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Heme/Onc Flashcards

1
Q

How does Factor V Leiden cause hypercoagulable state?

A

Usually activated protein C proteolytically inactivates Va (and VIIIa). Va Leiden doesn’t get cleaved as well. Furthermore, Va helps prothrombin - >thrombin.

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2
Q

How prevent tumor lysis syndrome?

A

Hydration and hypouricemic agents like allopurinol (xanthinse oxidase inhibitor) or rasburicase (urate oxidase which makes uric acid into allantoin)

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3
Q

Hydroxyurea tx for sickle cell?

A

Increases Hb F synthesis by unknown mechanism. Use for those w/ freq. pain crisis.

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4
Q

HUS

A

Microangiopathic hemolytic anemia, thrombocytopenia, renal insufficiency. Typically after EHEC O157:H7 -> hemorrhagic diarrhea and cramping, undercooked beef/unpasteurized milk. Endothelial injury > isolated activation of PLT = micro thrombi -> schistocytes w/o coagulation system activation (DIC).

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5
Q

HbC?

A

Glutamic acid -> Lysine (Neg to POS). Less movt non electrophoresis.

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6
Q

FFP vs. Cryoprecipitate

A

FFP contains all coagulation factors. Cryo only contains cold-soluble proteins (VIII, fibrinogen, vWF, vitronectin, XIII). Cold F-Eight von Vitronectin!

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7
Q

High dose ADH affects coagulation how?

A

Increases factor VIII activity in pts with Hemophilia A and von Willebrand disease.

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8
Q

Von willebrand Disease

A

AD with variable penetrance. vWF is mediator of platelet adhesion. Absence leads to function factor VIII and pot deficiency = inc. PTT and inc. bleeding time.

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9
Q

Where does 2,3-DPG bind?

A

To the two beta subunits of HbA after Hgb is deoxygenated. HbF (2 alpha, 2 gamma) does NOT bind to 2,3-DPG as well, so binds to O2 with HIGHER affinity (usu. bad, except helpful for HbF).

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10
Q

Polycythemia vera

A

Plethoric face, splenomegaly, peptic ulceration, itching, gouty arthritis. Mutation in JAK2 = non-receptor tyrosine kinase associated with EPO receptor. Constiutive kinase activation -> inc. production of blood cells.

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11
Q

Vincristine, bleomycin, doxorubicin, cyclophosphamide side effects

A

Vincristine - neurotoxicity. Bleomycin - pulmonary fibrosis and flagellate skin discoloration, doxo - CHF, cyclo - hemorrhagic cystitis.

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12
Q

Precursor B-ALL vs T-ALL immunophenotypes

A

TdT+, CD10+, CD19+ vs. all T-cell (CD2,3,4,5,7,8), TdT, and CD1a

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13
Q

Mature B-cell leukemia immunophenotypes

A

CD19 and co-express CD5 (T-cell)

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14
Q

Hemophilia A vs. B

A

VIII vs. IX. Both have isolated PTT elongation.

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15
Q

Desmopressin acetate effect on clotting?

A

Releases vWF and VIII (think Hemophilia A) from the endothelium.

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16
Q

Plummer-Vinson/Patterson Kelly Syndrome

A

Formation of esophageal webs 2/2 to Fe-deficiency anemia -> dsyphagia. Disfigured fingernails are also specific for Fe-deficiency anemia. Atrophic glossitis

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17
Q

How do parasethesias occur after pRBC transfer?

A

Citrate in transfusions can chelate Ca+ –> hypocalcemia. Requires massive transfusions (5-6L/24h)

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18
Q

Reticulocyte characteristic

A

Immature RBC that is slightly LARGER and BLUER (2/2 ribosomal RNA). Lacks cell nucleus.

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19
Q

BCR-ABL

A

CML (chromosome 9 to chromosome 22). Imatinib.

