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drugs list Flashcards

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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
K+ channel agonists: mechanism of action
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
26
K+ channel agonists: clinical uses
hypertension, but only severe hypertension.
27
COX inhibitor: mechanism of action
blocks COX which synthesises TXA2 and PG12. TXA2 aggregates platelets and PG12 forms prostaglandins
28
COX inhibitor: effects
less clot formation, vasodilation, anti-inflammatory
29
COX inhibitor: clinical uses
arthritis, acute pain
30
P2Y12 antagonists: mechanism of action
irreversibly antagonising the platelet P2Y12 receptor, preventing binding of ADP
31
P2Y12 antagonists: effects
reduced platelet aggregation and reaction of platelets to stimuli
32
P2Y12 antagonists: clinical uses
prevent heart attack/stroke, unstable angina, acute coronary syndrome
33
GPIIb-GPIIIa antagonists: mechanism of action
prevent platelet aggregation by blocking glycoprotein IIb/IIIa receptors on the platelet plasma membranes and inhibit fibrinogen binding
34
GPIIb-GPIIIa antagonists: clinical uses
management of acute coronary syndromes such as unstable angina and MI
35
heparin mechanism of action:
binds reversibly to ATIII (antithrombin) leads to inactivation of clotting factors IIa and Xa
36
heparin: clinical uses
prevention and treatment of venous thrombosis and pulmonary embolism after Mi, and unstable angina
37
Vitamin K antagonists: mechanism of action
inhibit vitamin k dependent epoxide reductase activity which is required for synthesis of clotting factors
38
vitamin K antagonists: clinical uses
venous thrombosis, pulmonary embolism, thromboembolic complications, recurrent MI and stroke
39
fibrinolytics: mechanism of action
dissolve blood clots by activating plasminogen which forms plasmin. plasmin breaks links between fibrin molecules in blood clots.
40
class 1 antiarrhythmics: mechanism of action
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
strength of class 1A sodium channel blockers?
moderate blockage, increases effective refractory period
42
strength of class 1B sodium channel blockers?
weak blockade, decreases effective refractory period
43
strength of class 1C sodium channel blockers?
strong blockade, no effect on the ERP
44
class 3 antiarrhythmics: mechanism of action
blocks re entry by binding to and blocking K+ channels responsible for repolarisation, prolonging the regractory period
45
class 3 antiarrhythmics: clinical uses
suppressing tachyarrhythmias
46
corticosteroids: mechanism of action
produce anti-inflammatory effects by inhibiting or activating transcription of genes encoding proteins involved in regulating inflammation
47
calcineurin inhibitors: mechanism of action
reduce interleukin-2 production and IL-2 receptor expression, leading to a reduction in T-cell activation. exert immunosuppressive effects.
48
calcineurin inhibitors: clinical uses
treating inflammatory skin conditions
49
antihistamines: mechanism of action
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
antihistamines: clinical uses
allergies
51
leukotriene receptor antagonists: mechanism of action
blocks action of leukotriene D4 in the lungs resulting in decreased inflammation and smooth muscle relaxation
52
anti-emetics: mechanism of action
highly specific & selective 5-HT3 receptor antagonist, blocks initiation of vomiting reflex
53
anti-emetics: clinical uses
treatment of nausea and vomiting caused by chemotherapy drugs
54
nitrogen mustards: mechanism of action
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
DNA polymerase inhibitor: mechanism of action
acyclovir is converted to its triphosphate form which compeitively inhibits viral dna polymerase.
56
DNA polymerase inhibitor: clinical uses
herpes, decreases pain and speeds healing of sores and blisters
57
neuraminidase inhibitor: mechanism of action
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
neuraminidase inhibitor: clinical uses`
flu virus
59
CCR5 antagonist: mechanism of action
prevent HIV-1 from entering and infecting immune cells by blocking CCR5 cell surface receptors.
60
CCR5 antagonist: clinical uses
HIV
61
fusion inhibitor: mechanism of action
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
fusion inhibitor: clinical uses
decreases amount of HIV in the blood
63
reverse transcriptase inhibitors: mechanism of action
RTIs blocks reverse transcriptase enzyme function and prevents completion of synthesis of the double stranded viral DNA - prevents HIV from multiplying.
64
reverse transcriptase inhibitors: clinical uses
treats HIV infection or AIDS
65
integrase inhibitors: mechanism of action
inhibits the activity of HIV-1 integrade which impedes insertion of HIV-1 dna into the host cell genome
66
integrase inhibitors: clinical uses
treatment of HIV
67
protease inhibitors: mechanism of action
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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