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FirstAID > Hematology/Oncology > Flashcards

Hematology/Oncology Flashcards

1
Q

Erythrocytosis
Anisocytosis
Poikilocytosis
Reticulocyte

A
  • Erythrocytosis = polycythemia = increased RBCs
  • Anisocytosis = varying sizes
  • Poikilocytosis = varying shapes
  • Reticulocyte = immature RBC
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2
Q

Spectrin

A

supplies the biconcavity/flexibility of RBCs

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3
Q

1/3 of platelets are stored in?

A

Spleen (lifespan = 8-10 days)

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4
Q

Causes of polycythemia/erythrocytosis?

A
  • Any time have increased EPO (hypoxia, renal cell carcinoma, HCC, pheochromocytoma, hemangioblastoma)
  • Down’s babies at birth
  • Polycythemia vera –> have increased RBCs, but normal EPO
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5
Q

Barr bodies

A

=inactivated X in neutrophils

–>seen in all women + KF men

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6
Q

When do you see hypersegmented polymorphic neutrophils?

A

-Vitamin B12/Folate deficiency

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7
Q

Neutrophil chemotactic factors?

A
  • Leukotriene B4
  • IL-8
  • C5a
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8
Q

CD14 = cell marker for?

A

Macrophages

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9
Q

Causes of Eosinophilia?

A
  • DNA-CAAPA:
  • Drugs
  • Neoplastic
  • Asthma (and Churg-Strauss)
  • Collagen Vascular diseases
  • Allergic processes
  • Addison’s (adrenal insufficiency)
  • Parasites (invasive)
  • Acute Interstitial Nephritis
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10
Q

Phagocytes:

  • in brain
  • in tissue
  • in liver
  • in joints
A
  • brain = microglia
  • tissue = macrophages
  • liver = kupffer cells
  • joints = A-cells
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11
Q

Mast cells vs Basophils?

A

Both are similar, mediate allergic rxn

  • Basophils in Blood
  • Mast cells in tissue

-mast cells are involved in type 1 hypersensitivity rxns

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12
Q

Langerhans cells

A
  • dendritic cells on skin and mucous membranes
  • act as professional APCs
  • possess Birbeck granules = racquet-shaped intracytoplasmic granules
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13
Q

Main inducers of primary antibody response?

A

Dendritic cells = professional APCs

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14
Q

clock-face chromatin

A

Plasma cells (B cells differentiate into plasma cells; plasma cells produce lots of antibody specific to a particular antigen)

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15
Q

plasma cell neoplasm?

A

Multiple Myeloma –> make a whole bunch of one particular type of B cell, all making one type of antibody (so see monoclonal antibody spike)

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16
Q

CD3

A

on ALL T-cells

  • ->Th also have CD4
  • ->Cytotoxic also have CD8
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17
Q

anti-AB antibodies (Ig type?)

A

-IgM –> don’t cross placenta

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18
Q

anti-Rh antibodies (Ig type?)

A

=IgG –> can cross placenta and cause hemolytic disease of newborn (erythroblastosis fetalis) if fetus is Rh+

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19
Q

Blood type A (example)

A
  • have A antigen on RBC surface

- B antibody in plasma

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20
Q

erythroplastosis fetalis

  • cause?
  • symptoms?
  • hypersensitivity type?
  • how to prevent?
A
  • type 2 hypersensitivity rxn
  • cause: Rh- mother exposed to Rh+ fetal blood during delivery; makes anti-Rh IgG –> can cross placenta in subsequent pregancies, causing hemolytic disease of newborn in next fetus who is Rh+
  • Symptoms in infant: hepatosplenomegaly, severe anemia, jaundice, demise/death
  • Treat/Prophylaxis = give mother Rhogam = Rho (D) Ig at first delivery to prevent all future erythroblastosis
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21
Q

Deficiency of Factor VIII?

A

Hemophilia A

“Aight”

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22
Q

Deficiency of Factor IX?

A

Hemophilia B

“Benine”

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23
Q

Vitamin K deficiency?

A

decreased synthesis of “diSCo 1972”

  • proteins C and S
  • Factors X, IX, VII, II (10, 9, 7, 2)

*Vitamin K normally catalyzes carboxylation of glutamic acid residues on proteins involved with blood clotting

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24
Q

Vitamin K antagonist?

A

Warfarin

–>acts by inhibiting Epoxide Reductase (vitamin K–>activated vitamin K)

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25
Q

Antithrombin inhibits?

A

Antithrombin inhibits:

  • thrombin
  • factors VIIa, IXa, Xa, XIa, XIIa
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26
Q

Drug that activates antithrombin?

