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Fennel the Cat Step 2 > Step 2 Heme/Onc > Flashcards

Step 2 Heme/Onc Flashcards

1
Q

Heparin: MOA and Corresponding lab

A

Activates antithombin, therefore inhibiting thrombin and preventing conversion of fibrinogen to fibrin. Active in common pathway. Checked by checking PTT. Antidote is protamine sulfate. LMWH has more effect on factor Xa and LMWH does not increase PTT

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2
Q

Warfarin: MOA and Corresponding lab

A

Inhibits vitamin K epoxide reductase thereby inhibiting synthesis of K-dependent clotting factors II, VII, IX, X, C and S. Check lab with PT and INR. Therapeutic target for INR=2-3. Rapid reversal =FFP or Vitamin K. Warfarin is teratogenic

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3
Q

tPA: MOA and Corresponding lab

A

Aids conversion of plasminogen to plasmin, which breaks down fibrin. Increases PT and PTT. treat toxicity with aminocaproic acid

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4
Q

ApiXaban, and RivaroXaban: MOA and lab?

A

Factor Xa Inhibitors: PT/PTT not monitored. No reversal agent

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5
Q

LMWH (enox)

A

Mainly inhibits factor Xa. Antifactor Xa can be monitored but enox is typically not monitored. Protamine is less effective at reversal

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6
Q

Direct thrombin inhibitors (Dabigatran and argatroban)

A

Directly inhibits factor II/thrombin) No lab monitoring. Idaracizumab can reverse dabigatran.

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7
Q

3 types of hemophilia, deficient clotting factors. PDT

A

A: XIII, B: IX, C:XI. Pts will have elevated PTT. Best initial test: mixing study. Tx: factor replacement or desmopressin, which releases factor VIII from endothelial cells

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8
Q

VWD PDT

A

Autosomal defect or deficiency in platelets. Often presents in childhood with recurrent and mucosal bleeding. Lab: increased bleeding time. +/- increased PTT. PT and plt count will be NL. Most accurate test: Ristocetin cofactor assay (that will show decreased agglutination) and vWF antigen level. Tx: DDAVP. Note: ASA increases bleed risk in pts w VWD.

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9
Q

3 common hypercoaguable states?

A

Factor V leiden, HIT (a rapid 50% drop in PLTs), antiphospholipid syndrome.

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10
Q

How long do you treat pts a hypercoaguable state who have had a DVT or PT? With what?

A

heparin immediately, followed by 3-6 months of warfarin for first event. if second event, 6-12 months of warfarin, if 3rd, lifelong anticoag is needed.

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11
Q

Diagnstic clinical features of DIC?

A

Thrombosis and hemorrhage. DIC is an acquired coagulopathy caused by deposition of fibrin in small blood vessels leading to thrombosis and end-organ damage. Depletion of clotting factors and platelets leads to a bleeding diathesis. Common associations with DIC: OB complications, sepsis, neoplasms, acute promyelocytic leukemia, pancreatitis, hemolysis, vascular disorders (aortic aneurysm), massive trauma, drug reactions, acidosis and ARDS. DIC may be confused w liver disease but unlike liver dz, factor VIII is depressed.

Clinical presentation: acute: bleeding from venipuncture sites, bleeding into organs, ecchymoses and petichiae. Chronic: bruising and mucosal bleeding, thrombophelbitis, renal dysfunction, and transiend nrueologic syndromes.

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12
Q

TTP PDT. 5 sx that should be a tip off:

A

Deficiency of vWF-cleaving enzyme adamts-13, results in platelet microthrombi. RBCs are fragmented by contact w microthrombi, leading to hemolysis (microangiopathic hemolytic anemia). Maintain high suspicion if 3 out of 5 symptoms are present: FAT RN
1. Fever
2. Anemia: microangiopathic hemolytic anemia
3. Thromboytopenia
4. Renal changes
5. Neurologic Changes (delerium, seizure, stroke)
Clinical dx: presence of schistocytes.
Tx: plasma exchange. PLT transfusion is contraindicated as can worsen condition.

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13
Q

3 causes of micorangiopathic hemolytic anemia?

