Final Flashcards

1
Q

Where can you see neutrophilia

A

CML, leukemia, sickle cell
Secondary disosrders: infection, inflammation, smoking, stress, asplenia and medications (corticosteroids lithium and exogenous growth factors), CSF secreting tumors (bronchogenic carcinoma)

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2
Q

How do neutrophils change with infection

A

Increase in marginated pool, decrease in circulating, increase in tissue

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3
Q

How do neutrophils change with epi

A

Increased circulating pool, decreased marginated pool, decreased in tissue

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4
Q

How do neutrophils change with steroids

A

Equal circulating and marginated pool

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5
Q

How does leukocyte adhesion deficiency affect neutrophils

A

Increase in circulating pool, low marginated pool, low in tissues

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6
Q

What are causes of acute vs chronic neutrophilia

A

Acute: physical stimuli, emotional stimuli, infection (localized or systemic, bacterial, mycotic, rickettsial, some viral), inflammation or necrosis (burns, trauma, gout, vasculitis), drugs
Chronic: heme disorders (chronic hemolysis, asplenia*, myeloproliferative disorders), endocrine disorders (thyroid storm, ACTH overproduction), drugs, malignancy (gastric or bronchogenic), inflammation and infection

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7
Q

What is the workflow for evaluation of neutrophilia

A

Repeat counts; if persistent examine smear for leukocrythroblastosis -> if yes, BM exam for tumor, granulomas, CML; if no -> look for signs of fever or infection -> if no, serological for AID, peripheral blood for BCR-ABL and JAK2, potential drugs, smoking

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8
Q

What are the causes of eosinophilia

A

Parasite infections (trichinella), allergic rhinitis, atopic dermatitis, urticaria, fungal allergy, asthma, meds (abx, NSAIDs, antipsychotics), bronchiectasis/cardiac failure

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9
Q

What should basophilia always trigger evaluation for

A

CML and PV

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10
Q

What drugs cause neutropenia

A

Cephalosporins, clindamycin, gentamicin, sulfonamides, tetracyclines, vancomycin, carbamazepine, mephenytoin, phenytoin, anti depressants (amitriptylene), H2 blockers (ranitidine), antimalarials, antithyroid, CV drugs (hydralazine, captopril, propranolol), diuretics (thiazides), antipsychotics (chlorpromazine), allopurinol

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11
Q

What is the suggested workup for neutropenia

A

If fever and ANC <500 give abx; if new -> see if isolated or pancytopenia -> if isolated do BM exam, if pan measure B12; if BM exam reveals abnormal cytogenetics, myelodysplasic, if LGL by flow then LGL if normal then idiopathic; if not new see if FH -> check for ELANE mutation (cyclic neutropenia)

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12
Q

What is lymphopenia

A

Lymphocyte count <1500

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13
Q

What are the causes of lymphopenia

A

Congenital immunodeficiency diseases (SCID, CVID, ATM, wiskott-Aldrich), aplastic anemia, infections, iatrogenic (chemo, glucocorticoids)

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14
Q

What is monocytopenia seen in

A

Hairy cell leukemia even in absence of hair cells on smear, do flow cytometry for markers (CD11c and CD103)

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15
Q

What conditions have low hemoglobin but normal hematocrit

A

Thalassemia

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16
Q

What is the definition of anemia

A

Hemoglobin <12 in females and <13 in males

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17
Q

How do you calculate mea corpuscular hemoglobin and mean corpuscular hemoglobin concentration

A

MCH: hemoglobin/red cell count
MCHC: hemoglobin/hct

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18
Q

What does increased reticulocyte count suggest in terms of anemia

A

Either blood loss or response to therapy; low reticulocyte count indicates iron deficiency or folate/b1 efficiency or low. EPO

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19
Q

What are acanthocytes associated with

A

Liver disease

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20
Q

What are echinocytes associated with

A

End stage renal dz

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21
Q

What is the evaluation of someone with anemia

A

Look at reticulocyte count; if high and bleeding, due to blood loss, if high and no bleeding do a smear - if schistocytes (microangiopathy), spherocytes (hereditary spherocytosis or warm abs), sickle cell, bite cells (G6PD), target (thalassemia), inclusions (malaria); if reticulocyte count low do peripheral smear - if microcytic (iron def, thalassemia, sideroblastic), normocytic (aplasia, marrow infiltration, Renal dz, inflammation, chronic dz), if macrocytic (B12 def, folate def, Myelodysplasia, drug toxicity, alcohol)

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22
Q

What is the treatment for aplastic anemia

A

Offer HSC transplant for <40; if not eligible, immunosuppressive therapy with antithymocyte globulin and cyclosporine

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23
Q

What drugs can cause microcytic anemia

A

Alcohol, lead, chloramphenicol, isoniazid - via reducing heme synthesis

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24
Q

What is pagophagia

A

Craving for ice seen with iron deficiency

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25
Q

Why is ferritin not useful in diagnosing inflammation related anemia

A

Ferritin is an acute phase reactant

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26
Q

Where is intramedullary hemolysis seen

A

Thalassemia

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27
Q

What is characteristic of methemoglobinuria

A

Contains ferric ions which causes pO2 values higher than expected in relation to percent oxygen saturation

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28
Q

What drugs should not be used in patients with G6PD deficiency

A

Dapsone, methylene blue, nitrofurantoin, phenylhydrazine, primaquine, sulfamethoxazole, sulfapyridine

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29
Q

What is nonmegaloblastic macrocytosis associated with

A

Liver disease

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30
Q

What does inflammation do to erythropoeisis

A

Decreases it; hepcidin increases which decreases iron

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31
Q

What do you treat babies who test positive for sickle cell with

A

5 years of prophylactic penicillin (or macrolide if allergy)

