Cardiovascular/blood drugs

Question 1

Furosemide

Answer 1

Loop diuretic

Inhibits the Na-K-Cl pump in the ascending loop of henle. This means there is no ionic resorption and water follows increased salt concentration in filtrate. Blood volume is decreased

Hyponatremia and hypokalemia, dehydration

Question 2

Carvedilol

Bisoprolol

Answer 2

Beta-adrenoreceptor antagonists

Inhibit normal sympathetic activation of the b1 adrenoreceptor. This reduces heart rate and contractility

Used to treat heart failure, angina associated hypertension

Question 3

Ramipril

Answer 3

ACE inhibitor

Inhibit the formation of angiotensin II via inhibition of ACE. Angiotensin II is a vasoconstrictor, meaning inhibition reduces blood pressure. Aldosterone production also inhibited, meaning more water and H20 excreted from the kidney

Bradykinin induced cough, renal impairment, dizziness

Question 4

Valsartan

Candesartan

Answer 4

Angiotensin II receptor blockers

Inhibits vasoconstrictory action of angiotensin II. Decreases aldosterone production, meaning more water and Na+ excretion from kidney

Good for use in ACE intolerant patients

Question 5

Spironolactone

Eplerenone

Answer 5

Aldosterone receptor antagonists

Prevents Na+ and H20 resorption from the renal tubules, hence decreases blood pressure

Electrolyte imbalance and hyperkalaemia (spironolactone)

Question 6

Ivabradine

Answer 6

Cardiotonic agent

Acts on the If ion current produced in the SA node. This blocks cardiac pacemaker function and slows heart rate

Bradycardia and luminous phenomena

Question 7

GTN

Answer 7

Vasodilator

Prodrug converted to NO in vascular endothelium. NO increases cGMP production. cGMP causes myosin dephosphorylation and smooth muscle relaxation. Lowers blood pressure

Headaches and hypotension

Question 8

Aspirin

Answer 8

Non selective NSAID

Inhibits COX-1 and modifies COX-2 enzymes. Less prostaglandin and thromboxane A2 production, meaning platelet aggregation inhibited

Aspirin induced asthma, haemorrhage, bronchospasm

Question 9

Ticagrelor

Answer 9

Platelet activation inhibitor

An anti-thrombotic drug that blocks the P2Y ADP receptor, meaning platelets cannot be activated

Dyspnoea
Hematoma

Question 10

Atorvastatin

Answer 10

Statin

Competitive inhibitor of HMG-CoA reductase enzyme. This enzyme catalyses the rate limiting step in de novo cholesterol synthesis. Also decreases amount of LDL in blood

Joint pain, loose stools, indigestion

Question 11

Amlodipine

Felodipine

Answer 11

Ca2+ channel blocker (dihydropyridine family)

Inhibits movement of Ca2+ into vascular smooth muscle and cardiac muscle cells, inhibiting vasoconstriction

Dihydropyridines have greater affinity for calcium channels in VSMCs

Peripheral oedema, flushing, palpitations

Question 12

Indapamide

Bendrofluazide

Answer 12

Thiazide-like diuretics

Inhibit the NaCl cotransporter at the distal convoluted tubule. This blocks salt resorption and hence decreases blood volume

No adverse side effects of note

Question 13

Doxazosin

Answer 13

a1 adrenoreceptor antagonist

a1 receptor responsible for vasoconstriction of SMCs. Blocking activation induces vasodilation

Postdural hypotension

Question 14

What is the difference between calcium channel blockers and calcium receptor antagonists?

Answer 14

Ca2+ channel blockers - antagonise ion channels that prevent Ca2+ influx into smooth muscle cells E.g amlodipine

Ca2+ receptor antagonists- drugs that block the activation of receptors that lead to an increase in intracellular [Ca2+]. E.g. Doxazocin and Valsartan

Question 15

What makes carvedilol an ideal candidate for use to treat hypertension associated with angina/MI?

Answer 15

Binds a1, b1 and b2 receptors equally

Question 16

Warfarin

Answer 16

Vitamin K antagonist

Binds vitamin K reductase meaning vitamin K cannot be recycled back into its active form. This inhibits the formation of clotting factors 2,7,9 and 10

Interactions with everything via cytochrome p450 mechanism

Question 17

How do NSAIDS interact with warfarin to alter INR? (2 mechanisms)

Answer 17

Increase serum warfarin via cytochrome p450 interaction

NSAIDS inhibit COX2, leading to less thromboxane-a2 production. This impairs platelet activation

Question 18

What lifestyle factors affect INR? How?

Answer 18

Leafy green vegetables (increase vitamin K)
Binge drinking inhibits warfarin metabolism
Chronic drinking induces warfarin metabolism

Question 19

How is the effect of warfarin reversed?

Answer 19

Vitamin K adminstration

Question 20

How do DOACs differ from Warfarin in their dosing regimes?

Answer 20

DOACS - fixed regime

Warfarin - Based on INR

Question 21

What is the name of the only DOAC that can be reversed? What is the name of the reversal agent?

Answer 21

Dabigatran

Praxbind

Question 22

What is the mechanism of action of Dabigatran?

Answer 22

Thrombin inhibitor

Question 23

What is the mechanism of action of Apixaban?

Answer 23

F10a inhibitor

Question 24

What is the mechanism of action of Edoxaban?

Answer 24

F10a inhibitor

Question 25

What is the mechanism of action of Rivaroxaban?

Answer 25

F10a inhibitor

Question 26

What is tissue plasminogen factor (TPF)? What is it used for?

Answer 26

An enzyme that activates plasmin and hence clot degradation

Used as a thrombolytic drug in the treatment of severe pulmonary embolism/DVT

Question 27

Tranexamic acid

Answer 27

Anti-fibrinolytic drug used in treatment of pre-hospital and surgical trauma

Lysine analogue that binds to plasminogen, inhibiting plasmin production and hence fibrin degradation