Cardiovascular System Flashcards

1
Q

What is atheroma?

A

A degenerative condition affecting large and medium sized arteries.

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2
Q

Name the arteries affected by atheroma in the heart, brain, kidney, intestine and limbs?

A

Coronary, carotid, renal, mesenteric, iliac

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3
Q

How does atheroma develop?

A

It begins with damage to the endothelium of vessel lumen which allows LDL to enter the intima

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4
Q

What happens when lipids enter the intima?

A

They are phagocytosed by macrophages and form a fatty streak

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5
Q

What is the effect of oxidised lipids?

A

These are worse for the cell wall as they oxygen free radicals are particularly damaging

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6
Q

What is lipid plaque?

A

Small amounts of lipid released by macrophages

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7
Q

How is fibrolipid plaque formed?

A

Macrophages secrete cytokines which cause myelofibroblasts to secrete collagen- this causes initial damage to elastic lamina and also covers the plaque surface

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8
Q

What are muscle fibres replaced with?

A

Collagen

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9
Q

What happens the surface of the fibro-lipid plaque?

A

It ulcerates- ulceration exposes collagen with fibrin-platelet thrombus formation

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10
Q

What is the cause of the thinning of media in atheroma?

A

Leads to weakness and inelasticity

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11
Q

What are the risk factors for atheroma?

A

Adverse lipid profile, diabetes, smoking,obesity

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12
Q

What is the role of HDL in protection from atheroma?

A

It reduces free cholesterol and inhibits LDL oxidation

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13
Q

What is the role of endothelial damage in atheroma?

A

Activation of atherogenesis

1) release of growth factors
2) oxidative stress
3) exposure of monocyte adhesion molecules

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14
Q

What are the 3 main consequences of atheroma?

A

1) reduction in size of vessel lumen
2) thrombus formation
3) weakening of vessel walls

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15
Q

Complications of atheroma?

A
Is hammock heart disease
Cerebrovascular disease (stroke) 
Renal artery stenosis
Infarcted bowel
Peripheral vascular disease- gangrene
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16
Q

What is an MI

A

Constriction of blood supply to the heart

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17
Q

What change would you expect in an ecg for MI?

A

And elevated ST segment

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18
Q

What is creating kinase?

A

An enzyme released from myocardial and skeletal muscle cells

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19
Q

How soon after an MI would you see raised creatine kinase? And when would it return to normal?

A

3-6hrs. 3 days

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20
Q

What is troponin?

A

Calcium binding complex in muscle incorporating T and I

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21
Q

How soon after an MI would you see raised troponin and how long will it remain raised?

A

3 hours, last 8 days

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22
Q

What is one problem of troponin over CK?

A

Troponin is expensive to measure

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23
Q

Difference between troponin I and T?

A

I is specific to cardiac troponin

T may cross react with troponin in other tissues

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24
Q

What would troponin be in a patient with acute coronary syndrome?

A

Within reference range

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25
Q

What would troponin be in patients with non ST elevation MI

A

Raised

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26
Q

What is the increased risk of MI or death in patients with non st elevation MI and raised troponin?

A

2 to 3 fold within 3 months

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27
Q

What is the normal CK range or men and women?

A

24-170 U/L and 24-194 U/L in men

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28
Q

What is normal troponin level?

A
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29
Q

What is the prevalence of chronic heart failure and what is the mortality at 5 years?

A

1-2% and 50% mortality at 5 years

30
Q

What is he presentation of chronic heart failure?

A

Shortness of breath and/or ankle oedema

31
Q

Risk factors of chronic heart failure?

A

Previous MI, hypertension,alcohol and drug abuse

32
Q

What is an echocardiogram?

A

An ultrasound examination of heart chambers and coronary blood flow

33
Q

What is a coronary angiography?

A

Catheter passed up the aorta to the right coronary artery and a dye is added that can be seen radiographically

34
Q

What is B type natriuretic peptide (BNP) and how is it formed?

A

Derived from the precursor protein peptide-proBNP- cleaved into biologically active BNP and inactive n-terminal BNP (NT-proBNP)

35
Q

Where is BNP primarily synthesised?

A

Ventricular myocardium

36
Q

What are the actions of BNP? (5)

A
Increase in glomerular filtration rate
Inhibition of sodium resorption
Natriuresis( excretion of Na) and diuresis (excretion of water) 
Vascular smooth muscle relaxation
Reduced blood pressure
37
Q

What is the clinical use ofBNP?

