MOHDIII - Unit 2 > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

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1
Q

Assessment of intrinsic pathway

A
  • partial thromboplastin time (PTT or APTT)
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2
Q

Assessment of extrinsic pathway

A
  • prothrombin time (PT)
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3
Q

How to do prothrombin time

A
  • add thromboplastin and calcium to plasma
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4
Q

Prothrombin time uses

A
  • monitor warfarin (coumadin) therapy
  • evaluate liver disease
  • evaluate vitamin K deficiency
  • evaluate disseminated intravascular coagulation (DIC)
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5
Q

International normalized ratio (INR)

A
  • uses international sensitivity index (ISI) to normalize PT time
  • ISI=measure of the sensitivity of the thromboplastin the lab is using
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6
Q

How to do PTT

A
  • add activator, calcium, & phospholipid to plasma
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7
Q

Reasons for prolonged PTT

A
  • heparin
  • factor deficiency that may cause bleeding
  • factor deficiency w/ no clinical significance (factor XII)
  • specific factor inhibitor - most commonly to factor VIII
  • antiphospholipid antibody
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8
Q

Mixing study

A
  • used in evaluation of a prolonged PTT or PT
  • patients sample mixed w/ equal volume of normal plasma
  • correction to normal = FACTOR deficiency
  • continued prolongation = INHIBITOR (aka antibody)
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9
Q

Fibrinogen

A
  • measured by addition of thrombin to plasma
  • may have either quantitative or qualitative abnormalities of fibrinogen
  • DECREASED in DIC, liver disease, congenital absence of fibrinogen
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10
Q

D-dimer

A
  • D-dimer assay detects excess generation of cross linked fibrin by plasmin
  • useful in evaluation of DIC
  • used in evaluation of venous thrombosis & pulmonary embolism
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11
Q

PFA-100 closure times

A
  • evaluates platelets
    1. col/epi & col/ADP - normal = no platelet abnormality
    2. col/epi long & col/ADP normal = aspirin effect
    3. col/epi & col/ADP abnormal = platelet defect or von willebrand disease
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12
Q

Causes of hemorrhage

A
  • trauma, tumor, ulcer, necrosis, depletion of hemostatic factors
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13
Q

Petechia

A
  • pinpoint hemorrhages in skin

- sign of platelet disorder

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14
Q

Purpura

A
  • slightly larger hemorrhages than petechia
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15
Q

Ecchymoses

A
  • large areas of hemorrhage into skin

- aka large bruises

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16
Q

Hematoma

A
  • localized collection of clotted blood into a space or potential space
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17
Q

Platelet

A
  • produced in marrow from megakaryocytes
  • normal number 150,000-450,000/uL
  • remain in circulation 7-10 days
  • QUANTITATIVE problems more common than qualitative
  • typically causes mucocutaneous bleeding
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18
Q

Platelet counts & bleeding risk

A
  • minimal bleeding: >50,000
  • minor bleeding: 20-50,000
  • spontaneous:
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19
Q

Thrombocytopenia causes

A
  • decreased platelet production
  • ineffective platelet production
  • splenic sequestration of platelets
  • increased peripheral destruction
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20
Q

Bone marrow appearance in aplastic anemia

A
  • all FAT no cells
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21
Q

Increased platelet destruction causes

A
  • non immune destruction: DIC, other microangiopathic hemolytic anemias
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22
Q

Immune mediated thrombocytopenia

A
  • alloimmune destruction: maternal fetal incompatability, blood transfusion
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23
Q

Drug induced thrombocytopenia

A
  • drug or metabolite attached to platelet surface
  • development of antibodies to platelet-drug complex
  • platelets removed by macrophages in liver/spleen
  • QUININE is prototypic drug
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24
Q

