Pharmacology Flashcards

1
Q

Which drug inhibits Vitamin K dependant factor?

  • A ) Abciximab
  • B ) Aspirin
  • C ) Clopidogrel
  • D ) Dabigatran
  • E ) GbII/IIIa inhibitors
  • F ) Heparin
  • G ) Paracetamol
  • H ) Rivaroxaban
  • I ) Streptokinase
  • J ) Warfarin
A

Which drug inhibits Vitamin K dependant factor?

= J) Warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
A
  • *Answer: Phenytoin**
  • *Explanation:** About one-third of children whose mothers are taking this drug during pregnancy typically have intrauterine growth restriction with a small head and develop minor dysmorphic craniofacial features and limb defects including hypoplastic nails and distal phalanges
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A

Answer: Inhibit reabsorption of Na+ and Cl- in DCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
A
  • *Answer: MAOIs**
  • *Explanation:** MAOIs destroy the function of MAO -> unrestricted diet could increase the available tyramine. Tyramine is a naturally occurring trace amine derived from the amino acid tyrosine. Tyramine acts as a catecholamine releasing agent. Notably, it is unable to cross the blood-brain barrier, resulting in only non-psychoactive peripheral sympathomimetic effects following ingestion. A hypertensive crisis can result, however, from ingestion of tyramine-rich foods in conjunction with monoamine oxidase inhibitors (MAOIs).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
A

Answer: bronchospasm : β2 agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
A

Answer: NSAIDs (Indomethacin)

Explanation: Although Colchicine has been used to treat acute gout since the sixth century and is of proven efficacy, it should rarely be prescribed as a primary treatment because of its toxicity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
A

Answer: Clopidogrel

Explanation: ADP receptor inhibitors (e.g. clopidogrel and prasugrel) work by inhibiting platelet aggregation. This irreverisbly blocks ADP receptors, which in turn prevents expression of glycoprotein IIb/IIIa on the platelet surface. It is used in the management of ACS and during coronary stenting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
A

Answer: Blurred vision, dry mouth, urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
A

Answer: 4-5 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
A

Answer: Cephalosporins
Cephalosporins are beta-lactam antibiotics that inhibit cell wall synthesis and are therefore bactericidal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
A

Answer: Vitamin B6, peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
A

Answer: Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
A

Answer: Celecoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
A

Answer: Drowsiness, sedation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The ECG shown below is most commonly seen in what type of drug overdose?

  • A) Amphetamines
  • B) Cocaine
  • C) Paracetamol
  • D) SSRIs and SNRIs
  • E) TCAs
A

Answer: TCAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
A

Answer: antagonist, Vitamin K reductase

Explanation: Warfarin antagonises Vitamin K reductase, a co-enzyme that reduces activation of factors II, VII, IX and X. It initially has a pro-coagulant effect by inhibiting protein C and S; therefore it’s important to use heparin for atleast 48 hours until a therapeutic INR range has been reached.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
A

Answer: Postural hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
A

Answer: Hyperkalaemia

Explanation: Digoxin directly inhibits Na+/K+ ATP-ase in the sodium/potassium pump of the non-pacemaker cells of the heart and the smooth muscle of vessels. This means that there will be a slow leak of potassium outwards, and a slow leak of sodium inwards. The presence of hyperkalaemia is an earlier indicator of digitalis toxicity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
A

Answer: Flumazenil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q
A

Answer: Benzodiazepine receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
A

Answer: Via stimulation at the M2 receptor of the vagus nerve

Explanation: Digoxin exhibits its anti-arrhythmic effects via vagal nerve stimulation at the M2 receptor.

It does block Na+/K+ ATP-ase, but this increases cardiac inotropy.

