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Renal > Drug-drug and drug-disease interactions > Flashcards

Drug-drug and drug-disease interactions Flashcards

1
Q

Types of drugs to consider

A
  • Prescribed drugs
  • Herbal remedies
  • OTC medications
  • Dietart factors
  • Lifestyle factors
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2
Q

What is drug interaction?

A

Modification of one drug’s actions by another

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3
Q

Individual variations to drugs

A
  • Loss of efficacy
  • Unexpected side-effects or toxicity
  • Types of variability are pharmacokinetic (different conc. of drug reaching site of action) and pharmacodynamic (different degree of response)
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4
Q

Effect on medication of being child

A
  • Drug metabolism slower - organs are immature
  • Renal excretion less efficient
  • Drug sensitivity changes
  • Body fat to mass changes
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5
Q

Effect on medication of being elderly

A
  • Failing organ function decreases drug metabolism
  • Renal excretion less efficient
  • Drug sensitivity changes as receptor numbers deplete
  • Poly-pharmacy and co-morbidities
  • Body fat and mass changes
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6
Q

Effect on medication of being pregnant

A
  • Decrease in plasma protein binding
  • Increased plasma volume and extracellular fluid
  • Increased cardiac output - increased renal blood flow and GFR = increased renal drug elimination
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7
Q

Pharmaco-genetics

A

how different individual genotypes relate to different drug responses

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8
Q

Pharmaco-genomics

A

pharmaco-genetics applied to whole human genome

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9
Q

Mixed function oxidases

A
  • Found in liver, often referred to as cytochrome P450 family
  • Good at breaking down meducations
  • Changes toxicity and effectiveness of drug
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10
Q

Ethnicity and drug response

A
  • Genetic differences account for some variations
  • Diet also important
  • ACEi not used in afro-caribbean background because of angio-oedema
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11
Q

CYP 1A2

A

Increases/decreases anti-psychotic drugs metabolism

Increases adverse reaction of traduce dyskinesia

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12
Q

CYP 2C9

A

Increases/decreases warfarin, phenytoin and losartan metabolism
Increases adverse reaction of bleeding, toxicity, ataxia and confusion

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13
Q

CYP 2C19

A

Increases/decreases diazepam, omeprazole metabolism

Increases adverse effects of prolonged sedation and acid suppression

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14
Q

CYP 2D6

A

Increases/decreases B-blockers metabolism

Increases adverse reaction to excessive bradycardia

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15
Q

Har,ful drug interactions

A
  • 15% of adverse drug reactions
  • Elderly, hepatic/renal impairment, polypharmacy (on multiple drugs) and pts on drug with narrow therapeutic range (phenytoin) are at increased risk
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16
Q

Pharmacodynamics

A
  • Agonism at receptor - 2 drugs of same/similar class (e.g. opioids competing for receptor)
  • Antagonism at receptor - opiate analgesics and naloxone, B-blockers and beta2 agonists
  • Non-selective nature of drug - antidepressants intercta with many receptor subtypes
  • Enhanced effect by other means - increased digoxin toxicity by hypokalaemia caused by loop diuretic e.g. furosemide
17
Q

Pharmacokinetics

A
  • ADME - 4 stages of pharmacokinetics (absorption, distribution, metabolism, excretion)
  • Parenterally = passes first pass metabolism
  • Excreted in urine and bile
18
Q

Absorption

A
  • Changes in gut motility - opiates and atropine slow gut down - Cmax and Tmax
  • Metoclopramide speeds gut up - Cmax and Tmax
  • Interfere with absorption and enterhepatic circulation - calcium salts bind tetracyclines in gut, cholestyramine binds warfarin and digoxin, activated charcoal binds drugs in gut after overdose
19
Q

Distribution

A
  • Many drugs alter distribution by displacing another drug from plasma or tissue binding sites
  • Causes transient increases in unbound drug
  • Subsequently corrected by increased elimination
  • Total drug concentration reduced but free value recovers at steady state
20
Q

