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IHO > Exam Final > Flashcards

Exam Final Flashcards

1
Q

Three main mechanisms for bleeding disorders

A
  1. blood vessel fragility/damage
  2. platelet deficiency or dysfunction
  3. Derangement of coagulation pathway
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2
Q

Vessel wall abnormality bleeding

A
  • common but serious cause of bleeding
  • small hemorrhages- petechiae and purpura of skin and mucous membranes
  • PT, PTT, and platelets normal
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3
Q

Infection source of Vessel wall abnormality bleeding

A

meningococcus and other septicemia, microbial damage to microvasculature or DIC - petechiae/purpura

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4
Q

Drug reaction sources of Vessel wall abnormality bleeding

A

Drug induced immune complex in vessel wall and hypersensitivity vasculitis (leukocytoclastic) - palpable purpura

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5
Q

Scurvy and Ehlers-Danlos source of Vessel wall abnormality bleeding

A

Collagen defects weaken vessel wall- easier breaking of vessels

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6
Q

Henoch-Schonlein purpura source of Vessel wall abnormality bleeding

A
  • systemic immune disorder, deposited immune complexes in vessels throughout the body - rash, abdominal pain, arthralgia, acute glomerulonephritis
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7
Q

Perivascular amyloid source of Vessel wall abnormality bleeding

A

Causes muco-cutaneous petechiae

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8
Q

What is considered thrombocytopenia?

A

Platelet count less that 100,000/uL

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9
Q

What platelet level can aggravate posttraumatic bleeding?

A
  • 20,000-50,000/uL
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10
Q

What platelet level is associated with spontaneous bleeding?

A

<20,000/uL

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11
Q

thrombocytopenia bleeding usually involves

A

Small vessels: skin, mucous membranes of GI/GU tract, intracranial bleeds are the most severe complications

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12
Q

Four categories of thrombocytopenia

A
  1. Decreased platelet production (aplastic anemia, leukemia, drug, HIV, EtOH)
  2. decreased platelet survival/increased consumption (immune ITP, non-immune DIC or thrombo. microangiopathy)
  3. Platelet sequestration (spleen 30-35% of bodies platelets, 80-90% with splenomegaly)
  4. Dilution (massive transfusion, viable platelets decrease with time in stored blood)
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13
Q

Chronic Immune Thrombocytopenic Purpura (ITP)

A
  • autoantibody mediated platelet destruction (usually to GP2b3a or 1b9, majority IgG
  • Secondary: predisposing condition (SLE, HIV, CLL)
  • Primary: idiopathic ( exclusion of secondary)
  • splenectomy improves thrombocytopenia due to decreased phagocytosis and sequestration and decreased autoantibodies by decreasing plasma cells
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14
Q

What is seen morphologically in ITP?

A
  • normal size spleen, sinusoidal congestion and enlarged lymph follicles
  • BM: modestly increased numbers of megakaryocytes, immature/not specific indicating increased thrombopoiesis
  • PBS: abnormally large platelets (megathrombocytes)
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15
Q

What are the clinical presentations of ITP?

A
  • Female, under 40
    -insidious bleeding onset, skin and mucosal surfaces
  • Hx of nosebleeds, easy bruising, gum bleeding, bruising from minor trauma
  • Subarachnoid hemorrhage
  • splenomegaly/lymphadenopathy RARE, suggests secondary to B cell neoplasm
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16
Q

Treatment for ITP

A
  • Glucocorticoids first line, may relapse a year or more later
  • IVIg or anti-CD20 used in relapse
  • Splenectomy
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17
Q

Acute immune thrombocytopenic purpura

A
  • Autoantibodies to platelets
  • disease of CHILDHOOD
    -abrupt onset 1-2 weeks post self-limited viral illness trigger
  • usually resolves after 6 months
  • glucocorticoids only if thrombocytopenia is severe
  • 205 develop chronic ITP
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18
Q

Drug induced thrombocytopenia

A
  • Direct effect or immune mediated
  • quinine, quinidine, vancomycin bind platelet glycoproteins creating antigenic determinants recognized by antibodies
  • platelet inhibitory drugs bind GP2b3a and create and immunogenic epitope
  • heparin induced thrombocytopenia
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19
Q

