Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 Revision > Y2S1 Pharmacology > Flashcards

Y2S1 Pharmacology Flashcards

1
Q

What is the mechanism of action of dipyridamole?

A

Inhibits platelet phosphodiesterase → increased cAMP → inhibition of platelet activation

AND

Inhibits thromboxane A2 synthesis

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

Name 3 P2Y12 receptor antagonists

A
  1. Clopidogrel
  2. Prasugrel
  3. Ticagrelor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does antagonism of the P2Y12 receptor inhibit platelet aggregation?

A

Antagonism of the P2Y12 (ADP) receptor → increased adenylate cyclase → increased cAMP → decreased platelet aggregation

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

What is the difference in mechanism of clopidogrel and prasugrel, and ticagrelor?

A

The active metabolite of the thienopyridines (clopidogrel, prasugrel) irreversibly binds to the platelet P2Y12 receptor and inhibits platelet aggregation for the life of the platelet

Ticagrelor binds reversibly to the P2Y12 receptor.

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

Name 3 glycoprotein IIb/IIIa inhibitors

A

Abciximab

Eptifibatide

Tirofiban

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

How do glycoprotein IIb/IIIa inhibitors reduce platelet aggregation?

A

They prevent the binding of fibrinogen to platelets by occupying glycoprotein IIb/IIIa receptor, thereby blocking platelet aggregation

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

Name 4 classes of medications that affect platelet adhesion and activation

A
  1. COX inhibitors
  2. Phosphodiesterase inhibitors
  3. P2Y12 receptor antagonists
  4. GP-IIb/IIIa receptor antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name 3 low molecular weight heparins

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

What is the mechanism of heparins?

A

Bind to and activate antithrombin III → inactivation of clotting factors IIa (thrombin) and Xa

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

What is the major difference between the mechanism of heparin and low-molecular-weight heparins (LMWH)?

A

LMWHs have stronger effects on factor Xa

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

Which medication is used to reverse the action of heparins?

A

Protamine

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

What is the mechanism of protamine?

A

Rapidly forms a stable complex with heparin - “chemical antagonist”

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

Name 2 direct thrombin inhibitors

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

Which medication is used to reverse the effects of dabigatran?

A

Ibarucizumab

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

What is the mechanism of idarucizumab?

A

Humanised monoclonal antibody fragment binds with dabigatran → stable inactive complex → reverses anticoagulant effect

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

Name 3 factor Xa inhibitors?

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

What is the mechanism of warfarin?

A

Vitamin K reductase inhibitor

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

The concentration of which clotting factors are affected by warfarin?

A

II, VII, IX, X

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

Which laboratory test is used to monitor coagulation in patients on warfarin?

A

International normalised ratio (INR)

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

Which laboratory measurement is used to determine the international normalised ratio?

A

Prothrombin time

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

What is used to reverse the actions of warfarin?

A

Vitamin K

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

What is the mechanism of tranexamic acid?

A

Inhibits breakdown of clots by blocking binding of plasminogen and plasmin to fibrin

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

What is the mechanism of cyclophosphamide?

A

Alkylating agent - interferes with transcription and DNA replication

AND is an immunosuppressant, having cytotoxic effects on lymphocytes

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

What is the mechanism of methotrexate?

A

Folic acid antagonist. Inhibits DNA synthesis and cell replication

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

What is the mechanism of fludarabine?

A

Purine antimetabolite → inhibits DNA synthesis → apoptosis

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

What is the mechanism of 5-fluorouracil?

A

Pyrimidine antimetabolite → inhibits DNA synthesis → apoptosis

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

Name 6 adverse effects of cytotoxic chemotherapy drugs

A
  1. Myelosuppression
  2. Poor wound healing
  3. Alopecia
  4. Damage to the gastrointestinal epithelium
  5. Growth depression
  6. Sterility

Other: teratogenicity, carcinogenicity

These effects occur because chemotherapy targets all rapidly dividing cells

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

What is the mechanism of cetuximab?

