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An atheroma is the manifestation of fibrous tissue and lipid deposits on arterial walls. It can affect all arteries except brachial and renal (diabetics may have this). It mainly occurs at bifurcations. There are different stages, related to clinical effects:
- Lumenal narrowing: ischaemia
- Lumenal occlusion: infarction
- Embolism: ischaemia and infarction
- Weakened wall: aneurysm
- Occlusion of the coronary arteries causes chest pain on exertion – Angina
- Thrombotic occlusion of the artery- infarction
- Thrombosis over the carotid arteries may release a small emboli, when these travel to the brain they cause a TIA
- Thrombotic occlusion of a cerebral artery leads to infarct and stroke
- Atheroma of the femoral artery causes reduced blood supply to the lower limbs; the patient has pain in their calf when they walk which is relieved by rest. This is claudication.
- Thrombosis may develop over an atheroma plaque and the femoral artery causing infarct- Gangrene
- Lack of blood causes pain and diarrhoea- Ischaemic colitis
- Thrombosis may occur on an achromous plaque in the mesenteric arteries causing infarction- Ischaemic enteritis
- The renal arteries are usually spared severe atheroma but in diabetic patients, the origin of the renal artery is affected. The kidney gradually becomes atrophic due to chronic ischemia. The under perfused kidney releases renin resulting in renal hypertension, with consequent risk of heart failure and stroke.
A diagram of the renin angiotensin aldosterone axis, which helps the body control blood pressure.
- Response-to-injury hypothesis - Chronic endothelial injury leading to endothelial dysfunction
- Lipid hypothesis - Initial accumulation of atherogenic plasma-derived lipoproteins. High plasma LDL cholesterol may promote accumulation of cholesterol in the intima and ultimately plaques.
- Inflammation- Macrophages produce various intercellular communication molecules which promote various aspects of inflammation. Lymphocytes accumulate, and fibroblasts proliferate and produce collagen
- High plasma LDL
- High sat fat diet
- Sedentary lifestyle
- Low birth weight
- Low social class
A thrombus is a solid mass of blood constituents formed within the vascular system whereas a clot is coagulation within or outside the vascular system.
A thrombus is made up of
- Platelets with dense granules for aggregation and alpha granules for adhesion
Contact with damaged endothelium or atheromatous plaque triggers the coagulation cascade, converting fibrinogen to fibrin.
Things that promote thrombus formation are:
- Endothelium damage
- Abnormal blood flow
- Hypercoagulability states- immobility, post op, genetic
Types of thrombi:
- Thrombi can occlude a vessel which may result in necrosis of the part served (infarction).
- Mural thrombus can release fragments (emboli) which can travel in the bloodstream to block distal vessels.
- Thrombus on heart valves due to infection can also embolism.
- Thrombolysis - Thrombosis can be cleared by the fibrinolytic system. Plasminogen activator released from endothelial cells converts plasminogen to plasmin which dissolves fibrin.
- Recanalisation - Thrombosis can undergo recanalization. Endothelial cells grow out from the vessel wall and create new channels through the thrombus.
- Embolism - Thrombosis can throw off emboli which can occlude distal vessels
- Fibrosis (Reorganisation) - Thrombosis can simply be organised i.e undergo fibrous tissue replacement
- Smoking- causes platelets to become sticky
- MI, infective endocarditis
- Atrial fibrillation
- Damage to valve endothelium
- Fibrinogen is increased post op
A mass of material in the blood which can lodge in a vessel and block its lumen
Can be made up of:
- Amniotic fluid
- Foreign matter
Embolism to the lungs (pulmonary arteries) originates in the deep veins.
Embolism to organs and limbs originates in the heart or large arteries
- Embolism to the lungs (pulmonary arteries) originates in the deep veins.
- Embolism to organs and limbs originates in the heart or large arteries
- Large emboli effectively occlude the circulation, and sudden death occurs.
- Medium emboli cause occlusion of a branch of the pulmonary artery by a medium sized embolus. Infarction often results. A healthy person with a good circulation may not develop infarction due to the dual blood supply of the lungs and anastomoses
- Occlusion of small pulmonary arteries usually doesn’t result in infarct. However if extensive in addition to multiple they may cause pulmonary hypertension and/or cor pulmonale
Ischaemia & Infarction
Ischemia: Organs or tissues has perfusion lower than its metabolic need
Infarction: tissue death caused by a local lack of oxygen due to destruction of the tissues blood supply
The changes that occur:
- Biochemical alterations
- Ultra structural changes
- Light microscopic changes
- Gross morphological changes
Hypoxia causes anaerobic glycolysis increasing free radicals and lactate. These results in membrane peroxidation and destruction, metal ions are released damaging adjacent cells.