HIV associated thrombocytopenia

A
  • one of the most common hematologic issues in HIV infection
  • impaired production and increased destruction
  • CD4 and CXCR4, HIV receptor and co receptor found on megakaryocytes
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20
Q

Thrombotic thrombocytopenic purpura (TTP)

A
  • pentad of fever, thrombocytopenia, microangiopathic hemolytic anemia, transient neurological defects, and renal failure
  • associated with deficiency in plasma emzyme ADAMTS13, von willebrand factor metalloprotease which degrades VHMW multimers of vWF
  • high platelet consumption –> low count
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21
Q

Hemolytic Uremia Syndrome (HUS)

A
  • absence of neurologic symptoms, prominence of renal failure, and occurrence in children
  • Strong association with infectious gastroenteritis (e.coli O157:H7)
  • Toxin alters endothelial function resulting in platelet activation and aggregation
  • Bloody diarrhea is the first symptom
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22
Q

Inherited disorders of platelet dysfunction

A
  1. Defects of platelet adhesion
  2. Defects of platelet aggregation
  3. Disorders of platelet secretion
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23
Q

Bernard-Soulier syndrome

A
  • inherited defect of platelet function
  • autosomal recessive
  • defect of platelet adhesion to sub-endothelial matrix, defect of GP complex 1b-9, poor binding to VWF
  • abnormally large platelets
  • variable, severe bleeding
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24
Q

Glanzmann thrombasthenia

A
  • inherited defect of platelet function
  • autosomal recessive
  • platelets fail to aggregate in response to ADP, collagen, epinephrine, or thrombin
  • deficiency of GP 2b3a
  • often severe bleeding tendency
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25
Q

Aspirin and non-steroidal leading to acquired defects of platelet function

A
  • COX inhibitors –> no TXA2 or PGI2 (needed for platelet aggregation and granule release
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26
Q

Uremia leading to acquired defect of platelet function

A
  • Decreased GP1b complexes, poor adhesion
  • reduced platelet function involving adhesion, granule secretion, and aggregation
  • reduced fibrinogen binding, poor aggregation
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27
Q

Hemophilia A

A
  • most common hereditary disorder associated with life threatening bleeding
  • mutated factor 8 (essential for factor 9 in the clotting cascade)
  • X-linked recessive affecting males and homozygous females
  • severity of bleeding depends on level of factor 8 activity
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28
Q

Symptoms of hemophilia A

A
  • Easy bruising and massive bleeding with trauma
  • spontaneous hemarthrosis leading to debilitating joint deformities
  • Prolonged PTT, normal PT (intrinsic pathway defect)
  • Treat with infusion of recombinant factor 8
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29
Q

Hemophilia B

A
  • Severe factor 9 deficiency
  • X-linked recessive
  • variable severity
  • prolonged PTT, normal PT (intrinsic pathway defect)
  • treat with infusion of recombinant factor 9
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30
Q

Von Willebrand Disease

A
  • The most inherited bleeding disorder (1% of US adults)
  • autosomal dominant
  • mild bleeding tendency, unnoticed until procedure or other increased requirement for hemostasis
  • presents with epistaxis/mucous membrane bleeding, menorrhagia, excess wound bleeding
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31
Q

Type 1 Von Willebrand Disease

A
  • quantitative defect in vWF
  • Autosomal dominant, mild-moderate severity
  • spectrum of mutations resulting in poor maturation of the vWF proteins or its rapid clearance
  • 70% of all cases, incomplete penetrance and variable expression
  • Mild disease
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32
Q

Type 2 Von Willebrand disease

A
  • Qualitative defects in vWF
  • autosomal dominant, missense mutations inhibit multimer formation
  • Severe subtypes
  • 25% of all cases
  • mild-moderate bleeding
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33
Q

Type 3 Von Willebrand disease

A
  • quantitative defect in vWF
  • Autosomal recessive, very low level of vWF
  • severe deficiency
  • marked effect on factor 8, bleeding resembles hemophilia
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34
Q

Von Willebrand counts

A
  • normal platelet count, defect in platelet function
  • active vWF decreased because vWF stabilizes factor 8, a secondary decrease of factor 8 occurs
  • prolonged PTT in types 1 and 3
  • can pretreat with factor 8 and vWF prior to surgery or dental work
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35
Q

