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Step 1 > Hem Onc > Flashcards

Hem Onc Flashcards

1
Q

What are the platelet receptors for vWF and fibrinogen respectively?

A

vWF - GPIb. Fibrinogen - GPIIb/IIIa

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2
Q

How do reticulocytes show up under Wright-Giemsa stain and why?

A

Blue due to ribosomal RNA presence

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3
Q

What causes the green color in most pus and sputum?

A

Myeloperoxidase from neutrophils (contains heme)

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4
Q

What is the most common cause of hypersegmented PMNs?

A

Folate deficiency

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5
Q

Causes of eosinophilia

A

NAACP. Neoplastic, Asthma, Allergic process, Collagen vascular disease, Parasites

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6
Q

How does induction therapy work?

A

Prevents allergies by inducing blocking antibody (IgG against allergen) by introducing small amounts of allergen over time. Prevents IgE-mast cell interaction

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7
Q

What type of antibodies are anti-AB and anti-Rh respectively?

A

Anti-AB are IgM, anti-rh are IgG

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8
Q

What factor is specifically measured by the PT?

A

VII

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9
Q

What factors does antithrombin inhibit?

A

7, 9, 10, 11, 12

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10
Q

What factors do protein C and S inhibit?

A

5 and 8 (but not 5 leiden)

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11
Q

Between the PT and aPTT which measures the intrinsic pathway and which the extrinsic?

A

PT measures extrinsic, aPTT measures intrinsic

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12
Q

Pathology associated with spur cells (acanthocytes)

A

Liver disease, abetalipoproteinemia

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13
Q

Pathology associated with basophilic stippling

A

Thalassemias, Anemia of chronic disease, Iron deficiency, Lead poisoning (w/ hypochromic microcytic anemia)

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14
Q

Pathology associated with bite cells

A

G6PD deficiency

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15
Q

Pathology associated with schistocytes, helmet cells

A

DIC, TTP/HUS, Traumatic hemolysis

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16
Q

3 causes of DIC

A

Gram negative sepsis, Acute pancreatitis, Burn injury

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17
Q

Common cause of TTP/HUS

A

E Coli 0157 (ask about a recent diarrheal illness)

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18
Q

Pathology associated with teardrop cells

A

Bone marrow infiltration (eg. myelofibrosis)

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19
Q

Pathology associated with target cells

A

HbC, Asplenia, Liver disease, Thalassemia

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20
Q

Pathology associated with Heinz bodies

A

Alpha-thal, G6PD deficiency. Due to oxidation of iron from ferrous to ferric denaturing hemoglobin

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21
Q

Pathology associated with Howell-Jolly bodies

A

Function hyposplenia or asplenia. Due to basophilic nuclear remnants in RBCs

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22
Q

Types of alpha thalassemias

A

4 gene deletion - Hb Barts (g4) is incompatible with life. 3 gene deletion - HbH disease (b4). 1-2 gene deletion - no significant anemia

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23
Q

How do you confirm the diagnosis of b-thal minor?

A

Increased HbA2 (>3.5 percent) on electrophoresis

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24
Q

What is increased in major and minor b-thal?

A

HbF

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25
Q

X-ray finding in b-thal major

A

Crew cut skull x-ray (marrow expansion). Also Chipmunk facies

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26
Q

What heme synthesis enzymes are inhibited by lead?

A

ALA dehydratase and ferrochelatase

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27
Q

Lines on gingivae and epiphyses on x-ray, encephalopathy and erythrocyte basophilic stippling, abdominal colic, sideroblastic anemia, wrist and food drop

A

Lead poisoning

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28
Q

Treatment for lead poisoning

A

EDTA and Dimercaprol. Succimer for kids

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29
Q

Defect and genetics in sideroblastic anemia

A

X-linked defect in gamma-ALA synthase. Can also be caused by alcohol and lead. Will find increased iron, normal TIBC, increased ferritin

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30
Q

Treatment for sideroblastic anemia

A

Pyridoxine (B6)

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31
Q

What leads to thalassemias?

A

Mutations that cause defective mRNA processing (a mutation 3 bases upstream of start codon interferes w mRNA binding to ribosome)

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32
Q

How do you distinguish folate deficiency from B12 deficiency.

A

B12 will come with neuro signs. Also, normal methylmalonic acid in folate def, but increased in B12 def

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33
Q

What compound is found in increased levels in both folate and B12 deficiency?

A

Homocysteine

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34
Q

What are the main spinal cord areas targeted by B12 deficiency?

A

Posterior columns (vibration/proprio) and lateral corticospinal tract (spasticity)

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35
Q

How do you distinguish B12 deficiency from tabes dorsalis?

A

Lateral corticospinal tract affected in B12 deficiency but not in tabes dorsalis

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36
Q

A few drugs that cause nonmegaloblastic macrocytic anemia (3)

A

5-FU, AZT, hydroxyurea

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37
Q

Findings in intravascular hemolysis

A

Decreased haptoglobin, increased LDH, hemoglobin in urine

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38
Q

Findings in extravascular hemolysis

A

Increased LDH and increased unconjugated bilirubin

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39
Q

How do you calculate corrected reticulocyte count?

