Pahtology of arterial circulation Flashcards
Learning outcomes
Define ischaemia and infarction; giving clinical examples and causal factors
•Define atheroma and explain the pathogenesis of atheroma
•Explain arterial thrombosis as a complication of atheroma
•Define aneurysm and outline the clinicopathological characteristics of: Abdominal Aortic Aneurysm, Dissecting aneurysm, Berry aneurysm, Charcot-Bouchard aneurysm
•Define vasculitis and give clinical examples
Ischaemia vs infarction
Ischaemia-
Result of impaired blood flow/ perfusion of tissue such that it is deprived of vital nutrients (esp oxygen)
Reversible
Effects depend on duration and metabolic demands of affected tissue
Infarction (lesion = infarct) -
Necrosis of tissues as result of ischaemia
Irreversible
Tissues vary in ability to repair/regenerate (fibrous scarring or sometimes tissue regeneration)
Ischaemia vs infarction- factors
Depends on many factors
- Nature of blood supply- lung/liver (dual blood supplies- pulm/bronch artery and hep/portal artery- relatively resistant to infarction) versus spleen/kidney (end-arterial vascular obstruction- usually leads to tissue death)
- Rate of development of occlusion- slow vs fast- slow if there is no time to develop alternate perfusion pathways- COLLATERAL CIRCULATIONS
- Vulnerability of tissue to hypoxia- neurones (irreversible after 3-4 mins) and myocardium 20-30 min ischaemia vs skeletal muscle and fibroblasts (many hours)
- O2 content of blood- anaemia+ hypoxia vs normal
In anaemic patient, increased susceptibility to hypoxia (blood carries less oxygen)
Myocardial ischaemia and infarction
normal artery > uncomplicated atheroma >
1. Significant fixed lesion: stable angina
2. Ustable angina > acute MI
unstable plaque- Acute Coronary Syndrome
Ischaemic Heart Disease (IHD)
- A spectrum of clinico-pathological entities including
- – Angina
- – Myocardial infarction: occlusion in L or R coronary artery (run in epicardial fat) > infarction of this part of left ventricle or branch
- – Sudden death
- Imbalance between demand for O2 and itssupply by coronary arteries
- Mainly due to atheroma and its complications but other factors such as vascular spasm and anaemia can contribute
Ischaemia vs infarction
Acute limb Ischaemia- peripheral vascular disease- intermittent claudication
•Paraesthesia (pins and needles)
•Pallor (mottled colouration)
•Pulselessness
•Paralysis
•Poikilothermia (coolness) (or
Perishingly cold)
(In order of mild > moderate > severe ischaemia > infarction)
Brain- TIA > Cerebral Infarct (ischaemic attack)
Heart- Stable angina> unstable angina> MI
Acute coronary syndrome can be severe isc or Infarct
Leg- Intermittent claudication > acute limb ischaemia ( patient prevents initially w severe isc which, if untreated, can rapdily evolve into infarction)
Peripheral vascular disease> Mild Isc > Infarct
Atherosclerosis
ATHEROMA -Focal accumulation of lipid in the intima of arteries
•from the Greek -“athero”,-gruel, or wax, corresponding to the necrotic core area at the base of the atherosclerotic plaque,
“sclerosis” - hardening, or induration, referring to the fibrous cap of the plaque’s luminal edge.
Atheromas are lipid rich, containing foamy macrophages and cholestrol
Structure of arterties- •Intima-single layer of endothelium with thin layer of connective tissue •Internal elastic lamina •Media •External elastic lamina •Adventitia
Atheroma formation
Injury to endothelium (e.g smoking) > tissue response of vessel wall > atheroma formation
•ENDOTHELIAL CELL INJURY -allows LDL-CHOLESTEROL to leak into the intima.
•AN INFLAMMATORY REACTION occurs in which macrophages are present.
•Macrophages accumulate lipid in cytoplasm-FOAM CELL
•Smooth muscle cells migrate into the intima.
•Lipid- laden macrophages die, spilling lipid into a “lipid c o r e ”.
Attempted tissue repair-proliferation of smooth muscle cells producing collagen, elastin –FIBROUS CAP formation
•Neovascularisation at periphery of plaque (may lead to haemorrhage)
•Increase in plaque volume by organisation of small microthrombi that form on the surface
•Dystrophic calcification may occur
Evolution of a plaque, and the 3 types of atheromatous plaques
Fatty streak > atherosclerotic plaque > lumen narrowing, atherothrombotic occlusion, embolisation
(In descending order of evolution)
Fatty Streaks
•– Linear elevations composed of lipid –laden (foamy) macrophages
Fibrolipid Plaque
•– Bigger lesions with fat and fibrosis, and with fibroblasts present
Complicated Lesion •– Narrowing •– Endothelial erosion with thrombosis •– Plaque rupture and fissuring (bleeding) •– Aneurysm formation •– Also embolic phenomena
Aetiology of atheroma
Multifactorial
Non modifiable risk factors
-Family history, increasing age, male gender
Modifiable risk factors
-Hyperlipidaemia, hypertension, obesity, smoking, diabetes mellitus
Uncertain risk factors
- Many
Complications of atheroma
- Acute arterial occlusion secondary to plaque rupture and thrombosis
- Progressive luminal narrowing producing ischaemia of organ
- Erosion of media by plaque leading to aneurysm formation
- Dislodgement of plague thrombus or of plaque core constituents to produce emboli
Aneurysm and different types of aneurysm
•Localised, permanent abnormal dilatation of blood vessel (or left ventricle e.g. Post MI)
-from Greek aneurusma, aneurunein to dilate, eurunein to widen
Types of Aneurysm
- Atherosclerotic
- Dissecting
- Berry
- Capillary Micro-aneurysms (Charcot-Bouchard Aneurysms)
- Luetic (Syphilitic)-Ascending aorta or arch of aorta
- False Aneurysm-a blood filled space that forms round a blood vessel usually after a traumatic injury or perforating rupture
Atherosclerotic aneurysm of the abdominal aorta ( AAA)
•Most common and clinically significant type of atherosclerotic aneurysm
-Complications
•Erosion and replacement of the media by an adjacent complicated atheroma
•Bigger than 5.5cmin diameter –greater risk of rupture
•Thrombus formation may lead to emboli
- May extend into iliac arteries leading to
•Thickening of walls
•Decrease in lumen
•Peripheral Vascular Disease
AAA rupture
Classical Triad 1.Pain in the flank or back, 2.Hypotension 3.Pulsatile abdominal mass • Not all present with these symptoms SURGICAL EMERGENCY -The death rate after rupture is about 80 % because many patients die before they reach hospital.
screening programme targeted to 65+ males and smokers
Dissecting Aortic Aneurysm
- Blood is forced through a tear in intima•Haematoma in the media-propagated along blood vessel
- Sharp, tearing pain
- Classifications basedoninvolvement/non-involvementof ascendingaorta
Possible Outcomes of Dissecting Aortic Aneurysm
- Blood ruptures through adventita-massive haemorrhage into pericardium , pleural cavity , other structures
- Blood re-enters aortic lumen-Double-barrelled aorta
- Blood may extend down tributary arteries-compresses lumen-results in end-organ infarction
