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Hem/Onc > General HO 0502Q > Flashcards

General HO 0502Q Flashcards

1
Q

HIT

A

more common w/ unfractionated heparin.
leads to paradoxical thrombosis.

avoid HMW and LMW heparin.

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2
Q

argatroban

A

direct thrombin inhibitor - bind thrombin active site. does not require AT III for action.

used to treat HIT.

other DTIs: hirudin, lepirudin

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3
Q

dx of febrile URI followed by sudden appearance of red, flushed cheeks 2-5 days later in child?

A

erythema infectiosum (parvovirus B19) - rash related to IC deposition once serum IgM and IgG levels are high enough

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4
Q

where does parvovirus B19 replicate?

A

BONE MARROW.

tropic for erythroid precursor cells (bld group P Ag [globoside] serves as receptor)

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5
Q

what appears as parvovirus face rash disappears?

A

reticular lacelike pattern on trunk and extremities

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6
Q

JAK2

A

non-receptor tyrosine kinase assoc. with EPO receptor (type I cytokine receptor)

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7
Q

which Abs are essential for classical complement pathway after binding C1?

A

IgG and IgM.

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8
Q

which Ab is more effective in activating complement cascade?

A

IgM (pentameric structure)

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9
Q

dysphagia and disfigured fingernails (spoon nails/koilonychia) are specific for….?

A

iron deficiency anemia

*dysphagia often due to esoph. webs (Plummer Vinson syndrome)

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10
Q

common features of all types of anemia

A 
malaise
fatigue
pallor
decreased exercise capacity
CHF
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11
Q

tx of iron deficiency anemia

A

oral iron prep

*may add vit C to improve oral iron absorption

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12
Q

what supplement reduces erythroid precursor apoptosis in folate deficiency?

A

THYMIDINE
activates thymidine kinase salvage pathway.
increases dTMP levels.

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13
Q

X-linked recessive inheritance

A

affected males always produce unaffected sons, carrier daughters.

carrier females have 50% chance of producing affected son, carrier daughter.

ex: G6PD deficiency

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14
Q

ferritin

A

intracellular iron-binding protein.
stores iron inside enterocyte.
iron is eventually excreted in stool as enterocytes are sloughed.

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15
Q

ferroportin

A

iron transporter on basolateral enterocyte surface.

allows iron to enter circulation.

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16
Q

transferrin

A

iron-binding transport protein that binds free iron in circ.
eventually becomes internalized after interacting with transferrin receptor on cell.

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17
Q

what regulates the diff routes taken by iron?

A

HEPCIDIN - acute phase reactant made in LIVER by hepatocytes

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18
Q

hepcidin action on ferroportin

A

causes internalization and degradation of ferroportin.

results in decreased basolateral iron transport in intestine. inhibits release of iron by macrophages

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19
Q

what increases hepcidin synthesis?

A

high iron levels.

inflamm conditions.

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20
Q

lactoferrin

A

secreted by renal tubular cells.
binds free iron in urine for possible metabolic use.

*very limited role in iron metabolism

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21
Q

AL amyloidosis

A

assoc. with multiple myeloma and other monoclonal plasma cell dyscrasias.

derived from monoclonal Ig light chains.
deposit in kidney, heart, tongue, nervous system.

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22
Q

serious adverse effect of ganciclovir

A

NEUTROPENIA
increased incidence w/ co-admin of zidovudine. both drugs affect DNA synthesis of hematopoietic stem cells and result in BM suppression

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23
Q

mitotic index is Burkitt lymphoma

A

high value.

aka proliferation fraction (Ki-67)

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24
Q

how does radiation induce DNA damage?

A

through dsDNA breaks and formation of oxygen free radicals.

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25
Q

common cause of extramedullary hematopoiesis

A

severe chronic hemolytic anemia

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26
Q

skel abnormalities due to EM hematopoiesis

A

expanding mass of progenitor cells in BM thins out bony cortex and impairs bone growth…

pathologic fx
maxillary overgrowth and frontal bossing (chipmunk facies)

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27
Q

Bruton’s agammaglobulinemia

A

X-linked deficiency of all antibodies and low B cell counts due to defect in B cell maturation.
T cell numbers and functions are intact.

absent germinal centers.

