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Flashcards in Cardiovascular Diseases 1 Deck (64):
1

Inadequate blood supply to the myocardium

Ischaemic heart disease

2

What degree of coronary artery stenosis is insufficient at rest?

>90%

3

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

During diastole

4

3 types of angina pectoris

Stable/typical
Variant/prinzmetal
Crescendo/unstable

5

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

Stable

6

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

Varient/prinzmetal

7

What type of angina is often due to plaque disruption?

Crescendo/unstable

8

3 causes of acute coronary syndrome?

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

9

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

Subendocardial
Transmural

10

Is subendocardial MI associated with ST elevation?

No

11

Causes of subendocardial MI

Stable atheromatous occlusion
Acute hypotensive episode

12

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

Transmural

13

How do transmural MIs heal?

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

14

Causes of transmural MIs

Coronary atheroma and thrombus

15

Gross appearance of heart tissue

Normal/dark

16

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

Yellow, infarct centre

17

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

Hyperaemic border, yellow centre

18

Gross appearance of heart tissue

Red/grey

19

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

Scar

20

Microscopic appearance of heart tissue

Necrosis and neutrophils

21

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

More necrosis and neutrophils

22

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

Macrophages

23

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

Granulation tissue

24

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

Collagen scar

25

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

3-7 days- infiltrated with macrophages

26

Name 3 blood markers of cardiac myocyte damage

Troponins T&I
Creatinine Kinase
Myoglobin

27

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

Myoglobin, CKMB, Troponin

28

When do troponin levels peak post MI?

12 hours

29

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

Renal failure
PE
Heart failure
Myocarditis

30

How does troponin prevent muscle contraction?

binds to actin and stops in binding to tropomyosin

31

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

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

32

7 complications of MIs

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

33

In familial hypercholesterolaemia, what are the specific genes affected?

low density lipoprotein receptor gene
apolipoprotein B

34

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

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

What is the difference between primary and secondary hypertension

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

Which is more common, primary or secondary hypertension?

Primary (accounts for 95%)

37

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

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

38

What are the 3 main organs affected by hypertension?

Kidneys, heart and brain

39

Describe the pathogenesis of hypertensive heart disease

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

What is a normal LV thickness?

18mm

41

What BP categorises as a bypertensive crisis?

>180/120 mmHg

42

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

Hypertensive crisis

43

What are the 3 main effects of a hypertensive crisis

Acute hypertensive encephalopathy
Renal failure
Retinal haemorrhages

44

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

Acute hypertensive encephalopathy

45

3 causes of pulmonary hypertension

COPD
Fibrosis (interstitial lung diseases)
Emboli or thrombosis

46

Pulmonary hypertension occurs secondary to what

LV failure

47

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

Framingham heart study

48

Where is renin synthesises, stored and released from?

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

49

What does renin do?

Cleaves angiotensinogen to angiotensin 1

50

WHere is angiotensin 1 converted to active angiotensin 2?

In many tissues, especially lung

51

Role of angiotensin 2

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

52

What effect does aldosterone have on the body?

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

53

Excessive aldosterone secretion

Conn's syndrome

54

Causes of conn's syndrome

Adrenocorticol adenoma
Micronodular hyperplasia

55

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

Aldosterone increases, renin decreases to compensate.

56

Result of Conn's syndrome

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

57

How do you diagnose conn's syndrome?

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

58

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

Phaeochromocytoma

59

Effects of phaeochromocytoma

Pallor, headaches, sweating, nervousness, hypertension

60

How do you diagnose phaeochromocytoma?

24hr urine collection for adrenal metabolites

61

Treatment for phaeochromocytoma?

Surgery

62

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

Cushing's disease

63

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

Cushing's syndrome- cotisol from any source.
Cusching's disease- cortisol from adrenal cortex

64

Causes of cushing's syndrome

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