Flashcards in 5. Circulatory Pathology Deck (41):
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.
What is von Willebrand disease?
Inherited bleeding disorder characterized by either a deficiency or qualitative defect in von Willebrand factor.
Where is von Willebrand factor produced?
By endothelial cells and megakaryocytes.
What is the treatment for type I (mild) cases of von Willebrand disease?
Desmopressin (an antidiuretic hormone (ADH) analog), which releases vWF from Weibel Palade bodies of endothelial cells.
What is thrombosis?
Pathologic formation of an intravascular fibirn-platelet thombus.
What does Thrombus have that blood clot doesn't?
Blood clots lacks platelets and lines of Zahn and has no definite shape.
What is an embolism?
Any intravascular mass that has been carried down the bloodstream from its site of origin, resulting in the occlusion of a vessel.
What is Caisson diseaes?
A gas embolism caused by decompression sickness.
What vessels make up the dual blood supply to the lungs?
Pulmonary artery and bornchial arteries.
What is a paradoxical emboli?
Any venous embolus that gain access to the systemic circulation by crossing over from the right to the left side of the heart through a septal defect.
Where do anemic infarcts like to strike?
AKA pale or white color infarcts, they like to strike in solid organs with a single blood supply such as kidney, spleen and heart.
Where do hemorrhagic infarcts like to strike?
AKA red color infarcts, they like to strike organs with dual blood supply or collateral circulation such as the lungs or intestines. They also occur in venous occlusion like testicular torsion.
What is a shock?
It is characterized by vascular collapse and widespread hypoperfusion of cells an tissue due to reduced blood volume, cardiac output, or vascular tone.
What type of bacteria produces spetic shock?
What is neurogenic shock and causes it?
Generalized vasodilation; anetheisia or brain/spinal cord injury.
What happens in "shock lungs"?
Lungs undergo diffuse alveolar damage.
What happens in "shock liver"?
Liver undergoes centrilobular necrosis.