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

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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

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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)

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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

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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)

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Bacillary Angiomatosis

Bacillary Angiomatosis

Causative agent

•    Bartonella henselae and Bartonella quintana

Clinical manifestations

•    Opportunistic infection of immunocompromised patients

•    Manifest as vascular proliferations that clinically resemble tumours

•    Involve skin, bone, brain and other organs

•    Cutaneous involvement marked by one or more red papules and nodules or rounded cutaneous masses

Histologic features

•    Characterized by tumour-like growth pattern

•    Involves capillary proliferation that exhibit protuberant epithelioid endothelial cells with nuclear atypia and mitoses

•    Numerous stromal neutrophils, nuclear dust and purplish granular material consisting of the causative bacteria

Histologic differential diagnosis

•    Kaposi sarcoma

•    Pyogenic granuloma

•    Angiosarcoma

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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

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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

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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

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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

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