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Hematology Oncology > Hematology > Flashcards

Hematology Flashcards

0
Q

Heparin and warfarin MOA

A

Heparin: increases Antithrombin III levels, affects intrinsic pathway and decreases fibrinogen levels
Warfarin: inhibits vitamin K activated factors- 10, 9, 7, 2 and Protein C and S

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1
Q

What lab value measures heparin vs. warfarin?

A

Heparin: PTT
Warfarin: PT

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2
Q

Intrinsic pathway

A

XII -> XI -> IX -> VIII -> X

Factor X is where intrinsic and extrinsic collide

X -> V -> II -> XIII -> Fibrin to crosslinked fibrin
Factor II also converts fibrinogen to fibrin

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3
Q

Extrinsic pathway

A

III helps convert VII -> VIIa -> X

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4
Q

Antidote for heparin and warfarin

A

Heparin: protamine sulfate
Warfarin: Vitamin K, fresh frozen plasma

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5
Q

Enoxaparin MOA

A

Inhibits Factor X

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6
Q

Platelet dysfunction vs coagulation dysfunction manifestation

A

Platelet dysfunction: petechiae

Coagulation dysfunction: hemarthroses

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7
Q

Hemophilia: inheritance and types

A 
X linked recessive
A: Factor VIII dysfunction
B: Factor IX dysfunction
C: Factor XI dysfunction
Factor VII deficiency: PT elevation only
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8
Q

Mixing study

A

Mix patient’s blood with normal blood. If the PTT corrects, it’s likely dysfunctional factors that are causing the disease. If it doesn’t, there’s an antibody present

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9
Q

Hemophilia characterization

A

Mild: >5% normal levels of factors
Moderate: 1-3% normal levels of factors
Severe: <1% normal levels of factors

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10
Q

Cryoprecipitate

A

Mainly factor VIII and fibrinogen
Small concentrations of factor XIII, vWF, and fibronectin
It is a more concentrated source of factor VIII and fibrinogen than FFP
Good for treatment of Hemophilia A (Factor VIII deficiency)

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11
Q

Mild hemophilia tx

A

DDAVP

-vasopressin is an ADH analog which increases the amount of factor VIII in the blood

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12
Q

von Willebrands disease inheritance

A

Autosomal dominant disease with low levels of vWF and Factor VIII (carried by vWF)

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13
Q

Diagnosis of von Willebrands disease

A

PT is normal. PTT and bleeding time may increase 2/2 decreased Factor VIII levels
Ristocetin cofactor assay: measures the capacity of vWF to aggregate platelets

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14
Q

Bernard Soulier syndrome

A

Deficiency of GpIb (a receptor on platelets which binds to vWF)

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15
Q

Glanzmann’s thrombasthenia

A

GP IIb/IIIa deficiency (GP IIb/IIIa is a receptor on platelets which binds to fibrinogen. The fibrinogen binds to two different receptors on different platelets, allowing platelets to aggregate)

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16
Q

Clopidogrel mechanism of action

A

Irreversibly blocks the ADP receptor

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17
Q

Most common thrombophilias

A

Thrombophilia = hypercoaguable state

Most common = Factor V Leiden

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18
Q

Sickle cell disease

A

Hereditary disease of RBCs, causing them to sickle
Sludging and occlusion of arterial vasculature can lead to stroke
-due to malformed RBCs

Tx: Exchange transfusion
-DO NOT USE FIBRINOLYTICS OR ANTI-COAGS

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19
Q

Antiphospholipid syndrome

A

Hypercoaguable state
VDRL +
Causes thrombocytopenia and prolonged PTT
Tx: LMWH or Coumadin

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20
Q

Lepirudin MOA

A

Direct thrombin inhibitor

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21
Q

Danaparoid (MOA)

