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UWorld Journal > Heme and Onc > Flashcards

Heme and Onc Flashcards

1
Q

complications of lead poisoning

A
  • neurologic (cognitive impairment, irritability)
  • GI (constipation, abdominal pain)
  • renal (interstitial nephritis)
  • hematologic (anemia)
  • lead lines on gingivae (Burton lines) and on metaphyses of long bones on x-ray
  • erythrocyte basophilic stippling
  • drops-wrist and foot drop
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2
Q

most of the cutaneous lymph from the umbilicus down, including the anus below the dentate line, drains to the ______________

A

superficial inguinal lymph nodes

exceptions: glans penis and posterior calf, which drain to the deep inguinal nodes

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3
Q

sickle cell patients have increased risk for bacteriemia due to

A

Streptococcus pneumoniae and Hemophilus influenza

because these patients become functionally asplenic

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4
Q

function of hepcidin

A

polypeptide synthesized by liver that acts as the central regulator of iron homeostasis

low hepcidin levels increase intestinal iron absorption and stimulate iron release by macrophages

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5
Q

what is the Kozak consensus sequence

A

occurs on eukaryotic mRNA and defined as: (gcc)gccRccAUGG, R is either adenine or guanine

sequence helps initiate translation at the methionine start codon (AUG)

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6
Q

appearance of RBC in beta thalassemia

A

hypochromic, microcytic anemia

-increased central pallor, anisopoikilocytosis (variation in size and shape), target cells, tearrop cells, nucleated red cell precursors, and basophilic stippling

unpaired alpha chains precipitate within red cells and cause membrane damage, leading to ineffective erythropoiesis and extravascular hemolysis

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7
Q

how come hepatitis B can integrates its DNA into the host genome but hepatitis C can’t

A

because hep C is an RNA virus that lacks reverse transcriptase to help it integrate its DNA into the host genome

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8
Q

function of von Willebrand factor

A

binds glycoprotein (GP) Ib receptors on platelet membrane and mediates platelet aggregation and adhesion to subendothelial collagen

also serves as a carrier for factor VII and stabilizes it

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9
Q

characteristics of inflammatory breast cancer

A

dermal lymphatic invasion by breast carcinoma

poor prognosis

peau d’orange: erythematous, itchy breast rash with skin texture changes analogous to an orange peel

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10
Q

what is bleeding due to heparin toxicity treated with

A

protamine sulfate

can’t be used for warfarin overdose

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11
Q

what to use for warfarin overdose

A

vitamin K (takes time)

fresh frozen plasma

can’t be used for heparin overdose

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12
Q

how does cyanide toxicity work? and how is it treated?

A

toxicity: bind ferric iron (Fe3+) with high affinity, inhibiting cytochrome c oxidase in mitochondria (needed for oxidative phosphorylation)–> lactic acidosis and death
treat: inhaled amyl nitrite

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13
Q

how does inhaled amyl nitrite treat cyanide poisoning?

A

it oxidizes ferrous iron (Fe2+) in hemoglobin to ferric iron (Fe3+), generating methemoglobin

methemoglobin can’t carry oxygen but has high affinity for cyanide

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14
Q

hemorrhagic cystitis is an adverse reaction to which two drugs

A

cyclophosphamide or irosfamide (nitrogen mustard-based chemotherapy) from the urinary excretion of the toxic metabolite acrolein

can be prevented by aggressive hydration, bladder irrigation, and administration of mesna (binds acrolein)

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15
Q

Gianzmann thrombassthenia

A

autosomal recessive disorder that is caused by a deficient or defective glycoprotein (GP) IIb/IIIa on platelet surfaces.

presents in childhood with mucocutaneous bleeding

peripheral smear snows no platelet clumping

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16
Q

mechanism of action of abciximab

A

blocker of GP IIb/IIIa receptor, which normally promotes platelet binding to fibrinogen

treat unstable angina and acute coronary syndrome

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17
Q

BRCA1 and BRCA2 are tumor suppressor genes involved in what process

A

repair of double-stranded DNA breaks

mutation- autosomal dominant with variable penetrance

increased risk of developing breast and ovarian cancer

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18
Q

characteristic of polycythemia vera

A

primary polycythemia

increased RBCs

intense itching after hot shower, erythromelalgia (severe, burning pain and red-blue coloration) due to episodic blood clots in vessels of extremities

decreased erythropoeitin

treat: phlebotomy, hydroxyurea, ruxolitinib (JAK1/2 inhibitor)

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19
Q

why do you need to check G6PD levels before administering dapsone?

