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EXAM > Hematology, Oncology, immune > Flashcards

Hematology, Oncology, immune Flashcards

1
Q

Describe HL

A

Localized single group of nodes. Prognosis is better than NHL. Characterized by reed sternberg cells.&raquo_space;55 years age. 50% cases assoc with EBV. Symptoms include low grade fever, night sweats, weight loss.

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2
Q

Describe NHL

A

More common. Multiple peripheral nodes. Involve B cells. 20-40 years age. Assoc with HIV. Fewer constitutional symptoms compared to HL

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3
Q

Reed sternberg cells found in?

A

HL. Binucleate “owl eyes” that are CD15 and CD30 B cell origin. Modular sclerosing form most common (which is one out of four subtypes of HL)

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4
Q

Describe IgA

A

Prevents attachment of bacteria/virus to mucus membrane
Does NOT fix complement
Crosses epithelial cells
Released in secretions

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5
Q

Describe IgG

A

2 DELAYED response to antigens
Fixes complement
CROSS placenta
Most abundant in serum

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6
Q

Describe IgE

A

Bind mast cells and basophils
Mediate hypersensitivity
lowest concentration

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7
Q

Describe IGM

A

1 IMMEDIATE response to antigen
Does NOT cross placenta
Fixes complement

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8
Q

Describe IL1-12

A

“HOT T-bone stEAK”

IL8- neutrophils chemotactic factor
IL10- INHIBITS inflammation
IL12- T cell maturation, NK cells

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9
Q

Which cytokines are secreted by macrophages?

A

IL-1,6,8,12,TNF alpha

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10
Q

Cytokines secreted by T cells?

A

IL-2,3

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11
Q

Cytokines released from Th2 cells

A

IL-4,5,10

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12
Q

Describe interferons

A

Part of innate host defense with viruses. Cells that act locally on uninfected cells “priming” cells for viral defense. ACTIVATES RNAse l and PK–> apoptosis

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13
Q

Describe steps of platelet plug formation (primary hemostasis) in platelet… INJURY, ADHESION, ACTIVATION, AGGREGATION

A

INJURY, VWF binds to exposed collagen– ADHESION, platelets bind to VWF via GplB at site of specific injury– platelet release ADP and Ca (for coagulation cascade)– ADP helps platelets adhere to endothelium– ACTIVATION, ADP binding to Hpllb/IIIa expression at platelet surface–AGGREGATION, fibrinogen binds to GpIIb/IIIa receptors and links platelets. balance between pro-aggregation and anti-aggregation factors – temp plus stops bleeding.

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14
Q

Describe coagulation cascade, where is hemophilia A/B?

A

Hemo A- factor VIII, Hemo B- factor IX

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15
Q

Describe platelet plug formation/ thrombogenesis and where does ASA, clopidogrel, abciximab act. Where are the deficiencies?

A

ASA inhibited cyclooxygenase (TXA2 synthesis), clopidogrel inhibits GPIIb/GPIIa expression. Abciximab inhibits GPIIB/GPIIa directly. Deficiencies vWF, Bernard soulier, glanzmann.

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16
Q

Describe microcytic anemias <80

A

Not a lot of RBX and the existing RBC are small. HEMOGLOBIN problem! Iron deficiency, ACD, thalassemia (inherited abnormality), lead poisoning, sideroblastic anemia (iron get in but can’t get out).

17
Q

Iron deficiency can lead to…

A

Conjunctivial pallor under eyes, and Plummer Vinson syndrome associate with iron deficiency, esophageal webs, and strophic glossitis.

18
Q

Describe alpha and beta thalassemia

A

Alpha is alpha globulin deletions cause decrease in alpha globin synthesis in asian and African populations.

Beta is point mutations causing decrease in beta globulin synthesis in Mediterranean pop.

19
Q

Describe macrocytic anemia

A

Due to folate and B12 deficiency. Megaloblastic is errors in blood DNA production. Folate, b12, robotic aciduria. Non magloblastic include liver dz, alcoholism, reticulocytosis.