A

Raised in heart attack

38
Q

If a patient has normal BNP - what does this rule out?

A

Chronic heart failure

39
Q

What 2 drugs can cause a fall in BNP?

A

Diuretics and antihypertensive drugs

40
Q

What is digoxin used for?

A

Atrial fibrilation and sometimes heart failure

41
Q

What are toxic effects of digoxin?

A

Nausea and vomiting. Bradycardia (slow heart rate)

42
Q

What’s the therapeutic range for digoxin?

A

1-2 micrograms/L. Must measure 6 h after dose given

43
Q

Hat effect does hypokalaemia have on digoxin

A

Makes it more toxic

44
Q

What is amiodarone used to treat?

A

Cardiac arythmias

45
Q

Side effects of amiodarone

?

A

Alters TFTs . Reduces conversion of t4 to t3. Can develop hypo and hyperthyroidism

46
Q

What is the use of diuretics?

A

Heart failure and hypertension

47
Q

Side effect of diuretics

A

Hyperkalaemia and hypo

48
Q

Name three antihypertensive drugs?

A

Angiotensin converting enzyme inhibitor, thiazides, statins

49
Q

What is hypertension?

A

Systolic blood pressure > 140mm Hg

Diastolic blood pressure >90mm Hg

50
Q

A diastolic BP in the range of what is associated with increased risk of ischaemic heart disease

A

70-110

51
Q

What controls blood pressure- how is cascade triggered?

A

Renin-angiotensin system. Triggered by release of renin from the kidneys in response to a fall in blood pressure

52
Q

What is the role of the sympathetic nervous system in blood pressure?

A

Regulation of vascular tone in the resistance arteries

53
Q

If someone has early onset hypertension or resistant hypertension what should u test for?

A

Underlying endocrine issues

54
Q

Biochemical measuring of patients with hypertension should include what 3 steps?

A

1) check for side effects of antihypertensive drugs
2) check for development of other hypertensive drugs
3) check for development of other cardiovascular risk factors

55
Q

Name antihypertensive drugs?

A
Thiazides diuretics 
Beta blockers 
Calcium antagonists
Ace inhibitors 
Angiotensin receptor antagonists
56
Q

Early onset hypertension combined with electrolyte abnormalities could suggest what?

A

Conns syndrome (aldosterone excess)

57
Q

Early onset hypertension combined with episodic headaches, sweating and palpitations is associated with what?

A

Phaechromacytoma (catecholamine excess)

58
Q

What is aldosterone responsible for?

A

Reabsorption of sodium in exchange for k and h

59
Q

What would be The effect of excess aldosterone of potassium, hydrogen and sodium?

A

Hypokalaemia
Alkalosis (low blood h ion)
High sodium

60
Q

In conns syndrome would you expect to see raised renin levels?

A

No, just aldosterone. Aldosterone/renin will be more than 850

61
Q

What causes hypertension in conns syndrome?

A

Increased sodium reabsorption results in increased water reabsorption and excess exrtracellular volume - hypertension

62
Q

Why is renin normal/low in conns syndrome

A

Hypertension suppresses renin secretion from kidneys

63
Q

Primary hyperaldosterone is shown by….

A

High aldosterone and low renin

64
Q

Secondary aldosterone indicated by….

A

High aldosterone but normal renin. Could be due to antihypertensive drugs

65
Q

WHat is spironalactone?

A

Competitive antagonist of aldosterone receptors

66
Q

Treatment of hyperaldosterone

A

Excision of unilateral adenomas

67
Q

What causes pahechromacytoma?

A

Catecholamine secreting tumour of neuroectodermal tissue

68
Q

What percentage of pahechromacytoma share found outside of the adrenal medulla?

A

10%

69
Q

How do you screen for phaeochromacytoma?

A

24 h urinary catecholamines to measure adrenaline, noradrenaline and metanephrines

70
Q

How do you treat phaeochromacytoma ?

A

With surgery or hypertensive drugs

71
Q

What are foam cells?

A

Cells containing phagocytosed cholesterol

72
Q

What is a risk of statins?

A

Rhabdomyolysis- destruction of striated muscle cells. muscle pain, liver damage and kidney failure