Drug treatment for complex heart disease Flashcards

1
Q

Define myocardial infarction

A

Irreversible necrosis of heart muscle secondary to prolonged ischaemia

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2
Q

4 particularly prevelant risk factors for MI

A

High blood pressure
High blood cholesterol
Diabetes
Family history of premature CAD

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3
Q

Function of thrombolytics

A

Clot buster

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4
Q

What is tissue plasminogen activator

A

Fibrinolytic agent found in endothelial cells
Exhibits significant fibrin specificity and affinity binding of tpa and plasminogen to fibrin induces conformational change
faciliates conversion of plasminogen to plasmin clot dissolves

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5
Q

What inhibits conversion of plasminogen to plasmin

A

Plasminogen activator inhibitor 1 (PAI 1)

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6
Q

What activates conversion of plasminogen to plasmin

A

tissue plasminogen activate t-PA

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7
Q

What inhibits conversion of plasmin to fibrin

A

Thrombin activatable fibrinolysis inhibitor (TAFI)

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8
Q

What inhibits conversion of fibrin to thrombin

A

FDPs

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9
Q

Simple mechanism of aspirin

A

Irreversible inhibitor of COX
Platelets cannot make new proteins as lack nucleus
Stops thromboxane production

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10
Q

What is thromboxane

A

Potent platelet stimulator

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11
Q

How are side effects minimised when a low dose of aspirin is gievn

A

Low dose inhibits platelets in portal blood so is rapidly destroyed in systemic circulation

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12
Q

When is aspirin contraindicated

A

Children <16 y old

Small risk of fulminant liver failure

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13
Q

When is aspirin cautioned

A

Bleeding diathesis

Severe hypertension

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14
Q

Why is aspirin given to pregnant women and what are potential side effects

A

To reduce risk of pre-eclampsia

Small risk of closure of DA which could lead to PPHN

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15
Q

Can you use aspirin when breast feeding

A

Small amounts get into breast milk- avoid due to risk of Reyes syndrome

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16
Q

Can you give aspirin to patients with liver disease?

A

Avoid due to bleeding risk

Often auto-anticoagulated due to reduced clotting factors

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17
Q

Can you given aspirin to patients with renal disease

A

Increased risk of bleeding

Salt and water retention

18
Q

Why are beta blockers used for patients with AMI?

A

BBs reduces infarct size and early mortality when started early
Lowers risk of death when continued long term

19
Q

Where are beta 1 receptors found

A

Heart and kidney

20
Q

Where are beta 2 receptors found

A

Lungs, peripheral blood vessels, skeletal muscle

21
Q

Action of beta blockers on the kidney?

A

Blocks beta 1 receptors
Inhibits renin release
Reduces RAAS

22
Q

Action of beta blockers of the heart

A

Blocks beta 1 receptors on SAN reduces heart rate (negative chronotrophic effect(
blockage of beta 1 in myocardium reduces contractibility (negative inotropic effect(

23
Q

Action of beta blockers on the central and peripheral nervous system

A

Blockage of beta-receptors in the brainsteam and of prejunctional beta receptors in the periphery inhibits release of neurotrasmitters and decreases sympathetic nervous system activity

24
Q

Give three examples of cardioselective beta blockers

A

atenolol
bisoprolol
metoprolol

25
Q

Name a beta blocker which acts as a local anaesthetic and anti-arrhythmic effect

A

sotalol

26
Q

Name a beta blocker with partial agonist activity

A

Pindolol

27
Q

What risks are associated with a mother using beta blockers during pregnancy?

A

Intra-uterine growth restriction
Neonatal hypoglycaemia
Bradycardia

28
Q

Can you be on beta blockers as a breast feeding mother?

A

Infants should be monitored as small chance of toxicity. However, usually too small amount to affect infants

29
Q

Can you use beta blockers if you have renal disease

A

Sometimes

Some beta blockers are renally excreted and accumulate in renal failure

30
Q

What is the rate limiting step in cholesterol synthesis

A

HMG-coA

31
Q

What are statins

A

Competitive natural or synthetic inhibitors of HMG-coA

32
Q

What is propranolol and where does it act

A

Beta antagonist

Acts to prevent renin release

33
Q

Where does aliskiren act?

A

Conversion of angiotensinogen to angiotensin 1

anti hypertensive

34
Q

Where does captopril act?

A

Angiotensin 1 to angiotensin 2 (ACE inhibitor)

anti hypertensive

35
Q

Where does losartan act?

A

Blocks AT1 receptors

anti hypertensive

36
Q

How do ACE inhibitors work?

A

Competitive inhibitor of plasma ACE enzyme, preventing conversion of angiotensin 1 to active 2
leads to vasodilation by preventing ang 2 constriction
effects greatest when RAAS ssytem is up

37
Q

True or false- most ACE inhibitors are pro drugs that require conversion to active form

A

TRUE

38
Q

Describe the events that occur after an MI which can lead to ventricular remodelling and myocardial dysfunction

A
  • Survivors of MI have significant risk of future cardiovascular events
  • Infarct expansion due to thinning and stretching of infarct zone
  • Significant left ventricular dilation can begin within 3 hours
  • Remodelling process begins with myocyte necrosis and formation of fibrotic scar.
  • Followed by elongation of infarcted segment and then dilation and hypertrophy of border zone ventricular myocardium
39
Q

Basic mechanism of clopidogrel?

A

P2Y12a inhibitor

Further inhibits platelet aggregation

40
Q

What is the role of thrombolytics?

A

Immediately stop ongoing infusion of thrombolytic drug

Stop all antiplatelet and anticoagulant therapies

41
Q

7 side effects of ADRs

A
Bronchospasm
Bradycardia
Hypotension
Memory
Diabetogenis
Erectile dysfunction
Worsens psoriasis
42
Q

What is the main affect of ACE inhibitors

A

Dry irritant cough