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Clinical Pathology > Lecture 8: Platelets and coagulation II: secondary hemostasis and fibrinolysis > Flashcards

Lecture 8: Platelets and coagulation II: secondary hemostasis and fibrinolysis Flashcards

1
Q

What occurs during secondary hemostasis

A
  1. Coagulation system activation and platelet activation at injury
  2. Fibrin clot
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2
Q

most coagulation proteins are synthesized by the __

A

liver

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3
Q

what would factor X be called in active form

A

Xa (add “a” for active form)

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4
Q

what are the vitamin K dependent coagulation factors

A

X, XI, VII, II

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5
Q

what are the key players in extrinsic coagulation pathway

A
  1. Tissue factor/factor III
  2. Factor VII
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6
Q

what lab test do you use to evaluate extrinsic pathway (VII and III)

A

PT- prolonged if factors deficient

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7
Q

in extrinsic pathway: in presence of tissue factor, ___ is activated to __

A

VII activated to VIIa

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8
Q

in extrinsic pathway: VIIa in presence of __ and __ activates factor __ to __ to begin common pathway

A

TF and Ca2+, activates X to Xa

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9
Q

what does the common pathway generate

A

thrombin—> fibrin clot

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10
Q

what are the key players in intrinsic coagulation pathway

A

XII, XII, IX, VIII

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11
Q

what lab test do you run to test intrinsic pathway

A

PTT—> prolonged if factors XII, XI, IX, and VIII low

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12
Q

In intrinsic pathway: thrombin generated by extrinsic pathway activates __ into __ and __ into __

A

XI to XIa and VIII to VIIIa

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13
Q

in intrinsic pathway: factor XIa with ca2+ cleaves __ into __

A

IX and IXa

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14
Q

In intrinsic pathway: IXa with Ca2+ and accessory factor VIIIa cleave __ into __ to start common pathway

A

X into Xa

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15
Q

common pathway begins with activation of factor __ via intrinsic and extrinsic pathways

A

factor X

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16
Q

in common pathway there is conversion of__ into __

A

fibrinogen (factor I) into fibrin (factor Ia)

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17
Q

fibrin Ia polymerizes with other fibrin monomers to form __

A

soft clot

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18
Q

XIIIa (needs ca2+) crosslinks with fibrin stands of soft clot to form __

A

hard clot

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19
Q

what is Fibrinolysis and what does it prevent

A

breakdown of fibrin clots formed at tissue injury
Prevents thrombosis

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20
Q

Fibrinolysis initiated concurrently with __

A

fibrin production during vessel injury

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21
Q

the fibrin clot is removed by the proteolytic action of __

A

plasmin

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22
Q

what is inactive precursor of plasmin

A

plasminogen

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23
Q

plasmin lyses fibrinogen and fibrin into fragments known as __

A

fibrin degradation products (FDPs)

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24
Q

___ are FDPs specifically from degredation of hard clot

A

d-dimers

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25
Q

increased plasma levels of ___ indicate increase Fibrinolysis, secondary to increased clotting and is __

A

FDPS, pathological

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26
Q

what is the major control of inhibiting coagulation to prevent thrombosis

A

antithrombin

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27
Q

antithrombin is produced by __

A

liver

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28
Q

acquired antithrombin deficiency can occur due to __ or ___

A

increased consumption (DIC), or increased loss (protein losing nephropathy)

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29
Q

what blood tube is used to evaluate hemostasis

A

blue top

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30
Q

what would a prolonged PT test indicate

A
  1. deficiency in extrinsic factors- typically VII
  2. Deficiency in common pathway factors: fibrinogen, thrombin, V, X
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31
Q

what would a prolonged PTT test indicate

A
  1. Deficiency in intrinsic factors- XII, XI, IX, VIII
  2. Deficiency in common pathway factors
  3. Increased concentrations of inhibitors (heparin therapy)
32
Q

what is the PIVKA test

A

proteins induced by vitamin K antagonism/absence

33
Q

what is PIVKA test used for

A

indicator of vitamin K deficiency—> decrease X, IX, VII, II

34
Q

increased FDP’s or d-dimers indicates excessive __

A

fibrinolysis

35
Q

D-dimer tests are most specific and sensitive for ___

A

lysis of hard clot

36
Q

will D-dimers increase or decrease with DIC and thrombosis

37
Q

what are some signs of coagulopathies

A
  1. Excessive hemorrhage after trauma or sx
  2. Ecchymoses and purpura
  3. Hematomas
  4. Hemarthrosis
  5. Hemorrhage into body cavities
38
Q

What are the causes of coagulopathies and which most common

A
  1. Most common: decreased production of coagulation factors
  2. Increased consumption or loss of factors
  3. Production of abnormal molecules
39
Q

isolated deficiencies in factor __ and __ can be asymptomatic or cause mild bleeding problems

40
Q

deficiencies in factors __, __ or __ cause more severe problems

A

VIII, IX, or common pathway

41
Q

what is the most common inherited coagulopathy

A

hemophilia A

42
Q

what causes hemophilia A

A

deficiency or defective factor VIII

43
Q

what species most commonly gets hemophilia A

44
Q

Who is clinically affected by hemophilia A: males or females

A

sex linked recessive
Males clinical
Females carriers

45
Q

what are results of PTT, PT, and factor VIII: coagulant activity for hemophilia A

A
  1. Prolonged PTT
  2. Normal PT
  3. Decreased factor VIII: coagulant activity
46
Q

what is cause of hemophilia B

A

deficiency or defective factor IX

47
Q

what are PTT, PT and factor IX: coagulant activity for hemophilia B

A
  1. Prolonged PTT
  2. Normal PT
  3. Decreased factor IX: coagulant activity
48
Q

what is tx for hemophilia A and B

A

transfusion of fresh plasma, fresh-frozen plasma, cryoprecipiate or cryosupernatant for acute bleeding episodes