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32
Q

What are the risks assoc with sickle cell trait

A

Sudden death with extreme exercise

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33
Q

What is the anemia seen with sickle cell

A

Normocytic normochromic; increased reticulocyte count; if microcytic suggests sickle cell beta thalassemia or coninherited alpha thalassemia

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34
Q

What kind of murmur can be caused by anemia

A

Systolic

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35
Q

What are the effects of hydroxyurea

A

Increases HbF, lowers neutrophils, hydrates erythrocytes, macrocytosis, lower reticulocyte count

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36
Q

When should exchange transfusions be used in sickle cell

A

To manage acute complications; reduces iron overload (rather than transfusion)

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37
Q

What are ACE inhibitors used for in sickle cell

A

Prevent kidney dz by lowering intraglomerular pressure; also lowers protein excretion (used in patients with sickle cell and albuminuria even in abscence of HTN)

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38
Q

What vitamins supplement must be given to sickle cell patient

A

Folic acid

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39
Q

What drugs are linked to ITP

A

Quinidine, rifampin, TMP-SMX, phenytoin, gold

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40
Q

What screening is required for all patients with ITP

A

HIV

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41
Q

What is the treatment for ITP

A

Glucocorticoids and IV immune globulin

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42
Q

If there are schistocytes on a peripheral blood smear, can ITP be a diagnosis

A

No; will be TTP, DIC or HELLP; when measuring platelets make sure to exclude clumpin

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43
Q

What should be administered if patient has HIT

A

Direct thrombin inhibitors (lepirudin or argatroban)

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44
Q

What is the 4T score for diagnosis of HIT

A

-thrombocytopenia:2 points (platelet count fall >50%), 1 point (platelet count fall 30-50% or nadir 10k-19k)), 0 points (platelet fall <30% or nadir <10,000)
-timing of fall: onset btw 5-10 das 2 points, onset after 10 days 1 point, <4 days 0 points
-thrombosis: new thrombosis, skin necrosis 2 points, progressive or recurrent thrombosis, nonnecrotizing skin lesions 1 point, no thrombosis 0 points
-other causes for thrombocytopenia: none 2 points, possible 1 point, definite 0 points
Score 0-3: low probability, 4-5 intermediate, 6-8 high

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45
Q

Should you transfuse platelets in untreated TTP-HUS

A

No; associated with stroke and acute kidney injury

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46
Q

What is the treatment for essential thrombocythemia

A

If <60 with no hx of thromboembolic event, and platelet count <1 million follow without therapy; those not in this category treated with hydroxyurea and low dose aspirin (if need greater platelet reaction, give pegylated IFN-alpha or anagrelide)

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47
Q

What are causes of reactive thrombocytosis

A

Iron deficiency, inflammation, cancer, infection

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48
Q

What is the Ann Arbor staging system for lymphoma

A
  • stage I: involvement of single LN region or single extranodal organ
  • stage II: involvement of 2 or more LN regions or lymphatic structures on same side of diaphragm; or involvement of limited contiguous extranodal sites (IIE)
  • STage III: involvement of LN regions or lymphoid structures on both sides of the diaphragm (if involves spleen IIIS)
  • Stage IV: diffuse or disseminated involvement of one or more extranodal Organs with or without LN involvement
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49
Q

What should patients with HL receive before starting treatment

A

EKG and pulm function; women should receive fertility preservation counseling

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50
Q

What are prognostic risk factors for HL therapy

A

Increased ESR, male, >40, stage IV dz, bulky mediastinal LAD

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51
Q

What is the treatment for Hodgkin

A

ABVD

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52
Q

What is patient management after treatment of HL

A

For first 3 years, seen every 3-6 months; in 4th and 5th year every 6 months and annually thereafter

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53
Q

What should be included in follow up for HL survivors

A

CBC, thyroid function, annual infuenza shot if received bleomycin or chest radiation; breast cancer screening beginning 8-10 years post radiation or at age 40

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54
Q

What should all patients with NHL be tested for

A

HIV and hep C

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55
Q

What is the prognosis of 8;21 AML

A

Good in adults, poor in kids; RUNX1/AML1 gene

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56
Q

What is the abnormality seen in AMML

A

Inversion 16 or translocation 16;16; abnormal eosinophils with large and irregular basophilic granules and positivity for chloroacetate esterase; KIT mutation confers poor prognosis; RUNX1/CBFB

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57
Q

Where is translocations involving 11q seen

A

Acute monocytic leukemia ; poor prognosis unless have 9;11 mutation; involves KMTA/MLL

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58
Q

What are the most common mutations seen in AML

A

FLT3(most common in APL and AML with normal karyotype) - assoc with poor prognosis
NPM1 - favorable
CEBPA - favorable

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59
Q

What is the standard chemo induction for AML

A

3 days of daunorubicin or idarubicin, and 7 days of continuous infusion of cytarabine; can cause tumor lysis syndrome; if neutropenic fever, give abx, if persists, give antifungals

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60
Q

What is the definition of remission for AML

A

Normalized blood counts, <5% BM blasts, normalization of karytoype

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61
Q

what are the treatments for AML and ALL

A
  • AML: induction = 3+7 anthracyclin and ara-c; consolidation: high dose ara-c (HDAC); maintenance: promyelocytic leukemia only - ATRA
  • ALL: induction - vincristine/prednisone + others; consolidation: multiple agents plus CNS prophylaxis (MTX or ara-c), maintenance: 6MP and MTX
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62
Q

