Chapter 1 Flashcards
- purplish red, pinpoint hemorrhagic spots in the skin caused by loss of capillary ability to withstand normal blood pressure and trauma.
Petechiae
- produced by hemorrhage of blood into small areas of skin, mucous membranes, and other tissues.
Purpura
First appears red-purple the turns brownish yellow
Purpura
- a form of purpura in which blood escapes into large areas of skin or mucous membranes, but not into deep tissue.
Ecchymosis
Appears Black/blue then turns greenish brown to yellow
Ecchymosis
- nosebleed
Epistaxis
- leakage of blood into a joint cavity
Hemarthrosis
- vomiting of blood
Hematemesis
- expectoration of blood secondary to hemorrhage in the larynx, trachea, bronchi or lungs
Hemoptysis
- a swelling or tumor in the tissues or a body cavity that contains clotted blood
Hematoma
- in vivo blood clot causing vascular occlusion and tissue ischemia
Thrombus
- formation, presence of a clot in a blood vessel
Thrombosis
- presence of intact red cells in the urine
Hematuria
- presence of hemoglobin in the urine
Hemoglobinuria
- passage of dark tarry stool containing decomposing blood.
Melena
- excessive menstrual bleeding
Menorrhagia
- passage of blood in feces
Hematochezia
Hemostasis- a complex mechanism that
1. retains the blood within the[?] during periods of injury
2. localizes the reaction involved to the [?] of injury
3. repairs and re-establishes [?] through the injured vessels
vascular system
site
blood flow
Three Hemostatic Components:
Extravascular components
Vascular components
Intravascular components
Play a part in hemostasis by providing back pressure on the injured vessel through swelling and entrapment of escaped blood
Extravascular components
Extravascular components Depends on the
• [?] of surrounding tissue
• [?] of tissue
• [?] of the surrounding tissue
bulk or amount
type
tone
Vascular components Depends on:
Size of the [?]
Amount of [?] within their wall
Integrity of the [?]
blood vessels
smooth muscle
endothelial cell lining
Platelets and biochemicals in the plasma
Intravascular components
STAGES OF HEMOSTASIS
Primary Hemostasis
Secondary Hemostasis
(compare the walls of the arteries from that of the veins and capillaries)
Primary Hemostasis Involves
- Vasoconstriction
- Platelet adhesion, release reaction & aggregation
• Activated by desquamation and small injuries to blood vessels
Primary Hemostasis
Procoagulant substances are exposed or released by damaged or activated endothelial cells
Primary Hemostasis
• Involves vascular intima and platelets
Primary Hemostasis
- Rapid, short-lived response
Primary Hemostasis
- Ends with platelet plug formation
Primary Hemostasis
Do platelets have role in secondary hemostasis?
Involves activation of a series of plasma proteins in the coagulation system until fibrin clot formation
Secondary Hemostasis
Activated by large injuries to blood vessels and surrounding tissues
Secondary Hemostasis
→ Tissue factor exposed on cell membranes
Secondary Hemostasis
Involves platelets and coagulation system
Secondary Hemostasis
Delayed, long-term response
Secondary Hemostasis
Naturally occurring inhibitors in blood will block activated coagulation factors so that widespread coagulation does not occur
Secondary Hemostasis
Fibrinolysis
Secondary Hemostasis
Slow breakdown & removal of fibrin clot as healing of the injured vessel occurs
Fibrinolysis
Inhibits platelet activation
Prostacyclin (PGI2)
Stimulates vasodilation
Prostacyclin (PGI2)
Anticoagulant
Prostacyclin (PGI2)
Heparan sulfate
Thrombomodulin (Endothelial protein C receptor)
Tissue factor pathway inhibitor (TFPI)
Fibronolytic
Thrombomodulin (Endothelial protein C receptor)
Tissue plasminogen activator (tPA)
Reduces blood flow rate’
Adenosine
Procoagulant
von Willebrand factor (VWF) (Weibel-Palade bodies)
Adhesion molecules
• Coats the endothelial cell surface and weakly enhances activity of antithrombin-Ill
Heparan sulfate
• Endothelial surface receptor for thrombin (binds and inactivates thrombin)
Thrombomodulin (Endothelial protein C receptor)
• Enhances anticoagulant and fibrinolytic action of protein C
Thrombomodulin (Endothelial protein C receptor)
• Controls activation of the extrinsic pathway
Tissue factor pathway inhibitor (TFPI)
• Converts plasminogen to plasmin
Tissue plasminogen activator (tPA)
• Stimulates vasodilation
Adenosine
• Required for platelet adhesion to site of vessel injury
von Willebrand factor (VWF)
(Weibel-Palade bodies)
• P-selectin; Intercellular adhesion molecules (ICAMs)
Adhesion molecules
• Platelet endothelial cell adhesion molecules (PECAMs)
Adhesion molecules
- help cells stick to each other and to their surroundings
• Platelet endothelial cell adhesion molecules (PECAMs)
