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Clinical Pathology G > Cardiovascular disease 1 > Flashcards

Cardiovascular disease 1 Flashcards

1
Q

What is ischaemic heart disease?

A

Inadequate blood supply to the myocardium

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2
Q

What are the causes of ischaemic heart disease?

A

reduced coronary blood flow, usually atheroma +/- thrombus
myocardial hypertrophy, usually due to systemic hypertension
Any imbalance in supply vs demand

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3
Q

What is the pathogenesis of ischaemic heart disease?

A

Acute and/or chronic ischaemia
Autoregulation of coronary blood flow breaks down if > 75% occlusion
>90% stenosis may be insufficient at rest
Low diastolic flow especially sub-endocardial
Active aerobic metabolism of cardiac muscle-60 secs of ischaemia before function lost
Myocyte dysfunction/death from ischaemia
Damage is reversible in 20-30 mins

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4
Q

What are the features of angina pectoris?

A

typical/stable- fixed obstruction, predictable relationship to exertion
variant/Prinzmetal-coronary artery spasm
crescendo/unstable- often due to plaque disruption

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5
Q

What are the features of acute coronary syndrome?

A

acute myocardial infarction (+/- ECG ST elevation)

crescendo/unstable angina

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6
Q

What is subendocardial myocardial infarction?

A

The subendocardial myocardium is relatively poorly perfused under normal conditions
If there is
stable atheromanous occlusion of the coronary circulation
an acute hypotensive episode
Then the subendocardial myocardium can infarct without any acute coronary occlusion

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7
Q

What would the morphology of MI be like at

A

macro - normal/dark

micro - necrosis and neutrophils

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8
Q

What would the morphology of MI be like at 1-2 days?

A

macro - yellow infarct centre

micro - More necrosis and neutrophils

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9
Q

What would the morphology of MI be like at 3-7 days?

A

macro - Hyperaemic border, yellow centre

micro - macrophages

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10
Q

What would the morphology of MI be like at 1-3 weeks?

A

macro - red/grey

micro - granulation tissue

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11
Q

What would the morphology of MI be like at 3-6 weeks?

A

macro - scar

micro - collagen scar

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12
Q

Describe how cardiac myocyte damage affects troponins T and I?

A

detectable 2 – 3h, peaks at 12h, detectable to 7 days

raised post MI but also in pulmonary embolism, heart failure, & myocarditis.

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13
Q

Describe how cardiac myocyte damage affects creatine kinase?

A

detectable 2 – 3h, peaks at 10-24h, detectable to 3 days

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14
Q

Describe how cardiac myocyte damage affects myoglobin?

A

peak at 2h but also released from damaged skeletal muscle

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15
Q

Describe how cardiac myocyte damage affects Lactate dehydrogenase isoenzyme 1?

A

peaks at 3days, detectable to 14days

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16
Q

Describe how cardiac myocyte damage affects Aspartate transaminase?

A

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

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17
Q

What are the 3 subtypes of creatine kinase?

A

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

18
Q

What is the prognosis following an MI?

A

20% 1-2h mortality – sudden cardiac death

19
Q

List the possible complications of MI

A

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

20
Q

What are the features of chronic ischaemic heart disease?

A

Coronary artery atheroma produces relative myocardial ischaemia & angina pectoris on exertion
Risk of sudden death or MI
Cardiac hypertrophy and dilatation

21
Q

What are the 2 most common mutations found in familial hypercholesterolaemia?

A 
Low density lipoprotein receptor gene (1 in 500)
Apolipoprotein B (1 in 1000)
22
Q

What happens to people with heterozygous mutations?

A

develop xanthomas – tendons, perioccular, corneal arcus – and early atherosclerosis
Early primary treatment with statins (hydroxymethyglutaryl CoA reductase inhibitors) is effective

(Treatment of homozygotes is more complex and less effective)

23
Q

What is primary hypertension?

A

95% people with hypertension - no discernible cause

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

Cardiac baroreceptors
Renin-angiotensin- aldosterone system
Kinin-kallikrekin system
Naturetic peptides
Adrenergic receptor system
Autocrine factors produced by blood vessels
Autonomic nervous system
24
Q

What is secondary hypertension?