By inhibiting the Na+/K+ ATPase, cardiac glycosides cause intracellular sodium concentration to increase. This enhances the ability for the cell to depolarise, and leads to an accumulation of intracellular calcium via the Na+/Ca2+ exchange system. In the heart, increased intracellular calcium causes more calcium to be released by the sarcoplasmic reticulum, thereby making more calcium available to bind to troponin-C, which increases contractility (inotropy).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
A

Answer: Verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
A

Answer: administration of N-acetylcysteine, glutathione

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
A

Answer: QTc; torsades de pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
A

Answer: Streptokinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
A

Answer: Early distal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
A

Answer: Thromboxane A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
A

Answer: Aspirin

Explanation: Aspirin’s anti-platelet action works by blocking the synthesis of thromboxane A2 from arachidonic acid in platelets (it does this by irreversibly inhibiting cyclooxygenase). Thromboxane A2 stimulates phospholipase C, which increases calcium levels and causes platelet aggregation. Aspirin also has analgesic, anti-inflammatory, and antipyretic actions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
A

Answer: Prednisone

Explanation: The patient’s history and symptoms indicate that he was most likely suffering from steroid-induced cataract development. Long-term therapy with a high dose of glucocorticoids has been associated with the development of posterior subcapsular cataracts, which occur in about 20% of patients treated for 1 year or more. Mifepristone and fludrocortisone are not used to treat rheumatoid arthritis, nor do they cause cataracts. Methotrexate, azathioprine, and cyclophosphamide are sometimes used to treat rheumatoid arthritis, but they do not cause cataract formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q
A

Answer: Clozapine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q
A

Answer: Lithium

Lithium is a common medication prescribed for bipolar depression. One complication of this medication is lithium nephropathy, which usually presents within the first month.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q
A

Answer: Rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
A

Answer: Polymixins

Polymixins are highly toxic antibiotics that destroy cell membranes. They have powerful gram-negative activity and are used for pseudomonas otitis externa (topical) and pseudomonas pneumonia in CF patients (nebulised).

34
Q
A

Answer: Theophylline

35
Q
A

= A

36
Q
A

Answer: Selegiline

37
Q
A

Answer: Monoamine oxidase and Aldehyde dehydrogenase

38
Q
A

Answer: Haloperidol

39
Q
A

Answer: Dexamethasone

Corticosteroids significantly reduce hearing loss and neurological sequelae but do not reduce overall mortality.

40
Q
A

Answer: Sedation

  • Sedation is a result of blocking H1 receptors.
  • Urinary retention, dry mouth, and blurred vision all occur due to blocking M receptors.
  • Postural hypotension occurs due to blocking alpha-1 receptors.
41
Q
A

Answer: Competitively antagonises acetylcholine action on muscarine receptors.

42
Q
A

Answer: Nifidepine

Dihydropyridine calcium channel blockers, such as nifidepine, mainly affect arterial vascular smooth muscle.

43
Q
A

Answer: Cyproheptadine

In patients with significant agitation and neuromuscular excitation, oral cyproheptadine may be used; a H1-, 5-HT1A-, and 5-HT2A-receptor antagonist.

In patients with severe serotonin toxicity who are unable to take oral medications, chlorpromazine may be used as an alternative drug for sedation.

44
Q
A

Answer: Bromocriptine

45
Q
A

Answer: Phenytoin and carbamazepine

46
Q
A

Answer: It is polar and metabolises in the periphery

Although there is no cure for Parkinson’s disease, many medications are available to control the symptoms. Some of these drugs will boost the production of dopamine in the brain. Others mimic the effects of dopamine. Interestingly, dopamine itself is not used. This is because the dopamine molecule is too polar to cross the blood-brain barrier, and thus cannot enter the brain. The most common treatment used contains the chemical L-dopa. This molecule is also polar, however, because it is an amino acid it is recognised by proteins that carry amino acids across the blood-brain barrier. L-dopa is therefore safely transported across the interface.

47
Q
A

Answer: Ipratropium

48
Q
A

Answer: Miosis

DUMBELS: Diarrhoea, Urination, Miosis, Bronchoconstriction, Excitation (of skeletal muscle and CNS), Lacrimation, Salivation/Sweating

49
Q
A

Answer: Anticholinergics

50
Q
A

Answer: inhibiting constriction of the efferent arteriole

51
Q
A

Answer: They are contraindicated in patients with renal impairment

Bisphosphonates are most commonly used to treat patients with osteoporosis because they are antiresorptive agents and act on osteoclasts to decrease or stop the resorption of the bone. They can pass into breast milk and, therefore, should not be used by patients who are breastfeeding. They also cause esophageal erosions and should be used with caution in patients with gastrointestinal diseases. The older generation of bisphosphonates (eg, etidronate) caused osteomalacia when used in continuous mode and in high dosages; however, the newest medications in this class (eg, alendronate, risedronate) are safer and have not been shown to cause this complication.

