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drugs and disease > drugs list > Flashcards

drugs list Flashcards

1
Q

statins: mechanism of action

A

inhibit HMG-CoA reductase to increase removal of apo-b containing lipoproteins in the liver, and reduce synthesis and secretion of them too.

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2
Q

statins: clinical uses

A

high colesterol, cardiovascular disease, atherosclerosis, risk of strokes and heart attacks

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3
Q

ace inhibitors: drug class

A

antihypertensive drugs

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4
Q

ace inhibitors: mechanism of action

A

interferes with the renin angiotensin system by inhibiting production of angiotensin 2 which is a vasoconstrictor

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5
Q

ace inhibitors: effects

A

dilates arteries and veins by blocking ang2 and inhibiting bradykinin metabolism.
blocks effects of ang2 on sympathetic nerve release.
inhibits cardiac remodelling associated with hypertension, heart failure and MI

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6
Q

ace inhibitors: clinical uses

A

hypertension, heart failure and MI

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7
Q

angiotensin receptor blockers: mechanism

A

block type 1 angiotensin2 receptors (AT1) on blood vessels and other tissues. these receptors are coupled to the gq protein and IP3 signal pathway

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8
Q

angiotensin receptor blockers: effects

A

dilate arteries and veins so reduce pressure, preload and afterload.
down regulate sympathetic adrenergic activity.
inhibit remodelling of the heart

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9
Q

angiotensin receptor blockers: clinical uses

A

hypertension and heart failure

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10
Q

renin inhibitors: mechanism of action

A

bind to active site of renin and inhibit the binding of renin to ang, blocks formation of ang1

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11
Q

renin inhibitors: effects

A

vasodilation, reduced pressure, decreased sympathetic adrenergic activity, inhibits remodelling

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12
Q

renin inhibitors: clinical uses

A

hypertension

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13
Q

calcium channel blockers: mechanism of action

A

bind to L-type calcium channels on vascular smooth muscle and cardiac tissue and block ca entry into muscle cells

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14
Q

calcium channel blockers: effects

A

vascular smooth muscle relaxation, decreased myocardial force and decreased heart rate. decrease firing rate of pacemaker sites.

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15
Q

calcium channel blockers: clinical uses

A

hypertension, angina, arrythmias

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16
Q

a1 adrenoceptor antagonists: mechanism of action

A

blocks binding of NA to smooth muscle receptors and inhibit contraction

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17
Q

a1 adrenoceptor antagonists: clinical uses

A

treatment of hypertension in combination with other anti-hypertensives

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18
Q

thiazide like diuretics: mechanism of action

A

inhibit na-cl transport in distal convuluted tubule, preventing reabsorption of sodium and chloride

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19
Q

thiazide like diuretics: clinical uses

A

hypertension

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20
Q

K+ sparing diuretics: mechanism of action

A

antagonise the actions of aldosterone at the distal segment of the distal tubule (aldosterone receptor antagonists)

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21
Q

beta blockers: mechanism of action

A

competitive antagonists that block the receptor sites for catecholamines on adrenergic beta receptors of the sympathetic nervous system

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22
Q

beta blockers: effects

A

decrease arterial blood volume by reducing cardiac output,
inhibit renin release by kidneys so decrease in ang2 and aldosterone,
reduce heart rate, contractility and arterial pressure.

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23
Q

beta blockers: clinical uses

A

hypertension, angina, myocardiac infarction, arrhythmias, heart failure

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24
Q

a2 adrenoceptor agonists: mechanism of action

A

bind to a2 adrenoceptors to inhibit release noradrenaline

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25
Q

K+ channel agonists: mechanism of action

A

activate atp sensitive K+ channels in vascular smooth muscle. opening these hyperpolarises the smooth myscle so closes ca channels. less calcium causes relaxation and dilation

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26
Q

K+ channel agonists: clinical uses

A

hypertension, but only severe hypertension.

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27
Q

COX inhibitor: mechanism of action

A

blocks COX which synthesises TXA2 and PG12. TXA2 aggregates platelets and PG12 forms prostaglandins

28
Q

COX inhibitor: effects

A

less clot formation, vasodilation, anti-inflammatory

29
Q

COX inhibitor: clinical uses

A

arthritis, acute pain

30
Q

P2Y12 antagonists: mechanism of action

A

irreversibly antagonising the platelet P2Y12 receptor, preventing binding of ADP

31
Q

P2Y12 antagonists: effects

A

reduced platelet aggregation and reaction of platelets to stimuli

32
Q

P2Y12 antagonists: clinical uses

A

prevent heart attack/stroke, unstable angina, acute coronary syndrome

33
Q

GPIIb-GPIIIa antagonists: mechanism of action

A

prevent platelet aggregation by blocking glycoprotein IIb/IIIa receptors on the platelet plasma membranes and inhibit fibrinogen binding