A

Direct thrombin inhibitor

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22
Q

DIC vs TTP vs ITP MOA

A

DIC: deposition of fibrin in small vessels leads to thrombosis and depletion of clotting factors and platelets. Platelet microthrombi block off small blood vessels
TTP: Platelet microthrombi block off small blood vessels
ITP: IgG antibodies against patient’s platelets are formed and destroy platelets. NO MICROTHROMBI PRESENT

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23
Q

DIC associated disorders

A

Sepsis, acidosis, drug reactions, massive trauma, ARDS, intravascular hemolysis
OB complications
Neoplasms, APML

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24
Q

DIC vs liver disease

A

DIC: Factor VIII is depleted also, while in liver disease factor VIII is normal (because Factor VIII is made by endothelial cells)

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25
Q

DIC Tx

A

Reverse underlying cause, RBC and platelet transfusion

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26
Q

Microangiopathic hemolytic anemia

A

Caused by DIC, TTP, and HUS
Basically, small microthrombi of platelets deposit in small blood vessels and RBCs shear when they go through them
Causes hemolysis and fragmented RBCs (schistocytes)

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27
Q

5 common symptoms of TTP

A 
TTP = idiopathic activation of platelets leading to microthrombi and microangiopathic hemolytic anemia. TTP definition is MAHA + end-organ ischemia
5 common si/sx:
-thrombocytopenia
-MAHA
-neuro changes (delirium, sz, stroke)
-impaired renal function
-fever
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28
Q

TTP vs HUS

A

HUS occurs after an E Coli infection
Both = MAHA + end-organ damage
HUS has much worse renal failure

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29
Q

Treatment of TTP

A

Steroids to decrease microthrombus formation
Plasmapharesis
DO NOT REPLACE PLATELETS

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30
Q

ITP

A

IgG antibodies against patient’s platelets causes thrombocytopenia
BM production of platelets increases (increased megakaryocytes in the BM)

Sx: mild, no systemic sx; some bruising, petechiae, hematuria, hematemesis, melena

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31
Q

ITP associated with what diseases:

A

lymphoma, leukemia, SLE, HIV, HCV

32
Q

Most common pediatric cause of renal failure

A

HUS

33
Q

Treatment of ITP

A

Most cases remit (in childhood)
Symptomatic bleeding: corticosteroids, high dose IVIG, and splenectomy
-PLATELET TRANSFUSION IS NOT HELPFUL

34
Q

Differential diagnosis for thrombocytopenia

A 
HIT SHOC:
HIT/HUS
ITP
TTP/Treatment (ie meds)
Splenomegaly
Hereditary (ie Wiskott Aldrich syndrome)
Other causes ie malignancy
Chemotherapy
35
Q

What are bands on a differential?

A

Bands = precursor to neutophils, eosinophils, basophils

36
Q

Retic > 2.5

A

Hemolysis or hemorrhage

37
Q

What type of anemia is pyridoxine deficiency?

A

Can cause sideroblastic anemia if INH is given without pyridoxine (microcytic or normocytic)

38
Q

Physical exam findings of Fe deficiency anemia

A

Glossitis, angular cheilitis, and koilonychia (spoon nails)

39
Q

Fe deficiency vs ACD labs

A

Fe deficiency:

  • Serum Fe: decreased
  • Ferritin: decreased
  • Transferrin/TIBC: increased
  • serum transferrin receptor: increased

ACD:

  • Serum Fe: decreased
  • TIBC/transferrin: decreased
  • ferritin: increased
  • serum transferrin receptor: normal
40
Q

Acquired sideroblastic anemia

A

Defective heme synthesis 2/2 pyridoxine dependent impairment ie INH
Dimorphic RBCs: both hypochromic and monochromic
Tx: B6

Labs: normal Fe, decreased TIBC

41
Q

Cobalamin

A

B12

42
Q

What cells produce intrinsic factor?

