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Clinical Pathology > 28 - Cardiovascular Disease 1 > Flashcards

28 - Cardiovascular Disease 1 Flashcards

1
Q

Ischaemic heart disease - definition

A

Inadequate blood supply to the myocardium via atheroma/ thrombus/ myocardial hypertropy

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2
Q

Ischaemic heart disease - pathogenesis

A

Acute & chronic

Autoregulation of coronary blood flow breaks down if

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3
Q

Ischaemic heart disease - syndromes

A

Angina pectoris
Acute coronary syndrome
Sudden cardiac death
Chronic ischaemic heart disease

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4
Q

Angina pectoris - types

A

Typical/stable - fixed obstructable, predictable on exertion
Variant/Prinzmetal - coronary artery spasm, unpredictable
Crescendo/unstable - red flag syndrome due to plaque disruption

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5
Q

Acute coronary syndrome

A 
Acute MI (+/- ECG ST elevation)
Crescendo/unstable angina
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6
Q

Acute ischaemia - causes and why

A

Atheroma + acute thrombosis / haemorrhage

Lipid rich plaques at most risk

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7
Q

Acute ischaemia - what is it?

A

Regional transmural myocardial infarction

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8
Q

Acute ischaemia - management

A

Thrombolysis

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9
Q

Acute ischaemia - Diagnosis

A

Clinical
ECG
Blood cardiac proteins

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10
Q

Subendocardial myocardial infarction - why is that region vulnerable?

A

subendocardial most vulnerable due to less blood going to it as capillaries run over endocardium

Can infarct without any acute coronary occlusion

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11
Q

Subendocardial myocardial infarction - ST elevation?

A

Rarely

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12
Q

Blood markers of cardiac myocyte damage - troponins T&I

A

Detectable 2-3hrs peaks at 12h detectable at 7 days.

Raised post-MI but also in PE, heart failure & myocarditis

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13
Q

Blood markers of cardiac myocyte damage - Creatine kinase

A

Detectable 2-3hrs, peaks at 10-24hrs, detectable to 3 days

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14
Q

Blood markers of cardiac myocyte damage - Myoglobin

A

peak at 2hrs but also released from damaged skeletal muscle

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15
Q

Blood markers of cardiac myocyte damage - lactate dehydrogenase isoenzyme 1

A

Peaks at 3 days, detectable to 14 days

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16
Q

Blood markers of cardiac myocyte damage - aspartate transaminase

A

Also present in liver so less useful as a marker of myocardial damage

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17
Q

Blood markers of cardiac myocyte damage - most useful/only one used?

A

Troponin

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18
Q

Blood markers of cardiac myocyte damage - creatine kinase subtypes

A

CK MM - muscle
CK BB - brain, lung
CK MB - cardiac, possibly muscle

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19
Q

Familial hypercholesterolaemia - commonest mutations

A 
Low density lipoprotein receptor gene (1in500)
Apolipoprotein B (1 in 1000)

Note homozygous more severe

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20
Q

Whats a xanthoma and egs.

A

Tendons
Periocular
Corneal arcus
Early atherosclerosis

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21
Q

Which is more common - primary hypertension or secondary?

A

Primary (95%)

Main secondary is hyperthyroidism

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22
Q

Renin cycle

A

Synthesised, stored and release in juxtaglomerular apparatus in the wall of afferent renal arterioles.

Cleaves Angiotensinogen to Ang I
Ang I is converted to active Ang II in many tissues

23
Q

Ang II facts

A

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

24
Q

Aldosterone facts

A

Physiological mineralocorticoid
Renal action causes sodium and water retention
Circulating blood volume increases

25
Q

Conn’s syndrome - causes and why

A

Caused by excess aldosterone secretion

Why: adrenocortical adenoma, micronodular hyperplasia, renal sodium&water hypertension, elevated aldosterone w/ low renin, potassium loss (via muscle weakness.

26
Q

Conn’s syndrome - diagnosis

A

Diagnose by CT scan of adrenals in presence of metabolic abnormalities

27
Q

Phaeochromocytoma - what is it? what causes the symptoms?

