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Modules > Coagulation > Flashcards

Coagulation Flashcards

1
Q

Normal INR

A

0.8-1.2

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2
Q

Warfarin INR

A

2-3

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3
Q

Normal PTT

A

22-35 seconds

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4
Q

Vit K dependent factors

A

2,7,9,10

Protein C and S

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5
Q

Normal PT

A

Less than 14

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6
Q

Which coagulation factor is not produced by the liver?

A

Factor 8, made by epithelial cells

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7
Q

Mixing study

A

1:1 mix of patient blood and normal blood
Ordered after elevated PT or PTT
If it corrects- deficiency in factors
If doesn’t correct- inhibits factors

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8
Q

What are the three main anti- platelet factors made by endothelial cells?

A
  1. NO- vasodilates, inhibits aggregation
  2. PgI2- vasodilates, inhibits aggregation
  3. ADPhosphotase- degrades ADP which is released by dense granules and activates platelets
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9
Q

What are the three major anticoagulant factors made my endothelial cells?

A
  1. Heparin like molecules- activated anti thrombin 3
  2. Thrombomodulin- binds thrombin and makes it activate protein C which together with protein S ( also made by endothelial cells) inactivated factors V and VIII
  3. TFPI
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10
Q

What anti fibrinolytic factor do endothelial cells secrete when activated?

A

Plasminogen activator inhibitors (PAI)

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11
Q

What are the receptors on platelets

A
  1. Gp1b- binds vwf
  2. GpIIb/IIIa- binds fibrin and links platelets
  3. GpVI- binds collagen
  4. P2Y12 and P2Y1- bind ADP
  5. PAR-1- binds thrombin
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12
Q

Contents of alpha granules

A

White on EM

VwF, fV, fibrinogen, fVIII, PDGF, TGFb, RANTES (attracts monocytes)

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13
Q

Contents of dense bodies

A

ADP/ATP, Ca, serotonin

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14
Q

What other constituents are there in platelets besides granules?

A

Microtubles under membrane help it change shape

Has the capacity to make TXA2 when activates which aggregates platelets and causes vasoconstriction

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15
Q

Why does aspirin lower risk of thrombosis if it blocks prostacyclin and thromboxane synthesis?

A

Platelets cannot make more COX because can’t synthesize new profit while endothelial cells can so endothelial cells can overcome the blockade

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16
Q

What are the non clotting cascade effects of thrombin and how are they propagated?

A

Thrombin activates PARs ( protease activated receptors) by cleaving the seven transmembrane protein and thus activating a G coupled cascade

  1. Platelet activation and txa2 secretion
  2. Endothelial activation to generate leukocyte adhesion molecules and tPA and NO and PGI2
  3. Increase leukocyte adhesion to endothelium
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17
Q

Anti thrombin action

A

Bind heparin like molecules on endothelial cells or heparin drug
Inhibits factors 9,10,11,12

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18
Q

Protein c and s action

A

Vit K dependant ( with 2,7,9,10)

Inhibit factor 8 and 5

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19
Q

What are fibrin split products and how are they used?

A

Fibrin breakdown by plasmin results in D-dimers which can be used to diagnose DIC, DVT, or PE

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20
Q

How does plasminogen become plasmin

A

Factor 12
tPA- made by endothelial cells, most active when bound to fibrin which limits its action to recent thrombi
uPA(urokinase) - in plasma, can be cleaved to active form by streptokinases

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21
Q

How is free plasmin controlled

A

Bound to a2 anti plasmin in blood

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22
Q

What endothelial cell product blocks the fibrinolytic cascade?

A

Plasminogen activator inhibitors
Activity increase by inflammatory cytokines esp IFN y and probably responsible for intravascular thrombosis in severe inflammation

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23
Q

Primary hypercoagulability

A

Inherited

  1. Leiden/ factor V mutation- makes resistant to protein C , increased risk venous thrombosis, change of aa residue
  2. Prothrombin mutation- g to a substitution, increases prothrombin synthesis, increase risk venous thrombosis
  3. Congenitally elevated homocysteine

Heterozygotes not that bad off until they have additionally acquired risk like bedrest, pregnancy, long airplane ride