A

Heparin

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27
Q

Coagulase

A

Produced by S. aureus

–>can convert fibrinogen–>fibrin

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28
Q

tPA, Streptokinase, Urokinase:

A

All facilitate: plasminogen–> plasmin

so, stimulate breakdown of clots!

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29
Q

vWF receptor on platelets? Fibrinogen receptor on platelets?

A
  • vWF –> GpIb
  • Fibrinogen –> GpIIb/IIIa

***vWF and Fibrinogen are both inside platelets

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30
Q

ESR in pregnancy?

A

increased

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31
Q

Decreased ESR:

A
  • polycythemia
  • sickle cell anemia
  • CHF
  • microcytosis
  • hypofibrinogenemia
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32
Q

Spur cell (Acanthocyte)

A

Liver disease, Abetalipoproteinemia

–>irregularly spiked RBCs

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33
Q

basophilic stippling

A

TAIL:

  • Thalassemias
  • Anemia of chronic disease
  • Iron deficiency
  • LEAD poisoning!

–>have denatured RNA within RBCs

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34
Q

type of anemia caused by folate or B12 deficiency?

A

Macrocytic, Megaloblastic anemia

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35
Q

iron deficiency anemia + esophageal web + atrophic glossitis?

A

Plummer-Vinson syndrome

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36
Q

“crew cut” on skull x-ray?

A

Bone Marrow expansion –> see in beta-thal major

  • thalassemias
  • Sickle cell disease
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37
Q

chipmunk facies

A

beta-thal major

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38
Q

Ringed sideroblasts

A

sideroblastic anemia = defect in heme synthesis (x-linked defect in ALA synthase gene)
-treat with B6 (Pyridoxine)

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39
Q

Lead poisoning symptoms: LEEAADDS

A
  • Lead lines on gingivae (Burton’s lines) and on epiphyses of long bones on x-ray
  • Encephalopathy
  • Erythrocyte basophilic stippling
  • Abdominal colic
  • Anemia (sideroblastic anemia)
  • Drops (wrist and foot drop)
  • Dimercaprol and EDTA = treatment
  • Succimer = treatment for kids
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40
Q

Dimercaprol

A

treatment for lead poisoning (also EDTA)

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41
Q

Succimer

A

=treatment for kids with lead poisoning (“SUCks to be a kid with lead poisoning”)

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42
Q

Hypersegmented neutrophils + glossitis +
increased homocysteine and:
-normal methylmalonic acid?
-increased methylmalonic acid?

A
  • if normal methylmalonic acid: Folate deficiency
  • if increased methylmalonic acid: B12 deficiency

***both cause megaloblastic macrocytic anemia (so have impaired DNA synthesis and ineffective erythropoiesis = pancytopenia)

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43
Q

Megaloblastic anemia that’s not correctable by vitamin B12 or Folate?

A

–> Orotic Aciduria

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44
Q

Pancytopenia =

A
  • Anemia
  • Neutropenia
  • Thromboctyopenia
45
Q

Fanconi’s anemia

A

DNA repair defect –> get aplastic anemia

NOT the same as Fanconi’s syndrome = proximal tubule reabsorption defect in kidneys!

46
Q

Why anemia in kidney disease?

A

decreased EPO –> decreased hematopoiesis

47
Q

Aplastic anemia

A
  • Pancytopenia

- Normal cell morphology, but hypocellular bone marrow with fatty infiltration

48
Q

Hemolytic anemia in a newborn?

A

Pyruvate kinase deficiency –> decreased ATP –> rigid RBCs

49
Q

HbC defect

A

Glutamic acid-to-lysine mutation

*pts with HbSC (1 of each mutant gene) have milder disease than HbSS pts (full sickle cell)

50
Q

older pt, unexplaned anemia:

A

must rule out colon cancer

51
Q

reversible etiologies of sideroblastic anemia?

A
  • alcohol

- lead

52
Q

what vitamin should be supplemented in vegans/vegetarians?

A

B12 (may get deficiency –> megaloblastic anemia)

53
Q

Hepcidin

A

released by liver, binds ferroportin on intestinal mucosal cells and macrophages
-increased in cases of inflammation: increased hepcidin–>decrease release of iron from macrophages

*this is what happens in anemia of chronic disease: decreased iron, decreased TIBC, increased ferritin

54
Q

decreased iron + decreased TIBC + increased ferritin

A

anemia of chronic disease (inflammation–> increased hepcidin –> decreased release of iron from macrophages

55
Q

Cause of hereditary spherocytosis?

A
  • extravascular intrinsic hemolytic normocytic anemia
  • caused by defect in proteins interacting with RBC membrane skeleton and plasma membrane (ankyrin, band 3, protein 4.2, spectrin)
  • premature removal of RBCs by spleen –> splenomegaly, aplastic crisis; eventually need splenectomy
56
Q

Labs for PNH (paroxysmal nocturnal hemoglobinuria)?

