Coagulation Disorders

Front 1

vascular response

Back 1

when a blood vessel is injured an immediate localvasoconstrictive response occurs

Front 2

platelet response

Back 2

platelets are activated when they are exposed to interstitial collagen from an injured blood vessel

Front 3

plasmaclotting factors

Back 3

plasma proteins circulation in plasma until activated

Front 4

platelets

Back 4

small fragments of cells, round in shape
lifespan is 8-10 days
150,000- 400,000 mm3

Front 5

thrombopoietin

Back 5

produces platelets

Front 6

intrinsic pathway

Back 6

activated by collagen exposure from endothelial njury when the BLOOD VESSEL is damaged

Front 7

extrinsic pathway

Back 7

initiated when tissue thromboplastin is released extravascularly from injured tissues

Front 8

where are clotting factors made?

Back 8

liver

Front 9

end product of clotting cascade

Back 9

fibrin clot

Front 10

fibrinolysis

Back 10

breakdown of a clots

uses plasmin and plasminogen

Front 11

plasmin

Back 11

dissolves protein

Front 12

plasminogen

Back 12

precursor of plasmin

Front 13

antithrombins

Back 13

neutralizes clotting factors by forming a complex with them

Front 14

thrombocytosis

Back 14

presence of high platelet count

Front 15

thrombocytopenia

Back 15

reduction of platelets below 150,000mm3

Front 16

aPTT

Back 16

measure intrinsic side of coagulation cascade measure clotting factors, longer with use of heparin
30-45 sec

Front 17

PT

Back 17

measures extrinsic side

12-15 sec

Front 18

INR

Back 18

international normalized ratio:
standardized system of reporting PT based on a reference calibration model and calculated by comparing the patients PT w/ a control value

2-3

Front 19

four general causes of hemorrhagic disorders

Back 19

weak vessels, decreased platelets, decreased clotting factors, excessive or insufficient fibrinolysis

Front 20

hemophilia

Back 20

X linked inheritance pattern; deficiency of antihemphilia factor [factorVIII]
usually seen in males

Front 21

inheritance pattern of hemophilla

Back 21

female carriers will transmit the genetic defect to 50% of sons and 50% of daughters will be carriers

men will not transmit to their sons, but ALL of their daughters will be carriers

Front 22

hemophilia newborn S/S

Back 22

excessive bleeding after circumcision

Front 23

hemophilia young children S/S

Back 23

slow persistent prolonged bleeding from minor injuries, uncontrollable bleeding afte dental extractions or irritaion of gingival, GI bleeds from ulcers

Front 24

hemophilia lab profile

Back 24

PT= normal
platelet count= normal
thrombin count=normal
PTT= prolonged! ONLY effects intrinsic system
bleeding time= prolonged

Front 25

Demospressin Acetate [DDAVP]

Back 25

used to treat mild hemophilia

stimulates an increase in factor VIII and vWF

Front 26

treatments for hemophilia

Back 26

DDVAP, antifibrinolytic therapy and epsilon aminocaproic acid, controlling bleeding

Front 27

treatment for epistaxis

Back 27

sit up, lean forward, apply pressure continuoulsy for at least 10 minutes, insert cotton or wdded tissue into each nostril and apply cold

Front 28

hemiarthrosis

Back 28

blood leaks into the joints

Front 29

Immune Thrombocytopenic Purpura

Back 29

the most common acquired thrombocytopenia
platlets are coated with antibodies, so when they reach the spleen the are recognized as forgien and are destroyed by macrophages

only survive 1-3 days instead of 8-10

Front 30

Petechiae

Back 30

small, flat, pinpointed red or reddish brown micro hemorrhages.
when platelet count is low RBCs may leak out of the blood vessels and inthe the skin

Front 31

Purpura

Back 31

when petechiae are numberous, results in reddish skin bruise

Front 32

Ecchymoses

Back 32

larger purplish lesions caused by hemmorrhage

Front 33

S/S of ITP

Back 33

bleeding [epistaxis, gums], prolonged bleeding

Front 34

Tx of ITP

Back 34

corticosteriods [supress phagocytic response of splenic macrophages], IV immunoglobulin, splenectomy, platelet transfusion

Front 35

nursing considerations for ITP

Back 35

tell patient to report any minor bleed, avoid IM or subq, count sanitary napkins during menses, teach parents how to deal with bleeding events

Front 36

Risk factors for thrombus formation

Back 36

Atherosclerosis, venous statis, venous endothelial injury, hypercoagulability [pregnant women], atrial fib

Front 37

embolous

Back 37

mobile clots that generally do not stop movin until they lodge at a narrowed part of the circulatory system

Front 38

arterial thrombus

Back 38

cascade begins with platelts adhering to vessel wall; result is decreased perfusion of tissues

Front 39

venous thrombus

Back 39

occurs b/c of sluggish blood flow, clot forms w/ elongated tail, parts break off and become emboli

Front 40

3 general causes of venous thrombus

Back 40

venous stasis, hypercoagulability, venous endothelial injury

Front 41

5 interventions for DVT

Back 41

ROM exercises, IPC devices, early ambulation, avoid pillows, change position

Front 42

S/S of DVT

Back 42

extremity pain, warm skin, erythema, positive homan's sign, edema

Front 43

S/S of pulmonary embolism

Back 43

anxiety, sudden dyspnea, tachypnea, or tachycardia, pleuritic chest pain, hemptysis, crackles, n/v, cyanosis

Front 44

tx of PE

Back 44

administer O2, turn, cough, deep breathing, morphine

drugs used: heparin, warfarin, thrombolytic agents

Front 45

aspirin

Back 45

supresses platelet aggregation, inhibits thromboxane A