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MRCP Revision > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

MOA of Pilocarpine? (Indication: Glaucoma)

A

Stimulation of muscarinic cholinergic receptors to increase aqueous humour outflow resulting in ciliary contraction (contraction of the iris), which will increase aqueous humour outflow, miosis, and accommodation.

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2
Q

MOA Latanoprost? (Indication Glaucoma)

A

Increasing uveoscleral outflow of aqueous humour by activating prostaglandin receptors

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3
Q

MOA: Dorzolamide? (Indication glaucoma)

A

Reduce the production of aqueous humour by inhibition of carbonic anhydrase

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4
Q

Mechanism of Aspirin?

A

irreversibly inhibits cyclooxygenase-1 (COX-1) enzyme which inhibits the production of thromboxane A2

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5
Q

MOA of Ciclosporin and Tacrolimus?

A

inhibit calcineurin thus decreasing IL-2

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6
Q

MOA Fleclanide?

A

potent sodium channel blocker (specifically the Nav1.5 sodium channels

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7
Q

MOA of LMWH?

A

Low-molecular weight heparin activates antithrombin III. Forms a complex that inhibits factor Xa

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8
Q

Digoxin:
MOI?
Indications?
Notable SEs?

A

inhibition of the Na+/K+ ATPase pump (Slows rate via AV and positive inotropic affect)
Rate control, symptoms in HF (specific indications)
SE = arrythmias, confusion, yellow/green vision, gynaecomastia

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9
Q

INDUCERS of cytochrome P450 (PC BRASS)

A

Phenytoin, Carbamazepine, Barbiturates, Rifampicin, Alcohol (chronic), Sulphonylurea, Smoking,

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10
Q

Inhibitors of cytochrome P450 (CRACK AMIGOS)

A

Cimetidine, Ritonavir, Amiodarone, Ciprofloxacilin, Ketoconazole, Acute alcohol use, Macrolides, Isoniazid, Grapefruit juice, Omeprazole, Sulfonamides

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11
Q

MOI Pilocarpine?

A

Muscuranic Agonist

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12
Q

Pharmacokinetics: what is phase 1 metabolism?

A

oxidation - Addition of oxygen or removal of hydrogen atom
reduction - Gain of electrons or hydrogen atoms
hydrolysis - add water to a drug molecule resulting in its breakdown to more polarised forms

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13
Q

Pharmacokinetics: what is phase 2 metabolism? (Conjugation)

A

Products are typically inactive and excreted in urine or bile

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14
Q

What is first past metabolism?

A

a phenomenon where the concentration of a drug is greatly reduced before it reaches the systemic circulation due to hepatic metabolism. As a consequence much larger doses are need orally than if given by other routes

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15
Q

What is zero order kinetics?

A

describes metabolism which is independent of the concentration of the reactant. This is due to metabolic pathways becoming saturated resulting in a constant amount of drug being eliminated per unit time

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16
Q

T/F 50% UK population are deficient in Acetylator status which affects metabolism of key drugs?

A

True
Drugs affected:
isoniazid
procainamide
hydralazine
dapsone
sulfasalazine

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17
Q

Mnemonic for zero order kinetics:
Zero Alcohol Is Allowed

A

Police (Phenytoin)
Stop (Salicylate)
Heavy (Heparin)
Drinkers (Ethanol)

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18
Q

Mnemonic for drugs affected by acetylator status:
SHIPpeD

A

Sulfosalazine. Hydralazine. Isoniazid. Procainamide. Dapsone

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19
Q

Mnemonic for first past metabolism drugs:
Nitrates Have A Very Large Pre Systemic Intake

A

Nitrates, hydrocortisone, aspirin, verapamil, lignocaine, propranolol, iSoSorbide dinitrate, Isoprenaline, Testosterone

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20
Q

MOA of Quinolones (e.g. ciprofloxacilin)

A

Inhibits DNA synthesis by inhibiting topoisomerase

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21
Q

MOA Macrolides (e.g. Clarithromycin)

A

Binds to 50S subunit, inhibiting translocation (movement of tRNA from acceptor site to peptidyl site)

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22
Q

MOA of tetracyclines (e.g. doxycycline)

A

Binds to 30S subunit blocking binding of aminoacyl-tRNA

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23
Q

MOA Aminoglycosides? (Gentamicin)

A

Binds to 30S subunit causing misreading of mRNA

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24
Q

MOA of Penicilins, cephalosporins, carbapenems?

A

Inhibit the cross-linking of peptidoglycans in bacterial cell walls

25
Q

MOA Metronidazole?

A

DNA Damage

26
Q

MOA Sulphonamides, trimethoprim?

A

Inhibits folic acid formation

27
Q

MOA Rifampicin?

A

Inhibits RNA synthesis

28
Q

What drug is indicated, when you suspect adrenaline induced ischaemia during local infiltration?