A

(Hct / 45) x [Retic Count]. If polychromasia present, divide result by 2

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40
Q

What is the main regulator of iron in the body?

A

Hepcidin

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41
Q

Major causes of aplastic anemia

A

Benzene, chloramphenicol, alkylating agents, antimetabolites, parvo B19, EBV, HIV, HCV, Fanconis anemia, Immune mediated (often follows acute hepatitis)

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42
Q

Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection

A

Aplastic anemia

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43
Q

What GI related effect does hemolytic anemia predispose to?

A

Pigmented gallstones

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44
Q

What test would you run (besides a CBC) if you suspect spherocytosis and what would be the result?

A

Osmotic fragility. RBCs will lyse in hypotonic saline

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45
Q

Treatment for hereditary spherocytosis

A

Splenectomy

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46
Q

Genetics of G6PD deficiency

A

X-linked

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47
Q

Back pain with hemoglobinuria a few days later. RBCs with heinz bodies and bite cells

A

G6PD deficiency

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48
Q

Cause of intrinsic hemolytic normocytic anemia in newborn (and most common associated finding)

A

Pyruvate kinase deficiency. Will find splenic hypertrophy from increased work

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49
Q

What substitution gives HbC?

A

Glutamic acid to lysine at position 6

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50
Q

Labs and complications of PNH

A

Increased urine hemosiderin. Complications - thrombosis

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51
Q

What substitution causes HbS?

A

Glutamic acid for valine at position 6

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52
Q

X-ray findings of sickle cell anemia

A

Crew cut

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53
Q

What is the immediate effect of an HbS mutation?

A

Hydrophobic interactions among hemoglobin molecules with HbS are altered

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54
Q

What causes autosplenectomy in sickle cell patients?

A

Vascular occlusion in the spleen

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55
Q

Most common complications of sickle cell related to microorganisms

A

Aplastic crisis (parvo B19) and osteomyelitis (salmonella, followed by s aureus and e coli)

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56
Q

How do children with sickle cell often present?

A

Dactylitis (painful swelling of the hand)

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57
Q

How would kidney problems in a sickle cell patient present

A

Either rapid onset hematuria (renal papillary necrosis) or microhematuria (medullary infarcts)

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58
Q

Treatment for sickle cell and how it helps

A

Hydroxyurea increases HbF. Give oxygen in crises. Last resort is bone marrow transplantation

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59
Q

Put the following in order of how far they travel on electrophoresis: HbA, HbC, HbS

A

(Least far to farthest) HbC, HbS, HbA

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60
Q

What composes warm agglutinins and what conditions are they seen in?

A

IgG. SLE, CLL, alpha-methyldopa and other drugs

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61
Q

What composes cold agglutinins and in what conditions are they seen

A

IgM. CLL, Mycoplasma pneumonia, infectious mono

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62
Q

Conditions in which microangiopathic anemia is seen

A

DIC, TTP-HUS, SLE, malignant hypertension. Will see schistocytes

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63
Q

Iron studies in pregnancy/OCP use

A

Serum iron nl, Transferrin up, Ferritin nl, Transferrin sat down

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64
Q

Iron findings in lead poisoning

A

Serum iron up, transferrin down, ferritin nl, transferrin sat up

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65
Q

What gene is mutation in PNH?

A

PIG-A (a GPI anchor)

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66
Q

In what condition will a CD55/CD59 deficiency be seen?

A

PNH (GPI anchor is necessary for CD55/59 attachment)

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67
Q

Hemolytic anemia, hypercoagulability, decreased blood counts

A

Suspect PNH

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68
Q

Headache, memory loss, demyelination

A

Lead poisoning (adult)

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69
Q

Defect in AIP

A

Porphobilinogen deaminase (aka uroporphyrinogen-I-synthase)

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70
Q

What is the rate limiting step in heme synthesis?

A

ALA synthase (first step). Defective in x-linked sideroblastic anemia

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71
Q

Painful abdomen, red-wine colored urine, polyneuropathy, psychologic disturbances, recent medication change.

A

AIP

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72
Q

What is the treatment for AIP?