A

to prevent hemolytic anemia in those with G6PD deficiency

Dapsone puts oxidative stress on body

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20
Q

where does isotype switching of immunoglobulins occur?

A

germinal centers of lymph nodes and requires interaction of CD40 receptor on B-cells with the CD4- ligand CD154) expressed by activated T-cells

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21
Q

difference between topoisomerase I and topoisomerase II

A

I- makes single-stranded nicks to relieve negative supercoiling

II-induces transient breaks in both DNA strands simultaneously to relieve both positive and negative supercoiling

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22
Q

mechanism of action of etoposide

A

chemotherapeutic agent that inhibits the sealing activity of topoisomerase II

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23
Q

what is negative selection in T cell maturation?

A

eliminate T cells that bind to self MHC or self antigens with overly high affinity

occurs in thymic medullla

prevent autoimmunity

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24
Q

leukocyte adhesion process- step 1

A

1) margination: increased vascular leakage in microvasculature leads to hemoconcentration and decreased wall shear stress, improving contact of neutrophils with endothelial lining

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25
Q

leukocyte adhesion process-step 2

A

2) rolling: neutrophils roll on endothelium via loos binding of sialylated carbohydrate groups such as Sialyl Lewis X or PSGL-1 to L-selectin on neutrophils or E-selectin/P-selectin on endothelial cells

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26
Q

leukocyte adhesion process-step 3

A

3) activation: slow rolling allows leukocytes to sample chemokines secreted by inflamed tissue. this activates integrins by inducing signaling cascade that results in conformational change in integrins necessary for binding

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27
Q

leukocyte adhesion process-step 4

A

tight adhesion and crawling: neutrophils become firmly attached to endothelium via binding of CD18 beta 2 integrins (Mac-1 and LFA-1) to intercellular adhesion molecule-1 (ICAM-1) on endothelial cells

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28
Q

leukocyte adhesion process- step 5

A

transmigration: neutrophils eventually migrate out of the vasculature by squeezing between cells via integrin attachments and adherence to platelet endothelial cell adhesion molecule 1 (PECAM-1)

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29
Q

mechanism of action of rivaroxaban and apixaban

A

oral anticoagulant that directly inhibits factor Xa

used in venous venous thromboembolism and atrial fibrillation

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30
Q

what are cytokeratins

A

proteins that help form the keratin-containing intermediate filaments that make up the cytoskeleton of almost all epithelial

marker for epithelial-derived tumors

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31
Q

classic triad of paroxysmal nocturnal hemoglobinuria

A

hemolytic anemia (hemoglobinuria), pancytopenia, and thrombosis at atypical sites

due to a gene defect that leads to uncontrolled complement-mediated hemolysis

chronic hemolysis–> iron deposition in the kidney (hemosiderosis)

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32
Q

sickling episodes of sickle cell disease results in hemolysis, which leads to

A

increased indirect bilirubin and lactate dehydrogenase

decreased levels of haptoglobin

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33
Q

what are Reed-Sternberg cells

A

giant binucleated cell derived from germinal center B-lymphocytes and are the neoplastic cells of Hodgkin lymphoma

owl’s eyes

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34
Q

association between vitamin B12 and folate deficiency and treatment

A

moderate improvement in the hemoglobin level often occurs when a deficiency in vitamin B12 is treated with folate, or vice versa

treatment of vitamin B12 deficiency with folate alone can actually worsen neurologic dysfunction

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35
Q

characteristic laboratory abnormalities of hemolytic uremic syndrome

A

decreased hemoglobin and platelet count and increased bleeding time, lactate dehydrogenase, bilirubin, BUN, and creatinine

HUS –> acute kidney injury, microangiopathic hemolytic anemia, and thrombocytopenia

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36
Q

how does bone metastases assists in cancer diagnosis?