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28
Q

paracortical zone of LN

A

internal to cortex.
mainly has T cells and dendritic cells.
dendritic cells present Ag to T cells here.

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29
Q

causes of non-EBV infectious mono

A

CMV
HIV
toxoplasmosis

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30
Q

procarcinogens enter body and are metabolized by…?

A

most chemicals are metabolized by P450 MONOOXYGENASE in hepatic microsomes and endoplasmic reticulum in various tissues

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31
Q

factor Xa inhibitors

A

anticoagulants with specific activity against factor Xa WITHOUT antithrombin activity

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32
Q

lab changes seen with factor Xa inhibitors

A

increase PT and aPTT.

NO CHANGE to TT.

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33
Q

what effect does heparin and other drugs that directly inhibit thrombin formation have on TT?

A

prolonged TT

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34
Q

steroid abuse

A 
erythrocytosis
abn testicular size, function
hepatic abnormalities
deepened voice
male pattern baldness
acne

*competitive athletes

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35
Q

androgen effect on RBC

A

stimulates RBC production (higher Hct)

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36
Q

MTX for ectopic preg

A

DOC for <6WGA

toxic to rapidly dividing cells of trophoblast

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37
Q

MTX molecule

A

similar to folic acid structure.

converted to POLYGLUTAMATE form inside target cell (keeps it in cell)

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38
Q

what modification allows folate and recycled DHF to be stored within cells?

A

polyglutamation

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39
Q

what is PABA (para-aminobenzoic acid)?

A

folic acid precursor in prokaryotes

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40
Q

what drug is a chemical analogue of PABA?

A

sulfonamide Abx - inhibit dihydropteroate synthetase to prevent bact conversion of PABA to folic acid

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41
Q

PI3K/Akt/mTOR pathway

A

intracellular signaling pathway - antiapoptosis, cellular proliferation, angiogenesis

mutations in any component contribute to cancer pathogenesis

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42
Q

aplastic anemia presentation

A

pancytopenia
low reticulocyte count
NO splenomegaly

43
Q

aplastic anemia labs

A

“dry” BM aspirate.

marrow replaced by fat cells and fibrous stroma

44
Q

myelophthisic anemia

A

caused by SPACE-OCCUPYING lesions in BM. all hematopoietic lines affected.

*common cause: metastatic carcinoma with fibrosis

45
Q

Hb action in lungs

A

binds O2, releases protons

46
Q

Hb action in tissues

A

releases O2

acquires protons

47
Q

where in body does Hb become completely saturated with O2?

A

LUNGS

high pO2 in alveoli increases O2 binding to Hb, causes release of protons.

48
Q

what is the mech of Hb release of oxygen in the TISSUES?

A

high proton conc (due to high Co2, converted to bicarb and protons by carbonic anhydrase) in tissues protonates amino groups of Hb subunits – subunits form salt/ionic bridges that STABILIZE DEOXY Hb and decreases Hb affinity for O2

49
Q

what stabilizes deoxyHb (favors decreased Hb affinity for O2)?

A
  1. salt bridges between N-terminal histidine residues in each globulin
  2. ionic bonding of 2,3 DPG to two beta subunits
50
Q

Rb protein

A

prolif signals activate cyclin-dependent kinase 4, which hyperphosphorylates Rb to make it INACTIVE. this allows unregulated transition from G1 to S phase of cell cycle

*hypophosphorylated = active. hyperphosphorylated = inactive.

51
Q

E2F transcription factor

A

released by hyperphosphorylated Rb to allow cell progression from G1 to S phase

52
Q

what happens when E2F TF is bound?

A

hypophosphorylated Rb + E2F complex INHIBITS transcription of genes for G1-S transition

53
Q

what would increased activity of DHF reductase and DNA polymerase indicate?