Factor defects secondary to liver disease

A
  • most clotting factors synthesized in the liver
  • decreased production of anticoagulants also occurs
  • patients risk for thrombotic and bleeding compliactions
  • liver disease can cause prolonged PT and PTT
  • all vitamin K dependent proteins decrease (2, 7, 9, 10)
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36
Q

Vitamin K deficiency

A
  • leafy green veg or intestinal flora synthesis
  • ## deficiency is seen in very ill patients subsisting on parenteral nutrition after 4-6 weeks, or alcoholics
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37
Q

What is DIC?

A
  • acute, subacute or chronic thrombo-hemorrhagic disorder characterized by excess activation of coagulation and the formation of thrombi in the microvasculature
  • consumption of clotting factors, fibrin, and platelets
  • secondary activation of fibrinolysis
  • can present with tissue hypoxia due to micro-thrombi in microvasculature, hemorrhage due to deficiency of factors and activation of fibrinolysis
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38
Q

What are the two main mechanisms that trigger DIC?

A

1.) release of tissue factor or other pro-coagulant (OB complications, burn injuries, adenocarcinoma mucin activating factor 10)
2.) Widespread injury to endothelial cells

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39
Q

What is DIC most likely associated with?

A
  1. OB complications (placental/fetal procoagulants or amniotic fluids entering circulation
  2. Malignant neoplasms (adenocarcinoma, APML-AML M3)
  3. Sepsis (bacterial endotoxin activating factor 7 or decreasing thrombomodulin)
  4. major trauma/burns/extensive surgery (release of tissue factor/factor 3)
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40
Q

Waterhouse-Friderichsen syndrome -DIC

A
  • meningococci from blood, spinal fluid, or throat
  • circulatory collapse- hypotension
  • extensive purpura shock, prostration, cyanosis
  • hemorrhagic destruction of adrenal gland
  • characteristic up and down fever
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41
Q

Osler Weber Rendu syndrome

A
  • autosomal dominant
  • red spider-like lesions on oral and nasal mucosa
  • dilated capillaries cause bleeding
  • dilated vessels present in skin, lips, tongue, and GI
  • Iron deficiency anemia
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42
Q

Senile purpura

A
  • normal finding in elderly
  • results from impaired collagen production and capillary fragility
  • non-palpable purpura in areas of trauma
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43
Q

What treatment is commonly given in platelet disorders?

A
  • Fresh frozen plasma (has all the clotting factors) is used in all coagulation disorders
  • Cryoprecipitate: mostly factors 8, 13, vWF, fibronectin, and fibrinogen
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44
Q

Fanconi’s anemia:

A

Bone marrow failure, thrombocytopenia and macrocytes

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45
Q

Neonatal thrombocytopenia

A

antibodies to fetus platelet antigens

46
Q

Acute ITP

A
  • Children (2-6 years)
  • following a viral infection (URTI)
  • abrupt and easy bruising, petechiae, nosebleeds, and bleeding from mucous membranes
  • platelet count <20,000
  • 95% spontaneous remission
  • treatment: corticosteroids
47
Q

ITP mech and labs

A
  • phagocytosis of antibody coats platelets by splenic macrophages
  • IgG type antibodies
  • lab finding: low platelets, increased megakaryocytes
  • no splenic enlargement, no fever
48
Q

Chronic ITP

A
  • young women, 20-40 years
  • associated with HIV, SLE, and CLL
  • gradual onset of bleeding symptoms
  • normocellular, increased megakaryocytes
  • platelet count <100,000
  • Treatment: corticosteroids, splenectomy
49
Q

Common features between TTP, HUS, and DIC

A
  • microthrombi throughout the vasculature, consuming platelets and causing thrombocytopenia
  • microangiopathic hemolytic anemia (MAHA)
  • schistocytes on PBS
50
Q

What is seen on a peripheral smear of TTP?

A
  • decreased platelet count (thrombocytopenia)
  • normal PT and aPTT
  • increased Bleeding time
  • schistocytes and reticulocytes
51
Q

What are trigger mechanisms of DIC?