A

Tumour of adrenal medulla

Presents due to secretion of vasoconstrictive catecholamines - AD and NA

28
Q

Phaeochromocytoma - clinical presentation

A 
Pallor
Headaches
Sweating
Nervousness
Hypertension
29
Q

Phaeochromocytoma - diagnosis

A

24hr urine collection for AD metabolites

30
Q

Cushing’s disease - what is it? + effects

A

Overproduction of cortisol by adrenal cortex

Potentiating SNS and has mineralocorticoid (aldosterone-like) action of kidneys causing hypertension

31
Q

Cushing’s disease - causes

A

Adrenocortical neoplasm usually an adenoma

A pituitary adenoma (80% cause) or paraneoplastic effect of other neoplasms (small lung cell carcinomas).

The other neoplasms produce adrenocorticotrophic hormone that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol

32
Q

Hypertension - effects

A

CV - hypertensive heart disease
Renal failure
Cerebrovascular incident

33
Q

Hypertension - hypertensive heart disease

A

Systemic hypertension leads to increased LV blood pressure -> LV hypertrophy
When pressure is too great LV fails to pump blood at normal rate and dilates

34
Q

Hypertension - renal effects

A

Vascular changes:
Arterial intimal fibroelastosis
Hyaline arteriolosclerosis

Slow deterioration in renal function leading to failure

35
Q

Hypertensive cerebrovascular disease

A

Hypertensive encephalopathy
Increased risk of rupture of abnormal arteries - atheromatous (intracerebral haemorrhage); berry aneurysm of the circle of Willis (subarachnoid haemorrhage)

36
Q

Hypertension - hypertensive crisis

A

BP >180/120

37
Q

Hypertension - hypertensive crisis clinical presentation

A

Acute hypertensive encephalopathy
Renal failure
Retinal haemorrhages

Urgent treatment

38
Q

Hypertension - acute hypertensive encephalopathy

A

Clincopathological syndrome
Diffuse cerebral dysfunction - confusion, vomiting, convulsions, coma and death
Rapid intervention required to reduce accompanying raised intracranial pressure

39
Q

Pulmonary hypertension - caused by

A

Loss of pulm. vasculature
2* to LV failure
Systemic to pulm. art. shunting
Primary or idiopathic

40
Q

Pulmonary hypertension - causes

A

Increased RV work to pump blood
RV myocardium hypertrophy initially w/o dilation
Later dilation and systemic venous congestion as RV failure develops

41
Q

What is Framingham risk score?

A

Calculates an individual’s risk of CVD based on multiple risk factors and algorithms

42
Q

Other risk assessment systems

A

SCORE
QRISK2
Joint British societies risk prediction charts

43
Q

What is renin? Where is it made and released from?

A

Synthesised, stored in and released from juxtaglomerular apparatus in wall of afferent arteriole of kidney

44
Q

What does renin do?

A

Cleaves angiotensinogen to angiotensin I

45
Q

Where is Ang1 cleaved?

A

AngII in many tissues

46
Q

What is AngII and what does it do?

A

Potent vasoconstrictor
Very short half-life
Stimulates adrenal cortex to produce aldosterone

47
Q

What is aldosterone?

A

Physiological mineralocorticoid

Causes sodium, and in turn, water retention

Increases blood volume

48
Q

What is Conn’s syndrome?

A

Excess aldosterone secretion

Adrenocortical adenoma

Renal sodium and Na retention

Elevated aldosterone and low renin

Potassium loss

49
Q

What does potassium loss cause?

A

Muscular weakness
Cardiac arrhythmias
Parasthaesesia
Metabolic alkalosis

50
Q

Phaeochromocytoma - what is it?

A

Tumour of adrenal medulla

Secretion of vasoconstrictive catecholamines - AD & NA

51
Q

Phaeochromocytoma clinical presentation

A 
Pallor
Headaches
Sweating
Nervousness
Hypertension
52
Q

Phaeochromocytoma diagnosis

A

24hr urine collection of AD metabolites

53
Q

Cushing’s disease

A

Overproduction of cortisol by adrenal cortex

Caused by: pituitary adenoma (80%)

Adenocortical neoplasm - usually adenoma

Paraneoplastic effect of neoplasms

54
Q

How would another neoplasm cause cushing’s disease?

A

Produce adrenocorticotrophic hormone that stimulates zona fasciculata cells of the adrenal cortex to produce cortisol

Clinical Pathology (65 decks)

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