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Clinical Pathology > Cardiovascular Diseases 1 > Flashcards

Cardiovascular Diseases 1 Flashcards

1
Q

Inadequate blood supply to the myocardium

A

Ischaemic heart disease

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2
Q

What degree of coronary artery stenosis is insufficient at rest?

A

> 90%

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3
Q

At what stage in the heart cycle does most perfusion occur?

A

During diastole

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4
Q

3 types of angina pectoris

A

Stable/typical
Variant/prinzmetal
Crescendo/unstable

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5
Q

What type of angina is a fixed obstruction, predictable and related to exertion

A

Stable

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6
Q

What type of angina is due to a coronary artery spasm?

A

Varient/prinzmetal

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7
Q

What type of angina is often due to plaque disruption?

A

Crescendo/unstable

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8
Q

3 causes of acute coronary syndrome?

A

Acute MI with ST elevation
Acute MI without ST elevation
Unstable/crescendo angina

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9
Q

Give 2 types of MI, based on what area of the heart is affected

A

Subendocardial

Transmural

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10
Q

Is subendocardial MI associated with ST elevation?

A

No

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11
Q

Causes of subendocardial MI

A

Stable atheromatous occlusion

Acute hypotensive episode

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12
Q

What type of MI is caused by a sudden blockage that kills the whole wall?

A

Transmural

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13
Q

How do transmural MIs heal?

A

By scarring and fibrosis- no regeneration of myocytes and no contractile function

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14
Q

Causes of transmural MIs

A

Coronary atheroma and thrombus

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15
Q

Gross appearance of heart tissue

A

Normal/dark

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16
Q

Gross appearance of heart tissue 1-2 days after an MI

A

Yellow, infarct centre

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17
Q

Gross appearance of heart tissue 3-7 days after an MI

A

Hyperaemic border, yellow centre

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18
Q

Gross appearance of heart tissue

A

Red/grey

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19
Q

Gross appearance of heart tissue 3-6 weeks after an MI

A

Scar

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20
Q

Microscopic appearance of heart tissue

A

Necrosis and neutrophils

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21
Q

Microscopic appearance of heart tissue 1-2 days after an MI

A

More necrosis and neutrophils

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22
Q

Microscopic appearance of heart tissue 3-7 days after an MI

A

Macrophages

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23
Q

Microscopic appearance of heart tissue 1-3 weeks after an MI

A

Granulation tissue

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24
Q

Microscopic appearance of heart tissue 3-6 weeks after an MI

A

Collagen scar

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25
Q

At what point after an MI is the heart tissue the weakest?

A

3-7 days- infiltrated with macrophages

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26
Q

Name 3 blood markers of cardiac myocyte damage

A

Troponins T&I
Creatinine Kinase
Myoglobin

27
Q

Name the blood markers of cardiac myocyte damage in order of their appearance in the blood post MI

A

Myoglobin, CKMB, Troponin

28
Q

When do troponin levels peak post MI?

29
Q

When else can troponin levels be high in the blood, other than post MI?

A

Renal failure
PE
Heart failure
Myocarditis

30
Q

How does troponin prevent muscle contraction?

A

binds to actin and stops in binding to tropomyosin

31
Q

What are the 3 sybtypes of creatinine kinase and which tissues are they found in?

A

CKMM-cardiac and skeletal muscle
CKBB-brain, lung
CKMB-mainly cardiac, also skeletal muscle

32
Q

7 complications of MIs

A 
Contractile dysfunction and chronic cardiac failure
infarct extension
pericarditis
arrhythmias
mural thrombus
ventricular aneurysm
myocardial rupture
33
Q

In familial hypercholesterolaemia, what are the specific genes affected?

A

low density lipoprotein receptor gene

apolipoprotein B

34
Q

What is the result when the LDL receptor gene is not functional?