34
Q

GPIIb-GPIIIa antagonists: clinical uses

A

management of acute coronary syndromes such as unstable angina and MI

35
Q

heparin mechanism of action:

A

binds reversibly to ATIII (antithrombin) leads to inactivation of clotting factors IIa and Xa

36
Q

heparin: clinical uses

A

prevention and treatment of venous thrombosis and pulmonary embolism after Mi, and unstable angina

37
Q

Vitamin K antagonists: mechanism of action

A

inhibit vitamin k dependent epoxide reductase activity which is required for synthesis of clotting factors

38
Q

vitamin K antagonists: clinical uses

A

venous thrombosis, pulmonary embolism, thromboembolic complications, recurrent MI and stroke

39
Q

fibrinolytics: mechanism of action

A

dissolve blood clots by activating plasminogen which forms plasmin. plasmin breaks links between fibrin molecules in blood clots.

40
Q

class 1 antiarrhythmics: mechanism of action

A

bind to and block the sodium channels responsible for rapid depolarisation of fast response cardiac action potentials. leads to decrease in amplitude of action potential and decrease in conduction velocity

41
Q

strength of class 1A sodium channel blockers?

A

moderate blockage, increases effective refractory period

42
Q

strength of class 1B sodium channel blockers?

A

weak blockade, decreases effective refractory period

43
Q

strength of class 1C sodium channel blockers?

A

strong blockade, no effect on the ERP

44
Q

class 3 antiarrhythmics: mechanism of action

A

blocks re entry by binding to and blocking K+ channels responsible for repolarisation, prolonging the regractory period

45
Q

class 3 antiarrhythmics: clinical uses

A

suppressing tachyarrhythmias

46
Q

corticosteroids: mechanism of action

A

produce anti-inflammatory effects by inhibiting or activating transcription of genes encoding proteins involved in regulating inflammation

47
Q

calcineurin inhibitors: mechanism of action

A

reduce interleukin-2 production and IL-2 receptor expression, leading to a reduction in T-cell activation. exert immunosuppressive effects.

48
Q

calcineurin inhibitors: clinical uses

A

treating inflammatory skin conditions

49
Q

antihistamines: mechanism of action

A

cross the bbb into the CNS and competitively antagonise H1-receptors and reduce the release of proinflammatory mediators from mast cells and basophils, reduce expression of adhesion molecules

50
Q

antihistamines: clinical uses

A

allergies

51
Q

leukotriene receptor antagonists: mechanism of action

A

blocks action of leukotriene D4 in the lungs resulting in decreased inflammation and smooth muscle relaxation

52
Q

anti-emetics: mechanism of action

A

highly specific & selective 5-HT3 receptor antagonist, blocks initiation of vomiting reflex

53
Q

anti-emetics: clinical uses

A

treatment of nausea and vomiting caused by chemotherapy drugs

54
Q

nitrogen mustards: mechanism of action

A

form cyclic aminium ions by intramolecular displacement of the chloride by the amine nitrogen. this then alkylates dna once it is attached by the n7 nucleophilic center on guanine base

55
Q

DNA polymerase inhibitor: mechanism of action

A

acyclovir is converted to its triphosphate form which compeitively inhibits viral dna polymerase.

56
Q

DNA polymerase inhibitor: clinical uses

A

herpes, decreases pain and speeds healing of sores and blisters

57
Q

neuraminidase inhibitor: mechanism of action

A

inhibit budding of ‘flu virus’ by inhibiting neuraminidase enzyme responsible for breaking bonds between viral coat and host cell membrane - prevents new viral particles being released

58
Q

neuraminidase inhibitor: clinical uses`

A

flu virus

59
Q

CCR5 antagonist: mechanism of action

A

prevent HIV-1 from entering and infecting immune cells by blocking CCR5 cell surface receptors.

60
Q

CCR5 antagonist: clinical uses

A

HIV

61
Q

fusion inhibitor: mechanism of action

A

binds to first HR1 repeat in the gp41 subunit of the viral envelope glycoprotein and prevents conformational changes required for the fusion of viral and cellular membranes

62
Q

fusion inhibitor: clinical uses

A

decreases amount of HIV in the blood

63
Q

reverse transcriptase inhibitors: mechanism of action

A

RTIs blocks reverse transcriptase enzyme function and prevents completion of synthesis of the double stranded viral DNA - prevents HIV from multiplying.

64
Q

reverse transcriptase inhibitors: clinical uses

A

treats HIV infection or AIDS

65
Q

integrase inhibitors: mechanism of action

A

inhibits the activity of HIV-1 integrade which impedes insertion of HIV-1 dna into the host cell genome

66
Q

integrase inhibitors: clinical uses

A

treatment of HIV

67
Q

protease inhibitors: mechanism of action

A

binds tot he protease active site and inhibits the activity of the enzyme, prevents cleavage of the viral polyproteins resulting in the formation of immature virus particles

drugs and disease (2 decks)

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