CP28 - Cardiovascular Disease 1 Flashcards
what is ischaemic heart disease
inadequate blood supply to the myocardium - any imbalance in supply vs demand
what is the pathogenesis of ischaemic heart disease
acute/chronic ischaemia
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 minutes
what are the different ischaemic heart disease syndromes
angina pectoris
acute coronary syndrome,
sudden cardiac death,
chronic ischaemic heart disease
what are the different types 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 different types of acute coronary syndrome
acute MI (+/- ECG ST elevation)
crescendo/unstable angina
how can subendocardial myocardial infarction take place?
- subendocardial myocardium is relatively poorly perfused even under normal conditions
- if there is a stable atheromanous occlusion of the coronary circulation/an acute hypertension episode
- then the subendocardial myocardium can infarct without any acute coronary occlusion
what is the different between subendocardial and transmural MI?
subendocardial - only affect the subendocardium whereas the transmural affect the entire area of the heart
what does the myocardium look like macroscopically and histologically in less thank 24 hours of occurrence?
Macro - normal/dark
Histo - necorsis + neutrophils
what does the myocardium look like macroscopically and histologically in less thank 1-2 days of occurrence?
Macro - yellow infarct centre
Histo - necrosis + neutrophils
what does the myocardium look like macroscopically and histologically in less thank 3-7 days of occurrence?
macro - hyperaemic border, yellow centre
histo - macrophages
what does the myocardium look like macroscopically and histologically in less thank 1-3 weeks of occurrence?
macro - red/gray
histo - granulation tissue
what does the myocardium look like macroscopically and histologically in less thank 3-6 weeks of occurrence?
macro - scar
histo - collagen scarr
what are some blood markers which can be used to detect myocyte damage
troponins T & I
creatine kinase MB
Myoglobin
lactate dehydrogenase isoenzyme 1
aspartate transaminase
when is troponins T & I detectable ?
detectable 2 – 3h, peaks at 12h, detectable to 7 days
raised post MI but also in pulmonary embolism, heart failure, & myocarditis.
when is creatine kinase MB detectable?
detectable 2 – 3h, peaks at 10-24h, detectable to 3 days
when is myoglobin detectable?
peak at 2h but also released from damaged skeletal muscle
when is lactate dehydrogenase isoenzyme 1 detectable?
peaks at 3 days and detectable up to 14 days
what are some complications for MI?
- contractile dysfunction and chronic cardiac failure
- arrhythmias
- infarct extension
- myocardial rupture
- pericarditis - Dressler’s syndrome
- mural thrombus
- ventricular aneurysm
what is familial hypercholesterolaemia
- mutation in genes which involved in cholestrerol metabolism
- low density lipoprotein receptor gene, Apolipoprotein B
what is primary hypertension?
usually benign, idiopathic
what can cause primary hypertension
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 a common pathway for hypertension?
All inherited and acquired forms of share increased net salt balance as a common pathway.
Increased intravascular volume and volume delivery to the heart augment cardiac output and therefore blood pressure.
The resulting tissue perfusion exceeds metabolic demand, leading t autoregulation of blood flow to increased vasoconstriction to reduce blood flow
This results in a steady-state hemodynamic pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output.
what are some examples for secondary hypertension?
renal
endocrine - Cushing Syndrome, primary aldosteronism, phaeochromocyotma - neurotumour present in the medulla of the adrenal glands and so secrete large amount of adrenaline and noradrenaline
cardiovascular - coarction of the aorta, increased intravascular volume, increased cardiac output
neurologic - raised intracranial pressure, acute stress, sleep apnoea
what are some effects for hypertension?
cardiovascular - hypertensive heart disease
renal - renal failure
cerebrovascular - cerebrovascular accident
where does the left side of the heart pump blood to?
Left - aorta - body
Right - to the lungs
what can happen to the heart if the systemic pressure is too high
leads to increased left ventricular blood pressure
the left ventricle undergoes hypertrophy initially without dilation in response to increased work needed to pump blood
if pressure too hight then left ventricle fails to pump and can cause sudden death
what can happen to the kidney if hypertension exists
arterial intimal fibroelastosis, hyaline arteriolosclerosis - slow deterioration in renal function leading to chronic renal failure
what can happen to the brain should hypertension be present?
hypertensive encephalopathy
increased risk of rupture abnormal arteries (atheromatous - intracerebral haemorrhage), berry aneurysm of the circle of willis (subarachnoid haemorrhage)
what is another name for hypertensive crisis?
malignant hypertension
what is the presentation for malignant hypertenison?
acute hypertensive encephalopathy, renal failure, retinal haemorrhages
what is acute hypertensive encephalopathy?
Diffuse cerebral dysfunction - confusion, vomiting, convulsion, coma and death
what can cause pulmonary hypertension?
loss of pulmonary vasculature - chronic obstructive lung disease, pulomary interstital fibrosis, PE, under ventilated alveoli
secondary to left ventricular failure
what does pulmonary hypertension cause?
increased right ventricle workload, right ventricular myocardial hypertrophy initially without dilation, later dilation and systemic venous congestion as right ventricular failure develops
