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Category Archives: Vascular
Shock
Shock
Different types of shock
1. cardiogenic (pump failure from myocardial infarctionI)
2. hypovolemic (hemorrhage)
3. septic shock (infection with gram negative bacterium)
Histology of shock in major organs:
Brain: ischemic encephalopathy
Heart: subendocardial hemorrhage, contraction band necrosis
Lungs: resistant
Liver: fatty change, CPC later
Adrenal: cortical fat depletion
Gastrointestine: hemorrhagic enteropathy
Kidneys: acute tubular necrosis
Posted in Vascular
Tagged , Cardiogenic shock, Hemorrhage, Hemorrhagic shock, Hypovolemic shock, Infection and shock, Pump failure, Septic shock, Shock, Shock histology
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Infarction Factors
Infarction
Factors that influence the development of an infarct
1. rate of occlusion
2. vulnerability of the tissue to hypoxia
3. oxygen tension of blood
4. nature of the vascular supply
Posted in Vascular
Tagged , Factors that influence infarct, Infarct size, Infarction, Infarction factors
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Embolism
Embolism
Different types of emboli
1. Pulmonary embolism (PE)
2. Systemic embolism (arterial)
3. Fat embolism
4. Air embolism
5. Amniotic fluid embolism
Pulmonary Embolism
Pulmonary Embolism Complications
1. sudden death
2. hemorrhage (medium sized arteries)
3. infarction (arterioles)
4. pulmonary hypertension and right hear failure
Systemic Arterial Embolism
Causes of systemic arterial emboli
1. mural thrombus in the heart
2. valvular vegetation
3. atherosclerotic plaque
4. aneurysm
Fat Embolism
Causes of fat emboli
1. Fracture of long bones
2. Soft tissue trauma and/or burns
Air Embolism
Main cause of air embolism
1. Decompression sickness (rapid ascent from water)
Amniotic Fluid Embolism
What is it and how does it occur?
- tear in the placental membrane and uterine vessels
Classic histologic finding:
- squames in the pulmonary circulation
- also see edema and diffuse alveolar damage (DAD)
Posted in Vascular
Tagged , Air embolus, Amniotic fluid embolus, Bone marrow embolus, Emboli, Embolism, Embolus, Fat embolus, Pulmonary thromboembolus, Systemic thromboembolus, Thrombus
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Thrombosis
Thrombosis
Primary and secondary hypercoagulable states
Primary (Factor V mutation, Protein S or C deficiency, Antithrombin III)
Secondary (Stasis, DIC, Cancer, MI)
Virchow’s triad:
1. stasis
2. hypercoagulability
3. endothelial injury
Venous thrombosis
1. Resolution
2. Embolization
3. Organization and incorporation into wall
4. Recanalization
Arterial versus venous thrombi
Arterial thrombosis
- aorta or heart (lines of Zahn)
- retrograde propagation
- occlusive
Venous thrombosis
- extend with direction of blood flow
- also occlusive
Posted in Vascular
Tagged , Antithrombin III, Arterial thrombosis, Arterial versus venous thrombi, Factor V mutation, Primary hypercoagulable states, Protein C deficiency, Protein S deficiency, Secondary hypercoagulable states, Stasis, Thrombosis, Venous thrombosis, Virchows triad, Virchow’s triad
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Hemorrhage
HEMORRHAGE
Different types of hemorrhage depending on the size of the hemorrhage.