A

increased DNA synthesis

54
Q

what kind of cells are the ATYPICAL LYMPHOCTES seen in infectious mono?

A

activated CD8+ cytotoxic T cells

destroy virally infected B cells

55
Q

what is CD14?

A

surface marker of monocytes, macrophages.

receptor for LPS, which activates macrophage.

56
Q

scenarios for CO poisoning

A
  1. emission for cars in poorly ventilated spaces

2. faulty home heater

57
Q

tx of CO toxicity

A

100% or hyperbaric oxygen

58
Q

CO action

A

inhaled CO rapidly diffuses across alv memb to bind heme-bound iron (carboxyHb)

CO decreases O2 content of bld by occupying O2 bindings sites

CO also alters Hb conformation to relaxed form (inhibits release of O2 in tissues)

59
Q

how does CO change oxygen dissociation curve?

A

CO also alters Hb conformation to relaxed form (inhibits release of O2 in tissues)

LEFT shift in curve.
tissue hypoxia via deficient O2 unloading

60
Q

2,3 DPG

A

binds Hb in pocket formed by the two beta chains - forms ionic bonds with beta subunits of DEOXY form

61
Q

what type of Hb cannot interact with 2,3 DPG?

A

fetal Hb (serine instead of histidine. no beta chains) - much higher affinity for O2. needs to extract O2 from maternal Hb in placenta.

62
Q

process of liver uptake of unconj bilirubin

A

PASSIVE - organic anion transporting polypeptide (OATP)

63
Q

process of liver secretion of conj bilirubin

A

ACTIVE - MRP2 organic ion transporter/ATP-binding cassette protein

some passive through hepatocyte OATP

64
Q

what is unconj bilirubin complexed to in circ?

A

serum albumin - UCB is insoluble in water. tightly complexed to albumin in circ. CANNOT be excreted in urine.

65
Q

which form of bilirubin is freely excreted in urine?

A

conjugated bilirubin - water soluble, non toxic. loosely bound to albumin.

66
Q

mechs that produce unconj hyperbilirbuinemia

A
  1. excessive production of bili
  2. reduced hepatocyte uptake
  3. impaired conjugation
67
Q

mechs that produce conj hyperbilirubinemia

A
  1. decreased hepatocellular excretion

2. impaired bile flow

68
Q

host cell receptor : virion/virion protein binding

A
  1. CD4 : HIV gp120
  2. CD21 : EBV gp350
  3. erythrocyte P Ag : parvovirus B19
69
Q

EBV transmission

A

oropharyngeal secretions

70
Q

herpesvirus entry into host cell requires…?

A

initial contact with GAG chains on host cell surface proteoglycans

71
Q

resistance to activated prot C

A

factor V Leiden = atypical venous thrombosis

72
Q

ondansetron for chemo-induced nausea/vomiting

A

inhibits serotonin 5HT3 receptors which are located peripherally in presynaptic nerve terminals of vagus n. in GI tract - also present centrally in chemoreceptor trigger zone (area postrema) and solitary nucleus

73
Q

filgrastim

A

G-CSF analog that stimulates proliferation/differentiation of granulocytes.

used to minimize granulocytopenia after myelosuppressive chem.

74
Q

prevention of tumor lysis syndrome (electrolyte disturbances, acute renal failure)

A

ALLOPURINOL

along with hydration and alkalinization of urine

75
Q

major clin manifestations of factor V Leiden

A
  1. DVT
  2. cerebral vein thrombosis
  3. recurrent pregnancy loss
76
Q

pathogenesis of thrombophilia in factor V Leiden

A
  1. increased coagulation (thrombin prod)

2. decreased anticoagulation (activated prot C resistance)

77
Q

what is used to prevent primary/secondary coronary artery events and ischemic strokes in pts who have had a TIA?

A

daily low-dose aspirin

78
Q

presentation of TIA

A

sudden onset of focal numbness and tingling, fully resolved in minutes.

ddx: seizure, migraine, anxiety, hypoglycemia

79
Q

at low doses, aspirin mainly inhibits….?

