Flashcards in Cardiovascular diseases Deck (35):
What is ischaemic heart disease?
Inadequate blood supply to the myocardium
What are the main causes of ischaemic heart disease?
- Atherosclerosis and/or thrombus*
- Myocardium hypertrophy due to systemic hypertension
- any imbalance in supply vs demand
At what % occlusion does auto regulation of the coronary arteries breaks down?
At what % occlusion does auto regulation of coronary arteries break down at rest?
What happens with acute cardiac ischaemia?
Myocyte dysfunction/death due to blood flow and loss of aerobic metabolism
What is the length of time where damage is reversible with ischaemia?
At what point in the cardiac cycle doe cardiac perfusion occur?
What are the 3 types off angina pectoris?
Stable/typical - fixed dysfunction and predictable symptoms
Variant/prinxmetal - coronary artery spasm - effects less predictable
Crescendo/unstable - red flag - usually due to plaque disruption - worsening symptoms, unpredictable (MI risk = high)
What two syndromes come under acute coronary syndrome?
MI - irreversible damage of myocytes
Crescendo/unstable angina (similar - treated in same way)
There are two types of MI - what are they?
Subendocardial - non full thickness** (most vulnerable region - poorly perfused)
Transmural - regional (kills entire wall)
What is the main characteristic of subendocarial infarction?
Doesn't need acute coronary occlusion to occur MISMATCH BETWEEN DEMAND AND SUPPLY
- because it is normally poorly perfused, can occur with stable atherosclerotic occlusion of coronary circulation and following a hypotensive episode
What are subendocardial MIs also referred to as?
Non-ST elevation MI
Why are transmural MIs so debilitating?
Death of large region (entire wall) - results in necrosis, fibrosis and formation of fibrous (collagen) scar - cannot pump properly (loss of specialised tissue)
Name the 5 stages of MI morphology (24hrs -6 weeks)
24hrs - normal
1-2 days - pale, oedema with myocyte necrosis and neutrophils
3-4 days - yellow with haemorrhagic edge, myocyte necrosis with macrophage invasion
1-2 weeks - pale, thin (red/grey) - granulation tissue then fibrosis
3-6 weeks - fibrotic scar formation (collagen) (can't tell how old it is after 4 weeks)
What are the 2 main markers of cardiac damage?
TROPONIN T and I (detectable after 2-3 hrs, peaks at 12, detectable for 1 week)
CREATINE KINASE MB - detectable 2-3h, peaks 10-24 hrs, detectable for 3 days
Also myoglobin (peaks 2hrs) but non-specific - skeletal muscle too
What are the 3 subtypes of creatine kinase
CK MM - skeletal muscle and cardiac
CK BB - brain and lung
CK MB - mainly cardiac but also skeletal
Name some of the complications of MI
-Contractile dysfunction and chronic heart failure
-VF, arrhythmias, sudden cardiac death
- Myocardial rupture
- Ventricular aneurysm
- Mural thrombus - stroke!
- Autoimmune pericarditis (Dressler's syndrome) (3 day mark - neutrophil inflammatory response)
What is chronic ischaemic heart disease characterised by?
Hypertrophy and dilatation
What can chronic IHD cause?
Sudden death/MI/angina pectoralis on exertion
what is hypercholestroaemia and what are the most common types?
Mutations of genes involved in cholesterol metabolism
LDL receptor (1 in 500)
Apolipoprotein B (1 in 1000)
What do individuals with heterozygotic hypercholesterolaemia develop?
- cholesterol deposit (foam cells to endothelium - atherosclerosis)
- tendon, perioccular, corneus arcus, early atherosclerosis
What are considered abnormal diastolic and systolic BPs?
Diastolic = above 90 mmHg
Systemic = above 140 mmHg
What is the effect of hypertension on the heart?
LV hypertrophy without dilatation (initially then subsequent dilatation when it fails to pump blood sufficiently - final stage)
What is the main effect of hypertension on the renal system?
Slow deterioration of renal function - chronic renal failure (damage to vessels - arterial intimal fibroelastosis)
Kidneys have stippled appearance
What can hypertension cause in the brain? (hypertensive cerebrovascular disease)
What is acute hypertensive crisis and what does it cause?
Rapid increase in BP above 180/120 mmHg
Causes organ failure - hypertensive encephalopathy (brain - confusion, vomiting, convulsions, coma/death), renal failure and retinal haemorrhage
What is pulmonary hypertension and what is it caused by?
- Increased pressure in pulmonary vasculature
Caused by loss of pulmonary vasculature
- chronic obstructive lung disease
- pul thrombi/emboli
- reduced alveoli vent
- Interstitial lung disease
What does pulmonary hypertension cause?
- Increased pulmonary resistance (OEDEMA)
- Increase RV work to pump blood
- RV hypertrophy and later dilatation as RV failure occurs
Name some causes of secondary hypertension
Renal - acute glomerulonephritis, chronic renal disease, polycystic kidneys
Endocrine - Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, hyperthyroidism
CV - coarticulation of aorta
- Angiotensinogen converted to Angiotensin I by renin (produced in juxtaloglomerular apparatus in kidney)
- angiotensin I converted to angiotensin II (lungs many - why ACE inhibitors cause chronic cough) - potent vasoconstrictor
- angiotensin II also stimulate adrenal cortex release of aldosterone (Na and H2O retention - increased circulating volume and increased BP)
What is CONNS syndrome and how is it caused?
Excess aldosterone secretion from adrenal cortex
Usually adrenocortical carcinoma/adenoma
How is CONNS syndrome characterised and what does it cause?
high aldosterone with low renin
High BP (Na and H2O retention)
K loss - metabolic alkalosis, muscle weakness, arrhythmia
What is pheochromocytoma and what does it cause?
Tumour of the adrenal medulla
Excessive synthesis and secretion of catecholamines - increase adrenaline/NA - increases vasoconstriction and BP
What is cushing's disease and what is it mostly caused by?
Overproduction of CORTISOL from adrenal cortex
Caused by pituitary adenoma (80%), adrenocortical adenoma or paraneoplastic effect of other neoplasms