A

increased urine hemosiderin

57
Q

complication of PNH?

A

thrombosis

58
Q

Treatment for sickle cell anemia?

A
  • Hydroxyurea –> increases HbF

- Bone marrow transplant = ultimately

59
Q

Coomb’s positive anemia?

A

autoimmune hemolytic anemia (ie warm agglutinin or cold agglutinin anemias)

60
Q

microangiopathic anemia

A
  • see schistocytes
  • RBCs damaged when passing through obstructed or narrowed vessel lumina
  • see in: DIC, TTP-HUS, SLE, malignant HTN; prosthetic valves, aortic stenosis…
61
Q

rate limiter of heme synthesis?

A

ALA synthase (delta-aminolevulinic acid synthase)

62
Q

effect of heme on ALA synthase activity

A

low heme–> increased ALA synthase

lots of heme–>decreased ALA synthase

63
Q

Rate limiter of heme synthesis

A

ALA synthase (requires B6!)

64
Q

tea-colored urine + blistering cutaneous photosensitivity?

A
  • Porphyria cutanea tarda (most common porphyria)
  • d/t deficiency of Uroporphyrinogen Decarboxylase (needed for heme synthesis); get accumulation of Uroporphyrin (hence the tea-colored urine)
65
Q

painful abdomen + red-wine colored urine + polyneuropathy + psych disturbances; precipitated by drugs:

A

Acute Intermittent Porphyria

  • d/t deficiency of Porphobilinogen Deaminase (aka uroporphyrinogen-I-synthase)
  • accumulate Porphobilinogen, ALA, and uroporphyrin (in urine)
66
Q

Treatment for Acute Intermittent Porphyria?

A

-Glucose and Heme –> inhibit ALA synthase

67
Q

Defect in factors I, II, V, VII, X –>?

A

increased PT (extrinsic pathway defect)

68
Q

Defect in all factors EXCEPT VII and XIII?

A

increased PTT

69
Q

Defects in platelet plug formation?

A

increased BT (bleeding time)

70
Q

Bernard-Soulier disease:

  • defect
  • labs (BT =bleeding time; PC=platelet count)
A

defect in Gp1b–> so vWF can’t bind platelets for platelet plug formation

  • increased BT
  • decreased PC
71
Q

Glanzmann’s thrombasthenia:

  • defect?
  • BT/PC?
A
  • defect in GpIIb/IIIa –> platelets can’t link to eachother, so no platelet aggregation for platelet plug formation
  • increased BT
  • no effect on PC
72
Q

ITP = Idiopathic Thrombocytopenic Purpura:

  • defect?
  • labs?
A
  • defect:have anti-GpIIb/IIIa antibodies–> antibodies bind platelets –> complex gets consumed by splenic macrophages
  • increased BT
  • decreased PC
  • also have increased megakaryocytes (trying to make more platelets!)
73
Q

TTP = Thrombotic Thrombocytopenic Purpura

  • defect?
  • labs?
A

deficiency of vWF metallprotease –> decreased degradation of vWF multimers: so: increased vWF multimers–> increased platelet aggregation and thrombosis–> decreased platelet survival

  • increased BT
  • decreased PC
  • schistocytes
  • increased LDH
74
Q

Affect of aspirin on BT/PC?

A

increased BT
no effect on PC
(like Glanzmann’s)

75
Q

All platelet disorders effects on BT/PC?

A
  • all increase BT

- all decrease PC, except Glanzmann’s

76
Q

most common inherited bleeding disorder?

A

von Willebrand’s disease

77
Q

PC, BT, PT, PTT findings in von Willebrand’s disease?

A
  • increased BT
  • increased or normal PTT (depends on severity)
  • normal PC and PT
78
Q

-treatment for von-Willebrand’s disease?

A

DDAVP = Desmopressin (releases vWF stored in endothelium)

79
Q

PC, BT, PT, PTT findings in DIC?

-other lab findings?

A
  • decreased PC
  • increased BT
  • increased PT
  • increased PTT

-also: schistocytes, increased D-dimers (fibrin split products), decreased fibrinogen, decreased factors V and VIII)

80
Q

Causes of DIC?

A

“STOP Making New Thrombi”

  • Sepsis
  • Trauma
  • Obstetric complications
  • acute Pancreatitis
  • Malignancy
  • Nephrotic syndrome
  • Transfusion
81
Q

Factor V Leiden

A

most common cause of inherited hypercoagulability

-production of mutant factor V, that can’t be degraded by protein C

82
Q

Cryoprecipitate

A

contains fibrinogen, factor, VIII, factor XIII

-used to treat coagulation factor deficiencies (if deficient in fibrinogen or factor VIII)

83
Q

CD30+ and CD15+ cells of B-cell origin?

