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Urinary system > Clinical pharmacology in renal disease > Flashcards

Clinical pharmacology in renal disease Flashcards

1
Q

List the functions of the kidneys

A
  • Excretion of metabolic waste products
  • Regulation of extracellular volume
  • Regulation of ionic concentration
  • Regulation of physiological pH
  • The metabolism of hormones such as insulin and vit D
  • Excretion of active drugs or their metabolites
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2
Q

What side effects are associated with gentamicin?

A

– Gentamicin may cause renal or ototoxicity

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3
Q

What side effects are associated with digoxin?

A

– Digoxin may cause arrhythmia, nausea or death

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4
Q

What side effects are associated with lithium?

A

– Lithium may cause renal toxicity and death

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5
Q

What side effects are associated with tacrolimus?

A

– Tacrolimus may cause renal and CNS toxicity

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6
Q

What effect does GFR in renal impairment have on pharmacokinetics?

A

Increased half life of drugs due to decreased excretion (GFR is reduced in renal impairment)

This leads to accumulation

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7
Q

How do you combat an increased half life of a drug in the renal impaired?

A

– Reduce dosage
– Increase dose interval
– Therapeutic drug monitoring (TDM) - Monitor blood levels for toxic drugs like gentamicin, lithium, digoxin, vancomycin

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8
Q

Give some examples of drugs closely monitored due to their toxicity?

A

gentamicin
lithium
digoxin
vancomycin

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9
Q

Describe the pharmacodynamic effects in renal impairment

A

Renal disease alters the actions of drugs on the tissues

  • The blood brain barrier becomes more permeable and the brain becomes more sensitive to tranquillisers, sedatives and opiates
  • Circulatory volume may be reduced making the patient sensitive to antihypertensive agents ACEIs or α-blockers
  • There may be an increased tendency to bleed beware warfarin or NSAIDs
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10
Q

When renal impairment causes the BBB to become more permeable, the brain becomes more sensitive to what drugs?

A

tranquillisers, sedatives and opiates

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11
Q

What are the effects of renal impairment on the pharmacology of drugs?

A

Dramatic alterations in pharmacokinetics
• Increased t1/2
• Build up of drug or metabolites
• Decrease in protein binding (more free drug available)

Alteration in Pharmacodynamics
• Increased sensitivity to pharmacological action
• Increased sensitivity to toxicity and ADRs

Increased sensitivity to the toxic effects of combined therapy

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12
Q

What drugs should be ideally used in patients with renal impairment?

A

– Have a high therapeutic index and

– Are metabolised by the liver with the production of non-toxic metabolites

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13
Q

What hypertension drugs are affected by renal impairment?

A
  • ACEIs are commonly recommended however they can produce severe acute renal dysfunction and are not used in women of childbearing age
  • Direct vasodilators can produce profound hypotension and salt and water retention
  • Thiazides/thiazide-type diuretics may precipitate gout
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14
Q

How can drug induced renal disease present?

A

Salt and water abnormalities
– Dehydration – can cause renal impairment
– Oedema

Acute renal failure
– Acute tubular necrosis
– Acute interstitial nephritis

Chronic renal failure

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15
Q

Define acute renal failure

A
  • Definition - a sudden deterioration in renal function which results in a rapid rise in creatinine
  • Urine volume falls to < 400ml/day in 40% of patients
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16
Q

What are the 3 categories for causes of acute renal failure?

A
  • Prerenal – dehydration (diuretics)
  • Renal or Intrinsic – nephrotoxicity (gentamicin)
  • Post renal or Obstructive
17
Q

List some pre-renal causes of drug induced renal disease

A

Water and electrolyte abnormalities
• Diuretics, laxatives, lithium, NSAIDs

Increased catabolism
• Steroids, tertracyclines

Vascular occlusion
• Oestrogens/ OCP – not as prevalent now due to lower doses

18
Q

List the 3 types of intrinsic acute renal failure

A
  • Acute tubular necrosis (ATN)
  • Acute interstitial nephritis
  • Thrombotic microangiopathy
19
Q

Describe acute tubular necrosis

A
  • Occurs very rapidly
  • ATN is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. Common causes of ATN include low blood pressure and use of nephrotoxic drugs.
20
Q

List some drugs that cause acute tubular necrosis

A
  • Aminoglycoside antibiotics
  • Amphotericin B
  • Cisplatin - causes renal failure in up to 25% of patients after a single dose
  • Radiocontrast agents
  • Statin drugs given in combination with immunosuppressive agents such as cyclosporin can cause renal failure
21
Q