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20
Q

t(8;14)

A

Burkitt lymphoma

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21
Q

Acute promyelocytic leukemia

A

Subset of AML. Can present with persistent infection and COAGULOPATHY -> hemorrhagic signs and symptoms. Biopsy with promyelocytes with intracytoplasmia AUER rods. t(15;17) -> alpha RETINOIC acid receptor w/ PML.

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22
Q

Histopath of follicular lymphoma?

A

LN biopsy shows aggregates of packed follicles. Mostly centrocytes > centroblasts (larger). T(14;18) w/ BCL-2 over-expression.

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23
Q

ITP vs. DIC?

A

ITP has ISOLATED thrombocytopenia (dec. plt count and increased bleeding time). DIC has throbocytopenia, INC PT, PTT, DEC plasma fibrinogen, and RBC fragmentation.

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24
Q

TTP vs. HUS?

A

Disease spectrum w/ pentad of fever, neuro, ARF, thrombocytopenia, microangiopathic hemolytic anemia. TTP adults w/ neuro. HUS children with renal. NO COAG involvement.

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25
Q

Osmotic fragility test

A

Spherocytes are more susceptible to hypertonic saline. Sickle cells are NOT.

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26
Q

Complications of hereditary spherocytosis?

A

Pigment gallstones, asplastic crises 2/2 parvovirus B19

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27
Q

What are the important platelet receptors?

A

GpIb for vWF receptor. GpIIb/IIIa for fibrinogen receptor.

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28
Q

What granules do platelets carry?

A

Dense granules (ADP and Ca2). Alpha granules (vWF, fibrinogen)

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29
Q

Hypersegmented polys?

A

Vitamin B12/folate deficiency

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30
Q

Surface marker for macrophages?

A

CD13, CD14, CD15, CD64

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31
Q

Causes of eosinophilia?

A

NAACP = Neoplasia, Asthma, Allergic processes, Connective tissue diseases, Parasites

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32
Q

Basophil function?

A

Mediates allergic reaction. Basophilic granules contain heparin, histamine, leukotrienes (SRS-A: “slow reacting substance of anaphylaxis”)

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33
Q

What drug prevents mast cell degranulation?

A

Cromolyn sodium

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34
Q

B lymphocyte CD’s?

A

CD 19, CD20.

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35
Q

Treatment to prevent hemolytic disease of the newborn?

A

Rho(D) immune globulin. Which is IgG (there CAN cross placenta but doesn’t cause disease b/c it is in low levels….) Apparently IgG > IgM, so that’s why they use IgG.

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36
Q

Roles of bradykinin

A

Vasodilation, increased permeability, and increased pain. Produced by cleavage of HMWK by kallikrein

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37
Q

Fibrin vs. Plasmin?

A

Fibrin is used for making clots. Plasmin is used to break said clots.

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38
Q

What coagulation factors does IIa activate?

A

Factors VIII, V, and XIII.

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39
Q

Extrinsic pathway key?

A

TF:VIIa

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40
Q

At what point do the intrinsic and extrinsic pathways coalesce?

A

In activating factor X. Because factor X (w/ Ca, PL, and Va) activates II.

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41
Q

Factor V Leiden mutation?

A

Produces a factor V that is RESISTANT to CLEAVAGE by Protein C.

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42
Q

Protein C pathway?

A

Activated via thrombin-thrombomodulin complex, then with Protein S, cleaves and inactivates Va and VIIIa. “Chad Ocho Cinco.”

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43
Q

What factors does anti-thrombin inhibits?

A

1972 + XI and XII.

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44
Q

Walk me through platelet plug formation.

A

Exposed collagen. vWF binds to it. Attracts PLT via GpIb receptor inducing release of ADP and Ca2+. ADP induces GpIIb/IIIa receptor expression, which attracts fibrinogen to LINK platelets. Now it’s a fight between TXA2 and PGI2/NO.

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45
Q

Ristocetin

A

Activates Gp1B-vWF interaction.