52
Q
A

Answer: Quinolones

  • Quinolones - DNA gyrase inhibition
  • Tetracyclines - Ribosomal subunit inhibition
  • Carbepenem - Inhibition of cell wall synthesis
  • Cephalosporins - Inhibition of cell wall synthesis
  • Macrolides - Ribosomal subunit inhibition

Other antibiotics that interfere with DNA include: quinolones, metronidazole, cotrimoxazole, rifampicin, and fusidic acid.

53
Q
A

Answer: Ceftriaxone

Cell-membrane inhibitors are almost all excreted renally. Ceftriaxone is the only cell-membrane inhibitor that is eliminated hepatically. This is useful to know, as it concentrates in the gallbladder and can be used in the treatment of cholecystitis.

54
Q
A

Answer: conjugation

55
Q
A

Answer: Mimic dopamine transmission at the postsynapse

56
Q
A

Answer: Salmeterol

The question is asking for a prolonged method of therapy which is salmeterol -> long-acting (8–12h). Salbutamol has the same MoA but it is short acting.

57
Q
A

Answer: Digoxin-specific antibody Fab fragments

58
Q
A

Answer: Sulfonyureas

59
Q
A

Answer: Heparin

60
Q
A

Answer: Xa

61
Q
A

Answer: Xa

Potentiates the action of ATIII, increasing inhibition of Xa and IIa, but (unlike unfractionated heparin) in a 4:1 ratio.

62
Q
A

Answer: Xa

63
Q
A

Answer: Draw a stat paracetamol level and administer NAC.

Survival from a paracetamol overdose is generally considered to be 100% in cases receiving NAC within 8 hours of exposure. Efficacy declines after this point. The threshold for potential paracetamol-induced hepatic injury in adults is >10g or >200 mg/kg (whichever is less) within 24 hours. With an unknown amount, a toxic dose should be presumed.

64
Q
A

Answer: Cytochrome P-450

65
Q
A

Answer: Kidney injury occurs by metabolite other than NAPQI

66
Q
A

Answer: Clopidogrel

67
Q
A

Answer: Heparin

68
Q
A

Answer: Thrombomodulin

69
Q
A

Answer: Antithrombin

70
Q
A

Answer: Protamine sulfate

71
Q
A

Answer: Vitamin K

72
Q
A

Answer: Aspirin

73
Q
A

Answer: Factor Xa

74
Q
A

Answer: Activation of D2 receptors (Bromocriptine)

75
Q
A

Answer: Reversible inhibition of COMT (Entacapone)

76
Q
A

Answer: Carbidopa

77
Q
A

Answer: Carbimazole

78
Q
  • A) Administer a nonsteroidal anti-inflammatory drug (NSAID)
  • B) Administer chewable aspirin (325mg) and activate the cardiac catheterization team
  • C) Administer IV thrombolytic therapy
  • D) Administer IV heparin bolus followed by an infusion for 48 hours
  • E) Admit to the CCU to rule out myocardial infarction and perform stress testing in the morning
A

Answer: Administer a nonsteroidal anti-inflammatory drug (NSAID)

The patient’s clinical history is consistent with acute pericarditis, likely viral in nature. The ECG supports this diagnosis, with findings of PR-segment depression as well as concave ST-segment elevation in a large territory that does not follow a coronary artery distribution. An NSAID should be administered to alleviate the patient’s chest discomfort. Atrial fibrillation was incidentally found on physical examination at the time of presentation. Atrial fibrillation is not an uncommon finding in patients with pericarditis and may resolve on its own after the inflammatory process subsides. The use of anticoagulation in this young woman with no significant risk factors for stroke or thromboembolism would be of little benefit, and it may be harmful given that the patient might have a pericardial effusion associated with pericarditis, which can be worsened by anticoagulation. The patient is not experiencing an acute MI; therefore, IV thrombolytic therapy and aspirin and cardiac catheterization are not indicated.

79
Q
A

Answer: Allopurinol

Allopurinol is a xanthine oxidase inhibitor and it should be used as first-line urate-lowering therapy.

80
Q
A

Answer: Somatostatin analogue
Somatostatin analogues such as ocreotide are used to treat acromegaly.