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FU17 Hematology > Coagulation And Platelet Disorders > Flashcards

Coagulation And Platelet Disorders Flashcards

1
Q

Complex interaction b/t progocagulant and anticoagulant factors, mediated by vascular endothelial cells

A

Normal hemostasis

Localized fibrin/platelet plug prevents blood loss while keeping clot fro extending beyond injured area

Blood plug and prevention of clotting to non injured sites

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2
Q

Major players in coagulation

A

Endothelial cells
Subendothelial matrix
VWF
Platelets

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3
Q

Endothelial cells coagulation fxn

A

Secrete small amount of NO, ADPase, and prostacyclin = inhibition and vasodilation

When damaged = production ceases, begin producing procoagant and tissue factor

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4
Q

What causes platelet capture and activation

A

Sub-endothelial matrix/TF exposure

This is facilitated by vonWillebrand’s factor

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5
Q

VonWillebran’d factor

A

Large molecule synthesized in multimeric strings in EC and megakaryocytes

Circulates in plasma and becomes bound to exposed subE matrix

Loosely adhere platelets at site of injury, causing platelets to slow roll along vessel

factor 8 carrier

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6
Q

Binding of vWF causes

A

Binding occurs at the GPIIb/IIIa receptor

Conformational change of the receptor –> ACTIVATED

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7
Q

Hormone that mediates platelet suppply

A

Thrombopoeetin

From liver, kidney, muscle, BM

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8
Q

Platelet activation causes:

A

Recruitment of addition platelets (via thromboxane A2)

Vasoconstriction (thromboxane A2 and serotonin)

Fibrin formation

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9
Q

Imp. Molecules in the platelet membrane (3)

A
  1. Glycoprotein IIb/IIIa (binds platelets, fibrinogen, vWF)
  2. Phospholipids
  3. Absorbed coagulation factors
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10
Q

Granules in platelet cytoplasm contain (3)

A
  1. Hemostais mediators (fibrinogen, plasminogen, coat factors)
  2. Vasoconstrictors
  3. Platelet derived growth factors
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11
Q

Minimum req. platelet counts:

Prevention of spontaneous bleeding

A

10-20,0000

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12
Q

Minimum req. platelet counts:

Central line insertion

A

20-50,0000

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13
Q

Minimum req. platelet counts:

Administration of therapeutic anticoagulant

A

30-50,000

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14
Q

Minimum req. platelet counts:

Minor surgery

A

50-80,000

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15
Q

Minimum req. platelet counts:

Major surgery

A

80,000-100,000

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16
Q

Major site of coagulation factor synthesis

A

Liver

Some of the coagulation factors and natural anticoagulants are vitamin K dependent

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17
Q

Limiters of clot formation

A

Anti-thrombin III

Protein C and S

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18
Q

Anti-platelet agents

5

A
  1. Aspirin
  2. NSAIDS
  3. COX-2 Inhibitors
  4. Thienopyridines
  5. GP IIb/IIIa inhibitors
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19
Q

Aspirin

A

Permanently inhibits COX-1 for life of platelet

Prevents it from making thromboxane A2 (no platelet accumulation)

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20
Q

NSAIDs

A

Reversible and competitive binding to COX-1

Anti platelet effects depend on drug concentration, varies over time

Given 2 hrs after ASA so not to dampen aspirin effect

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21
Q

COX-2 Inhibitors

A

Thought to be platelet neutral (only targeting leukocytes)

Decreases production of prostacyclin so can cause stroke, HTN, MI j

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22
Q

Thienopyridine

A

Impair platelet aggregation by inhibiting ADP biding to platelets and ADP activation of GP 2b/3a receptor

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23
Q

Thienopyridine indications

A

CAD, unstable angina, acute coronary syndrome, acute MI

Clopidogril - TIA, stroke

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24
Q

Coagulation medications (5)

A
  1. Direct thrombin inhibitors
  2. Heparin
  3. LMWH
  4. Xa Inhibitors
  5. Warfarin/Coumadin
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25
Q

Direct thrombin Inhibitors indications

A

Leprudin and argatroban are sub q/IV for HIT

Pradaxa is for clot prevention, AFib, DVT, PE

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26
Q

Heparin

A

Acceleration of ability of ATIII to inactivate thrombin and clotting factors

No NEW clots are formed

Administered as a drip

Measured with a PTT

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27
Q

LMWH

A

Acceleration of ability of AT III to inhibition activation of X

Less effect on platelets, more stable, Sub Q, no monitoring

But must consider renal clearance

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28
Q

Indications of Xa

A

Prophylaxis of thromboembolism in Afib

DVT/PE

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29
Q

Warfarin

A

Vitamin K antagonist, decreses synthesis of vitamin K dependent clotting factors

Monitored with PT/INR

Dosed with therapeutic middle dose (INR of 2.0-3.0)

Reversed with FFP or Vitamin K injection

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30
Q

Arterial problem, which drugs?

