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
Antero-septal infarct - which leads will you see this in?
V1, V3
26
Antero-apical infarct - which leads will you see this in?
V3, V4
27
Occlusion of which artery most commonly causes inferior and septal infarcts?
Right coronary artery
28
Occlusion of which artery most commonly causes an anterior MI?
LAD
29
What anti-platelet therapy would you most commonly use following a CABG?
Aspirin - if it cannot be used then clopidogrel
30
Can ramipril be used in pregnancy?
No