A

Parietal cells in the GI tract

43
Q

Folate stores length vs. B12

A

Folate: 4 months
B12: years

44
Q

B12 deficiency: sx other than anemia

A

Neuro sx: deymyelinating disorder causing motor, sensory, autonomic, and/or neuropsychiatric dysfunction
-aka subacute combined degeneration of the cord

45
Q

What infection can cause B12 deficiency?

A

Diphyllobothrium latum: tapeworm

46
Q

Schilling test

A

Ingestion of radiolabeled cobalamin:

  • First give pt unlabeled B12 IM to saturate all B12 receptors in the liver
  • Then give an oral challenge of radiolabeled B12. If everything is normal, the B12 will be absorbed in the GI tract, but the liver is unable to use it so it should pass through into the urine. Radiolabeled B12 in the urine = positive test, meaning that pt has nutritional B12 deficiency
  • No radiolabeled B12 in the urine means pt may have pernicious anemia, bacterial overgrowth, or pancreatic enzyme deficiency; give B12 with IF and check urine, with antibiotics and check urine, and with pancreatic enzymes and check urine
47
Q

Diagnosis of B12 and folate deficiency

A

B12: elevated MMA and homocysteine, increased LDH
Folate: normal MMA, elevated homocysteine, normal LDH

48
Q

G6PD deficiency

A

X-linked recessive hemolytic anemia

Increased sensitivity to oxidative stress

49
Q

Paroxysmal nocturnal hemoglobinuria

A

Hemolytic anemia
Increased blood cell sensitivity to complement activation
Patients are prone to thrombotic events

50
Q

Hereditary spherocytosis

-what is it, how to diagnose, what to supplement these patients with

A

Abnormality of the RBC membrane, leading to spherocytes on smear which lack areas of central pallor
Dx: with a osmotic fragility test (these RBCs are more fragile)

Supplement with folate

51
Q

Autoimmune RBC destruction

A

2/2 EBC, mycoplasma, CLL, rheumatoid disease, or medications

52
Q

How does hemolytic anemia present differently than anemia?

A

Jaundice, low haptoglobin, elevated indirect bilirubin, elevated LDH
Urine is dark with hemoglobinuria
Increased excretion of urinary and fecal urobilinogen
Elevated retic count

53
Q

G6PD stressors

A

Infection, quinidine, nitrofurantoin, fava beans, antimalarials, dapsone, sulfonamides, metabolic acidosis

54
Q

Coombs test

A

Direct: Pt’s RBCs are washed to remove any unbound antibodies and mixed with antihuman antibodies (aka Coombs reagent); the antihuman antibodies bind the pt’s anti-RBC antibodies on multiple RBCs and cause agglutination = + test

Indirect: Patient’s serum is collected (which contains anti-RBC antibodies) and mixed with donor RBCs; The donor RBCs will bind to the pt’s antibodies; Antihuman antibodies are added (Coombs reagent) and these will agglutinate the mixture already

the big difference is where the RBCs are from

55
Q

Causes of aplastic anemia

A

Fanconi’s anemia (congenital), Parvovirus B19, HIV, toxins (drugs, cleaning solvents), and radiation

56
Q

Aplastic anemia: hx/PE, Dx, Tx

A

Hx/PE:
-pancytopenia: pallor, weakness, tendency to infection, petechiae, bruising, bleeding

Dx: BM biopsy shows hypocellularity and space occupied by fat

Tx: blood transfusion + stem cell transplant

  • immunosuppresion with cyclosporine A and antithymocyte globulin
  • infections are major cause of mortality
57
Q

Fanconi’s anemia

A

Hereditary aplastic anemia

PE: cafe au lait spots, short stature, radial/thumb hypoplasia/aplasia

58
Q

Sickle Cell Disease

-genetics and affected protein

A

Genetics: autosomal recessive disorder

Affected protein: B chain of hemoglobin

59
Q

Symptoms of sickle cell disease

A

Dactylitis, cholelithiasis, increased cardiac output (cardiomegaly and murmur), delayed growth, splenic infarction (predisposes to pneumococcal sepsis), acute chest syndrome (pneumonia and pulmonary infarct), pain crises (triggers: cold temp, dehydration, infection)

