Vascular disease Flashcards
(34 cards)
Define arterosclerosis/arteriosclerosis
Thickening and hardening of wall of artery/arteriole
Define atheroma
Important disease of L and M arteries in high pressure system of systemic arterial system.
NEVER VENOUS
Define atherosclerosis
Arteriosclerosis due to atheroma
Outline the impacts of hypertension
Replacement of wall structure by amorphous hyaline material
Decreased lumen size and less response to endocrine stimuli
Hypertrophy of media, fibroelastic thickening of SM intima, elastic lamina reduplication
Outline the consequences of hypertension
Decreased lumen size, reduced flow, ischaemic changes in tissues
Increased rigidity of vessel wall, loss of elasticity
unreactive to vasodilators
How does age affect atheroma?
Worsens with age
Which layers of the artery wall is affected first?
Tunica intima then media
Describe the stages of atheroma
- Blood lipids migrate to the intima, forms damaged endothelium
- Lipids phagocytosed by macrophages in intima (oxidised LDLs)
- Formation of raised fatty streak
- Lipids released from MP form lipid plaque
- MPs secrete cytokines, stim myofibroblasts to secrete collagen- early damage in elastic lamina and media
- Collagen covers plaque surface- forms fibroliquid plaque
- Muscle fibres replaced by collagen
Lipids in intima are calcified, surface of fibrolipid plaque ulcerates due to endo loss - Initiates coagulation cascade- blood clot
- Thinning of media- weakness and inactivity
- Complicated atheroma
List examples of the consequences of atheroma
Coronary arteries- angina
Leg arteries- intermittent claudication (leg cramps)
Mesenteric arteries- ischaemic colitis
Cerebral and verterbral arteries- cerebral ischaemic events
Describe the causes of atheroma within infarcted tissue
Occlusion by atheroma, atheroma and thrombus, atheroma and plaque fissure, occlusion by embolus
Describe the six changes that occur within infarcted tissue
0-12 hrs: early cell death
12-24 hrs: Necrotic tissue visible microscopically
24-72 hrs: Acute inflam reaction
3-14 days: macrophagic removal of debris and vascular granulation tissue formation
14-21 days: fibrovascular granulation tissue formation
21-56 days: scar forms and cauterisation (healing)
Describe venous infarction
Occurs when entire venous drainage from an organ or tissue is and remains obstructed
Describe two causes of venous infarction
Testis infection- torsion
Bowel infection- volvulus, hernia
Describe the mechanism by which tissue necrosis occurs due to venous infarction
Veins obstructed by extrinsic pressure
Tissue congested with blood
Venules and caps engorged with blood that can’t escape
Pressure in venules and caps increases-rupture
leakage of blood
Arterial blood can’t enter
Tissues become congested and necrotic
Outline changes that occur in infarcted tissue, use MI as an example
MI- necrosis of heart muscle due to occlusion of supplying coronary artery
Outcome- sudden death, survival- infarct replaced by granulation tissue- fibrous scar
Death due to problems in infarct healing process
Describe 2 late complications of MI
Ventricular aneurysm
Chronic LVF
Describe 5 early complications of MI
SUDDEN DEATH due to cardiac disarrhythmia/acute LV failure
Rupture of myocardium- HAEMOPERICARDIUM
Rupture of papillary muscle- acute valve failure- LVF
Mural thrombus on infant- embolism-stroke
Define thrombus
Normal physiological mechanism to prevent bleeding when a vessel wall is breached
Becomes pathological when not controlled by fibrinolysis
Describe the process of thrombosis
- Vessel wall breached
- Circulating platelets aggregate- plug gap and release factors to trigger coagulation cascade
- Coag cascade converts fibrinogen- insoluble fibrin
- Long fibrin mols bind together platelets and entrap RBCs and WBCs- form a haemostatic plug
Describe the process of fibrinolysis
Fibrin holds thrombus together, if broken down thrombus dissolves: FIBRINOLYSIS
- Plasma contains inactive plasminogen (becomes activated)- plasmin
- Plasmin fragments convert fibrin into fibrin degradation products
- Plasminogen- plasmin by plasminogen activators (t-PA) secreted by endo cells
- tPA and plasminogen bind to fibrin- degrades fibrin
- Controls size of thrombus
Describe how pathological thrombus occurs
Thrombus enlarges beyond vessel healing requirements
Physically affect bv and blood flow- intrinsic fibrinolytic system incapable of controlling size
- Fibrinolysis fails- thrombus grows by ACCRETION of layer on layer
- If it continues, brown-red mass produced in vessel lumen
What is Virchow’s triad
hint: DSC
Factors that predispose to thrombus formation:
- Damage to bv wall
- Slow turbulent blood flow (stasis)
Change in blood character eg more platelets, RBCs, viscocity
What are the common causes of pathological arterial thrombus
Vessel wall damage eg atheroma, coronary artery
What are the main causes of pathological venous thrombosis?
Stasis eg DVT- tenderness, pitted oedema, embolism
