Hem Exam 3

Front 1

Thrombophilla

Back 1

Congenital or acquired abnormality and increase clots

Front 2

Thrombus

Back 2

Forms a blood clot and remains there, is the final product of the blood coagulation step in hemostasis

Front 3

Thrombosis

Back 3

Formation of a platelet and/or fibrin mass within a vessel

Front 4

Hypercoagulability

Back 4

Recurrent thrombosis in patients <45 years old
Patients with a positive family history
Recurrent spontaneous thromboses
Thrombosis is unusual sites
Heparin resistance
Protein C and S deficiency
Throombosis associated with pregnancy and estrogen therapy
Unexplained recurrent pregnancy loss.

Front 5

Antithrobin III

Back 5

Naturally occurring inhibitor to thrombin Factors XII, XI, IX, and X, which binds it 1:1 when heparin is present the reaction between AT3 and thrombin occurs 1000x faster. Antithrobin III and Heparin is produced by mast cells located by the pericapallary connective tissue throughout the body. Acquired newborns, liver disease, inc consumption-acute thrombosis, DIC high dose estrogen birthcontrol, and treatment oral anticoagulation.

Front 6

Protein C

Back 6

Vit K dependent inhibitor, Thrombinthrombomodulin activates protein C with protein S inactivates factor V and VIII. Protien C < 50%  venous thrombosis

Front 7

Protein

Back 7

Vit K dependant cofactor of protein C to inactivate Factor V and VIII
Protein S bounds to C4b-binding protein , free, and any conditions that inc acute phace reactant C4bwill decrease free Protein S risk of thrombosis.

Front 8

Describe the clinical significance of factor V Leiden

Back 8

Inherited thrombotic disorder, substituting arginine with glutamine at position 506 of the factor V gene Normal coagulation scheme, once protein C is activated, it works to inactivate factors V and VIII, to inhibit the clotting mechanism. The mutated factor V leiden, impedes the degration of factor V by protein C, causing activated protein C resistance. Deep vein thrombosis or other hypercoagulability condtions.

Front 9

Thrombocytopenia

Back 9

Decrease platelet count is caused by a number of factors. Decrease production of platelets usually accounts for the pathophysiology of most quantitative defects in platelets

Hint 9

Antibody/PF4/Heparin complex attached to platlet activates platelet thrombosis
Heparin develop HIT

Front 10

Thromocytosis

Back 10

Platelet count greater than 450X 10^9/L. The cause for an increased platelet count may be primary or secondary. A primary thrombocytosis is seen in myeloproliferative disorders.

Hint 10

Bleeding 25% patients-plt missing granules. Abnormal plt aggregation, Essential thrombocytosis, Uncontrolled megakaryocytes inc plts.

Front 11

Petechiae

Back 11

Small red spots, <3mm, blood leaks thru capillary endothelial cells, Extremities; not painful

Front 12

Purpura

Back 12

Means purple, refers to petechiae and ecchymoses

Front 13

Ecchymosis

Back 13

Bruises >3mm red-purple-yellow green, blood escapes thru endothelium, into intact subcutaneoustissue, painful and tender.

Front 14

Hematoma

Back 14

Blood leaks from open vessel, collects under intact skin, blue or purple slightly raised occur in any organ or tissue, may be a clot.

Front 15

Qantitative platelet disorders

Back 15

Reference range 150-440 x 10^9/L
Thrombocytopenia #1 cause of bleeding
Clinical symptoms seen <50 X 10^9/L
<30 X 10^9/L-petechiae, menorrhagia, spontaneous brusing, w/little trauma
<10 X 10^9/L –severe bleeding into CNS may be fetal mucous membranes-GI nose

Front 16

Examples of causes due to increased platelet destruction

Back 16

DIC: severe infection (gram negative septicemia)
cancer
major trauma/surgery (tissue damage)
Obstetrics: amniotic fluid embolism, septic abortion, retained dead fetus.

Front 17

Decreased platelet production and decreased platelet function.

Back 17

bone marrow examination to look for Ý or ß megakaryocytes
ß platelet production (ß # of megakaryocytes) : marrow infiltration (malignant disease), marrow hypoplasia (aplastic anemia, ETOH), congenital cause (rare)
Ineffective production (abnormal megakaryocytes): myeodysplastic syndromes, megaloblastic anemia

Front 18

Describe Quantitative platelet disorders:

Back 18

Reference range 150-440 x 10^9/L
Thrombocytopenia #1 cause of bleeding
Clinical symptoms seen <50 X 10^9/L
<30 X 10^9/L-petechiae, menorrhagia, spontaneous brusing, w/little trauma <10 X 10^9/L –severe bleeding into CNS may be fetal mucous membranes-GI nose

Front 19

Explain the effect of aspirin on platelets

Back 19

Acetylates cyclooxygenase, prevents release of ADP from dense bodies, prevents release of Thromboxane A2, BT may inc 1-2 minutes in a normal person. Plt aggregation-no secondary wave.

Front 20

THROMBOTIC

Back 20

Substituting arginine with glutamine at position 506 of the factor V gene Normal coagulation scheme, once protein C is activated, it works to inactivate factors V and VIII, to inhibit the clotting mechanism. The mutated factor V leiden, impedes the degration of factor V by protein C, causing activated protein C resistance. Deep vein thrombosis or other hypercoagulability condtions.

Front 21

THROMBOCYTOPENIC PURPURA

Back 21

Platelet aggregation on microvascular endothelium
Adults 10-50 yrs, female >male
Unknown cause-infections, pregnancy
W/o treatment 90% fatality due to multiorgan failure.
Damage to endothelial lining of small vessels enhanced plt aggregation or platelet activation  endothelial damage
Multiple hyaline
CNS symptoms severe
Microanglopathic hemolytic anemia
fever

Front 22

HEMOLYTIC UREMIC SYNDROME

Back 22

TCP, Acute renal failure
Children <5 yrs old
Few days after shigella or E.Coli

Front 23

DIC

Back 23

Always secondary response to a primary disease process
Alteration of hemostasis