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61 Cards in this Set
- Front
- Back
EDEMA
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An abnormal accumulation of fluid in the intercellular spaces or body cavities.
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Anasarca (dropsy)
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generalized edema especially evident in subcutaneous tissues (pitting edema).
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Ascites
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collection of edema in the peritoneal cavity.
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Hydrothorax
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edema in the pleural cavity
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Pericardial infusion
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or hydropericardium - edema of the pericardium
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Causes of Edema
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Lowered plasma colloid oncotic pressure.
Elevated hydrostatic pressure. Increased permeability of the endothelium. Lymphatic blockage. |
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Generalized Edema found primarily in:
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Congestive heart failure (CHF) - edema most severe in lower extremities.
Renal disease - nephrotic syndrome with proteinuria, hypoproteinemia, edema - edema generalized throughout body, greater than CHF edema, and identified by edema of the face especially of eyelids. Cirrhosis of the liver - results particularly in ascites. Other causes: starvation, malabsorption syndromes, toxemia, hypothyroidism, estrogen (sodium retention). |
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Localized edema found primarily in:
(TEST QUESTION) |
-Impaired venous drainage
-Localized increase in vascular permeability -Lymphatic obstruction |
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Gross Pathological changes of edema
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Pitting edema
Organs are enlarged, pale, heavier than normal. Tense capsules which upon sectioning have a glistening appearance In brain, edema results in flattened, swollen gyri with compressed ventricles. In lung, edema generally found in lower lobes - sectioning results in the escape of a frothy, sanguineous fluid. |
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Microscopic Pathological changes of edema
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Granular acidophilic interstitial precipitate.
Separation of cellular and fribillar elements In brain, swelling of intercellular and perivascular spaces. In lung, widening of septal walls and presence of a granular pink precipitate within the alveoli. |
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HYPEREMIA & CONGESTION
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Increased volume of blood in an affected tissue or part.
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Active hyperemia
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Results from an increased flow of blood into capillary beds because of arteriolar dilation. This occurs by:
-Increase in functional activity of a tissue. -Neurogenic mechanisms -Heat -Hormones and other vasodilators |
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HEMORRHAGE
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Escape of blood from the cardiovascular system
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Types of hemorrhage
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Hematoma - localized collection of blood.
Petechiae - minute capillary hemorrhages. Purpura - up to 1 cm. Ecchymoses - large, blotchy hemorrhages. |
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Passive hyperemia (congestion)
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Results from decreased venous drainage. This occurs in:
-Heart failure -Venous obstruction |
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Gross Patholoogical Changes in hyperemia
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Most obvious in lungs, liver, and spleen.
-Organs excessively bloody. In liver, results in “nutmeg liver”; in spleen, splenomegaly. |
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Microscopic Patholoogical Changes in hyperemia
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-Lungs have enlarged and engorged capillaries with “heat failure” cells.
-Liver has central hemorrhagic necrosis. -Spleen has enlarged and engorged sinusoids with hemosiderin deposits. |
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Hematuria
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blood in urine
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Melana
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blood in stools
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Hematamensis
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vomiting of blood
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Hemoptysis
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expectoration of blood
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Epistaxis
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nose bleed
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THROMBOSIS
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Formation of a solid mass from constituents of the blood within the vascular system.
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THROMBOSIS
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Formation of a solid mass from constituents of the blood within the vascular system.
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Factors involved in thrombogenesis: Endothelial injury
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Decreases sulfated mucopolysaccharides, plasminogen activator, PGI2, and other substances to degrade platelet-aggregating agents.
Promotes platelet adhesion and activates clotting factors by exposing circulation to subendothelial collagen. |
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Factors involved in thrombogenesis: Alteration in normal blood flow
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-occurs with stasis or turbulence.
-Bring platelets in contact with endothelium. -Prevent liver from clearing activated coagulation factors. -Damage endothelial cells. -Loss of normal velocity prevents thrombi from being washed away. |
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Factors involved in thrombogenesis: Hypercoagulability
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in prolonged rest, CA, serious illness, estrogens
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Thrombogenesis
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-Endothelial injury.
-Platelet adherence and activation of plasma clotting system. -Granule release and prostaglandin release by platelets. -Platelet aggregation and vasoconstriction from primary hemostatic plug. -Formation of secondary hemostatic plug (viscous metamorphosis) from thrombin, fibrin, and rbc’s. -Plasminogen activator and antithrombin reduce rapid clotting. -Clot retraction and fibrinolysis reduce size of clot. -Organization. -Endothelial regeneration. |
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Primary Hemostasis ( clot forming)
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1)Platelet adhesion
2)Shape change 3)Granule release (ADP, TXA2) 4)Recruitment 5)Aggregation (hemostatic plug) |
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SECONDARY HEMOSTASIS
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1) Tissue Factor
2) Phospholipid complex expression 3) Thrombin activation 4) Fibrin polymerization |
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Vichow’s triad in thrombosis:
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Endothelial injury, hypercoagulability, and abnormal blood flow, all lead to thrombosis
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Appearance of arterial thrombi
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“white or conglutination thrombi” - composed primarily of platelets and fibrin with mixed layer of rbc’s (lines of Zahn) -
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Appearance of venus (phlebothromboses) thrombi
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“stasis or red coagulation thrombi” - origin attached to endothelium and appears gelatinous yet friable - contains fibrin - swells vein - related to cancer as Trousseau’s sign (migratory thrombophlebitis).
