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FRACP Exam > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is a phase 1 clinical trial?

A

Test the toxicitiy of the drug/ maximum tolerated dose/determine side effects

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2
Q

What is a phase 2 clinical trial?

A

Determine the best dose schedule/dosing regime/determine activity

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3
Q

What is a phase 3 clinical trial?

A

Determine outcomes of the drug - progression free survival, tumou response rate ectr

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4
Q

What is phase 4 clinical trial?

A

Post-marketing monitoring - ongoing adverse effects ect

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5
Q

Formula for bioavailability

A

F(po)=AUC(po)/AUC(IV)

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6
Q

Formula for T1/2

A

T1/2= (VDx0.693)/Cl

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7
Q

Formula for loading dose

A

LD= VDx target concentration (divided by PO bioavail if PO drug)

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8
Q

What are the units for clearance?

A

Volume/Time ( e.g L/min)

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9
Q

How do you calculate therapeutic index?

A

TI= Adverse effect at EC50/Therapeutic effect at EC50

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10
Q

Volume of distribution is measued in what unit?

A

Volume = so if given VD as L/Kg - need to multiply by body weight to get the unit as L only

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11
Q

How do you calculate VD (without T1/2)

A

VD = absorption/Plasma concentration.

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12
Q

What happens to VD if lipid or water ?

A

Lipid soluble- VD increase
Water soluble- VD decreased

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13
Q

How to calculate steady state concentration?

A

CPss= F/dosing interval

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14
Q

What is bioequivalence?

A

90% confidence intervals need to be within 80-125% of the Cmax or AUC of the original drug.

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15
Q

HLA for abacavir metabolism?

A

B57:01 - TEN

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16
Q

Why cant you use tamoxifen and SSRI?

A

Tamox activated by CYP2D6, SSRI inhibit 2D6 –> tamoxifen not metabolised to active form

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17
Q

What are substrates for CYP3A4?

A

Ciclosporin, warfarin, midazolam, oestrogen

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18
Q

What are substrates for P-glycoprotein?

A

Dabigatran, digoxin

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19
Q

What are CYP2D6 substrates?

A

Codeine, tramadol, tamoxifen

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20
Q

What activates clopidogrel?

A

CYP2C19 - there is genetic variation in this so its ineffective in some

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21
Q

What are INDUCERS of CYP3A4

A

St johns wart, carbamazipine, phenytoin, rifampicin

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22
Q

What is the importance of an inducer?

A

LOWER the drug concentration by INCREASING metabolism.

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23
Q

What are CYP3A4 inhibitors?

A

Itrakonazole, ketoconazole, macrolides, ritonavir

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24
Q

What is the importance of CYP Inhibitors?

A

INCREASE drug concentration by REDUCED metabolism

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25
Q

What enzyme is important in Azathioprine metabolism?

A

TMPT activity - low TPMP = give lower dose

25
Q

What enzyme is important in Azathioprine metabolism?

A

TMPT activity - low TPMP = need lower dose.
Otherwise make excess 6TGN leading to toxicities like marrow supression

26
Q

What is the main elimination of digoxin and dabigatran?

A

Excreted unchanged = RENAL

27
Q

What are the PK changes in the elderly?

A

Reduced renal flow = increased conc drugs with high FU
Higher fat = Inc VD for lipophilic drugs -> inc T1/2 (e.g benzos)
Reduced Water - Reduced VD for hydrophilic drgs - Gent

28
Q

What are the features of Anti-depressant withdrawal?

A

F- flu-like symptoms
Insomnia
Nausea
Imbalance
Sensory disturbances
Hyperarousal

29
Q

How do ACEi cause angioedema?

A

ACE metabolises bradykinin into degradation product, inhibition of this + lack of C1 esterase in familial angioedema

30
Q

What happens to levels of valporate, phenytoin, leveteracetam and lamotragine in pregnancy?

A

Levles reduced either due to increased metabolism by BYP incudction or increased renal clearance

31
Q

What effect does cirrhosis have on metabolism of drugs?

