17 - Drug treatments for complex heart conditions

Question 1

What are thrombolytics

Answer 1

Clot busters indicated for MI

Question 2

Side effects of thrombolytics

Answer 2

Haemorrhage
Short half-life
Bleeding diathesis

Question 3

Cryoprecipitate

Answer 3

Antifibrinilytic

Question 4

Tranexamic acid

Answer 4

antifibrinolytic

Question 5

Reverse anti-platelet effects drug

Answer 5

DDAVP (desmopressin)

Platelets

Question 6

Reverse anti-coagulant effects

Answer 6

Protamine

Question 7

Examples of thrombolytics

Answer 7

Strptokinase
Urokinase
Alteplase
(synthetic tpa)

Question 8

MoA of Aspirin

Answer 8

Irreversible COX-2 inhibitor
Stops thromboxame production
Inhibits platelets for a lifecycle

Question 9

What does thromboxane do

Answer 9

Proaggregant and vasoconstrictor

Question 10

Why does aspirin have minimal side effects

Answer 10

It is rapidly destroyed in the systemic circulation

Question 11

Why do other NSAIDs increase the risk of cvs events

Answer 11

Inhibition of COX in macula densa

Leads to water and sodium retention

Question 12

What is aspirin contraindicated in

Answer 12

children under 16

liver disease

Question 13

Can you give aspirin in breastfeeding and why not

Answer 13

No

Reyes syndrome

Question 14

Effects of beta blockers

Answer 14

Reduces infarct size and early mortality

Lowers risk of death long term

Question 15

Mechanism of action of BB

Answer 15

 Competitively antagonise effects of sympathetic nerve stimulation
 Or circulating catecholamines at B-adrenoceptors

Question 16

Where are B1 receptors found+ the effects

Answer 16

• Kidney: inhibit renin release, reduce RAAS

* Heart: SA node, reduces HR and in myocardium decrease cardiac contractility (negative inotropic effect)

Question 17

Examples of BB

Answer 17

Atenolol, bisprolol and metoprolol

Question 18

SE of BB

Answer 18

 Bronchospasm
 Bradycardia
Memory/sleep problems
 Erectile dysfunction

Question 19

MoA of statins

Answer 19

o HMG-coA reductase is the rate limiting step in cholesterol synthesis
o Statins are competitive natural or synthetic inhibitors

Question 20

Non-cholesterol effects of statins

Answer 20

	Decrease macrophage number
	Increase smooth muscle cell maturation
	Increase interstitial collagen
	Decrease matrix metalloproteinase expression
	Decrease TF expression
	Reduce Oxidative stress

Question 21

How do statins decrease plasma cholesterol levels

Answer 21

 Uptake of cholesterol from plasma
 More LDL receptors
 Less synthesis in liver

Question 22

Side effects of statins

Answer 22

	Increases likelihood of developing diabetes
	Sleep disturbances
	Hepatitis 
	Jaundice
	Muscle toxicity

Question 23

Example of ACE-Inhibitor

Answer 23

Ramipril

Question 24

MoA of ACE inhibitor

Answer 24

o Competitive inhibitor of plasma ACE enzyme, preventing conversion of (inactive) angiotensin I to (active) angiotensin II
o Leads to vasodilatation by preventing AngII constriction
o Additional effects on fibrinolysis (Reduction in plasma plasminogen activator inhibitor-1)

Question 25

Absorption, metabolism and excretion of ACE-I

Answer 25

o Absorption – Well absorbed (50-60%)
o Metabolism – Hepatic to the active form ramiprilat
o Excretion – 60% urine

Question 26

Side effects of ACE-I

Answer 26

	Dry irritant cough – bradykinin accumulation
	Angioedema – kinin potentiation 
	Hyperkalaemia
	Hypotension 
	Impairment of renal function

Question 27

• Clopidogrel MOA

Answer 27

P2Y12a inhibitor – further inhibits platelet aggregation

Question 28

GTN MoA

Answer 28

NO donor, to relieve any residual exertional chest pain (angina)