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Year 2 Clinical Pathology > Cardiovascular disease 1 > Flashcards

Cardiovascular disease 1 Flashcards

1
Q

What is the definition of ischeamic heart disease?

A

Inadequate blood supply to the myocardium due to any imbalance in supply vs. demand

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2
Q

For what 2 main reasons could someone have inadequate blood supply to the myocardium?

A

1) Reduced coronary blood flow - usually atheroma - with or without thrombus
2) Myocardial hypertrophy, usually due to systemic hypertension

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3
Q

Why does diastolic insufficiency occur in IHD?

A

Most perfusion of the heart occurs during diastole when the aortic valve is closed and there is a degree of back flow into the cusps - in IHD during diastole is when the relative O2 deficit is at its worst

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4
Q

What is loss of autoregulation in IHD, at what percentage of occlusion does it occur?

A

Autoregulation of the vessels is dilation and constriction according to demand, vessels lose autoregulation when they cannot dilate sufficiently to allow enough blood through - this happens at >75% occlusion

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5
Q

At what percentage of stenosis is blood supply to the heart insufficient at rest?

A

> 90%

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6
Q

In which type of IHD is low diastolic flow particularly apparent?

A

Sub endocardial

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7
Q

How many seconds of ischemia are possible before function of the myocardium is lost?

A

60 secs

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8
Q

What happens to the myocardium if ischaemic for more than 60 secs?

A

Get myocyte dysfunction and death from ischemia

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9
Q

After how many minutes of ischemia is the damage to the myocardium irreversible?

A

20-30 mins

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10
Q

Name 4 common ischemic heart disease syndromes?

A

1) Angina pectoris
2) Acute coronary syndrome
3) Sudden cardiac death
4) Chronic ischaemic heart disease

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11
Q

What are the 3 types of angina?

A

1) Typical/stable - fixed obstruction, predictable relationship to exertion
2) Variant/Prinzmetal - coronary artery spasm
3) Crescendo/ unstable - often due to plaques disruption and small emboli, pain is getting worse and more unpredictable

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12
Q

Which of the 3 types of angina is a red flag and requires urgent treatment?

A

Crescendo/unstable angina

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13
Q

What classifies a cardiac infarct?

A

Loss of myocytes

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14
Q

What are the 2 acute coronary syndromes?

A

1) Acute myocardial infarction (+/- ECG ST elevation)

2) Crescendo/unstable angina

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15
Q

Why does a subendocardial myocardial infarction commonly occur without any acute coronary occlusion?

A

1) The subendocardial myocardium is relatively poorly perfused in normal conditions (far from coronary vessels and far from heart chamber for direct diffusion)
2) If there is a stable angina or an acute hypotensive episode…
3) The subendocardial myocardium can infarct without any acute coronary occlusion
Subendocardial MIs are different to your typical MIs

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16
Q

What is a transmural myocardial infarction?

A

Severe occlusion of the coronary vessel leads to death of myocytes across all layers of the myocardium

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17
Q

What would be the gross and microscopic appearance of an infarct less than 24 hours old?

A

Microscopic - necrosis and neutrophils

Gross - normal/dark

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18
Q

What would be the gross appearance of an infarct which was:

a) 1-2 days old
b) 3-7 days old
c) 1-3 weeks old
d) 3-6 weeks old

A 
Gross appearance
1-2 days = yellow infarct center
3-7 days = hyperaemic border, yellow center
1-3 weeks = red/grey
3-6 weeks = scar
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19
Q

What would be the microscopic appearance of an infarct which was:

a) 1-2 days old
b) 3-7 days old
c) 1-3 weeks old
d) 3-6 weeks old

A

1-2 days = more necrosis and neutrophils (than

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20
Q

What are the 5 blood markers of cardiac myocyte damage?

A

1) Troponins T and I
2) Creatine kinase MB
3) Myoglobin
4) Lactate dehydrogenase isoenzyme 1
5) Aspartate transaminase

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21
Q

Which blood marker is most commonly used post MI, when does it peak, for how many days is it raised?

A

Troponin

Detectable after 2-3 hours, peaks at 12 hours and detectable for up to 7 days

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22
Q

In what 3 other conditions is troponin raised?

A

1) heart failure
2) Myocarditis
3) PE

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23
Q

Creatine Kinase MB is detectable how may hours post MI and peaks when, when can you detect it til?

A

Detectable 2-3 hours post MI for up to 3 days

Peaks at 10-24 hours

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24
Q

Myoglobin peaks when post MI, why is it not the most useful?

