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DWT exam 2 > More clin path > Flashcards

More clin path Flashcards

1
Q

requirements for hemostasis

A
  1. intact and healthy vessels
  2. normal platelet numbers
  3. normal platelet function
  4. normal amount and function of clotting factors
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2
Q

petechiae and echymoses

A

pin point red spots on skin/mucus membranes
indicating problem with platelets

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3
Q

megakaryocytes

A

in bone marrow
pinched off parts of cytoplasm containing granules turns into platelets

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4
Q

thromboxane A2 and ADP

A

activates platelets

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5
Q

vonWillebrands factor

A

platlets bind to receptor on vWF when exposed

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6
Q

platelets

A

from cytoplasm of metakaryocytes
binds to vWF and fibrinogen (cross linking)
+ charge to bind to - charge

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7
Q

automated platelet count

A

hematology analyzer
pro: quick and easy
cons: clumping = false decrease

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8
Q

estimated platelet count

A

stained blood smear
pro: cheap, small sample volume, subjective if clumping
cons: clumping, time and technical skill

look at monolayer under 100x objective
multiply number in field by 15,000

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9
Q

thrombopathy

A

platelets are not working properly
can be extrinsic or intrinsic

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10
Q

extrinsic platelet thrombopathy

A

something from outside the platelet is not working
most common: vonWillebrands disease
diagnosis:
* normal platelet count, PT, PTT
* prolonged buccal mucosal bleeding time (BMBT)
* measure vWF

problem with PRIMARY hemostasis

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11
Q

intrinisc hereditary thrombopathy

A
  • uncommon
  • various mechanisms
  • specialized testing

diagnosis
* bleeding, poor clot formation, normal platelets, normal PT/PTT, normal vWF

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12
Q

intrinsic acquired thrombopathy

A

drugs: COX inhibitors (NSAIDs, steroids), b-lactam antbiotics, calcium channel blockers
uremia (renal failure, toxins in circulation impairs platelets)
DIC: fibrin and fibrinogen in excess interfere with platelts
liver dz
infections

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13
Q

thrombocytopenia main causes

A

Sequestration
Decreased Production
Utilization/consumption
Destruction

SPUD

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14
Q

sequestration thrombocytopenia

A

platelets trapped in spleen
splenomegaly

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15
Q

decreased production thrombocytopenia

A

selective and generalized marrow injury
severy thrombocytopenia

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16
Q

utilization/consumption thrombocytopenia

A

DIC (hypercoagulation forms microclots, then runs out and hemorrhage)
moderate thrombocytopenia
schistocytes/fragmenatation RBCs

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17
Q

destruction thrombocytopenia

A

severe
immune mediated usually
infection, drugs

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18
Q

Thrombocytosis causes

A

Not Neoplasia (Common)
* Physiologic/Excitement (splenic contraction)
* Inflammation (reactive, most common)
* Hemorrhage (regeneration)
* Iron deficiency
* Vincristine
* Glucocorticoids

Neoplasia (rare)
* Essential Thrombocythemia (Chronic megakaryocytic leukemia)
* >1,000,000/uL

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19
Q

Where are clotting factors produced?

A

liver

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20
Q

coagulation factor I

A

fibrinogen

21
Q

coagulation factor II

A

thrombin

22
Q

coagulation factor III

A

tissue factor (TF)

23
Q

Coagulation factor VIII 8

A

factor A

24
Q

coagulation factor IX 9

A

factor B

25
Q

Intrinsic coagulation pathway

A

inside the blood vessel
initiated by contact with - charged substances (exposed collagen, platelet, endotoxins)

26
Q

extrinsic coag cascade

A

things outside of the blood vessel (ex tissue factor III)

27
Q

Intrinsic cascade coagulation factors

A

12 > 11> 9 > 8

Its not $12, its $11.9

28
Q

common coagulation cascade factors

A

10 > 5 > 2 > 1

each one decrease by ~ 1/2
29
Q

common coagulation cascade factors

A

10 > 5 > 2 > 1

each one decrease by ~ 1/2
30
Q

extrinsic coag pathway factors

A

3 > 7

31
Q

vitamin K dependent factors

A

2, 7, 9, 10

32
Q

which vit k dependent coag factor has the shortest half life?

A

7
will shoe deficiency first

33
Q

blue top tube

A

contains citrate, stops clotting

34
Q

coagulation test for intrinsic and common cascades?

A

Activated clotting time (ACT): not as sensitive, can do at clinic
Partial thromboplastin time (PTT): must go to lab

35
Q

coagulation test for extrinsic and common cascades?

A

Prothrombin time (PT)

36
Q

coagulation test for fibrinogen concentration?

A

Thrombin time (TT)

37
Q

prolonged PTT/ACT, normal PT

A

Problems with intrinsic pathway
usually hemophilia A (8) or B (9)

38
Q

prolonged PT, normal PTT/ACT

A

problem with extrinsic pathway
factor 7 or 3 (TF) deficiency
early vit K deficiency (7 has shortest half life)

39
Q

prolonged TT

A

Fibrinogen deficiency/dysfunction
Thrombin inactivation
liver failure, DIC
NOT vit k deficiency

40
Q

Increased PTT/ACT and PT

A

vit K deficiency (if normal TT)
DIC (schistocytes, thrombocytopenia, increased TT, increased D dimers)
liver failure (low other liver products- glucose, BUN, albumin, cholesterol)

41
Q

Causes of intravascular coagulation

A

Thrombosis:
Initially unbalanced hemostasis
Virchow’s triad
* Stasis of blood flow
* Endothelial injury
* Hypercoagulability

Inciting processes
* Congestive heart failure
* Heartworm
* Protein-losing nephropathy

DIC
Initially balanced hemostasis
Massive coagulation initiation
* Massive TF exposure or release

Inciting processes
* Trauma
* Cancer
* Shock
* Sepsis

42
Q

DIC causes

A

Initially balanced hemostasis
Massive coagulation initiation
* Massive TF exposure or release

Inciting processes
* Trauma
* Cancer
* Shock
* Sepsis

TISSUE FACTOR

43
Q

Thrombosis causes

A

Initially unbalanced hemostasis
Virchow’s triad
* Stasis of blood flow
* Endothelial injury
* Hypercoagulability

Inciting processes
* Congestive heart failure
* Heartworm
* Protein-losing nephropathy

44
Q

plasminogen activator

A

in endothelial cells
converts plasminogen into plasmin
plasmin chops up fibrin and makes d dimers

45
Q

fibrinogenolysis/fibrinolysis

A
  1. plasma activator released from endothelial cells
  2. PA cleaves plasminogen into plasmin
  3. plasmin breaks down fibrin and fibrinogen into D dimers and fibrin degredation factors (FDP)
46
Q

increased fibrin degredation products

A

fibrin and fibrinogen degredation products
increased when there is plasmin mediated cleavage of fibrinogen/fibrin
increase = clot formation and breakdown
suggest DIC

47
Q

increased D dimers

A

specific type of fibrin degredation product
suggest clot formation and breakdown
suggest DIC

48
Q

heparin

A

anticoagulant

49
Q

antithrombin III

A

MOST POTENT antihemostasis protein in body
destroys thrombin
anticoagulant
amplified by heparin
lose by: Protein-losing disorders
* Protein-losing nephropathy (PLN)
* Protein-losing enteropathy (PLE)

DWT exam 2 (22 decks)

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