A

HUS, TTP and DIC

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14
Q

DDX for thrombocytopenia

A 
HIT SHOC
HIT or HUS
ITP
TTP or Treatment/meds
Splenomegaly
Hereditary (Wiskott-Aldrich Syndrome)
Other (malignancy)
Chemo
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15
Q

PDT for Immune thrombocytopenic purpura

A

ITP can accure follow a viral illness with abrupt onset of hemorrhagic complications. Commonly affects kids 2-6 yo. Chronically, there is insitious onset of sx or incidential thrombocytopenia. Affects adults 20-40 yo.
Diagnosis of exclusion. CPC, smear. If PLTs>30,000, and no bleeding, no tx necessary
If PLT<30m000 or bleeding: steroids or IVIG. Other tx if plt does not improve=ritux, splenectomy, or thrombopoietin receptor agnoist (romiplostim or eltrombopag).

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16
Q

Microcytic Anemia DDX:

A

TAILS: Thalassemias, ACD, Iron-deficiency, Lead, Sideroblastic

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17
Q

G6PD Deficiency triggers, best test, what will smear show?

A

G6PD deficiency leaves RBCs susceptible to hemolytic anemia, causing a normocytic anemia with increased retic. Common triggers: sulfa drugs, antimalarials, infections, fava beans. Best initial test=CBC w smear showing hemoltic anemia w bite cells and heniz bodies. Most accurate test is G6pD level a month after epidoe.

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18
Q

Most accurate test for PNH?

A

Absence of CD55/CD59 on flow cytometry. PNH is a normocytic anemia with intrinsic hemolysis (increased retics).

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19
Q

Warm AIHA and Cold AIHA. Acc’d Abs?

A

Warm: IgG, assc’d w SLE, CLL, drugs.
Cold: IgM, assc’d with mycoplasma and mono.
COLD MOM
warm Tx=steroids if severe
Cold=aboid cold and rituximab (anti CD20 Ab).

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20
Q

Hemoglobinuria predisposes to what renal issue?

A

ATN and renal failure

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21
Q

Symptoms for acute intermittent porphyria? 5 P’s

A 
Painful abdomen
Port-wine urine
Polyneuropathy
Psych disturbances
Precipitated by drugs

best initial test: urine and plasma porphyrin levels
Aboid triggers and provide symptomatic treatment. High doses of glusocse decrease heme synthesis during attacks.

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22
Q

3 types of transfusion reactions? timing + mechanism+ tx?

A

Febrile nonhemolytic reaction: fever, chills, malaise 1-6 hours post-transfusion. Caused by cytokine formation during storage of blood. Stop transfusion and give tylenol

Allergic: Prominent urticaria caused by Ab formation against donor proteins. give antihistamines. If severe reaction, stop transfusion and give epi.

Hemolytic transfusion reaction: Fever, chills, nausea, flusing, buring at IV site, tachucardia, hypotension during or shortly after transfusion. Caused by preformed or formed Abs against donor srythrocytes due to ABO mismatch or RHD antigens. Stop transfusion and give fluids.

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23
Q

Elderly man w hypochromic, microcytic anemia is asx. labS?

A

FOBT and sigmoidoscopy, suspect CRC.

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24
Q

Most common inherited cause of hypercoagulability

A

Factor V leiden mutation

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25
Q

most common inherited bleeding disorder

A

VWD

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26
Q

Most common inherited hemolytic anemia + diagnostic test?

A

hereditary spherocytosis. osmotic fragility test.

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27
Q

What type of anemia causes pure RBC aplasia?

A

Diamond-Blackfan anemia

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28
Q

Anemia associated with absent radii and thumbs, diffuse hyperpigmentation, cafe-au-lait spots, microcephaly, and pancytopenia?

A

Fanconi anemia

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29
Q

Medications and viruses that lead to aplastic anemia.

A

Chloramphenicol, sulfonamides, radiation, HIV, chemo, hepatitis, parvo, EBV

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30
Q

How to distinguish primary vs. secondary polycythemia?

A

Both will have increaed HCT and RBC mass but primary /polycythemia vera will have a normal O2 sat and low EPO levels

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31
Q

HUS triad?

A

Anemia, Thrombocytopenia and acute renal failure

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32
Q

TTP tx?

A

Emergent plasmapheresis, steroids, antiplatelet drugs. PLT transfusion is contraindicated

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33
Q

ITP tx in kids

A

usually supportive care only. But if severe, steroids and IVIG

34
Q

Which of the following are increased in DIC: fibrin split products, D-dimer, fibrinogen, platelets, and hematocrit?