What is IKZF1 alterations seen in

A

ALL with Ph chrom; poor prognosis

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63
Q

What are the 2 groups of ALL with hyperdiploidy

A

A group with 1-4 extra chrom (47-50) and more commonly more than 50 chrom - more common in kids (X, 21, 10, 14, 17,18, 4, 6); gain of 5 and 17q is poor prognosis; 4 10 17 good prognosis

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64
Q

What is the 1;19 translocation seen in

A

Kids with B cell ALL; CD10, CD19, CD34-, CD9

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65
Q

What is 8;14 seen in besides burkitt

A

Mature B cell ALL: high incidence of CNS involvement or abndominal LN involvement

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66
Q

What is the follow up for CML

A

1-2 weeks during initiation of imatinib; once stable blood counts, every month

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67
Q

What is the Rai staging system for CLL

A

Stage 0 - asymptomatic with lymphocytosis
Stage I: lymphocytosis with LAD
Stage II: lymphocytosis, LAD and HSM
Stage III: anemia
Stage IV: thrombocytopenia ; last 2 have mean survival of <2 years

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68
Q

What is the Binet staging system for CLL

A

Based on # of LN sites involved
Stage A: fewer than 3 sites
Stage B:3 or more sites - survival of 7 years
Stage C: anemia or thrombocytopenia; survival < 2 years

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69
Q

What can complicate CLL

A

Prone to autoimmune disease development; autoimmune thrombocytopenia or hemolytic anemia

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70
Q

What are the markers for hairy cell

A

CD22, 25, 103; also express tartrate resistant acid phosphatase

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71
Q

What is the treatment for hairy cell leukemia

A

Splenectomy; cladribine and deoxycoformycin; chemo refractory responds to vemurafenib (BRAF inhibitor)

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72
Q

What drugs can cause myelodysplastic syndromes

A
Alkylating agents (busulfan, nitrosurea, procarbazine) - latency 5-7 years
Topoisomerase inhibitors: 2 year latency
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73
Q

What alterations are seen in myelodysplastic syndromes

A

Euploidy mostly; loss of 5,7, 20 or trisomy 8

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74
Q

What mutation is seen specifically in MDS (not AML)

A

SF3B1 (RNA splicing machinery) - favorable outcome

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75
Q

What causes diamond Blackfan anemia

A

5q deletion

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76
Q

What is the treatment for MDS

A

If asymptomatic, nothing; if anemic, transfusion, azacitidine(hypomethylating agent) can prolong survival and delay time of formation to leukemia - give to patients with poor prognosis and symptomatic

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77
Q

What is lenalidomide used for

A

Thalidomide derivative; reversing anemia in MDS with 5q deletion; side effect: mylosuppresion and increased risk of thrombosis

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78
Q

What treatment can be given for MDS in patients with HLA-DR15

A

ATG, cyclosporine and anti-CD52 mab (alemtuzumab)

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79
Q

What is primary myelofibrosis

A

Proliferation of dysplastic megakaryocytes that produce factors that stimulate collagen formation leading to BM fibrosis

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80
Q

What mutations are seen in primary myelofibrosis

A

JAK2, MPL (thrombopoietin receptor), CAL

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81
Q

What factors are overproduced in primary myelofibrosis

A

TGFeta, tissue inhibitors of metalloproteinases; osteoprotegrin (osteoclasts inhibitor)

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82
Q

What can the extramedullary hematopoeisis of primary myelofibrosis cause

A

Ascites, portal or intracranial HTN, intestinal or ureteral obstrution, pericardial tamponade, spinal cord compression, skin nodules

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83
Q

What is the treatment for primary myelofibrosis

A

No definitive therapy; danazol used for anemia; hydroxyurea to control splenomegaly; allopurinol to control hyperuricemia; IFN alpha in early dz; ruxolitinib imrpvoes sx and prolongs survival (JAK2 inhibitor)

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84
Q

What is significant about the pruritis seen with PCV

A

Worsens after a warm bath

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85
Q

What is the treatment for PCV

A

Phlebotomy weekly (want Hb <15);if >60 or prior thrombosis - give hydroxyurea; also manage stroke risk ie: tobacco cessation, management of lipids, and BP control

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86
Q

What is does the evaluation of MM begin with

A

Serum protein electrophoresis and urine protein electrophoresis on 24 hr urine sample

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87
Q

What is the most common CBC abnormality seen in MM

A

Normochromic anemia

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88
Q

Do you do bone scans for MM

A

No - use conventional radiography instead

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89
Q

What is used to determine prognosis of MM

A

Beta 2 microglobin level and serum lactate DH level

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90
Q

What are markers of poor prognosis of MM

A

Chrom 13 deletion, elevated B2, hypoalbuminemia and >50% plasma cells on BM aspirate

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91
Q

What is the staging for MM

A

Stage I: low B2 and normal albumin

Stage III B2 >5.5 poor prognosis

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92
Q

When can you not give HSC transplant for people with MM

A

If progressive kidney dz, decompensated cirrhosis, and class III or IV heart failure

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93
Q

What is the initiation treatment for HSC as a treatment for MM

A

High dose dexamethasone and thalidomide *require prophylaxis treatment for DVT with spirit, low molecular weight heparin or warfarin

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94
Q

What should be given to prevent complications of MM

A

Pneumococcal and influenza vaccine, TMP SMX to prevent pneumocystis pneumonia; acyclovir if receiving bortezomib; bisphosphonates to all patients (pamidronate or zoledronate)but limited to 2 years

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95
Q

What do MM patients with back pain need

A

MRI to rule out spinal cord compression

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96
Q

What mutations are seen in WM

A

MYD88, CXCR4, ARID1A, CD79

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97
Q

What are the markers for WM

A

IgM, CD19, CD20 and CD22 positive; CD10 and CD23 neg

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98
Q

What is the presence of CXCR4 associated with

A

Higher BM dz burden and higher incidence of hyperviscosity

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99
Q

What is the treatment for WM

A

Plasmapharesis; ibrutinib in patients with sx - targets bruton tyrosine kinase; can also use rituximab, bendamustine, cyclophosphamide, or bortezomib