A

Antiplatelet

ASA or theianopyridine

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31
Q

Venous problems, which coagulant?

A

NOACs, Coumadin

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32
Q

Small vessel bleeds typically causes

A

Petechiae

Most often in GI, mucous membranes, skin

Occurs in PLATELET def.

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33
Q

Large vessel bleeding typically produces

A

Purpura and hematomas

Occur in muscles, solid organs, joints

FACTOR issue

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34
Q

Labs for blood evaluation (6)

A

CBC

PT/INR

PTT

Blood smear

Platelet count

Bone marrow biopsy

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35
Q

Vascular puppy

A

Disorders of blood vessels

Caused by structural integrity of blood vessel or by inflammation of vessel

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36
Q

Structural integrity problems that might cause vascular purpura

A

Senile purpura
Steroid induced
Scurvy
Congenital causes

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37
Q

Causes of vasculitis

A 
Viral infection (EBV, HIV, hepatitis) 
Aseptic vasculitis (medicine hypersentivity) 
Septic vasculitis 
Connective tissue disease (SLE, RA) 
Muscular disease
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38
Q

Causes of thrombocytopenia (3)

A
  1. Splenic sequestration
  2. Decreased platelet production
  3. Rapid death/utilization
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39
Q

Causes of decreased platelet production (5)

A
  1. Medications
  2. Nutritional disorders
  3. Bone marrow disease
  4. Myelodysplasia
  5. Congenital dz
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40
Q

Medications that decrease platelet production

A

Cytotoxic or immunosuppressive meds (cancer, autoimmune)

Thiazides, alcohol, BC

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41
Q

Myelodysplasia

A

Replacement of platelet progenitor cells with dysplastic cells

If with fibrosis – myelofibrosis

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42
Q

Splenomegaly and thrombocytopenia

A

Increased trapping, causes plasma levels of 50-100k

Typically in liver dz, CML, and malignancies with spleen

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43
Q

Peripheral planet destruction causes

A
  1. Immune mediated

2. Non immune mediated

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44
Q

Immune mediated peripheral platelet destruction

A

Platelet is coated with anti-platelet auto-abs

Then it is cleared from circulation by spleen

Shortens lifespan

45
Q

4 types of quantitative deficient platelets

A
  1. ITP
  2. HIT
  3. TTP
  4. HUS
46
Q

Immune thrombocytopenic purpura

A

Ig-autoantibodies to platelets (formed alone or 2 to other dz)

Coat platelets, increased trapping, and phagocytosis in red pulp of spleen

Can be pediatric or adult

47
Q

Pediatric ITP

A

Occurs acutely (following nonspecific viral illness - URI or Gasteroenteritis)

Common in children 1-6, male predominance

Recover spontaneously (steroid IVIG can be used to shorten)

Mostly resmmsion w/o recurrence (can do splenectomy if not gone)

48
Q

Adult ITP

A

Indisputable onset, unlikely to spontaneously resolve

Likely chronic

MC ink 30-40, 2:1 F:M

Have to rule out meds, diseases, and myelodysplastic dz

49
Q

Adult ITP presentation

A

Typically not systemically ill

Will NOT look sick

Determine if there is possible hemorrhage

50
Q

Adult ITP diagnosis

A

Isolated thrombocytopenia (no other abnormal cell lines, < 20 k)

Normal peripheral smear

51
Q

ITP treament

A

Goal: return platelet count to level high enough to prevent bleeding

NO CURE

Withdrawal of possible causative drug or control underlying dz

Treat w/ corticosteroid

52
Q

Corticosteroid and ITP

A

Decreases platelet autoantibodies production

Decreases splenic sequestration

Stabilizes vascular endothelium (less bleeding)

Best results if mixed with rituximab

53
Q

Additional ITP trement (2)

A

IVIG (sometimes with steroids, decreases autoantibodies and macrophage activity)

Splenectomy (good for acute)

