetes insipidus

First line in African Americans

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54
Q

MAO HCTZ

A

Inhibits reabsorption NaCl (in early segment of distal convoluted tubule)and H20
Promoting urine production

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55
Q

Indications HTCZ

A

Edema, mild to moderate hypertension

56
Q

Edema HCTZ

A

Moderate heart failure to decrease excess fluid in the system
Need proper renal function for meds to work

57
Q

Mild to moderate hypertension HCTZ

A

Lower bp by reducing blood volume and reducing arterial resistance. Along or in combo with hypertensive meds.
First line African Americans

58
Q

Side effects HCTZ

A 
Hypokalemia
Hyponatremia
Dehydration
Hyperglycemia
Gout
59
Q

HCTZ allergy

A

Sulfa allergy

60
Q

HCTZ pregnancy and breast feeding

A

NO
It will be excreted in breast milk
Also category B risk during pregnancy
Diuretics may reduce overall circulating volume and reduce blood flow to the placenta leading to the risk of birth defects. For this reason , diuretics like HCTZ are often avoided as first line agents

61
Q

K sparing diuretics

A

Diuretic which do not promote the secretion of potassium into the urine

62
Q

How do k sparing diuretics work

A

Competing with aldosterone for binding sites or directly blocking epithelial Na channels (ENaC)

63
Q

Indication or k sparing diuretics

A

CHF , hypertension and combined with other diuretics to Counter hypokalemia which they may cause

64
Q

Spironolactone

A

K sparing diuretic

Treats hyperaldosteronism

65
Q

Side effects k sparing diuretics

A

Hypercalcemia, which may lead to arrhythmias and muscle weakness, as wel as spironolactone induced gynecomastia

66
Q

Indication for k sparing diuretics

A

CHF, hypertension
Hypokalemia
Hyperaldosteronism

67
Q

What k sparing diuretic treats hyperaldosteronism

A

Spironolactone bc it is a competitive aldosterone receptor antagonist

68
Q

MOA k sparing diuretics at the collecting tubule

A

Antagonize aldosterone or na channels

69
Q

Amigo ride and triamterene

A

Block the apical sodium channel decrease na reabsorption

70
Q

Spironolactone and eplerenone

A

Compete with aldosterone for binding to intracellular receptors causing:

  1. Decreased gene expression and reduced synthesis of a protein mediator that activates na channels int he apical membrane
  2. Decreased na/k/atpase pumps in the basolateral membrane
71
Q

What is spironolactone used for

A

Heart failure, as cites, hypertension, hypokalemia, hyperaldosteronism

Also antiadronergic as it blocks androgen binding through various mechanisms

Competitive aldosterone receptor antagonist(competes for intracellular mineralocorticoid receptors in late distal tubule or collecting tubule decreasing reabsorption of na and water while decreasing secretion of k)

72
Q

__ is a similar drug to spironolactone

A

Eplerenone

73
Q

Amiloride and triamterene

A

K sparing diuretics which act in the distal tubule of collecting tubule to decrease k loss by excreting their actions on epithelial sodium channels

Block ENaC to prevent its reabsorption in collecting tubules. Na is not reabsorbed and k is not exchanged or wanted into collecting tubule lumen

74
Q

Side effects k sparing diuretics

A

Hyperkalemia

Gynecomastia

75
Q

Signs of hyperkalemia

A

Muscle weakness and fatal arrhythmias

76
Q

Gynecomastia with spironolactone

A

Antiandrogen effects and weak progesterone effects

77
Q

Spironolactone (aldactone)

A

K sparing diuretic. Opposite effects as aldosterone as it promotes k retention and na excretion

78
Q

Spironolactone produces minimal ___ bc the excreted sodium is quickly reabsorbed by the nephron

A

Diuresis

May take 48 hours

79
Q

MOA spironolactone

A

Na and water retention and k excretion

Blocks effect of aldosterone and increases k reabsorption and sodium excretion

80
Q

Why is potassium (spironolactone) retention important for cardiac patients

A

Elevated potassium can lead to dysarrhythmias. To maintain an ion balance in the nephron as potassium is retained, na will be excreted

81
Q

Indications for spironolactone

A

Hypertension, edema, heart failure

82
Q

Why use spironolactone for heart failure

A

Blocking aldosterone receptors int he heart and blood vessels, along with decreasing fluid and retaining k.

Aldosterone has harmful effects on the heart, so blocking it provides beneficial results in HF patients

83
Q

Side effects spironolactone

A

Hyperkalemia and endocrine effects

84
Q

Why get endocrine effects with spironolactone

A

Structure is derived from a steroid structure bc of this spironolactone can cause menstrual irregularities, deeming of the voice and gynecomastia

85
Q

Why avoid potassium supplements on spironolactone

A

It increases k reabsorption can lead to hyperkalemia if not watched

86
Q

ACE inhibitor

A

Treat hypertension, CHF, and diabetic nephropathy

87
Q

Worry about ACE inhibitors

A

Toxicities

88
Q

What are toxicities of ACE inhibitors

A

Cough, angioedema, K changes, taste changes, hypotension, pregnancy changes, rash increased renin, lower angiotensin II, also hyperkalemia(bc lower aldosterone)

89
Q

How remember ACE inhibitors toxicities

A

CARTOPRIL

90
Q

Why cough on ACE inhibitor

A

Increased bradykinin

91
Q

Angioedema ACE inhibitors

A

Increased bradykinin

Seen in patients with genetic predisposition to degrade bradykinin more slowly

92
Q

ACE inhibitors and potassium changes (hyperkalemia)

