Coagulopathy Flashcards

1
Q

Factor I deficiency
- Deficiency
- Results of routine screening tests

A

-Afibrinogenemia; hypofibrinogenimia; dysfibrinogenemia
- Increase PT, PTT, ACT
- decrease to normal fibrinogen

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2
Q

Factor II deficiency

A
  • Hypoprothrombinemia
  • Increase PT, ATT, ACT
  • Normal fibrinogen
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3
Q

Factor VII deficiency

A
  • Hypoproconvertinemia
  • Increase PT
  • Normal PTT, ACT, fibrinogen
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4
Q

Factor VIII deficiency

A
  • Hemophilia A
  • Increase PTT, ACT
  • Normal PT, fibrinogen
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5
Q

Factor IX deficiency

A
  • Hemophilia B (Christmas disease)
  • Increase PTT, ACT
  • Normal PT, fibrinogen
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6
Q

Factor X deficiency

A
  • Stuart-Prower deficiency
  • Increase PT, PTT, ACT
  • Normal fibrnogen
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7
Q

Factor XI deficiency

A
  • Hemophilia C
  • Increase PTT, ACT
  • Normal PT, fibrinogen
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8
Q

Factor XII deficiency

A
  • Hageman trait
  • Incrase PTT, ACT
  • Normal PT, fibrinogen
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9
Q

Factor XIII deficiency

A
  • Normal PT, APP, ACT, Fibrinogen
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10
Q

Factor II, VII, IX, and X deficiency

A
  • Combined vitamin K-dependent factor deficiency.
  • Doc in Devon Rex, 1 lab
  • Increase PT, PTT, ACT
  • Normal fibrinogen
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11
Q

Tranexamic acid and aminocaproic acid: MOA

A

Lysine analogues, they exert their mechanism of action by competitively binding C-terminal lysine sites on plasminogen. As a result of lysine analogue binding plasminogen is prevented from binding fibrin and plasmin formation is inhibited.

inhibiting plasminogen activators and preventing plasmin from degrading fibrin clots, thus stabilizing clots against fibrinolysis

SE: Hpotension and gastrointestinal signs, weakness, myonecrosis, myoglobinuria and rhabdomyolysis are dose dependent adverse reactions (in human aminocarproic acid).
Vomiting at high dose (TXA).

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12
Q

Bernard–Soulier syndrome
- type of defect
- specific mechanism
- breed affected
- clinical relevance

A
  • Extrinsic Adhesion
  • GPIb/V/IX deficiency
  • Cocker spaniel
  • Severe bleeding
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13
Q

Glanzmann thrombasthenia
- type of defect
- specific mechanism
- breed affected
- clinical relevance

A
  • Intrinsic Aggregation
  • Absence or deficiency of GPIIbIIIa
  • Great Pyrenees and otterhounds
  • Spontaneous mucosal haemorrhage
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14
Q

Scott Syndrome
- type of defect
- specific mechanism
- breed affected
- clinical relevance

A
  • Intrinsic Procoagulant deficiency
  • Impaired PS externalisation
  • ⇓ prothrombinase
  • German shepherd dog
  • Postoperative haemorrhage and epistaxis
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15
Q

P2Y12 receptor disorder
- type of defect
- specific mechanism
- breed affected
- clinical relevance

A
  • Intrinsic Prevention of agonist action
  • Impaired binding of ADP → reduced fibrinogen binding
  • Greater Swiss mountain dog
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16
Q

Ca1DAG-GEFI thrombopathia
- type of defect
- specific mechanism
- breed affected
- clinical relevance

A
  • Intrinsic Signalling Prevents GPIIb-IIIa conformation change for fibrinogen binding
  • Basset hound, Landseer and spitz
17
Q

Chediak-Higashi
- type of defect
- specific mechanism
- breed affected
- clinical relevance

A

-Intrinsic Granular storage pool deficiency Agonist deficiency.
-Absent aggregation response to collagen
- Persian cats
- Prolonged bleeding times

18
Q

Delta-storage pool disease
- type of defect
- specific mechanism
- breed affected
- clinical relevance

A

-Intrinsic Granular storage pool deficiency
-Dense granule deficiency of ADP
-American cocker spaniel
-Postoperative haemorrhage

19
Q

Type I vWD
- Breeds affected
- Multimer concentration
- Multimeric size
- Clinical importance
- Diagnosis

A
  • Doberman, corgi, Airedale terrier, and various others breeds
  • Low Full spectrum of sizes
  • Mild to moderate bleeding tendency
  • Dx: Genetic test, Plasma vWF antigen ELISA (Borderline: 50 to 69% Abnormal:0 to 49%, not specific for vWD), Plasma vWF CBA ELISA (CBA in normal/type 1 dogs=50 to 170%)
20
Q

Type II vWD
- Breeds affected
- Multimer concentration
- Multimeric size
- Clinical importance

A

-German short haired pointer
-Variable Absence of large multimers
-Moderate to severe bleeding tendency
-DX: Plasma vWF CBA ELISA Type 2 dogs typically >2.0

21
Q

Type III vWD
- Breeds affected
- Multimer concentration
- Multimeric size
- Clinical importance

A
  • Dutch kooiker, Scottish terrier, Shetland sheepdog
  • Marked reduction or absence of all multimers N/A
  • Mild to severe bleeding
  • Dx: Plasma vWF antigen ELISA (Borderline: 50 to 69% Abnormal:0 to 49%, not specific for vWD)
22
Q

Platelet count WNL, aPTT long, PT - WNL, Fibrinogen -WNL. DDX?

A

Intrinsic factor defects:
Factor VIII (hemophilia A)
Factor IX (hemophilia B)
Factor XI
Contact pathway factors:
Factor XII (Hageman trait)
Prekallikrein
HMW kininogen

23
Q

Platelet count WNL, PT long, aPTT - WNL, Fibrnogen WNL - DDX?

A

Fac VII deficiency

24
Q

Platelet count - WNL, aPTT and PT long, fibrinogen - WNL

A

Common pathway or combined defects:
Common path:
- Fac II
- Fac V
- Fac X

Combined vit K def
- Fac II, VI, IX, X

25
Q

Platelet count - WNL, aPTT, PT, Fib - long

A

Fibrinogen deficiency

26
Q

Platelet count WNL, coag panel WNL

A

vWD
(platelet function defects)
(fibrinolysis defects)
(nonhemostatic defect)

27
Q

Type I hypersenstivity
- Immune reactant
- Antigen
-Effector mechanism
- Example

A
  • IgE
  • Soluble antigen
  • MCT activation
  • Allergic diz, analphylaxis, some drug allergies
28
Q

Type II hypersensitivity (cytotoxic)
- Immune reactant
- Antigen
-Effector mechanism
- Example

A
  • IgG
    -Cell or matrix, cell surface receptor
    -Complement FcR+ cells (phagocytes, NK cells)
  • Some drug allergies, Myasthenia gravis, IMHA, ITP
29
Q

Type III hypersentivitiy
(immune complex)
- Immune reactant
- Antigen
-Effector mechanism
- Example

A

-IgG
-Soluble antigen
-Complement, phagocytes
- Systemic lupus, Leishmania, IMGN

30
Q

Type IV hypersensitivity
(immune reactant - Th1 cells)
- Antigen
-Effector mechanism
- Example

A

-Soluble antigen
-Macrophage activation
-TB reaction

31
Q

Type IV hypersensitivity
(immune reactant - Th2 cells)
- Antigen
-Effector mechanism
- Example

A
  • Soluble antigen
  • IgE production, eosinophil activation, mastocytosis
  • Chronic asthma, chronic allergic rhinitis
32
Q
A