A

osteolytic (lucent): due to osteoclast stimulation, tend to represent aggressive cancer

osteoblastic (sclerotic): due to osteoblasts, indicates a more indolent course

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37
Q

how does chronic myelogenous leukemia (CML) differs from leukocytosis

A

have decreased leukocyte (neutrophil) alkaline phosphatase while that is normal or elevated in a leukemoid reaction

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38
Q

presentation f von Willebrand disease

A

lifelong history of mucosal bleeding, including gingival bleeding, epistaxis, and/or menorrhagia

normal platelet levels but porlonged bleeding time due to impaired platelet functioning

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39
Q

2 important functions of van Willebrand factor

A
  • promotes platelet adhesion by binding and crosslinking platelet glycoproteins (primarily GpIb) with exposed collagen underneath damaged endothelium
  • protective carrier protein for factor VIII
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40
Q

heinz bodies are found in which anemia type

A

G6PD deficiency

heinz bodies: dark, intracellular inclusion that stain with supravital stain and represent hemoglobin that has denatured/precipitated from oxidative stress

41
Q

t(14;18) chromosomal translocation is associated with what gene expression abnormalities

A

Bcl-2 overexpression

Bcl-2 is a protooncogene becasue it has anti-apoptotic effects–> allow cells to live

associated with follicular lymphoma

42
Q

acute intermittent porphyria

A

autosomal dominant condition caused by porphobilinogen deaminase deficiency

minority present with acute attacks characterized by abdominal pain and vomiting, peripheral neuropathy, neuropsychological symptoms, and reddish-brown urine

treat with IV glucose or heme preparations, which down-regulate ALA synthase activity

43
Q

characteristic of hairy cell leukemia

A

indolent B-cell neoplasm

middled-aged men, bone marrow failure and infiltration into the reticuloendothelial system

massive splenomegaly

“dry tap” unsuccessful bone marrow aspiration

lymphocytes with cytoplasmic projects

44
Q

how can G6PD deficiency present with hemolytic anemia?

A

need NADPH to keep glutathione reduced to detoxifies free radicals and peroxides

so when NADPH is low in RBC–> hemolytic anemia due to RBC poor defense against oxidizing agent

need G6PD to make NADPH

45
Q

difference between direct factor Xa inhibitors and direct thrombin inhibitors

A

factor Xa: apixaban, rivaroxaban)-increase the prothrombin and activated partial thromboplastin times but do not affect the thrombin time

thrombin (dabigatran) prolong aPTT, PT, and TT

46
Q

why do patients with significant renal dysfunction have excessive bleeding

A

due in part to accumulation of uremic toxins int eh circulation

prolonged bleeding time with normal platelet count, prothrombin time (PT), and activated partial thromboplastin time (aPTT)

47
Q

how does sickle cell anemia lead to fibrosis and atrophy f the spleen?

A

repetitive splenic infarctions caused by splenic microvessel occlusioin

48
Q

multiple myeloma characteristics

A

bone marrow sample compased of greater than 30% of plasma cells

-median age of diagnosis= 70

49
Q

symptoms of multiple myeloma

A
  • normocytic and normochromic anemia due to replacement of bone marrow with malignant plasma cells
  • secretion of IL-1 and IL-6 activates osteoclasts–> bone resorption –> osteopenia
  • hypercalcemia
  • increased susceptibility to infection
  • AL amyloid due to accumulation of monoclonal immunoglobulin light chains
  • renal failure due to infiltrationcof kidney by plasma cells, amyloid, Bence-Jones cases in tubules, hypercalcemia, and inflammation
50
Q

auer rods stain positively for

A

myeloperoxidase

they are deformed azurophilic granules found in the cytoplasm of cytoplasm of the myeloblasts

found in AML M3 (acute promyeloctic leukemia)