A

Reed-Sternberg cells

84
Q

Most common Hodgkin’s lymphoma? Prognosis?

A
  • Nodular Sclerosing
  • Excelent prognosis (b/c Lymphocytes»>R-S cells)
  • see collagen banding in lymph node
  • mostly young adults
85
Q

t(8;14) c-myc gene

A

Burkitt’s lymphoma (non-Hodgkin lymphoma; neoplasm of mature B cells)

86
Q

Most common adult non-Hodgkin lymphoma?

A

Diffuse large B-cell lymphoma

–>20% of cases are in kids though

87
Q

t(11;14); affects cyclin D regulatory gene

A

Mantle Cell Lymphoma

-affects older males; poor prognosis

88
Q

t(14;18) bcl-2 overexpression

A
  • Follicular Lymphoma
  • affects adults
  • indolent course, but difficult to cure
  • bcl-2 inhibits apoptosis (normally; it’s a proto-oncogene)
89
Q

Lymphoma caused by HTLV-1?

A

Adult T-cell lymphoma

  • ->adults present with cutaneous lesions
  • ->aggressive
90
Q

Mycosis fungoides/Sezary syndrome

A
  • mature T-cell lymphoma; adults present with cutaneous lesions
  • indolent
91
Q

Bence-Jones protein

A

Multiple Myeloma

-Ig light chains in urine (don’t see on urinalysis though)

92
Q

Rouleaux formation

A

Multiple Myeloma

93
Q

most common primary tumor arising within bone in elderly?

A

Multiple Myeloma

94
Q

CRAB symptoms of Multiple Myeloma:

A
  • hyperCalcemia
  • Renal insufficiency
  • Anemia
  • Bone lytic lesions/Back pain
95
Q

Down syndrome pts: increased risk of which cancers?

A
  • ALL

- AML

96
Q

stains TRAP positive (tartrate-resistant acid phosphatase)

A

Hairy cell leukemia

-mature B-cell tumor in elderly; cells have filamentous, hairlike projections

97
Q

Age group affected by ALL?

A

<15 years old

  • most responsive to therapy
  • may spread to CNS and testes
  • t(12;21) = better prognosis
98
Q

Hallmark of Acute Leukemias?

A
  • lots of blast cells (>20% blasts)

- rapid onset and progression

99
Q

Auer rods

A

AML = t(15;17)

-responds to vitamin A

100
Q

Which leukemia can be treated with Vitamin A?

A

AML

  • t(15;17)
  • auer rods
101
Q

t(9,22), bcr-abl

A

Philadelphia chromosome

  • CML
  • 30-60 yrs old
  • more mature cells (<5% blasts); insidious onset
  • resonds to imatinib = bcr-abl tyrosine kinase inhibitor
102
Q

Imatinib

A

treatment for CML

-inhibits bcr-abl tyrosine kinase

103
Q

Teardrop cell

A

Myelofibrosis

  • ->fibrosis of bone marrow (
  • ->bone marrow is crying because it’s fibrosed :(
104
Q 
JAK2 mutations: positive/negative?
Philadelphia chromosome?
-polycythemia vera
-essential thromboyctopenia
-myelofibrosis
-CML
A
  • JAK2:
  • positive in polycythemia vera, essential thrombocytosis, myelofibrosis
  • negative in CML
  • Philadelphia:
  • only positive in CML
105
Q

thombolytics mechanism? (streptokinase, urokinase, tPA, APSAC)

A

aid conversion of plasminogen–>plasmin, which cleaves thrombin and fibrin clots

106
Q

Affect of aspirin on BT, PT, PTT

A

increased BT

-no effect on PT, PTT

107
Q

Ticlopidine toxicity?

A

-Neutropenia (should monitor CBC during first few months of trtmt)
(Ticlopidine = ADP-receptor blocker, so inhibits platelt aggregation; like Clopidogrel)

108
Q

Drug side effect = tinnitus?

A

Aspirin!

109
Q

Raloxifene vs Tamoxifen: Which is better for osteoporosis prevention?

A
  • both are SERMs
  • ->antagonists in breast (treat breast cancer)
  • ->agonists in bone (bone-building)
  • Tamoxifen may increase risk of endometrial carcinoma, b/c it’s a partial endometrial agonist
  • Raloxifene is an endometrial antagonist, so no increased risk of endometrial carcinoma; so, better choice for osteoporosis trtmnt

FirstAID (24 decks)

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