A

Decreased angiotensin also leads to decreased aldosterone

93
Q

Taste chance ACE inhibitor

A

Sulfhydryl group found in ACE inhibitors

High doses of captopril

94
Q

AcE inhibitors and pregnancy

A

Still birth, fetal renal damage, congenital malformations

95
Q

Rash and ACe inhibitors

A

Captopril

Associated with sulfhydryl group found in ACE inhibitors

96
Q

Increased renin ACE inhibitors

A

Due to negative feedback of angiotensin I to angiotensin II conversion

97
Q

Lower angiotensin II ACE inhibitors

A

Inhibits angiotensin converting enzyme, which is responsible for the conversion of angiotensinI to angiostatin II

98
Q

ACE inhibitors

A

Antihypertensive drugs that work by inhibiting the renin angiotensin aldosterone system

99
Q

How do ACE inhibitors lower bp

A

Inhibiting angiotensin converting enzyme and decreasing the amount of angiotensin II and aldosterone
-get lowered arteriolar resistance, increased venous capacity
-decrease cardiac output and index and stroke volume
Natriuresis is increased, while there is a decreased resistance in the blood vessels of the kidney

100
Q

Side effect ACE inhibitors

A

Bradykinin, which display as persistent dry cough

101
Q

Suffix of ACE inhibitors

A

Pril

102
Q

Indication for ACE inhibitors

A

Hypertension, CHF (with left ventricular systolic dysfunction), angina, cardiac ischemia, post MI patients diabetic nephropathy

103
Q

MOA ACE inhibitors

A

Inhibit ACE

Decrease GFR-inhibits constriction of efferentarteriole

104
Q

ACE

A

Secreted by the lungs and kidneys. Converts angiotensin I to II to activate AT1 receptors in the adrenal cortex. Leads to lowered aldosterone levels too

105
Q

What happens when angiotensin II binds to AT1 receptor

A

Vascular NADpH oxidase, superoxide, adhesion molecules, PAI-1
CARDIOVASCULR TOXICITY

106
Q

What happens when angiotensin II bindsto AT2

A

Increase eNOS, NO, PGI2, EDHF, t-PA, PKC, cGMP

CARDIOVASCULAR PROTECTION

107
Q

What does bradykinin do

A

Increase eNOS, NO, PGI2, EDHF, tPA, and CARDIOVASCULAR PROTECTION

108
Q

What does angiotensin 2 do

A

Constricts efferent arterioles increasing GFR

109
Q

Why increased concentration of renin with ACE inhibitors

A

Bc negative feedback of angiotensin I to angiotensin II conversion

110
Q

Side effects ACE inhibitors

A

Increased bradykinin cough

Potent vasodilator

111
Q

Angiotensin receptor blockers (ARBs)

A

Similar in effect to ACE inhibitors but do not result in increased level of bradykinin and are not as likely to cause persistent dry cough as a side effect

112
Q

Indication for ARB

A

Intolerant to ACE inhibitor

113
Q

Suffix ARB

A

Sartan

114
Q

What do ARBs treat

A

Hypertension, CHF, slow progression of ice tic nephropathy

115
Q

How do ARB work

A

Block angiotensin II receptors

116
Q

Side effect ARB

A

Hyperkalemia due to interference with the renin angiotensin aldosterone system

117
Q

Indications ARB

A

Hypertension, CHF, diabetic nephropathy

118
Q

Hypertension and ARB

A

Intolerant to ACE inhibitor

Block angiotensin II at AT! Leading to vasopressin and aldosterone reduction, reducing BP

119
Q

CHF ARB

A

Candesartan

120
Q

Diabetic nephropathy ARB

A

Delay the progression

121
Q

MOA ARB

A

Block activation of angiotensin II AT1 receptors without effecting bradykinin levels

122
Q

Result of angiotensin II AT1 receptors being blocked without effecting bradykinin

A

Vasodilation and reduction of vasopressin secretion and reduction of aldosterone production and secretion

123
Q

Side effects ARB

A

Hyperkalemia

-

124
Q

Pregnancy and ARB

A

Not major human. Teratogens but are generally avoided in all trimesters of pregnancy due to the risk of adverse effects
In all trimesters

125
Q

Erythropoietin (epoetin Alfa, exogenous, procrit)

A

Recombinant growth hormone that is similar to human erythropoietin and stimulates the production of rbc in the bone marrow. This drug is indicated for patients with anemia secondary to health conditions such as chronic renal failure or chemotherapy treated cancers.

126
Q

MOA epo

A

Stimulates RBC production from bone marrow

This increases patients hemoglobin, hematocrit and reticulocyte counts.

127
Q

On epo the patient must have adequate intake of what

A

Iron, folic acid, and vitamin B12 in order to maximize the effectiveness of epo

128
Q

Indications epo

A

Chronic Rena failure and anemia

129
Q

Why epo with chronic renal failure

A

Kidneys make epo

130
Q

Side effects epo

A

Increased risk of thrombosis
Pelvic and limb pain
Hypertension

131
Q

Epo and increased risk of thrombosis ,stroke, MI

A

Ok

132
Q

Hypertension and EPO

A

Increases rbc production , hemoglobin and hematocrit monitor BP

133
Q

Why shouldn’t you shake a vial of epo

A

Denature glycoproteins and inactivate medication

134
Q

Why monitor hog weekly on epo

A

Idk

135
Q

Why may epo accelerate tumor progression

A

Promotes angiogenesis

Do not give to people with leukemia or other myeloid malignancies

136
Q

Who should not take epo

A

Cancer patients not receiving radiation or chemotherapy bc of tumor acceleration

Pharmacology (52 decks)

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