A

Fibrin split products and D-dimer are elevated. Plts, fibrinogen and hematocrit are decreased.

35
Q

A 9yo w hemarthrosis and PTT increased w/ nl PT and bleeding time. Dx? Tx?

A

Hemophilia A or B. Consider mixing study, consider sesmopressin for Hemo. A

36
Q

14 yo w prolonged BT after dental procedure, nl PT, increased PTT. Dx? Tx?

A

vWD. tx w desmopressin, FFP or cryoprecipitate.

37
Q

60 yo AA man w bone pain. work up for multiple myeloma might reveal?

A

lytic lesions in skull and long bones., serum protein analysis w M-spike, Benge Jones proteinuria

38
Q

Reed sternberg cells present in what dz?

A

Hodgkin lymphoma

39
Q

10 yo w b-cell cymptoms and anterior mediastinal mass. Dx?

A

NHL

40
Q

80 yo man w fatigue, lymphadenopathy, spelnmegaly and isollated lymphocytosis. Suspected dx?

A

CLL

41
Q

Pt w fatigue found to have increased MCV and decreased Hb. DDX?

A

folate, B12, alcohol,

42
Q

late, life-threatening complication of CML

A

Blast crisis (fever, bone pain, splenomegaly, and pancytopenia)

43
Q

Auer rods on blood smear

A

AML

44
Q

AML sybtype associated w DIC?

A

M3. Tx w retinoic acid

45
Q

Electrolyte changes in tumor lysis syndrome?

A

Hyper Phos, Hyper K, Hypoca, Hyperuricemia

46
Q

50 yo w early satiety, splenomegaly, bleeding and t(9,22)?

A

CML

47
Q

Pt w ANC of 1000 a fever? best next step?

A

broad-spectrum ABX

48
Q

10 yo with Sickle cell dz presents w bone pain. Mangamenet?

A

O2, hydration, pain management, if severe, transfuse

49
Q

Significant cause of morbidity in thalassemia patients?

A

Iron overload. Tx=deferoxamine

50
Q

15 yo presents with WBC of 56,000 following dx of mono. MD orders a leukocyte alk phos to distinguish between a leukemoid reaction and malignancy. What do you expect?

A

The leukocyte alk phos (LAP) would be elevated in a mono patient. In contrast, LAP would be decreaesd in a pateient with a hematologic malignancy

51
Q

Common lab finding in patients w CLL?

A

Lymphocytosis (increased NK, T or B ells)

52
Q

Common lab finding in patients w CML

A

Increased granulocytes. (neutrophils, eosinophils, basophils)

53
Q

40 yo w fatigue, hepatosplenomegaly, peripheral smear shows myeloblasts w kidney shaped nuclei and prominent nucleoli. Dx?

A

AML. Think MPO+ and Auer rods present. Fine granules in myeloblasts.

54
Q

40 yo w weight loss and splenomegaly. CBC shows high WBC count. LDH, Urate, and B12 levels are high. Most accurate test? Dx?

A

CML. Most accurate test: t(9:22) cia PCR or FISH.

55
Q

PDT for hairy cell leukemia

A

P: pancytopenia, splenomegaly, fatigue, petechiae, bruising, infection (esp. w MAC), abd. pain, early satiety
Best initial test: CBC w smear showing mononuclear cells w mnay cytoplasmic projections (hairy cells) that stain w TRAP (tartrate-resistant acid phosphatase.
T: cladribine, alternatives include splenectomy and IFN-alpha

56
Q

NHL vs. HL. Nodal involvement of each? Cell line distinctions? Epi?

A

NHL has many peripheral nodes involved, can have extranodal and non-contiguous spread. HL involves a single group of localized nodes, spreads contiguously, rarely involves extranodal sites.
NHL comprised mainly of B-cells, rarely T.
HL has Ree-Sternberg cells (owl eyes). Distinct CD 15+ and CD30+ cells.
NHL peak incidence 65-75.
HL bimodal age distribution of old and young.
NHL assc’d w HIV and autoimmune conditions.
HL associated with EBV.

57
Q

When are lymphnodes more likely to be benign?