A

Glucose and heme (they inhibit ALA synthase)

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73
Q

Defect in porphyria cutanea tarda

A

Uroporphyrinogen decarboxylase

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74
Q

Blistering cutaneous photosensitivity

A

Porphyria cutanea tarda (the most common porphyria)

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75
Q

List the substance that accumulates in each of the following - lead poisoning, AIP, porhyria cutanea tarda

A

Lead poisoning - protoporhyrin (in blood), AIP - porphobilinogen, ALA uroporphyrin (in urine), PCT - uroporphyrin (tea-colored urine)

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76
Q

Defect and genetics in Hemophilia A and B

A

X-recessive. A - 8, B - 9

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77
Q

Bleeding studies in hemophilia A and B

A

Increased PTT, normal PT, normal bleeding time

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78
Q

Defect and labs in Bernard-Soulier disease

A

Defect in platelet plug formation due to decreased GP1b (platelets cant bind vWF). Decreased platelet count, increased bleeding time

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79
Q

Defect and labs in Glanzmanns thrombasthenia

A

Decreased GpIIb/IIIa leads to defect in platelet-to-platelet aggregation. No change in platelet count, increased BT

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80
Q

Defect and labs in ITP

A

Anti-GPIIb/IIIa antibodies (platelet-Ab complex consumed by splenic macrophages). Decreased platelet count, increased bleeding time, increased megakaryocytes

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81
Q

Defect and labs in TTP

A

Deficiency of ADMTS13 leads to decreased degradation of vWF multimers (increased platelet aggregation and thrombosis). Low platelet count, high BT, schistocytes, high LDH

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82
Q

Neurologic and renal symptoms, fever, thrombocytopenia, microangiopathic hemolytic anemia

A

TTP

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83
Q

What bleeding abnormalities would be found in patients who have missed their dialysis a while and why?

A

Very long BT with normal platelet count, PT, and PTT. Uremia causes qualitative platelet d/o

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84
Q

vWF disease primarily affects binding of what to what?

A

Platelets to collagen (due to decreased levels of vWF)

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85
Q

Treatment for vWF disease and why

A

DDAVP. Releases vWF stored in endothelium

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86
Q

Labs in vWF disease

A

PC normal, BT high, PT normal, PTT normal or high

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87
Q

Labs in DIC

A

PC low, BT high, PT high, PTT high

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88
Q

Causes of DIC (7)

A

Sepsis, Trauma, Obstetric complications, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion

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89
Q

What is the most common cause of inherited hypercoagulability and how does the defect cause a problem?

A

Factor V Leiden. It cannot be degraded by protien C

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90
Q

What deficiency increases the chance of thrombotic skin necrosis after warfarin administration?

A

Protein C or S deficiency

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91
Q

How do you distinguish leukemia from leukemoid reaction?

A

High leukocyte alkaline phosphatase in leukemoid reaction

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92
Q

Which lymphoma is a localized single group of nodes with contiguous spread?

A

Hodgkins

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93
Q

Which lymphoma includes B symptoms most often

A

Hodgkins

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94
Q

Which lymphoma involves noncontiguous spread?

A

NHL

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95
Q

What is the relationship of Reed-Sternberg cell presence to diagnosis of Hodgkins?

A

Necessary but not sufficient

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96
Q

List the types of Hodgkins lymphoma from best prognosis (also most common) to worst prognosis (also least common)

A

Nodular sclerosing (most common, best prognosis), Mixed cellularity, Lymphocyte predominant, Lymphocyte depleted (least common, worst prognosis)

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97
Q

Starry sky appearance

A

Burkitts lymphoma. Due to lymphocytes interspersed with macrophages

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98
Q

What is the most common NHL and in whom does it usually occur?

A

Diffuse large B-cell. Usually older adults, but 20 percent in children

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99
Q

Mantle cell lymphoma marker and epidemiology

A

Older males, CD5 positive

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100
Q

What parts of the world are most affected by adult t-cell lymphoma and what is the causal agent?

A

HTLV-1. Japan, West Africa, Caribbean

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101
Q

What is the marker with mycosis fungoides/Sezary and how does it present?

A

CD4+. May present with cutaneous patches/nodules

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102
Q

Hypercalcemia, constipation, renal insufficiency, anemia, fatigue, back pain

A

Multiple myeloma (will also see lytic bone lesions)

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103
Q

What will you find in the kidney with multiple myeloma?

A

Atrophic tubules and eosinophilic casts

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104
Q

Bence Jones protein

A

Ig light chains in the urine. Usually have a Kappa-Kappa configuration

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105
Q

Markers in ALL

A

CALLA and TdT+

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106
Q

Mediastinal mass causing respiratory symptoms and SVC syndrome in a child

A

Consider ALL

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107
Q

What yields a better prognosis in ALL?

A

t(12,21)

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108
Q

What lymphoma and leukemia are the same disease and what is the difference between them?

A

Small Lymphocytic Lymphoma and CLL. CLL has increased peripheral blood lymphocytosis

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109
Q

Marker for hairy cell leukemia

A

TRAP

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110
Q

Auer rods

A

AML (common APL which is M3). Release leads to DIC

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111
Q

Treatment for APL (AML M3)

A

ATRA (vitamin A) induces differentiation of myeloblasts

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112
Q

CML translocation (give chrosomes and genes)

A

t(9,22). BCR-ABL

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113
Q

Burkitts translocation (give chrosomes and genes)

A

t(8,14). C-Myc activation

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114
Q

Follicular lymphoma translocation (give chrosomes and genes)

A

t(14,18). BCL-2 Activation

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115
Q

APL (AML M3) translocation (give chrosomes and genes)

A

t(15,17)

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116
Q

Ewings sarcoma translocation (give chrosomes and genes)

A

t(11,22)

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117
Q

Mantle cell lymphoma translocation (give chrosomes and genes)

A

t(11,14)

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118
Q

Markers in Langerhans cell histiocytosis (LCH)

A

S-100 and CD1a

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119
Q

What are JAK2 mutations associated with?

