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Heme boards > Other > Flashcards

Other Flashcards

1
Q

Management of acute GVHD affecting the GI tract

A
  • nonabsorbable oral steroid (budesonide)
    + systemic glucocorticoid
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2
Q

Management of erythrocytosis in patient with transplanted kidney

A

ACE inhibitor

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3
Q

Most common mutations in CMML

A
  • TET2
  • SRSF2
  • ASXL1
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4
Q

CMML treatment

A

IF high risk, HMA bridge to transplant
IF low risk, observation
Once needing treatment HMA vs. hydrea

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5
Q

Pathophysiology of cerebellar neurotoxicity with cytarabine

A

Widespread loss of purkinje fibers

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6
Q

clinical benefit of early vs. delayed transplant in myeloma

A

PFS alone

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7
Q

DOAC management perioperatively

A
  • IF urgent surgery, reverse DOAC
  • IF low/moderate bleeding risk, hold for one day before
  • IF high bleeding risk, omit 2 days before
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8
Q

Definition of GVHD overlap syndrome

A

simultaneous features of both chronic and acute GVHD

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9
Q

Advanted of BuCy conditioning vs. BuFlu

A
  • reduced time to t cell engraftment
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10
Q

Burr cells on peripheral smear

A

see photo

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11
Q

Burr cell differential

A
  • ESRD
  • Liver disease
  • Pyruvate kinase deficiency
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12
Q

PKD inheritance

A

autosomal recessive

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13
Q

drug contrandicated with methotrexate

A

NSAIDS (reduce renal clearance)

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14
Q

Site of hematopoiesis in gestation at 5/6 months

A

l*iver
bone marrow

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15
Q

Peripheral smear of hereditary stomatocytosis

A
  • see photo online
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16
Q

Management of patient on ganciclovir for CMV and levels are uptrending

A

Continue (takes 1-2 weeks for levels to decline after starting treatment)

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17
Q

Management of acquired VWF deficiency

A

recombinant VWF

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18
Q

What is idecabtagene?

A

idecabtagene vicleucel (ide-cel)

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19
Q

Least important antigen for hemolytic transfusion reaction

A

Lewis antigen

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20
Q

Etiology of CLL patient treated with FCR and presenting with dry cough, fever, hypoxia

A

PJP oneumonia

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21
Q

Other SE of IVIG to be aware of

A

aseptic meningitis

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22
Q

What to do if you’ve caused hyperviscosity in LPL patient with rituximab

A

PLEX

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23
Q

What to think with prolonged thrombin time

A

low fibrinogen

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24
Q

Gaucher disease treatment

A

IF cytopenias or significant splenomegaly, enzyme replacement therapy

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25
Q

idelalisib mechanism

A
  • inhibits phosphorylated MTOR
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26
Q

Letermovir SE’s

A
  • AKI
  • pneumonia
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27
Q

Preferred systemic therapy for NLPHL

A

R-CHOP

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28
Q

Sweet syndrome clinical features

A

abrupt appearance of painful, edematous, and erythematous papules, plaques, or nodules on the skin + fever + neutrophilia

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29
Q

WHIM syndrome

A

Warts, Hypogammaglobulinemia, Infections, Myelokathexis
- severe neutropenia

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30
Q

Management of symptomatic gastric MALT that is negative for h pylori

A

rituximab

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31
Q

Management of cirrhosis from iron overload

A

liver transplantation

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32
Q

Management of hemolytic anemia post liver transplant

A
  • transfuse donor type RBCs
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33
Q

Function of hepcidin

A
  • degrades ferroportin
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34
Q

Next step if patient develops thrombocytopenia post ritiximab

A
  • check EBV/HCV serologies
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35
Q

Second line for FL

A
  • if early relapse/aggressive disease, CAR-T
  • if late relapse and BR frontline, R-CHOP
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36
Q

Post transfusion purpura presentation

A

Severe thrombocytopenia after a platelet transfusion

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37
Q

Next steps if patient has detectable HPA-1a antibodies in the serum

A
  • only transfuse HPA-1a negative RBCs
  • *washed and resuspended RBCs (you need to remove any platelets that are HPA-1a positive and may have contaminated RBCs)
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38
Q

Preferred CAR-T products for ALL

A

IF age >25, Brexi-cell (Zuma-3)
IF age up to 25 years, tisa-cel (approval)

