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BPT Written > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

CYP3A4 inducers

A 
D - Dexamethasone
R - Rifampicin
J - St John’s Wort
A - Chronic Alcohol 
P - Phenytoin and Carbimazole

Inducer = increase rate of another drug’s metabolism

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2
Q

CYP3A4 inhibitors

A 
G - Grapefruit juice
R - Ritonavir
A - Azoles
C - CCBs
E - Erythromycin/ Clarithromycin
O - Omemprazole
C - Cimetidine

Inhibitor = inhibits metabolism of another drug (i.e. co-prescribed medication level can rise)

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3
Q

How many half lives does it take to reach steady state?

A

5 half lives (97%)

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4
Q

Formula for half life of a drug?

A

T1/2 = 0.693 x Vd/Cl

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5
Q

What is the formula for maintenance infusion rate of a drug?

A

DR = CL x Css

DR = maintenance dose rate (mg/hr)
CL = Clearance (L/hour)
CSS = steady state drug concentration (mg/L)
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6
Q

What is the formula for the loading dose of a drug?

A

Loading dose = Vd x target plasma concentration

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7
Q

What is the formula for volume of distribution?

A

Vd = amount of drug in body (A) / plasma drug concentration (C)

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8
Q

What is the formula for bioavailability?

A

Non-IV AUC / IV AUC

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9
Q

Pharmacokinetics

A

What the body does to the drug
Describes the relationship between the dose and the unbound drug concentration at the site of action and the time course of drug concentration in the body

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10
Q

Pharmacodynamics

A

What the drug does to the body
Describes the relationship between the unbound drug concentration at the receptor and the drug response (i.e. therapeutic effect)

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11
Q

Drug disposition

A

Absorption, distribution, metabolism, excretion

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12
Q

Parameters in pharmacokinetics

A

Clearance (CL) - efficacy of elimination of a drug from the body
Volume of distribution (V) - relationship between drug concentration in the blood and drug in the tissue at the site of action
Half life

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13
Q

Definition of Clearance

A

The volume of blood cleared per unit time

Determines the maintenance dose rate required to achieve target plasma concentration at steady state

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14
Q

Formula for extraction ratio

A

Extraction ratio = 1 - (concentration out / concentration in)

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15
Q

Definition of steady state

A

Situation at which the rate of drug administration is equal to the rate of drug elimination
At steady state: elimination = maintenance dose rate

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16
Q

Definition of elimination

A

Amount of drug eliminated per unit time ‘mg/hr’
Directly proportional to the plasma drug concentration
Directly proportional to the clearance

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17
Q

Statin muscle related adverse events

A

Risk is substantially increased when taking statins metabolised by CYP3A4 e.g. Lovastatin, Simvastatin and Atorvastatin
Less risk with Pravastatin
Taking other drugs that INHIBIT CYP3A4 increase risk
Risk is greater at higher doses
SLO1B1 gene
Onset usually weeks to months after initiation

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18
Q

Reduced capacity to metabolise codeine related to which cytochrome?

A

Reduced activity of P450 2D6

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19
Q

Thiopurine methyltransferase (TPMT) homozygous deficient patients

A

Azathioprine, mercatopurine and thioguanine are all pro drugs that are inactivated by TPMT

Low TPMT activity = high 6GTN levels = severe myelosuppression (need dose reduction)

High TMPT activity = low 6GTN levels = less therapeutic efficacy

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20
Q

Typical dose dependent (type A) adverse drug reaction to Cholinesterase inhibitors?

A

Bradycardia

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21
Q

Clinically significant interactions with grapefruit juice

A

Amiodarone, atorvastatin, cyclosporine, felodipine, simvastatin, tacrolimus

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22
Q

Factors increasing risk of muscle disorders with simvastatin and atorvastatin

A

CYP3A4 inhibitors
Disease states: DM, hypothyroidism, renal and hepatic disease
Advanced age
High dose
Medicines inhibiting metabolism by other means e.g. gemfibrozil

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23
Q

Zero order kinetics

A

Alcohol
Aspirin
Phenytoin
Theophylline

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24
Q

Hepatic clearance

A

hepatic clearance = Hepatic blood flow x extraction ratio

High hepatic extraction ratio: morphine, GTN, propranolol, CCB, haloperidol, antidepressants

Low hepatic extraction ratio: NSAIDs, diazepam, carbamazepine, phenytoin, warfarin

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25
Q

What has the greatest impact on drug metabolism in old age.