Heparin induced thrombocytopeina

A
  • caused by antibody directed against heparin & platelet factor 4
  • causes platelet AGGREGATION & thrombocytopenia
  • may cause life threatening THROMBOSIS
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25
Acute immune thrombocytopenia purpura
- CHILDREN: 2-6 yrs old - antecedent viral illness - increased incidence in fall/winter - ABRUPT onset - self limited course, most completely recover - Rx: steroids, IV IgG, Rh immune globulin
26
Chronic immune thrombocytopenia purpura
- ADULTS: 20-40 yrs old - FEMALES greater than males, 3:1 - GRADUAL onset - remission and RELAPSES over years
27
Thrombotic thrombocytopenia purpura
- PENTAD of features: *microangiopathic hemolytic anemia*, *thrombocytopenia*, neurologic abnormalities, fever, renal dysfunction
28
TTP histologic findings
- thrombi w/in glomerular capillaries | - schistocytes in peripheral blood
29
TTP etiology & treatment
- deficiency of a protease (ADAMTS13): cleaves large von willebrand multimers - multimers aggregate platelets leading to thrombi - treatment: plasmapheresis & infusion of fresh frozen plasma * *FATAL unless they undergo treatment**
30
Drug induced platelet dysfuntion
- aspirin: IRREVERSIBLY acetylates COX - NSAIDs: REVERSIBLY inhibit COX - clopidogrel: blocks ADP receptor (P2Y12)
31
Disease-related platelet dysfunction
- uremia: global platelet dysfunction - paraproteins (plasma cell myeloma) - myeloproliferative disorders - after extracorporeal platelet circulation (cardiac bypass pump)
32
Hemophilia A (classic hemophilia)
- factor VIII deficiency - sex linked: men effected, women carriers - incidence: 1/10,000 males - MOST common hereditary disease - most severe hemophiliacs have inversion mutation in X chromosome
33
Type of bleeding with hemophilia
- bleeding into JOINTS, hematomas
34
Signs & symptoms of severe hemophilia
- delayed bleeding from small wounds b/c platelets are normal - hematomas, hemarthrosis, hematuria - joint destruction & muscle atrophy - death from bleeding into vital areas, complications of therapy - lab abnormalities: prolonged PTT, normal PT, normal PFA-100
35
Treatment of hemophilia
- treatment of hemophilia A is factor VIII replacement | - 5-15% of patients will develop factor VIII inhibitor (antibody)
36
Hemophilia B
- factor IX deficiency - sex linked, incidence: 1/50,000 males - cause: failure of synthesis or synthesis of defective factor IX - treatment: factor IX - lab abnormalities: prolonged PTT, normal PT
37
Other coagulation factor deficiencies
- most are rare | - deficiency in factor XII: benign disorder, NO increased risk of bleeding, prolonged PTT
38
Von willebrand disease
- autosomal dominant - deficiency of von willebrand factor - relatively common (1% population): bleeding occurs in less than 10% of these patients - signs/symptoms: mucocutaneous bleeding, epistaxis, menorrhagia
39
Diagnosis of von willebrand disease
- prolonged PFA-100 closure time - decreased factor VIII level - decreased von willebrand factor antigen activity
40
Subtypes of von willebrand disease
Type I: 70% moderate reduction in vWF levels in plasma Type II: qualitative defects in vWF Type III: autosomal recessive-vWF absent, present like hemophiliacs
41
Treatment of von Willebrand disease
- avoid aspirin - DDAVP (desmopressin), synthetic analog of vasopressin - humate P: contains factor VII and vWF
42
Changes in hemostasis in liver disease (vWF & factor VIII)
- increased levels of vWF & factor VIII due to endothelial cell activation
43
Lab abnormalities in liver disease
- increased PT, PTT - increased D-dimers/FDPs (don't clear them) - decreased fibrinogen level - increased factor VIII level - decreased platelet count
44
Treatment for liver disease
- fresh frozen plasma but don't just treat numbers
45
Disseminated Intravascular Coagulation (DIC)
- intravascular thrombin formation - deposition of fibrin in microvasculature - inhibitors consumed (AT, protein C/S) but fail to control process - fibrinolysis initiated, fails to remove all the fibrin - platelet consumption
46
Signs of DIC
- schistocytes due to thrombosis and vascular occlusion | - increased bleeding due to platelet consumption
47
Causes of DIC
- sepsis, trauma, cancer (AML) - obstetrical complications - vascular disorders - toxins: SNAKE VENOM, drugs
48
Lab abnormalities in DIC
- increased PT, PTT - decreased fibrinogen - increased D-dimer/FDPs - decreased platelet count - fragmented RBCs in blood smear
49
Treatment of DIC
- treat UNDERLYING disorder | - blood product replacement in patients who are bleeding
50
Factors requiring vitamin K
- II, VII, IX, X | - protein C & S
51
Vitamin K deficiency
- hemorrhagic disease of newborn (HDN): prevented by giving vitamin K at birth - warfarin (coumadin) - oral antibiotic therapy: decreased gut flora - poor absorption of vitamin K: biliary tract obstruction, bowel disease
52
Acquired coagulation abnormalities
- post Op state, bed rest, pregnancy, oral contraceptives, myeloproliferative disorders, cancer, antiphospholipid antibody syndrome (lupus anticoagulant)
53
Antiphospholipid antibody syndrome
- most common cause of acquired thrombophilia - development of antibodies against plasma proteins w/ affinity for anionic phospholipids: most commonly Beta2-glycoprotein 1
54
Antiphospholipid antibody syndrome: clinical findings
- venous/arterial thrombosis - recurrent fetal loss - thrombocytopenia
55
Lupus anticoagulant
- antibody that prolongs phospholipid dependent coagulation tests (PTT) - may occur in presence OR absence of SLE - INCREASED risk of clotting even with increased PTT
56
Factor V Leiden
- mutation in factor V: unable to be cleaved by activated protein C - prevalence: 3-7% in caucasians - heterozygous state: only a mild risk factor
57
Inherited thrombophilias
- prothrombin gene mutation: increased prothrombin - protein C or S deficiency - anithrombin deficiency - hyperhomocyteinemia - dysfibrinogenemia
58
Clinical features of thrombophilic patient
- FAMILY HISTORY of thrombosis - thrombosis at young age - idiopathic thrombosis - thrombosis in an unusual site
59
Morphology of thrombi
- arterial thrombi: platelets & fibrin (WHITE thrombus) - venous thrombi: cellular elements & thrombin (RED thrombus) - mural thrombus: attached to wall (LINES OF ZAHN imply thrombus at site of blood flow)
60
Fates of thrombus
- propagation: extension leading to vessel obstruction - embolization: travel to other sites - dissolution: removed by fibrinolysis - organization: ingrowth of endothelial cells, smooth muscle fibroblasts, vascular flow may be re-established
61
Clotting cascade pathways
- intrinsic: factors VIII, IX, XI, XII - extrinsic: factor VII - common: factor X & II (thrombin)
MOHDIII - Unit 2
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