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Case 10: Urinary System > Pharmacology: Renal & Drugs > Flashcards

Pharmacology: Renal & Drugs Flashcards

1
Q

What is the most common route for drug/metabolite elimination

A

Kidneys

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2
Q

What occurs during renal failure with drug concentration

A

Drugs/active metabolites can accumulate & cause toxicity

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3
Q

What is 3 processes of drug elimination

A
  1. Glomerular filtration rate
  2. Passive tubular reabsoprtion
  3. Active tubular secretion
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4
Q

What is the equation for total renal elimination of a drug

A

Filtration + secretion - reabsorption

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5
Q

What 3 drugs are metabolized in the kidneys

A
  1. Insulin
  2. Vitamin D activation
  3. Kidneys produce EPO
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6
Q

What is the consequence of renal failure & diabetics use

A

Decrease insulin dosage

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7
Q

What is the consequence of renal failure & vitamin D use

A

Give vitamin D in active form

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8
Q

What is the consequence of renal failure & anaemia use

A

EPO can not be produced & exogenous EPO must be administered

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9
Q

What is the 2 criteria’s for prescribing in renal failure

A
  1. Check if drug can be used
  2. Dose adjustment
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10
Q

What diuretics dose must be adjusted in renal failure & how

A

Loop diuretic & increase dosage

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11
Q

What markers are used to monitor renal function

A

eGFR
Creatinine

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12
Q

What is a way of clearing drugs from system

A

Dialysis

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13
Q

What drugs should be used w/ caution in renal failure

A

Drugs that increase potassium

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14
Q

What does mechanism does loop diuretics inhibit

A

NK2Cl transporter

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15
Q

Where does loop diuretics work

A

Thick ascending limb

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16
Q

What is the efficacy of loop diuretics

A

High ceiling effect, the higher the dose the higher the effect

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17
Q

What drugs is an example of a loop diuretic

A

Furosemide

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18
Q

What is the 5 adverse effects w/ loop diuretics

A
  1. Hypokalaemia due to blocking of trasporter
  2. Decreased magnesium due to less potassium transport
  3. Increase urate due to inhibition of efflux MRP4 transporter
  4. Hypersensitivity
  5. Ototoxicity
19
Q

What is the best route to administer furosemide

A

IV as variable oral bioavailability

20
Q

What is the 3 clinical indicators of furosemide use

A
  1. Moderate-severe fluid overload
  2. IV in pulmonary oedema
  3. HPT w/ renal failure
21
Q

What does mechanism does thiazide diuretics inhibit

A

Na/Cl transporter

22
Q

Where does thiazide diuretics work

A

At the DCT

23
Q

What is the efficacy of thiazide diuretic

A

Moderate w/ maximal diuresis

24
Q

What is the 5 adverse effects of thiazide diuretics

A
  1. Hypokalaemia
  2. Hyponatraemia
  3. Increase urate
  4. Impaired glucose tolerance
  5. Slight increase LDL & TG
25
Q

What is the 3 clinical indicators of thiazide use

A
  1. HPT
  2. Mild-moderate fluid overload
  3. Synergy w/ loop diuretics (can cause over diuresis)
26
Q

What is the 4 clinical indicators of aldosterone antagonist diuretic use

A
  1. Primary hyperaldosteronism
  2. Secondary hyperaldosteronism & increased fluid (cardiac failure, nephrotic syndrome & cirrhosis)
  3. Refractory HPT
  4. Synergy w/ loop/thiazide diuretic to balance K loss
27
Q

What is the 2 adverse effects of aldosterone antagonist diuretics

A
  1. Hyperkalaemia
  2. Gynecomastia
28
Q

What is the efficacy of aldosterone antagonist diuretic

A

Low-moderate

29
Q

What is an example of aldosterone antagonist diuretic

A

Spironolactone (steroid aldosterone antagonist)

30
Q

How does aldosterone antagonist work & where

A

K sparing diuretic by reducing Na reabsorption at collecting duct

31
Q

What diuretics should not be used in renal failure

A

Potassium sparing diuretics

32
Q

What is the 2 benefits of ACE-I in renal failure

A

Slow/prevent progression of renal failure, especially in diabetes
Reduce proteinuria in nephrotic syndrome

33
Q

What is the 2 harms of ACE-I in renal fialure

A

Risk of ­K+ in renal failure
Can cause pre-renal failure by inhibiting angiotensin mediated constriction of efferent arteriole (e.g., bilateral renal artery stenosis, with NSAIDs, hypovolaemia)

34
Q

What 2 hormones normal maintain renal blood flow

A
  1. Prostaglandin mediate vasodilation in afferent arteriole
  2. Angiotensin 2 mediate vasoconstriction in efferent arteriole
35
Q

When does prostaglandin have a effect on renal blood flow

A

Decrease effective circulating volume

36
Q

What is the 2 mechanism of drug induced nephrotoxicity in pre-renal failure

A
  1. Hypovolaemia
  2. Reduce renal blood flow or pressure
37
Q

What 2 factors reduce renal blood flow or pressure

A

NSAIDS block vasodilation prostaglandin that causes vasoconstriction
ACE-I dilate efferent arteriole

38
Q

What 2 drugs causes drug induced nephrotoxicity in acute tubular necrosis

A

Amino-glycoside & amphotericin B

39
Q

What is important when giving drugs that can cause acute tubular necrosis

A

Monitor renal function

40
Q

What is the 2 mechanism of drug induced nephrotoxicity in interstitial nephritis

A
  1. Hypersensitivity reaction
  2. AKI
41
Q

What is the 2 effect of NSAIDS on the kidneys

A

Block prostaglandin synthesis which dilate afferent glomerular arteriole that reduce renal blood flow & GFR
Increase NaCl & water reabsorption leading to fluid overload

42
Q

What renal disease can NSAIDs cause

A

Interstitial nephritis

43
Q

What is the 3 uncommon mechanisms of nephrotoxicity

A
  1. Obstruction
  2. Nephrotic syndrome
  3. Thrombotic angiopathy
44
Q

What is the 3 types of obstruction that can cause nephrotoxicity

A
  1. Crystals
  2. Retroperitoneal fibrosis
  3. Papillary necrosis

Case 10: Urinary System (8 decks)

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