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46
Q

Drugs inhibiting ADP induction of GpIIb/IIIa receptor expression

A

Clopidogrel, ticlopidine, prasugrel, ticagrelor

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47
Q

Glanzmann thrombasthenia

A

Deficiency in GpIIb/IIIa

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48
Q

Bernard-Soulier syndrome

A

Deficiency in Gp1B

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49
Q

Causes of decreased ESR?

A

Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia.

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50
Q

Acanthocyte

A

Spiny, “spur cell.” Liver disease, abetalipoproteinemia

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51
Q

Basophilic stippling

A

Anemia of chronic disease, alcohol abuse, lead poisoning, thalassemias

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52
Q

Schistocyte

A

“Helmet” cell. DIC, TTP/HUS, traumatic hemolysis (e.g. mechanical heart valve)

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53
Q

Teardrop cell

A

Bone marrow infiltration

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54
Q

Target cell

A

HbC disease, Asplenia, Liver disease, Thalassemia

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55
Q

Heinz bodies

A

Seen in G6PD w/ crystal violet stin.

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56
Q

Howell-Jolley bodies

A

Basophilic nuclear remnants usu. removed by functioning splenic macrophages. May be sign of hyposplenia/asplenia

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57
Q

Etiological differences between alpha and beta-thalassemias?

A

Alpha thalassemias are due to the deletion of the four alpha globin genes. Beta thalamssemias are often due to mutations of splicing/promoting problems that decrease the amount of Beta-globin synthesis. Alpha not seen on electrophoresis but Beta does.

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58
Q

Lead poisoning physical findings and lab findings?

A

Burton lines (Gingivae) and lead lines on long-bones. Wrist/foot drop. Sideroblastic microcytic anemia. Accumulated protoporhyrin and d-ALA

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59
Q

Lead poisoning mech and treatment?

A

Mech - inhibits ferrochelatase and ALA dehydratase -> decreased heme synthesis and increased RBC protoporphyrin. Tx = EDTA and dimercaprol.

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60
Q

Causes of sideroblastic anemia?

A

EtOH (mitochondrial damage), vitamin B6 deficiency/INH (ALA synthase problem), X-linked defect in ALA synthase gene, lead poisoning. Tx = pyridoxine

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61
Q

Lab differences between B9 and B12 deficiency?

A

B12 involved in making methionine from homocysteine and well as in making methylmalonic acid into succinyl-CoA. Therefore, B12 deficiency will have increased homocysteine and methylmalonic acid. B9 deficiency will have increased homocysteine (because folate needed to make methionine) but NORMAL methylmalonic acid.

62
Q

Mechanisms of anemia of chronic disease?

A

Increased ferritin b/c of storage of Fe away from blood to prevent bacterial growth. TIBC/transferrin low. Low Fe.

63
Q

Labs for hereditary spherocytosis

A

Positive osmotic fragility test. Eosin-5-maleiimide binding test.

64
Q

Labs for paroxysmal noctural hemoglobunuria?

A

Commbs NEG hemolytic anemia, pancytopenia, CD55 [decay-accerlerating factor] and CD59 [MAC inhibitory protein] NEG RBC’s on flow cytometry.

65
Q

Paroxysmal nocturnal hemoglobunuria?

A

INTRAvascular hemolytic anemia. Complement mediated lysis (b/c of impaired synthesis of GPI anchor for membrane protecting factor). Acquired mutation in hematopoietic stem cell that increases incidence of acute leukemias.

66
Q

Warm vs. cold agglutinin autoimmune hemolytic anemias?

A

Cold are IgM. Acute anemia triggered by cold seen in CLL, mycoplasma or mono infectious. Warm are IgG and seen in SLE, CLL or methyldopa.

67
Q

Direct Coomb’s vs. Indirect Coomb’s

A

Direct look for stuff on RBC’s. So anti-Ig Ab for Ig’s on RBCs. Indirect adds normal RBC’s to serum to see if there’s anti-RBC surface Ig’s.

68
Q

Causes of neutropenia?

A

Sepsis, drugs (chemo), aplastic anemia, SLE, radiation

69
Q

Causes of lymphopenia?