51
Q

hydroxyurea for sickle cell disease

A

drug that increases fetal hemoglobin synthesis

52
Q

B-cell vs T-cell acute lymphoblastic leukemia

A

ALL= most common malignancy of childhood

B is approximately 70-80% of all cases of ALL

T present with mediastinal mass that cause respiratory symptoms, dysphagia, or superior vena cava syndrome

53
Q

in what ways are selective COX2 inhibitors better than non-selective COX inhibitors

A

selective COX 2 inhibitors have potent anti-inflammatory effects without the side effects of bleeding and GI ulceration

do not impair platelet function because platelets predominantly express COX 1

54
Q

porphyria cutanea tarda (PCT) cause and presentations

A

most common disorder of porphyrin (heme) synthesis

uroporphyrinogen decarboxylase deficiency

early stage: neuropsychiatric manifestations without photosensitivity

late: derangements lead to photosensitivity–> vesicle and blister formation on sun exposed area

55
Q

difference between unfractionated heparin vs. low molecular weight heparin (LMWH)

A

only unfractionated heparin has a pentasaccharid chain long enough (>18 saccharid units) ot bind to both antithrombin and thrombin

unfractionated heparin has EQUAL activity against factor Xa and thrombin, while LMWH has greater activity against Factor Xa than thrombin

56
Q

tumor lysis syndrome- what is it and how to prevent it

A

oncologic emergency that develop during chemotherapy because large numbers of tumor cells are destroyed in a short period, so lots of intracellular ions are released into serum along with nuclei acids (catabolized into uric acid)

prevent with hydration and use of hypouricemic agents such as allopurinol or rasburicase (convert uric acid into more soluble metabolites

57
Q

how do you treat heparin-induced thrombocytopenia (HIT)

A

direct thrombin inhibitors (DTIs) such as argatroban

avoid all forms of heparin in these patients

58
Q

why are prothrombin time and partial thromboplastin time normal in hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) and abnormal in DIC

A

because the coagulation system is not activated in HUS-TTP

59
Q

Li-Fraumeni syndrome- mutation and what types of cancers

A

autosomal dominant mutation in TP53, gene that codes for tumor suppressor protein p53

sarcoma, breast, leukemia, and adrenal cancer (SBLA mnemonic)

60
Q

role of p53

A

arrest cells with mutant DNA in the G1/S stage of cell cycle until he damage is repaired

61
Q

what is pure red cell aplasia

A

rare form of marrow failure characterized by severe hypoplasia of marrow erythroid elements in the setting of normal granulopoiesis and thrombopoiesis

associated with thymoma, lymphocytic leukemias, and parvovirus B19 infection

62
Q

mechanism of action of enoxaparin

A

low-molecular-weight heparin that functions like heparin in that it binds and activates antithrombin III (AT III)

63
Q

heparins mechanism of action

A

increases the effect of the naturally occurring anticoagulant antithrombin III (AT III)

unfractionated and low molecular weight heparins are commonly used for DVT prevention in inpatient settings

64
Q

sideroblastic anemia- causes

A

results from an inability to form heme molecules in the motochondria–> leading to iron deposition inside the mitochondria (forming a ringed sideroblast)

chronic alcoholism, lead poisoning, copper deficiency, and certain meds (isoniazid, chloramphenicol, linezolid), myelodyplastic syndrome

65
Q

how does lead poisoning lead to sideroblastic anemia

A

inhibits two key enzymes in the heme synthesis pathway:
- ferrochelatase (last enzyme in heme synthesis to help incorporate iron into protoporphyrin–> buildup of iron and protoporphyrin