IHD Risk Factors
- Dyslipidemia: high VLDL and low HDL
- Diabetes mellitus
- Family history of premature coronary artery disease
- Obesity and lack of exercise
- Male sex and increasing age
- Others: eg. Homocysteinemia
Even after clot is removed there is a problem with reperfusion:
- Endothelium blebs
- Platelet aggregation
- Neutrophil plugs
- Swollen monocytes
- Rouleaux formation
Onset of irreversible damage is 30 minutes after occlusion of artery; this is when lactate becomes too high and ATP too low.
A sustained diastolic pressure greater than 90 mm Hg or a sustained systolic pressure in excess of 140 mm Hg is considered to constitute hypertension.
Hypertension can cause:
- Hyaline arteriosclerosis: This vascular lesion consists of a homogeneous pink hyaline thickening of the arterioles with loss of underlying structural detail and with narrowing of the lumen
- Hyperplastic arteriosclerosis: Concentric laminated thickening of the arteriolar walls
- Left ventricular hypertrophy
- increased risk of cerebral haemorrhage
- Ischaemia of nephron units
Malignant hypertension is defined as a diastolic pressure >130 mm Hg
The causes of malignant hypertension are:
- Renal disease
- Accelerated essential hypertension
This may cause: fibrinoid necrosis, haemorrhage, thrombosis. Mainly effects kidneys, eyes, brain.
An aneurysm is a localized abnormal dilatation of a blood vessel
Common sites of aneurysms are the:
- Microaneuryms may be seen in the retina and kidney
Types of Aneurysm:
- Atherosclerosis: eg, aortic aneurysms
- Cystic medial degeneration of arterial wall
- Congenital defects: potentiating berry aneurysms in the brain
- Mycotic aneurysm: septic embolus in a vessel, extension of an adjacent suppurative process, circulating organisms affecting the wall of the vessel
- Syphilitic aneurysm: Syphilitic infection of the vasa vasorum of the thoracic aorta
- Aneurysms due to vasculitides
- Capillary Microaneurysms- hypertension and diabetes
- Rupture into the peritoneal cavity retroperitoneum.
- Embolism from associated atheroma
- Erosion of adjacent vertebrae or compression of the ureter
- Pulsating abdominal mass
- Cardiac Tamponade
- Aortic insufficiency
- Myocardial infraction
- Extension of dissection into the great arteries of the neck, coronary arteries and mesenteric arteries
- Left: pulmonary congestion and oedema - breathlessness
- Right: peripheral oedema hepatic congestion, raised JVP
- Congestive: Right & Left
- Stenosis: failure of valve to open properly decreasing forward blood flow
- Insufficiency: failure of valve to close properly allowing reversible flow
Causes liver congestion and lung/peripheral oedema Mitral:
- Stenosis: rheumatic heart disease
- Regurgitation: infective endocarditis, prolapse, rupture of papillary muscle/ chordae tendinae
- Stenosis: senile calcification, congenital
- Regurgitation: infective endocarditis, rheumatic heart disease, connective tissue disorders
Rheumatic Heart Disease:
- Acute immunologically mediated multisystem inflammatory disease that occurs a few weeks after a group A streptococcus pharyngitis
- May develop into a chronic condition, this is the organisation of acute inflammation
- Aschoff bodies- eosinophilic swollen collagen surrounded by T cells and macrophages which may cause pericarditis
- Maccallum plaques- fibrin deposition and necrosis which sit small verrucae of fibrin and inflammatory cells, exacerbated by regurgitation streams
- M proteins of staphylococci cross react with glycoproteins of the heart
- Polyarthritis of large joints
- Sydenham’s cholera
- Colonization or iunvasion of the heart valves (commonly mitral valve) or the mural endocardium by a microbe leading to the formation of bulky, friable vegetations composed of thrombotic debris and organisms destroying underlying tissue
- Mainly caused by strep viridans but in IV drug users may be staph aureus
- Fever, chills, fatigue, weight loss, glomeurolnephritis, splenomegaly
- Micro-emboli- sublingual haemorrhage, janeways lesions, oslers nodes, roth spots in retina
- Emboli- septic to other organs