A

HIV, DiGeorge, SCID, SLE, steroids, radiation, sepsis, post-op

70
Q

HbC disease?

A

Glutamic acid-to-lysine in Beta-globin. Leads to a hemolytic normocytic anemia.

71
Q

Acute intermittent porphyria

A

HMB synthase = porphoilinogen deaminase deficiency. 5 P’s - painful abdomen, port wine-colored urine, polyneuropathy, psychological disturbances, precipitated by drugs, EtOh, and starvation. Tx = glucose and heme which inhibits ALA synthase. Build-up of porphobilinogen, d-ALA, and coporphobilinogen (urine)

72
Q

Porphyria cutanea tarda

A

Uroporphyrinogen decarboxylase deficiency. Most common. Uroporphyrin build-up in urine (tea-colored). Blistering cutaneous photosensitivity.

73
Q

Treatment for paroxysmal nocturnal hemoglobinuria?

A

Eculizumab - Ab against complement

74
Q

Warfarin mechanism?

A

Inhibits vitamin K dependent carboxylation of glutamic acid residues of clotting factors 1972.

75
Q

Heparin mechanism?

A

Increases effect of naturally occurring anticoagulant antithrombin-III by binding to it -> conformational change -> increased antithrombin binding and neutralization of THROMBIN (II) and Xa. Unfractionated heparin has greater inactivating of thrombin than LMWH b/c of longer pentasaccharide chain.

76
Q

Defects in what factors only lead to increased PT and not increased PTT?

A

VII, then the common pathway = X, V, II, I. B/c PTT is intrinsic while PT is extrinsic (add TF with Ca2+)

77
Q

Platelet abnormality symptoms

A

Mucous membrane bleeding, epistaxis, petechiae, purpura, inc. bleeding time, possibly a decreased platelet count

78
Q

Bernard-Soulier vs. Glanzmann thrombasthenia labs?

A

GpIb vs. GpIIb/IIIa defect. Thrombocytopenia in B-S but not in Glanzmann. Both will have increased bleeding times. No change in PT or PTT. Glanzmann will show poor PLT clumping on blood smear.

79
Q

Etio of thrombotic thrombocytopenic purpura?

A

Inhibition or deficiency in ADAMTS13 = vWF metalloprotease that degrades vWF multimers. Large multimers -> increased PLT adhesion and thrombosis but DEC. PLT survival

80
Q

TTP labs?

A

Schistocytes, increased LDH. Dec. PLT count. Inc. Bleeding time.

81
Q

How do you diagnose von Willebrand disease?

A

Ristocetin cofactor assay. Ristocetin activates GpIb-vWF interaction. So vWF disease patients will have DCREASED agglutination.

82
Q

Treatment for von Willebrands?

A

DDAVP which releases vWF stored in endothelium. (Desmopressin acetate)

83
Q

Etios of DIC

A

STOP Making New Thrombi = Sepsis (gram neg), Trauma, OB comps, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion

84
Q

DIC labs

A

decreased PLT count. Inc. BT, PT, PTT. Inc. fibrin-split product (D-dimers), dec. fibrinogen, dec. factors V and VIII.

85
Q

Skin and subcutaneous tissue NECROSIS after warfarin?

A

Protein C deficiency. (Unable to inactivate V and VIII) -> thrombotic skin necrosis

86
Q

Antithrombin deficiency etios

A

Genetic. Renal failure/nephrotic syndrome can lead to antithrombin loss in the urine leading to increased factors II and X.

87
Q

Hodgkin’s lymphoma vs. Non-Hodgkin’s Lymphoma

A

Localized single group of nodes vs. multiple, peripheral nodes w/ extra nodal involvement. Reed-Sternberg vs. B-cell. Bimodal vs. Peak at 20-40. EBV association vs. ?HIV + immunosuppression. B signs (wt loss, fever, night sweats) vs. fewer constitutional symptoms

88
Q

Reed-Sternberg CD?