20
Q

Describe normocytic anemia

A

Hemolytic due to intrinsic or extrinsic (environmental factors). Or non-hemolytic. Nonhemolytic: ACD, aplastic anemia, CKD, iron deficiency. Hemolytic intrinsic: RBC membrane defect (hereditary spherocytosis), RBC enzyme deficiency (G6PD PK), hBC defect, paroxysmal nocturnal hburia, SCA. Hemolytic extrinsic: autoimmune, microangiopathic, macroangiopathic, infections.

21
Q

Draw out lane values of anemia including Fe deficiency, Chronic dz, hemochromatosis of Serum iron, transferrin TIBC, ferritin.

A

Draw

22
Q

Describe leukopenias

A

Decrease in WBC..
Neutropenia- seen in sepsis/postinfection. <1500
Lymphopenia- seen in HIV, digeorge syndrome. <1500

23
Q

Describe heme synthesis, porphyria, lead poisoning.

A

Porphyria is defect in heme synthesis leading to accumulation of heme precursors. Lead inhibits specific enzymes needed in heme synthesis.

24
Q

Lead poisoning affected enzyme, accumulate substrate, symptoms

A

Ferrochelatase and ALA dehyratase. Protoporphyrin accumualted. Children= mental deterioration via lead pain. Adults=demyelination

25
Q

Acute intermittent porphyria. Affected enzyme, accumulated substrate, symptoms

A

Porphyobilinogen deaminase enzyme. Porphobilinogen accumulated. 5P’s symptoms painful abdomen, port-wine urine, polyneuropathy, psychological disturbances, precipitated by drugs. Tx. Glucose and heme.

26
Q

Porphyria cutaneous Tara. Affected enzyme. Accumulated substrate, symptoms

A

Uroporphyrinogen decaroxylase. Uroporphyrin accumulated. Blisters and Most Common porphyria.

27
Q

Draw out heme synthesis.

A

Draw

28
Q

Basophilic stippling

A

BASICally ACiD Alcohol is LeThal. ACD, alcohol abuse, lead poisoning, thalassemia.

29
Q

Describe multiple myeloma “monoclonal M protein spike”

A

Think CRAB: hypercalcemia, renal insufficiency, anemia, bone lyrics lesions/back pain.

30
Q

Chromosomal translocations 9:22, 8:14, 11:14, 14:18, 15:17

A

Philly/CML (BCR able gene), burkitts, mantel cell hyperplasia, follicular lymphoma, AML.

31
Q

Describe types of NHL

A

Burkitts lymphoma (8:14), diffuse large B cell (14;18)MOST common , mantle cell (11:14), follicular (14:18).

32
Q

Describe chronic myeloproliferative disorders and examples

A

JAK2 is involved in hematopoietic growth factor signaling. Mutations lead to myeloproliferative disorders other than CML. I.e. Polycythemia Vera (erythromelalgia, intense itching after hot shower), essential thrombocytosis (overproduction of abnormal platelets–> bleeding). Myelofibrosis (teardrop RBC)

33
Q

Heparin Vs. Warfarin

A

HEPARIN: route parenteral, site of action is blood, speed is rapid, actives antithrombin which DEC actions if IIa and factor Xs. Duration of actions is hours. Tx of overdose protamine and monitor PTT (intrinsic pathway). Doesn’t cross placenta. WARFARIN: route oral, site of action liver, speed is slow, impairs synthesis of Vit K dependent clotting factors, duration is days. Tx of overdose IV vitamin K or fresh frozen plasma. Monitor with PT/INR (extrinsic pathway). Cross placenta

34
Q

Draw cancer drug cell cycle. Include antimetabolites, etoposide, bleomycin, vinca alkaloids/taxol

A

Draw

35
Q

Draw common chemotoxicities “man” include cisplatin, vincristine, bleomycin,doxorubicin, trastuzumab, cyclophosphamide, 5FU, 6MP, methotrexate.

A

Draw

EXAM (13 decks)

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