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Systems: Urinary AB > Clinical Pharmacology > Flashcards

Clinical Pharmacology Flashcards

1
Q

What are 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 a small number of drugs such as insulin and vit D
  • Excretion of active drugs or their metabolites
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2
Q

What will there be a rapid build up of if renal function is impaired?

A
  • Active drug

- Toxic or active metabolites

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3
Q

What type of drugs do not present a problem in renal impairment?

A

Drug or metabolites which have a high therapeutic index or low toxicity such as benzylpenicillin

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4
Q

What can drugs/metabolites which have a narrow therapeutic index cause in renal impairment?

A

Toxicity or death

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5
Q

What can gentamicin cause?

A

Renal or ototoxicity

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6
Q

What can digoxin cause?

A

Arrhythmia, nausea or death

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7
Q

What can lithium cause?

A

Renal toxicity and death

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8
Q

What can tacrolimus cause?

A

Renal and CNS toxicity

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9
Q

What may dramatically influence the pharmacokinetics or pharmacodynamics of the drugs?

A

Renal function

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10
Q

Why do we worry about renal impairment in people in hospital?

A
  • Sick
  • Volume depleted
  • Hypotensive
  • Prescribed a large number of potentially reno-toxic agents
  • All factors interact to generate de novo renal impairment or worsen pre existing renal impairment/toxicity
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11
Q

What are the 3 mechanisms of renal excretion?

A
  • Glomerular filtration
  • Passive tubular reabsorption
  • Active tubular secretion
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12
Q

What will changes in mechanisms of renal excretion due to disease, age or drug therapy change?

A

Will automatically change drug pharmacokinetics and pharmacodynamics

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13
Q

Why does renal impairment prolong the half life of certain drugs?

A
  • All drugs and their metabolites are filtered at the glomerulus
  • Renal impairment will therefore prolong the half life of all drugs or their metabolites cleared by this route
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14
Q

What care needs to be taken due to the prolonged half life of drugs in renal impairment?

A

Prolongation of half-life means that extra care must be taken when using drugs with a low therapeutic index in the presence of renal impairment

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15
Q

Give examples of high half-life differs for certain drugs in renal impairment

A
  • Benzylpen 0.5h>8h
  • Gentamicins 2.5h>50h
  • Atenolol 6h>100h
  • Digoxin 36h>120h
  • Glibenclamide 10h>100h
  • Chlopropramide 36h>200h
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16
Q

What does a reduction in GFR result in?

A
  • Reduced clearance of drugs by the kidney resulting in accumulation
  • Protein binding is reduced
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17
Q

What must be carried out during drug administration in someone with reduced GFR clearance?

A
  • Reduce dosage
  • Increased dose interval
  • TDM monitor blood levels for toxic drugs like gentamicin, lithium, digoxin and vancomycin
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18
Q

In what ways does renal disease alter the actions of drugs on the tissues?

A
  • 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 a-blockers
  • There may be an increased tendency to bleed beware warfarin or NSAIDs
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19
Q

How can the direct nephrotoxic actions of drugs be described in patients with renal disease?

A

Synergistic

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20
Q

When will gentamicin toxicity be unmasked?

A

When used in conjunction with furosemide or lithium

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21
Q

How can renal impairment alter pharmacokinetics?

A
  • Increase t1/2
  • Build up of drugs or metabolites
  • Decreases in protein binding. So more free drug available
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22
Q

How can renal impairment alter pharmacodynamics?

A
  • Increased sensitivity to pharmacological action

- Increased sensitivity to toxicity and ADRs

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23
Q

How can renal impairment affect combined therapies?

A

Can increase the sensitivity to the toxic effects of combined therapy

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24
Q

What do we need to know about drugs before administering them to patients with renal impairment?

A
  • Drugs which can be safely used with decreased eGFR

- Drugs which have a narrow therapeutic index may present problems

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25
Q

What considerations need to be made when prescribing in impaired renal function?

A
  • Risk/benefit ratio
  • Severity of possible side effects
  • Severity of toxicity
  • The availability of TDM
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26
Q

Ideally if a patient suffers from renal impairment we should use drugs which:

A
  • Have a high therapeutic index

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

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27
Q

Why is hypertension common in renal disease?

A
  • Hypertension causes renal damage

- Renal damage causes hypertension

28
Q

What types of drugs would usually be used for hypertension?

A
  • Thiazide type diuretics
  • CCBs
  • ACEIs
29
Q

Why are conventional anti-hypertensives a problem in renal disease?

A
  • They have a low GFR, hyperuricaemia

- They are more sensitive to the hypotensive actions of Antihypertensives

30
Q

What is the solution to hypertension in renal disease?

A

We can tackle the problem in two ways.

  • Use drugs which are totally metabolised by the liver or else where in the body (ACEI are potentially nephrotoxic)
  • Use reduced dose of the drug with longer dosing periods. i.e. atenolol 25mg/day or on alternate days.
31
Q

What can ACEI cause?

A

Severe acute renal dysfunction

32
Q

What can direct vasodilators cause?

A

Profound hypotension and salt and water retention

33
Q

What can thiazide type diuretics cause?

A

Precipitate gout

34
Q

What is a common cause of morbidity and mortality in hospitalised patients when it comes to the kidneys?

A

Adverse drug reaction that affect the kidneys as toxic renal effects often remain silent until too late

35
Q

How do kidneys get damaged by drugs?

A
  • The kidney is particularly vulnerable to drugs and other agents that cause renal damage
  • Any drug in the blood will eventually reach kidneys
  • May potentially cause drug-induced renal failure
  • If the drug is primarily cleared by the kidney, it will be increasingly concentrated as it is moves from the glomerulus and along the renal tubules
  • The concentrated drug exposes the kidney tissue to far greater drug concentration per surface area
36
Q

What types of renal damage can occur?