A
  • release of tissue factor
  • exposed to circulation after vascular damage
  • released after exposure to cytokines
  • endotoxin (as in gram negative sepsis)
52
Q

Clinical features of DIC

A
  • Bleeding
  • microangiopathic hemolytic anemia (schistocytes)
    -Respiratory dyspnea and cyanosis
  • Neurological signs and symptoms
  • oliguria and acute RF
53
Q

Lab findings of DIC

A
  • Prolonged PT and PTT
  • decreased fibrinogen (best test for predicting prognosis)
  • thrombocytopenia
  • Prolonged bleeding time
  • Fibrinolysis test: presence of FDPs and D-Dimers (Most sensitive overall test for DIC)
  • Schistocytes
  • treatment: Heparin, FFPs
54
Q

Treatment of Hemophilia A

A
  • Mild disease: desmopressin acetate (increases factor 8 synthesis) acts on endothelial cells
  • Severe disease: recombinant factor 8
55
Q

What cab cause vitamin K deficiency?

A
  • neonates: lack of bacterial colonization for vit K synthesis
  • Antibiotic Rx: sterilizes bowel, MCC in hospitalized patients
  • Fat malabsorption: ex. CF, pancreatitis, IBDs
  • Warfarin
56
Q

VKBD

A
  • vitamin K deficiency bleeding (newborns)
  • Hemorrhagic disease of newborn (HDN)
  • neonates require injection at birth, vit K not present in breast milk
57
Q

Virchow’s triad

A
  • three primary abnormalities leading to thrombosis
  • leading causes of death: MI, stroke, PE
    1. endothelial injury
    2. stasis or turbulent blood flow
    3. hypercoagulability of the blood
58
Q
  1. Endothelial injury
A
  • leads to platelet aggregation, underlies arterial thrombosis formation where high flow rate impedes clot formation
  • cardiac/arterial clots are rich in platelets
  • platelet adherence and activation are necessary for thrombus formation under high shear stress and flow in arteries
59
Q
  1. alterations in normal blood flow (turbulence)
A
  • normal flow is laminar
  • turbulence creates endothelial injury leading to local pockets of stasis which is a major contributor to venous thrombosis
60
Q
  1. Hypercoagulability (thrombophilia)
A
  • any disorder of blood predisposing to thrombosis
  • typically venous thrombosis
  • Primary: genetic (point mutation factor 5, Leiden mutation)
  • Secondary: acquired, multifactorial (antiphospholipid antibody syndrome, heparin induced, smoking, etc)
61
Q

Features of Factor 5 Leiden and prothrombin mutations

A
  • heterozygosity = mild/moderate risk of thrombosis
  • increased risk in settings of other risk factors including: pregnancy, prolonged bed rest, and long airline travel
62
Q

When should inherited hypercoagulability be considered?

A
  • in patients under 50 who present with thrombosis, even when acquired risk factors are present (5-8% of the US population has a genetic risk factor for thrombosis)
63
Q

Heparin induced thrombocytopenia syndrome

A
  • occurs after administration of unfractionated heparin (LMWH less common)
  • induces antibodies that recognize complexes of heparin and platelet factor 4 on the surface
  • these antibodies result in platelet activation, aggregation, and consumption
  • endothelial damage also occurs leading to prothrombotic state
64
Q

Type 1 heparin induced thrombocytopenia

A
  • rapid onset, little clinical impact, sometimes resolves despite continued therapy
  • direct platelet aggregation effect
65
Q

Type 2 heparin induced thrombocytopenia

A

-less common, 5-14 days after the start of therapy, can lead to life threatening venous and arterial thrombosis
- caused by antibody that recognize complexes of heparin and platelet factor 4 on the surface of platelet granules
- DISCONTINUE HEPARIN
- clots in large arteries, limb loss, DVT, fatal PE

66
Q

Antiphospholipid antibody syndrome

A
  • previously lupus anticoagulant syndrome
  • recurrent venous and arterial thromboses
  • repeated miscarriages (failed placental development)
  • DVT, PE, bowel infarction, cardiac valve vegetation, etc
67
Q

What can be seen in 24% of Antiphospholipid antibody syndrome?