60
Q

Osteomyelitis in sickle cell disease

A

Most common: S aureus
Very prone to Salmonella also
Increased risk of AVN of the hipt

61
Q

Target cells

A

sickle cell disease

62
Q

Treatment of sickle cell disease

A

Hydroxyurea, which stimulates fetal hemoglobin production

63
Q

Treatment of vaso-occlusive reactions in sickle cell disease

A

Pain management, aggressive hydration, incentive spirometry, and keeping sickle cell variant < 40%
-this will keep VOD from progressing to acute chest syndrome

64
Q

Alpha vs beta thalassemia

A

Alpha: affects one or more of 4 alpha-globin chains
Beta: affects one or both of 2 beta-globin chains

65
Q

Types of thalassemia

A

B-thal major: absent both B-globin genes; severe microcytic anemia and need chronic transfusions or marrow transplant

B-thal minor: 1 of 2 B-globin genes; asymptomatic, but cells are microcytic and hypochromic

Hydrops fetalis: 0/4 alpha-chains; patients die in utero

Hemoglobin H disease: 1/4 alpha chains present; severe hypochromic, microctyic anemia; chronic hemolysis, splenomegaly, jaundice, and cholelithiasis; elevated reticulocyte count

a-thal trait: 2/4 alpha chains; low MCV, but asymptomatic

Silent carrier: 3/4 alpha chains present; no signs or symptoms of dz

66
Q

Fe chelator

A

Deferoxamine

67
Q

Hyperviscosity syndrome

A

2/2 erythrocytosis

Easy bruising/bleeding, blurred vision, pruritis after a warm bath, hsm, CHF, neuro abnormalities

68
Q

Causes of primary erythrocytosis

A

Polycythemia vera, hypoxia (smoking, high altitudes, restrictive lung dz, fetal hypoxia), tumors (EPO producing tumor)

69
Q

PCV pathophysiology

A

Clonal proliferation of a pluripoitent marrow stem cell 2/2 JAK2 mutation; all marrow lines increase, RBCs more than others
Low EPO levels

70
Q

Polycythemia vera treatment

A

Cytoreductive drugs: hydroxyurea, interferon

-ASA also because PCV is prothrombotic

71
Q

Types of blood transfusion reactions

A

Nonhemolytic febrile reaction
Minor allergic reaction
Hemolytic transfusion reaction

72
Q

Nonhemolytic febrile reaction

A

Cytokine formation during storage of blood
Fevers, chills, rigors, malaise 1-6 hours after transfusion
Stop transfusion and give acetaminophen

73
Q

Minor allergic reaction to blood transfusion

A

Antibody formation against donor proteins, after receiving plasma containing product

p/w prominent urticaria

Tx: antihistamines; if the reaction is severe, may need to stop and give epinephrine

74
Q

Hemolytic transfusion reaction

A

Antibody formation against donor erythrocytes, results from ABO incompatibility or from minor Ag mismatch

p/w fevers, chills, nausea, flushing, burning at IV site, tachycardia, hypotension shortly after transfusion; can cause hemoglobinuria which can lead to ATN and renal failure

Tx: stop transfusion immediately; give IVF and maintain UO

75
Q

Leukocyte alkaline phosphatase

A

Increased in leukemoid reactions

Decreased in hematologic malignancies

76
Q

Porphyria

A

Congenital abnormality of heme production which leads to accumulation of porphyrins

Photodermatitis
Neruopsychiatric complaints
Visceral complaints: usually colicky abdominal pain and seizures

PE: tachycardia, skin erythema and blisters, areflexia, and nonspecific abdominal exam

Erythropoietic porphyria: hemolytic anemia

77
Q

Porphyria triggers

A

EtOH, OCPs, barbiturates

78
Q

Pink urine

A

porphyria

Hematology Oncology (3 decks)

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