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39
Q

Other poor prognosticator in AML

A
  • monosomal karyotype
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40
Q

Polymorphic PTLD management

A
  • Single agent rituximab + reduction of immunosuppression
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41
Q

Monomorphic PTLD management

A

IF minimally symptomatic/more indolent lymphoma, single agent rituxan
IF DLBCL/more aggressive lymphatic, R-CHOP

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42
Q

Factor VII deficiency perioperative treatment for procedure with significant bleeding risk

A

recombinant activated factor VII (novoseven) 15-30 mcg/kg q12h

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43
Q

Factor XII deficiency coags

A
  • prolonged apTT
44
Q

Factor deficiencies with prolonged aPTT

A

8,9,11 and 12

45
Q

prekallikrein and HMWK deficiency bleeding phenotype

A

No bleeding diasthesis,
just prolonged aPTT

46
Q

Bleeding phenotype of hemophilia carriers

A
  • can have bleeding, depends on level
47
Q

peripartum management of hemophilia carrier

A
  • depends on baseline factor level
  • IF <50 need factor
48
Q

Enzyme involved in Xa inhibitor metabolism

A

CYP3A4

49
Q

Result of mixing study in VWD

A

corrects (it’s factor VIII deficiency that causes the aPTT prolongation)

50
Q

Other causes of protein s deficiency

A
  • Liver disease (synthesized by hepatocytes) →
  • Acute thrombosis →
  • Pregnancy → nearly all pregnant people have decreased, physiologic protein s
  • OCP’s/estrogen treatment
    ***Any comorbid illness that causes an acute phase response can lower the level of free protein S →
  • DIC →
    Anticoagulants: Warfarin, NOAC treatment →
    *Nephrotic syndrome →
    *HIV
51
Q

Other causes of antithrombin deficiency

A

Liver disease →
Nephrotic syndrome (protein loss) →
Surgery and trauma → Modest fall in AT levels + nadir around post-op D3
Meds → asparaginase
Heparin therapy → up to 30% reduction
*OCP or estrogen treatment

52
Q

Other clinical presentations of HITT aside from clotting

A
  • skin necrosis at the site of heparin injections
  • venous limb gangrene (eg patient presents with swollen and ischemic hand after cardiac surgery)
53
Q

Cardiac surgery for patient with history of HITT

A
  • IF ELISA is negative, rechallenge
  • IF ELISA is positive, PLEX before
54
Q

Blood type of mother with greatest risk of hemolytic disease of newborn if father is A+

A
  • 0+
55
Q

Additional antigens sickle cell patients need matching for

A

C, E, and Kell

56
Q

How to differentiate alpha thal trait vs. beta thal trait

A

beta thal = A2 greater than 3.5

57
Q

hemoglobin S trait on hgb electrophoresis

A

S of about 30%

58
Q

Drugs precipitating G6PD

A
  • sulfonylureas
  • rasburicase
  • phenazypyridine (pyridium)
    *fluoroquinolones
    *dabrafenib
59
Q

Copper deficiency clinical features

A

*ringed sideroblasts on marrow
- cytopenias
- neurologic deficits

60
Q

PKD clinical features

A
  • *echinocytes on peripheral smear
  • congenital hemolysis
    *Pyruvate kinase can be low normal
    *elevated hexokinase
61
Q

Labs for PKD

A
  • increased bisphosphoglyceric acid (2,3 BPG)
62
Q

Treatment of AIP refractory to medical therapy

A

Liver transplant

63
Q

function of erythroferrone

A

Decreases hepcidin production

64
Q

Physiology of iron overload in MDS and other states of ineffective erythropoeis

A
  • body senses inadequate iron so so increases erythroferrone production, which downregulates hepcidin to increase iron absorption
65
Q

Ferroportin mutation is seen in what

A

hemochromatosis

66
Q

AICD physiology

A

increased IL-6 production, which increases hepcidin production

67
Q

Clinical features of congenital erythropoietic porphyria

A

bald + skin is peeling off + peeing red + brown teeth/Alopecia + friable skin + red urine + pink to brown pigmented teeth. Huge vat of urine to his right/very high levels of uroporphyrin.