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100
Q

What is POEMS syndrome

A

Polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes

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101
Q

What is the diagnostic criteria for POEMS

A

All of the following must be met:
Polyneuropathy, monoclonal plasma cell proliferative disorder, any one off the following (sclerotic bone lesions, castelman’s dz, elevated VEGF), any one off the following (organomegaly -HSM or LAD, extravascular volume overload, endocrinopathy, skin Changes, papilldema, or thrombocytosis/polycythemia)

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102
Q

What is gamma heavy chain dz

A

Franklin dz; LAD, ever, anemia, malaise, HSM, and weakness, *palatal edema resulting from involvement of waldeyer’s ring; reacts with anti-IgG but not antilight chain; die of infection; usually rapid downhill course

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103
Q

What is alpha heavy chain dz

A

Seligmann dz; most common heavy chain dz; related to Mediterranean lymphoma (where intestinal parasites are common); infilatration of lymphocytes in lamia propria of small intestine; no hyperviscosity; no light chains; present with chronic diarrhea, weight loss, and malabsorption mesenteric and paraaortic LAD; IPSID assoc with campylobacter

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104
Q

What is mu heavy chain dz

A

Subset of CLL; presence of vacuoles in malignant lymphocytes; diagnosis required ultracentrifugation or gel filtration to confirm nonreactivity of paraprotein with light chain;; treated same as CLL

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105
Q

What is AA amyloid

A

Composed of acute phase reactant protein serum amyloid A - occurs chronic inflammation or infection (secondary amyloidosis)

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106
Q

What tissue should you test to confirm diagnosis of systemic amyloidosis

A

Abdominal fat

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107
Q

How does renal amyloidosis manifest

A

Proteinuria and hypoalbuminemia, secondary hypercholesterolemia, hypertriglyceridemia, edema, anasarca

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108
Q

What is the leading cause of death of amyloidosis

A

Cardiac failure

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109
Q

What is raccoon eye sign indicative of

A

AL amyloidosis

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110
Q

How do you treat AL amyloidosis

A

Dexamethasone, high dose melphalan followed by HSC transplant

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111
Q

How do you manage nephrotic syndrome caused by amyloidosis

A

Diuretics, supportive stockings, albumin

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112
Q

What meds are contraindicated in amyloidosis

A

Beta blockers digitalis and calcium channel blockers

113
Q

What activates secondary Hemostasis

A

Tissue factor binding Factor VII

114
Q

What can measure increased bleeding time as a result of liver dz

A

Levels of fibrinogen, fibrinogen degradation products and D dimmer

115
Q

What can cause prolonged PT

A

Warfarin, factor VII deficiency, vitamin K def, liver dz

116
Q

What can cause a prolonged PTT

A

Heparin; lupus anticoagulant, vWD, factor VIII, IX, XI, XII def

117
Q

What can cause prolonged PT and PTT

A

Heparin, warfarin, DIC, liver dz, factor V or X, prothrombin, or fibrinogen def

118
Q

What can cause increased thrombin time

A

Heparin, direct thrombin inhibitor, factor Xa inbhitor, fibrin degradation product

119
Q

At what platelet level does spontaneous bleeding occur

A

<10k

120
Q

What are the factor Xa inhibitors

A

Fondaparinux, rivaroxaban, apixaban

121
Q

What are the direct thrombin inhibitors

A

Argatroban, lepirudin, dabigatran

122
Q

What coagulapathies will cause an increase in PT/INR

A

Liver dz, vit K def DIC

123
Q

What is a cause of acquired inhibitors of clotting factors

A

Phenytoin, sulfa drugs, penicillin, malignancy, autoimmune disorders; present with tissue hematomas but not hemarthrosis

124
Q

What does IV vitamin K in crease the risk of

A

Anaphylaxis use FFP if need urgent correction

125
Q

What do you manage INR in patients taking vitamin K antagonists

A

Withhold drug if <5; if >5 but <9 add oral vit K; if >9 use FFP or recombinant factor VII

126
Q

What can you do to reverse direct thrombin inhibitors

A

Fluid and blood products if bleeding moderately; can use hemodialysis; severe bleeding use prothrombin complex concentrations or factor VII

127
Q

How do you reverse factor Xa inhibitors

A

Bleeding - discontinue; hemodialysis does NOT work; give PCC or recombinant factor VII

128
Q

What is the most common infection associated with DIC

A

Gram negative sepsis

129
Q

What does factor V Leiden mutation cause

A

Protein C resistance (cant inactivate 5 and 8)

130
Q

How is protein C deficiency inherited

A

AR; causes warfarin induced skin necrosis

131
Q

How is protein S inherited

A

AD; cofactor to protein C so also leads to less protein C activity (increased fibrin)

132
Q

What is the inheritance pattern of antithrombin deficiency

A

AD *suspect if clot does not respond to heparin

133
Q

What factors does antithrombin decrease the production of

A

XII, XI, X, IX and II

134
Q

What causes hyperhomocystinuria

A

Inherited mutation in MTHFR

135
Q

What is the most common form of acquired thrombophilia

A

Antiphospholipid ab syndrome

136
Q

What can cause acquired hyperhomocysteinemia

A

B6, B12, and folate deficiency

137
Q

Should you screen children under 15 for thrombophilia if they are asymptomatic

A

No

138
Q

What are the factors that suggest an increased risk for inherited thrombophilia

A

Thrombosis <50 years old, hx of recurrent thrombosis, first degree relatives with thrombosis, unusual site of thrombosis (mesenteric, splenic, portal, hepatic, cerebral, UE), thrombotic event during pregnancy or postpartum, thrombotic event while taking OCP, hx of recurrent pregnancy loss