A

Chronic myeloproliferative disorders

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120
Q

What types of cells are increased in polycythemia vera?

A

RBCs, WBCs and platelets

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121
Q

Causes of ectopic erythropoietin (5)

A

RCC, Wilms tumor, cyst, HCC, hydronephrosis

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122
Q

Enoxaparin

A

Low molecular weight heparin. Act more on Xa, better bioavability, 2-4x longer half life. No monitoring necessary but not easily reversible

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123
Q

How does HIT work?

A

Heparin binds platelet factor IV causing antibody production which binds and activates platelets

124
Q

Lepirudin and Bivalirudin

A

Direct thrombin inhibitors

125
Q

Which one crosses the placenta, heparin or warfarin?

A

Warfarin. (Just remember that heparin is natural to the body, so it cant cause problems in pregnancy)

126
Q

Fondaparineux

A

Pentasaccharide Xa inhibitor

127
Q

Streptokinase

A

Thrombolytic

128
Q

APSAC (anistreplase)

A

Thrombolytic

129
Q

What change in the platelet count do thrombolytics cause?

A

None

130
Q

What do you treat thrombolytic toxicity with?

A

Aminocaproic acid (an inhibitor of fibrinolysis)

131
Q

What effect does aspirin have on blood studies?

A

Increased BT, no change in PT or PTT

132
Q

Clopidogrel and Ticlopidine

A

Irreversibly block ADP receptors and inhibit platelet aggregation. Prevent IIb/IIIa expression.

133
Q

What hematologic drug has a side effect that may present with fever and mouth ulcers?

A

Ticlopidine (neutropenia)

134
Q

Cilostazol and dipyridamole

A

PDE III inhibitor (increased cAMP in platelets inhibits aggregation). Also vasodilate

135
Q

Abciximab

A

Monoclonal antibody to IIb/IIIa receptor

136
Q

Anticancer drugs acting on the S phase

A

Antimetabolites and etoposide

137
Q

Anticancer drugs acting on the G2 phase

A

Etoposide and Bleomycin

138
Q

Anticancer drugs acting on the M phase

A

Vinca alkaloids and taxols

139
Q

What do you give to reverse methotrexate effects?

A

Leucovorin

140
Q

What do you give to reverse 5-FU effects?

A

Thymidine (not leucovorin)

141
Q

Cytarabine (ara-C)

A

Pyrimidine analog (inhibits DNA pol)

142
Q

Dactinomycin

A

Intercalates DNA. Use in childhood tumors

143
Q

Doxorubicin and daunorubicin

A

Generates free radicals, intercalates DNA. Use in Hodgkins. Cardiotoxicity (prevent with dexrazoxane), alopecia

144
Q

Bleomycin

A

Free radical formation, DNA breaks. Pulmonary fibrosis, skin changes

145
Q

Etoposide, teniposide

A

Inhibits topoisomerase II (causes DNA degradation). Myelosuppression, GI irritation, alopecia

146
Q

Cyclophosphamide and ifosfamide

A

X-link DNA. Bioactivation by liver. Prevent hemorrhagic cystitis with mesna (binds metabolite)

147
Q

Carmustine, lomustine, semustine, streptozocin

A

Alkylating agents. GBM. Dizziness, ataxia

148
Q

Busulfan

A

Alkylating agent. CML. Pulmonary fibrosis, hyperpigmentation

149
Q

Vincristine and Vinblastine

A

Block MT polymerization. Neurotoxic and paralytic ileus (vincristine), myelosuppression (vinblastine)

150
Q

Paclitaxel (and other taxols)

A

Hyperstabilize MTs. Ovarian and breast carcinomas. Myelosuppression and hypersensitivity

151
Q

Cisplastin, carboplatin

A

Alkylating-like agents. Cross link DNA. Nephrotoxic (prevent with amifostine), acoustic nerve damage, chloride diuresis

152
Q

What is the most commonly used glucocorticoid in cancer chemotherapy

A

Prednisone (may induce apoptosis)

153
Q

Tamoxifen and raloxifene

A

SERMs. Antagonists in breast and agonists in bone. May increase risk of endometrial ca (tamoxifen)

154
Q

Trastuzumab

A

Antibody to Her-2. Cardiotoxicity

155
Q

Imatinib

A

BCR-ABL inhibitor. Fluid retention

156
Q

Most common chemotherapy causing cardiotoxicity

A

Doxorubicin

157
Q

Most common chemotherapy causing myelosuppression

A

5-FU, 6-MP and Methotrexate

158
Q

Aput tumors

A

S-100 positive. Melanoma, small cell of lung, bronchial carcinoid, carcinoid tumor, neuroblastoma

159
Q

Young girl with necrotic mass coming out of her vagina. Vimentin and keratin negative, desmin positive.

