Coag & hemostasis

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  1. Assessment of Primary hemostasis (tests)
    • Bleeding Time
    • &
    • Platelet Aggregation Studies
  2. Secondary Hemostasis (tests)
    Screens: PT & PTT

    • Mixing Studies
    • Factor Assays
  3. Primary hemostasis involves what
    • Vascular system 
    • Platelets

    For the formation of the platelet plug
  4. Secondary hemostasis involves
    • Coagulation system
    • Fibrinolysis system

    to form a thrombus
  5. Acute ITP
    Antibody mediated platelet destruction.

    • Occurs in children
    • Rapid onset
    • Hx of infection
  6. Acute ITP lab findings
    Plt < 20k

    Duration <6mos
  7. Acute ITP Treatment
    • Maybe no treatment
    • Prevent intracranial hemorrhage
    • IVIG, RhIg, or Corticosteroids
  8. Chronic ITP
    • Occurs in women 2x more frequently
    • May be secondary condition
  9. Chronic ITP lab findings
    • Plt <30k
    • enlarged Plt's

    Duration >6mos
  10. Chronic ITP Treatment
    • Corticosteroids
    • IVIG, Rhig
    • Splenectomy 

    • Refractory ITP: 
    • - Rituximad
    • - Immunosuppressive agents
    • - Plasma Exchange ***
  11. Acquired: TTP (Thrombotic Thrombocytopenic purpura)
    Thromboticc microangiopathy

    • Acute deficiency of vWf cleaving ADAMTS13 leading to accumulation of ultra large vWF multimers. 
    •  

    Etiology: 

     - Congenital: Upshaw Shulman, MUtation of ADAMTS13 gene

    - Idiopathic: Autoantibody formation to ADAMTS13
  12. TTP clinical presentation
    • 1. MAHA
    • 2. Thrombocytopenia
    • 3. Fever
    • 4. Neurolgoical abnormalities
    • 5. Renal dysfunction
  13. TTP Lab findings
    • Plt <60k
    • Elevated LDH, ibili, & retic
    • Schistocytes

    * Normal PT, PTT, & Dimer
  14. TTP Treatment
    • Plasma Exchange
    •  - Removes UL vWF & anti-ADAMTS13
    •  - Provides ADAMTS13
    •  
    • *** Platelet transfusion may worsen situation!
  15. HUS
    Hemolytic Uremic Syndrome
    Endothelial damage causing plt's associated thrombosis& vessel obstruction, MAHA, & renal failure.

    Occus mostly in children secondary to E. coli O157:H7 - Undercooked meat

    • Atypical reasons:
    • Secondary to S. pneumoniae infection, genetic causes, medications, and pregnancy
  16. Clinical presentation of HUS
    • Hemolytic anemia
    • Renal failure
  17. HUS lab findings
    • Plt < 60k
    • Schistocytes
    • Giant Plt's
    • Low haptoglobin

    Elevated Retic, LDH, & IBili

    Normal PT, PTT & Neg DAT
  18. HUS Treatment
    Suppoprtive & antibiotics
  19. PTP

    Post transfusion purpura
    Antibody mediated platelet destruction

    Most common anti-HPA-1a

    Destroys antigen pos and neg plt's.
  20. PTP clinical presentation
    • 2-14 post transfusion
    • Bruising
    • Mucosal bleeding
    • Purpuric rash
    • possible fever
  21. PTP lab findings
    Severe thrombocytopenia 

    Could lead to life threatening hemorrhage

    Identify platelet specific alloantibody
  22. PTP Treatment
    • IVIG
    • Splenectomy
    • Plasma Exchange

    Future: transfuse antgien neg plt's
  23. HIT
    Heparin Induced Thrombocytopenis
    • Immune mediated
    • caused by IgG antibody against heparin & plt Factor 4 complex
  24. HIT clinical presentation
    • Thobosis
    • Skin lesions at heparin injection site
  25. HIT lab findings
    • Decreased plt (20 - 50 k)
    • Increased anti-heparin/PF4 antibody

    Platelet Agg to confirm
  26. HIT Treatment
    • Discontinue heparin
    • Use alternative anticoagulant
    • Direct thrombin inhibitors
  27. PFA

    Platelet Function Analysis
    Assesses platelet function - Measures time for plt's to form a plug

    • Affected by :
    • low plt counts & /or activity
    • Inadequate plasma on vWF
    • Inadequate Hct
  28. Fibrinolysis
    • Breakdown of formed blood clots
    • Keeps thrombi from getting too large
    • Aids in wound healing.