139
Q

What can artificially decrease protein C and S levels

A

Warfarin

140
Q

When should yo discontinue anticoagulation in patients heterozygous for factor V Leiden or prothrombin G20210A mutation

A

3-6 months; extend therapy only if cancer, persistently elevated anticardiolipin abs, or antithrombin deficiency

141
Q

Has vitamin B or folic acid helped with VTEs in hyperhomocystinemia

A

Nope

142
Q

What are unna boots

A

Compressive dressings treated with agents to decrease edema and promote healing of ulcers caused by venous stasis

143
Q

What is the Wells score

A

Prediction of DVT

144
Q

What test should patients with low clinical likelihood of DVT undergo

A

D dimer (negative will rule out DVT); if D dimer is positive then do US Doppler

145
Q

What is unique to lymphedema

A

Toe edema

146
Q

How do you treat DVT

A

Unfractionated or low molecular weight heparin (outpatient); long term with warfarin - overlap with heparin for 5 days and until INR has reached therapeutic range (2-3) for 2 measurements taken 24 hrs apart *treamtent for min of 3 months

147
Q

What is the only test that can exclude PE

A

Totally normal V/Q

148
Q

Do V/Q scans use contrast

A

No

149
Q

What is the Wells criteria for DVT

A
  • active cancer: point
  • bedridden >3 days or major surgery within 4 weeks:1 point
  • calf swelling >3cm: 1 point
  • collateral superficial veins:1 point
  • entire leg swollen: point
  • localized tenderness along deep venous system: 1 point
  • pitting edema confined to sx leg: 1 point
  • paralysis of LE: 1 point
  • previous DVT: 1 point
  • alternative diagnosis to DVT as likely or more likely: -2
150
Q

What do scores from the Wells criteria indicate

A

0 or lower: d-dimer testing; negative means no DVT and no further testing; if positive -> US

  • 1-2: moderate risk; do high sensitivity d-dimer; neg rules out DVT; positive -> US
  • 3 or higher suggest DVT is likely
151
Q

What lifestyle habit can cause neutrophilia

A

Smoking

152
Q

When is pain in LN after drinking beer reported

A

Hodgkin

153
Q

Radiation can cause all Leukemias except …..

A

CLL

154
Q

What is sweet’s syndrome

A

Aka acute febrile neutrophilic dermatitis; cutaneous manifestation of AML; bx demonstrates myeloblasts in dermis; treatment is management of AML

155
Q

Where is gingival hypertrophy seen

A

M4 and M5 variants of AML

156
Q

What are the physiologic responses to anemia

A

Increased CO, shunting of blood to vital tissues, increased concentration of 2,3 DPG in RBCs (shifts to right - affinity for oxygen reduced)

157
Q

How do you calculate MCHC

A

Hgb/Hct

158
Q

What is the cutoff for microcytic, normocytic Nd mcrocytic anemia

A

Micro <2.5th percentile

Macro >97.5 percentile

159
Q

What is the cutoff for MCHC (hypo or hyper)

A

Hypo <32; hyper >35

160
Q

What are the causes of anemia in the neonate

A
  • blood loss
  • Immune hemolytic anemia (pos direct Coombs, indirect bilirubin, normocytic anemia, elevated reticulocyte count)
  • congenital hemolytic anemia: G6PD def(Heinz bodies and bite cells), pyruvate kinase def (spur cells)
  • congenital infection: *parvovirus
  • diamond Blackfan syndrome: macrocytic anemia with low reticulocyte count; congenital pure red cell aplasia (increased apoptosis of precursors)
  • fanconi anemia: macrocytic, reticulocytopenia, thrombocytopenia, leukopenia; *most common form of inherited aplastic anemia; progresses to pancytopenia
161
Q

What are the causes of anemia in infancy and toddlers

A
  • iron deficiency anemia; target cells; microscopic loss in blood due to milk
  • chronic infection: normocytic; low transferrin; Ferritin can be elevated
  • blood loss
  • disorder of Hb structure: thalassemia (low mentzer index - MCV/RBC count if >13 iron def <13 thalassemia, Hb, basophilic stippling); sickle cell
  • RBC enzyme defects
  • acquired hemolytic anemia
  • transient eythroblastopenia of childhood
  • *lead poisoning - microcytic hypochromic; basophilic stippling
162
Q

What are the causes o anemia in late childhood and adolescence

A
  • iron deficiency

- chronic dz

163
Q

What does normal reticulocyte count rule out

A

Fanconi, diamond Blackfan syndrome, congenital infections

164
Q

What history would suggest transient erythroblastopenia of childhood

A

Recent viral infection

165
Q

Where do you see Howell jolly bodies

A

Hereditary spherocytosis; AD

166
Q

What are the most common types of pediatric cancers

A

0-14: leukemia

15-19: lymphoma

167
Q

What are B sx

A

Fever >39, weight loss >10% body weight over 6 months, drenching night sweats

168
Q

What should any patient with suspected HL undergo before LN biopsy

A

Chest radiography to rule out mediastinal mass

169
Q

What can increase a child’s risk for NHL

A

SCID
Wiskott-Aldrich syndrome: X linked recessive; recurrent Sino pulm infections and ear infections, severe atopic dermatitis, bleeding secondary to thrombocytopenia
Ataxia telangiectasia
Bloom syndrome