A

COX1

80
Q

what is Samter’s triad?

A
  1. asthma
  2. aspirin hypersensitivity (nasal sx, bronchospasm, facial flushing)
  3. nasal polyposis
  • occurs in asthmatics treated w/ ASA
  • due to overproduction of leukotrienes that occurs when ASA blocks COX and diverts precursors into lipooxygenase pathway
81
Q

salicylism

A

caused by very high dose ASA.
vertigo, tinnitus, hearing loss.
also stimulates resp drive (hyperpnea).

82
Q

why is there an even greater increased risk of GI bleeding with high dose ASA?

A

loss of gastric cytoprotection in addition to impaired plt aggregation

83
Q

multidrug resistance gene (MDR1) in human tumor cells

A

codes for P glycoprotein, a transmemb ATP-dependent efflux pump protein that has broad specificity for hydrophobic cmpds.

reduces influx of drugs into cytosol AND increases efflux from cytosol - thereby preventing action of chemotherapeutic agents

84
Q

differential cyanosis restricted to lower body (in child) suggests….?

A

PDA with late-onset reversal of shunt.

*whole body cyanosis occurs with shunt reversal in pts with septal defects or TOF

85
Q

does coarctation of aorta cause cyanosis?

A

NOOOOO - it can limit lower extremity exercise tolerance but does not cause cyanosis

86
Q

what causes differential cyanosis?

A

reduced arterial oxygen saturation in distal aorta compared to that in aorta proximal to left subclavian artery – right to left shunting of bld through PDA into junction between aortic arch and descending aorta

87
Q

most common cause of aortic stenosis

A

degenerative (senile) calcification of aortic valve leaflets

88
Q

pulsus parvus et tardus

A

small and slow rise in carotid pulse during systole

*seen in aortic stenosis

89
Q

how does hydroxyurea help sickle cell disease?

A

increase HbF by unknown mech

90
Q

which sickle cell pts are treated with hydroxyurea?

A

pts with frequent pain crises

91
Q

Gardos channel blockers in sickle cell tx

A

calcium-dependent (Gardos) potassium channel regulates K and H2O transport through RBC memb.

blocked channel = prevent RBC dehydration = reduce HbS polymerization.

92
Q

BM in megaloblastic anemia

A

HYPERCELLULAR but megaloblastic erythroid precursors are quickly destroyed in BM before entering circ

93
Q

hyperplastic arteriolosclerosis mechanism in hypertensive crisis

A

laminated SMCs and reduplicated BMs.

renal arteriolar stenosis decreases glom perfusion and GFR, thus activating RAAS.

94
Q

presentation of aplastic anemia

A

pancytopenia.

NO SPLENOMEGALY.

95
Q

BM in aplastic anemia

A

HYPOcellular. replaced by fat cells, fibrous stroma.

96
Q

what should be ruled out first in a pt with iron deficiency anemia?

A

bld loss, esp in GI tract…. esp in adult males and postmenopausal women

*upper GI endoscopy + colonoscopy

97
Q

hemorrhagic disease of newborn

A

cutaneous, GI, and intracranial bleeding.
PRETERM INFANTS at risk.
prevent with VIT K (parenteral at birth + supp in formulas)

98
Q

what does breast milk from women with healthy diets lack?

A

vit K and D

*D deficiency manifests around 6 mos.
K deficiency can be life-threatening w/in first week of life.

99
Q

when do maturing erythrocytes lose their ability to synthesize heme?

A

when they lose their mitochondria

100
Q

where in the body is heme synthesized?

A

everywhere but mainly in RBCs and hepatocytes

101
Q

what do hepatocytes use heme in?

A

P450 system

102
Q

what is the major determinant of prognosis for bladder carcinoma?

A

tumor penetration of bladder wall

103
Q

do sickle cell TRAIT RBCs sickle when sodium metabisulfite is added?

A

yes….

all other parameters normal.

104
Q

HbS in sickle cell trait

A

35-40% HbS

> 50% HbA**

Hem/Onc (9 decks)

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