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24
Q

Secondary hypercoagulability

A
  1. Stasis or vascular injury
  2. Hyperestrogenic states- oral contraceptives and pregnancy, increase hepatic synthesis of coag factors and decreased synthesis of anti thrombin III
  3. Cancers - tumors can release procoagulant products like mucin from adenocarcinoma
  4. Age- lower PGI2
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25
Q

What are the additives for a PT

A

plasma, Ca, thromboplastin (brain extract)

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26
Q

What are the additive for PTT

A

plasma, Ca, kaolin (XII activator), and cephalin (phospholipid layer substitute)

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27
Q

DDx for bleeding due to vascular instability/fragility

A
  1. vit C deficiency
  2. systemic amyloidosis
  3. Chronic glucocorticoid use
  4. inherited conditions of connective tissue
  5. vasculitides (meningococcemia, infective endocarditis, rickettsial disease, typhoid, and HSP)
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28
Q

Clinical characteristics of bleeding due to vascular fragility

A

spontaneous petechiae and ecchymoses of skin and mucous membrane

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29
Q

Clinical characteristics of platelet disorder

A

easy bruising, nosebleeds, excessive bleeding from minor trauma, menorrhagia

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30
Q

Clinical characteristics of coagulation disorder

A

bleeding in joints and lower extremities (areas subject to trauma)

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31
Q

Waterhouse-Friderischsen syndrome

A

Massive bleeding into adrenals associated with severe bacterial infection (Neisseria meningitidis) and DIC

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32
Q

Sheehan syndrome

A

Postpartum pituitary necrosis (bleed or DIC after delivery)
Agalactorhea, amenorhea or oligomenorrhea, hypothyroidsm, Addison’s, gonadatropin changes

Can result as hyponatremia acutely after delivery due to ADH hypersecretion (normal K)
acute hypoglycemia because of lack of cortisol

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33
Q

Chronic ITP

A

Chronic immune throbocytopenic purpura
women between 20-40
Antibodies against GpIIb/IIIa or GpIb/IX in 80% of cases
IgG coated platelets destroyed in spleen (also produces IgG), splenectomy beneficial
Increased megakaryocytes in bone marrow
Petechiae, easy brusing, epistaxis, gum bleeding, hemorrhage after minor trauma

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34
Q

Acute ITP

A

Acute immune thrombocytopenic purpura

Self limited, children, after viral infections

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35
Q

HIT

A

Heparin Induced Thrombocytopenia
Unfractionated heparin –> 1,2 weeks
IgG antibodies to factor 4 on platelets
Leads to platelet activation–> thrombosis –> venous and arterial thrombosis with thrombocytopenia
Cycle of activation and degradation
Discontinue heparin
Less common with low molecular weight heparin

36
Q

How do you clinically differentiate HUS and TTP?

A

HUS doesn’t cause neurological problems, occurs more often in children, and is characterized by acute renal failure

37
Q

What is the TTP pentad?

A
  1. Fever
  2. thrombocytopenia
  3. microangiopathic hemolytic anemia
  4. neurological deficits
  5. renal failure
38
Q

Pathophysiology of TTP

A

Acquired (autoantibodies) or inherited mutation in ADAMTS-13
ADAMTS is a metalloprotease that degrades very high molecular weight vWF
In absence of ADAMTS, large multimers of vWF accumulate in the blood and form platelet microaggregates throughout the microcirculation

39
Q

Virchow’s triad

A

Risk for thrombus

  1. Hypercoagulability
  2. Endothelial injury
  3. Changes in flow (e.g. stasis)
40
Q

Role of liver in coagulation

A

synthesizes all coagulation factors except III and VIII; also responsible for removing activated coagulation factors
hepatic parenchymal disease causes complex hemorrhagic diatheses
early liver disease see a decrease in PT
later liver disease decrease in PTT

41
Q

Where does vWF come from

A

Endothelial cells within cytoplasmic granules called Weibel Palade bodies
(when released binds to collagen in subepithelium and factor VIII in the plasma)

42
Q

vW Disease

A

AD European clotting disorder

Type I: quantity of circulating vWF decreased (also insig decrease in factor VIII which vWF stabilizes)

Type II: selective loss of high molecular weight vWF multimers (most active form) IIa: not made; IIb: dysfunctional and degraded by the liver (can cause mild chronic thrombocytopenia

