Hemodynamic Disorders

Question 1

Hyperemia

Answer 1

Active process resulting from arteriolar dilation and increased blood inflow. Hyperemic tissues are redder than normal.

Question 2

Congestion

Answer 2

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.

Question 3

Edema

Answer 3

An accumulation of interstitial fluid within tissues.

Question 4

Anasarca

Answer 4

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

Question 5

Vascular hydrostatic pressure

Answer 5

Pressure that fluid in the blood vessels exerts on the wall of the vessel. An increase can lead to edema.

Question 6

Plasma Osmotic Pressure

Answer 6

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.

Question 7

Transudate

Answer 7

Protein poor edema fluid. usually accumulates int eh setting on inc. hydrostatic pressure or dec. plasma colloid pressure.

Question 8

Exudate

Answer 8

Protein-rich edematous fluid caused by increased vascular permeability. Inflammatory edema.

Question 9

Increased Hydrostatic Pressure

Answer 9

Can be caused by local increases, such as DVT, or generalized increases such as congestive heart failure.

Question 10

Reduced Plasma Osmotic pressure

Answer 10

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.

Question 11

Lymphatic obstruction

Answer 11

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.

Question 12

Excessive Sodium and water retention

Answer 12

Can lead to edema by increasing hydrostatic pressure and reducing plasma osmotic pressure. Example: post-streptococcal glomerulonephritis and acute renal failure.

Question 13

Hemorrhage

Answer 13

Extravasation of blood from vessels.

Question 14

Hematoma

Answer 14

hemorrhage which accumulates within a tissue.

Question 15

Petechiae

Answer 15

Minute (1-2 mm) hemorrhages into the skin, mucous membranes, or serosal surfaces. Can be caused by Therombocytopenia, defective platelets, Vitamin C deficiency.

Question 16

Purpura

Answer 16

3-5 mm hemorrhages. Can be caused by vasculitis and increased vascular fragility. Low platelets, Vitamin C, etc.

Question 17

Ecchymoses

Answer 17

1-2 cm subcutaneous hemorrhages. Bruises. Change color as hemoglobin is converted to bilirubin and eventually hemosiderin.

Question 18

Fatal hemorrhage

Answer 18

• Site is important, i.e. subarachnoid or subdural hemorrhage
• Speed is important
• Volume is important, about 20% can cause shock.

Question 19

Thrombosis

Answer 19

formation of blood clot within non-traumatized intact vessels

Question 20

Hemostasis

Answer 20

Regulated processes that result in blood clot formation.

Question 21

Sequence of hemostasis

Answer 21

1. Arteriolar vasoconstriction
2. Primary hemostasis, formation of the platelet plug
3. Secondary hemostasis, deposition of fibrin
4. Clot stabilization and resorption

Question 22

Arteriolar Vasoconstriction

Answer 22

Reflex action, markedly reduces bloodflow to the injured area. Mediated by neurogenic mechanisms and local secretion of endothelin

Question 23

Primary Homeostasis

Answer 23

Disruption of endothelium exposes vonWilebrand Factor and collagen which promote platelet adherence. Platelets then release secretory granules which recruit more platelets.

Question 24

Secondary hemostasis

Answer 24

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.

Question 25

Clot Stabilization

Answer 25

Polymerized fibrin and platelets undergo contraction to form a solid, permanent plug.

Question 26

Clot resorption

Answer 26

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.

Question 27

Von Willebrand Factor

Answer 27

Released by injured epithelia to recruit platelets by bridging the gap between platelet surface receptor glycoprotein Ib (GpIb) and exposed collagen.

Question 28

Prothrombin Time (PT)

Answer 28

Assesses the function of the proteins in the extrinsic and common pathways (Factors 7, 10, 5, and 2, and fibrinogen)

Question 29

Partial Thromboplastin Time (PTT)

Answer 29

Screens the function of proteins in the intrinsic and common pathways (factors 12, 11, 9, 8, 10, 5, 2, and fibrinogen)

Question 30

Plasmin

Answer 30

Enzyme that breaks down fibrin and interferes with its polymerization

Question 31

D-dimers

Answer 31

Breakdown product of fibrinogen useful as a clinical marker of several thrombotic states.

Question 32

T-PA, tissue plasminogen activator

Answer 32

Most important plasminogen activator, most active when bound to fibrin. Useful therapeutically after thrombosis

Question 33

Heparin-like molecules

Answer 33

Bind and activate antithrombin III, which inhibits thrombin and other coagulation factors.

Question 34

Thrombomodulin and endothelial protein C receptor

Answer 34

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.

Question 35

Virchow’s triad

Answer 35

Primary abnormalities that lead to intravascular thrombosis:
Endothelial injury
Stasis or turbulent blood flow
Hyper coagulability

Question 36

Endothelial injury

Answer 36

Can trigger thrombosis by exposing vWF and tissue factor.

Question 37

Turbulence

Answer 37

Chaotic blood flow, can cause endothelial injury or dysfunction, and can form countercurrents and local pockets of stasis.

Question 38

Hypercoagulability

Answer 38

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.

Question 39

Propagation of thrombus

Answer 39

Thrombus enlarges increasing odds of occlusion or embolization.

Question 40

Embolization of thrombus

Answer 40

Thrombus is dislodged, all or in part, and is transported elsewhere where it may become lodged. Ex. DVT leading to PE.

Question 41

Dissolution of Thrombus

Answer 41

Activation of fibrinolytic factors may lead to rapid shrinkage and complete dissolution.

Question 42

Organization and recanalization

Answer 42

Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts.

Question 43

Embolism

Answer 43

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.

Question 44

Infarction

Answer 44

An area of ischemic necrosis caused by occlusion of the vascular supply.

Question 45

Shock

Answer 45

A state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia.

Question 46

Cardiogenic shock

Answer 46

Results from low cardiac output as a result of myocardial pump failure.

Question 47

Hypovolemic shock

Answer 47

Results from low cardiac output due to loss of blood or plasma volume.

Question 48

Septic shock

Answer 48

triggered by microbial infections.