chap 10 - bleeding and clotting disorders

Question 1

thrombocytosis

Answer 1

too many

Question 2

idiopathic thrombocytopenic purpura (ITP)

Answer 2

• associated with platelet antibodies
• bone marrow infiltration by leukemic cells or metastatic carcinoma

Question 3

secondary thrombocytopenia

Answer 3

damage to bone marrow from drugs or chemicals
- bone marrow infiltration by leukemic or metastatic carcinoma

Question 4

hemo

Answer 4

blood

Question 5

sta

Answer 5

remain

Question 6

hemostasis

Answer 6

stoppage of bleeding
- process is rapid and localized in response to external injury

Question 7

primary players in hemostasis:

Answer 7

blood vessels, platelets, coagulation proteins - clotting factors

Question 8

where are clotting factors made?

Answer 8

liver

Question 9

phases of hemostasis

Answer 9

phase 1: vasoconstriction
phase 2: platelet plug
phase 3: clot

Question 10

where does the clot come from

Answer 10

coagulation proteins, makes a fiber that reinforces the platelets

Question 11

safe and effective hemostasis

Answer 11

components of hemostasis are always circulating in the blood, but don’t want activation unless injury
- we only want it when we have an injury
how stop?
- intact endothelial cells inhibit platelet adherence and blood coagulation

Question 12

hemostasis phase 1

Answer 12

injury to endothelial cells promotes clot formation
- vasoconstriction
- narrows the lumen of the vessel to minimize the loss of blood
- brings the hemostatic components to the blood (platelets and plasma proteins) into closer proximity to the vessel wall

Question 13

hemostasis phase 2

Answer 13

platelet plug
- thrombocytes
at rest = minimal interaction with blood vessel wall
when stimulated by collagen exposure function to:
– plug the defect = round and sticky
- aggregation
– secretion of active substances
– release vasoconstrictors
– cause more platelets to aggregate

Question 14

secretions from platelets

Answer 14

ADP
- shape change
- stimulate release thromboxane A2
thromboxane A2
- positive feedback - amplifies the initial aggregation of platelets into a large platelet mass
- vasoactive amines
- epinephrine
- coagulation factors

Question 15

hemostasis phase 3

Answer 15

• coagulation
• two pathways
  extrinsic = tissue factor (found inside some cells)
  intrinsic
• need: calcium, vitamin K –> activates some of the coagulation proteins

Question 16

fibrin

Answer 16

final outcome of coagulation, help support the platelet plug

Question 17

platelets and coagulation factors

Answer 17

• distinct but complementary and mutually dependent
  
  • platelets interact with coagulation factors
    
    • provide binding sites
  • thrombin activates platelets

Question 18

coagulation inhibitors

Answer 18

• counterbalance coagulation factors
  
  • restrict clot from getting too big

Question 19

plasminogen

Answer 19

activated by tissue plasminogen activator (TPA) - TPA is released by endothelial cells
- plasmin dissolves fibrin
- used clinically in disorders such as a stroke - TPA would dissolve the clot in the stroke – restoring blood flow

Question 20

most frequent and serious problems

Answer 20

trauma
- most common cause of hemorrhage
- injury to larger vessels may require significant medical treatment
- virchows triangle = inappropriate activation
- coagulation disorder
- disseminated intravascular coagulation (DIC)

Question 21

epistaxis

Answer 21

constant nose bleeds

Question 22

menorrhagia

Answer 22

abnormal menstrual cycle

Question 23

hematuria

Answer 23

coughing up blood

Question 24

hematochezia

Answer 24

blood in the stool

Question 25

petechiae

Answer 25

tiny pinpoint hemorrhages

Question 26

hematoma

Answer 26

large bruise

Question 27

signs and symptoms of bleeding and clotting disorders

Answer 27

- epistaxis, menorrhagia, hematuria, hematochezia, bleeding into tissues and joints, excessive brusing - petechiae, hematoma

Question 28

tests for bleeding and clotting disorders

Answer 28

CBC, fibrinogen assay, prothrombin time (test for extrinsic pathway), activated partial thromboplastin time (tests for deficiencies in the intrinsic pathways of coagulation mechanism)

Question 29

a wide range of diseases can result in:

Answer 29

injury to vessels, disorders of platelet number or function, derangements of the coagulation cascade

Question 30

thrombocytopenia

Answer 30

too little platelets causes = genetics, acquired (radiation), disease (leukemia), autoimmune, hypersplenism - leads to petechiae

Question 31

thrombocytosis

Answer 31

too many platelets - more common causes of thrombocytosis - transient increase in platelets following - trauma - operations - childbirth risk for abnormal clotting

Question 32

thrombosis

Answer 32

inappropriate activation of blood coagulation - contributed by: endothelial cell injury, abnormal blood flow (stasis or turbulence), hypercoagulability - can occur in: arteries or veins consequences: - deep vein thrombosis - pulmonary embolism - stroke - heart attack

Question 33

treatment for thrombosis

Answer 33

anticoagulants - warfarin (coumadin) - reduced amount of vitamin K availability - decrease risk of clot formation - heparin - inactivates thrombin - antiplatelets - aspirin - inhibits A2 formation - plavix

Question 34

genetic coagulation disorders

Answer 34

hemophilia = too little

Question 35

acquired coagulation disorders (too little)

Answer 35

liver disease, lack of vitamin K

Question 36

what could cause a lack of vitamin K?

Answer 36

could be due to taking long term antibiotics that wipe out the healthy bacteria in your gut, a lot of vitamin K is housed in the GI tract

Question 37

hemophilia

Answer 37

lack of coagulation factor - spontaneous or traumatic subcutaneous bleeding - blood in the urine - bleeding in the mouth, lips, tongue - bleeding into the joints, CNS, GI tract - genetics - x linked

Question 38

treatment for hemophilia

Answer 38

whole blood transfusions or can be treated with the missing factor - can restore the pathway