A

Embryonal rhabdomyosarcoma (most common sarcoma of children)

160
Q

What type of tumor tends to be found in the midline?

A

Teratomas

161
Q

Most common site for lymphomas not in a lymph node

A

Stomach (H pylori)

162
Q

Most common lymphoma

A

Follicular B cell

163
Q

What is the presentation of hydatidiform moles and when do they present?

A

First trimester, signs of preeclampsia (HTN, proteinuria, edema)

164
Q

Which type of hydatidiform mole can progress to cancer and what type of cancer?

A

Complete (46XX), choriocarcinoma. Partial (69 chromosomes) does not progress to cancer

165
Q

Which vessel in the fetus has the highest O2 concentration?

A

Umbilical vein

166
Q

What is seen in a hydatidiform mole that is not seen in a choriocarcinoma?

A

Chorionic villus

167
Q

What hormones does the synctiotrophoblast (or a hydatidiform mole or choriocarcinoma) secrete?

A

B-hCG and hPL

168
Q

Choristoma

A

Heterotopic tissue (i.e. pancreatic tissue in the GI tract)

169
Q

How many doubling times does it take to get a tumor that can be detected clinically?

A

About 30 doublings

170
Q

What types of cancer tend to spread to lymph nodes before going hematogenous?

A

Carcinomas (sarcomas can go directly hematogenous)

171
Q

What carcinoma breaks the rule and goes directly hematogenous (without stopping in a lymph node first)?

A

Follicular carcinoma of the thyroid

172
Q

In what organ is primary cancer more common than metastasis?

A

Kidney (renal adenocarcinoma)

173
Q

What lab abnormality will likely be seen in metastasized prostate cancer?

A

Increased alkaline phosphate (because prostate carcinoma is blastic to bone)

174
Q

What is seen on EM of a vascular malignancy?

A

Wibble palad bodies (have vWF in them)

175
Q

Steps in oncogenesis (and define each)

A

Initiation (mutation), Promotion (multiple copies of mutation are made), Progression (sub-specialization)

176
Q

What type of mutation is responsible for loss of function in all TS genes?

A

Point mutation

177
Q

Why is hepatocellular carcinoma common in Asia?

A

Because hepatitis B and aflatoxin (aspergillus) are common

178
Q

What is the cause of the rapidly increasing incidence of primary CNS lymphoma?

A

HIV

179
Q

Associations with UVA and UVB light

A

UVA - black light (contributes to skin cancer indirectly, less dangerous), UVB - skin cancers (basal cell, squamous cell, melanoma), UVB - thymidine dimers

180
Q

What metal is associated with skin cancer?

A

Arsenic

181
Q

Most common cause of white eye reflex

A

Congenital cataract (CMV, rubella, corticosteroids, Cushings). Rb is notable, but less common

182
Q

What is the basic rule for BCC and SCC?

A

Upper lip and above is BCC, lower lip and down is SCC

183
Q

What is the only bacterium associated with cancer?

A

H pylori

184
Q

What is the general rule for colon cancer symptoms?

A

Left side obstructs, right side bleeds (watch for anemia with right side)

185
Q

What can metastasize to virchows node besides gastric cancer?

A

Pancreatic

186
Q

Trousseaus sign

A

Superficial migratory thrombophlebitis due to carcinoma of the head of the pancreas

187
Q

Two common hematologic findings in cancer patients

A

Hypercoagulability and thrombocytosis

188
Q

Most common cause of fever in cancer patients

A

Gram negative infection (e coli from indwelling catheter, pseudomonas from respirator, also s aureus from catheter even though its gram positive)

189
Q

What is the most common paraneoplastic syndrome?

A

Hypercalcemia

190
Q

Cancers that PTHrP

A

Squamous of the lung and RCC

191
Q

What are two skin signs that if they show up quickly might signal cancer, and which cancer do they signal?

A

Acanthosis nigricans and seborrheic keratosis. Quick development may signal gastroadenocarcinoma

192
Q

What collagen vascular disease is associated with cancer and which cancers?

A

Dermatomyositis - leukemia, lymphoma and lung cancer. Can get patches on knuckles (goltrins patches)

193
Q

What endocarditis is associated with cancer and which cancers?

A

Marantic (nonbacterial thrombotic) endocarditis. Mucuous producing cancers (eg colon). Be careful, they can embolize

194
Q

What tumor can convert calcitonin to amyloid?

A

Medullary carcinoma of the thyroid

195
Q

What tumors is AFP associated with?

A

Yolk sac tumor and HCC

196
Q

How can CEA (marker for colon cancer) cause problems outside the colon?