CC: spontaneous mucosal bleeding; increased bleeding from wounds; menorrhagia

43
Q

Hemophilia A

A

X linked mutation in gene encoding factor VIII
Variety of mutations = various degrees of clinical manifestation, females with bleeds due to unfavorable lyonization
Mild (5-20% fVIII); Moderate (1-5% fVIII), Severe (

44
Q

Hemophilia B

A

X linked mutation in factor 9
Clinically indistinguishable from Hemophilia A but less common, definitions of severity the same
Lab: increase PTT, assays for factor 9 decreased
Treat: recombinant factor 9

45
Q

HUS

A

EColi OH157: H7 bacteria
Shiga like toxin–> damages endothelial cells –> platelets aggregate
CC: bloody diarrhea-> few days later acute renal failure and microangiopathic anemia
- 10% are cases of inherited mutations or autoantibodies that lead to a deficiency in factor H, I, or CD46 which are negative regulators of the complement cascade ; loss of factors causes uncontrolled complement activation;
- Other exposures: drugs or radiation that damage endothelial cells

46
Q

Homan’s sign

A

calf pain on dorsiflexion, sign of DVT

47
Q

DDx for DVT

A
  1. Baker’s cyst (popliteal cyst cause by swelling of sinovial bursa in knee joint)
  2. Inflammatory process (Cellulitis, phlebitis, thrombophlebitis)
  3. Generalized edema (Renal failure, CSF)
  4. Musculoskeletal issues (Fracture, Hematoma, Muscle injury, Arthritis )
48
Q

Antithrombin deficiency

A
  1. Type I AT: decreased levels of AT

2. Type II AT: normal levels of AT with reduced functionality

49
Q

Protein C deficiency

A

Type I: reduced gene expression and thus reduced functional activity
Type II: protein with reduced functional activity
At a higher risk for warfarin skin necrosis (clotting in microvasculature)

50
Q

Oral contraceptives and clotting

A

Estrogen is a sterile steriod that can change gene expression of proteins including clotting factors

51
Q

Pregnancy and Clots

A 
Hypercoagulable state (increase in fibrinogen, thrombin, decreases protein S)
Warfarin is teratogenic
52
Q

Antiphospholipid antibodies

A

Antiphospholipid syndrome
Autoantibodies directed against plasma proteins bound to anionic phospholipids
1. SLE or other rheumatic diseases (activates thrombin)
2. Anti cardiolipin antibody (inhibits protein C)
3. Anti b2 glucoprotein -1
Increased risk for venous and arterial thrombosis and fetal loss
Can get false positives if infected with syphilis
Prolonged PTT suggest lupus anticoagulant
Mixing study doesn’t correct PTT

53
Q

Trousseau Syndrome

A

Thrombophlebitis migrans associated with underlying malignancy (solid tumors like pancreas, ovary, primary liver, and brain)
Tissue factor produced by tumor cells and monocytes

54
Q

Essential thrombocythemia (ET)

A

Sustained platelet count > 450,0000
JAK2 mutation (protein that signals production and proliferation of megakaryocytes)
Bone marrow biopsy should reveal increased megakaryocytes

55
Q

Red thrombus + treatment

A

Venous thrombus: PE or DVT

anticoagulants

56
Q

White thrombus + treatment

A

Arterial thrombus : MI or Stroke

Anti-platelet agent

57
Q

Long term complication of PE

A

chronic thromboembolic pulmonary hypertension

58
Q

Long term complication of DVT

A

Post thrombotic syndrome (veins collapse, swelling and pain)

59
Q

Submassive PE

A

hemodynamically stable

oxygen and anticoagulant

60
Q

Massive PE

A

hemodynamically unstable , treat with tPA

61
Q

Warfarin/Coumadin reversal

A

Fresh frozen plasma (FFP)

Vit K

62
Q

Different types of Heparin

A
  1. LMWH: purified for low molecular weight, Enoxaparin, Dalteparin, Tinzaparin; mild IIa inactivation (medium chain), monitor with anti XA; stop drug + protamine suflate, sc
  2. Heparin: pig products, unfractionated; strong IIa inactivation (long chain), monitor with PTT; stop drug to stop, iv
  3. Fondaparinux: synthetic pentasaccaride (no IIa inactivation, short chain); monitor with anti-10a ; stop drug + protamine sulfate (high dose), sc
63
Q

