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Cardiovascular Conditions (JBR) > Myocardial Infarction > Flashcards

Myocardial Infarction Flashcards

1
Q

What is a myocardial infarction?

A

Supply-led ischaemia caused by plaque rupture, fissure, thrombosis

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2
Q

How does a fatty streak develop?

A

Injury of blood vessel endothelium
Uptake of LDL from the blood into artery’s tunica intima
LDL oxidised - OXLDL
Monocyte migrate across endothelium & differentiate into macrophages
Macrophages take up OXLDL (scavenger receptors) and convert them to cholesterol-laden foam cells - form fatty streaks

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3
Q

How do fatty streaks progress to atheromatous plaques?

A

Various cell types release inflammatory substances that cause cell division and proliferation of smooth muscle cells and collagen deposition

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4
Q

How do atheromatous plaques develop into atheroma?

A 
Lipid core (product of dead foam cells) 
Fibrous cap (smooth muscle + collagen) 
= Atheroma
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5
Q

How do platelets become activated in primary homeostasis?

A

Damage to vessel
Expose collagen and TF in sub endothelial matrix
Collagen binds to vWF + platelet glycoprotein binds
Platelet binds to collagen (integral + GPVI receptors)
Platelet activated

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6
Q

How does platelet activation facilitate ADP binding to platelet for further platelet activation?

A 
Activated platelet extends pseudopodia & synthesises TXA2 - binds platelet
Mediator release (5-HT, ADP, vWF, factor V
Vasoconstriction + 5-HT release (indirect & direct)
ADP binds to platelet & activates further platelets
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7
Q

What is a pseudopodia?

A

Temporary membrane extension)

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8
Q

What is TXA2?

A 
Thromboxane 2 
(aka arachidonic acid)
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9
Q

Where are 5-HT and ADP released from in primary haemostasis?

A

Dense granules

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10
Q

Where are factor V and vWF released from in primary homeostasis?

A

Alpha granules

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11
Q

What is the effect of ADP binding to platelet in primary homeostasis - how does it facilitate coagulation?

A

Activates further platelets
Increase platelet receptor expression
Expose phospholipids on platelet surface to facilitate coagulation

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12
Q

What occurs during the initiation phase of the coagulation cascade?

A 
Vascular injury
TF-bearing cells bind to and activate Factor VIIa
Activates factor X to Xa
Xa + Va (co-factor) convert II to IIa 
= small amount of thrombin
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13
Q

What is II?

A

Prothrombin

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14
Q

What is IIa?

A

Thrombin

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15
Q

What happens during the amplification phase of the coagulation cascade?

A

II activates platelets
Release factor V from platelet a-granules + release factor VII from vWF
Thrombin activates Factor XIa - forms complex with factor VIIIa - causing II-IIa conversion
= burst of thrombin production

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16
Q

What is the name of the complex formed between factor XIa and VIIIa?

A

Tenase

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17
Q

What happens during the fibrin formation phase of the coagulation cascade?

A

IIa cleaves fibrinogen forming fragments
Spontaneously polymerise to form fibrin
Factor VIIIa cross-links polymer to form fibrin fibre network = solid clot

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18
Q

What is thrombosis?

A

Pathological haemostasis

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19
Q

Thrombosis is highly unlikely in the arterial unless what? why?

A

Aterosclerosis or other cause of stasis

Blood flow normally laminar

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20
Q

What is an arterial (white) thrombus?

A

Mainly platelets in the fibrin mesh; forms embolus if detached that often lodges in an artery - primary treated with anti-platelets

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21
Q

What is a venous (red) thrombus?

A

red thrombus: white head, jelly-like red tail, fibrin rich

if detaches forms an embolus that usually lodges in the lung (pulmonary embolism)

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22
Q

White thrombi are mainly treated with?

A

Antiplatelets

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23
Q

Red thrombi are mainly treated with?

A

Anticoagulants

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24
Q

What makes up Virchow’s Triad?

A

Endothelial injury
Hypercoagulability
Stasis of blood flow

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25
Q

Ischaemia leads to?

A

Infarction

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26
Q

Infarction is?

A

Death of tissue

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27
Q

How does insufficient ATP for ATP generation cause cell death?

A

Increase calcium stimulating ATPase
Phospholipase - membrane image
Proteases - membrane and cytoskeleton damage
Endonuclease - DNA damage/breakdown
Mitochondrial permeability- release pro-death factors

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28
Q

What re symptoms & signs of an MI?

A

Severe central crushing pain radiating to the jaw and (esp. left) arm(s)
Similar to angina attack but more severe + not received by GTN
Associated with sweating, causes & (often) vomiting

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29
Q

Which ECG change is observed in the first few hours?

A

ST elevation

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30
Q

Which ECG change is observed in 1st day?

A

T wave inversion and Q waves

New onset LBBB

31
Q

ST elevation in leads II, III and aVF is?

A

Inferior MI

32
Q

ST elevation in leads V1-V6 is?

A

Anterior MI

33
Q

ST elevation in leads V1-V4 is?

A

Anteroseptal MI

34
Q

ST elevation in leads I, aVL, V1-V6 is?