A

CEA-Ag complexes can deposit in the kidney and cause diffuse membranous glumerulonephritis (a nephrotic syndrome)

197
Q

Most common benign and malignant primary CNS tumors in kids

A

Benign - cerebellar cystic astrocytoma (most common overall), malignant - medulloblastoma

198
Q

Most common cancers in men and women respectively

A

Men - prostate, lung, colon. Women - breast, lung, colon

199
Q

Most common infection transmitted by accidental needle stick in the hospital

A

Hepatitis B

200
Q

How long does it take after anemia develops to get an elevated reticulocyte count?

A

5-7 days

201
Q

What is the cutoff for an expected reticulocyte count in anemia?

A

Corrected retic count should be 3 percent or greater

202
Q

What is the most common cause for failure of the Hb and Hct to go up sufficiently after transfusion?

A

GI bleed (which is most common cause of anemia worldwide)

203
Q

Where are iron, folate and B12 absorbed respectively?

A

Iron - Duodenum, Folate - jejunum, B12 - terminal ileum

204
Q

What is the most common cause of malabsorption and what areas does it affect?

A

Celiac sprue. Duodenum and jejunum

205
Q

What finding on a blood smear is an important marker for alcoholism?

A

Target cells (due to altered cholesterol concentration)

206
Q

What is the relationship between transferrin and TIBC?

A

They are the same

207
Q

What determines the number of cell divisions an RBC precursor undergoes when developing in the marrow?

A

Hb concentration

208
Q

4 globins and the 3 normal hemoglobins

A

Globins - A, B, D, G. HbA is 2A2B, HbA2 is 2A2D, HbF is 2A2G

209
Q

Whats the best way to distinguish between IDA and anemia of chronic disease?

A

ACD - high ferritin levels, IDA - high TIBC (transferrin)

210
Q

What is the inhibitory neurotransmitter in the spinal cord?

A

Glycine

211
Q

3 causes of sideroblastic anemias

A

Alcohol, Vitamin B6 deficiency, Lead poisoning

212
Q

EM findings in alcoholism

A

Megamitochondria (alcohol is an uncoupling agent and screws up mitochondria)

213
Q

What causes a ringed sideroblast?

A

Iron that enters the mitochondria but cant get out (because its not properly assembled into heme)

214
Q

Primary populations for alpha thalassemia

A

Far easterners and blacks

215
Q

What will be the results of Hb electrophoresis in alpha thalassemia?

A

Normal. Alpha globin is required in all the normal hemoglobins (HbA, HbA2 and HbF) so they are all equally decreased

216
Q

Why is the rate of choriocarcinoma high in the far east?

A

Because the higher incidence of alpha-thal leads to spontaneous abortion (Hb Barts) which predisposes to choriocarcinoma

217
Q

Treatment for alpha thalassemia

A

None. Do not give iron

218
Q

Populations in which beta thal is common

A

Blacks, greeks, italians

219
Q

What will you see on Hb electrophoresis in beta thal?

A

Decrease in HbA, increase in HbA2 and HbF

220
Q

Most common cause of iron deficiency anemia in a newborn

A

Bleeding meckels diverticulum

221
Q

What causes cerebral edema in lead poisoning?

A

Buildup of delta-lemavinylinic acid

222
Q

Common lead poisoning scenarios

A

Child - eating paint. Adults - automobile shop (batteries), moonshine (made in old radiator), pottery painter (lead based paint)

223
Q

Iron studies in alpha and beta thal

A

Serum iron - normal, TIBC - high, Saturation - high, Ferritin - high

224
Q

What are the two main jobs of B12?

A

Transfer methyl group from folate to homocysteine (to make methionine) and helping with odd chain FA metabolism

225
Q

How does B12 deficiency lead to neurologic symptoms?

A

Succinyl CoA builds up (failure of odd chain FA metabolism) and screws up myelin

226
Q

What drug inhibits intestinal conjugase and what is the effect of this?

A

Phenytoin. This significantly reduces folate absorption (conjugase has to turn polyglutamate to monoglutamate folate)

227
Q

What two substances inhibit folate absorption?

A

OCPs and alcohol

228
Q

How many lobes does a PMN have to have to be called hypersegmented?

A

5 or more

229
Q

Drugs that cause aplastic anemia

A

Chloramphenical, indomethacin, phenylbutazone, thyroid drugs

230
Q

Do you get hemoglobinuria in intravascular hemolysis, extravascular hemolysis, or both?

A

Intravascular only

231
Q

Which type of hemolysis more typically produces jaundice, intravascular or extravascular?

A

Extravascular

232
Q

Most common causes of intrinsic hemolysis

A

MAD. Membrane defect (spherocytosis, PNH), Abnormal Hb (SC), Deficiency of enzyme (G6PD)

233
Q

In sickle cell disease, what percentage of a cells hemoglobin has to be sickled for the cell to sickle?

A

60 percent

234
Q

What is the most common cause of death in a child with sickle cell disease

A

Strep pneumo sepsis

235
Q

At what age does sickle cell disease typically present?

