Myocardial Infarction - 206 Flashcards

1
Q

What is the role of chylomicrons?

A

They carry fats from the intestine. In the liver they release triglycerides and some cholesterol

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2
Q

What do HDLs do?

A

Transport cholesterol back to the liver for excretion

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3
Q

What hormone stimulates an increase in uptake of fatty acids by liver cells in response to increased blood conc. of FAs after a meal?

A

Insulin

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4
Q

Some fatty acids are taken up by the liver and converted into what? What happens next?

A

VLDLs. These are secreted into plasma and converted into IDLs, which are then converted to LDLs and fatty acids

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5
Q

There are many different types of hyperlipidaemia. Familial hypercholesterolaemia belongs to which category? Which category does diabetes fall into?

A
FH = Type IIa
Diabetes = Type V
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6
Q

What is the ideal cholesterol level in the blood?

A

5mmol/L

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7
Q

Familial hypercholesterolaemia is what kind of disorder? Which chromosome? What is the mutation in? What clinical sign is virtually diagnostic?

A

Autosomal dominant disorder of chromosome 19. Mutation in LDL receptor.
Tendon xanthomata are virtually diagnostic.

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8
Q

What is the 1st line treatment for Familial hypercholesterolaemia?

A

Statins -> they alter the balance of cholesterol and increase removal of LDL and IDL.
Fibrates are 2nd line -> increase HDL. *caution in renal impairment

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9
Q

What kind of arteries are atheromas found in?

A

Elastic arteries and medium/large muscular arteries

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10
Q

Describe the morphology of an atheromatous plaque (basic terms)

A

Core of lipid (surrounded with macrophages. Within INTIMAL layer). Connective tissue capsule (mostly collagen)

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11
Q

What cells are the only cells capable of protecting against plaque rupture?

A

Vascular smooth muscle cells -> they have stabilising effects

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12
Q

Why should statins be taken in the evenings?

A

Cholesterol synthesis is most active at night

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13
Q

What does total cholesterol have to be above to diagnose familial hypercholesterolaemia? What other signs/symptoms must be present?

A

Above 7.5mmol/L

Tendon xanthoma in patient or 1st degree relative

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14
Q

Is the incubation period for atherosclerotic disease long or short?

A

Long - foam cells and fatty streak can be seen from 1st decade of life

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15
Q

Partial thickness ischaemia causes what ECG changes?

A

ST depression

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16
Q

Full thickness ischaemia can cause what ECG changes?

A

ST elevation

17
Q

What causes pathological Q waves?

A

Where the region of heart muscle has died it becomes pathologically ‘silent’. This causes the Q waves and signifies a full thickness infarct.

18
Q

Percutaneous coronary intervention is indicated for what type of MI?

A

STEMI. If PCI not available iv thrombolytic (fibrinolytic) drugs can be used

19
Q

How does aspirin work?

A

Irreversibly binds to COX-1. Causes vasodilation

20
Q

Minutes after an MI - what does the ecg look like?

A

Increased ST segments , tall pointed T waves facing infarcted area

21
Q

Hours after an MI - what does the ecg show?

A

Pathological Q waves, inverted T waves

22
Q

Days after an MI - how does the ecg look now?

A

Normal ST segments

23
Q

Inferior infarct - which leads will you see this in?

A

II, III and aVF

24
Q

Lateral infarct - which leads will you see this in?

A

I, aVL, V5, V6

25
Q

Antero-septal infarct - which leads will you see this in?

A

V1, V3

26
Q

Antero-apical infarct - which leads will you see this in?

A

V3, V4

27
Q

Occlusion of which artery most commonly causes inferior and septal infarcts?

A

Right coronary artery

28
Q

Occlusion of which artery most commonly causes an anterior MI?

A

LAD

29
Q

What anti-platelet therapy would you most commonly use following a CABG?

A

Aspirin - if it cannot be used then clopidogrel

30
Q

Can ramipril be used in pregnancy?

A

No