A

Anterolateral MI

35
Q

Creatinine kinase peaks within?

A

24 hours

36
Q

Troponin I and T are highly specific to?

A

Cardiac necrosis

37
Q

What are complications post-MI?

A 
Cardiac rupture
Dressler's syndrome
VSD
Mitral valve regurgitation
Left ventricular aneurysm formation
Mural thrombosis +/- septum emboli
Inflammation
Acute pericarditis
38
Q

What is Dressler’s Syndrome?

A

Type of pericarditis that occurs many (6) weeks after an MI

39
Q

What is the pathophysiology behind Dressler’s syndrome?

A

Damaged heart releases previously un-encountered material stimulating an immune response

40
Q

What are non-pharmacological guidelines to secondary preventative measures?

A

No smoking
Healthy diet
Regular aerobic exercise

41
Q

What should be the aimed cholesterol level?

A

<4 mmol/L

42
Q

What is the aimed BP?

A

<140/86

43
Q

In organ damage diabetes, renal disease and/or organ damage; target BP is?

A

135/80

44
Q

What drug regimen is recommended post-MI?

A 
Consider warfarin for 3 months if large anterior MI
Aspirin
Beta-blocker
ACEI
Statin
?Clopidogrel
45
Q

What is the mechanism of warfarin?

A

Blocks clotting factors II, VII, IX and X

Prevent new thrombosis by binding to hepatic vitamin K reductase preventing conversion of epoxide to active hydroquinone

46
Q

How is warfarin administered?

A

PO

47
Q

What is warfarin’s onset of action?

A

2-3 days

48
Q

Why does warfarin take a while to take actionß

A

Inactive factors replace active gamma-carboylated factors that are slowly cleared from plasma

49
Q

What may be added to warfarin for rapid anticoagulatory effect?

A

Heparin

50
Q

Warfarin has a low therapeutic index. Patients need to be monitored using the?

A

INR

51
Q

What are side effects of warfarin?

A

Haemmorhage

52
Q

What potentiates the risk of haemorrhage with warfarin treatment?

A

Liver disease
Increased metabolic rate
Drug interaction (aspirin/NSAIDs)
Reduction of vitamin K

53
Q

Why do NSAIDs potentiate warfarin haemorrhage risk?

A

Inhibit platelet function

54
Q

What do you give a patient if they overdose on warfarin?

A

Vitamin K

55
Q

What is the mechanism of aspirin?

A

Irreversibly blocks cyclo-oxygenase (COX) in platelets and anti-thrombotic prostaglandin I2 in endothelial cells
Endothelial cells can produce new COX; platelets can’t resulting in anti-thrombotic dominance

56
Q

Giving aspirin inhibits TXA2 synthesis for 7-10 days. Why?

A

Irreversible blockage of COX - all platelets need to be replaced; takes 7-10 days

57
Q

What is an example of a beta-blocker used?

A

Bisoprolol

58
Q

What is an example of a statin?

A

Simvastatin

59
Q

A statin aims to..?

A

Reduce total and LDL cholesterol
Reduce triglycerides
Slightly increase HDL
Decrease inflammation, reverse endothelial dysfunction, decrease thrombosis, stabilise atherosclerotic plaques

60
Q

What is the mechanism of a statin?

A

Competitive inhibitor of HMG-CoA reductase - rate limiting step in cholesterol synthesis

61
Q

How do you administer a statin?

A

PO

62
Q

What are the side effects of a statin?

A

Myositis

Rarely rnhabdomylosis

63
Q

A statin shouldn’t be prescribed in?

A

Pregnancy

64
Q

What is the mechanism of clopidogrel?

A

Forms disulphide bond to P24-12 receptor
Irreversible inhibitor
Prevents ADP activating platelets

65
Q

How do you administer clopidogrel?

A

PO

66
Q

Clopidogrel has a synergistic effect with?

A

Aspirin

67
Q

What are the side effects of clopidogrel?

A

Dyspepsia, abdo pain, diarrhoea, bleeding disorders

68
Q

What is the pathogenesis of atheroma?

A

Endothelial injury causes trans-endothelia migration
Macrophages stimulate lipid uptake which along with smooth muscle proliferation and collagen and fibrin acccumulation forms a fibro-fatty plaque

69
Q

What are the risk factors for atheroma

A 
Smoking 
Hypertension
Hyperlipidaemia
Diabetes
Old age
Male sex 
Genetics (rare)
70
Q

What are complications of atheroma?

A 
Stenosis
Thrombosis
Aneurysm
Dissection 
Embolism
71
Q

What is used to reopen occluded arteries in an acute MI or stroke? (rarely used)

A

Fibrinolytics

72
Q

What is an example of a fibrinolytic that decreases mortality in acute MI?

A

Streptokinase (admin IV)

73
Q

How can overdose of streptokinase be controlled?

A

Oral Tranexamic acid (inhibits plasminogen activation)

74
Q

Streptokinase should not be given if the patient has had a recent ______ infection

A

Strep

Cardiovascular Conditions (JBR) (20 decks)

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