28 - Cardiovascular Disease 1 Flashcards
Ischaemic heart disease - definition
Inadequate blood supply to the myocardium via atheroma/ thrombus/ myocardial hypertropy
Ischaemic heart disease - pathogenesis
Acute & chronic
Autoregulation of coronary blood flow breaks down if
Ischaemic heart disease - syndromes
Angina pectoris
Acute coronary syndrome
Sudden cardiac death
Chronic ischaemic heart disease
Angina pectoris - types
Typical/stable - fixed obstructable, predictable on exertion
Variant/Prinzmetal - coronary artery spasm, unpredictable
Crescendo/unstable - red flag syndrome due to plaque disruption
Acute coronary syndrome
Acute MI (+/- ECG ST elevation) Crescendo/unstable angina
Acute ischaemia - causes and why
Atheroma + acute thrombosis / haemorrhage
Lipid rich plaques at most risk
Acute ischaemia - what is it?
Regional transmural myocardial infarction
Acute ischaemia - management
Thrombolysis
Acute ischaemia - Diagnosis
Clinical
ECG
Blood cardiac proteins
Subendocardial myocardial infarction - why is that region vulnerable?
subendocardial most vulnerable due to less blood going to it as capillaries run over endocardium
Can infarct without any acute coronary occlusion
Subendocardial myocardial infarction - ST elevation?
Rarely
Blood markers of cardiac myocyte damage - troponins T&I
Detectable 2-3hrs peaks at 12h detectable at 7 days.
Raised post-MI but also in PE, heart failure & myocarditis
Blood markers of cardiac myocyte damage - Creatine kinase
Detectable 2-3hrs, peaks at 10-24hrs, detectable to 3 days
Blood markers of cardiac myocyte damage - Myoglobin
peak at 2hrs but also released from damaged skeletal muscle
Blood markers of cardiac myocyte damage - lactate dehydrogenase isoenzyme 1
Peaks at 3 days, detectable to 14 days
Blood markers of cardiac myocyte damage - aspartate transaminase
Also present in liver so less useful as a marker of myocardial damage
Blood markers of cardiac myocyte damage - most useful/only one used?
Troponin
Blood markers of cardiac myocyte damage - creatine kinase subtypes
CK MM - muscle
CK BB - brain, lung
CK MB - cardiac, possibly muscle
Familial hypercholesterolaemia - commonest mutations
Low density lipoprotein receptor gene (1in500) Apolipoprotein B (1 in 1000)
Note homozygous more severe
Whats a xanthoma and egs.
Tendons
Periocular
Corneal arcus
Early atherosclerosis
Which is more common - primary hypertension or secondary?
Primary (95%)
Main secondary is hyperthyroidism
Renin cycle
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
Ang II facts
potent natural vasoconstrictor
V. short half life
Stimulates adrenal cortex to produce aldosterone
Aldosterone facts
Physiological mineralocorticoid
Renal action causes sodium and water retention
Circulating blood volume increases
Conn’s syndrome - causes and why
Caused by excess aldosterone secretion
Why: adrenocortical adenoma, micronodular hyperplasia, renal sodium&water hypertension, elevated aldosterone w/ low renin, potassium loss (via muscle weakness.
Conn’s syndrome - diagnosis
Diagnose by CT scan of adrenals in presence of metabolic abnormalities
Phaeochromocytoma - what is it? what causes the symptoms?
Tumour of adrenal medulla
Presents due to secretion of vasoconstrictive catecholamines - AD and NA
Phaeochromocytoma - clinical presentation
Pallor Headaches Sweating Nervousness Hypertension
Phaeochromocytoma - diagnosis
24hr urine collection for AD metabolites
Cushing’s disease - what is it? + effects
Overproduction of cortisol by adrenal cortex
Potentiating SNS and has mineralocorticoid (aldosterone-like) action of kidneys causing hypertension
Cushing’s disease - causes
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
Hypertension - effects
CV - hypertensive heart disease
Renal failure
Cerebrovascular incident
Hypertension - hypertensive heart disease
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
Hypertension - renal effects
Vascular changes:
Arterial intimal fibroelastosis
Hyaline arteriolosclerosis
Slow deterioration in renal function leading to failure
Hypertensive cerebrovascular disease
Hypertensive encephalopathy
Increased risk of rupture of abnormal arteries - atheromatous (intracerebral haemorrhage); berry aneurysm of the circle of Willis (subarachnoid haemorrhage)
Hypertension - hypertensive crisis
BP >180/120
Hypertension - hypertensive crisis clinical presentation
Acute hypertensive encephalopathy
Renal failure
Retinal haemorrhages
Urgent treatment
Hypertension - acute hypertensive encephalopathy
Clincopathological syndrome
Diffuse cerebral dysfunction - confusion, vomiting, convulsions, coma and death
Rapid intervention required to reduce accompanying raised intracranial pressure
Pulmonary hypertension - caused by
Loss of pulm. vasculature
2* to LV failure
Systemic to pulm. art. shunting
Primary or idiopathic
Pulmonary hypertension - causes
Increased RV work to pump blood
RV myocardium hypertrophy initially w/o dilation
Later dilation and systemic venous congestion as RV failure develops
What is Framingham risk score?
Calculates an individual’s risk of CVD based on multiple risk factors and algorithms
Other risk assessment systems
SCORE
QRISK2
Joint British societies risk prediction charts
What is renin? Where is it made and released from?
Synthesised, stored in and released from juxtaglomerular apparatus in wall of afferent arteriole of kidney
What does renin do?
Cleaves angiotensinogen to angiotensin I
Where is Ang1 cleaved?
AngII in many tissues
What is AngII and what does it do?
Potent vasoconstrictor
Very short half-life
Stimulates adrenal cortex to produce aldosterone
What is aldosterone?
Physiological mineralocorticoid
Causes sodium, and in turn, water retention
Increases blood volume
What is Conn’s syndrome?
Excess aldosterone secretion
Adrenocortical adenoma
Renal sodium and Na retention
Elevated aldosterone and low renin
Potassium loss
What does potassium loss cause?
Muscular weakness
Cardiac arrhythmias
Parasthaesesia
Metabolic alkalosis
Phaeochromocytoma - what is it?
Tumour of adrenal medulla
Secretion of vasoconstrictive catecholamines - AD & NA
Phaeochromocytoma clinical presentation
Pallor Headaches Sweating Nervousness Hypertension
Phaeochromocytoma diagnosis
24hr urine collection of AD metabolites
Cushing’s disease
Overproduction of cortisol by adrenal cortex
Caused by: pituitary adenoma (80%)
Adenocortical neoplasm - usually adenoma
Paraneoplastic effect of neoplasms
How would another neoplasm cause cushing’s disease?
Produce adrenocorticotrophic hormone that stimulates zona fasciculata cells of the adrenal cortex to produce cortisol
