Flashcards in Cardiovascular disease 1 Deck (41):
What is ischaemic heart disease?
Inadequate blood supply to the myocardium
What are the causes of ischaemic heart disease?
reduced coronary blood flow, usually atheroma +/- thrombus
myocardial hypertrophy, usually due to systemic hypertension
Any imbalance in supply vs demand
What is the pathogenesis of ischaemic heart disease?
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
What are the features of angina pectoris?
typical/stable- fixed obstruction, predictable relationship to exertion
variant/Prinzmetal-coronary artery spasm
crescendo/unstable- often due to plaque disruption
What are the features of acute coronary syndrome?
acute myocardial infarction (+/- ECG ST elevation)
What is subendocardial myocardial infarction?
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
What would the morphology of MI be like at
macro - normal/dark
micro - necrosis and neutrophils
What would the morphology of MI be like at 1-2 days?
macro - yellow infarct centre
micro - More necrosis and neutrophils
What would the morphology of MI be like at 3-7 days?
macro - Hyperaemic border, yellow centre
micro - macrophages
What would the morphology of MI be like at 1-3 weeks?
macro - red/grey
micro - granulation tissue
What would the morphology of MI be like at 3-6 weeks?
macro - scar
micro - collagen scar
Describe how cardiac myocyte damage affects troponins T and I?
detectable 2 – 3h, peaks at 12h, detectable to 7 days
raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
Describe how cardiac myocyte damage affects creatine kinase?
detectable 2 – 3h, peaks at 10-24h, detectable to 3 days
Describe how cardiac myocyte damage affects myoglobin?
peak at 2h but also released from damaged skeletal muscle
Describe how cardiac myocyte damage affects Lactate dehydrogenase isoenzyme 1?
peaks at 3days, detectable to 14days
Describe how cardiac myocyte damage affects Aspartate transaminase?
Also present in liver so less useful as a marker of myocardial damage
What are the 3 subtypes of creatine kinase?
CK MM- muscle (cardiac and skeletal)
CK BB-brain, lung
CK MB- mainly cardiac, also skeletal muscle
What is the prognosis following an MI?
20% 1-2h mortality – sudden cardiac death
List the possible complications of MI
Contractile dysfunction and chronic cardiac failure
Infarct extension (free wall, septum, papillary muscle)
Pericarditis- Dressler's syndrome
What are the features of chronic ischaemic heart disease?
Coronary artery atheroma produces relative myocardial ischaemia & angina pectoris on exertion
Risk of sudden death or MI
Cardiac hypertrophy and dilatation
What are the 2 most common mutations found in familial hypercholesterolaemia?
Low density lipoprotein receptor gene (1 in 500)
Apolipoprotein B (1 in 1000)
What happens to people with heterozygous mutations?
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)
What is primary hypertension?
95% people with hypertension - no discernible cause
Likely many physiological systems interacting over long periods of time with minor dysfunctions
Renin-angiotensin- aldosterone system
Adrenergic receptor system
Autocrine factors produced by blood vessels
Autonomic nervous system
What is secondary hypertension?
5% - identifiable cause of high blood pressure
Chronic renal disease
Renal artery stenosis inc fibromuscular dysplasia
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)
Pregnancy – pre-eclampsia if severe
Renin – producing tumour
Coarctation of the aorta
Increased intravascular volume
Increased cardiac output
Raised intracranial pressure
Acute stress ( including surgery )
What are the pathological effects of hypertension?
Cardiovascular - Hypertensive heart disease
Renal - Renal failure
Cerebrovascular - Cerebrovascular accident
What are the features of hypertensive heart disease?
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
Describe the renal effects of hypertension
Vascular changes in essential hypertension
Arterial intimal fibroelastosis
Slow deterioration in renal function leading to chronic renal failure
Describe the cerebrovascular effects of hypertension
Increased risk of rupture abnormal arteries
atheromatous (intracerebral haemorrhage)
berry aneurysm of the Circle of Willis (subarachnoid haemorrhage)
What is a hypertensive crisis? (aka malignant hypertension)
Clinically signs & symptoms of organ damage
- acute hypertensive encephalopathy
- renal failure
- retinal haemorrhages
Requires urgent treatment to preserve organ function
What is acute hypertensive encephalopathy?
Diffuse cerebral dysfunction
Confusion, vomiting, convulsions, coma and death
Rapid Intervention is required to reduce the accompanying raised intracranial pressure
What is pulmonary hypertension caused by?
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
What does pulmonary hypertension cause?
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
What are the risk factors for cardiovascular disease?
High blood cholesterol
Low blood high density lipoproteins
Obesity – especially central obesity
High alcohol use
Ethnicity – south Asian
What are some cardiovascular risk assessment systems?
Framingham risk score
Whats is Conn's syndrome?
Caused by excess aldosterone secretion
Usually due to adrenocortical adenoma
Possibly micronodular hyperplasia
Renal sodium and water retention
Elevated aldosterone, low renin
- Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis
How is Conn's Syndrome diagnosed?
Diagnose by CT scan of adrenals in presence of these metabolic abnormalities
What is a Phaeochromocytoma?
Tumour of the adrenal medulla
Presents due to secretion of vasoconstrictive catecholamines – adrenaline and noradrenaline
What are the symptoms of a Phaeochromocytoma?
How is Phaeochromocytoma diagnosed?
Diagnosed by 24hr urine collection for adrenaline metabolites
What is Cushing's disease?
Overproduction of cortisol by adrenal cortex