Direct Thrombin inhibitors

A

Hirudin, lepirudin, desirudin (sub Q) , bivalirudin (shortest half life), argatroban (cleared by liver)
Unlike heparin they bind directly to thrombin rather than binding antithrombin first
Monitor via PTT
Discontinue DTI to reverse

64
Q

New oral anticoagulants

A

Xa inhibitors, po
Rivaroxaban, Apixaban, Edoxoban
12-18 hr half life, no monitoring required, no reversal agent yet

65
Q

Acute submassive PE steps

A
  1. Anticoagulate
  2. Risk stratify for thrombolysis (Evaluate RV enlargement, consider in select cases if no contraindication)
  3. Convert to an chronic anticoagulant (if UFH iv or LMWH sc, convert to warfarin or NOAC- except in pregnancy(teratogenic ) and cancer (complex))
66
Q

Provoking factors from VTE

A

Major: surgery, trauma, hospitalization, plaster cast immobalization
Minor: Estrogen, Pregnancy, Travel > 8 hrs
If provoked treat with anticoagulants for 3-6 mos

67
Q

Unprovoked VTE

A

anticoagulants at least 3-6 months

DASH (scoring system for higher risk of recurrance (D-Dimer, Age (

68
Q

Hemophilia B Leyden

A

Severe in childhood but less severe after puberty due to an androgen responsive promoter mutation

69
Q

Hemophillia C

A

Factor 11
Ashkenazi Jews
Clinically relevant

70
Q

Complications of Hemophilia

A

Hemophilic arthropathy (result of repeat bleeds)
HIV/hep C infections from transfusions
Factor VIII/IX autoimmune response against recombinants
Poor dental health
Obesity and Cardiovascular disease(lifestyle, tell people not to get exercise)

71
Q

Bleeding history

A
  1. Episodes of bleeding
  2. Surgeries (dental surgery most important)
  3. Transfusions
  4. Medications
  5. Family Histor
  6. Menses/ Pregnancy/ complications
72
Q

vWF tests

A
  1. PFA-100 (quantitative test where platelets are activated and you see how long it takes them to plug a capillary)
  2. vWF antigen : amount
  3. Ristocetin cofactor (vWF: RCo) tests activity
  4. Factor VIII activity (how well it stabilized factor VIII)
73
Q

vWD type 1

A

vWF antigen = vwF: RCo (activity matches amount of protein, partial quantitative decrease in vWF and factor VIII)

74
Q

vWF type 2 A

A

vWF: RCo/ vWF: Ag

75
Q

vWF type 2 B

A

vWF: RCo/ vWF: Ag

spontaneous aggultination, low large multimers

76
Q

vWF type 2 M

A

vWF: RCo/ vWF: Ag

poor agglutination, normal large multimers

77
Q

vWF type 2 N

A

vWF: RCo/ vWF: Ag

Issue with factor VIII binding

78
Q

vWF type 3

A

complete lack of vWF (vWF: Rco and vWF: Ag very very low)

79
Q

Treatment of vWD

A

Desmopressin (DDAVP): analog of vasopressin, induces endothelial cells to release vWF into blood
Antifibrinolytics

80
Q

What is the effect of having a type O blood type in clotting

A

lower levels of vWF

less of a DVT risk

81
Q

Function of Bradykinin

A
  1. Vasodilation
  2. Permeability
  3. Pain
    HMWK —-> Bradykinin (activated by kallikrein, inactivated by ACE)
82
Q

Drugs that cause acquired/qualitative platelet defects

A
  1. Aspirin
  2. Clopidogrel/Plavix (block P2Y12)
  3. NSAIDS/ibprofen (cox like aspirin but reversible)
  4. Prasugrel (also a P2Y12 inhibitor)
83
Q

Gray platelet syndrome

A

Abnormal alpha granule formation and secretion

Peripheral smear shows gray platelets rather than the purple stain

84
Q

Hirudin derivatives

A

Direct thrombin inhibitors
univalent: Hirudin “rudins”
divalent: agratroban, -gatrans
short 1/2 life so can just discontinue

85
Q

NOACs

A

Direct Xa inhibitors
Rivaroxaban, apixaban, edoxoban
no monitoring
long half life with no reversal agent

86
Q

Warfarin heparin bridge protocol

A

both for 5 day and INR 2 for 24 hrs

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