  • deta-ALA dehydratase: converts delta-ALA to porphobilinogen to make porphyrin –> buildup of delta-ALA
66
Q

what medication is associated with sideroblastic anemia

A

isoniazid–> can also cause vitamin B6 deficiency–> peripheral neuropathy

67
Q

how to diagnose sideroblastic anemia

A

bone-marrow examination with Prussian blue stain

68
Q

what is hereditary spherocytosis

A

autosomal dominant hemolytic anemia that result from an abnormality in the RBC membrane characterized by defects in the membrane proteins such as ankyrin (most common), spectrin, or band 3

have increased MCHC due to mild dehydration of the RBC

69
Q

mechanism of action of desmopressin (DDAVP)

A

synthetic analog of vasopressin that increases circulating factor VIII and endothelial secretion of vWF to stop bleeding

can be used to treat von Willebrand factor deficiency and mild hemophilia A

70
Q

beta-thalassemia is due to what abnormal cellular process

A

alternate RNA splicing–> can lead to cancer, dementia, and epilepsy

71
Q

how can blood transfusions lead to hypocalcemia

A

whole blood transfusions or packed RBCs may develop elevated plasma levels of citrate (substance added to stored blood

citrate chelates Ca2+ and magnesium and may reduce their plasma levels, causing paresthesias

72
Q

methotrexate mechanism of action

A

folic acid antagonist used to treat ectopic pregnancy

competitively inhibits the enzyme dihydrofolate (DHF) reductase, which catalyzes the synthesis of tetrahydrofolate–> inhibition of DHF reducatase causes the intermediate DHF to accumulate intracellularly

73
Q

how does radiation do to metastatic cells

A

induces DNA damage through DNA double-strand fractures and formation of oxygen free radicals

74
Q

how does cancer cells gain resistance to chemotherapy

A

human multidrug resistance (MDR1) gene codes for P-glycoprotein, a transmembrane ATP-dependent efflux pump protein that can reduce the influx of drugs into the cytosol and can increase efflux form the cytosol, thereby preventing the action of chemotherapeutic agents

75
Q

target of rituximab

A

CD20

a monoclonal antibody directed against the CD20 antigen

treatment for B-cell non-Hodgkin lymphoma, CLL, rheumatoid arthritis, and idiopathic thrombocytopenic purpura

76
Q

how come tumors taht harbor KRAS mutations are resistant to treatment with anti-EGFR drugs (eg, ctuximab, panitumumab)

A

KRAS is an activating mutation that lead to constitutive activation of the epidermal growth factor receptor (EGFR) pathway, promoting increased cell proliferation and growth

77
Q

how is tumor necrosis factor-alpha associated with muscle wasting?

A

thought to mediate paraneoplastic cachexia in humans by suppressing appetite and increasing basal metabolic rate

78
Q

why can’t maturing erythrocytes synthesize heme

A

need mitochondria to produce heme

79
Q

when does sickling occur?

A

HbS aggregates in deoxygenated state

under conditions associated with anoxia including low pH and high levels of 2,3-bisphosphoglycerate

80
Q

result of vitamin K deficiency

A

life-threatening bleeding diathesis, such as intracranial hemorrhage and profuse bleeding from the GI tract, umbilicus, and surgical sites

81
Q

Kaposi’s sarcosma is associated with

A

Human herpes virus type 8

presents as blue-violet or brownish skin plaques on the extremities and mucous membranes of HIV-positive patients

82
Q

side effect of ganciclovir

A

neutropenia

risk increased with co-administration of zidovudine or trimethoprim-sulfamethoxazole

83
Q

how can RBC sickle in sickle cell anemia?

A

HbS contains a mutation that replaces glutamic acid with valine at the 6th amino acid position of the beta globin chain

promotes hydrophobic interaction among Hb molecules –> HbS polymerization and erythrocyte sickling

84
Q

association between chronic hemolysis and gallstone formation

A

chronic hemolysis increase the amount of unconjugated bilirubin in bile, which promotes calcium bilirubinate precipitation and leads to black pigment stone

pigmented gallstones are a complication of any hemolytic anemia

85
Q

how does warfarin-induced skin necrosis occur

A

inhibition of vitamin K-dependent gamma-carboxylation of clotting factors-> procoagulant effect

-> interrupt blood flow to skin and lead to skin necrosis, particularly in patients with protein C or S deficiency

86
Q

what is the Haldane effect? what is the Bohr effect?

