Pharmacology Drug MOA dose etc

Question 1

Describe the mechanism of actions for Adrenaline

Answer 1

Binding to the adrenergic receptors of the sympathetic system causing a response.
A1- vascular smooth muscle constriction
B1- cardiac muscle causing increase strength of contraction, aswell as increase in Rate.
B2- smooth muscle in the lungs causing relaxation

Question 2

Dose of ADR

Answer 2

Life Threat Asthma= 500mcg Bolus

Question 3

Describe the mechanisms of action for ATROPINE

Answer 3

Atropine is an M2 receptor antagoist

Binding to the muscarinic 2 receptors of the parasympathetic nervous system (Specifically vagus nerve) acting as an antagonist therefore blocking the receptor site leading to an unopposed sympathetic nervous system reaction leading to an increase in heart rate.

Question 4

Dose and route for Atropine?

Answer 4

600mcg undiluted bolus repeat 1 minute max dose 3mg

Question 5

Describe the mechanism of action for salbutamol

Answer 5

Salbutamol is a B2 agonist binding to beta two receptors in the smooth muscle of bronchial leading to Bronchial smooth muscle relaxation

Salbutamol is a sympathomimetic drug and a B2 agonist which causes an,
- ^ in cAMP
- v in Ca2+
- v in actin & myosin interaction
- leading to bronchodilation

Question 6

Describe the mechanism of action for glyceryl trinitrate

Answer 6

Glyceryl trinitrate is a pro drug converted into nitric oxide defuses into the smooth muscle of the coronary arteries increasing CGMP causing phosphorylation of the SERCA pump leading to relaxation of the muscle it also inhibits phosphorylation of the myosin light chain decreasing the interaction between myosin and actin therefore decreasing muscle construction

GTN is a
o Nitrate and a Pro-drug
oI works as a Vasodilator
o & undergoes de-nitration to form Nitric Oxide (NO)
o NO goes into smooth muscles of vessels
o Increases cGMP
o Decreases Ca2+
o Decreases actin and myosin interaction
Causes vasodilation

Question 7

Describe the MOA for Ipratropium

Answer 7

Ipratropium bromide is an anticholenergic binding to muscurinic three receptors in the airways.
M3 Antagonist, blocks Ach from binding to M3r causing a
- v in Ca2+
- blocks PNS activity, allowing the SNS to take over
- causing bronchodilation
- and blocks mucus producing cells

Question 8

MOA of fexofenadine and loratadine

Answer 8

Fexofenadine is a selective H1 receptor antagonist

Question 9

MOA for amiodarone

Answer 9

Amiodarone is a class three Anti arrhythmic working primarily as a K channel blocker in phase three of the cardiac action potential. extending the plateau pahse devrease heart rate

Question 10

MOA adenosine

Answer 10

Acts on Adenosine 1 receptors within the AV node reducing conduction time through the AV node

Stimulates A1 adenosine recpeter and opens ACh senstive K+ channels. By

Question 11

MOA of aspirin

Answer 11

Anti platelet medication works by inhibiting the conversion of AA into Prostaglandins as well TXA2 by blocking the cox 1-2 enzyme decreasing the stimulation of the Gq pathway decreasing platelet aggregation.

Question 12

MOA for clopidagrel

Answer 12

Anti platelet medication works as a P2y12 receptor antagonist blocking ADP from binding to the receptor inhibiting the G Inhibatory protien pathway leading to a decrease in platelet activation

Question 13

Dose route for clopidogrel

Answer 13

300mg Oral no repeat

Question 14

MOA TXA

Answer 14

TXA inhibits plasminogen to be activated into plasmin by tissue plasminogen activator leading to an increase in fibrin and a clot can form

o Anti-fibrinolytic
o Binds to lysine receptors as an antagonist
o Blocks to activation of plasminogen to plasmin
o Inhibits tissue bound plasmin to cleave fibrin
o Prevents clot degradation

Question 15

Whats the dose for TXA

Answer 15

1g/10ml
1g is max dose

Question 16

MOA of tenectaplase

Answer 16

Temectaplase is a tissue plasminogen activator (tpa) increasing the conversion of plasminogen to plasmin. Plasmin breaks down fibrin clot
Plasmin eats clot

Question 17

MOA Enoxaparin

Answer 17

Enoxaparin is a low molecular weight heprin anti coagulation used to inhibit factor ten in the clotting cascade. leading to a decrease in fibrin leading to a decrease in clot

Question 18

MOA Heprin

Answer 18

Heprin is an anticoagulant used to inhibit the activation of factor two and factor Ten in the clotting cascade ultimatly leading to a decrease in fibrinogen converting to fibrin decrease clots.

o Anti-coagulant drug
o Low molecular weight heparin
o binds to anti-thrombin, allowing anti-thrombin to bind to factor Xa (10a).
o deactivates factor Xa, which inhibits the coagulation cascade.
o Thrombin is not converted to fibrinogen
o Thus fibrin is not activated
o Fibrin mesh does not form
o Platelet plug remains unstable

Question 19

MOA of Digoxin

Answer 19

· inhibits the sodium/potassium ATPase pump on cardio myocytes.