Metabolism

A
  • 2 phase metabolism for many drugs
  • Liver is main site of metabolism
  • Drug → derivative → conjugate
  • Phase 1: CYP450 family, low substrate specificity metabolises a wide range of drugs
  • Phase 2: e.g. glucuronidation increases solubility and allows easier renal elimination , converted to active metabolite
21
Q

Enzyme inducing drugs

A
  • Warfarin and carbamezapine
  • Increased activity of cytochrome family
  • Warfarin metabolised quicker = failure of treatment
  • Drugs that induce CYP450 increase metabolism of other drugs and increase own metabolism
  • Carbamezapine induces CYP3A4 - warfarin is metabolised and carbamezepine causes faster warfarin clearance, reduced anticoagulant activity, therapy failure
22
Q

CYP 450 induction

A
  • Slow onset (1-2 weeks) because new enzyme production induced
  • Induction persists some time after stopping inducing drug and whilst enzyme levels normalise
  • Removing inducer will disturb equilibrium
  • Warfarin may have been adjusted so INR is stable despite interaction
  • Removal leads to reduced CYP3A4 activity - warfarin metabolism slows over 1-2 weeks, warfarin levels climb, risk of over-anticoagulation and bleeding
23
Q

Herbal remedy for depression

A

St John’s Wort

24
Q

Why is St John’s Wort dangerous

A

increases metabolism of oral contraceptive, digoxin, phenytoin, warfarin

25
Q

CYP 450 inducers

A 
Anticonvulsants
Antibiotics
Steroids
Alcohol
St John's Wort
HIV therapies
26
Q

Macrolide antibiotics and warfarin

A
  • All antibiotics kill gut bacteria - vit K falls, increased anticoagulant effect, increased INR
  • Macrolide antibiotics (clarithromycin) - inhibit CYP450, warfarin metabolism reduced, increased INR
27
Q

CYP 450 inhibition

A
  • Relatively quick onset
  • Related to half life and clearance of drug and plasma concentration at time of interaction
  • Usual effect is reduced metabolism of drugs - increased effect and toxicity
28
Q

CYP 450 inhibitors

A 
Anti-arrythmics
Antibiotics
Anti-ulcers
Antidepressants
HIV drugs
Statins
Sodium valproate
29
Q

QTc interval prolongation

A
  • Increased risk of lethal cardiac arrhythmia
  • Drugs may prolong this interval and cause torsade des pointes
  • Leads to PEA
  • Genetic and acquired forms
  • Ion channels and sympathetic abnormalities
  • QTc lengthened by anti-arrythmics
  • Another drugs prolong QT
  • Any drug impairs metabolism of QTc prolonging drug may cause long QT
30
Q

Drugs increasing risk of long QTs

A
  • Anti-arrythmics - quinidine, aotalol
  • Antibiotics - macrolides (erythromycin, clarithromycin)
  • Anti-fungal agents
  • Anti-histamines
  • Psychotropic drugs
  • Motility agents
31
Q

Hepatic disease

A

Decreased clearance of hepatically metabolised drugs
Decreased CYP450 activity
Increase half life and toxicity - classic is opiates in cirrhotic patients

32
Q

Renal disease

A

Reduced clearance of renal excreted drugs - digoxin
Increased electrolyte and fluid distributions = increased toxicity
Nephrotoxic drugs worsen renal function

33
Q

Cardiac disease

A

Decreased metabolism of drugs dependent on hepatic blood flow
Increased response to cardiovascular drugs

34
Q

Other diseases

A

Exacerbation of asthma by beta-blockers and NSAIDs

Decreased seizure threshold with some antibiotics like ciprofloxacin

35
Q

Grapefruit juice

A
  • Inhibits CYP450 isoenzymes
  • Decreased clearance of many drugs - simvastatin, amiodarone and terfenadine (long QT)
  • May lead to increased exposure of drugs
36
Q

Cranberry juice

A
  • Treats urinary sepsis
  • Inhibits bacterial adherence to urothelium
  • Inhibits CYP2C9 isoform - decreased clearance of warfarin, increased anticoagulant effect, increased risk of haemorrhage, pt should be advised not to drink if on warfarin

Renal (26 decks)

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