Hemodynamic Disorders Flashcards
Hyperemia
Active process resulting from arteriolar dilation and increased blood inflow. Hyperemic tissues are redder than normal.
Congestion
Passive process resulting from impaired outflow of venous blood from a tissue. Congested tissues may display cyanosis. Longstanding congestion may cause edema and focal hemorrhages from secondary tissue fibrosis.
Edema
An accumulation of interstitial fluid within tissues.
Anasarca
Severe generalized edema marked by profound swelling of subcutaneous tissues and accumulation of fluid in body cavities.
Vascular hydrostatic pressure
Pressure that fluid in the blood vessels exerts on the wall of the vessel. An increase can lead to edema.
Plasma Osmotic Pressure
Concentration of the plasma which osmotically regulate fluid in the blood vessel. A decrease can lead to edema. Usually slightly less than the hydrostatic pressure, leading to some drainage into the lymph system.
Transudate
Protein poor edema fluid. usually accumulates int eh setting on inc. hydrostatic pressure or dec. plasma colloid pressure.
Exudate
Protein-rich edematous fluid caused by increased vascular permeability. Inflammatory edema.
Increased Hydrostatic Pressure
Can be caused by local increases, such as DVT, or generalized increases such as congestive heart failure.
Reduced Plasma Osmotic pressure
Reduction of plasma albumin concentrations leads to decreased colloid osmotic pressure and loss of fluid from circulation. Examples include nephrotic syndrome where albumin is lost from the blood, and Liver cirrhosis where albumin synthesis is reduced.
Lymphatic obstruction
Obstrution of lymphatic drainage compromises absorption of fluid from interstitial spaces. Example: Elephantiasis from infection of filariasis produces fibrosis in inguinal lymphnodes, and massive edema in lower limb.
Excessive Sodium and water retention
Can lead to edema by increasing hydrostatic pressure and reducing plasma osmotic pressure. Example: post-streptococcal glomerulonephritis and acute renal failure.
Hemorrhage
Extravasation of blood from vessels.
Hematoma
hemorrhage which accumulates within a tissue.
Petechiae
Minute (1-2 mm) hemorrhages into the skin, mucous membranes, or serosal surfaces. Can be caused by Therombocytopenia, defective platelets, Vitamin C deficiency.
Purpura
3-5 mm hemorrhages. Can be caused by vasculitis and increased vascular fragility. Low platelets, Vitamin C, etc.
Ecchymoses
1-2 cm subcutaneous hemorrhages. Bruises. Change color as hemoglobin is converted to bilirubin and eventually hemosiderin.
Fatal hemorrhage
- Site is important, i.e. subarachnoid or subdural hemorrhage
- Speed is important
- Volume is important, about 20% can cause shock.
Thrombosis
formation of blood clot within non-traumatized intact vessels
Hemostasis
Regulated processes that result in blood clot formation.
Sequence of hemostasis
- Arteriolar vasoconstriction
- Primary hemostasis, formation of the platelet plug
- Secondary hemostasis, deposition of fibrin
- Clot stabilization and resorption
Arteriolar Vasoconstriction
Reflex action, markedly reduces bloodflow to the injured area. Mediated by neurogenic mechanisms and local secretion of endothelin
Primary Homeostasis
Disruption of endothelium exposes vonWilebrand Factor and collagen which promote platelet adherence. Platelets then release secretory granules which recruit more platelets.
Secondary hemostasis
Injury exposes tissue factor, which binds and activates Factor VII, catalyzing the thrombin generation cascade. Thrombin cleaves fibrinogen into fibrin, creating a meshwork clot. This consolidates the platelet plug.
Clot Stabilization
Polymerized fibrin and platelets undergo contraction to form a solid, permanent plug.
Clot resorption
Counter regulatory mechanisms, like t-PA which blocks fibrinolysis, and thrombomodulin, which clocks the coagulation cascade, are set in motion to limit clotting and eventually start tissue repair.
Von Willebrand Factor
Released by injured epithelia to recruit platelets by bridging the gap between platelet surface receptor glycoprotein Ib (GpIb) and exposed collagen.
Prothrombin Time (PT)
Assesses the function of the proteins in the extrinsic and common pathways (Factors 7, 10, 5, and 2, and fibrinogen)
Partial Thromboplastin Time (PTT)
Screens the function of proteins in the intrinsic and common pathways (factors 12, 11, 9, 8, 10, 5, 2, and fibrinogen)
Plasmin
Enzyme that breaks down fibrin and interferes with its polymerization
D-dimers
Breakdown product of fibrinogen useful as a clinical marker of several thrombotic states.
T-PA, tissue plasminogen activator
Most important plasminogen activator, most active when bound to fibrin. Useful therapeutically after thrombosis
Heparin-like molecules
Bind and activate antithrombin III, which inhibits thrombin and other coagulation factors.
Thrombomodulin and endothelial protein C receptor
Binds thrombin and Protein C into a complex on the cell surface, stopping thrombin from activating coagulation and instead activates the Protein C/Protein S complex that inhibits coagulation factors 5a and 7a.
Virchow’s triad
Primary abnormalities that lead to intravascular thrombosis:
Endothelial injury
Stasis or turbulent blood flow
Hyper coagulability
Endothelial injury
Can trigger thrombosis by exposing vWF and tissue factor.
Turbulence
Chaotic blood flow, can cause endothelial injury or dysfunction, and can form countercurrents and local pockets of stasis.
Hypercoagulability
Abnormally high tendency of the blood to clot, typically caused by alteration in coagulation factors. Underlying risk for venous thrombosis. Both genetic and acquired disorders.
Propagation of thrombus
Thrombus enlarges increasing odds of occlusion or embolization.
Embolization of thrombus
Thrombus is dislodged, all or in part, and is transported elsewhere where it may become lodged. Ex. DVT leading to PE.
Dissolution of Thrombus
Activation of fibrinolytic factors may lead to rapid shrinkage and complete dissolution.
Organization and recanalization
Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts.
Embolism
A detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site, where it often causes infarction.
Infarction
An area of ischemic necrosis caused by occlusion of the vascular supply.
Shock
A state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia.
Cardiogenic shock
Results from low cardiac output as a result of myocardial pump failure.
Hypovolemic shock
Results from low cardiac output due to loss of blood or plasma volume.
Septic shock
triggered by microbial infections.
