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B SL ext. > 1 Myocardial Infarction > Flashcards

1 Myocardial Infarction Flashcards

1
Q

Define an MI

A

Ischaemic necrosis of the myocardium as a result of acute occlusion of a coronary artery

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2
Q

What is included in the clinical definition of MI?

A
  1. Symptoms - characteristic of myocardial pain
  2. ECG changes - characteristic of myocardial infarct/ischaemia
  3. Cardiac enzymes - evidence for cardiac myocyte necrosis (without enzymes → Acute Coronary Syndrome)
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3
Q

What is unstable angina and how should it be treated?

A

Change in character, duration, frequency, severity of chest pain

Treat as acute coronary syndrome

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4
Q

Name some common causes of MI

A

Atheroma,

Hypercoagulability,

Aortic dissection - flap occlusion,

Coronary artery dissection/aneurysm

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5
Q

What are the major symptoms of MI?

A

Chest pain - ususally sudden onset, crushing, >20 mins, may radiate

Sweating

Pallor

Nausea

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7
Q

What are the signs of MI?

A

Excess sympathetic tone - Tachycardia, Hypertension

or Excess parasympathetic tone - Bradycardia and Hypotension

Impaired left ventricle function → hypotension, lung crackles, murmur

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8
Q

What are the stages of ECG changes in MI?

A

ST depression - not always there - ischaemia + partial occlusion

T wave peaking - ischaemia (or hyperkalaemia)

ST elevation - ischaemia + total artery occlusion

T wave inversion - ST segment slowly → baseline

Q wave development

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9
Q

What is indicative of a LBBB?

A

Wide QRS

Broad +/- notched R wave - prolonged upstroke in V5, V6 (and 1, AVL)

Left axis deviation may/may not be present

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10
Q

What are the major cardiac enzymes implicated in MI?

A

Troponin (T or I)

Released within 4-6 hours, raised up 2 weeks after Infarction (but also rises in PE, septicaemia, renal failure, cardiac trauma)

Other enzymes: MB creatinine kinase, Lactate dehydrogenase-1

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11
Q

What is the immediate treatment of MI?

A

AMONAC

Antiemetic, Morphine, O2, Nitrate, Aspirin, Clopidogrel

Cyclizine, Morphine/Diamorphine, GTN, Aspirin, Clopidogrel

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12
Q

What is the treatment for STEMIs?

A

Reperfusion therapy <12 hours

Immediate Percutaneous Coronary Intervention (PCI) - most effective <90 mins

or

Thrombolysis

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13
Q

What does Percutaneous Coronary Intervention involve?

A

Balloon Angioplasty +/- stenting, with drugs:

Glycoprotein IIb/IIIa Inhibitors (Abciximab, Eptifibatide) - Antiplatelet - reduce risk of immediate vascular obstruction

Unfractioned Heparin

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14
Q

What does thrombolysis involve?

A

Recombinant tissue plasminogen activator: Plasminogen → Plasmin → Break down fibrin

Telecteplase

Given with LMWH

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15
Q

What is the treatment and management for an NSTEMI?

A

LMWH, or unfractioned Heparin

Take troponin 12 hours after onset

GRACE system >3% CV event risk → Coronary angiography +/- PCI (within 96 hours)

<3% → non-invasive ischaemia testing

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16
Q

For confirmed MI, what drugs should be given?

A

MI5 (AABCS)

Aspirin - Antiplatelet

ACE inhibitor - Decrease BP and cardiac workload

Beta blocker - Bisoprolol - Slow HR and contractility

Clopidogrel - Antiplatelet

Statin - Lower cholesterol

Also warfarin/fondaparinux (anticoagulants) and Insulin if required

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17
Q

Where are atheromas distributed?

A

Patchily in elastic arteries and large/medium muscular arteries

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18
Q

What are the layers of the arterial wall structure?

A

Intima - Endothelium (simple squamous), basal lamina, subendothelial connective tissue

Media - thickest, smooth muscle, elastic and collagen fibres

Adventitia - thin outer layer to prevent overstretch - contains vasa vasorum, nervi vascularis

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19
Q

What is the structure of a plaque?

A
  1. Fibrous cap - made of smooth muscle, with collagen and elastin
  2. Shoulder regions - accumulation of foam cells and T lymphocytes
  3. Lipid core - oxidised LDL and cholesterol, cell debris and some foam cells
  4. Weak vessel wall under plaque due to degeneration of vessel media
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20
Q

What are the stages of plaque development?

A
  1. LDLs damage and enter the endothelium
  2. Monocytes attracted
  3. Foam cells die
  4. Cytokines encourage smooth muscle to form fibrous cap
  5. Continued growth and development of nectrotic core
  6. Deterioration of plaque
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21
Q

How do LDLs damage and enter the endothelium?

A

Monocytes release free radicals → oxidise LDLs

oxLDL → damages endothelium at points of high shear stress and bind to basement membrane proteoglycans

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22
Q

How are monocytes attracted in plaque development?