A

Peaks at 2 hours

Less useful as also released from skeletal muscle

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25
Q

Lactate dehydrogenase isoenzyme 1 peaks how many days post MI and is detectable for how many?

A

Peaks at 3 days, detectable for up to 14 days

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26
Q

Why is aspartate transaminase a less useful blood marker of cardiac myocyte damage?

A

Because its also present in the liver

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27
Q

What are the 3 subtypes of creatine kinase, where is each mostly found?

A

1) CK MM - muscle (cardiac and skeletal)
2) CK BB - brain, lung
3) CK MB - mainly cardiac, also skeletal muscle

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28
Q

On the basis of what 3 factors is a diagnosis of MI made?

A

1) Clinical
2) ECG
3) Blood cardiac proteins

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29
Q

What percentage of people die from sudden cardiac death immediately post MI?

A

20%

30
Q

What are the 7 common complications of MI?

A

1) Contractile dysfunction and chronic cardiac failure
2) Arrhythmias
3) Infarct extension (free wall, septum, papillary muscle)
4) Myocardial rupture
5) Pericarditis - Dressler’s syndrome
6) Mural thrombus
7) Ventricular aneurysm

31
Q

What is Dressler’s syndrome?

A

Secondary form of pericarditis following damage to the heart or pericardium - believed to be caused by immune response following such injury

32
Q

What is the term for blood filling the pericardial sac?

A

Haemopericardium

33
Q

What is chronic ischaemic heart disease?

A

Coronary atheroma produces relative myocardial ischemia and angina pectoris on exertion

34
Q

What is the main risk with CIHD and what 2 things does it lead to?

A

Risk of sudden death or MI

Leads to cardiac hypertrophy and dilatation

35
Q

What is familial hypercholesterolaemia?

A

Mutations in genes involved in cholesterol metabolism

36
Q

Which 2 genes are most commonly mutated in familial hypercholesterolaemia?

A

1) LDL receptor gene

2) Apolipoprotein B

37
Q

What are the 3 main clinical signs seen in familial hypercholesterolaemia heterozygotes?

A

1) Xanthomas - cholesterol deposits in tendons
2) Corneal arcus
3) Early atheroscelrosis

38
Q

What is the treatment for familial hypercholesterolaemia heterozygotes?

A

Statins

39
Q

How does the treatment for homozygotes for familial hypercholesterolaemia differ to that for heterozygotes?

A

More complex and less effective

40
Q

Blood pressure is physiologically regulated to fulfil what 2 functions?

A

1) Ensure the perfusion of organs is sufficient to maintain function
2) Prevent higher flow that exceeds metabolic demands, increases damage to blood vessels and thus organs

41
Q

What is considered normal BP?

A

120/80

42
Q

What is considered abnormal BP?

A

Sustained systolic 140

43
Q

What percentage of cases of hypertension are primary ie. idiopathic?

A

95%

44
Q

Why is it difficult to identify individuals susceptible to primary hypertension?

A

Likely caused by many physiological systems interacting over long periods of time with minor dysfunctions

45
Q

How is the hypothesis that all essential (primary) hypertension share the common pathway of positive sodium balance (ie increased salt intake) explained?

A

1) Positive sodium balance leads to increased IV volume and volume delivery to the heart augmenting cardiac output and thus pressure
2) Tissue perfusion thus exceeds metabolic demand leading to autoregulation of blood flow to increase vasoconstriction to reduce blood flow
3) This results in a pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output

46
Q

Name the 4 classes of causes of secondary hypertension?

A

1) Renal
2) Cardiovascular
3) Endocrine
4) Neurologic

47
Q

Name 3 important endocrine causes of secondary hypertension?

A

1) Cushings syndrome (overproduction of steroids)
2) Primary aldosteronism (excess aldosterone)
3) Phaemochromocytoma (tumour of adrenal glands resulting in overproduction of adrenaline and noradrenaline)

48
Q

Describe hypertensive heart disease?

A
  • Systemic hypertension leads to increased LV BP
  • LV hypertrophy without dilatation initially in response to increased work needed to pump blood
  • When the pressure is too great the LV fails to pump blood at normal rate and dilates
  • Recognized cause of sudden death
49
Q

What are the main renal effects of hypertension?

A

Get vascular changes in primary hypertension:
- arterial intimal fibroelastosis
- Hyaline arteriosclerosis
Slow deterioration in renal function leading to chronic renal failure

50
Q

What is hypertensive cerebrovascular disease?