A

Monoclonal antibody targeted against epidermal growth factor receptor (EGFR) → inhibits proliferation and inducing apoptosis of tumour cells that over-express EGFR

E.g. colorectal, non-small cell lung and head and neck cancer

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

What is the mechanism of erlotinib?

A

Reversible inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase

Intracellular kinase activity drives downstream signalling of tumours

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

What is the mechanism of pembrolizumab?

A

Inhibits the binding of programmed cell death protein 1 (PD-1) to its ligands on tumour cells

This reactivates cytotoxic T cells and anti-tumour immunity

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

What is the mechanism of medroxyprogesterone acetate?

A

Activates progesterone receptors in the endometrium → antiproliferative effects against endometrial cancer

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

What is the mechanism of letrozole?

A

Reversible inhibition of aromatase in the adrenal cortex → decreased oestrogen synthesis

Used for oestrogen-receptor-positive breast cancer in post-menopausal women

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

Why is letrozole only used in post-menopausal women?

A

A reduction of oestrogen synthesis by the adrenal cortex causes a compensatory increase in ovarian oestrogen production in pre-menopausal women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which drug is used to stimulate neutrophil production?

A

Granulocyte-colony stimulating factor - filgrastim/pegfilgrastim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which disease-modifying anti-rheumatoid drug (DMARD) is first-line?

A

Methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the mechanism of cyclosporine?

A

Calcineurin inhibitor

Calcineurin usually stimulates the production of interleukin‑2 and other cytokines, which normally stimulate T cell proliferation and differentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the mechanism of tacrolimus?

A

Calcineurin inhibitor

Calcineurin usually stimulates the production of interleukin‑2 and other cytokines, which normally stimulate T cell proliferation and differentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the mechanism of azathioprine?

A

Purine antimetabolite

Interferes with purine synthesis, inducing DNA damage that impairs proliferation and function of B and T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the mechanism of mycophenylate?

A

Inhibits inosine monophosphate dehydrogenase → decreased guanosine synthesis → suppresses lymphocyte proliferation and antibody formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

List 6 immunosuppressants or immunomodulators that are used for rheumatoid arthritis

A

Cyclosporine

Tacrolimus

Azathioprine

Mycophenolate

Hydroxychloroquine

Infliximab

Corticosteroids

Tofacitinib

Methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the mechanism of infliximab?

A

Tumour necrosis factor alpha antagonist

TNF-alpha is a cytokine released by various immune cells, including T helper cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which enzyme converts histadine into histamine?

A

Histadine decarboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the main mechanism of antihistamines?

A

Histamine inverse agonist - binds to histamine receptors and stabilises them in their inactive form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Name 4 effects of antihistamines

A
  1. Reduced mast cell release of histamine
  2. Reduced recruitment of immune cells
  3. Reduced itch, pain and sneezing
  4. Reduced vasodilation

Other: reduce bronchoconstriction

45
Q

What is the major difference between first and second generation antihistamines?

A

First generation antihistamines more readily cross the BBB, causing sedaion

46
Q

Name 3 first-generation antihistamines

A
  1. Diphenhydramine
  2. Promethazine
  3. Doxylamine
47
Q

Name 2 second-generation antihistamines

A
  1. Loratadine
  2. Fexofenadine
48
Q

Name 3 antiresorptive drugs used for osteoporosis

A

Alendronate, pamidronate, etidronate (bisphosphonate)

Raloxifen, tamoxifen (SERM)

Denosumab (RANKL inhibitor)

49
Q

Name an anabolic agent used for osteoporosis

A

Teriparatide (recombinant PTH)

50
Q

What is the mechanism of bisphosphonates?

A

Induces apoptosis in osteoclasts

51
Q

Name a simple bisphosphonate

A

Etidronate

52
Q

Name 2 amino bisphosphonates

A
  1. Alendronate
  2. Pamidronate
53
Q

How do simple and amino bisphosphonates differ in their mechanism of action?

A

Simple - are incorporated into ATP analogues in osteoclasts → apoptosis

Amino - interfere with the anchoring of cell surface protein to the osteoclast membrane → decreased osteoclast attachment → apoptosis

54
Q

How does oestrogen decrease osteoclast proliferation?