170
Q

What are the subtypes of NHL in kids

A

Burkitt, lymphoblastic, diffuse large B cell, anaplastic large cell

171
Q

What does survival of pediatric NHL depend on

A

Pathological subtype, tumor burden (reflected by serum LDH), presence or absence of CNS dz and sites of met spread

172
Q

What is the definition of LAD

A

LN that are abnormal in number, size or consistency

173
Q

Where are common spots for LAD

A

Cervical, supraclavicular, axillary , inguinal

174
Q

What is considered an enlarged LN

A

> 2cm

175
Q

What does the quality of the LN tell you about your diagnosis

A
  • tender, warm, red, fluctuant: lymphadenitis
  • soft, mobile, smooth: benign
  • firm and rubbery: lymphoma
  • fixed and matted: malignancy or TB
176
Q

When should you biopsy LN in a kid

A

If nodes never get better after watchful waiting, if after 4-6 weeks of abx nodes don’t improve, right away if supraclavicular nodes consistent with malignancy are palpated

177
Q

How do you treat MRSA

A

Bactrim, clindamycin, vancomycin

178
Q

How do you treat cat scratch dz

A

Azithromycin, TMP-SMX, rifampin, ciprofloxin

179
Q

What are the manifestations of cat scratch dz

A

Visceral involvement, parinaud’s syndrome (conjunctivitis, preauricular adenitis, conjunctival granuloma), neuroretinits, encephalopathy, transverse myelitis, radiculitis, cerebellar ataxia

180
Q

What tumors are seen in each area of the mediastinum

A

Anterior: thymoma, teratoma, lymphoma
Middle: LN from met or granuloma, pleuropericardial and bronchogenic cysts
Posterior: neurogenic tumors, meningocele, esophageal lesions, gastroenteric cyst

181
Q

What do neuroblastomas produce

A

Catcholamines; check urine VMA and HVA

182
Q

What is WAGR

A

Wilms tumor, Aniridia, genital anomalies, mental retardation

183
Q

What is beckith wiedeman syndrome

A

Enlargement of body organs, macroglossia, hemi hypertrophy, ompalocole, WT2 mutation; increased risk of wilms tumor

184
Q

How does wilms tumor present

A

Large ab mass, hematuria, pain in ab, intestinal obstrution, HTN, pulm met

185
Q

How do you calculate ANC

A

%neutrophils + %bands x WBC / 100

186
Q

What is the definition of neutropenia

A

ANC <1500; severe if <500

187
Q

What is severe congenital neutropenia (kostmann syndrome)

A

Life threatening pyogenic infections; defect in myeloid dif; AR; ANC <200 since birth increased risk of AML ELA-2 mutation

188
Q

What is cyclic neutropenia

A

Cyclic fever, oral ulcers, gingivitis, periodontal dz, recurrent bacterial infections; AD; ANC <200 for 3-7 days every 3 weeks; ELA-2 mutation; no increased risk for malignancy

189
Q

What is schwachman-diamond syndrome

A

Triad: neutropenia, exocrine pancreases insufficiency, skeletal abnormalities; defects in neutrophil migration; AR; low serum trypsinogen, elevated fecal at, rib cage abnormalities, short stature, SBDS mutation increase risk for myelodysplastic syndrome or leukemia

190
Q

What is fanconi anemia

A

Bone marrow failure syndrome; GU and skeletal abnormalities, increased chromosome fragility; neutropenia

191
Q

What is leukocyte adhesion deficiency

A

Delayed separation of umbilical cord (>3 weeks); recurrent bacterial and fungal infections without pus; poor wound healing, periodontal dz; AR

192
Q

What is hyper-IgE or job syndrome

A

Severe eczema, bacterial infections of skin and lung; defect in chemotaxis, eosinophilia

193
Q

What is chronic granulomatous dz

A

Recurrent purulent infections with fungal or bacterial catalase positive organisms; cant generate superoxide; diagnosed with nitroblue tetrazolium test; X linked

194
Q

What viruses cause neutropenia

A

HIV, parvovirus, EBV, CMV, influenza

195
Q

What is the most common cause of neutropenia in infancy and childhood

A

Primary autoimmune neutropenia

196
Q

What platelet count would impair primary Hemostasis

A

<75 k

197
Q

What platelet count would lead to spontaneous bleeding

A

<50k

198
Q

What platelet count can cause significant bleeding

A

<20k

199
Q

What platelet count could cause life threatening hemorrhage

A

<10k

200
Q

What are the most common causes of fetal and neonatal thrombocytopenia

A

Alloimmune, congenital infection, aneuploidy, autoimmune, placental insufficiency, perinatal asphyxia, DIC

201
Q

What are the destructive thrombocytopenias

A
  • primary platelet consumption syndromes: idiopathic thrombocytopenia purpura
  • immunologic: HUS
  • nonimmunologic: TTP
  • combined platelet and fibrinogen consumption syndromes: DIC, Kassabach-Merritt
  • specific to neonate: HELLP
202
Q

What are the impaired or ineffective production of platelet causes of thrombocytopenia in kids

A
  • congenital and hereditary disorders: TAR syndrome, fanconi aplastic anemia
  • primary hematologic processes: Wiskott-Aldrich syndrome
  • acquired: marrow infiltrative process, nutritional deficiency
203
Q

What would you think of for a child with petechiae, thrombocytopenia but otherwise normal CBC

A

Meds, portal HTN, early aplastic process like fanconi anemia; kids would be sick with increased platelet destruction

204
Q

What should you think of in a kid with eczema, recurrent infections and small platelets

A

Wiskott aldrich

205
Q

What is the most common cause of isolated thrombocytopenia in otherwise well children

A

Acute ITP

206
Q

Do we treat acute ITP

A

Not usually; but can with IVIG, prednisone or anti-D immunoglobulin in RH-

207
Q

What is kasabach Merritt syndrome

A

Thrombocytopenia and hypofibrinogenemia secondary to hemangiomas and intravascular coagulation