    Plasminogen activated to plasmin, degrades fibrinogen, 5, 8, & 13, No fibrin formation occurs. The breakdown of fibrin.
  29. Hemophilia A (F8) - Etiology & Clinical presentations
    • X-linked recessive
    • Decreased or absent F8
    • Varies in severity

    • Delayed bleeding
    • Hemathroses
    • easy bruising
    • Mucous membrane bleeding
    • GI bleeding
    • Hematuria
    • Spontaneous hemorrhage
  30. Hemophilia A (F8) Lab findings
    • Prolonged PTT
    • Decreased F8 assay
  31. Hemophilia A (F8) Treatment
    • IV F8 concentrates
    • DDAVP - mild cases

    Porcine F8 for those with antibodies
  32. Hemophilia B (F9) etiology & clinical presentations
    X-linked recessive

    • Increased bleeding: mucosa, GI, hematuria, spontatneous, hemathroses, 
    • Easy bruising
  33. Hemophilia B (F9) Lab findings
    • Prolonged PTT
    • Decreased F9 assay
  34. Hemophilia B (F9) Treatment
    • IV F9  concentrates
    • Plasma
    • PCC
  35. Fibrinogen Disorders and their clinical presentations
    • Afibrinogenemia - most severe
    • Dysfibrinogemia - moderate
    • Hypofibrinogenemia - less severe

    • Umbilical cord bleeding
    • Mucosal bleeding
    • Hemathroses
    • Intracranial hemorrhage
    • Miscarriages
    • Delayed wound healing
  36. Fibrinogen disorders Lab findings
    • Afibrinogenemia: 
    • Prolonged: PT, PTT, BT, & TT
    • Absent fibrinogen

    • Dys:
    • Prolonged TT
    • Prolonged Reptilase time

    • Hypo: 
    • Prolonged TT
    • Low fibrinogen
  37. Fibrinogen Disorder Treaments
    • Cryo
    • Fibrinogen concentrates
  38. Von Willebrand Disease
    • Autosomal Recessive  - typical 
    • May also be autosomal dominant
    • Both sexes affected equally
    • 3 different types (1, 2, & 3)

    Defect in platelet adhesion at the vascular site of injury.

    • Increased bleeding 
    • Mucosal Bleeding
  39. Type 1 vWD lab findings and treatment
    • Quantitative defect of vWF
    • Decreased F8, 
    • <50% Ristocetin
    • <70% vWF antigen
    • *slight prolonged PTT
    • Increased BT

    • TREATMENT: 
    • DDAVP - may stimulate the release of vWF from vascular endothelium
  40. Type 2 A&B vWD
    Qualitative defect

    • <50% Ristocetin
    • <70% vWF antigen
    • Increased BT
    • *Decreased PLT

    • Treatment: DDAVP (type 2a)
    •                  F8, Amicar (Type 2b)
  41. Type 3 vWD lab findings and treatment
    Complete absence of vWF

    • <5% F8
    • <10% Rostocetin cofactor & vWF antigen
    • Increased BT & PTT*
    • *No agg with RIPA

    • Treatment:
    • DDAVP, F8, Amicar
  42. vWD additional info
    Platelet transfusion is inappropriate since the defects are in the plasma protein and patients platelets function normally.
  43. DDAVP
    Causes the release of vWF from the endothelial cells and into circulation, thus increasing plt. adhesion

    ***DDAVP should NOT be given in patients with type 2b and platelet type vWD
  44. Vitamin K Deficiency
    Vit. K is essential for: 

    2, 7, 9, & 10

    Most commonly a result of warfarin

    Increased bleeding episodes
  45. Vitamin K Def lab findings & Treatment
    • Prolonged PT & PTT
    • Low Vit. K

    • Treatment:
    • IM Vitamin K - for no excessive bleeding
    • IV - Vit K - CNS or GI bleeding
    • Plasma -  severe bleeding
    • PCC - severe bleeding and warfarin reversal
  46. Liver Disease
    • Decreased production of coag factors
    • maladsorption of vit K. 
    • Platelet dysfunction
    • May lead to DIC
  47. Liver Disease Lab findings & treatment
    • Prolonged PT & PTT (PT is more thant PTT)
    • Decreased PLT, Protein C & S along with miscellaneous factors. (F8 is not affected)

    Differentiate from DIC with DIMER - Dimer is neg with Liver disease.

    • TREATMENT:
    • Vitamin K
    • Plasma
    • DDAVP
    • PCC
  48. Define DIC and list Etiologies
    Is the process of systemic uncontrollable clotting that can cause microthrombi with simultaneous lysis of the clots that causes bleeding.

    • Sepsis
    • Trauma
    • Burns
    • Hemolytic transfusion reactions
    • Acute promyelocytic leukemia
    • OB issues (placenta abruptus, amniotic fluid embolism, ecampsia, retained fetus)
    • Liver disease
    • Some cardiac prosthetic devices
  49. DIC Laboratory findings
    • Low:
    • Platelet
    • H&H
    • Fibrinogen <150 (<100 - bleeding risk)
    • AT (<80% risk of thrombosis)
    • Plasminogen
    • Factor activity levels

    • High:
    • FDP's
    • Dimers
    • PT
    • PTT
    • TT

    • Other:
    • Schistocytes
  50. DIC Treatment
    • Identify the underlying cause and treat
    • Maintain blood volume & hemostatic function
    • Cryo >100 mg/dL
    • AT/Protein C
    • Heparin  (for thrombosis risk)
    • RBC's, Plasma, Platelets

Card Set Information

Author:
Kwalke12
ID:
335264
Filename:
Coag & hemostasis
Updated:
2017-10-20 20:33:38
Tags:
coag coagulation hemostasis
Folders:
Coag & Hemostasis
Description:
Coagualtion Hemostasis Disorders, treatment, & lab findings
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