54
Q

drug induced immune thrombocytopenia

A

immune mediated platelet destruction due to Abs produced against a DRUG

Abs cross react with platelet Ags – platelet is collateral damage

very sudden, but can also be recovered quickly with DQ drug

55
Q

drugs that typically cause drug induced thrombocytopenia

A
  1. quinidine, quinine (not commonly used)
  2. ABX 9pcn, sulfa, cephalosporins, vanco
  3. anti HTN- thiazide, ACEI
  4. cimetidine
  5. tegretol, dilantin
  6. benzos, halloo, lithium
  7. plavix
56
Q

heparin induced thrombocytopenia

A

similar to drug induced, but catastrophic thrombotic complications

taking heparin, develop immune mediated thrombocytopenia (50-100k)

binding of these auto-abs to platelets also activates them so they clot

57
Q

what is the immune complex actually against in HIT?

A

IgG anti-Heparin- platelet/factor 4 complex

58
Q

pts more likely to get HIT

A

serum surgical patients

esp. CPB

platlet counts begin to decline around 5-4 days after initiation

59
Q

how is HIT detected?

A

HIPA serum assay

specific but not sensitive (if positive confirmed, if negative might still be)

60
Q

HIT treatment

A

discontinue heparin, never give again

can use DTI or anti-coagulant

61
Q

two major functions of vWF

A
  1. binds to platelets at site of injury

2. carries and stabilizes factor 8

62
Q

vWF disease

A

deficiency or dysfunction of vWF that limited platelet adhesion to vessel wall

causes deficiency of factor 8 –> increased bleeding

63
Q

vWF disease epidemiology

A

1% of population

M:F are 1:1

greater s/s may occur in women

64
Q

s/s of vWF d

A

excessive bleeding (heavy periods, gum bleed, easy bruising)

delayed bleeding

worse with ASA

65
Q

diagnosis of vWFd

A

prolonged PTT (factor 8) normal PT

measure vWF levels directly

66
Q

everyday treatment of vWFd

A

avoid ASA and limit activities that result in sig. bleeding

FFP is effective but not recommended

anti-fibrinolytic

birth control

67
Q

surgery or sig. bleeding treatment of vWFd

A

DDAVP

can use Factor VIII concentrate w/ vWF (donated factor 8)

68
Q

DDAVP

A

given to vWFd patients before surgery

stimulates vWF release from platelets –raises them to the adequate levels

69
Q

anti-fibrinolytics used in vWFd treatment

A

aminocaproic acid (Amicar)

Tranexamic acid (Listed, Cyklokapron)

70
Q

uremia

A

renal failure causes platelet dysfunction by an unknown mechanism

71
Q

dilution thrombocytopenia

A

follows massive blood product transfusion after trauma or surgery

CPB is also damaging (only temporary)

72
Q

hemophilia deficiencies in which factors

A 
Factor VIII (A) 
Factor IX (B, christmas disease)

Factor XI (C)

73
Q

Hemophilia factor level

Severe

A

<1%

74
Q

Hemophilia factor level

Moderate

A

1-5%

75
Q

Hemophilia factor level

Mild

A

5-40%

76
Q

Can women get hemophilia?

A

Not genetically – only males.

Can get acquired

77
Q

Hemophilia pathophysiology

A

No factor 8/9 so unable to produce proper amounts of thrombin

Severe bleeding from even minor injury – but typically following surgery or trauma, spontaneous

78
Q

Hemophilia bleeding where?

A

Joints (hemarthrosis)

Deep parts of body (GI, CNS, muscles, GU, pulmonary, cardio)

79
Q

Hemarthrosis

A

Hallmark of hemophilia

Inflammation of synoveal membrane

Causes permenant joint deformation, severe pain, loss of mobility

80
Q

Hemophilia labs

A

PTT normal/prolonged

PT normal

Specific factor assays will be very low

81
Q

Hemophilia treatment

A

Recombinant coagulation plasmid factors

Avoid ASA

82
Q

Acquired hemophilia

A

Spontaneous development of autoantibody to own clotting factors

Develops hemophilia

Male or female

83
Q

DIC is associated with what conditions

A

Sepsis (esp. gram - bc endotoxins)

Malignancy

Liver disease

Severe trauma/obstetrics

84
Q

Procoagulant substrate DIC

A
  1. Bacterial lipopolysaccharide
  2. Tissue factor (sepsis or trauma)
  3. Proteolytic enzymes (cancer or placenta)
85
Q