A

Benign usually = from infection

Benign nodes are generally bilateral, <1cm, mobile, nontender in viral infxn and tender in bacterial infxn

58
Q

PDT for Multiple Myeloma

A

P:
Mnemonic: MM=CRAB: hyperCalcemia, Renal involvement, Anemia, Bone pain (lytic lesions)

D: best initial test=SPEP showing IgG or IgA (resulting in M spike)

Most accurate test: bone bx showing > 10% monoclonal CD 138+ plasma cells.
Also CBC shows rouleax, urinalysis may show Bence Jones protein. Total protein:albumin gap is often elevated.

Tx: pts<70 can be tx w autologous bone marrow transplant
older than 0=melphalan (an oral alkylating agent) and prednisone

59
Q

What is a monoclonal expansion of plasma cells that is asymptomatic and may eventually lead to multiple myeloma?

A

MGUS

60
Q

What renal syndrome may result from multiple myeloma?

A

adult Fanconi syndrome can develop due to renal tubule damage

61
Q

PDT for Waldenstrom Macroglobulinemia

A

P: malignant monoclonal gammopathy w eelevated IgM levels and hyperviscosity syndrome. Pts present w lethargy, weight loss, Rayaud, neuro problems including mental status changes, sensorimotor peripheral neuropathy and blurry vision (engorged blood vessels can be noted on eye exam). MGUS is a precusor.
Dx: one Bx and aspirate. Abnormal plasma cells w Dutcher Bodies (PAS+ IgM deposits around nucleus). SPEP, and UPEP can also be used. labs may also reveal: elevated ESR, urate, LDH and Alk Phos

T: Chemo for underlying malignancy

62
Q

3 disorders that involve elevated IgM?

A

Cryoglobulinemia, Waldenstrom macroglobulinemia, and cold agglutinins. Note that cryoglobulinemia is most common in HCV and has systemic signs such as joint pain and renal involvement whereas cold agglutinins cause numbness upon cold exposure and are seen w EBV, mycoplasma infxn and Waldenstrom.

63
Q

ANC cutoff?

A

<1500

64
Q

Causes of secondary eosinophilia

A

NAACP: Neoplasm, Allergies, Asthma, Collagen vascular disease, Parasites

65
Q

level for eosinophilia?

A

Absoloute eosinophil count>350/mm

66
Q

Xeroderma pigmentosum. Associated Neoplasm?

A

squamous cell and basal cell carcinomas of the skin

67
Q

Actinic keratosis

A

squamous cell carcinoma of skin

68
Q

Multiple dysplastic nevi

A

malignant melanoma

69
Q

Down syndrome

A

ALL

70
Q

Immunodeficiencies

A

Malignant lymphomas

71
Q

AIDS

A

NHL and KS

72
Q

Autoimmune diseases (myasthenia gravis)

A

benign and malignant thymomas

73
Q

chronic atrophic gastritis, pernicious anemia, postsurgical gastric remnants

A

gastric adenocarcinoma

74
Q

Barret esophagus (chronic GI reflus)

A

esophageal adenocarcinoma

75
Q

Plummer-Vinson syndrome (atrophic glossitis, esophageal webs, anemia, all due to iron deficiency)

A

squamous cell carcinoma of the esophagus

76
Q

Acanthosis nigricans

A

visceral malignancy (stomach, lung, breast, uterus)

77
Q

Tuperous sclerosis (facial angiofibroma, seizures, mental retartadation)

A

astrocytoma and cardia rhabdomyoma

78
Q

Paget Disease of bone

A

secondary ostepsarcoma and fibrosarcoma

79
Q

Pt w recent splenectomy surgery. now w increased plt count. dx?

A

Secondary (reactive) thrombocythemia. Spleen removes old plts and spleen is now gone. therefore elevated plts.

80
Q

5 Ps of acute intermittent porphyria?

A

“five P’s” of acute intermittent porphyria: Painful abdomen, Polyneuropathy, Psychologic disturbances, Precipitated by drugs/alcohol, and Purple pee.

81
Q

PDT for myelodysplastic syndrome

A

Epi: Hamatopoietic stem cell neoplasm
Risk increases with older age, previous chemotherapy
May transform to acute leukemia
P: Cytopenias (anemia, leukopenia, thrombocytpenia). HSM & lymphadenopathy
D: Dysplastic WBC+RB (ovalomacrocytosis and neutrophil hyposegmentation)
BMB (hypercellular marrow)
T: Transfusion for cytopenias
Chemo
hematopoietic stem cell transplant

Fennel the Cat Step 2 (15 decks)

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