A

CD 15 and CD30.

89
Q

What subtypes of Hodgkins’ lymphoma have the best prognosis?

A

Lymphocyte-rich. Lymphocyte-mixed or depleted have poorest prognosis.

90
Q

Burkitt lymphoma

A

Adolescent/young adults. c-myc (8) + heavy-chain Ig (14). Histo is “Starry sky” = sheets of lymphocytes with interspersed macrophages. EBV. Jaw lesion endemic in Africa. FAST-growing tumor. Decent prog.

91
Q

Diffuse large b-cell lymphoma

A

Usually in older adults. t(14;18) = BCL2. Histo - large nuclei with open chromatin and prominent nucleoli. CD19, CD20. EBV, HHV-8. Rapidly enlarging often symptomatic mass at single nodal or extra nodal site. Decent prog.

92
Q

Mantle cell lymphoma

A

Older men. t(11;14) = cyclin D1 to heavy-chain Ig. Incurable. Fatigue, lymphadenopathy found to have generalized disease.

93
Q

Follicular lymphoma

A

Indolent course w/ remissions and recurrences. Fluctuating painless LN enlargement (waxing and waning). Abdominal mass. t(14;18) leading to over expression of BCL-2 (inhibits apoptosis). Centrocytes (cleaved nuclear outline) mixed with centroblasts. (large nucleoli)

94
Q

Adult T-cell lymphoma

A

Caused by HTLV-1. In adults. Cutaneous lesions, lytic bone lesions, hyperCa. Southern Japan and Carribbean. Extremely aggressive.

95
Q

Mycosis fungoides/Sezary syndrome

A

Cd4+ T-cells. Plaques/tumors. Sezary cells are the circulating cells. Incurable but indolent.

96
Q

Multiple Myeloma acronym

A

CRAB = hyperCalcemia, Renal insufficiency, Anemia, Bone lytic lesions/Back pain

97
Q

Multiple Myeloma findings

A

Infections, primary amyloidis, “punched-out” lytic lesions, M-spike on serum, Ig light chains in urine (not all MM’s secrete heavy chains found in serum electrophoresis), Rouleaux formation on smear, plasma cells w/ “clock face” chromatin and intracytoplasmic inclusions.

98
Q

Monoclonal gammopathy of undetermined significance

A

MGUS. A monoclonal expansion of plasma cells leading to a M spike < 3g/dL and BM with < 10% monoclonal plasma cells. 1-2% MM rate per year

99
Q

Waldenstrom macroglobulinemia

A

Unlike MM, the M-spike is due to IgM -> hyperviscosity but NO bone lesions

100
Q

Pseudo-Pelger-Huet anomaly

A

After chemo, sometimes you will see bilobed neutrophils that a thin piece of chromatin connecting the lobes

101
Q

ALL

A

Acute lymphoblastic leukemia/lymphoma. Within 3 months, fatigue, infection, bleeding, bone pain, splenomegaly, hepatomegaly, CNS. TdT, CD10+ (b-cells). Responsive to therapy. t(12;21) has better prognosis. T-cell ALL is more likely to present as a MEDIASTINAL mass -> resp, dysphagia, SVC syndrome. Down syndrome has 10-20x increased risk.

102
Q

Hairy cell leukemia

A

Indolent B-cell leukemia with hairlike cytoplasmic projections. CD19, CD20. CD11c and CD103. Older men. Stains TRAP. Marrow FIBROSIS = dry tap. Tx with caldribine (2-DA), which is an adenosine analog that is resistant to adenine deaminase. Excellent prognosis

103
Q

Small lymphocytic lymphoma (SLL)/chronic lymphocytic leukemia (CLL)

A

Different names for extent of peripheral involvement. Often asymptomatic or nonspecific symptoms. Infectioins. Autoimmune hemolytic anemia. Older age. CD20+, Cd5+ B-cell neoplasm. Often asymptomatic. SMUDGE cells in peripheral blood

104
Q

Acute myelogenous leukemia (AML)

A

Older. Myeloblasts on peripheral smear. RFs include chemo, radiation, myeloproliferative disorder. Promyelocytic leukemia responsive to vitamin A b/c it induces terminal differentiation and also has AUER rods.

