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Renal/Urology > Lecture 20 - Clinical Pharmacology of Renal Disease > Flashcards

Lecture 20 - Clinical Pharmacology of Renal Disease Flashcards

1
Q

How does renal disease affect clinical pharmacology?

A

Renal dysfunction –> rapid build up of active drug/toxic/active metabolites

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2
Q

What features of drugs make them okay to use in renal disease?

A

If the drug has a high therapeutic index or a low toxicity

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3
Q

Give egs of 4 drugs with narrow therapeutic indexes that should be avoided in renal disease and what may happen if the level of the drug goes above the therapeutic index

A

Gentamicin - renal/ototoxicity
Digoxin - arrhythmias, naussea, death
Lithium - renal toxicity, death
Tacrolimus - renal and CNS toxicity

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4
Q

What are the 3 methods of renal excretion?

A

Glomerular filtration
Passive tubular resorption
Active tubular secretion

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5
Q

Are all drugs/their metabolites filtered at the glomerulus? Which drugs aren’t if not?

A

Yes

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6
Q

Renal impairment prolongs what of every drug cleared by the kidneys?

A

Half life (so be careful using drugs with a low therapeutic index in renal impairment)

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7
Q

A reduction in GFR in kidney disease leads to what?

A

Reduced clearance of drugs –> accumulation

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8
Q

What must things must you consider when prescribing for someone with renal dsiease?

A

Reduce dose
Increase dose interval
TDM - monitor level, e.g. for gentamicin, lithium, digoxin etc.
Consider changing drug

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9
Q 
Renal disease alters the actions of drugs on different tissues. Describe the effect on:
- Blood brain barrier
- Circulatory volume
- Bleeding
in those with renal disease
A

Blood brain barrier becomes more permeable so pts more sensitive to tranquilisers/sedatives/opiates
Circulatory volume may be reduced, pt more sensitive to anti-HTNs
May be increased tendency to bleed, be aware of NSAIDs/warfarin

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10
Q

How is protein binding affected in kidney disease?

A

Can be reduced so more free drug is available

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11
Q

Ideally if a patient suffers from renal impairment we should use drugs that -

A

Have a high therapeutic index and are metabolised by the liver to non-toxic metabolites

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12
Q

What is the link between HTN and renal disease?

A

HTN causes renal disease and vice cersa

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13
Q

What is the issue with treating HTN in renal disease?

A

They are more sensitive to hypotensive actions of antihypertensive agents

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14
Q

What is the problem with using ACEi in renal disease?

A

They may produce severe acute gout

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15
Q

What is the issue with using direct vasodilators in renal disease?

A

May cause profound hypotension and salt and water retention

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16
Q

What is the issue with using thiazides/thiazide type diuretics in renal disease?

A

May precipitate gout

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17
Q

Drug induced renal toxicity can causes what 4 major syndromes?

A

Acute renal failure
Nephrotic syndrome
Renal tubular dysfunction with potassium wasting
Chronic renal failure

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18
Q

What is acute renal failure?

A

Sudden deterioriation in renal function leading to a rapid rise in creatinine

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19
Q

Who often gets acute renal failure?

A

Elderly pts who are sick, have poor fluid intake, on multiple meds + are not being monitored aggressively

20
Q

How is acute renal failure categorised?

A

Prerenal
Renal/intrinsic
Postrenal or obstructive

21
Q

What are causes of pre-renal drug induced renal failure?

A

Due to water and electrolyte abnormalities - diuretics, laxatives, NSAIDs, lithium

Due to increased catabolism - steroids, tetracyclines

Due to vascular occlusion - oestrogen/OCP

22
Q

What are the three types of intrinsic acute renal failure?

A

Acute tubular necrosis
Acute interstitial nephritis
Thrombotic microangiopathy

23
Q

What is the most common cause of AKI?

A

Acute tubular necrosis

24
Q

What is ATN?

A

Necrosis of the renal tubular epithelial cells leading to kidney dysfunction

25
Q

Is ATN reversible?

A

If treated in the early stages it can be

26
Q

What are the two main causes of ATN?

A

Ischaemia and nephrotoxins

27
Q

What things causing ischaemia may lead to ATN?

A

Shock

Sepsis

28
Q

What nephrotoxins may lead to ATN?

A 
Aminoglycosides
Myoglobin secondary to rhabdomyolysis
Radiocontrast agents
Lead
Cisplatin 
Amphotericin B
29
Q

What are features of ATN?

A

Raised urea, cr, K

Muddy brown casts in the urine

30
Q

What are the histopathological features of ATN?

A

Tubular epithelial necrosis - loss of nuclei and detachment of tubular cells from the basement membrane
Dilatation of tubules may occur
Necrotic cells obstruct the tubule lumen

31
Q

What are the three phases of ATN?

A

Oliguric
Polyuric
Recovery

32
Q

What are causes of acute interstitial nephritis?

A

Drugs (most common, esp antibiotics) - penicillin, rifampicin, NSAIDs, allopurinol, furosemide, omeprazole, cocaine
Systemic disease - SLE, sarcoidosis, Sjogren’s
Infection - Hanta virus, staphylococci

33
Q

What is the histopathology of acute interstitial nephritis?

A

Marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

34
Q

What are the clinical features of acute interstitial nephritis?

A

Fever, rash, arthalgia
Eosinophilia
Mild renal impairment
Hypertension

35
Q

What do you see when you investigate the urine of someone with acute interstitial nephritis?

A

Sterile pyuria

White cell casts

36
Q

What is the pathological hallmark of thrombotic microangiopathy?

A

Thrombi in the microvasculature of many organs

37
Q

What changes in the kidney occur in thrombotic microangiopathy?

A

Afferent arteriolar and glomerular thrombosis

38
Q

What drugs can precipitate thrombotic microangiopathy?

A 
Cyclosporin, tacrolimus
Chemotherapeutic agents, e.g. cisplatin, bleomycin
Clopidogrel
Quinine 
Oestrogen containing contraceptives
Cocaine
39
Q

What drugs are implicated in crystal formation in the urinary tract?

A 
Aciclovir, indinavir
Sulfonamides
Triamterene
Methotrexate
Vit C
40
Q

What drugs can cause a nephrotic syndrome?

A

Gold
NSAIDs
Penicillamine
Interferon

41
Q

What are the most recognised adverse renal effects of NSAIDs?

A 
Acute renal failure
Nephrotic syndrome
HTN
Hyperkalaemia
Papillary necrosis
42
Q

What is the most common type of NSAID induced acute renal failure resulting from?

A

Decreased synthesis of renal vasodilator prostaglandins –> reduced renal blood flow + reduced glomerular filtration

43
Q

What is the mechanism by which aminoglycosides are nephrotoxic?

A

Proximal tubular injury –> necrosis

44
Q

Define contrast media nephrotoxicity

A

25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media

45
Q

What are risk factors for contrast media nephrotoxicity?

A 
Known renal impairment (esp. diabetic nephropathy)
Age >70 years
Dehydration 
Cardiac failure
Use of nephrotoxic drugs, e.g. NSAIDs
46
Q

How long does contrast induced nephropathy tend to occur after administration?

A

2-5 days

47
Q

How can contrast media nephrotoxicity be prevented?

A

IV 0.9% NaCl at a rate of 1ml/kg/h for 12h pre and post procedure

Renal/Urology (29 decks)

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