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Appearance of post-mortem thrombi
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Postmortem clots - rubbery, gelatinous coagulum, moist homogenous - not attached to underlying wall - forms perfect cast of vessel and its branches.
“currant jelly” - cyanotic dark red. “chicken fat” - coagulated clear plasma over darker red cell settled area. |
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Types of Thrombus--Mural
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do not occlude lumen
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Types of Thrombus--Occlusive
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- fill lumen
Arterial - in frequency, coronary, cerebral, iliac, femoral Venous - in frequency, deep calf, femoral, popliteal, iliac |
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Types of Thrombus--Vegetations
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thrombi on valves of heart
Septic - contain bacterial infection Bland - non-bacterial |
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Types of Thrombus--Disseminated intravascular coagulations (DICs)
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microcirculatory thromboses
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EMBOLISM
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Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.
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Pulmonary Embolism
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-Most common and most lethal.
-95% arise from veins of the leg. -Large emboli cause sudden death by occluding the pulmonary artery or by blocking its bifurcation (saddle embolus). -Smaller emboli may cause infarction, cardiac, or circulating insufficiency with inadequate bronchial circulation. |
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Systemic Embolism
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-Emboli in arterial circulation.
-Arises from left side of the heart or thrombi in the aorta or major arteries. -Most often affects the brain, lower extremities, spleen, and kidneys. -Causes infarction of the affected organ. |
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Air or Gas Embolism (Caisson Disease)
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Formed by air or gasses.
Decompression sickness (Caisson Disease) occurs from nitrogen coming out of solution and forming bubble or gas emboli. “Bends” - patient doubles up with pain because of gas emboli in joints and skeletal muscles. “Chokes” - respiratory distress from emboli in the lungs. |
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Fat Emboli
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Trauma to fat-laden tissue, e.g. bone fracture ( bone marrow embolus )
Non-traumatic by emulsion instability of chylomicrons of fat. |
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Amniotic Embolism (amniotic fluid infusion).
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Originally believed to be caused by debris in amniotic fluid.
Now known to be a cause of disseminated intravascular coagulation (DIC) because of thromboplastin-like substances in amniotic fluid. |
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INFARCTION
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Localized area of ischemic necrosis in an organ or tissue resulting from occlusion of either its arterial supply or venous drainage.
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Types of Infarcts: Anemic (white)
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occur with arterial occlusions and in solid tissues - occurs in heart, spleen, and kidneys.
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Types of Infarcts: Hemorrhagic (red)
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occur with venous occlusions and in loose tissues with double circulation or previously congested - occurs in lung, intestine, brain, liver.
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Types of Infarcts : Septic
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presence of bacterial inflammation in area of necrosis.
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Types of Infarcts : Bland
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absence of bacterial inflammation
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Morphology of Infarcts: Gross
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Are wedge-shaped, apex toward focus of occlusion, external part of the organ forms the base.
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Factors Affecting Infarction Damage
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General status of the blood and cardiovascular system.
Anatomic patterns of arterial supply. Rate of development of occlusion - collateral circulation. Vulnerability of tissue to ischemia. |
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SHOCK
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A constellation of syndromes, all characterized by low profusion circulatory insufficiency leading to imbalance between the metabolic needs of vital organs and the available blood flow.
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Hypovolemic Shock
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Reduction in blood volume from external loss of blood plasma or water.
Reduction in blood volume from internal loss; e.g., massive exudation or internal hemorrhage. |
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Cardiogenic Shock
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Intrinsic myocardial damage from infarction or diffuse myocardial disease.
Extrinsic embarrassment of cardiac function from pulmonary embolus or cardiac tamponade. |
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Septic Shock
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Overwhelming gram-negative infections with endotoxemia (endotoxic shock).
Overwhelming gram-positive infections. |
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Morphology of Shock
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Results in generalized cellular damage.
Organs most affected are brain, heart, lungs, kidneys, also adrenal, GI tract, and liver. |
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Neurogenic Shock
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Clinical examples are anesthesia & spinal cord injury
principle mechanism is peripheral vasodialation with pooling of blood |
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In shock you get a cascade of cytokine mediators. Give some examples.
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LPS – TNF – IL1 – IL6/IL8 – NO, PAF (platelet activating factor)
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In low quantities these cytokine mediators lead to (what is the end result)
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monocyte/macrophage activation– endothelial cell activation – complement activation – then LOCAL INFLAMMATION
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In moderate quantities these cytokine mediators lead to (what is the end result)
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Moderate quantities result in fever—acute-phase reactants (fibrinogen; C-reactive protein; complement proteins B, C3, C4; alpha 2-acid glycoprotein, serum amyloid A, proteinase inhibitors, etc) leading to SYSTEMIC EFFECTS
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In high quantities these cytokine mediators lead to (what is the end result)
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High quantities you get low cardiac output, low peripheral resistance, blood, vessel injury, thrombosis, disseminated intravascular coagulation, adult respiratory distress syndrome and SEPTIC SHOCK
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