A
  • AKI
  • Acute tubular necrosis
  • Chronic kidney disease
  • Inflammatory disorders
37
Q

What forms does renal involvement commonly take?

A

Salt and water abnormalities

  • Dehydration
  • Oedema

AKI

  • Acute tubular necrosis
  • Acute interstitial nephritis

Chronic renal failure

38
Q

What may happen to patients subjected to unnecessary and radical surgery?

A

May die

39
Q

What are the 4 major syndrome that drug induced renal toxicity can cause?

A
  • Acute renal failure
  • Nephrotic syndrome
  • Renal tubular dysfunction with potassium wasting
  • Chronic renal failure
40
Q

Define ARF

A
  • A sudden detioration in renal function which results in a rapid rise in creatinine
  • Urine volume falls to < 400ml/day in 40% of patients.
41
Q

Who is usually affected by ARF?

A

Often elderly patients who are sick, have a poor fluid intake, who are on multiple medications and who are not being monitored aggressively.

42
Q

How can ARF be classified?

A
  • Prerenal
  • Renal or intrinsic
  • Post renal or obstructive
43
Q

What are pre-renal causes of ARF?

A

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

Increased catabolism
-Steroids, tetracycline’s

Vascular occlusion
-Oestrogens/OCP

44
Q

What are the 3 types of renal or intrinsic ARF?

A
  • Acute tubular necrosis
  • Acute interstitial nephritis
  • Thrombotic micro angiography
45
Q

What drugs can 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
46
Q

When does the onset of acute interstitial nephritis occur?

A

Onset after drug exposure 3-5 days with a second exposure, to as long as several weeks with a first exposure.

47
Q

How can the latency period vary in acute interstitial nephritis?

A

Latency period may be as short as 1 day with rifampicin, or as long as 18 months with an NSAID.

48
Q

What drugs are implicated in acute interstitial nephritis?

A
  • Penicillin’s
  • Cephalosporin’s
  • Cocaine
  • Sulphonamides
  • NSAIDs
  • Diuretics
  • Lithium
  • Ranitidine
  • Omeprazole
  • Captopril
  • Phenytoin
  • Valproic acid
  • Amphotericin B
  • Streptokinase
  • 5-aminosalicylates
  • Allopurinol
  • Rifampicin
  • Chinese herbs
49
Q

What can thrombotic microangiography cause?

A

Severe acute renal failure

50
Q

What is the pathological hallmark of thrombotic microangiography?

A

Thrombi in the microvasculature of many organs

51
Q

What changes occur in the kidney with thrombotic microangiography?

A

Afferent arteriolar and glomerular thrombosis

52
Q

What drugs can cause thrombotic microangiography?

A
  • Cyclosporin, tacrolimus
  • Chemotherapeutic agents mitomycin C bleomycin, cisplatin
  • Ticlopidine, clopidogrel
  • 19 estrogen-containing oral contraceptives
  • Quinine
  • Cocaine
53
Q

What sites can drug associated obstruction of urine outflow occur?

A
  • Within the tubules or the ureters (due to crystal formation)
  • Outside the ureters due to retroperitoneal fibrosis caused by agents such as methysergide.
54
Q

What drugs are implicated in crystal formation?

A
  • Acyclovir, indinavir
  • Sulfonamides,
  • Triamterene
  • Methotrexate,
  • Vitamin C in large doses (due to oxalate crystals).
  • Guaifenesin and ephedrine can also cause stones to form in kidneys
55
Q

What is nephrotic syndrome due to and marked by?

A

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

56
Q

What drugs are implicated in nephrotic syndrome?

A
  • Gold,
  • NSAIDs,
  • Penicillamine,
  • Interferon,
  • Captopril
57
Q

What are the recognised adverse renal effects of nonselective NSAIDs include:

A
  • Acute renal failure,
  • Nephrotic syndrome,
  • Hypertension,
  • Hyperkalemia,
  • Papillary necrosis
58
Q

What is the epidemiology of AKI?

A
  • 20% of hospital admissions due to AKI are drug related
  • Most are community acquired
  • AKI affects 7% of hospitalized patients, and 20-30% of critically ill patients,
59
Q

What drugs are responsible for hospital acquired renal insufficiency?

A
  • Aminoglycosides 18%
  • NSAIDs 13%
  • Piperacillin/tazobactam 7%
  • Amphotericin B 6%
  • Trimethoprim’s/sulfs 65
  • Cyclosporine 3%
  • ACEI 2%
  • Multiple nephrotoxins (>3) 2%
  • Ciprofloxacin, cis-platinum, acyclovir, ceftazidime 1%
60
Q

What does the most common type of NSAID induced acute renal failure result from?

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 blood flow is already reduced
61
Q

What type of reaction occurs in NSAID- induced acute allergic interstitial nephritis?

A

Idiosyncratic reaction

62
Q

What drugs are particularly prone to NSAID induced acute allergic interstitial nephritis?

A

Propionic acid derivatives (ibuprofen, naproxen and fenoprofen)

63
Q

What is NSAID-induced acute allergic interstitial nephritis associated with in 90% of cases?

A

Nephrotic syndrome

64
Q

What is the mechanism of aminoglycoside induced renal injury?

A

Proximal tubular injury leading to cell necrosis

65
Q

How can sepsis treatment lead to nephrotoxicity?

A

Aminoglycoside antibiotics, used in severe gram-negative sepsis, cause nephrotoxicity in 10% to 20% of therapeutic courses.

66
Q

What is the most common renal damage due to drugs?

A

Acute renal failure due to ATN is the most common and is due to aminoglycosides

Systems: Urinary AB (26 decks)

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