Cardiovascular system and diseases II Flashcards
what is atherosclerosis
hardening of arteries, causing thickening and loss of elasticity
- INTIMAL LESIONS can be atheromatous or fibrofatty, they protrude and obstruct the vascular lumens
where do atherosclerotic plaques generally develop
in elastic arteries (aorta, carotid) and large and medium sized muscular arteries (coronary)
atherosclerosis is associated with what
high LDL cholesterol
low HDL cholesterol
what are the non-modifiable risk factors associated with atherosclerosis (4 of them)
- age
- gender (m>f)
- positive family history
- genetic abnormality (ACE gene)
what are the modifiable risk factors associated with atherosclerosis (6 of them)
- hyperlipidaemia
- hypertension
- smoking
- Diabetes
- obesity
- physical inactivity
what is the pathological feature of atherosclerosis
what does it consist of
atherosclerotic PLAQUES
- consists of: raised lesion with a soft, yellow, grumous core of LIPID (mainly chol and chol esters) covered by a white FIBROUS CAP
describe the structure of atherosclerotic plaques
- superficial FIBROUS CAP: SMOOTH MUSCLE cells, dense collagen
- SHOULDER: cellular area cont MACROPHAGES, T CELLS, SMOOTH MUSCLE cells
- NECROTIC CORE: cont LIPID, DEAD CELL DEBRIS, FOAM CELLS, FIBRIN, variably organised THROMBUS and other plasma proteins
- CHOLESTEROL: often present as crystalline aggregates or CLEFTS
- NEOVASCULARISATION: at the periphery of lesion
what are the 3 principle components of a plaque
1) CELLS: smooth musc, macrophages, other leukocytes
2) EXTRACELLULAR MATRICES: collagen, elastin, proteoglycans
3) INTRACELLULAR and EXTRACELLULAR lipid
what is the morphology of the lesions
EARLIEST aortic atherosclerosis:
- fatty streaks
- lipid-filled foamy macrophages
- begin as multiple minutw flat yellow spots
ADVANCED complicated atherosclerosis in abdominal aorta:
- many lesions have ruptured
- become thrombosed
what are the key pathological events in atheroscleorsis
1) ENDOTHELIAL INJURY: inc vascular permeability, leukocyte adhesion and thrombosis
2) ACCUMULATION OF LIPOPROTEINS: mainly LDLin vessel wall
3) MONOCYTE ADHESION to the endothelium, followed by MIGRATION into the INTIMA and TRANSFORMATION into macrophages and foam cells
4)
what are the key pathological events in atheroscleorsis
1) ENDOTHELIAL INJURY: inc vascular permeability, leukocyte adhesion and thrombosis
2) ACCUMULATION OF LIPOPROTEINS: mainly LDLin vessel wall
3) MONOCYTE ADHESION to the endothelium, followed by MIGRATION into the INTIMA and TRANSFORMATION into macrophages and foam cells
4) PLATELET ADHESION
5) FACTOR RELEASE from activated platelets, macrophages and vascular cell walls –> SMC recruitment and further accumulation of macrophages
6) SMC proliferation and ECM production
7) Lipid accumulation both extracellulary and intracellularly (macrophages and SMCs)
what are the consequences of atherosclerotic plaques
1) RUPTURE, ULCERATION, EROSION of the intimal surface–> high thrombogenic substances –> THROMBOSIS
2) HAEMORRHAGE INTO A PLAQUE: rupture of the fibrous cap –> intra-plaque haemorrhage –> plaque rupture
3) ATHEROEMBOLISM: plaque rupture–> atherosclerotic debris into blood stream –> microemboli
4) ANEURYSM FORMATION: atherosclerosis-induced pressure, ischaemic atrophy, loss of eleatic tissue–> weakness –> aneurysmal dilation and potential rupture
what are the 3 clinical phase outocomes of an atheroscleotic plaque
1) rupture (can cause anyeurism and rupture)
2) occlusion (by thrombus)
3) stenosis (narrowing of vessel)
what are the outcomes of atheroscleotic diseases dependant on
- size of involved vessels
- relative stability of the plaque itself
- degree of degeneration (underlying arterial wall)
what are the MAJOR consequences of atherosclerotic diseases
- myocardial infarction (MI) (heart attack)
- cerebral infarction (stroke)