A

Reduced hepatic blood flow

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26
Q

Causes of impact of drug metabolism in old age?

A

Clearance
- CrCl declines 1% per year but serum Cr may be normal
- 40% reduction in blood flow, 30% reduction in liver mass
- age selective impairment of phase I > phase II
Vd
- decreased lean body mass, decreased body water, increased body fat (Vd decreased for water soluble drugs)
Half life: usually longer
Pharmacodynamics
- blunted homeostatic response
- impaired receptor systems e.g. cholinergic

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27
Q

Drugs and pregnancy

A

Increased HBF and RBF due to increased CO
Increased Vd
Decreased protein bindin

Isotretinoin: greatest risk in 1st trimester
Doxycycline: greatest risk in 3rd trimester

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28
Q

Inhibition p- glycoprotein leads to?

A

An increase in blood drug concentration

P-glycoprotein is an efflux pump

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29
Q

P-glycoprotein substrates

A 
Digoxin
Antineoplastic drugs ( docetaxel, vincristine)
Calcineurin inhibitors (cyclosporin, tacrolimus)
Macrolides (clarithromycin)
CCB (amlodipine)
Protease inhibitors 
Rivaroxaban
Ticagrelor
Loperamide 
Steroids
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30
Q

P-glycoprotein inhibitors

A 
Macrolides (clarithromycin, erythromycin)
Verapamil
Amiodarone
Ritonovir
Antifungals (e.g. itraconazole)
Ticagrelor
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31
Q

P-glycoprotein inducers

A

Rifampicin
St John’s Wort
Carbamazepine
Phenytoin

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32
Q

Stimulators receptors of alcohol

A

GABA-A
5-HT3
NMDA

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33
Q

Stimulators receptor of benzodiazepines

A

GABA-A

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34
Q

Stimulatory receptors of Cocaine

A

Binds to Dopamine transporter

Blocks dopamine re-uptake from synapse

35
Q

Stimulatory receptor of heroin

A

Mu-opioid receptors

36
Q

Methamphetamine

A

Binds to dopamine transporter

Blocks dopamine re-uptake from synapse

37
Q

Stimulatory receptor of nicotine

A

Nicotine can - stimulates dopamine release

38
Q

Hysteresis

A

Positive hysteresis: clockwise = tachyphylaxis

Negative hysteresis: anti-clockwise = drug distribution to site of action

39
Q

Adverse drug reactions

A 
SSRIs - platelet dysfunction 
Gentamicin - ototoxicity
Omeprazole - interstitial nephritis
Sitagliptin - pancreatitis 
Atypical antipsychotics - metabolic syndrome 
Anti convulsants - suicidality
40
Q

Type A ADR

A

Dose related
Frequent
Usually occurs in preclinical / trial phase
No immunological basis

41
Q

Type B ADR

A

Dose relationship unclear
Infrequent
Occurs post marketing
Immunological basis e.g. anaphylactic

42
Q

Severe skin reactions: DRESS

A

Drug Reaction Eosinophilia and Systemic Symptoms
Fever, rash organ involvement (liver, kidney then lungs)atypical lymphocytosis,
Lymphadenopathy, HHV-6 / EBV / CMV reactivation 3-8 weeks following initiation

43
Q

Stevens-Johnson Syndrome vs Toxic epidermal necrosis

A

SJS: 1-10% skin detachment
TEN: >30% skin detachment
SJS-TEN overlap: 10-30% skin detachment

44
Q

Acute generalised Exanthematous pustulosis

A

Widespread erythema followed by sterile pustules, fever, neutrophilia

45
Q

Drug-gene pairs

A

Azathioprine and TPMT
Warfarin and VKOR
Cetuximab and KRAS
Codeine and CYP2D6

46
Q

What drug will minimise cardiac toxicity in amitriptyline overdose?