A

Phentolamine (Competitive a-adrenoreceptor antagonist)

29
Q

MOA Metformin?

A

activation of the AMP-activated protein kinase (AMPK)

30
Q

Aetiology of heparin induced thrombocytopenia?

A

Antibodies against complexes of platelet factor 4 (PF4) and heparin

31
Q

Monitoring blood test for:
1) Unrationed Heparin
2) LMWH

A

1) APTT
2) Anti-factor Xa

32
Q

Infliximab:
Indication:
Target:

A

Crohns
TNFa

33
Q

Rituximab
Indication:
Target:

A

Non-Hodgkins
CD20

34
Q

Daratumumab
Indication:
Target:

A

Multiple Myeloma
CD38

35
Q

Alemtuzumab
Indication:
Target:

A

chronic lymphocytic leukaemia
CD52

36
Q

Trastuzumab (more commonly known as Herceptin)
Indication:
Target:

A

metastatic breast cancer
HER2

37
Q

What is the mechanism of aminoglycoside neprhotoxicity?

A

Acute tubular necrosis

38
Q

Pathophysiology of paracetamol induced hepatotoxicity?

A

Paracetamol overdose occurs when glutathione stores run-out leading to an increase in NAPQI (N-acetyl-p-benzoquinone imine)

39
Q

T/F Ciprofloxacilin side effects -> everything is increased (Fluid, BP, K+, Hair, Gums, Glucose)

A

True

40
Q

How does COCP use affect the incidence of the following cancers:
1) Breast + Cervical
2) Ovarian + Endometrial

A

1) Increased risk
2) Decreased risk

41
Q

Drugs which can be cleared with Hemodialysis (BLAST)

A

BARBITURATE
Lithium
Alcohol (inc methanol, ethylene glycerol)
Salicylates
Theophyllines

42
Q

MOA of heparin?

A

Enhances activity of circulating antithrombin

43
Q

1mg of prednisone is equivalent to how much hydrocortisone?

A

4mg hydrocortisone

44
Q

1mg Dexamethasone is equivalent to Hoe much prednisone?

A

7mg Prednisolone

45
Q

How do class one anti arrhythmias work?

A

Inhibit sodium channels
-Amiodarone/ Lidocaine/ Phenytoin / Flecainide

46
Q

How do class two anti arrhythmias work?

A

Beta blockers
-propranolol
-Esmolol

47
Q

How do class 3 anti arrhythmias work?

A

Potassium Channel Blocker
-Sotalol
-Amiodarone

48
Q

How do class 4 anti arrhythmias work?

A

Calcium channel blocker
-Verapamil
-Diltiazem

49
Q

How do class 5 anti arrhythmias work?

A

Unexplained
-Adenosine / Digoxin / K+ ions / Mg Ions

50
Q

MOA of furosemide?
(lasix)

A

Inhibiting chloride absorption in the ascending loop of Henle
(Lasix = lasts 6 hours)

51
Q

MOA of Bendroflumethaizide?

A

Inhibiting sodium absorption at the beginning of the DCT

52
Q

What is ‘DRESS’ syndrome?

A

Drug reaction with eosinophilia and systemic symptoms
-Triad: Extensive skin rash, pyrexia, organ involvement

53
Q

Cyanide Poisoning
-Presentation
-Signs
-Pathophysiology of poisoning
-Tx:

A

-Factory worker rescued from fire (burning plastics)
-Headache, bitter smell, red, ashen, hypoxic
-Inhibition of cytochrome C Oxidase leading to cessation of mitochondrial electron transfer chain
-IV Hydroxocobalamin
(Alternatives: inhaled amyl nitrate / IV Sodium thiosulfate)

54
Q

Where is the most common defect implicated in Catecholaminergic polymorphic ventricular tachycardia (VPVT)?
-Gene defect
-Inheritance pattern

A

-Ryanodine receptor (RYR2) found on myocardial sarcoplasmic reticulum
-Autosomal Dominant

55
Q

Brugada Syndrome
-Inheritance pattern
-Gene mutation

A

-Autosomal dominant
-SCN5a which encodes the myocardial sodium ion channel protein

56
Q

Congenital Cyanotic heart disease:
-Most common at birth
-Most common overall

A

-Transposition of the great arteries
-Fallots

57
Q

4 most common congenital acyanotic heart diseases?

A

-VSD
-ASD
-PDA
-Coarctation of the aorta

58
Q

Patient Ductus Arteriosus
-Acyanotic or cyanotic
-Where is the abnormal connection
-Management

A

-Acyanotic
-Pulmonary trunk and descending aorta
-Indomethacin
(However, may use prostaglandin E1 to keep open if awaiting surgical repair)

59
Q
A

MRCP Revision (17 decks)

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