68
Q

Congenital erythropoietic porphyria (CEP) treatment

A

Bone marrow transplant

69
Q

CNL clinical features

A

-neutrophil count can be very high, but is typically in the range of 20,000 to 35,000/microL
- otherwise normal blood counts
- no dysplasia in marrow and blast count 0-5%

70
Q

Bone marrow in systemic mastocytosis + immunophenotype

A
  • spindle shaped mast cells
  • CD117+, CD2+, CD25+
71
Q

management of hypereosinophilia with strongyloides travel hx

A
  • empiric abx
  • strongyloides antibody
  • bone marrow biopsy
  • pred 1 mg/kg (mitigate end organ damage from hypereosinophilia)
72
Q

Gaucher disease physiology + gene mutation

A
  • lysosomal storage disease
  • glucocerebroside (a sphingolipid, also known as glucosylceramide) accumulates in cells and certain organs.
73
Q

Managmeent of gaucher patient on imiglucerase with hypersensitivity reaction

A

Discontinue and start eliglustat

74
Q

Upshaw shulman management

A
  • recombinant ADAMTS13
  • IF not available, plasma infusion
75
Q

Management of pregnant Upshaw shulman patient

A

regularly scheduled plasma infusion

76
Q

Relapsed aplastic anemia management

A

alternative donor-HSCT

77
Q

Luspatercept indications in low risk MDS

A
  • SF3B1
    *ringed sideroblasts
78
Q

why do AYA patients do better with pediatric intensive regimens?

A
  • higher doses of nonmyelosuppressive drugs (asparaginase isn’t typically in adult regimens like Hyper-CVAD and isn’t very myelosuppressive)
79
Q

Unfavorable risk HL management

A
  • ABVD not XRT
80
Q

Advanced stage NPHL

A
  • rituximab based combination chemo
  • R-CHOP
81
Q

Relapsed ALL management

A
  • IF treatment refractory, blinatumomab or inotzumab if CD22 bridget to allo-HSCT
  • If treatment refractory, CAR-T
82
Q

blinatumomab target

A

CD19

83
Q

Consolidation for Ph- ALL who is MRD-

A

Blinatumomab alone (Preferred – Transplant related mortality offsets survival advantage)
Blinatumomab + chemo

84
Q

bexarotene SE’s to know

A
  • hypothyroidism
  • hyperlipidemia
85
Q

Brentuximab SE’s to know

A
  • peripheral neuropathy
  • pneumonitis
86
Q

Where does somatic hypermutation occur?

A

Germinal center of B-cell follices

87
Q

Defining high risk smoldering myeloma

A
  • 20/2/20
    *also cytogenetics (same as for myeloma)
88
Q

ET risk stratification

A
  • age >60
  • prior VTE
  • CV RF’s
    *JAK2 V617
89
Q

POEMS management with limited sclerotic lesions

A

Radiation

90
Q

CNL treatment

A

Jak inhibitors

91
Q

treatment for systemic POEMS

A

auto-HSCT

92
Q

Pathogen associated with chronic ibrutinib

A

Aspergillus

93
Q

CRS management

A

*remember that if mild (fever without hypotension or hypoxia), just supportive care without tocilizumab

94
Q

Most common BCR/ABL fusion protein in CML

A

p210
(picture matt in a net)

95
Q

Clinical features of T cell histiocyte-rich large b cell lymphoma

A
  • larger degree of infiltrating reactive T cells and macrophages
  • tend to be young with liver and bony involvement
96
Q

Copper deficiency MCV

A

microcytic

97
Q

Recommended duration of prophylactic lovenox for cancer patients

A

28 days of LMWH

98
Q

MYH9 inclusion bodies on peripheral smear

A
  • see photo online
99
Q

May Hegglin anomaly association

A

MYH9

100
Q

target hemoglobin level with red cell exchange in SCD

A

hgb of 10

101
Q

characteristic mixing study pattern of acquired hemophilia

A

prolongs at 1 hour and hten worsens at 2 hrs

102
Q

Management of pt with protein s deficiency determined during pregnancy

A

antepartum vigilance, postpartum prophylaxis

103
Q

Management of pregnant homozygous FVL or prothrombin patient

A

antepartum and postpartum prophylaxis

104
Q

Bridging key point with warfarin bridging

A

*You always need at least 5 days of overlap. If INR bumps, don’t hold

105
Q

Whole blood contains

A

Anti A and anti B

106
Q

Hereditary thrombophilia pts who need antepartum ppx

A
  • antithrombin deficiency
  • prothrombin gene mutation
  • homozygous FVL
107
Q

Monomorphic PTLD consistent w/ DLBCL management

A

upfront rituximab

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