- aortic aneurysms
- peripheral vascular disease (gangrene of the legs)
how severe is ischaemic heart disease
it is the LEADING CAUSE OF DEATH woldwide for both men and women
- In more than 90% of cases, the cause of myocardial ischemia is reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries
what are the clinical manifestations of ischaemic heart disease
- angina pectoris (chest pain)
- MYOCARDIAL INFARCTION (the most important form of IHD)
- heart failure
- sudden cardiac death
describe angina pectoris
what is it characterised by]
what is it caused by
- characterised by paroxysmal and ususally recurrent attacks
- substernal or precordial chest discomfort
- described as ‘constricting’, squeezing, choking or knifelike
- caused by TRANSIENT (15seconds to 15 mins) MYOCARDIAL ISCHAEMIA)
what are the patterns of angina pectoris
3 overlapping patterns:
1) stable or typical angina
2) variant (Prinzmental, vasospastic) angina
3) unstable (crescendo) angina
what is silent ischaemia
an ischaemic events are perceived by patients
what is MI - myocardial infarction
what is the pathogenesis
- heart attack
detah of cardiac muscle due to prolonged severe ischaemia - pathogenesis: coronary arterial occlusion
what are the causes of coronary arterial occlsion
- CORONARY ATHEROSCLEROSIS (90%)
- VASOSPASM (w/ or w/out coronary atherosclosis)
- EMBOLI (from the left atrium in association with atrial fibrillation)
- others
what are the clinical features of MI myocardial infarction
- most frequent symptom of acute myocardial infarction is severe chest pain (often develops suddenly but may build up gradually, and generally lasts for several hours)
- Pain is usually accompanied by profuse sweating, nausea and vomiting
- Many patients give a previous history of angina or non-specific chest pain in the weeks before the acute event
- in at least 10% of patients, myocardial infarction is painless or ‘silent’; this is particularly true in the elderly
what ecg changes occur in MI myocardial infarction
MINUTES AFTERWARDS: elevated ST
HOURS AFTERWARDS: virtually no S
DAYS: Q more pronounced, ST less defined
what is heart failure (HF)
Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation
what is HF often called
It is often called congestive heart failure (CHF), is a common, usually progressive condition with a poor prognosis
occurs when heart:
1) Is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or
2) Can do so only at an elevated filling pressure
what are the different forms of HF heart failure
1) acute
- myocardial infarction
2) chronic
- valvular defects
3) left HF
- hypertension, ischaemic heart disease
4) right HF
- severe pulmonary hypertension, secondary to left heart failure
describe left sided heart failre
what are the causes
the morphological and clincial effects of left sided heart failure often result from?
- Ischemic heart disease
- Hypertension
- Aortic and mitral valvular diseases
- Myocardial disease
result from:
1) congestion of the pulmonary circulation
2) stasis of blood in the left-sided chambers
3) hypoperfusion of tissues leading to organ dysfunction
what is the morphology of left heart failure
HEART: - Left ventricle hypertrophy and dilation, Left atrium dilation
LUNGS: Pulmonary congestion and oedema, Perivascular and interstitial oedema
- Interlobular septa
- Alveolar septa
Alveolar oedema
describe right sided heart failure
morphology
Most commonly a secondary consequence of left-sided heart failure due to increase in pressure in the pulmonary circulation
morphology:
Heart: Hypertrophy and dilation of the right atrium and ventricle
Liver: Congestive hepatomegaly
Spleen: Congestive splenomegaly
Lung: Pulmonary oedema, Accumulation of fluid in pleural, pericardial, or peritoneal spaces (effusions)
Oedema of the peripheral: Ankle (pedal) and pretibial oedema is a hallmark of right-sided heart failure
