L11 - Oedema,Thrombus, Embolus and Infarction Flashcards

1
Q

Oedema

A
  • Accumulation of excess fluid in the tissue is called oedema-local or general
  • This occurs if hydrostatic pressure in vessels increases ie more fluid leaves capillaries e.g. heart failure
  • More fluid leaves with reduced plasma oncotic (osmotic) pressurehypoproteinaemia-(recall transudate) e.g liver fails to produce albumin
  • More fluid leaves if vascular permeability is altered- acute inflammation (recall the gall bladder)
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2
Q

Pulmonary oedema

A

the accumulation of fluid in the alveoli of the lung. It is caused by increased hydrostatic pressure in the pulmonary vascular bed, resulting from failure of the left side of the heart- e.g cardiac hypertrophy

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3
Q

Subcutaneous oedema

A

is the accumulation of fluid in subcutaneous tissues. It is caused by increased hydrostatic pressure in the systemic venous system, resulting from failure of the right side of the heart

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4
Q

Haematoma

A

is an accumulation of blood within soft tissues. It is usually due to traumatic damage to vessels, but occasionally follows spontaneous rupture of diseased vessels.

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5
Q

What is haemorrhage caused by?

A
  • rupture of blood vessels
  • severe blood loss is usually caused by trauma to a major artery or vein, but may also result from bursting of a vessel weakened by disease.e.g. oesophageal varices
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6
Q

Petechiae

A
  • A small tissue haemorrhage that is 1 -2mm in diameter
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7
Q

Purpura

A
  • A small tissue haemorrhage that is 2 - 10nm in diameter
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8
Q

Thrombosis

A
  • A clotted mass of blood forming in the circulation is called a ‘thrombus‘
  • A thrombus is a structured, solid mass composed of blood constituents that forms in the cardiovascular system
  • Thrombosis, is due to activation of the normal blood coagulation system.
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9
Q

Factors contributing to thrombus formation

A
  • Damage to endothelium e.g. Atheromatous ulceration of an artery or damage to the endocardium in MI
  • Alterations in Blood flow e.g. turbulence in arteries (plaques) and stasis in veins (morbidity) interrupts the laminar flow of blood and allow platelets to come into contact with endothelium
  • Composition of blood OCP, smoking-sticky blood
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10
Q

4 main outcomes after thrombosis

A
  • The thrombus may enlarge along the vessel (a process termed propagation)
  • undergo lysis by the fibrinolytic system. The latter process may, in certain circumstances, be assisted by therapeutic administration of a fibrinolytic agent such as streptokinase.
  • There may be organization of the thrombus by ingrowth of granulation tissue from the vessel wall. Gradually the thrombus is replaced by granulation tissue, and new vascular channels develop, bridging the site of occlusion and re-establishing flow. This is termed recanalization.
  • Alternatively, fragments may break off the thrombus and be carried by the circulation to impact in other vessels, a process termed thromboembolism
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11
Q

Pulmonary embolus

A
  • Usually follows thrombosis in leg veins, often deep veins in calf.
  • Small pulmonary emboli impact in peripheral branches of pulmonary artery and cause pulmonary infarcts (often with clinical pleurisy).
  • Large pulmonary emboli may impact in, and obstruct, a major pulmonary artery, causing sudden death (massive pulmonary embolus).
  • A small pulmonary embolus (with infarction) may be followed by a much larger, fatal embolus (‘premonitary embolus’).
  • Prevention of leg vein thrombosis is the best way of preventing pulmonary embolus
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12
Q

Some clinical conditions predisposing to leg vein thrombosis

A
  • Immobility and bed rest.
  • Postoperative period.
  • Severe burns.
  • Cardiac failure
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13
Q

Other Emboli

A
  • Tumour
  • Bone Marrow
  • Air
  • Therapeutic
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14
Q

Infarction

A
  • Lack of perfusion of tissues by blood leads to infarction
  • Failure of adequate blood supply to a tissue causes cell damage through ischemia.
  • Tissue necrosis due to interference with local blood flow is termed infarction.
  • Blockage of an artery generally causes coagulative necrosis in the target organ the exception being Liquefactive necrosis in the brain
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15
Q

Body’s reaction to infarction

A
  • Systemic reaction to necrotic tissue
  • Fever and raised ESR
  • Neutrophilia
  • Enzymes from dead and dying cells
  • Aspartate transaminase AST, LDH, Creatine kinase from infarcts of the heart
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