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Hemato/Onco 2
UWORLD + FA Hematology and Oncology Review
| Question | Answer |
|---|---|
| What is drain by the Superficial Inguinal Nodes? | Cutaneous lymph from the umbilicus down, including the anus and below the dentate line. |
| What two cutaneous structures, below the umbilicus, do not drain into the Superficial Inguinal lymph nodes? | 1. Glans penis 2. Posterior calf |
| Bladder lymph drainage: | - Superior portion of bladder -----> External Iliac nodes - Inferior portion of bladder ----> Internal Iliac nodes |
| What is the lymph drainage of the Prostate? | It drains into the Internal Iliac nodes |
| Lymph from the testes is drain into? | Abdominal para aortic retroperitoneal lymph nodes |
| The upper third of the Rectum lymph fluid is drained into the ___________________________________ nodes. | Inferior Mesenteric Lymph |
| What are some structures which lymph node is drained into the Internal Iliac lymph nodes? | Inferior portion of the bladder and the Prostate. |
| What is RNA interference? | Biological process in which RNA molecules inhibit gene expression or TRANSLATION, by neutralizing targeted mRNA molecules. |
| What RNA type is targeted in RNA interference? | mRNA |
| What are examples of short non-coding RNA sequences? | microRNA and small interfering RNA |
| What are other names used to refer to RNA interference? | Co-suppression, Post-transcriptional gene silencing, adn quellung. |
| What is the main role for Cyclin-dependent kinases 4/6 (CKDs)? | Regulate the movement of cells from the G1----> S-phase |
| Mutations to the CKD 4/6 ---> | Unregulated cellular growth |
| What is a adverse effect seen in CKD 4/6 inhibition? | Inhibition growth of hematologic cells in bone marrow (neutropenia, anemia, or thrombocytopenia) |
| Why does CKD 4/6 inhibition cause decrease in some hematologic cell lineages? | It not only inhibits the growth of neoplastic cells, but also of hematopoietic cells in the bone marrow, due to its strong effect. |
| Common CKD 4/6 inhibitor? | Palbociclib |
| CKD 4/6 inhibition prevents the interaction between: | CYCLIN D and CKD 4/6 |
| What is the normal effect of Cyclin D and CKD 4/6 interaction? | It provides the Pi for phosphorylation of Rb, and allow progress of cell in to S-phase. |
| X-linked disorder. Affected father: | 1. Only has unaffected sons 2. Has all carrier daughters |
| What is the first wave of changes in DIC? | Marked by widespread of Coagulation cascade, leading to excessive Thrombin production and formation of microthrombi |
| After the increased production of Thrombin and formation of micro thrombin, in DIC, it is followed by: | Formation of Plasminogen to Plasmin, which results in Increased Fibrinolysis to clear the thrombi. |
| DIC pathogenesis process: | 1. Widespread of Coagulation cascade elements 2. Excessive Thrombin production 3. Excessive microthrombi formation 4. Conversion of Plasminogen into Plasmin 5. Increased Fibrinolysis to clear the thrombi |
| Lab results seen in DIC? | 1. Consumption of clotting factors -- Prolonged PT / PTT 2. Decrease in platelets --- Thrombocytopenia 3. Excessive Fibrinolysis -- Elevated D-dimer |
| What is a common vignette characteristic of a patient with DIC? | Bleeding or oozing from venipuncture/catheter sites |
| Bruton Agammaglobulinemia is: | X-R disorder; Defect in B-cell maturation, resulting in absence of mature B-cells with severe deficiency in ALL immunoglobulin types |
| How is the T-cell count and function of a patient with Bruton agammaglobulinemia? | Normal |
| What is the result on the absence of B-cells in Bruton agammaglobulinemia? | Primary lymphoid follicles an Germinal center will not form within the lymph nodes. |
| How is the Outer cortex of the Lymph node composed? | Mainly of primary and secondary follicles (B-cell rich regions) and a high number of CD4 T-cells, which allow T---B cell interaction. |
| Where is located the Paracortical Zone of the Lymph node? | Lies internal to the cortex of the lymph node |
| What cells are found tin the Paracortical Zone of the Lymph node? | T-lymphocytes and Dendritic cells |
| Monoclonal antibody directed against CD20? | Rituximab |
| Chimeric IgG1 antibody against TNF-alpha | Infliximab |
| Conditions or disorders usually treated with Infliximab? | Rheumatoid arthritis, Ankylosing spondylitis, and Crohn's disease |
| Cytokine used for the treatment of RCC and melanoma | IL-2 |
| Potent inhibitor of BCR/ALB protein tyrosine kinase | Imatinib |
| Monoclonal antibody against the platelet GP IIb/IIIa receptor | Abciximab |
| When is Abciximab used? | During angioplasty in patients with acute coronary syndrome |
| What occurs in Folate deficiency? | Inhibition of the synthesis of Nucleic acids, especially dTMP |
| What is the main nucleic acid inhibited in Folate deficiency? | dTMP |