A

Haldane: in the lungs, the binding of oxygen to hemoglobin drives the release of H+ and CO2 from hemoglobin

Bohr: in peripheral tissues, high concentrations of CO2 and H+ facilitate oxygen unloading from hemoglobin

87
Q

histology of Burkitt lymphoma

A

diffuse midium-sized lymphocytes and a high proliferation index represented by the high Di-67 fraction (approaching 100%)

“starry sky” appearance due to presence of benign macrophages

88
Q

plummer-vinson syndrome characteristics

A

dysphagia (esophageal web formation), iron deficiency anemia, koilonychia (spoon-shaped nailed) and shiny red tongue

symptoms resolve with iron supplementation

89
Q

mechanism of action of trastuzumab

A

monoclonal antibody used in management of patient with HER2-positive breast cancer

binds to portion of the extracellular domain of HER2 and prevents activation of a transmembrane tyrosine kinase

90
Q

what cause bruises to turn green

A

heme oxygenase converts heme to biliverdin, a pigment that causes the greenish color to develop in bruises several days after an injury

91
Q

how come you have to reduce the doses of 6-mercaptopurine if patients are also receiving xanthine oxidase inhibitor allopurinol?

A

because xanthine oxidase (XO) and thiopurin methyltransferase in the liver inactivate 6-mercaptopurine (cytotoxic purine analogs that inhibit de novo purine synthesis)

and since allopurinol is an XO inhibitor, it can increase concentration of 6-mercaptopurine

92
Q

how does c-Myc function?

A

functions as a transcription activator controlling cell proliferation, differentiation, and apoptosis

93
Q

retinoblastoma (Rb) tumor suppressor gene

A

encodes Rb protein to regulates cell cycle

active (hypophosphorylated) prevents damaged cells from passing G1 to S checkpoint

inactive (hyperphosphorylated) Rb protein allows the damaged cell to enter mitosis

abnormal phosphorylation leads to Rb inactivation

94
Q

with the exception of chronic myelogenous leukemia, the chronic myeloproliferative disorders (especially polycythemia vera) frequently harbor a mutation in the

A

nonreceptor cytoplasmic tyrosine kinase, Janus kinase 2 (JAK2)–> mutation leads to tyrosine phosphorylation activity and in the cytokine-independent activation of signal transducers and activators of transcription (STAT) proteins (JAK-STAT signaling pathway)

95
Q

how does the mutations lead to beta-thalassemia

A

mutation–> defective transcription, processing, and translation of beta-globin mRNA—> deficiency of the beta-globin chains

96
Q

clinical features that suggest malignant cause of back pain

A

worse at night, not relieved with rest or analgesics, advanced age, and systemic symptoms

common cancers that metastasize to bone: prostate, breast, kidney, thyroid, and lung

97
Q

hematologic side effects of chloramphenicol (suppresses bacterial protein synthesis by binding to the ribosomal 50S subunit and inhibit the peptidyl transferase enzyme

A

dose-related anemia, leukopenia, and/or thrombocytopenia that are reversible by withdrawing the medication

also cause dose-independent (idiosyncratic) aplastic anemia) which is severe and fatal without treatment (bone marrow transplant) and it is irreversible

98
Q

what does haptoglobin do?

A

serum protein that binds to free hemoglobin and promotes its uptake by the reticuloendothelial system

decrease when significant quantities of hemoglobin are released into circulation like in intravascular hemolysis

99
Q

protein mutated in hereditary hemochromatosis

A

HFE protein-normally interacts with transferrin receptor to sense iron stores level. if mutated, then falsely detect low iron levels and make the body accumulate more iron

inactivation of HFE–> decreased hepcidin (helps destroy ferroportin) synthesis by hepatocytes and increased DMT1 expression (divalent metal transporter so iron would be absorbed more in the intestinal lumen) by enterocytes

UWorld Journal (18 decks)

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