A

6-9 months

236
Q

Two x linked recessive enzyme deficiences

A

G6PD and Lesch-Nyhan

237
Q

What damages the RBCs in G6PD deficiency and what blood smear finding does it cause?

A

Peroxide damages hemoglobin, leading to Heinz bodies (Hb clumped together)

238
Q

What populations is G6PD typically seen in?

A

Same populations as beta thal - blacks, Greeks, Italians

239
Q

Two drugs most commonly used in G6PD questions

A

Primaquine and dapsone

240
Q

Which is more common, warm or cold agglutinins and what is the most common cause of it?

A

Warm. Most common cause is lupus

241
Q

Hypersensitivity reactions to penicillin

A

Rash - Type 1. Hemolytic anemia - Type 2

242
Q

How does methyldopa lead to hemolytic anemia?

A

It alters Rh antigens on RBCs and we end up making antibodies against our own Rh antigens

243
Q

How does quinidine lead to hemolytic anemia?

A

It forms immune complexes with IgM

244
Q

Three main drug induced autoimmune hemolytic anemias and the hypersensitivity type for each

A

PCN - type 2 (but rash is type 1), Methyldopa - type 2, Quinidine - type 3

245
Q

What is the most common cause of chronic intravascular hemolysis

A

Aortic stenosis

246
Q

What infection in kids can lead to such high WBC counts that we get concerned it might be ALL?

A

Pertussis. Viral infections can also do it

247
Q

What do we associated with atypical lymphocytes?

A

Mononucleosis - EBV

248
Q

What drug is associated with atypical lymphocytes?

A

Phenytoin

249
Q

What receptor does EBV use to infect B cells?

A

CD21

250
Q

Generalized painful lymphadenopathy, exudative tonsilitis, very high transaminases, spleen enlargement

A

EBV mono. Also get jaundice sometimes and spleen can rupture (no contact sports)

251
Q

What does the heterophile antibody test use and what does it test for?

A

Uses anti-horse or anti-sheep RBC antibodies to test for EBV mono

252
Q

What helminth infection does not cause eosinophilia?

A

Adult ascariasis (because they stick to the intestine and do not invade)

253
Q

Which leukemia is also a myeloproliferative disease?

A

CML

254
Q

Most common complication of polycythemia rubivera

A

Thrombosis (most commonly Budd-Chiari)

255
Q

4 Hs of polycythemia rubivera

A

Hyperviscosity, Hypovolemia, Histaminemia, Hyperuricemia

256
Q

A patient takes a shower and gets itchy all over his or her body

A

Polycythemia rubivera (the increased numbers of mast cells and basophils hang out in skin and degranulate more easily)

257
Q

What distinguishes between acute and chronic leukemia

A

Blasts less than 30 percent is chronic, greater than 30 percent is acute

258
Q

Leukemia in ages 0-14

A

ALL

259
Q

Leukemia in ages 15-39

A

AML

260
Q

Leukemia in ages 40-59

A

AML or CML (separate with bone marrow looking for blasts or philadelphia chromosome)

261
Q

Leukemia in 60 and over

A

CLL

262
Q

What stain can tell the difference between mature neutrophils and neoplastic neutrophils

A

Leukocyte Alkaline Phosphatase (LAP). Mature will take it up, neoplastic will not

263
Q

Kid with sternal tenderness, fever, generalized nontender lymphadenopathy, hepatosplenomegaly, normocytic anemia, WBC count 50,000

A

ALL. Most commonly CD10+, CALLA+. May be associated with Downs

264
Q

Elderly patient, smudge cells, normocytic anemia, hypogammaglobulinemia

A

CLL. High risk of infection (most common cause of death in CLL)

265
Q

What two tissues are resistant to invasion by cancer cells?

A

Cartilage and elastic tissue

266
Q

Langerhans cell histiocytosis looks like a tennis raquet on EM. What else has this look on EM?

A

Clostridium tetani spores

267
Q

Where in the lymph nodes are macrophages usually found?

A

In the sinuses

268
Q

Reed sternberg cells have an Owls eye appearance. What else has this appearance?

A

Giardia, CMV, aschoff nodules in rheumatic fever

269
Q

Woman with mass in anterior mediastinum and neck. Fatigue, night sweats, weight loss.

A

Nodular Sclerosing Hodgkins. Look for RS cells, be sure to rule out TB if she has a cough

270
Q

What do pts with Pompe disease typically die of?

A

Cardiac failure due to excess deposition of normal glycogen in the heart

271
Q

What do OCPs do that makes them thrombogenic

A

Increase synthesis of factors 5 and 8, increase synthesis of fibrinogen, inhibit antithrombin 3

272
Q

How does smoking lead to thrombogenesis?

A

Damages endothelial cells (exposing collagen to the clotting system)

273
Q

Where is vWF made?

A

Megakaryocytes and endothelial cells

274
Q

What are the effects of PGI2 and TXA2 respectively on blood vessel diameter?

