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Pharmacology Flashcards

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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
What has the greatest impact on drug metabolism in old age.
Reduced hepatic blood flow
26
Causes of impact of drug metabolism in old age?
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
27
Drugs and pregnancy
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
28
Inhibition p- glycoprotein leads to?
An increase in blood drug concentration | P-glycoprotein is an efflux pump
29
P-glycoprotein substrates
``` Digoxin Antineoplastic drugs ( docetaxel, vincristine) Calcineurin inhibitors (cyclosporin, tacrolimus) Macrolides (clarithromycin) CCB (amlodipine) Protease inhibitors Rivaroxaban Ticagrelor Loperamide Steroids ```
30
P-glycoprotein inhibitors
``` Macrolides (clarithromycin, erythromycin) Verapamil Amiodarone Ritonovir Antifungals (e.g. itraconazole) Ticagrelor ```
31
P-glycoprotein inducers
Rifampicin St John’s Wort Carbamazepine Phenytoin
32
Stimulators receptors of alcohol
GABA-A 5-HT3 NMDA
33
Stimulators receptor of benzodiazepines
GABA-A
34
Stimulatory receptors of Cocaine
Binds to Dopamine transporter | Blocks dopamine re-uptake from synapse
35
Stimulatory receptor of heroin
Mu-opioid receptors
36
Methamphetamine
Binds to dopamine transporter | Blocks dopamine re-uptake from synapse
37
Stimulatory receptor of nicotine
Nicotine can - stimulates dopamine release
38
Hysteresis
Positive hysteresis: clockwise = tachyphylaxis | Negative hysteresis: anti-clockwise = drug distribution to site of action
39
Adverse drug reactions
``` SSRIs - platelet dysfunction Gentamicin - ototoxicity Omeprazole - interstitial nephritis Sitagliptin - pancreatitis Atypical antipsychotics - metabolic syndrome Anti convulsants - suicidality ```
40
Type A ADR
Dose related Frequent Usually occurs in preclinical / trial phase No immunological basis
41
Type B ADR
Dose relationship unclear Infrequent Occurs post marketing Immunological basis e.g. anaphylactic
42
Severe skin reactions: DRESS
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
Stevens-Johnson Syndrome vs Toxic epidermal necrosis
SJS: 1-10% skin detachment TEN: >30% skin detachment SJS-TEN overlap: 10-30% skin detachment
44
Acute generalised Exanthematous pustulosis
Widespread erythema followed by sterile pustules, fever, neutrophilia
45
Drug-gene pairs
Azathioprine and TPMT Warfarin and VKOR Cetuximab and KRAS Codeine and CYP2D6
46
What drug will minimise cardiac toxicity in amitriptyline overdose?
Sodium bicarbonate - redistribution of unionised drug away from toxic component
47
MIC Type 1
Concentration dependent killing and prolonged persistent effects Aminoglycosides, daptomycin, fluroquinolones Goal of therapy = maximise concentrations PK/PD parameter: peak/MIC; 24h AUC/ MIC
48
MIC Type II
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
MIC Type III
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
Antioxidant required for conversion of paracetamol metabolite NAPQI to non-toxic substances?
Glutathione
51
MOA lumacaftor / Ivacaftor
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
Tenofovir - patterns of kidney injury
Proximal tubular dysfunction, AKI, CKD | Leads to increased creatinine, proteinuria, glycosuria, hypophosphatemia, acute tubular necrosis
53
Drugs that cause pulmonary fibrosis
``` Antineoplastic agents (Bleomycin, busulfan, cyclophosphamide) Nitrofurantoin Amiodarone Flecanide Penicillamine ```
54
Mechanism by which dobutamine increases cardiac output
Activation of beta adrenergic receptors
55
Ionotropes
Agents that increase myocardial contractility (inotropy) | E.g. adrenaline (beta receptors), dobutamine ( beta 1 and 2 receptors), isoprenaline, ephedrine
56
Vasopressors
Agents that cause vasoconstriction = increased systemic and/or pulmonary vascular resistance E.g. noradrenaline (alpha receptors), vasodilatory, metaraminol, vasopressin, methylene blue
57
Entresto (Sacubitril / Valsartan)
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
Medications that cause hyponatremia
Diuretics (esp indapamide and HCT) SSRIs (e.g. fluoxetine, sertraline) SNRIs (e.g. venlafaxine) Carbamazepine
59
THC MOA
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
Carbamazepine MOA
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
Aprepitant MOA
Antagonise substance P / neurokinin-1 receptors Augments antiemetic activity of 5-HT3 receptor antagonists Inhibits acute and delayed phases of chemotherapy induced emesis
62
Serotonin Syndrome
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
Drug-drug interactions
- 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
Glucagon indications
Beta blocker overdose with cardio genie shock or profound bradycardia unresponsive to atropine CCB overdose with heartblock unresponsive to calcium
65
Flumazenil
Competitive antagonist at benzodiazepine receptors Use in bento overdose DO NOT USE in mixed overdose with proconvulsant drugs (TCAs, antihistamines, amphetamines)
66
Anticholinergic (antimuscarinic) toxidrome
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
Location and action of alpha 1 receptors
Peripheral, renal and coronary circulation | Vasoconstriction
68
Location and action of beta 1 receptors
Heart | Increase contractility and HR
69
Location and action of beta 2 receptors
Lungs; peripheral and coronary circulation | Vasodilation, bronchodilation
70
Location and action of dopaminergic receptors
Mesenteric, renal, coronary arteries | Vasodilation
71
Aramine receptor and mechanism
Works solely on the alpha-adrenergic system | Peripheral vasoconstriction
72
Isoprenaline receptors and mechanism
Works solely on the beta-adrenergic system | Inotrophy and chronotrophy (causes tachycardia)
73
Neuroleptic malignant syndrome
``` Onset: days to weeks Neuromuscular findings: bradyreflexia, severe muscle rigidity, normal pupils Causative agents: dopamine antagonists Treatment: bromocriptine Resolution: days to weeks ```
74
Malignant hyperthermia
``` 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
Paracetamol overdose
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
Agonist vs antagonist
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
Phase I clinical trial
Focus on pharmacology - mode of delivery, dose finding, dosing schedule May include healthy participants
78
Phase II clinical trial
Focus on safety Also pharmacology and efficacy Usually subjects with disease, n<100
79
Phase III clinical trial
Focus on efficacy Subjects with disease n: 100-1000s Done after preliminary evidence suggests effectiveness of the drug
80
Phase IV clinical trial
Focus on long-term safety Post marketing surveillance E.g. use of registries
81
Carbamazepine and contraception
Carbamazepine can reduce efficacy of oral and implantable hormonal contraceptives by inducing cytochrome P450 enzymes, which increase clearance of sex hormones
82
Anticholinergic toxicity
Signs: delirium, tachycardia, dry, flushed skin, dilated pupils (mydriasis), myoclonus, increased temp, urinary retention Agents: TCAs, atropine, benztropine, antihistamines
83
Cholinergic toxicity
Signs: confusion, CNS depression, weakness, salivation, lacrimation, incontinence, GI cramping, emesis, diaphoresis, muscle fasiculations, miosis, hypotension, seizures

BPT Written (16 decks)

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