Hematology, Oncology, immune

Question 1

Describe HL

Answer 1

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.

Question 2

Describe NHL

Answer 2

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

Question 3

Reed sternberg cells found in?

Answer 3

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)

Question 4

Describe IgA

Answer 4

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

Question 5

Describe IgG

Answer 5

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

Question 6

Describe IgE

Answer 6

Bind mast cells and basophils
Mediate hypersensitivity
lowest concentration

Question 7

Describe IGM

Answer 7

1 IMMEDIATE response to antigen
Does NOT cross placenta
Fixes complement

Question 8

Describe IL1-12

Answer 8

“HOT T-bone stEAK”

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

Question 9

Which cytokines are secreted by macrophages?

Answer 9

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

Question 10

Cytokines secreted by T cells?

Answer 10

IL-2,3

Question 11

Cytokines released from Th2 cells

Answer 11

IL-4,5,10

Question 12

Describe interferons

Answer 12

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

Question 13

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

Answer 13

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.

Question 14

Describe coagulation cascade, where is hemophilia A/B?

Answer 14

Hemo A- factor VIII, Hemo B- factor IX

Question 15

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

Answer 15

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

Question 16

Describe microcytic anemias <80

Answer 16

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).

Question 17

Iron deficiency can lead to…

Answer 17

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

Question 18

Describe alpha and beta thalassemia

Answer 18

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.

Question 19

Describe macrocytic anemia

Answer 19

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

Question 20

Describe normocytic anemia

Answer 20

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.

Question 21

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

Answer 21

Draw

Question 22

Describe leukopenias

Answer 22

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

Question 23

Describe heme synthesis, porphyria, lead poisoning.

Answer 23

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

Question 24

Lead poisoning affected enzyme, accumulate substrate, symptoms

Answer 24

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

Question 25

Acute intermittent porphyria. Affected enzyme, accumulated substrate, symptoms

Answer 25

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

Question 26

Porphyria cutaneous Tara. Affected enzyme. Accumulated substrate, symptoms

Answer 26

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

Question 27

Draw out heme synthesis.

Answer 27

Draw

Question 28

Basophilic stippling

Answer 28

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

Question 29

Describe multiple myeloma "monoclonal M protein spike"

Answer 29

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

Question 30

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

Answer 30

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

Question 31

Describe types of NHL

Answer 31

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

Question 32

Describe chronic myeloproliferative disorders and examples

Answer 32

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)

Question 33

Heparin Vs. Warfarin

Answer 33

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

Question 34

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

Answer 34

Draw

Question 35

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

Answer 35

Draw