Week 3 - Heart And Blood Vessels Flashcards
What is atherosclerosis?
The progressive narrowing and hardening within an artery potentially resulting in a complete blockage
Why might atherosclerosis be caused?
- initiated by chronic injury to the endothelium –> resulting in chronic inflammation
- causes of injury - hyperlipidaemia, disturbed flow, smoking, hypertension
- then progresses as wbc, fat and blood constituents infiltrate injury. Lesion progression sustained by interaction between modified lipoproteins, macrophages, T cells and normal cellular constituents of the blood
What are the 6 stages of atheroma?
-initial lesion (isolated macrophage foam
cells)
-fatty streak lesion (mainly intracellular accumulation)
-intermediate lesion (type II changes with small extra cellular lipid pools)
-atheroma lesion (type II changes and core of EC lipid)
-fibroatheroma lesion (lipid core and fibrotic layers, or mainly calcified or mainly fibrotic)
-complicated lesion (surface defect, haematoma -haemorrhage, thrombus
Which arteries do heart attacks and angina (ischaemic heart disease) usually effect?
Coronary arteries
Which artery is an aneurysm most likely to effect?
The aorta
Which arteries may narrow, causing a stroke?
Carotid arteries
Atherosclerotic plaques develop slowly but what may they acutely cause symptoms due to?
- aneurysm and rupture
- thrombosis
- haematoma formation
- embolisation
- development of critical stenosis
What are collateral vessels?
Collateral vessels are extra blood vessels that connect portions of the same artery or link two different arteries. These alternate blood circulation routes develop in most people and are usually closed to the flow of blood. The collateral vessels can be microscopic or they may grow larger.
What is stenosis?
the abnormal narrowing of a passage in the body
Which way do atheromas usually grow?
Outward (away from lumen)
What causes thrombosis?
Rupture of the atheroma plaque’s fibrous cap
-allows blood coagulant factors to contact thrombogenic collagen found in the arterial extracellular matrix and tissue factor produced by macrophage-derived foam cells in the lipid core of lesions
What does atheroma plaque rupture often form?
The nidus for thrombi
Nidus - where something originates
What does the normal artery wall possess in order to resist thrombosis and lyse clots that begin to form?
-fibrinolytic or antithrombic mechanisms
(thrombomodulin, tissue and urikase-type plasminogen activators, heparan sulphate, proteoglycans, prostacyclin, nitric oxide)
When might the natural fibrinolytic or antithrombic mechanisms in the arteries not work?
When the clot overwhelms the endogenous fibrinolytic mechanisms - may propagate and lead to arterial occlusion
What do the consequences of arterial occlusion depend on?
- the degree of existing collateral vessels (pts with chronic multi vessel, occlusive coronary artery disease - these have often formed)
- in these circumstances, total occlusion may not cause MI
- pt with less advance disease and without substation stenotic lesions to provide a stimulus for collateral vessel formation - sudden plaque rupture and occlusion produces ST-segment elevation infarction
- MI/sudden death
What is ischaemic heart disease?
Imbalance between supply (perfusion) and demand of the heart for oxygenated blood
-not only low oxygen but also low nutrient substrates and inadequate removal of metabolites
What may cause a lower flow/not flow of oxygenated blood?
- atheroma
- embolism
- spasm
What may cause a higher demand for oxygen?
- thyrotoxicosis
- myocardial hypertrophy (e.g. Hypertension)
What are the fixed risk factors for ischaemic heart disease?
- positive family history
- male sex
- age
- genetic factors (like ACE gene deletion)
What are the signs and symptoms of ischaemic heart disease?
- Chest pain (often central, crushing, radiating to left arm or into jaw - elderly or diabetics may not get chest pain)
- SOB
- palpitations
- syncope - temporary loss of consciousness caused by a fall in BP
- nauseous, sweating, pale
What is the difference between stable and u stable angina?
Stable -
What conditions are under ACS - acute coronary syndrome?
Unstable angina
STEMI
NSTEMI
What’s the difference between STEMI AND NSTEMI?
-both MI
ST segment elevation myocardial infarction (STEMI) - most serious type of heart attack, where theres a long interruption to the blood supply, usually caused by a total blockage of the coronary artery, which can cause extensive damage to a large area of the heart.
non-ST segment elevation myocardial infarction (NSTEMI) - can be less serious because supply of blood to the heart is only partially blocked resulting in a smaller section of the heart being damaged (still regarded as a serious medical emergency)
What are the investigations conducted to text for angina and ACS?
Observations -BP, pulse, RR, sats Bloods - inc. cardiac enzymes Chest X-ray ECG Exercise tolerance test
What are the complication s that can occur because of an MI?
- cardiac arrest
- arrhythmias
- pericarditis
- valvular defects
- ventricular wall rupture
- DVT
- pulmonary embolus)
What is the immediate and common treatment for all ACS events and angina?
- oxygen
- pain relief
- aspirin
What is the most common treatments of angina?
Change of lifestyle, nitrates (dilates vasculature), B-blockers
What is the most common treatments for ACS?
Thrombolytic therapy, PTCA (percutaneous transluminal coronary angioplasty), CABG (coronary artery bypass graft), drugs
What is hyperlipidaemia?
High level of fat in the blood
- LDL cholestorol (bad) - delivered to peripheral tissues
- HDL cholesterol (good) -mobilises cholesterol from the tissues and transports it to the liver to be excreted in bile
How is hyperlipidaemia treated?
- reduce cholesterol and saturated fat in diet
- role of statins
Name some vascular diseases
Atherosclerosis, aneurysms, hypertension, diabetic vascular disease, vein diseases
What is cardiac failure?
Heart unable to pump blood at rate required for normal functioning
Resulting in:
- oedema (pulmonary and peripheral)
- tiredness
Initially the heart compensates -leading to cardiac hypertrophy and/or dilation and eventual inability to maintain normal function
State the causes of cardiac failure
Ischaemic heart disease, hypertension, valvular heart disease, arrhythmias, congenital heart disease