A

Sodium bicarbonate - redistribution of unionised drug away from toxic component

47
Q

MIC Type 1

A

Concentration dependent killing and prolonged persistent effects
Aminoglycosides, daptomycin, fluroquinolones
Goal of therapy = maximise concentrations
PK/PD parameter: peak/MIC; 24h AUC/ MIC

48
Q

MIC Type II

A

Time dependent killing and minimal persistent effects
Carbapenems, cephalosporins, erythromycin, linezolid, penicillins
Goal of therapy = maximise duration of exposure
PK/PD parameter: T>MIC

49
Q

MIC Type III

A

Time dependent killing and moderate to prolonged persistent effects
Azithromycin, clindamycin, tetracyclines, vancomycin
Goal of therapy = maximise amount of drug
PK/PD parameter: 24h AUC/MIC

50
Q

Antioxidant required for conversion of paracetamol metabolite NAPQI to non-toxic substances?

A

Glutathione

51
Q

MOA lumacaftor / Ivacaftor

A

Lumacaftor: improves the processing and conformational stability of F508del CFTR, enabling more of the mature CFTR protein to be successfully transported to the cell surface

Ivacaftor: CFTR potentiator that facilitates increased chloride transport by potentiaiting the channel open probability of the CFTR protein at the cell surface

Improves lung function by 3% inpatients homozygous for the F508del- CFTR mutation

52
Q

Tenofovir - patterns of kidney injury

A

Proximal tubular dysfunction, AKI, CKD

Leads to increased creatinine, proteinuria, glycosuria, hypophosphatemia, acute tubular necrosis

53
Q

Drugs that cause pulmonary fibrosis

A 
Antineoplastic agents (Bleomycin, busulfan, cyclophosphamide)
Nitrofurantoin 
Amiodarone 
Flecanide
Penicillamine
54
Q

Mechanism by which dobutamine increases cardiac output

A

Activation of beta adrenergic receptors

55
Q

Ionotropes

A

Agents that increase myocardial contractility (inotropy)

E.g. adrenaline (beta receptors), dobutamine ( beta 1 and 2 receptors), isoprenaline, ephedrine

56
Q

Vasopressors

A

Agents that cause vasoconstriction = increased systemic and/or pulmonary vascular resistance
E.g. noradrenaline (alpha receptors), vasodilatory, metaraminol, vasopressin, methylene blue

57
Q

Entresto (Sacubitril / Valsartan)

A

Angiotensin receptor-neprilysin inhibitor (ARNI)
Designed to block harmful effects of RAAS activation while raising levels of several endogenous vasoactive peptides (inc BNP, bradykinin and adrenomedullin) which are typically degraded by neprilysin

58
Q

Medications that cause hyponatremia

A

Diuretics (esp indapamide and HCT)
SSRIs (e.g. fluoxetine, sertraline)
SNRIs (e.g. venlafaxine)
Carbamazepine

59
Q

THC MOA

A

Partial agonist activity at the cannabinoid receptor CB1 (located in CNS)
Results in a decrease in the concentration of the secondary messenger molecule cAMP through inhibition of adenylate cyclise

60
Q

Carbamazepine MOA

A

Prevents repetitive neuronal discharges by blocking voltage-dependent and use-dependent sodium channels
HLAB*1502 allele = increased risk of SJS
Steady state plasma concentration may not be achieved for 2-4 weeks because of autoinduction of metabolism

61
Q

Aprepitant MOA

A

Antagonise substance P / neurokinin-1 receptors
Augments antiemetic activity of 5-HT3 receptor antagonists
Inhibits acute and delayed phases of chemotherapy induced emesis

62
Q

Serotonin Syndrome

A

Hunter Criteria
Onset 24hrs
Must have taken a serotonergic agent and meet ONE of the following conditions :
- spontaneous clonus
- inducible clonus PLUS agitation or diaphoresis
- ocular clonus PLUS agitation or diaphoresis
- tremor PLUS hyperreflexia
- hypertonia + temp >38 + ocular clonus or inducible clonus

63
Q

Drug-drug interactions

A
  • Tamoxifen and Paroxetine (CYP2D6 inhibitor)
  • Azathioprine and allopurinol (TMPT)
  • Simvastatin and Erythromycin (P450 3A4)
  • Omeprazole and Clopidogrel (omeprazole inhibits CYP2C19, reducing metabolism of clopidogrel)
64
Q

Glucagon indications

A

Beta blocker overdose with cardio genie shock or profound bradycardia unresponsive to atropine
CCB overdose with heartblock unresponsive to calcium