1. minute (1-2mm) petechiae (thrombocytopenia)
2. (>3mm) purpura (vasculitis)
3. larger (>1-2cm) ecchymoses/SQ hematomas/bruises
(trauma or above)
Posted in Vascular
Tagged , Bruise, Hematoma, Hemorrhage, Large hemorrhage, Minute hemorrhage, Petechiae, Purpura, Thrombocytopenia, Vasculitis
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Atherosclerosis Histology
Atherosclerosis Histology
Gross Features
- Key processes are intimal thickening and lipid accumulation
- An atheroma consists of a raised, focal lesion of the intima with a soft, yellow core of lipid (cholesterol and cholesterol esters) covered by a firm, white, fibrous cap
- Atheromatous plaques appear white to white-yellow and impinge on the arterial lumen
- Vary in size from 0.3-1.5 cm in diameter, but may coalesce to form larger masses
- Are eccentric, patchy and variable along the vessel length; are focal and sparsely distributed initially, but become more numerous and extensive as the disease progresses
- Mainly affects abdominal aorta, coronary arteries, popliteal arteries, internal carotid arteries and the vessels of the circle of Willis (in descending order)
Microscopic Histology Features
- Contain 3 principal components:
- Cells (SMCs, macrophages, other leukocytes)
- ECM (collagen, elastic fibers, proteoglycans)
- Intracellular and extracellular lipid
- Superficial fibrous cap is composed of SMCs and relatively dense ECM
- Beneath and to the side of the cap (the “shoulder”) is a cellular area consisting of SMCs, macrophages and T-lymphocytes
- Deep to the fibrous cap is a necrotic core containing a disorganized mass of lipid (cholesterol and cholesterol esters), cholesterol clefts, cell debris, foam cells, fibrin, variably organized thrombus and other plasma proteins
- The periphery of the lesion demonstrates neovascularisation
• Plaques continue to change and enlarge through cell death and degeneration, synthesis and remodelling of ECM, and organization of thrombus
• Atheromas also undergo calcification; patients with calcificied coronaries are at increased risk for coronary events
• Advanced atheromatous plaques can undergo the following changes:
- Focal rupture, erosion or ulceration: can induce thrombus formation or release of debris producing microemboli (cholesterol emboli)
- Hemorrhage into a plaque: may enlarge a plaque or induce its rupture
- Superimposed thrombosis: may partially or completely occlude the arterial lumen; may be incorporated into the plaque and enlarge it
- Aneurysmal dilatation: results from atherosclerosis-induced atrophy of the media with loss of elastic tissue causing weakness and a potential for rupture
Posted in Vascular
Tagged , Atheroma histology, Atherosclerosis features, Atherosclerosis gross features, Atherosclerosis histology
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Atherosclerosis Endothelial Cells
Atherosclerosis and Endothelial Cells
• Atherosclerosis thought to be a chronic inflammatory response of the arterial wall initiated by injury to the endothelium
• Lesion progression sustained by interaction between modified lipoproteins, lymphocytes, macrophages and normal cellular constituents of the arterial wall
• Pathogenesis thought to be due to:
- Chronic endothelial injury with resultant endothelial dysfunction results in increased permeability, leukocyte adhesion and thrombotic potential
- Accumulation of LDL in the vessel wall
- Oxidation of lipoproteins
- Adhesion of monocytes to endothelium, followed by migration into intima, and their transformation to macrophages and foam cells
- Platelet adhesion
- Release of factors from adherent platelets, macrophages or vascular cells causing migration of smooth muscle cells from the media to the intima
- Proliferation of SMCs and elaboration of ECM, resulting in accumulation of collagen and proteoglycans
- Extracellular and intracellular (within SMCs and macrophages) accumulation of lipids
• Human atherosclerotic lesions begin with intact endothelium.
• Cause of endothelial dysfunction could begin with harmful derivatives of cigarette smoke, homocysteine, viruses, or other infectious agents
• Two most important determinants of endothelial alteration are thought to be:
- Hemodynamic disturbances in normal circulatory function
- Adverse effects of hypercholesterolemia
• Lesion protected areas have normal laminar flow which blocks inflammatory mechanisms that mediate endothelial dysfunction and endothelial apoptosis
• Normal laminar flow also induces expression of genes (eg. superoxide dismutase) that protect against lesion development
Posted in Vascular
Tagged , Atheroma, atherosclerosis, Endothelial cell, Endothelial cells, Hypercholesterolemia
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Atherosclerosis Complications
Atherosclerosis Complications
• Myocardial infarction
• Cerebral infarction
• Aortic aneurysms
• Peripheral gangrene
• Mesenteric infarction, mesenteric occlusion
• Sudden cardiac death
• Chronic ischemic heart disease
• Ischemic encephalopathy
Posted in Vascular
Tagged , Aortic aneurysms, atherosclerosis, Atherosclerosis complications, Cerebral infarction, Myocardial infarction
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Atherosclerosis Risk Factors
Atherosclerosis Risk Factors
• Hypertension
• Smoking
• Hypercholesterolemia/hyperlipidemia
• Age
• Gender (males, postmenopausal females)
• Diabetes
• Family history
• Alcohol
• Obesity
• Physical inactivity
• Stress
• High carbohydrate intake
• Lipoprotein Lp(a)
• Hardened (trans)unsaturated fat intake
• Chlamydia pneumoniae
Posted in Vascular
Tagged , atherosclerosis, Atherosclerosis risk factors, Cardiac risk factors, Heart attack, risk factors
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