DIC pathophysiology

A

Coagulation and fibrinolysis are abnormally and massively activated – extensive thrombi formation and wide spread fibrinolysis

Reduced perfusion, thrombosis and bleeding (organ damage from acidic state)

86
Q

Arterial clots are where

A

Superimposed on ruptured arteriosclerotic plaque

Smaller clots

87
Q

Virchows triad

A
  1. Hyper coagulability
  2. Stasis
  3. Vessel damage

Causes of VENOUS clots

88
Q

Rare disease marked by formation of thrombi in microvasculature

A

Thrombotic Thrombocytopenic Purpura

Vasculature becomes hostile, rips vessels and clots form

89
Q

TTP is associated with what causes

A

Estrogens, drugs, pregnancy, infections

Adults 20-50, female predominance

90
Q

TTP cause

A

Acquired or inherited inability to cleave vWF molecules

Lack of ADAMTS13

Causes increased platelet adhesion and aggregation (w.o. coagulation)

91
Q

5 symptom presentation of TTP

A
  1. Fever (>105)
  2. Thrombocytopenia
  3. Microangiopathic hemolytic anemia (schistocytes, elevated LDH)
  4. Neurological symptoms (wax/wane aphasia, HA, LOC. Seizure)
  5. Renal insufficiency (elevated creatinine)
92
Q

TTP treamtnet

A

Plasmapheresis (replace bad plasma and donor)

Look for resolution of neurological changes, decrease LDH, and restore platelet count to >50k

Can also give steroid, rituximab

CI: platelet transfusions

93
Q

HUS

A

rare, similar to TTP but less neurological symptoms, more RENAL FAILURE

More likely to present in children

94
Q

HUS etiology

A

Viral or bacterial infection causing diarrheal illness -
Esp. Shigella or E. coli

Other infection, estrogen, post partum, immunosuppressive treatment

Can also be familial

95
Q

HUS lab picture

A

Similar to TTP
1. COOMBs neg – greater hemolytic anemia, schistocyte formation

  1. Greater renal failure, proteinuria, hematuria
  2. Less thrombocytopenia
96
Q

HUS treatment

A

DIC may be there

Supportive *fluids and treat infection

Hemodialysis to replace renal function

Can use Solaris

97
Q

Factor V Leiden

A

MC inherited disorder to cause VTE

Mutation that prevents Factor V from inactivation, so hyper coagulation

Heterozygous= 5x increased risk 
Homo= 90x risk
98
Q

You can have a genetic mutation in natural anticoagulant proteins

A

Extra clotting occurs

Can result increased loss or turnover leading to deficiency

Can cause hepatic disease, nephrotic syndrome

These are in ATIII, Protein C and S

99
Q

When do you suspect inherited thrombophlebitis

A
  1. Pt has strong family history of DVT/PE (esp. 1st degree relatives)
  2. Patients with VTE in odd locations
  3. Recurrent VTE (not explained by something else)
100
Q

Patients with inherited thrombophlia shold avoid

A

Estrogen/progesterone contraceptives

Immobilization

Smoking

Pregnancy

101
Q

Where do venous clots occur

A

Lower extremities, lg deep veins

Venous ultrasound to detect

102
Q

Venous clots are a ____ issue

A

FACTOR issue

Treated differently from arterial clot (platelet problem)

103
Q

When do yo do thrombophilia workup?

A
  1. After initial VTE if pt <45 and one relative has VTE
  2. Recurrence of VTE w/o risk factors
  3. Multiple VTE in unusual spots (portal, mesentaric, cerebral, hepatic veins)
104
Q

If discovered thrombophilia bc of genetic test

A

No prophylactic treatment or anti-platelet meds given

Avoid risk factors

105
Q

Treament if we discovered bc they clot

A
  1. Longer duration of anticoagulant after DVT/PE
106
Q

Thrombocytosis

A

Platelet count > 500k

  1. Reactive (cytokine driven)
  2. Autonomous over production by megakaryocyte
107
Q

Reactive thrombocytosis

A

Caused by infection, post operative status, malignancy, splenectormy and iron deficiency anemia or acute blood loss

Req. history, treat underlying cause or complications

108
Q

Thrombocytosis symptoms

A

Vasomotor symptoms (headache, lightheaded Ess., atypical chest pain, visual changes, numbers and tingling in fingers)

Bleeding

Thrombosis

FU17 Hematology (10 decks)

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