IV - Hemodynamic Disorders, Thrombosis and Shock Flashcards
Extravasation of fluid into interstitial spaces due to increases in vascular volume or pressure, decreases in plasma protein content or alterations in endothelial function.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
It is a severe and generalized edema with profound subcutaneous tissue swelling.
Anasarca(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.81
The edema fluid occuring with volume or pressure overload or under conditions of reduced plasma protein.
Transudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
Edema secondary to increased vascular permeability and inflammation.
Exudate(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.82
The serum protein most responsible for maintaining intravascular colloid osmotic pressure.
Albumin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
In breast cancer, infiltration and obstruction of superficial lymphatics can cause edema of the overlying skin, called _______ appearance.
Peau dā orange(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.83
Microscopically, it is reflected primarily as a clearing and separation of the extracellular matrix elements with subtle cell swelling.
Edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Diffuse edema usually more prominent in certain body areas as a result of the effects of gravity.
Dependent edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
True or false:Dependent edema is a prominent feature of left-sided heart failure.
False.Dependent edema is a feature of right-sided HF, while pulmonary congestion is a feature of left-sided HF.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Edema due to renal dysfunction which manifests disproportionately in tissues with loose connective tissue matrix, e.g. Eyelids.
Periorbital edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Finger pressure over significantly edematous subcutaneous tissue displacing the interstitial fluid, leaving a finger-shaped depression on the skin.
Pitting edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Condition wherein the lungs weigh 2-3x the normal, and on sectioning reveals frothy, sometimes blood-tinged mixture of air, fluid and extravasated red cells.
Pulmonary edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Condition wherein the brain is grossly swollen, with narrowed sulci and distended gyri showing signs of flattening against the underlying skull.
Brain edema(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
It is an active process resulting from augmented blood flow due to arteriolar dilation.
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
The affected tissue is redder than normal, because of engorgement with oxygenated blood.
Hyperemia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
It is a passive process resulting from impaired venous rturn out of a tissue.
Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Tissue has a blue-red color due to accumulation of hemoglobin in the affected tissue.
Congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.84
Characterized by alveolar capillaries engorged with blood, with associated alveolar septal edema or focal minute intra-alveolar hemorrhage.
Acute pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Pulmonary septa are thickened and fibrotic, with hemosiderin-laden macrophages in alveolar spaces.
Chronic pulmonary congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Hemosiderin- laden macrophages
Heart- failure cells(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
The central vein and sinusoids of the liver are distended with blood, with central hepatocyte degeneration. The periportal hepatocytes are better oxygenated.
Acute hepatic congestion(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
The central regions of the hepatic lobules are grossly red-brown and slightly depressed and are accentuated against the surrounding zones of uncongested tan, sometimes fatty liver (nutmeg liver).
Chronic passive congestion of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Presence of centrilobular necrosis with hepatocyte drop-out, hemorrhage and hemosirin-laden macrophages
CPC of the liver(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.85
Extravasation of blood from vessels into the extravasclar space.
Hemorrhage(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Accumulation of blood within a tissue.
Hematoma(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
1-2mm hemorrhages into skin, mucous membranes, or serosal surfaces.
Petechiae(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
3-5mm hemorrhages which can occur with trauma, vascular inflammation, or increased vascular fragility.
Purpura(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
1-2cm subcutaneous hematomas/bruises.
Ecchymoses (TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
It is a consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing the rapid formation of a localized hemostatic plug at the site of vascular injury.
Normal hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Pathologic form of hemostasis.
Thrombosis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
It occurs after an initial injury, as a result of reflex neurogenic mechanisms.
Arteriolar vasoconstriction(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
A potent endothelium-derived vasocontrictor.
Endothelin(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Receptors responsible for platelet adhesion.
GpIb receptors- plateletVon Willebrand factor - endothelium(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)
Deficiency of GpIb receptors.
Bernard-Soulier syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of GpIIb-IIIa receptors.
Glanzmann thrombasthenia(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Deficiency of Factor VIII.
Von Willebrand Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
It is a membrane-bound procoagulant glycoprotein synthesized by endothelium, which becomes exposed at the site of injury.
Thromboplastin/Factor III(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.88
Formation of a hemostatic plug due to platelet aggregation
Primary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
Hemostasis characterized by activation of thrombin through the coagulation cascade.
Secondary hemostasis(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.86
True or false:The primary aggregation of platelets is irreversible.
FalseReversible(TOPNOTCH)
Two substances essential for the formation of a primary hemostatic plug.
ADP and TXA2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.87
True or false:Activation of the coagultion cascade and subsequent thrombin formation is reversible.
FalseIrreversible(TOPNOTCH)
Substance that activates the coagulation proteins.
Calcium(TOPNOTCH)
Substance that medites further platelet aggregation and degranulation.
ADP(TOPNOTCH)
Substance that increases platelet activation and causes vasoconstriction. Synthesized by activated platelets.
TXA2(TOPNOTCH)
Most important initiator of the coagulation cascade.
Tissue factor(TOPNOTCH)