A

Damaged endothelium expresses cell surface adhesion molecules for monocytes

Macrophages migrate to subendothelium and take up oxLDL → Foam Cells

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23
Q

What happens when foam cells die?

A

They cannot process LDL, the debris realases further free radicals and attracts more monocytes/T cells

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24
Q

How is the fibrous cap formed?

A

Cytokines cause SMCs to migrate → intima

  1. Secrete collagen and elastin → forms cap
  2. Encourage angiogenesis into plaque
  3. Encourage further SMC migration into plaque/cap
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25
Q

How is the necrotic core formed?

A

Foam cells death → toxic free radicals and cytokines → induction of apoptosis

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26
Q

How does the plaque deteriorate?

A

Macrophage/Foam cells produce factors → SMC death and fibrous cap breakdown

Erosion: Cytokine-induced apoptosis and enzymes cutting basement membrane → endothelium erosion

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27
Q

How does thrombosis form?

A

Erosion/ rupture of the fibrous cap

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28
Q

How does rupture occur?

A

Unstable plaque development:

  1. Thin fibrous cap with few SMCs
  2. Increased inflammatory cell concentration (especially active macrophages instead of foam)
  3. Eroded epithelium
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29
Q

How does NO play a role in plaque formation?

A

Undersecretion

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30
Q

When is NO normally secreted? and what are its actions?

A

In response to shear stress

Vasodilation

Antiatherogenic - inhibits: SMC proliferation, monocyte attraction, LDL oxidation; and antiplatelet effects

Damaged endothelium less likely to be able to produce NO

31
Q

What are the sources of cholesterol?

A

Diet and synthesised by liver from Acety CoA

32
Q

How is cholesterol excreted?

A

Bile acids

33
Q

How is cholesterol regulated in the body?

A

Negative feedback - inhibits further synthesis of itself by inhibiting HMG-CoA reductase

Insulin/glucagon control - insulin → increases synthesis; glucagon → decreases synthesis

Long term control - inhibition of HMG-CoA reductase → decrease cholesterol

also: reduced cellular uptake by inhibition of cholesterol receptor expression

34
Q

What is the basic lipoprotein structure?

A

Non-polar lipid core - mostly TAGs and cholesterol esters

Polar (hydrophilic) outer coat

35
Q

What are the sources of cholesterol?

A

Diet and synthesised by liver from Acety CoA

36
Q

How is cholesterol excreted?

A

Bile acids

37
Q

How is cholesterol regulated in the body?

A

Negative feedback - inhibits further synthesis of itself by inhibiting HMG-CoA reductase

Insulin/glucagon control - insulin → increases synthesis; glucagon → decreases synthesis

Long term control - inhibition of HMG-CoA reductase → decrease cholesterol

also: reduced cellular uptake by inhibition of cholesterol receptor expression

38
Q

What is the basic lipoprotein structure?

A

Non-polar lipid core - mostly TAGs and cholesterol esters

Polar (hydrophilic) outer coat

39
Q

What is a chylomicron?

A

Takes TAGs from small intestine → tissues

40
Q

What do VLDLs do?

A

Take TAGs from liver → tissues

41
Q

What is IDL?

A

Remnant of VLDL and can form LDLs

42
Q

Diagram for major groups of lipoproteins and their actions

A
43
Q

What are LDLs?

A

Take cholesterol esters from IDL → tissues

44
Q

What is HDL?

A

Free cholesterol scavenger in periphery → liver

45
Q

How are long chain FAs transported from the intestine?

A

Converted to TAGs, packaged into chylomicrons → secreted into lacteals

(Exogenous pathway)

46
Q

Diagram for major groups of lipoproteins and their actions

A
47
Q

how are short and medium chain FAs transported from the intestine?

A

Secreted into bloodstream as FFAs

Increase in FFAs in blood → insulin secretion → encourage uptake by liver/muscle/tissue

Decrease FFAs in blood between meals → adipocyte release of FFAs

48
Q

What is a chylomicron?

A

Takes TAGs from small intestine → tissues

49
Q

What does the exogenous lipid transport pathway include?

A

Takes lipids from small intestine → tissues via chylomicrons

  1. Chylomicrons secreted into lymph system by intestinal mucosal cells
  2. Chylomicrons acquire apolipoproteins from HDL circulating in blood (apoC and apoE)
  3. CMs and TAGs broken down → FFAs by lipoprotein lipase (apoC) for the tissues to absorb
  4. Remnants taken up by liver (apoE)
50
Q

What is involved in the endogenous pathway?

A

Takes TAGs and Cholesterol to tissues via VLDL → IDL → LDL

  1. VLDL synthesised in the liver (TAGs + apolipoproteins/cholesterol)
  2. TAGs removed by lipoprotein lipase in capillaries → IDL
  3. Majority IDL donates apolipoproteins to HDL → becomes LDL
  4. LDL taken up by peripheral tissues (provide cholesterol)
51
Q

What does reverse cholesterol transport invovle?