A

5% - identifiable cause of high blood pressure

Renal

Acute glomerulonephritis
Chronic renal disease
Renal artery stenosis inc fibromuscular dysplasia
Renal vasculitis

Endocrine

Adrenocortical hormones ( Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, liquorice ingestion )
Exogenous chemicals ( glucocorticoids, oestrogen including pregnancy and oral contraceptives, monoamine oxidase inhibitors, amphetamines, cocaine)
Phaeochromocytoma
Acromegaly
Hypothyroidism
Hyperthyroidism
Pregnancy – pre-eclampsia if severe
Renin – producing tumour

Cardiovascular

Coarctation of the aorta
Polyarteritis nodosa
Increased intravascular volume
Increased cardiac output

Neurologic

Raised intracranial pressure
Acute stress ( including surgery )
Sleep apnoea
Psychogenic

25
Q

What are the pathological effects of hypertension?

A

Cardiovascular - Hypertensive heart disease
Renal - Renal failure
Cerebrovascular - Cerebrovascular accident

26
Q

What are the features of hypertensive heart disease?

A

Systemic hypertension leads to increased left ventricular blood pressure
Left ventricle hypertrophy without dilatation initially in response to increased work needed to pump blood
Recognized cause of sudden death
When the pressure is too great the left ventricle fails to pump blood at a normal rate and dilates

27
Q

Describe the renal effects of hypertension

A

Vascular changes in essential hypertension
Arterial intimal fibroelastosis
Hyaline arteriolosclerosis
Slow deterioration in renal function leading to chronic renal failure

28
Q

Describe the cerebrovascular effects of hypertension

A

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

29
Q

What is a hypertensive crisis? (aka malignant hypertension)

A

BP >180/120mmHg
Clinically signs & symptoms of organ damage
- acute hypertensive encephalopathy
- renal failure
- retinal haemorrhages
Requires urgent treatment to preserve organ function

30
Q

What is acute hypertensive encephalopathy?

A

Clincopathological syndrome
Diffuse cerebral dysfunction
Confusion, vomiting, convulsions, coma and death
Rapid Intervention is required to reduce the accompanying raised intracranial pressure

31
Q

What is pulmonary hypertension caused by?

A 
Loss of pulmonary vasculature
 - Chronic obstructive lung disease
 - Pulmonary interstitial fibrosis (interstitial lung diseases)
 - Pulmonary emboli or thrombosis
 - Under ventilated alveoli
Secondary to left ventricular failure
Systemic to pulmonary artery shunting
Primary or idiopathic
32
Q

What does pulmonary hypertension cause?

A

Increased right ventricular work to pump blood
Right ventricular myocardial hypertrophy initially without dilation
Later dilatation and systemic venous congestion as right ventricular failure develops

33
Q

What are the risk factors for cardiovascular disease?

A 
Gender
Hypertension
Smoking
High blood cholesterol
Low blood high density lipoproteins
Diabetes
Sedentary lifestyle
Obesity – especially central obesity
High alcohol use
Ethnicity – south Asian
34
Q

What are some cardiovascular risk assessment systems?

A

Framingham risk score

QRISK2

SCORE

35
Q

Whats is Conn’s syndrome?

A 
Caused by excess aldosterone secretion
Usually due to adrenocortical adenoma
Possibly micronodular hyperplasia
Renal sodium and water retention
 - Hypertension
Elevated aldosterone, low renin
Potassium loss
 - Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis
36
Q

How is Conn’s Syndrome diagnosed?

A

Diagnose by CT scan of adrenals in presence of these metabolic abnormalities

37
Q

What is a Phaeochromocytoma?

A

Tumour of the adrenal medulla

Presents due to secretion of vasoconstrictive catecholamines – adrenaline and noradrenaline

38
Q

What are the symptoms of a Phaeochromocytoma?

A 
Pallor
Headaches
Sweating
Nervousness
Hypertension
39
Q

How is Phaeochromocytoma diagnosed?

A

Diagnosed by 24hr urine collection for adrenaline metabolites

40
Q

What is Cushing’s disease?

A

Overproduction of cortisol by adrenal cortex

41
Q

What causes Cushing’s?

A

An adrenocortical neoplasm usually an adenoma
A pituitary adenoma (Cushing’s syndrome – 80% of cases)
or a paraneoplastic effect of other neoplasms (particularly small cell lung carcinoma) producing adrenocorticotrophic hormone that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol

Clinical Pathology G (23 decks)

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