Human Disease Ch 11

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1

hemostasis

stoppage of blood

process is rapid and localized

2

primary players in hemostasis

blood vessels

platelets

plasma proteins

ie coagulation proteins-involved in clot formation

3

three phases of hemostasis

vascular

platelet

coagulation (clotting)

4

vascular system

intact endothelial cells inhibit platelet adherence and blood coagulation

injury to endothelial cells promotes localized clot formation

5

first hase of vascular system

vasoconstriction

lumen of vessels narrows to minimize loss of blood

brings hemostatic components of the lood (platelets and plasma roteins) into closer proximity to vessel wall

collagen-enhances contact activation of platelets

6

von willebrand factor

made by endothelial cells

7

second phase of vascular system

plastlets ie platelets are the primary defense against bleeding

circulate in resting state

have minimal interaction with other blood components or the vessel walls

when stimulated by endothelial damage, platelets became activated they:

became round and sticky

aggregation-build a hemostatic plug

provide reaction surface for proteins that make fibrin

secretion of active substances

8

secretions from plateles

ADP-recruit more

vasoactive amines-epinephrine

thromboxane A2-amplifies the initial aggregation of platelets into a large platelet mass

9

coagulation

third phase of vascular system

two pathways for coagulation- extrinsic or intrinsic

nee- calcium and vitamin k

10

coagulation inhibitors

counterbalance coagulation factors

ie antithrombin

protein C- inactivates factors 5 and 7

11

disturbances of blood coagulation

four categories

1 abnormalities of small blood vessels

2 abnormalitiy of platelet formation

3. deficiency of one or more plasma coagulation factors

4. liberation of thromboplastic material into circulation

12

abnormality of small blood vessels

abnormal bleeding resulting from failure of small blood vessels to contract after tissue injury

13

thrombocytopenia

leads to spontaneous bleeding as a reaction to minor trauma

skin- reddish purple blotchy rash

may result from- decreased production due to toxins, radiation etc

increased platelets consumed

14

Von Willebrand disease

decrease in von willebrand factor

large protein molecules produced by endothelial cels-required for platelets to adhere to vessel wall at site of injury

VWF adheres to the damaged vessel wall, forms a framework that allws platelets and coagulation factors to adhere interact and form clots

15

hemophilia

x-linked hereditary disease affecting males

A-classic hemophilia-factor 7

B-Christmas disease-factor 9

16

hemophilia A

spontaneous or traumatic subcutaneous bleeding

blood in the urine

bleeding in mouth, lips, tongue

bleeding to the joints, CNS, GI tract

17

Phase 2

deficiency of prothrombin or factors required for the conversion of prothrombin into thrombin

ie liver disease

lack of vitamin K

18

Disseminated intravascular coagulation syndrome (DIC)

widespread blood clots

use up clotting factors and platelets-internal and external bleeding

microinfarcts

result of several pathological processes-snakebites ggram negative bacteria, or surgery

19

lab tests to evaluate hemostasis

platelet count

activated partial thrombloplastin time

prothrombin time

thrombin time= fibrinogen assay

20

anticoagulants

asprin

warfarin

heparin

21

asprin

inhibits thrombaxane A2 formation

22

warfarin

reduced amount of vitamin k availability

decrease risk clt formation

23

heparin

acutely

inactiviates thrombin