A
  • Livido reticularis (reticulated rash)
  • widespread in limbs, trunk, buttocks
  • higher prevelance in SLE
  • F>M
68
Q

What patients are diagnosed with Antiphospholipid antibody syndrome?

A
  • pts with thrombosis in association with Lupus anticoagulant (LA) or anticardiolipin antibody (ACL)
  • Primary: occurring in isolation
  • Secondary: associated with an autoimmune disease
69
Q

Testing for Lupus anticoagulant (LA)

A
  • 2 test 6-12 weeks apart
  • prolonged PTT, still abnormal after mixing 1:1 with normal plasma
  • all clotting factors present at least at the 50% level required for normal test, inhibitors still active below 50% so test is still prolonged
  • Normalizes with addition of phospholipid, which can overcome the inhibitory action of the antibody
70
Q

Testing for anticardiolipin antibody (ACL)

A
  • immunoassay
71
Q

What is the suspected antibody target for Antiphospholipid antibody?

A
  • beta2-glycoprotein 1, a plasma protein that interacts with endothelial cell surface and trophoblasts, and thrombin
72
Q

What is the treatment for antiphospholipid antibody syndrome?

A
  • anticoagulation and immunosuppression
73
Q

Thromboembolism is seen most commonly in which patients?

A
  • cancer (especially pancreatic, brain, advanced ovarian, lung, GI, or prostate)
  • catheterization and surgery are risk factors
  • Cancers can express tissue factor
  • trousseau syndrome
74
Q

Trousseau syndrome

A
  • episodes of vessel inflammation due to underlying clot which are recurring or appearing in different locations over time (migratory thrombophlebitis)
75
Q

Factor 5 Leiden mutation

A
  • autosomal dominant
  • 60% of patients have a hx of DVT
  • mutation renders factor 5 resistant to cleavage and resistant to inactivation by protein C (can be activated but not inactivated)
  • 5x higher thrombosis risk in heterozygotes
  • 50x higher thrombosis risk in homozygotes
76
Q

Anticoagulation deficiency: Protein C

A
  • type 1: low protein, low activity
  • type 2: normal protein, low activity
  • inherited (AD) or acquired (DIC, sepsis, cancer treatment, liver disease, warfarin)
77
Q

What can anticoagulation deficiency of protein C lead to?

A
  • warfarin necrosis
  • develops on initiation of treatment with Warfarin or other vitamin K antagonist
  • “double down” of initial warfarin decrease in protein C in combo with the deficiency
78
Q

Screening for thrombophilia

A
  • unprovoked episode of venous thromboembolism in individuals under 40
  • thrombosis in unusual sites (cerebral or mesenteric)
  • two or more first degree relatives with unprovoked thrombosis
  • three or more early pregnancy losses, or fetal deaths after 10 weeks gestation
79
Q

Lines of Zahn

A
  • alternating pale platelet rich and dark RBC rich layers, indicating thrombus formation in flowing blood, not present in post-mortem clot
  • seen in morphology of thrombus
80
Q

Arterial thrombosis

A
  • Frequently occlusive
  • coronary > cerebral > femoral
  • platelets and fibrin rich, fewer RBC, paler
  • Atherosclerotic plaque or vasculitis
81
Q

Venous thrombosis

A
  • almost always occlusive
  • lower extremity veins (90%), upper extremity, periprostatic venous plexus, ovarian and peri-uterine veins
  • Stasis
82
Q

4 Major events following the initial thrombus formation

A
  1. Propagation (thrombus accumulates additional platelets and fibrin)
  2. Embolization (thrombus dislodges and travels to another site)
  3. Dissolution (fibrinolysis and clot shrinkage)
  4. Organization and recanalization (small fibrous scars, small vascular channels reform)
83
Q

Red morphology Infarct

A
  • venous occlusion
  • loose spongy tissue
  • dual circulation
  • previously congested tissue
  • re-established flow into pale infarct
84
Q

White morphology infarct

A
  • arterial occlusion
  • firm tissue prevents blood seepage
  • single circulation- end arterial
  • no prior congestion
85
Q

Where are superficial venous thrombosis found?