A

(Hypertensive encephalopathy)
Increased risk of rupture to abnormal arteries:
- Atheromatous (circle of Willis)
- berry aneurysms of the circle of willis (SAH)

51
Q

How is a hypertensive crisis (malignant hypertension) defined?

A

BP >180/120

52
Q

A hypertensive crisis shows which 3 clinical signs of organ damage?

A

1) Acute hypertensive encephalopathy
2) Renal failure
3) Retinal haemorrhages
Requires urgent treatment to preserve organ function

53
Q

What are the 4 main symptoms of and acute hypertensive encephalopathy?

A 
Diffuse cerebral dysfunction:
1) Confusion 
2) Vomiting
3) Convulsions
4) Coma - death
(Rapid intervention is required to reduce the accompanying raised ICP)
54
Q

What is pulmonary hypertension?

A

Higher than normal pressure in the pulmonary artery

55
Q

What are the 4 main causes of pulmonary hypertension?

A

1) Loss of pulmonary vasculature (COPD, Interstitial lung disease, PE or thrombosis, under ventilated alveoli)
2) Secondary to LV failure
3) Systemic to pulmonary artery shunting
4) Primary or idiopathic

56
Q

What changes in the heart does pulmonary hypertension lead to?

A
  • Increased right ventricular work to pump blood
  • RV myocardial hypertrophy initially without dilation
  • Later dilatation and systemic venous congestion as RV failure develops
57
Q

Which ethnicity is a risk factor for CV disease?

A

South Asian

58
Q

What was the Framingham Heart Study?

A

Longitudinal population study to identify risk factors for CV disease

59
Q

What is the Framingham risk score and how can it be calculated?

A
  • Calculates an individuals risk of CV disease based on assessment of multiple risk factors
  • Can be calculated using computer algorithms or manually using a table
60
Q

Name 3 CV risk assessments other than the Framingham risk score?

A

1) SCORE - European society of cardiology
2) QRISK2
3) Joint British Societies risk prediction charts

61
Q

Where is Renin synthesised and stored, what is its role?

A
  • Synthesized, stored in and released from the juxtaglomerular apparatus in the wall of the afferent arterioles of the kidney (in response to low perfusion pressure)
  • Cleaves angiotensinogen to angiotensin 1
  • Angiotensin 1 is converted to angiotensin 2 in many tissues
62
Q

What effect does Angiotensin 2 have?

A
  • Potent vasoconstrictor with a very short half life

- Stimulates the adrenal cortex to produce aldosterone

63
Q

What is aldosterone, what effect does it have?

A
  • Physiological mineralocorticoid
  • Renal action causes sodium and thus water retention
  • Thus circulating blood volume increases
64
Q

What is Conn’s syndrome caused by?

A

Excess aldosterone secretion usually due to adrenocortical adenoma, possibly micronodular hyperplasia

65
Q

What are the 3 endocrine/electrolyte imbalances in Conn’s syndrome?

A

1) Renal sodium and water retention - hypertension
2) Elevated aldosterone, low renin
3) Potassium loss - muscular weakness, arrhythmias, paraesthesia, metabolic alkalosis

66
Q

How is Conn’s syndrome diagnosed?

A

CT scan of adrenals in presence of metabolic abnormalities of the disease

67
Q

What is phaeochromocytoma?

A

Tumour of the adrenal medulla

68
Q

What leads to the presenting symptoms of phaeochromocytoma?

A

Secretion of vasoconstrictive catechoamines - adrenaline and noradrenaline

69
Q

How is phaeochromocytoma diagnosed following presentation with symptoms?

A

24 hour urine collection for adrenaline metabolites

70
Q

What are the 5 main presenting symptoms of phaeochromocytoma?

A

1) Pallor
2) Headaches
3) Sweating
4) Nervousness
5) Hypertension

71
Q

What is Cushings disease?

A

Overproduction of cortisol by adrenal cortex - cortisol has many metabolic effects including potentiating SNS activity and aldosterone-like effects on the kidneys causing hypertension

72
Q

What are the 3 possible causes of Cushing’s syndrome?

A

1) An adrenocortical neoplasm - usually an adenoma
2) A pituitary adenoma
3) Paraneoplastic effect of other neoplasms (particularly small cell lung carcinoma) - producing adrenocorticotrophic hormone that stimulates the zona fasiculata cells of the adrenal cortex to produce cortisol)

Year 2 Clinical Pathology (64 decks)

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