Describe Acute interstitial nephritis

A
  • Intrinsic acute renal failure with onset after drug exposure 3-5 days, usually on second exposure, to as long as several weeks with a first exposure.
  • Latency period may be as short as 1 day with rifampicin, or as long as 18 months with an NSAID.
22
Q

List some drugs that cause acute interstitial nephritis

A
  • Penicillins
  • Cephalosporins
  • Cocaine
  • Sulfonamides
  • NSAIDs
  • Diuretics
  • Lithium
  • Ranitidine
  • Omeprazole
  • Captoprim
  • Phenytoin
  • Valproic acid
  • Amphotericin B
  • Streptokinase
  • 5-aminosalicylates
  • Allopurinol
  • Rifampin
  • Chinese herbs
23
Q

Describe Thrombotic microangiopathy

A

Type of intrinsic acute renal failure

  • Thrombotic microangiopathy can cause:
  • Severe acute renal failure.
  • Pathologic hallmark is thrombi in the microvasculature of many organs.
  • Changes in the kidney include afferent arteriolar and glomerular thrombosis
24
Q

List some drugs that cause thrombotic microangiopathy

A
  • Calcineurin inhibitors: cyclosporin, tacrolimus
  • Chemotherapeutic agents: mitomycin C, bleomycin, cisplatin
  • Inhibitors of platelet aggregation: ticlopidine, clopidogrel
  • 19 estrogen-containing oral contraceptives
  • Quinine
  • Cocaine
25
Q

List some drug related causes of post-renal or obstructive uropathy

A

Drug-associated obstruction of urine outflow can occur at several sites:
• Within the tubules or the ureters (due to crystal formation)
• Outside the ureters due to retroperitoneal fibrosis caused by agents such as methysergide

26
Q

List some drugs that can cause crystal formation within tubules or ureters of the kidneys

A
  • Acyclovir – cold sores
  • Indinavir
  • Sulfonamides
  • Triamterene
  • Methotrexate
  • Vitamin C in large doses (due to oxalate crystals) - supplements
  • Guaifenesin and ephedrine can also cause stones to form in kidneys
27
Q

Describe nephrotic syndrome

A

The nephrotic syndrome is due to glomerular dysfunction and marked by heavy proteinuria.

Nephrotic syndrome is a collection of symptoms due to kidney damage. This includes protein in the urine, low blood albumin levels, high blood lipids, and significant swelling. Other symptoms may include weight gain, feeling tired, and foamy urine. Complications may include blood clots, infections, and high blood pressure.

28
Q

List some drugs known to cause nephrotic syndrome

A
  • Gold - rheumatology
  • NSAIDs
  • penicillamine
  • Interferon
  • Captopril – rarely used now
29
Q

List the adverse renal effects associated with NSAID-induced nephropathy

A
  • Acute renal failure
  • Nephrotic syndrome
  • Hypertension
  • Hyperkalemia,
  • Papillary necrosis
30
Q

What % of hospital admissions due to AKI are drug related?

A

20%

31
Q

What % of hospitalised patients are affected by AKI?

A

7%

32
Q

What % of hospitalised patients who are critically ill are affected by AKI?

A

20-30% of critically ill patients

33
Q

What drug is responsible for most hospital acquired renal insufficiency?

A

Aminoglycosides

34
Q

Describe NSAID-induced pre-renal acute renal failure

A
  • The most common type of NSAID-induced acute renal failure results from decreased synthesis of renal vasodilator prostaglandins, which can lead to reduced renal blood flow and reduced glomerular filtration.
  • Patients become susceptible to acute renal failure if their renal blood flow is already reduced.
35
Q

Describe aminoglycoside induced renal injury

A
  • Aminoglycoside antibiotics, used in severe gram-negative sepsis, cause nephrotoxicity in 10% to 20% of therapeutic courses.
  • Mechanism is proximal tubular injury leading to cell necrosis.
36
Q

Describe NSAID-induced acute allergic interstitial nephritis

A
  • Idiosyncratic reaction
  • Particularly to the propionic acid derivatives (ibuprofen, naproxen, and fenoprofen),
  • Associated with nephrotic syndrome in about 90% of cases
37
Q

What is the most common form of AKI?

A

Acute tubular necrosis

Urinary system (22 decks)

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