A

Decreases the transcription of RANKL in osteoblasts

RANKL binds to the RANK receptor on osteoclast precursor, stimulating osteoclast maturation

55
Q

Name a selective estrogen receptor modulator (SERM)

A

Raloxifene

Tamoxifen

56
Q

How do SERMs modulate oestrogen?

A

Oestrogen receptor agonist in bone

Oestrogen receptor antagonist in the endometrium and breast

57
Q

What is the mechanism of denosumab?

A

Recombinant human monoclonal antibody that binds to and inhibits RANKL, decreasing the action of osteoclasts

58
Q

What is teriparatide?

A

Recombinant human PTH

Intermittent PTH has anabolic effects on bone

59
Q

How does teriparatide have anabolic effects on bone?

A
  1. Antiapoptotic effects on osteoblasts
  2. Induces osteoblast maturation
60
Q

How do cathepsin K inhibitors treat osteoporosis?

A

Cathepsin K degrades type 1 collagen, leading to bone degradation

Novel therapy e.g. odanacatib

61
Q

How do sclerostin inhibitors treat osteoporosis?

A

Sclerostin stimulates the production of RANKL by osteocytes, reducing bone formation and stimulating osteoclasts

62
Q

What is the mechanism of cinacalcet?

A

Enhances the sensitivity of PTH calcium-sensing receptors → decreases PTH release

63
Q

What is the mechanism of tissue plasminogen activator?

A

Activates plasmin, the enzyme responsible for the conversion of fibrin to fibrin degradation products

64
Q

Name a tissue plasminogen activator

A
  1. Alteplase

Other: reteplase, tenecteplase

65
Q

What is the difference in mechanism between urokinase-type plasminogen activator and recombinant tissue plasminogen activators?

A

Recombinant tPA is selective to fibrin-bound plasminogen

Urokinase does not discriminate between fibrin-bound plasminogen and plasma plasminogen → causes thrombolysis in clots and systemically

66
Q

What is the mechanism of tranexamic acid?

A

Lysin analogue → binds lysine binding site → blocks binding of plasminogen and plasmin to fibrin → inhibits breakdown of clots

67
Q

What is the mechanism of streptokinase?

A

Plasminogen activator

68
Q

Which antiepileptic drugs are sodium channel blockers?

A

Carbamazepine

Phenytoin

Lamotrigine

Sodium valproate

Topiramate

69
Q

Which antiepileptic drugs enhance GABA?

A

Benzodiazepines

Barbiturates

Gabapentin

Topiramate

Sodium valproate

70
Q

Which antiepileptic drugs are calcium channel blockers?

A

Ethosuximide

Sodium valproate

Clonazepam

71
Q

How do sodium-blocking antiepileptic medications target hyperexcitable neurons?

A

They are selective to highly active/excitable sodium channels - “use-dependent”

72
Q

What effect do sodium-channel blocking antiepileptics have on neuronal depolarisation?

A

Decrease rate of recovery of sodium channels, increasing the refractory period of neurons

This prevents repetitive neuronal firing

73
Q

What is the first-line medication for focal seizures?

A

Carbamazepine

74
Q

What is the first-line medication for generalised tonic-clonic seizures?

A

Sodium valproate

75
Q

What is the first line medication for pregnant women with focal seizures?

A

Lamotrigine

76
Q

Which medications are first-line for absence seizures?

A

Ethosuximide

Sodium valproate

77
Q

What is the mechanism of barbiturates?

A

Prolongs the duration of GABAA channel opening

78
Q

What is the mechanism of benzodiazepines?

A

Increases the frequency of GABAA channel opening

79
Q

What is the treatment of status epilepticus?

A

Benzodiazepines

80
Q

What is the mechanism of ethosuximide?

A

Blockage of low-threshold T-type calcium channels in thalamic neurons

81
Q

What are the 3 mechanisms of sodium valproate?