A

PGI2 is a vasodilator, TXA2 is a vasoconstrictor

275
Q

What is the main vasoconstrictor in Prinzmetals angina?

A

TXA2

276
Q

Both platelets and mast cells when activated release a preformed chemical then start making chemicals. What are these substances (give the preformed and manufactured for each platelets and mast cells)?

A

Platelets - preformed is ADP (and others), manufactured is TxA2. Mast cells - preformed is histamine (and 5HT and eosinophil chemotactic factor), manufactured is PGs and leukotrienes

277
Q

Are petechia, echymoses, and epistaxis more characteristic of platelet or coagulation abnormalities?

A

Platelet

278
Q

What procedure imposes the greatest hemostatic stress on the body?

A

Wisdom tooth extraction (good question to screen for coagulation disorders)

279
Q

What is the test for vWF disease?

A

Ristocetin cofactor assay (ristocetin wont cause platelets to clot if missing vWF)

280
Q

Factors of the common final pathway (in order)

A

10, 5, 2, 1

281
Q

Factors of the intrinsic pathway (in order)

A

12, 11, 9, 8. Then common final pathway (10, 5, 2, 1)

282
Q

Best test for DIC

A

D-dimer. Next best is fibrin split products

283
Q

How can you tell the difference between petechia and spider angioma (telangiectasia) on physical exam?

A

Petechia do not blanch but spiger angiomas will (because its an AV fistula)

284
Q

Kid with epistaxis and spots that do not blanch. Low platelet count

A

ITP

285
Q

Treatment for ITP

A

Cotricosteroids if severe, if not severe just leave it alone

286
Q

Two main causes of HUS

A

E coli O157H7 and Shigella toxin

287
Q

Main differences between vWF disease and Hemophilia A

A

1) Genetics (hemophilia A is XR and vWF is AD), 2) Number of deficiencies (hemophilia A its only 8 anticoagulant, vWF it is 8 Ag, 8 anticoagulant, and vWF), 3) vWF includes symptoms of platelet dysfunction

288
Q

Why is vWF disease often underdiagnosed in women?

A

Because OCPs cause increased synthesis of 8 Ag, 8 anticoagulant and vWF (the things deficient in vWF disease), which can mask the disease

289
Q

What is the difference between anti-AB and anti-A/anti-B?

A

Anti-AB is IgG whereas anti-A and anti-B are IgM

290
Q

Diseases associated with AB blood groups

A

A - gastric cancer, O - duodenal ulcer

291
Q

What antigen is missing in the black population which makes them less likely to get a malaria and which malaria?

A

Duffy antigen, reduces chances of getting plasmodium vivax

292
Q

G6PD, thalassemias, and SCD protect from which malaria?

A

Plasmodium falciparum

293
Q

What is the most common antibody in the US?

A

Anti-CMV

294
Q

What is the most common infection transmitted by blood transfusion?

A

CMV

295
Q

What is the most common type of hepatitis picked up from transfusion?

A

Hep C

296
Q

What causes febrile transfusion reactions?

A

HLA antibodies against leukocytes in donor blood

297
Q

Who is most at risk for febrile reaction with transfusion?

A

1) Patients who have been transfused before many times. 2) Women (may have picked up HLA Abs from fetal-maternal bleed)

298
Q

Which Ig is the most potent complement activator?

A

IgM. It will activate straight C1-C9 and you will get a MAC. Eg. hemolytic transfusion reactions (if wrong blood type given) happen very fast due to IgM

299
Q

What cells are responsible for delayed hemolytic transfusion reactions?

A

Memory B cells. Antibodies arent detected on cross-match because the memory B cells are dormant. But once they see an Ag on the transfused blood they start making Ab again

300
Q

Woman with a difficult delivery (abruptio placenta) one week ago returns with jaundice, anemia, and uncojugated hyperbilirubinemia

A

Delayed hemolytic transfusion reaction (assuming she was transfused)

301
Q

If someone has serious surgery and returns with jaundice how can you separate delayed hemolytic transfusion reaction from halothane and from hepatitis?

A

Delayed hemolytic transfusion - about 1 week, halothane - over a week, hepatitis - 6 to 8 weeks

302
Q

What type of hypersensitivity is involved in delayed hemolytic transfusion reactions?

A

Type 2

303
Q

Most common cause of jaundice in first 24 hours for a newborn

A

ABO incompatibility (physiologic jaundice of newborn starts at day 3)

304
Q

If a baby has ABO incompatability, what blood group must the mom be?

A

O (because anti-AB is the only one that is IgG and thus the only one that can cross the placenta)

305
Q

Which leads to a more serious hemolytic anemia, ABO incompatibility or Rh incompatibility?

A

Rh

306
Q

What other condition protects against Rh sensitization and how?

A

ABO incompatability. If fetal blood is both Rh and ABO incompatible and there is maternal fetal bleed at birth the anti-A and anti-B IgM will destroy cells so fast there wont be time for anti-Rh sensitization

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