A

LDLs are not taken in by the liver, so instead they are taken in by scavengers and settle underneath endothelial cells- contribute to atheroscerosis

35
Q

What is the difference between primary and secondary hypertension

A

primary hypertension develops over a long period of time due to obestiy, diabetes etc. Secondary hypertension develops much more rapidly and is the result of a condition or disease within the body e.g. renal complications, endocrime

36
Q

Which is more common, primary or secondary hypertension?

A

Primary (accounts for 95%)

37
Q

Too much sodium in the blood results in an increase in intravascular volume. As the perfusion exceeds metabolic demand, the body responds by vasoconstriction, resulting in a steady state haemodynamic pattern. Describe this pattern

A

Increase in blood pressure
Increase in systemic vascular resistance
Normal cardiac output

38
Q

What are the 3 main organs affected by hypertension?

A

Kidneys, heart and brain

39
Q

Describe the pathogenesis of hypertensive heart disease

A

Sytemic hypertension, Increase in LV blood pressure, LV hypertrophy without dilation initially in response to an increase in work load. Long term-dilation of LV.

40
Q

What is a normal LV thickness?

41
Q

What BP categorises as a bypertensive crisis?

A

> 180/120 mmHg

42
Q

Dramatic, immediate complications requiring urgent treatment. Results from primary or secondary hypertension

A

Hypertensive crisis

43
Q

What are the 3 main effects of a hypertensive crisis

A

Acute hypertensive encephalopathy
Renal failure
Retinal haemorrhages

44
Q

Diffuse cerebral dysfunction; confusion, vomiting, convulsions, coma and death

A

Acute hypertensive encephalopathy

45
Q

3 causes of pulmonary hypertension

A

COPD
Fibrosis (interstitial lung diseases)
Emboli or thrombosis

46
Q

Pulmonary hypertension occurs secondary to what

A

LV failure

47
Q

Longitudinal study to identify cardiovascular risk factors- calculates an individual risk

A

Framingham heart study

48
Q

Where is renin synthesises, stored and released from?

A

The juxtaglomerular apparatus in the wall of the afferent arterioles in the kidney

49
Q

What does renin do?

A

Cleaves angiotensinogen to angiotensin 1

50
Q

WHere is angiotensin 1 converted to active angiotensin 2?

A

In many tissues, especially lung

51
Q

Role of angiotensin 2

A

Potent natural vasoconstrictor. V.short half life. Stimulates adrenal cortex to produce aldosterone

52
Q

What effect does aldosterone have on the body?

A

It is a physiological mineralocorticoid. It acts on the kidneys and causes Na+ and thus water retention. Circulating blood volume increases.

53
Q

Excessive aldosterone secretion

A

Conn’s syndrome

54
Q

Causes of conn’s syndrome

A

Adrenocorticol adenoma

Micronodular hyperplasia

55
Q

What effects does conn’s syndrome have on aldosterone and renin concentrations

A

Aldosterone increases, renin decreases to compensate.

56
Q

Result of Conn’s syndrome

A

Gain sodium, lose potassium- muscular weakness, cardiac arrhythmias, metabolic alkalosis

57
Q

How do you diagnose conn’s syndrome?

A

CT scan of adrenals in presence of metabolic abnormalities (increase in aldosterone, decrease in renin)

58
Q

Tymour of the adrenal medulla, secretes vasoactive catecholamines- adrenaline and noradrenaline

A

Phaeochromocytoma

59
Q

Effects of phaeochromocytoma

A

Pallor, headaches, sweating, nervousness, hypertension

60
Q

How do you diagnose phaeochromocytoma?

A

24hr urine collection for adrenal metabolites

61
Q

Treatment for phaeochromocytoma?

62
Q

Overproduction of cortisol by adrenal cortex- caused by oversecretion of ACTH

A

Cushing’s disease

63
Q

How is cushing’s disease different from cushing’s syndrome?

A

Cushing’s syndrome- cotisol from any source.

Cusching’s disease- cortisol from adrenal cortex

64
Q

Causes of cushing’s syndrome

A

Adrenocorticol neoplasm (usually an adenoma)
Pituitary adenoma
Paraneoplastic effect of other neoplasms

Clinical Pathology (53 decks)

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