A

Transports free/used cholesterol back to the liver

HDL scavengers: free cholesterol in peripheries → liver

Provides apolipoproteins to CMs, VLDL, IDL

52
Q

What is xanthelasma?

A

Yellow flat plaques on upper/lower eyelids - lipid-containing macrophages condensing around the socket

Usually due to high cholesterol/atheromatous disease

53
Q

What is corneal arcus?

A

Grey opaque line surrounding margin of cornea

Common in Type II Diabetes

54
Q

What is the pathophysiology of Familial Hypercholesterolaemia?

A

Genetic disorder - autosomal dominant, though varying effect with homo/heterozygous

Causes LDL Receptor dysfunction - prevents proper uptake of LDL by cells

55
Q

What investigations can be used for diagnosis of Familial Hypercholesterolaemia?

A

Bloods

Total cholesterol >7.5mmol/l

LDL >4.9mmol/l

Plus tendon xanthoma → diagnosis

56
Q

What is the treatment for Familial Hypercholesterolaemia?

A

Diet/lifestyle

Treatment of associated conditions

Statins - decrease cholesterol synthesis and increase LDL uptake; increase atherosclerotic plaque stability

Fibrates - decrease hepatic secretion + increase peripheral uptake → decrease serum triglyceride

Increase gallstone risk by increasing choleseterol content of bile

57
Q

What is the clinical definition of familial hypercholesterolaemia?

A

Increased total cholesterol or LDL

+ Tendon Xanthoma in patient or close relative

58
Q

how are short and medium chain FAs transported from the intestine?

A

Secreted into bloodstream as FFAs

Increase in FFAs in blood → insulin secretion → encourage uptake by liver/muscle/tissue

Decrease FFAs in blood between meals → adipocyte release of FFAs

59
Q

What is the treatment for Familial Hypercholesterolaemia?

A

Diet/lifestyle

Treatment of associated conditions

Statins - decrease cholesterol synthesis and increase LDL uptake; increase atherosclerotic plaque stability

Fibrates - decrease hepatic secretion + increase peripheral uptake → decrease serum triglyceride

Increase gallstone risk by increasing choleseterol content of bile

60
Q

What investigations can be used for diagnosis of Familial Hypercholesterolaemia?

A

Bloods

Total cholesterol >7.5mmol/l

LDL >4.9mmol/l

Plus tendon xanthoma → diagnosis

61
Q

What is the pathophysiology of Familial Hypercholesterolaemia?

A

Genetic disorder - autosomal dominant, though varying effect with homo/heterozygous

Causes LDL Receptor dysfunction - prevents proper uptake of LDL by cells

62
Q

What is corneal arcus?

A

Grey opaque line surrounding margin of cornea

Common in Type II Diabetes

63
Q

What is xanthelasma?

A

Yellow flat plaques on upper/lower eyelids - lipid-containing macrophages condensing around the socket

Usually due to high cholesterol/atheromatous disease

64
Q

What is the clinical definition of familial hypercholesterolaemia?

A

Increased total cholesterol or LDL

+ Tendon Xanthoma in patient or close relative

65
Q

What does reverse cholesterol transport invovle?

A

Transports free/used cholesterol back to the liver

HDL scavengers: free cholesterol in peripheries → liver

Provides apolipoproteins to CMs, VLDL, IDL

66
Q

What is involved in the endogenous pathway?

A

Takes TAGs and Cholesterol to tissues via VLDL → IDL → LDL

  1. VLDL synthesised in the liver (TAGs + apolipoproteins/cholesterol)
  2. TAGs removed by lipoprotein lipase in capillaries → IDL
  3. Majority IDL donates apolipoproteins to HDL → becomes LDL
  4. LDL taken up by peripheral tissues (provide cholesterol)
67
Q

What does the exogenous lipid transport pathway include?

A

Takes lipids from small intestine → tissues via chylomicrons

  1. Chylomicrons secreted into lymph system by intestinal mucosal cells
  2. Chylomicrons acquire apolipoproteins from HDL circulating in blood (apoC and apoE)
  3. CMs and TAGs broken down → FFAs by lipoprotein lipase (apoC) for the tissues to absorb
  4. Remnants taken up by liver (apoE)
68
Q

How are long chain FAs transported from the intestine?

A

Converted to TAGs, packaged into chylomicrons → secreted into lacteals

(Exogenous pathway)

69
Q

What is HDL?

A

Free cholesterol scavenger in periphery → liver

70
Q

What are LDLs?

A

Take cholesterol esters from IDL → tissues

71
Q

What is IDL?

A

Remnant of VLDL and can form LDLs

72
Q

What do VLDLs do?

A

Take TAGs from liver → tissues

B SL ext. (3 decks)

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