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AS - N935 Advanced Patho II > Coagulation Disorders > Flashcards

Coagulation Disorders Flashcards

1
Q

Intrinsic Pathway

A 
AMPLIFIES
Contact activation 
Damaged surface
XII → XIIa
XI → XIa
IX → IXa
VIII → VIIIa
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2
Q

Extrinsic Pathway

A

Initial pathway
Tissue factor (III) + VII → X
PT 12-14sec
INR 0.9-1.2

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3
Q

Coagulation Cascade

A
  1. Vasoconstriction
  2. Platelet plug
  3. Blood clot
  4. Dissolution
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4
Q

Common Pathway

A

X → II → I
Prothrombin II → thrombin (IIa)
Fibrinogen I → fibrin Ia
CLOT

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5
Q

Single-Factor Deficiencies & Anesthesia

A

Treatment depends on deficiency severity
Several products available - factor concentrates, recombinant factors, FFP, gene therapy
Replacement therapy effect duration depends on each factor turnover time

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6
Q

Coagulation Disorders

A 
Hereditary
- Hemophilia A
- Hemophilia B
- Von Willebrand disease
Acquired
- Vitamin K deficiency
- Liver disease
- DIC
- Autoantibodies
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7
Q

Hemophilia A

A

Factor VIII gene dependent on X chromosome
Inherited or gene mutation
Severe hemophilia - inversion or deletion
< 1% VIII activity
Mild 6-30%
Diagnosis - prolonged aPTT, specific factor, & gene testing

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8
Q

Hemophilia A & Anesthesia

A

Hematology consult
Factor VIII level at least >50% prior to surgery
Mild DDAVP 30-90min prior to surgery
Moderate to severe admin VIII concentrate
Half-life 12hrs
FFP & cryo
Consider TXA as adjunct

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9
Q

Hemophilia B

A

Factor IX deficiency
Christmas factor
X-linked
Less common
Severe bleeding IX <1%
Mild 5-40% often not detected until surgery or dental procedure
Diagnosis - prolonged aPTT, specific factor, & gene testing

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10
Q

Hemophilia B & Anesthesia

A 
Similar to Hemophilia A
Hematology consult
Replacement therapy including recombinant factor IX, purified IX, prothrombin complex concentrate PCCs contain II, VII, IX, & X 
↑risk thrombotic events 
Continue replacement therapy 
Factor IX half-life 18-24hrs
Consider TXA as adjunct
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11
Q

Von Willebrand Disease

A

Most common congenital bleeding disorder in the world
Disorders caused by quantitative and/or qualitative defect
vWF mediates platelet adhesion & prolongs factor VIII half-life

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12
Q

Von Willebrand

Synthesis & Storage

A

Endothelial cells

Platelets

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13
Q

Von Willebrand

Hemostasis

A

Dual role affecting both platelet function & coagulation

  1. Platelet adhesion GIb
  2. Platelet aggregation GIIB/IIIa
  3. Factor VIII carrier molecule & factor IX co-factor
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14
Q

Von Willebrand Type 1

A

Most common 60-70%
Mild to moderate vWF level reduction
Mild bleeding symptoms - easy bruising & nosebleeds
Responsive to DDAVP

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15
Q

Von Willebrand Type 2

A

Qualitative defect vWF
9-30% patients
4 subtypes

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16
Q

Von Willebrand Type 3

A

< 1% patients
Nearly undetectable
Severe quantitative phenotype

17
Q

Von Willebrand

Platelet-Pseudo Type

A

Defect in platelet GIb receptor

18
Q

Von Willebrand Disease

Replacement Therapy Goals

A

Major - maintain factor VIII level >50% 1wk
Minor - maintain factor VIII level >50% 1-3 days & 20-30% additional 4-7 days
Dental extraction - single infusion to achieve factor VIII level >50%
DDAVP prior to procedure (type 1)
Spontaneous or post-traumatic bleeding - single infusion 20-40u/kg

19
Q

FFP

A

Fresh frozen plasma

Prothrombin (II), V, VII, VIII, IX, X, XI, XIII, vWF

20
Q

Cryoprecipitate

A

Fibrinogen, VIII, XIII, vWF

21
Q

PCCs

A

Prothrombin (II), VII, IX, X

22
Q

Factor Concentrates

A 
VIII
IX
X
XIII
vWF
23
Q

DIC

A

Disseminated Intravascular Coagulation
Thrombin generated in response to insulting factor (endotoxins or amniotic fluid embolism)
Intravascular clotting then disseminates
Blood clots throughout the body causing end-organ dysfunction
Coagulation factors are depleted & platelets become used up → dysfunction
Fibrinolysis activated & results in bleeding

24
Q

DIC S/S

A 
Widespread clot formation
- Chest pain
- SOB
- Leg pain (DVT)
- Difficulty speaking or moving
- ST changes
Patients present w/ clotting or bleeding or both
Hemorrhages simultaneously w/ microcirculation thrombosis
25
Q

DIC Causes

A 
Sepsis - bacterial, viral, or fungal
Surgery or trauma
Cancer - more chronic, insidious onset, often leukemia
Pregnancy complications - amniotic fluid bolus or HELLP syndrome
Snake bites - venom
Frostbite
Burns
Transfusion reaction
26
Q

Acute DIC

A

Coagulation & fibrinolysis dysregulation
Widespread clotting w/ resultant bleeding
- Fibrin deposits as thrombosis in circulation
- Platelet depletion & clotting factors
Tissue factor present on multiple cell surfaces (endothelial, macrophages, monocytes) & tissues (lung, brain, placenta)
- Exposed & released
- Bind w/ factor VIIa & activates IX & X to form thrombin & fibrin in the common final pathway

27
Q

Fibrinolysis

A 
Creates fibrin degradation products
- Inhibit platelet aggregation
- Antithrombin activity
- Impair fibrin polymerization
All contribute to bleeding
28
Q

DIC

Lab Values

A

Coagulation inhibitors consumed
↓inhibitor levels permit additional clotting
↑clotting factors → clotting
Thrombocytopenia d/t platelet consumption
Dysfunctional platelets d/t inflammatory processes

↓platelets & dysfunction
↓fibrinogen 
↑PT/INR
↑PTT
↑d-dimer
TEGs & ROTEMs
29
Q

Thrombin

A

Potent pro-inflammatory protein & platelet aggregator
Excessive & unregulated → coagulation factors consumption ↑fibrinolysis
Platelets & clotting factors depletion
→ fibrin degradation products
Thrombotic complications

30
Q

Throbomodulin

A

Binds to thrombin ↓pro-inflammatory response
Limited clinical trials
Direct thrombin inhibitors (no RCTs)

31
Q

DIC Treatment

A 
Identify
Treat the underlying condition
- Infection - antibiotics
- Trauma - resuscitation
Supportive therapy - platelets, cryoprecipitate, fibrinogen concentrate, FFP, Heparin (controversial), TXA, PCCs
32
Q

Heparin

A

Controversial therapy
Variable outcomes as DIC treatment
Reserved in early or highly prothrombotic states
↑risk additional bleeding
Reduces end-organ dysfunction
Discontinue when overt bleeding occurs
Difficult to monitor b/c PTT already prolonged d/t coagulation factor consumption

33
Q

TXA

A 
Tranexamic acid (antifibrinolytic)
CRASH-2 trial

AS - N935 Advanced Patho II (20 decks)

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