49
Q

what is the most common inherited factor deficiency in cats

A

Factor XII deficiency

50
Q

t or f: cats with factor XII deficiency are asymptomatic

51
Q

what is PTT and PT for factor XII deficiency

A
  1. Prolonged PTT
    2, normal PT
52
Q

what are the causes of acquired coagulopathies

A
  1. Liver disease
  2. Toxins: vitamin K rodenticides
  3. Venom
  4. DIC
53
Q

how does hepatic disease cause acquired coagulopathies

A
  1. Decrease production of clotting factors
  2. Decrease vitamin K recycling
  3. Decrease FDP and coagulation inhibitor clearance
  4. Decrease bile acid secretion
54
Q

decreased FDP and coagulation inhibitor clearance in hepatic disease predisposes to __

55
Q

how does decreased bile acid secretion in hepatic disease cause coagulopathies

A

decreased vitamin K absorption—> inactive clotting factors

56
Q

what are the causes of vitamin K deficiency/ antagonism

A
  1. Anticoagulant rodenticide
  2. Moldy sweet clover
57
Q

what are the results for PT, PTT and PIVKA for vitamin K antagonism/ deficiency

A
  1. Prolonged PT first
  2. Followed by prolonged PTT
  3. Prolonged PIVKA
58
Q

DIC results in increased __ of coagulation factors

A

consumption

59
Q

t or f: DIC is primary disease

A

false- always secondary to systemic disease

60
Q

what is pathophysiology of DIC

A
  1. Early DIC: hypercoaguable state
  2. Late DIC: hypocoagulable state
61
Q

what is net result of DIC

A

hemorrhage and combined risk of thrombosis

62
Q

what are the causes of DIC resulting in hemorrhage and thrombosis

A
  1. Coagulation factor depletion—> hemorrhage
  2. Fibrinogen depletion—> hemorrhage
  3. Inhibition of platelets by FDPs—> hemorrhage
  4. Excessive antithrombin depletion—>thrombosis
63
Q

to dx DIC you must have 3 of the following:

A
  1. Thrombocytopenia
  2. Decreased fibrinogen
  3. Increased FDPs or D-dimers
  4. Decreased antithrombin
  5. Prolonged PT, PTT, and ACT
64
Q

what are the RBC morphology changes on blood smear associated with DIC

A

associated with fragmentary injury: keratocytes, schistocytes, +/- acanthocytes

65
Q

define thromboembolic disease

A

Thrombus forms and continues unabated by mechanisms that usually cause dissolution of plug after its served its purpose

66
Q

what are some causes of thromboembolic disease

A
  1. Infectious (heart worm)
  2. Cardiac disease
    3, neoplasia
  3. Protein losing nephropathy, protein losing enteropathy, hepatic disease (decrease AT)
67
Q

what are some clinical signs of thromboembolic disease with saddle thrombi, pulmonary thromboembolism and renal infarct

A
  1. Rear limb weakness= saddle thrombi
  2. Dyspnea= pulmonary thromboembolism
  3. Hematuria= renal infarct
68
Q

what is most consistent finding for thromboembolic disease

A

decreased antithrombin

69
Q

case 1: 3yr Doberman hx of continued vaginal bleeding 8 weeks post parturition. PE: petechia on MM. following labwork. Classify erythron, leukon, bleeding disorder tests, and what are next steps

A

Erythron:
microcytic, hypochromic anemia—> iron deficiency anemia—> chronic hemorrhage

Leukon:
Inflammatory leukogram with concurrent stress

Prolonged BMBT- with platelet count WNL—> VWD- do antigen test

70
Q

case ex: 2yr, FS, mixed breed with hx of severe dyspnea, depression, dog has free run on farm at night. PE: muffled heart sounds, decreased lung sounds ventrally, weak pulses and hematomas noted on chest. Following blood work: characterize erythron, leukon, blood disorder tests and likely dx

A

erythron:
Normocytic, normochromic, non-regenerative anemia

Leukon: WNL

Prolonged PT and PTT, normal platelet count and FDPS—> ddx: anticoagulant rodenticide

71
Q

with DIC how is platelet count, BMBT, PTT, PT FDPs or D- dimers on blood work

A
  1. Platelet count: decreased
  2. BMBT: increased
  3. PTT and PT: increased
  4. FDPS and D-dimers: increased
72
Q

with thrombocytopenia how is platelet count, BMBT, PT, PTT, and FDPs and D-dimers appear on blood work

A
  1. Platelet count decreased
  2. BMBT increased
  3. PTT, PT, FDP or D- dimers: WNL
73
Q

with thrombocytopathy how is platelet count, BMBT, PTT, PT, and FDPs or D-dimer son blood work

A

1 platelet count: WNL
2. BMBT: increased
3. PTT, PT, FDP, D-dimers: WNL

74
Q

with vWD how is platelet count, BMBT, PTT, PT, FDPs or d-dimers on bloodwork

A
  1. Platelet count: wNL
  2. BMBT: increased
  3. PTT, PT, FDPs or D-dimers: WNL
75
Q

With liver disease how is platelet count, BMBT, PTT, PT, FDPS or d-dimers on blood work

A
  1. Platelets count: WNL
  2. BMBT: WNL
  3. PTT and PT: increased
  4. FDPs and D-dimers: WNL
76
Q

with vitamin K deficiency how is platelet count, BMBT, PTT, PT, FDP or d-dimers on blood work

A
  1. Platelet, BMBT, and FDP or d-dimers: WNL
  2. PTT and PT: increased

Clinical Pathology (12 decks)

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