A
  • saphenous vein with varicosities
  • local congestion, pain, swelling, tenderness (rarely embolize)
  • overlying skin at risk for ulceration
86
Q

Where are deep venous thrombosis found?

A
  • popliteal, femoral, iliac
  • more serious due to risk of PE
  • local symptoms not as pronounced with good collateral circulation
  • DVT 50% asymptomatic, only recognized following PE
  • often associated with hypercoagulable states
87
Q

Embolism

A
  • a detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site where it often causes tissue dysfunction or infarction
88
Q

Dislodged thrombi

A

Thromboembolism

89
Q

Atherosclerotic debris

A

cholesterol emboli

90
Q

Traumatic emboli

A

bone marrow fat embolism

91
Q

Shed carcinoma fragments

A

tumor emboli

92
Q

Nitrogen or other gas bubbles

A

Gas emboli

93
Q

Medical hardware

A

foreign body embolism

94
Q

What is used to measure level of anti-coagulation with dabigatran, rivaroxaban, apixaban

A

Chromomogenic Xa (factor 10) assay

95
Q

PFA-100

A
  • a useful way to measure platelet function
  • measures platelet response to ADP, collagen, and epinephrine
  • does not reveal etiology of platelet function defect
96
Q

How do you reverse aspirin?

A

Give platelets. Otherwise irreversible for the life of the platelets

97
Q

NSAIDs

A
  • ibuprofen, naproxen sodium, ketorolac, sulindac, indomethacin
  • reversible binding of platelets, wears off after 6-8 hours
98
Q

How do you reverse warfarin?

A
  • Time
  • Vitamin K
  • Fresh frozen plasma
99
Q

Rivaroxaban

A
  • oral factor 10 inhibitor (DOAC)
100
Q

Apixaban

A
  • oral factor 10 inhibitor (DOAC)
101
Q

Dabigatran

A
  • oral direct thrombin inhibitor, factor 2 (DOAC)
102
Q

Difference between FFP and cryoprecipitate

A
  • Fresh frozen plasma: contains all factors in normal levels
  • may be used to reverse warfarin or to replace factors lost in DIC and Liver disease
  • Cryoprecipitate: contains fibrinogen, vWF, factor 8, factor 13, and fibronectin
103
Q

What will you see in vascular/platelet defects?

A
  • prolonged bleeding
  • petechiae and easy bruising
  • <20,000 platelets, lower extremity petech.
  • skin and mucous membranes affected
  • non-recurrent bleeding
104
Q

What will you see in coagulation defects?

A
  • prolonged bleeding
  • deep hematomas
  • hemarthrosis
  • recurrent bleeding
105
Q

What are some hypercoagulable states?

A
  • post-operative
  • malignancy
  • immobilization
  • pregnancy/estrogen use
  • oral contraceptives/smoking
  • previous venous thromboembolism
  • HIT
  • TTP
  • Antiphospholipid antibody syndrome (APS)
106
Q

Appropriate duration of anticoagulation therapy for different patients:

A
  1. unprovoked non-life threatening DVT/PE: 3 months
  2. Life-threatening DVT/PE/arterial thrombosis: six months
  3. Second DVT/PE: six months-indefinite
  4. unprovoked DVT/PE with genetic mutation: indefinitely
107
Q

Why do you need a secondary drug when starting warfarin?

A
  • because it takes 4-5 days for warfarin to fully affect prothrombin (factor 2), and also decreases Protein C intitially causing MORE clotting
108
Q

What is the most common drug used as a bridge for Warfarin?

A
  • Argatroban
109
Q

What to use for Immune-mediated Thrombocytopenia?

A
  • Corticosteroids
  • Prednisone or Pulse dexamethasone
  • IVIg or Rhogam
  • Rituximab
  • thrombopoiesis agonist
110
Q

What test does antiphospholipid antibody interfere with?

A

INR measurement leading to false readings
- must follow chromogenic factor 10a instead of INR on Antiphospholipid antibody patients

111
Q

Acquired hemophilia A

A
  • acquired factor 8 inhibitor
  • must treat with Factor 7, giving more factor 8 will not work
112
Q

If the patient has pseudothrombocytopenia:

A
  • collect their blood in a blue top (heparin) rather than EDTA purple top

IHO (6 decks)

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