A

Fibrosis -> inc portal vein pressure –> reduced first pass metabolism/reduced hepatic flow, increased bioavailability

32
Q

How does portal vein thrombosis effect hepatic metabolism?

A

Reduced flow, reduced metabolism, reduced clearance, increased bioavailability

33
Q

How do you calculate hepatic clearance?

A

C; = hepatic flow ( Q) x extraction ratio

34
Q

Drugs with highhepatic ratio are rapidly broken down by liver enzymes, changes to what have the most significant effect on hepatic clearance?

A

Hepatic blood flow - cirrhoisis/ portal vein thrombosis, shock, heart failure

35
Q

Drugs with low hepatic ratio/clearance are not rapidly broken down in the liver, their metabolism is most sensitive to changes in what?

A

Enzyme induction/inhibition

36
Q

If you alkylate the urine, what does that do to basic drug excretion?

A

Increase excretion

37
Q

How to calculate VD?

A

Vd= Ab (amount of drug in the body)/CD ( concentration of drug)

38
Q

How to calculate Loading dose?

A

Loading Dose = VD x target Cp/ Bioavailability

39
Q

CL= ?

A

Cl = RE rate of elimination (mg/hr)/Cp concentration Mg/L)

40
Q

What is zero order kinetics?

A

The AMOUNT of drug eliminated is a set unit per time, in first order kinetics it is a set concentration per unit time

41
Q

What causes a high anion gap metabolic acidosis? MUDPILES

A

Methanol, Uremia, Diabetic ketoacidosis (or alcoholic ketoacidosis,) Paraldehyde, Iron (or Isoniazid,) Lactic acidosis, Ethylene glycol, and Salicylates

41
Q

What causes a high anion gap metabolic acidosis? MUDPILES

A

Methanol, Uremia, Diabetic ketoacidosis (or alcoholic ketoacidosis,) Paraldehyde, Iron (or Isoniazid,) Lactic acidosis, Ethylene glycol, and Salicylates

42
Q

What are the features of the anticholinergic toxidrome?

A

(TCAs) Dry mouth, dilated pupils, tachycardia, constipation, urinary retention, delirium, febrile

43
Q

What are the features of the cholinergic toxidrome? (organophosphate insectisides)

A

Bradycardia, miosis, rhinorrhoea, diarrhoea, diaphoresis, urinary and fecal incontinence, fasciculations, vomiting, sweating.

44
Q

What differentiates Neuroleptic malignant syndrome from serosonin syndrome?

A

LEAD pipe rigidity in NMS, not in SS

45
Q

TCA overdose syndrome?

A

Wide QRS from Na channel blockade, bradycardia, Seizures, drowsy, delirium, agitation, mydriasis

46
Q

How do you treat TCA overdose if wide QRS?

A

Sodium bicarb

47
Q

What are fatures of serotonin syndrome>

A

Mental status change, agitation, myoclonus, hyperreflexia, diaphoresis, trmor, incoordination (SSRI)

48
Q

What is the antidote for organophosphate poisoning?

A

Atropine

49
Q

What is the antidote for b-blocker OD?

A

Glucagon/ioprenalin

50
Q

What is the antidote for iron overdose?

A

Desferrioxamine

51
Q

What is the antidote for triocyclic overdose?

A

Bicarbonate

52
Q

What is the treatment of Methaemoglobinaemia?

A

Methylene blue

53
Q

What Cyp enzyme leads to production of NAPQI?

A

Cyp2E1

54
Q

What induced CYP2E1

A

Chronic alcoholism - leads to paracetamol toxicity as more is shunted down NAPQI pathway

55
Q

What inhibits CYP2E1?

A

Acute alcohol intake
Rifampin, phenytoin, crabamaz, barbiturates

56
Q

What is glutathione?

A

Active enzyme in NAC to breakdown NAPQI into non-toxic metabolites (cystine and mecapturic acid)

57
Q

How can you tell CCB fr Beta blocker OD?

A

CCB - high BSL, insulin release dependent on calcium channels normally
Beta block - get HYPOglycaemia

58
Q

What molecule is deficient in G6PD that protects against red cell oxidative stress?

A

Glutathione

FRACP Exam (15 decks)

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