BLEEDING DISORDERS CAUSED BY VASCULAR DEFECTS
Hereditary Connective Tissue Defects
• Sex-linked
- Ehlers-Danlos Syndrome
Caused by a defect in peptidase enzyme that converts procollagen to collagen
- Ehlers-Danlos Syndrome
• Characterized by hyperextensive joints and hyperplastic skin
- Ehlers-Danlos Syndrome
Laboratory findings: Normal Coagulation test and platelet function studies
- Ehlers-Danlos Syndrome
• Autosomal recessive
- Pseudoxanthoma elasticum
Characterized by calcified and structurally abnormal elastic fibers
- Pseudoxanthoma elasticum
Acquired Connective Tissue Defects
Importance of vitamin C: for the formation of the intact structure of the vascular basement membrane
- Vitamin C Deficiency (Scurvy)
Characterized by gingival bleeding
- Vitamin C Deficiency (Scurvy)
hemorrhage into subcutaneous tissues and muscles
- Vitamin C Deficiency (Scurvy)
Large hemorrhagic areas may develop just below the eyes
- Vitamin C Deficiency (Scurvy)
splinter-like hemorrhage may also appear in the fingernail beds
- Vitamin C Deficiency (Scurvy)
• Laboratory findings: CFT= usually positive
- Vitamin C Deficiency (Scurvy)
• Related with normal aging process
- Senile Purpura
• Laboratory findings: CFT= positive
- Senile Purpura
Bleeding time= normal or only slightly prolonged
- Senile Purpura
Hereditary Alteration of Vessel Wall Structure
Autosomal dominant trait characterized by thin-walled, focally disorganized and dilated blood vessels with a discontinuous endothelium appearing as red pinpoint lesions most commonly on the face, lips, tongue, mucous membranes of the mouth and nose, the ears, conjunctiva, palms and soles
- Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome)
Laboratory findings: Bleeding time, platelet function tests, Capillary Fragility test and coagulation tests are all normal
- Hereditary Hemorrhagic Telangiectasia (Rendu-Osler-Weber Syndrome)
What are telangiectasias?
Disorders associated with tumors composed of many vessels.
- Congenital Hemangiomata (Kasabach-Merritt Syndrome)
Formation of fibrin clots, platelet consumption and red cell destruction secondary to vascular obstruction occur at the site of tumor
- Congenital Hemangiomata (Kasabach-Merritt Syndrome)
Acquired Alterations of Vessel Wall Structure
Deposition of glycosylated proteins leading to thickening of capillary basement membrane affecting often the capillaries of the renal glomeruli and retina
- Diabetes Mellitus
Excessive amyloid deposit in small vessels
- Amyloidosis
Endothelial Damage
- Autoimmune Vascular Purpura
- Common drugs that induce purpura:
sulfonamides & iodides quinine, procaine, penicillin, aspirin, sedatives, coumarin
- May be due to development of antibodies to vessel wall components, development of immune complexes, and changes in vessel wall permeability.
a. Drug Induced Purpura
b. Allergic purpura/Anaphylactoid purpura
- associated with certain foods and drugs, cold temperature, insect bites and vaccinations.
b. Allergic purpura/Anaphylactoid purpura
Associated with bacterial; viral, Rickettsial and protozoal infections.
- Infectious Purpura
= associated with abdominal pain secondary to GIT hemorrhaging
Henoch’s Purpura
= associated with joint, especially in the knees, ankles and wrists
Schonlein’s Purpura
• Diameter:
2 - 4 um
• MPV (Mean Platelet Volume):
8 - 10 fL
• Reference platelet count:
150,000 - 450,000/pL
• Daily turnover:
35 X 10%/L (+/- 4.3)
• Lifespan:
8 - 11 days
• Function: maintenance of vascular integrity and blood coagulation
Platelet Factors
Plasma coagulation factor V
PF1
A globulin that inhibits antithrombin III; increases platelet aggregation and accelerates interaction of thrombin and fibrinogen (fibrinoplastic platelet factor)
PF2
A lipoprotein (phospholipid) found in platelet granules & membrane and required in 2 steps of the coagulation process
PF3
A glycoprotein stored in the alpha granules and is extruded during the platelet release reaction
PF4
Platelet fibrinogen
PF 5
A plasma inhibitor associated with platelets
PF 6
Cothromboplastin
PF7
Antithromboplastin factor
PF 8
Accelerator globulin stabilizing factor
PF9
Serotonin found in the dense granules
PF 10
aids in ADP-induced platelet aggregation and inhibits effect of heparin
P F 4
HMWK
Promote coagulation
Fibrinogen
Alpha granules
Factor V
Von Willebrand factor
ADP
Dense bodies
Promote aggregation
Calcium
Platelet factor 4
Alpha granules
Thrombospondin
Promote
Serotonin
Dense bodies
vasoconstriction
Promote vascular
Thromboaxane Az
precursors
Membrane phospholipids
Alpha granules
Platelet-derived growth factor
repair
Beta- thromboglobulin
Plasminogen
Alpha granules
Other systems
affected
02 - antip/asmin
C1 esterase inhibitor