| Folate deficiency lead to: | Defective DNA synthesis, which characteristically causes increased Apoptosis of Hematopoietic cells and Megaloblastic anemia. |
| What kind of supplementation can be given to treat Folate deficiency? | Thymidine supplementation |
| In patients with vitamin B9 deficiency, it is common to give ___________________, in order to bypass the affected enzyme and reduce ___________ _______________. | Thymidine; Erythroid cell apoptosis |
| By introducing Thymidine supplementation to a Folate deficient patient, it provides what benefit? | Reduction in Erythroid cell apoptosis |
| Major source of Nitrogen in the synthesis of Purine and Pyridine bases | Glutamine |
| What amino acid is associated with Endothelial cell injury and vascular inflammation? | Homocysteine |
| Why is Homocysteine elevated in Folate deficiency? | Due to impaired conversion of homocysteine into Methionine |
| Primary Myelofibrosis is: | a myeloproliferative disorder associated with the CLONAL expansion of MEGAKARYOCYTES |
| What symptom or manifestation accounts for most of the symptoms of Primary Myelofibrosis? | Bone Marrow fibrosis |
| What are the symptoms seen in Bone Marrow fibrosis? | Hepatosplenomegaly, cytopenias, and blood smear with Dacrocytes. |
| Primary Myelofibrosis usually has _______________________. | Dry Bone marrow aspiration |
| What is seen in Bone Marrow Biopsy of Primary Myelofibrosis? | Marked fibrosis with occasional cluster of atypical megakaryocytes. |
| What are the general and common causes for development of Aplastic anemia? | Injury from drugs, radiation and viruses to multipotent stem cells. |
| What are associative conditions of Aplastic anemia? | 1. Pancytopenia 2. Produndly hypocellular bone marrow that is infiltrated with adipose |
| Anemia of chronic disease (ACD): | Associated with HEPCIDIN - induced changes IRON metabolism that cause trapping within the macrophages. |
| What is Myelodysplasia? | Malignant stem cell cancer associated with the production of dysplastic atypical blood cells and cytopenias. |
| How is the Bone marrow composed in Myelodysplasia? | Hypercellular with multilineage dysplasia |
| Which cells produce EPO (erythropoietin)? | Peritubular fibroblasts el in the Renal cortex in response to decreased renal oxygen delivery |
| How does EPO increase RBC production? | Acts on Erythrocyte precursors in the bone marrow to increase RBC production. |
| What kind of patients may have damaged EPO-producing cells? | Chronic Kidney disease patients, resultingin Normocytic anemia. |
| What are Protoporphyrins? | Heme precursors; elevated in patients with IRON deficiency anemia. |
| What cells are involved in Multiple Myeloma development? | Plasma cells |
| In Multiple Myeloma, the plasma cells______________________ | Synthesize large amounts of monoclonal immunoglobulin or immunoglobulin fragments |
| Multiple Myeloma patients are susceptible to: | Proteasome inhibition, due to the large amount of proteins that they produce. |
| What is the result of Proteasome inhibition in Multiple Myeloma? | Accumulation of toxic intracellular and Pro-apoptotic proteins increases cellular apoptosis |
| Western blotting is used to ID _____________________. This technique is applied after the proteins are separated by ___________________. | Proteins; Electrophoresis |
| What is the essential difference between Western blotting and ELISA? | ELISA does not have previously separated proteins by Electrophoresis |
| Plasma cell malignancy that replicates in the bone marrow | Multiple Myeloma |
| What are the effects seen in Multiple Myeloma due to its replication in Bone marrow? | 1. Osteolytic bone lesions, 2. Bone destruction, 3. Hypercalcemia 4. Pathologic fractures |
| Histopathology of Multiple Myeloma: | Replacement of normal bone marrow with plasma cells and blasts |
| Squamous Lung carcinoma is associated with: | large, malignant cells containing Keratin with intercellular bridges |
| Round or polygonal cells with abundant clear cytoplasm | Renal Cell carcinoma |
| The PI3K/Akt/mTOR pathway is involved in: | 1. Anti-apoptosis 2. Cellular proliferation 3. Angiogenesis |
| PTEN is associated with the ______________________ pathway. | PI3K/Akt/mTOR |
| The conversion of PIP3 into PIP2 is done by actions of the _________. | PTEN |
| What are the functions of the Growth Factors? | 1. Stimulate cell proliferation by altering the expression of certain genes in the nucleus 2. After GF bins to its cell membrane receptor, signal transduction systems transfer the signal to the nucleus. |
| What are some common Signal Transduction systems? | 1. MAP-Kinase pathway 2. PI3K/Akt/mTOR pathway 3. Inositol phospholipid pathway 4. cAMP pathway 5. JAK/STAT pathway |
Created by:
rakomi
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