· This makes the cardio myocyte have a higher concentration of sodium.

· Because the cardio myocyte is already in higher concentration of sodium, it won’t use the sodium/calcium exchanger and store more calcium into the sarcoplasmic reticulum.

· This allows for more calcium to be used during cardiac action potential to increase force. Thus, increased inotropy.

· The SA and AV node are partially controlled by the vagus nerve.

· Digoxin stimulates or enhances the effects of the vagus nerve.

· Which means, increased amounts of digoxin will cause an increased vagus response, which will cause the SA node to fire slower, which causes the AV node to fire slower. Overall, decreasing heart rate or chronotropic effects.

https://youtu.be/ljm1JSubTOc

Question 20

MOA of Morphine

Answer 20

Morphine binds to mu, kappa and delta recpetors located in the CNS. binding to these sites inhibits transmission decreasing pain sensation

Question 21

MOA of Naloxone

Answer 21

Naloxine is an opioid receptor antagonist. Binding to opioid receptors blocking the effects of opioids

• Competitively antagonises opioids
• Binds to the opioid receptors mu as well as kappa and delta in the CNS
• Inhibits action of opioid analgesics
• Reduces respiratory depression, analgesia, miosis, bradycardia

Question 22

Describe MOA of Frusemide

Answer 22

Frusemide is a loop diuretics acting within the ascending loop of henle. Blocking the Na/K/Cl pump inhibiting the reaabsorbtion of ions threfore reducing water reabsorbtion within the nephrons

Question 23

MOA of hydrochlorothiazide (Thiazide diuretic)

Answer 23

Thiazide diuretics exert their diuretic effect via blockage of the sodium-chloride (Na/Cl) channel in the proximal segment of the distal convoluted tubule

Question 24

MOA of Benzodiazepines

Answer 24

BDZs act on GABA a receptors at an allosteric site. Increasing the effect of GABA

o Benzodiazepine
o Allosteric drug
o Enhances the effects of GABA
o Binds to benzodiazepine receptors
o Coupled with GABA receptors
o Stimulates Cl- channels to open
o Cl- floods into the cell
o Hyperpolarises it
o Blocks neurotransmission
o Causes CNS depression

Question 25

Ketamine MOA

Answer 25

Ketamine binds to the glutamate receptor NMDA angtagonising the receport blocking the excitory neurotransmiter.

Ketamine is an aesthetic/analgesic,
- it is an NMDA r antagonist
- blocks glutamate from binding to the NMDA r
- which blocks the excitatory neurotransmission
- preventing neuronal membrane depolarisation
- decreasing CNS activity
-blocking Ca2+ from continuing neurotransmission
- blocking pain signalling

Question 26

MOA of Glucagon

Answer 26

Glucagon binding to the glucagon receptors in the liver, GI tract, heart, pancreas, fat, adrenal glands, and kidneys activate adenylate cyclase, which in turn raises cAMP levels. cAMP stimulates glycogenolysis and glucogenesis, resulting in the release of glucose, primarily from liver glycogen stores

Question 27

MOA of Droperidol

Answer 27

Dopamine 1-2 receptor antagonist.
Blocks dopamine binding throughout parts of the brian leading to CNS depression.

Question 28

MOA of Sertraline and Fluocetine
(SSRI)

Answer 28

SSRIs antagonise the 5HT3 reuptake transporter. Increasing levels of 5HT3 within the synaptic cleft incraesing the amount of 5HT3 that cn be utilised

Question 29

Describe the MOA of Tricyclic antidepressant (Eg. Amitriptyline)

Answer 29

TCA antagonise the 5HT3 and Nor Adrenaline reuptake transportor, increasing the amount of 5HT3 and NE within the synaptic cleft. It also blocks muscurinic and histamin receptors on the post synamtic nerve termial.

Question 30

Describe the MOA of Mono amine oxidase inhibitors

Answer 30

MAO inhibitors inhibit the enzyme Monoamine oxidase from making 5HT3 NE and ADR from becoming an inactive metabolites. increasing the amount of catcheolamins from being repackaged into the vesicles.

Question 31

MOA of Olanzapine

Answer 31

Olanzapine is a D2 and 5HT2 receptor antagonist blocking these recpetors within the mesolimbic (reward) pathway.

The effect on the D2 receptors leads to a decrease in positive symptoms in patients, including hallucinations, delusions, and disorganized speech, thought, and behavior. Therefore olanzapine reverse these effects.

Question 32

MOA of Lignocaine

Answer 32

o Na+ channel blocker
o Local anaesthetic
o Blocks sodium movement
o Into local nerve cells
o Prevents the pain signalling (action potential) from continuing

Question 33

MOA of Lignocaine

Answer 33

o Na+ channel blocker
o Local anaesthetic
o Blocks sodium movement
o Into local nerve cells
o Prevents the pain signalling (action potential) from continuing