65
Q

Flumazenil

A

Competitive antagonist at benzodiazepine receptors
Use in bento overdose
DO NOT USE in mixed overdose with proconvulsant drugs (TCAs, antihistamines, amphetamines)

66
Q

Anticholinergic (antimuscarinic) toxidrome

A

Pure anticholinergic agents: atropine, benztropine, benzhexol
Drugs with anticyclone effects: TCAs, antihistamines, antipsychotics

Peripheral anticholinergic effects: dry skin, dry mouth, mydriasis, urinary retention, GI ileus
Central anticholinergic effects: hallucinations, delirium, agitation, agression

Antidotal therapy = physostigmine

67
Q

Location and action of alpha 1 receptors

A

Peripheral, renal and coronary circulation

Vasoconstriction

68
Q

Location and action of beta 1 receptors

A

Heart

Increase contractility and HR

69
Q

Location and action of beta 2 receptors

A

Lungs; peripheral and coronary circulation

Vasodilation, bronchodilation

70
Q

Location and action of dopaminergic receptors

A

Mesenteric, renal, coronary arteries

Vasodilation

71
Q

Aramine receptor and mechanism

A

Works solely on the alpha-adrenergic system

Peripheral vasoconstriction

72
Q

Isoprenaline receptors and mechanism

A

Works solely on the beta-adrenergic system

Inotrophy and chronotrophy (causes tachycardia)

73
Q

Neuroleptic malignant syndrome

A 
Onset: days to weeks
Neuromuscular findings: bradyreflexia, severe muscle rigidity, normal pupils
Causative agents: dopamine antagonists
Treatment: bromocriptine
Resolution: days to weeks
74
Q

Malignant hyperthermia

A 
Caused by mutation of the ryanodine receptor (type 1)
Criteria 
- respiratory acidosis
- Arrhythmia (tachycardia, VT, VF)
- Metabolic acidosis
- muscle rigidity 
- muscle breakdown ( CK >20,000; cola coloured urine, excess myoglobin, hyperK)
- increased temp
- family history 
- reversal with dantrolene
75
Q

Paracetamol overdose

A

Cytochrome P450 2E1 and 3A4 convert paracetamol to highly reactive intermediary metabolite NAPQI
Normally NAPQI is detoxified by conjugation with glutathione
In overdose, sulfate and glutathione pathways become saturated -> more paracetamol shunted to P450 system to produce NAPQI -> hepatocellular supply of glutathione become depleted
Therefore NAPQI remains in its toxic form in the liver

76
Q

Agonist vs antagonist

A

Agonist - enhances target receptor’s usual action
Full agonist - able to elicit maximal response with higher doses
Partial agonist - unable to elicit maximal response despite higher dose

Antagonist - inhibits target receptor’s usual action
Competitive antagonist - reversible binding; maximal dose CAN be reached with higher dose of agonist
Non-competitive agonist - non-reversible binding. Maximum effect CANNOT be achieved with higher dose of agonist

77
Q

Phase I clinical trial

A

Focus on pharmacology - mode of delivery, dose finding, dosing schedule
May include healthy participants

78
Q

Phase II clinical trial

A

Focus on safety
Also pharmacology and efficacy
Usually subjects with disease, n<100

79
Q

Phase III clinical trial

A

Focus on efficacy
Subjects with disease
n: 100-1000s
Done after preliminary evidence suggests effectiveness of the drug

80
Q

Phase IV clinical trial

A

Focus on long-term safety
Post marketing surveillance
E.g. use of registries

81
Q

Carbamazepine and contraception

A

Carbamazepine can reduce efficacy of oral and implantable hormonal contraceptives by inducing cytochrome P450 enzymes, which increase clearance of sex hormones

82
Q

Anticholinergic toxicity

A

Signs: delirium, tachycardia, dry, flushed skin, dilated pupils (mydriasis), myoclonus, increased temp, urinary retention

Agents: TCAs, atropine, benztropine, antihistamines

83
Q

Cholinergic toxicity

A

Signs: confusion, CNS depression, weakness, salivation, lacrimation, incontinence, GI cramping, emesis, diaphoresis, muscle fasiculations, miosis, hypotension, seizures

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