MOA

Question 1

Antihistamines MOA

Answer 1

Act on h 1 and 2 receptors on vasculature
Histamine antagonists competitively block h1 and 2 receptors, blocking histamine
Mast cell stabilisers block calcium channels essential for mast cell degranulation

Question 2

NSAIDS MOA

Answer 2

Acts on cox pathways
Block COX pathways inhibiting formation of cox products: prostglandins and thromboxane A2
Stops platelets sticking, vasodilation of vascular smooth muscle, decrease fever, blocks mild pain

Question 3

Corticosteroids MOA

Answer 3

Knocks out phospholipase a2 preventing the creation of arachidonic acid, blocking cox 1 and 2 and lipooxygenase pathways inhibiting formation of associated products such as:
Leukotrienes, prostaglandins, thromboxane a2

Question 4

Opioids MOA

Answer 4

Binds to u receptors at different levels of ascending pathway and areas of the brain concerned with pain perception resulting in blocked neuronal transmission of pain signals

Question 5

Narcotic antagonists MOA

Answer 5

Antagonises u receptors which blocks narcotic agonists binding to u receptors

Question 6

General anaesthetics MOA

Answer 6

Facilitate opening of K channels
Enhance activity of GABA
Inhibit activation of NMDA
Change lipid membrane structure

Question 7

Local anaesthetics MOA

Answer 7

Block nerve conduction via voltage gated sodium channel blocking preventing further AP formation and therefore propogation in the nerve cells as the channel has to be open for it to work

Question 8

Benzodiazepines MOA

Answer 8

Binds to GABAa BZR receptors and facilitates GABA binding increasing thr frequency of chloride channel opening

Question 9

Barbiturates MOA

Answer 9

Increase duration of chloride channel opening

Question 10

Z drugs MOA

Answer 10

Non benzo that binds to BDZ site on GABA receptor and has same inhibitory effect but is selective and short lived

Question 11

5 HT 1a receptor agonists MOA

Answer 11

Agonise inhibitory receptors to reduce the release of serotonin
Less serotonin release into synaptic cleft lowers neuronal transmission

Question 12

B receptor antagonists MOA

Answer 12

Reduce physical symptoms of anxiety by blocking b receptors

Question 13

Tricyclic antidepressants MOA

Answer 13

Block uptake of NA and serotonin by neurons. Competes for binding site on reuptake transport protein, stopping it from opening, resulting in elevation of synaptic concentrations of NA and serotonin
Can also block muscarinic, a1 adrenergic, histamine receptors

Question 14

Selective serotonin reuptake inhibitors (SSRIs) MOA

Answer 14

Inhibit reuptake of serotonin by competing for binding site on reuptake transport proteins

Question 15

Selective serotonin noradrenaline reuptake inhibitors (SSNRIs) MOA

Answer 15

Inhibit reuptake by competing for binding site on reuptake transport proteins stopping it from opening

Question 16

MOA inhibitors MOA

Answer 16

Inhibits moa enzymes that are responsible for metabolism of NA and serotonin found in mitochondria hence allowing a build up of neurotransmitter available for release

Question 17

Dopamine blockers - typical MOA

Answer 17

D2 receptor antagonist in cns blocking the action of dopamine to reduce the increased action of dopamine in pts with psychotic disorders

Question 18

Dopamine blockers - atypical MOA

Answer 18

Partially block action of d2 and 5HT1a receptors plus antagonist action 5HT2a

Question 19

B agonist MOA

Answer 19

Sympathetic response
Agonises b receptors at the postsynaptic ganglion, increasing the sympathetic nervous system tone: increased HR, conduction velocity, force pf contraction, bronchial dilation

Question 20

Muscarinic antagonist MOA

Answer 20

Parasympathetic response
Blocks ACh at postsynaptic ganglion, decreasing PNS tone: antislud, increased HR, conduction velocity, force of contraction, bronchial dilation

Question 21

Glutamate blockers MOA

Answer 21

Cns
Stabilised neuronal excitability on CNS via closing of t type calcium channels by blocking glutamate receptors on calcium channels that open them

Question 22

Sodium channel blockers MOA

Answer 22

Na channels on neurons in CNS

Blocks the frequency of opening of sodium channels therefore limiting repetitive firing of action potentials

Question 23

B antagonist MOA

Answer 23

Sympathetic b receptors
Blocks the binding of adrenaline/NA to receptor, blocking sympathetic tone
Class II reduce rate of sa node and slow conduction in the atria and av node and increase refractory period
Class III prolong the effective refractory period by prolonging AP duration
decrease myocardial contractility, cardiac output, O2 requirements, renin secretion and therefore levels of angiotensin II

Question 24

A antagonists MOA

Answer 24

antagonises a receptors on vascular smooth muscle causing the smooth muscle to relax and the vessels to dilate, therefore reducing venous return and CO therefore BP

Question 25

Calcium channel blockers MOA

Answer 25

Acts on cardiac and smooth muscle block voltage gated calcium channels in cardiac and smooth muscle, decreasing intracellular calcium levels leading to a reduction in muscle contraction (negative inotropic effect) decrease in cardiac contraction results in decreased CO, decreased BP in blood vessels, a decrease in calcium results in less contraction of vascular smooth muscle resulting in lowered venous return and CO and BP may slow the conduction of electrical activity in the heart by blocking the calcium channels during plateau phase resulting in negative chronotropic effect

Question 26

Potassium channel agonists MOA

Answer 26

Acts on smooth muscle activate K+ channels on smooth muscle (antagonist effect of ATP) to prevent closure resulting in hyperpolarisation and therefore relaxation of smooth muscle cells creating vasodilation

Question 27

Loop diuretics MOA

Answer 27

Act on kidney tubules inhibits reabsorption of Cl- and Na+ ions within the ascending limb of loop of henle Water follows Na+ so if Na+ is not retained and therefore excreted, water follows out of the body resulting in lowered blood volume and therefore BP

Question 28

Thiazide Diuretics MOA

Answer 28

inhibits reabsorption within the ascending limb and the distal convoluted tubule

Question 29

Potassium sparing Diuretics MOA

Answer 29

act on distal convoluted tubule | normalise K+ loss caused by other diuretics

Question 30

ACE inhibitors MOA

Answer 30

Act on juxtaglomerular apparatus in kidney blocks angiotensin converting enzyme which converts angiotensin I to II causing both vasoconstriction and release of aldosterone causing Na+ reabsorption by the kidneys, hence increasing blood volume and BP. by blocking this enzyme, it decreases BP

Question 31

Angiotensin II blockers MOA

Answer 31

AtI recrptors blocks AT1 receptors resulting in inhibition of angiotensin II angiotensin II causes vasoconstriction and release of aldosterone by blocking AT1 receptors, drops BP Doesn't effect plasma potassium concentration as ACE inhibitors do

Question 32

Nitrates MOA

Answer 32

Acts on smooth muscle taken up by vascular smooth muscle where the active form of nitric oxide activates enzymes that decrease intracellular Ca2+ levels causing vasodilation

Question 33

Anticoagulants MOA

Answer 33

Act on thrombin and vitamin k heparin: combines with anti-thrombin III forming a complex which inactivates thrombin factor IIa and others, preventing fibrin formation therefore stopping clots warfarin: intereferes with hepatic synthesis of vitamin K dependent clotting factors through inhibition of the vitamin K epoxide reductase complex 1

Question 34

Antiplatelets MOA

Answer 34

NSAIDS

Question 35

Thrombolytics MOA

Answer 35

dissolves clots by acting on the fibrinolytic system, converting plasminogen into plasmin plasmin is a fibrinolytic enzyme which digests or dissolves fibrin clots

Question 36

Muscle relaxants (depolarising) MOA

Answer 36

Acts on motor end plate of muscles nicotinic receptor agonists, maintaining a depolarised state of the motor end plate of muscle therefore preventing transmission of another AP Na+ channels remain open, motor end plate can no longer response to stimulus causing paralysis

Question 37

Muscle Relaxants (non-depolarising) MOA

Answer 37

Acts on pre and post synaptic nicotinic receptors competitely blocks ACh binding at post and presynaptic nicotinic receptors, blocking the condution across a synapse of an AP to the motor end plate. progressively weakens small muscles through to larger muscles before causing paralysis

Question 38

Antiemetics MOA

Answer 38

Acts on d2 receptors in CTZ and vomiting center antagonises D2 receptors located in the CTZ and vomiting center, inhibiting the action of N+V also has antihistamine and antimuscarinic properties metoclopramide accelerates gastric emptying, reduces reflux and enhances GIT motility

Question 39

B2 agonists MOA

Answer 39

stimulate B2 receptors in bronchial smooth muscle causing relaxation via increased cAMP

Question 40

muscarinic M3 antagonists MOA

Answer 40

blocks the action of ACh on M3 receptors M3 stimulation leads to increase cGMP which results in increased contraction and secretion blocking this prevents contraction and secretion

Question 41

Methyxanthines MOA

Answer 41

xanthine derivatives may act by inhibiting phosphodiesterase leading to a decrease in cAMP breakdown therefore leading to increase cAMP promotes bronchodilation via blockade of adenosine receptors

Question 42

Tetracycline Antidepressants MOA

Answer 42

inhibit presynaptic alpha 2 receptors, blocking release of transmitter into synaptic cleft

Question 43

Antifungals MOA

Answer 43

inhibit sterol synthesis in cell membrane of fungus, intereferes with permeability and transport functions

Question 44

Antivirals MOA

Answer 44

inhibits uncoating of virus and fusion of virus with host membrane cells interference with RNA and DNA synthesis and polymerase