A
  1. Prolongs recovery of sodium channels
  2. Inhibits thalamic T-type calcium channels
  3. Increases GABA production and reduces its breakdown → alteration in cellular resting membrane potentials
82
Q

What are the proposed mechanisms of migraines?

A
  1. Dilation of intracranial vessels (particularly meningeal vessels)
  2. Recurrent activation and sensitisation of the trigeminovascular pathway
  3. Reduced activation of descending pain inhibitory pathways
83
Q

What is the major drug class used to acutely stop migraines?

A

“Triptans” e.g. sumatriptan

84
Q

What is the mechanism of triptans?

A

Agonists at 5HT1B and 5HT1D receptors → vasoconstriction and enhancement of inhibitory descending pain pathways

85
Q
A
86
Q

What are contraindications to triptan use?

A

History of MI

Coronary artery disease

Peripheral vascular disease

Angina/coronary vasospasm

Uncontrolled hypertension

Stroke of TIA

Small risk of serious coronary events

87
Q

What are potential adverse effects of triptans?

A

Chest, jaw and throat tightness or tingling

Muscle pain and paresthesia

Flushing, dizziness, weakness

Transient increase in BP

Serious coronary events - rare

88
Q

Name 5 first-line medications for migraine prophylaxis

A
  1. Amitriptyline
  2. Candesartan
  3. Pizotifen
  4. Propranolol
  5. Topiramate

Other: sodium valproate, nortriptyline

89
Q

List 4 non-analgesic drugs used for neuropathic pain

A
  1. Amitriptyline
  2. Duloxetine
  3. Gabapentin
  4. Pregabalin
90
Q

How do tricyclic antidepressants treat neuropathic pain?

A

Promotion of descending inhibitory pain pathways

1. Inhibition of 5HT reuptake

2. Inhibition of NA reuptake

  1. Inhibition of post-synaptic histamine receptors
91
Q

Which drug is first-line for trigeminal neuralgia?

A

Carbamazepine

92
Q

What is the mechanism of capsaicin?

A

Transient receptor potential vanilloid type 1 (TRPV1) receptor agonist → substance P depletion → inhibits neuropathic pain

93
Q

What is the mechanism of lignocaine?

A

Voltage-gated sodium channel blocker → inhibition of conduction in peripheral nerves

94
Q

What is the mechanism of ketamine?

A

Polyamine antagonist (inhibits NMDA receptors) → anaesthesia

95
Q

What is the mechanism of macrogol?

A

Induces osmotic activity in the bowel (laxative)

96
Q

What is the mechanism of lactulose?

A

Induces osmotic activity in the bowel (laxative)

97
Q

What is the mechanism of senna?

A

Stimulatory laxative - directly stimulates nerve endings in colonic mucosa to increase intestinal motility

98
Q

What is the mechanism of ondansetron?

A

Central and peripheral 5HT3 receptor blockade → antiemetic

99
Q

What is the mechanism of metoclopramide?

A

Dopamine antagonist

100
Q

What is the mechanism of ranitidine?

A

Inhibits H2 receptors on parietal cells, reducing gastric acid secretion

101
Q

What is the mechanism of esomeprazole?

A

Proton pump inhibitor → reduces gastric acid secretion

102
Q

What is the mechanism of aluminium/magnesium hydroxide?

A

Antacid - neutralises stomach acid

103
Q

Which medication is used to reverse the effects of paracetamol overdose?

A

Acetylcysteine

104
Q

Which mediation is used to reverse opioid overdose?

A

Naloxone

105
Q

What is colchicine used for?

A

Relief of pain in acute gout

Reduces inflammation: inhibits neutrophil migration, chemotaxis, adhesion and phagocytosis in inflamed tissue. In gout, it reduces inflammatory reaction to urate crystals

106
Q

What is the mechanism of allopurinol?

A

Inhibits xanthine oxidase → reduces production of uric acid

107
Q

What is the mechanism of levodopa?

A

Dopamine precursor

108
Q

What is the mechanism of carbidopa?

A

Peripheral dopa decarboxylase inhibitor → reduce peripheral conversion of levodopa to dopamine

Y2 Revision (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions