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Therapeutics P2 > Exam 1 lecture 4 > Flashcards

Exam 1 lecture 4 Flashcards

1
Q

What are diuretics?

A

Agents that help get rid of sodium (naturesis) and water (diuresis)

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2
Q

Why do diuretics decrease BP?

A

because of a decrease in plasma volume.

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3
Q

What are some indication (uses) of diuretics

A

HTN
Edema
Heart failure
Acute renal failure

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4
Q

Is caffeine a diuretic

A

Not really, Only has a diuretc action for a short period of time, then body habituates to it.

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5
Q

Drugs usually target what type of transporter

A

Active

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6
Q

What are the classifications of diuretics based on MOA

A
  1. Inhibitors of carbonic anhydrase
  2. Osmotic diuresis
  3. Inhibitors of Na-K-2Cl symport
  4. inhibitors of Na-Cl symport
  5. Inhibitors of renal epithelial Na channels
  6. mineralocortecoid receptor antagonists
  7. vasopressin antagonists
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7
Q

WHat factors does glomerular filtration rate (GFR) depend on

A

Size of drug
extent of plasma protein binding of diuretic. (only unbound drug filtered)

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8
Q

carbonic anhydrase location

A

proximal tubule

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9
Q

example of carbonic anhydrase

A

acetazolamide

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10
Q

what do CAI do to Bicarbonate excretion

A

Increase urine output by increasing NaHCO3 excretion

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11
Q

What is an example of osmotic diuretic

A

Mannitol (increase h20 excretion)

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12
Q

How do Na-K-Cl inhibitors affect ions (loop diuretics)

A

Increase Na, K, CL excretion

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13
Q

What are Na-Cl inhibitors also known as

A

Thiazide diuretics

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14
Q

Mineralocorticoid receptor antagonists and inhibitors of renal epithelial Na channels work in what way

A

Increase K retention (K sparing)

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15
Q

CAI work in

A

PCT

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16
Q

Loop diuretics work in

A

Thick ascending limb

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17
Q

Why do diuretic drugs find it difficult to pass through glomerulus

A

Because they are protein bound (albumin).

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18
Q

If diuretics can not go into glomerulus, how do they get into tubules?

A

They undergo active drug secretion across to the proximal tubule

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19
Q

Where does active drug secretion happen

A

Proximal tubule

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20
Q

where does drug reabsorption happen?

A

Distal tubule

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21
Q

renal excretion of drugs is a major route of elimination for what percentage of drugs?

A

25-30%

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22
Q

Is the secretion of drugs in PCT active or passive

A

Active

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23
Q

What are the name of the transporters that aid in active secretion in proximal tubule

A

Organic anion transporter (OAT)
Organic cation transporter (OCT)

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24
Q

steps of active transport of drug into proximal tubule

A

Diffusion out of capillary into interstitial space
transport across basolateral membrane
secretion across luminal membrane

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25
Q

What are main sites for drug-drug interaction? WHY?

A

OAT/OCT transporters. SInce they are non selective, drugs can interact with each other here.

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26
Q

Some drugs that use OAT

A

Furosemide, penicillin, probenecid

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27
Q

How can we use the competition of drugs for these organic transporters therapeutically?

A

Like what probenecid + penicillin was used for in WW II, we can saturate the transporters in the kidney with another drug to increase the availability of the drug we want in the blood.

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28
Q

location of carbonic anhydrase inhibitors

A

Proximal tubule

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29
Q

what does carbonic anhydrase do?

A

Reabsorption of bicarbonate

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30
Q

What doe carbonic anhydrase inhibitors do?

A

block reabsorption of NaHCO3

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31
Q

example of CA-I

A

Acetazolamide (Diamox)

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32
Q

clinical use of CA-I

A

Acute mountain sickness
Diuretic (weak)

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33
Q

toxicities of CA-I

A

Hyperchloremic acidosis
renal potassium wasting

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34
Q

WHy are CA-I useful for mountain sickness

A

metabolic acidosis produced by excretion of bicarbonate counteracts the respiratory alkylosis that results from hyperventilation

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35
Q

Give an example of osmotic diuretic

A

Mannitol

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36
Q

what is mannitol? how does it work?

A

Mannitol is a large, pharmacologically inert molecule that is not reabsorbable. This forces water to rush into it.

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37
Q

location of osmotic diuretic action

A

proximal tubule and decending loop of henle

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38
Q

is mannitol IV or PO

A

IV

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39
Q

Orally active osmotic diuretics

A

glucose, glycine

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40
Q

Location of loop diuretic action?

A

ascending thick loop of henle

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41
Q

which transporter do loop diuretics affect?

A

Na, K, Cl symporter

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42
Q

T/F Loop diuretics must act on basolateral membrane for diuretic activity

A

False
must act on luminal membrane

43
Q

which are the most potent class of diuretics

A

loop diuretics

44
Q

Is energy required for Na-k-cl symporter?

A

No, K and Na are going down concentration gradient and they take Cl with them

45
Q

How is the gradient maintained in Na-K-Cl symporter

A

ATP-ase keeps pumping Na & K to keep gradient normal

46
Q

which class of diuretics lower urica acid

A

loop diuretics

47
Q

Loop diuretics also have weak _________ properties

48
Q

Give examples of loop diuretics

A

furosemide
bumetanide

49
Q

Most loop diuretics structure are derived from

A

sulfonamide groups

50
Q

which is the only loop diuretic that did not derive from sulfonamide

A

Ethacrynic acid

51
Q

use of loop diuretics

A

edema, HTN, heart failure

52
Q

what is the main toxicity of loop diuretics

A

Ototoxicity

53
Q

Effect of loop diuretics on potassium

A

Hypokalemia (potassium wasting)

54
Q

are loop diuretics potassium sparing or wasting

A

Potassium wasting

55
Q

location of action for thiazides

56
Q

What do thiazides target (transporter)

A

Na-Cl transporter

57
Q

Does the Na-Cl transporter in thiazides require ATP

A

No, Na is going down Concentration gradient and takes Cl with it. gradient is maintained by ATP-ase

58
Q

What percent of NA is reabsorbed from DCT

59
Q

thiazides structure derives from

A

sulfanilamide

60
Q

effect of thiazides on potassium

A

potassium wasting

61
Q

WHich two classes of diuretics are potassium wasting

A

Thiazides and loop diuretics

62
Q

examples of thiazides

A

Chlorothiazide, hydrochlorothiazide

63
Q

use of thiazide

A

HTN, HF, nephrogenic diabetes insipidus

64
Q

toxicities thiazides may cause

A

hypokalemia
hyperuricemia
impaired carbohydrate tolerance
hyperlipidemia

65
Q

why are loop diuretics more effective than thiazides

A

more Na is physiologically reabsorbed at loop of henle than at DCT

66
Q

Which two diuretics are potassium sparing

A

Inhibitors of renal epithelia Na channels
mineralcorticoid receptor antagonist (MRA)

67
Q

where do inhibitors of renal epithelia Na channels operate

A

Late distal tubule and collecting duct

68
Q

Which channel do inihitors of renal epithelia in NA channel act on

A

Na-k channels ( they are also used in combination with other diuretics)

69
Q

how do inhibitors of renal epithelia affect movement of K and Na

A

They inhibit K excretion and Na entrance

70
Q

examples of inhibitors of renal epithelia

A

Amiloride, triamtrene

71
Q

Clinical use of amiloride and triamtrene

A

Used in adjunctive tretament with thiazides and loop diuretics in HF and HTN

72
Q

Toxicities related to inhibitors of renal epithelia

A

hyperkalemia

73
Q

Contraindications while taking inhibitors of renal epithelia

A

K+ supplements
ACE inhibitors

74
Q

What are the only diuretics that do not act within the tubular lumen

A

MRA (mineralocorticoid receptor antagonists)

75
Q

Where do MRA drugs act

76
Q

What do mineralocortecoid receptors do?

A

Produce mRNA and produce Na channel

77
Q

MRA mechanism of action

A

Binds mineralocorticoid receptor in late distal tubule and collecting duct

78
Q

give an example of MRA drug

A

Spironolactone

79
Q

Uses of MRA drugs

A

HTN, HF
aldosteronism

80
Q

Toxicities related to using MRA drugs

A

Hyperkalcemia
gynecomastia

81
Q

Contraindications of MRA drugs

A

K supplements and ACE inhibitors

82
Q

K supplements and ACE inhibitors are contraindications related to which two diuretics

A

MRA and inhibitors of renal epithelia NA

83
Q

hyperkalemia is a toxicity related to which twodiuretics

A

The potassium sparing ones (MRA, inhibitors of renal epithelia)

84
Q

What is vasopressin

A

Antidiuretic hormone

85
Q

How to vasopressin antagonists work?

A

antagonize vasopressin

86
Q

main objective of vasopressin is to

A

increase BP

87
Q

Two vasopressins and their functions

A

V1- constrict blood vessels
V2- Fluid reabsorption from kidney

88
Q

mechanism by which Vasopressin increases renal conservation of H20

A

V2 receptors insert aquaporins into membrane, increasing permeability of water, causing BP to increase. Vasopressin blockers block this action

89
Q

Examples of vasopressin blockers

A

conivaptan
tolvaptan

90
Q

site of action if luminal side for drugs except for which two types

A

aldosterone inhibitors and vaptan inhibitors

91
Q

how does renal failure affect diuretic action

A

secretion of diuretics decrease with renal failure, reducing effectiveness.

92
Q

are diuretics secreted or filtered

93
Q

why are diuretics secreted and not filtered

A

because CA-I, thiazides and loop diuretics are highly bound to proteins

94
Q

hydrochlorothiazide effect on blood glucose

A

May increase it

95
Q

hydrochlorothiazide effect on ca

A

Decreases Calcium

96
Q

which one is more effective, increasing a dose for a single diuretic or combining diuretics with different mechanisms

A

Combining diuretics with different mechanisms

97
Q

explain braking phenomenon

A

diuretics decrease body weight due to Na excretion exceeding intake, this increases water excretion leading BW and ECFV to decrease. A new steady state is achieved when Na intake and excretion are equal but at a lower ECFV and weight. This results from activation of RAAS and SNS.

when diuretic is DX, BW and ECFV rise where Na intake exceeds excretion. New steady state reached.

98
Q

how do thiazides affect uric acid levels

A

thiazides increase uric acid

99
Q

amiloride causes hyper or hypo kalemia

A

Hyperkalemia

100
Q

Triamtrene effect on K

A

K increasing

101
Q

hydrochlorothiazide effect on Ca

A

Decreases Ca

102
Q

Hydrochlorothiazide effect on blood glucoseq

A

Increases BG

103
Q

what drug can furosemide not be used wuth

A

Gentamicin

Therapeutics P2 (41 decks)

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