105
Q

Chronic myelongenous leukemia (CML)

A

Adults. Philadelphia chromosome of t(9;22) BCR-ABL responding to imatinib. Can accelerate into a blast crisis (AML or ALL). Very low leukocyte alk phos (whereas HIGH leukocyte all phosphate in a leukomoid reaction)

106
Q

t(11;14)

A

Mantle cell

107
Q

t(14;18)

A

Follicular lymphoma

108
Q

Langerhans cell histiocytosis

A

Proliferative disorder of dendritic cells. Lytic bone lesions, skin rash, recurrent otitis media with mass in mastoid. S-100 and Cd1a. Birbeck granules on EM (“tennis rackets”)

109
Q

Myelofibrosis

A

Fibrotic obliteration of BM. TEARDROP RBC’s (dacrocytes) and immature myeloid cells.

110
Q

Heparin-induced thrombocytopenia (HIT)

A

IgG Ab’s against heparin-PLT factor 4 = complexes that lead to thrombosis and thrombocytopenia. Enlarged clot or new clot.

111
Q

Direct thrombin inhibitors

A

Argatroban, bivalirudin. Used for anti coagulating patients with HIT.

112
Q

Warfarin vs. heparin

A

Long-lasting vs. short-lasting. Not for pregnant women vs. doesn’t cross placenta. PT vs. PTT. P450 vs. not P450. Vitamin K/FFP vs. Protamine.

113
Q

Direct factor Xa inhibitors names and usage

A

Apixaban, rivaroxaban. Used for DVT/PE tx and ppx and stroke ppx in Afib patients. No monitoring for oral agents.

114
Q

Phosphodiesterase-3 (NOT 5) inhibitors

A

Cilostazol and dipyridamole. Increase cAMP in platelets and inhibit platelet aggregation. Used for claudication, coronary vasodilation, prevention of stroke or TIA a/ ASA, and angina ppx.

115
Q

G2 phase chemo drugs

A

Bleomycin and etoposide

116
Q

S phase chemo drugs

A

Etoposide and antimetabolites

117
Q

M phase chemo drugs

A

Vinca alkaloids and taxols

118
Q

Etoposide mechanism

A

Inhibits topoisomerase II

119
Q

Doxorubicin mechanism

A

DNA intercalator

120
Q

Cisplatin mechanism

A

Cross-links DNA

121
Q

Vinca alkaloids mechanism

A

Inhibit microtubule formation by binding Veta-tubulin. Vincristine and vinblastine.

122
Q

Paclitaxel mechanism

A

Inhibit MT disassembly by hyper stabilizing MT’s in M-phase. No Anaphase.

123
Q

MTX usage

A

Leukemias, lymphomas, chorioca, sarcoma. Abortion, ectopic pregnancy, RA, psoriasis, IBD.

124
Q

MTX toxicity

A

Myelosuppression reversible w/ lecuovorin (folinic acid). Maccrovesicular fatty change. Mucositis. Teratogenic.

125
Q

5-FU mechanism

A

Inhibits thymidylate synthase

126
Q

5-FU usage and tox

A

Colon ca, pancreatic ca, basal cell ca. Myelosuppresion (NOT reversible with leucovorin). Photosensitivity.

127
Q

Cytarabine mech, usage, and tox

A

Pyrimidine analog. Leuk/lymphomas. Leukopenia, thrombocytopenia, megaloblastic anemia.

128
Q

6-MP mech

A

PRPP glutamyl amidotransferase (first step in committed purine synthesis).

129
Q

6-MP usage and tox

A

Preventing organ rejection, RA, SLE, leukemia, IBD. Tox - BM, GI, liver. Increased toxicity with allopurinol b/c it is metabolized via xanthine oxidase.