208
Q

What are the lab finings in typical ITP

A

Normal WBC, normal reticulocyte count, normal RBC, negative Coombs

209
Q

What are the proteins involved in HIV

A
  • 2 positive ssRNA held tougher by P7
  • enclosed by capsid P24
  • RNA genome consists of 9 genes: gag, pol, env most important in making structural proteins for new virus particles
210
Q

What does the HIV capsid contain

A

Reverse transcriptase, integrate, protease

211
Q

How can HIV cause autoimmunity

A

Result of disordered cell immune function or B lymphocyte dysfunction; ie thrombocytopenia

212
Q

What are examples of allergic hypersensitivity reactions seen in AIDS

A

Eosinophilic pustular folliculitis (itchy red bump syndrome), increased hypersensitivity reaction to meds - fever and sunburn like rash with TMP-SMX

213
Q

What infections are seen at a CD4 count >500

A

Bacterial, TB, herpes simplex, herpes zoster, vagina candidiasis, hairy leukoplakia, kaposi

214
Q

What infections are seen at a CD4 count <200

A

Pneumocystosis, toxoplasmosis, cryptococcus, coccidiodes, cryptosporidosis, miliary TB, kaposi

215
Q

What infections are seen at a CD4 count <50

A

MAC, histoplasmosis, CMV retinitis, CNS lymphoma

216
Q

What do you see at CD4 <100

A

Cryptococcal, esophageal candidiasis, toxoplasmosis

217
Q

What is the testing for HIV

A

Immunoassay for HIV ab with test for p24 Ag; no western blot; positive result of HIV ab followed with testing of sample with HIV ab differentiation which confirms diagnosis BUT IF NEGATIVE, test with NAAT - if positive, then HIV, if neg initial test was false positive

218
Q

How often are CD4 counts measured

A

Every 3-6 months; if drops <200 start pneumocystis prophylactic therapy; if <100 MAC prophylaxis

219
Q

What tests the level of viral replication

A

HIV viral load

220
Q

How do you diagnosis pneumocystis

A

Chest XR; diffuse or perihilar infiltrates; don’t usually have pleural effusions (more bacterial, TB or kaposi); definitive diagnosis with wright-giemsa stain or fluorescence ab; bronchoalveolar lavage - if negative sputum but suspect pneumocystis

221
Q

What lab findings are consistent with pneumocystis pneumonia

A

Elevated LDH, serum beta glucan (more sensitive and specific), if see normal diffusing capacity of CO or no interstitial lung dz, pneumocystis unlikely, pneumothoraces (cystic appearing areas)

222
Q

What is the most common cause of pulm dz in HIV patients

A

Community acquired pneumonia

223
Q

What will you se on CT in toxoplasmosis

A

Subcortical lesions with predilection for basal ganglia

224
Q

What is the test for cryptococcal meningitis

A

Latex agglutination test of serum that detects CRAG

225
Q

What is a normal PT time

A

10-13; assesses extrinsic; factors II, V, VII, X and fibrinogen; *prolonged in warfarin or dicoumarol

226
Q

What is a normal PTT

A

25-40; tests factors VIII, IX, XI, XII prolonged in patients on heparin

227
Q

How do you treat vWD

A

Cryoprecipitate; DDAVP

228
Q

What can cause defects in platelet function

A

Uremia: impaired platelet adhesion
Dsproteinemias: interference with membrane function
Autoimmune

229
Q

What is prolonged with vit k deficiency

A

PT

230
Q

What is the defect in hereditary hemorrhagic telangiectasia

A

Endoglin; epistaxis most common symptom

231
Q

What is the clinical presentation of antithrombin III def

A

Variable from min sx to death from recurrrent PE;recurrent DVT, leg ulcers, etc; treat with prophylaxis anticoagulant and high doses of heparin if have DVT; replacement of anti thrombin III available if dont respond to heparin

232
Q

What does protein C do

A

Inactivate factor V and VIII

233
Q

How do you treat protein C and S def

A

Warfarin ***but most common cause of hypercoagulble state from def of these proteins is initiation of warfarin - depleted. Earlier than th other factors resulting in increase coagulation

234
Q

What is the treatment for factor V Leiden

A

If no prior episodes, monitor, DVT prophylaxis and risk reduction
Prior episodes life long anticoagulation

235
Q

What are associated features of antiphospholipd ab syndrome

A

Connective tissue dz; prolonged PTT that fails to correct with mixing studies

236
Q

How do you diagnose antiphospholipid ab syndrome

A

Prolonged PTT not corrected with mixing studies, neutralization of inhibitor with excess phospholipid; *dilute Russell viper venom time (DRVVT) may be more specific

237
Q

What is the treatment for antiphospholipid ab syndrome

A

No benefit if no hx of thromboembolic dz; with a hx, lifelong anticoauglation BUT NEED multiple positive tests over a 3-12month period; during pregnancy treat with SC heparin; hydroxychloroquine can help with APS and SLE

238
Q

What do you do for pseudothrombocytopenia

A

Repeat CBC in heparin or citrate tube

239
Q

What drugs can cause thrombocytopenia

A

Loop diuretics, H2 blockers, digoxin and abx

240
Q

What is liskers sign

A

Pain with percussion of anteriomedial tibia

241
Q

What is lowenergs sign

A

BP cuff applied to mid calf; pain when inflated to 80

242
Q

What drugs can cause hypercoagulability

A

Tamoxifen, bevacizumab, thalidomide and lenalidomide

243
Q

What conditions can affect d dimer levels

A

DVT/PE, stroke, age, malignancy, pregnancy, recent surgery, DIC, cocaine, connective tissue dz, hemodialysis

