Module 12-14 Flashcards Preview

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Flashcards in Module 12-14 Deck (28):
1

Petechiae

small red purpura or bruises that result from leakage from capilaries. They are less than 3mm in diameter. Prominent in extremeties d

2

Ecchymoses

Brusies larger than a centimeter usually caused by leakage from a blood vessel larger than a capillary. Red or purple and become yellow green as they heal.

3

Hematoma

Formed when blood leaks through a vessel and collects beneath the skin. Can occur in any organ. Color is blue or yellow, and area is slightly raised. Commonly called a bruise and is often the result of some sort of trauma including surgery.

4

Epistaxis

Nose bleed. Common in hemostatic defects of platelets. Can be caused by trauma or pathophysiology.

5

ITP

Immune thrombocytopenia. Destruction of platelets due to autoimmune Ab, and / or loss of self tolerance by CTLs or Tregs. Present only with thrombocytopenia, and due to difficulty in detecting platelet Ab diagnosis is typically made by exclusion. Treated with corticosteroids and IVIG.

6

DIC

Disseminated intravascular coagulopathy. Can be caused by sepsis, tumors / leukemias, trauma, transfusion and allergic reactions. Systemic coagulation and consumtion of clotting factors especially prothrombin. Can cause fatal bleeding and sometimes thrombosis.

7

consumption coagulopathy

A term sometimes used interchangeably with DIC, but which refers to the consumption of several clotting proteins and their inhibitors faster than they can be synthesized by the body, leading to a deficiency. This process explains the bleeding seen in DIC patients when systemic coagulation occurs in response to sepsis tumors and leukemia, burns, and trauma among others.

8

Acute phase protein:

These are proteins in the plasma which increase or decrease in response to inflammation. Some positive acute phase proteins are MBL, CRp, alpha 2 macroglobuilin (plasmin and thrombin inhibitor) ferritin, hepcidin, and haptoglobin. Negative acute phase proteins include albumin, transferrin, and antithrombin, and typically conserve energy and amino acids for the production of the positive phase proteins which combat inflammation.

9

screening testing

Screening tests measure secondary hemostasis and include the PT, APTT, TT, and quantitative fibrinogen test. These tests are cheap and easy to perform, and collectively cover a large portion of secondary hemostasis and are thus a good starting point for further reflexive testing

10

PPP

Platelet poor plasma or plasma with a platelet count of less than 10,000 per microliter. Obtained by spinning citrated blood at a low speed for 10-15 minutes. Useful for coagulation studies which requires some but not full amounts of platelets

11

Demarcation membrane system:

Internal membrane system not visible by light microscopy found in developing megakaryocytes. The system is composed of invaginations of the cytoplasmic membrane which aid in extracellular communication and eventually become the membrane of newly formed platelets.

12

endomitosis

Doubling of a cells DNA without nuclear or cytoplasmic division. In megakaryocytes it begins in the blast stage and is completed by phase II; can be 4N to 64N.

13

open canicular system

Channels leading from surface to interior which are formed from plasma membrane invaginations. Is the route of entry of external substances, exit route for granules, and provides extra membrane during platelet activation and shape change.

14

TUNNICA INTIMA

The innermost layer of endothelial tissue in consisting of one layer of vascular endothelial cells surrounded by a basement membrane and subendothelial connective tissue. VECs synthesize and secrete many of the signaling molecules responsible for maintaining hemostasis and initiating clot formation.

15

TUNICA MEDIA

Middle layer of endothelial tissue which is thicker in arteries than in veins which helps in blood pressure regulation. Consists of smooth muscle cells, and loose connective tissue composed of collagen, reticular fibers, and proteoglycans.

16

TUNICA ADVENTICIA

The outer coat of vascular endothelial tissue. Composed of collagen and oxygenating microvessels called the vasovarum. Fibroblasts also secrete fibers and matrix components. Usually thicker in venules.

17

gp 1B/IX

Is a complex of the glycoproteins GP1b, GPV and GPIX in a complex of 2:1:2. It is the major platelet receptor for VWF. GPV has unknown funtion and GPIX is required for efficient surface expression of GP1B. Other ligands include selectins and integrins found on activated platelets, VECS, and leukocytes. Functions in adhesion.

18

gpiib/IIIB


CD41/CD61: Is a complex of glycoproteins GPIIb/IIIa and is the major fibrinogen receptor. Also binds VWF, fibronectin, thrombospondin, vitronectin. Agonist binding converts it to a high affinity binding conformation required for platelet aggregation.


19

ARACHADONIC ACID

is produced by the activity of PLA2 on membrane lipids. AA is a precursor for the potent platelet activator thromboxane as well as prostacyclin both of which have cyclooxygenase as an intermediate enzyme.

20

ZYMOGEN

A zymogen is an enzyme which is produced in its inactive form and which is activated by another enzyme. Most factors in the coagulation cascade are zymogens,

21

COUMADIN

works by inhibiting the vitamin K dependent coagulation factors. Several factors in the cascade (II, VII, IX and X) need to be carboxylated in order to bind calcium (which is intimately involved in the cascade).
Mnemonic for vitamin k required clotting factors
Several tend to nicely stop cuts
7 10 9 2 s c

22

HEPARIN

Heparin works in a totally different fashion. It works by binding to antithrombin III (ATIII), which as you will recall is a natural anticoagulant that acts on a bunch of different factors on both sides of the cascade, but seems to have more of an effect on the intrinsic arm than it does on the extrinsic arm of coagulation. Heparin binds to ATIII, causing a conformational change that activates ATIII and potentiates its action

23

ANTITHROMBIN

SERPI family serine protease suicide inhibitor. Active against many members of coagulation cascade including thrombin. binds heparin like strucures in VECs, forms complex with thrombin, inactivates.

24

5 conditions associated hereditary thrombosis

antithrombin deficiency, protein S and C deficiency, prothrombin mutation, APCR

25

APCR mutation Factor 5 leiden thrombosis

a factor 5 mutation which makes in not sensitive to protein c. omozygotes are at significantly greater risk for thrombosis than heterozygotes, simply because the activated protein C resistance increases the amount of thrombin formed, thus amplifying fibrin formation. Heterozygotes are placed at higher risk only when subjected to conditions that precipitate acquired thrombosis, as in pregnancy or DIC. As quantity is not the issue here, a specific functional test for clotting time can evaluate Activated Protein C resistance. When Activated Protein C is added to plasma from a patient with this disorder, clotting time is not increased

26

antithrombin deficiency

antithrombin is a protein which inactivates thrombin and factor X. Natural cofactor is heparin sulfate. Heparin increases antithrombin by 1000. Quantitative defect leads to reduction in antithrombin qualitative is mutation in heparin binding site or active site. Quantitative defect homozygosity incompatible with life. Liver and kidney disease can cause thrombin def.

27

protein c deficiency

PC inhibits F5 and F8 in coagulation vitamin K

28

PS deficiency

C4BBP binds protein S keeping it inactive. Acute phase protein. Less protein S for clotting regulation in inflammation. Total or free PS deficiency. Qualitative defect has impaired function.

Type I PS deficiency is characterized by low total antigen, free antigen, and functional activity. Type II deficiency is characterized by normal concentration of both total and free antigen but decreased functional activity (dysfunctional molecule). Type III deficiency is characterized by normal total PS but a decreased free and functional PS concentration (reflecting either a high C4BP concentration

McKenzie, Shirlyn B.; Williams, Lynne. Clinical Laboratory Hematology (3rd Edition) (Pearson Clinical Laboratory Science Series) (Page 729). Prentice Hall. Kindle Edition.