130
Q

Dactinomycin

A

DNA intercalator. Wilms, ewing, rhabdo. Tox = myelosuppression

131
Q

Doxorubicin = Adriamycin

A

Intercalates DNA leading to breaks. Generates free radicals. SOLID tumors, leuekmias,lymphomas. Tox dilated cardiomyopathy, myelosuppresion, alopecia. Dexrazoxane (Fe chelator) used to prevent cardiotoxicity

132
Q

Bleomycin

A

Free radical formation causing DNA breaks. Testicular cancer, Hodgkin’s. Tox - pulmonary fibrosis, skin, mucositis.

133
Q

Names of alkylating agents?

A

Cyclophosphamide, ifosfamide, nitrosureas, busulfan

134
Q

Cyclophosphamide

A

Covalently binds DNA. Requires liver activation. Solid tumors, leuekemias, lymphomas, some brain ca. Myelosuppresion, hemorrhagic cystitis (mesna prevention)

135
Q

Nitrosureas

A

Carmustine, lomustine, semustine, streptozocin. Cross-link DNA. BRAIN tumors. CNS tox.

136
Q

Busulfan

A

CML or ablation before BM transplantation. Tox - severe myelosuppression, pulmonary fibrosis, hyperpigmentation.

137
Q

Vinca alkaloids usage and tox

A

Solid tumors, L/L. Vincristine has neurotox. Vinblastine has myelosuppresion.

138
Q

Paclitaxel and other taxol usage and tox

A

Ovarian and breast ca. Myelosuppresion, alopecia, hypersensitivity.

139
Q

Platin usages and tox.

A

Cis/carboplatin. Testicular, bladder, ovary, and lung. Nephro and acoustic nerve damage. Amifostine (free radical scavenger) and cl- diuresis to preotect kidneys.

140
Q

Etoposide usage and tox

A

Solid tumors, L/L. Tox - myelosuppresion, GI, alopecia

141
Q

Irinotecan, topotecan

A

Inhibits topoisomerase I to prevent DNA unwinding and replication.

142
Q

Hydroxyurea

A

Inhibits ribonucleotide reductase (s-phase). Melanoma, CML, sickle cell. BM suppresion and GI.

143
Q

Rituximab

A

Monoclonal Ab against CD20 (B-cell). Used for Non-hodgkin lymphoma, RA w/ MTX, ITP. Risk of PML

144
Q

Vemurafenib

A

Small molecule inhibitor of B-RAF kinase. Used for metastatic melanoma.

145
Q

Bevacizumab

A

Anti-VEGF monoclonal Ab. Used for solid tumors.

146
Q

Etios of aplastic anemia

A

Hep C. Chloramphenicol, indomethicin. Parvovirus. Radiation. Phenylbutozone, thyroid drugs.

147
Q

Main mediator of paraneoplastic cachexia?

A

TNF-alpha. Cytokine causing necrosis of tumors. Also involved with producing fever in a bacterial infection and releasing acute-phase reactants. Suppresses appetite, inhibits lipoprotein lipase, increases insulin resistance.

148
Q

TGF-beta vs. TNF-alpha?

A

TGF-beta’s role is the INHIBITION of inflammatory response. TGF-beta promotes inflammatory response.

149
Q

Carcinoid syndrome etiologies?

A

Intestinal carcinoid tumors that haven’t metastasizes will have their products degraded by the liver. Therefore, a metastatic tumor (liver, lung) will need to symptoms: flushing, dizziness, diarrhea, wheezing, R-sided valvular disease.

150
Q

Pure red cell aplasia

A

Rare form of BM failure. Severe hypoplasia of erythroid elements but NOT other elements. Associated with thymoma, B19 infection, lymphocytic leukemias.

151
Q

Thrombin time

A

Add thrombin to blood and see how long it takes for blood to clot. TT is prolonged with agents that directly or indirectly inhibit thrombin (e.g. heparin)

Step 1 (19 decks)

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