244
Q

What is the management of acute DVT or PE

A

Anticoagulate for 3 months then reassess

245
Q

How do you anticoagulate cancer patients

A

Low molecular weight heparin. (Enoxaparin)

246
Q

What are the cytogenic of myelodysplasias

A

Partial or total loss of chrom 5 or 7; inv 16, trisomy 8

247
Q

What lab abnormalities can you see with mylodysplasias

A

Elevated LDH, sometimes iron overload (increased serum ferritin, serum iron and TIBC normal)

248
Q

Which myelodysplastic syndrome has the lowest risk of conversion to AML

A

Refractory anemia with rings sideroblastic

249
Q

What is the treatment for B6 def

A

Replace for 6 months then repeat marrow; if no improvement patient has pyridoxine resistant sideroblastic anemia

250
Q

What are adverse prognostic features of myelodysplasias

A

Marrow blasts >5%, platelets <100,000, Hb <10, neutrophils <2500, age >60, *monosomy 7, hypodiploidy, multiple abnormalities

*5q deletion is favorable and responds to lenalidomide

251
Q

How do you treat iron overload in patients with myelodysplasias

A

Desferrioxamine or deferasirox

252
Q

At what EPO level should you not administer EPO

A

If serum EPO >500

253
Q

What can androgens be used to treat

A

Myelodysplasias

254
Q

Are corticosteroids used to treat myelodysplasias

A

NO

255
Q

What is low/intermediate therapy for myelodysplasias

A

Hypomethylating agents: azacitidine, decitabine

Lenalidomide: angiogenesis inhibitor for 5q deletion only

256
Q

What is high intensity therapy for myelodysplasias

A

AML induction style treatment

HSC transplant: if <60

257
Q

What will you see with myelofibrosis

A

Massive splenomegaly **Triad = leukoerythroblastic anemia, poikilocytosis and splenomegaly

258
Q

What is the most common cause of death in myelofibrosis

A

Overwhelming infection

259
Q

What can ruxolitinib be used to treat

A

Myelofibrosis; JAK inhibitor

260
Q

What are the labs of polycythemia Vera

A

Increased RBC, nucleated RBCs, elevated LAP, increased WBC or platelet counts

261
Q

What is the cause of death in polycythemia Vera

A

Progressive fibrosis - spent phase

262
Q

What could be on your differentials for polycythemia Vera

A

Hemoconcentration, pulm dz (smokers erythrocytosis), EPO producing tumors (RCC, neuroendocrine), hemoglobinopathy, living at high altitude (low FiO2)

263
Q

What is the definition of neutropenic fever

A

Temp >101.4 with ANC,500

264
Q

What agents cause neutropenic fever

A

Indwelling venous catheters - staph aureus and epidermidis, klebsilla
Fungal: candida, aspergillus, pneumocystis and toxoplasma

265
Q

What should you NOT do if a patient has neutropenic fever

A

No rectal exams

266
Q

What is the primary prophylaxis of neutropenic fever

A

-if <500 for >7 days; levofloxacin and ciprofloxacin; fluconazole (but no activity against aspergillus) so use echinocandins (caspofungin, micafungin, anidulafungin) but only IV

267
Q

What is secondary prophylaxis for neutropenic fever

A

Prevents RECURRENT infection; for patients with hx of prior fungal infection; voriconazole first line for aspergillus but cant give with cytarabine or fludarabine - severe neurotoxicity with vincristine so give 1 week prior to chemo and then start after chemo again; if continued during chemo amphotericin B or echinocandins can be used

268
Q

What is empiric therapy for neutropenic fever

A

When suspected neutropenic fever is occuring; IV abx given until ANC >1000 then switch to oral abx only if patient is afebrile and tolerating meals without emesis

*IV: piperacillin + tazobactam, carbapnm, ceftazidime, cefepime

269
Q

How do you adjust empiric abx based on specific data

A

If have cellulitis or pneumonia - vanc or linezolid
Gram neg: add aminoglycoside
Ab sx or suspected c diff: metronidazole

270
Q

What are the outpatient oral regimes for empiric treatment for neutropenic fever

A

Ciprofloxacin + amoxicillin/clavulanic acid

Empiric antifungal should be added if persistent or recurrent fever does not resolve after 5 days - give caspofungin

271
Q

What is low risk post op patient

A

<40 no risk factors; minor surgery

272
Q

What are the intermediate risk factors

A

Non ambulatory, active infection, active malignancy, non orthopedic surgery, history of VTE, stroke, CVC or PICC, IBD, prior immobilization pre op, obesity, age >50, OCP, hypercoagulability, nephrotic syndrome, burns, cellulitis, varicose veins, paresis, systolic heart failure ,COPD

273
Q

What agents can be used for post op antioagulation

A

LMWH (enoxaparin), fondaparinux, DOACs, warfarin

274
Q

When do you use LMWH

A

Most critical care patients, many surgical patients (4 weeks in ab/pelvic cancer surgery), orthopedic patients (twice daily 10 day min), bariatric surgery (twice daily)

275
Q

When do we use fondaparinux

A

Orthopedic patients (10 day min)

276
Q

When do we use rivaroxaban or apixaban (DOAC)

A

Orthopedic patients s/p THA o TKA for 12 days (knee) and 35 days for hip

277
Q

When do we use dabigatran (DOAC) direct thrombin inhibitor

A

Cleared by kidney so use for THA only if CrCl >30 ml/min.

278
Q

When do we use warfarin

A

Goal: INR 2.5; administer to orthopedics patients for 10 days; if high risk and THA, TKA or hip fracture, up to 1 month