Robbins [03] - Hemodynamic Disorders, Thromboembolism, and Shock

11th edition

An active process resulting from arteriolar dilation and increased blood inflow (e.g., at sites of inflammation or exercising skeletal muscle). Affected tissues are redder than normal due to engorgement with oxygenated blood.

Hyperemia

A passive process resulting from impaired outflow of venous blood from a tissue (systemically in cardiac failure, or locally in venous obstruction). Tissues appear blue-red (cyanosis) due to the accumulation of deoxygenated hemoglobin. Long-standing chronic congestion can lead to parenchymal cell death, secondary tissue fibrosis, and edema.

Congestion

Hemosiderin-laden macrophages found within the alveolar spaces in chronic pulmonary congestion. They are derived from the phagocytosis and degradation of red blood cells that have leaked from congested, engorged alveolar capillaries.

Heart Failure cells

The gross appearance of the liver in chronic passive hepatic congestion. Centrilobular regions are red-brown and depressed (due to hypoxia-induced necrosis and cell loss), accentuated by surrounding zones of uncongested, tan, sometimes fatty periportal hepatocytes.

Nutmeg liver

This is the accumulation of interstitial fluid within tissues.

Edema

The collection of extravascular fluid within body cavities (e.g., hydrothorax in the pleural cavity, hydropericardium in the pericardial cavity, and hydroperitoneum/ascites in the peritoneal cavity).

Effusion

Severe, generalized edema marked by profound swelling of subcutaneous tissues and the accumulation of fluid in multiple body cavities.

Anasarca

Protein-poor, non-inflammatory edema fluid caused by elevated vascular hydrostatic pressure or diminished colloid osmotic pressure (with normal vascular permeability).

Transudate

Protein-rich inflammatory edema fluid caused by increased vascular permeability.

Exudate

Starling forces alterations (edema pathways)

Increased hydrostatic pressure (d/t impaired venous return)

Reduced plasma osmotic pressure (drop in plasma albumin, decreased hepatic synthesis, or protein malnutrition)

Edema resulting from localized lymphatic obstruction that compromises the resorption of interstitial fluid. Examples include elephantiasis (via parasitic filariasis fibrosis of inguinal lymphatics) and peau d'orange (orange peel appearance of breast skin due to tumor infiltration of superficial lymphatics).

Lymphedema

The formation of initial platelet plug at the site of vascular injury, involving platelet adhesion, activation, conformational change, and aggregation.

Primary Hemostasis

The deposition of insoluble fibrin via the coagulation cascade, which polymerizes and cements the platelet plug into a stable secondary hemostatic plug.

Secondary Hemostasis

A plasma glycoprotein by endothelial cells and megakaryocytes that acts as an essential bridge between platelet surface receptor GpIb and exposed subendothelial collagen.

Von Willebrand Factor (vWF)

An inherited bleeding disorder caused by a deficiency of the platelet receptor GpIb, preventing proper platelet adhesion to vWF.

Bernard-Soulier Syndrome

An inherited bleeding disorder caused by a deficiency of the platelet integrin receptor GpIIb/IIIa, preventing platelet-to-platelet aggregation via fibrinogen bridging.

Glanzmann Thrombastenia

A membrane-bound glycoprotein expressed by subendothelial cells that binds Factor VII to initiate the extrinsic pathway of coagulation in vivo following vascular injury.

Tissue Factor (Thromboplastin)

The 3 primary abnormalities that lead to intravascular thrombosis: (1) Endothelial injury, (2) Stasis or turbulent blood flow, (3) Hypercoagulability

Virchow’s Triad

Alternating pale laminations (platelets and fibrin) and dark laminations (red blood cells) characteristic of thrombi formed in flowing blood, proving that a clot formed antemortem.

Lines of Zahn

Thrombi that occur within the lumens of the heart chambers or the aortic lumen, typically adhering to the wall without completely occluding the vessel.

Mural Thrombi

Blood clot formed after death; lacks Lines of Zahn, is gelatinous, and typically displays a dark red dependent portion “currant jelly” and a yellow supernatant layer “chicken fat.”

Postmortem Clot

The most common inherited cause of hypercoagulability, featuring a point mutation in the factor V gene that renders Factor Va resistant to cleavage and inactivation by Activated Protein C (APC).

Factor V Leiden Mutation

An autoimmune hypercoagulable state characterized by recurrent arterial or venous thromboses, repeated miscarriages, and the presence of antibodies against phospholipids or plasma protein bound to them (e.g., B2-glycoprotein I).

Antiphospholipid Syndrome (APAS)

A detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin, where it often causes tissue dysfunction or infarction.

Embolus

A large pulmonary embolus that occludes the main pulmonary artery bifurcation, bridging across both the left and right pulmonary arteries; frequently causes sudden death.

Saddle Embolus

A venous embolus that passes through an interatrial or interventricular defect (e.g., patent foramen ovale) into the systemic arterial circulation, bypassing the lungs.

Paradoxical Embolus

A form of gas embolism caused by a rapid decrease in atmospheric pressure, causing dissolved nitrogen to come out of solution as bubbles in the blood and musculoskeletal tissues “the bends.”

Decompression Sickness

An area of ischemic necrosis caused by the occlusion of either the arterial supply or the venous drainage of a particular tissue.

Infarction

An infarct that occurs in venous occlusions, loose tissues (like lungs), tissues with dual circulations (lungs, small intestine), or tissues previously congested, allowing blood to pool in the necrotic area.

Red (Hemorrhagic) Infarct

An infarct that occurs with arterial occlusions in solid organs with end-arterial circulations (heart, spleen, kidney), where tissue density limits the leakage of blood into the necrotic zone.

White (Anemic) Infarct

State of profound systemic hypoperfusion caused by a reduction in either effective circulating blood volume or cardiac output, resulting in widespread cellular hypoxia and tissue dysfunction.

Shock

Shock resulting from low cardiac output due to myocardial pump failure (myocardial infarction, ventricular arrhythmias, or cardiac tamponade)

Cardiogenic Shock

Shock resulting from low cardiac output due to a severe loss of blood volume or plasma volume (hemorrhage, severe burns, vomiting, or diarrhea)

Hypovolemic Shock

Shock triggered by systemic microbial infections, characterized by overwhelming endothelial cell activation, vasodilation, peripheral pooling of blood, DIC, and metabolic abnormalities.

Septic Shock

A thrombohemorrhagic disorder characterize by the widespread activation of coagulation, leading to microvascular thrombi consumption of clotting factors and platelets, paradoxically causing severe bleeding.

Disseminated Intravascular Coagulation (DIC)