5. Circulatory Pathology Flashcards
What is edema?
Precense of excess fluid in the intracellular space.
Describe transudate fluid.
Edema fluid with low protein content. Specific gravity
Describe exudate fluid.
Edema fluid with high protein content and cells. Specific gravity >1.020.
Describe the difference between active hyperemia versus passive hyperemia.
An excessive amount of blood in tissue or organ secondary to vadilation (active) or diminished venous outflow (passive).
What is hemostasis?
Sequence of events leading to cessation of bleeding by the formation of stable fibrin-platelet hemostatic plug.
What factor is on top of the extrinsic pathway?
Release of tissue factor from injured cells activates Factor VII.
What factor is on top of the intrinsic pathway?
Exposure of thrombogenic subendothelial collagen activates Factor XII.
Describe step 1 of platelet clotting.
Platelet adhesion: First von Willebrand factor (vWF) adheres to subendothelial collagen. Then platelets adhere to vWF glycoprotein Ib.
Describe step 2 of platelet clotting.
Platelet activation. Platelets undergo a shape change and degranulation occurs. Platelets synthesis of thromboxane A2 and memebrane expression of the phospholipid complex, which is an important platform for the coagulation cascade.
Describe step 3 of platelet clotting.
Platelet aggregation: Additional platelets are recruited from the blood stream. ADP and thromboxane A2 are potent mediators of aggregation. Platelets bind to each other by binding to fibrinogen using Gp IIb-IIIa.
What causes Bernard-Soulier Syndrome?
It’s an autosomal recessive disease where deficiency of platelet Gp Ib leads to defective platelet adhesion (Step 1).
What causes Glanzmann Thrombasthenia?
It’s an autosomal recessive disease where deficiency of Gp IIb-IIIa leads to defective platelet adhesion (Step 3).
What is Immune thrombocytopenia purpura (ITP)?
When antiplatelet antiboides are made in the spleen against platelet antigens such as Gp IIb-IIIa and Gp Ib-IX; platelets are destroyed peripherally in the spleen by macrophages, which have Fc receptors that bind IgG-coated platelets.The acute form is seen in children following a viral infection; it is self-limited. The chronic kind is seen in women in their childbearing years, and maybe seen as the first manifestation of lupus.
What is the treatment for Immune thrombocytopenia purpura (ITP)?
I. Corticosteroids, which decrease antibody production. II. Immunoglobulin therapy, which floods Fc receptors on splenic macrophages. III. Splenectomy, which removes the site of platelet desctruction and antibody production.
What is Thrombocytopenic purpura (TTP)?
Widespread formation of platelet thrombi with scant fibrin (hyaline thrombi). No activation of the coagulation system.
What are the pentad characteristic signs of Thrombocytopenic purpura (TTP)?
Fever, Thombocytopenia, Microangiopathic hemolytic anemia, Neurologic symptoms, Renal failure. [FTMNR]
What is Hemolytic uremic syndrome (HUS)?
It has a similar clinical pentad as TTP, it occurs most often in children after a gastroenteritis with bloody diarrhea; verotoxin-producing E. coli 0157:H7.
What does prothrombin time (PT) test for?
Test the extrinsic and common coagulation pathways. Factors VII, X, V, prothrombin, fibrinogen. [PT-E]
What does partial thromboplastin time (PTT) test for?
Test the intrinsic and common coagulation pathways. Factors XII, XI,IX, VIII, X, V, prothrombin, fibrinogen.
What does Thrombin time (TT) test for?
Adequate fibrinogen levels.
What does Fibrin degradation products (FDP) test for?
Fibrinolytic system; increased with DIC.
What causes hemophilia A?
AKA classic hemophelia, caused by the deficiency of factor XIII; X-linked recessive.
What causes Hemophila B?
AKA Christmas disease, caused by the deficiency of factor IX; X-linked recessive.
What factors of coagulation are affected in vitamin K deficiency?
Factors II, VII, IX, X. And protein C and S.
