Cardiovascular disease 1 Flashcards
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)
crescendo/unstable angina
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
Arrhythmias
Infarct extension (free wall, septum, papillary muscle)
Myocardial rupture
Pericarditis- Dressler’s syndrome
Mural thrombus
Ventricular aneurysm
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
Cardiac baroreceptors Renin-angiotensin- aldosterone system Kinin-kallikrekin system Naturetic peptides Adrenergic receptor system Autocrine factors produced by blood vessels Autonomic nervous system
What is secondary hypertension?
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
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
Hyaline arteriolosclerosis
Slow deterioration in renal function leading to chronic renal failure
Describe the cerebrovascular effects of hypertension
Hypertensive encephalopathy
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)
BP >180/120mmHg
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?
Clincopathological syndrome
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?
Gender Hypertension Smoking High blood cholesterol Low blood high density lipoproteins Diabetes Sedentary lifestyle Obesity – especially central obesity High alcohol use Ethnicity – south Asian
What are some cardiovascular risk assessment systems?
Framingham risk score
QRISK2
SCORE
Whats is Conn’s syndrome?
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
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?
Pallor Headaches Sweating Nervousness Hypertension
How is Phaeochromocytoma diagnosed?
Diagnosed by 24hr urine collection for adrenaline metabolites
What is Cushing’s disease?
Overproduction of cortisol by adrenal cortex
What causes Cushing’s?
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
