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10. What cancer causes “punched-out” lytic bone lesions that can be seen on x-ray? (FA p353) Multiple myelom M-spike increase in IgG common increase IgA – least common CRAB hypeRcalcemia Renal insufficiency Anemia cause by bone infiltration Bone and Back pain Bence Jones Proteins – Urine IgG Rouleaux formation
Walderstroms vs Multiple Myeloms Mspike is caused by IgM and have hyperviscocity
15. What are the common causes of eosinophilia? (FA p337) NAACP • Neoplasm • Asthma • Allergic process • Collagen vascular – polyarteritis nodosa • parasites
What substance activates the classic complement pathway? What substance activates the alternative compliment pathway? (FA p206) Classic complement pathway – IgG and IgM activate against gram negative bacteria Alternative Pathway is activated by microbial surfaces such as endotoxins or cell walls.
anticancer agent toxicity is increased by allopurinol 6-MP, purine analog, activated by HGPRTase
anticancer agent cardiotoxic; monitor patients using ejection fraction Doxorubicin (Adriamycin), free radicals break DNA, A in ABVD, Alopecia
anticancer agent blocks polymerization of tubulin Vincristine (neurotoxic) and Vinblastin (blasts bone marrow), blocks vines, part of MOPP,
anticancer agent hyperstabilizes polymerized microtubules Paclitaxel and other Taxols
anticancer agent known to cause hemorrhagic cystitis cyclophosphamide, isosfamide, X-link DNA,
crosses blood-brain barrier; used in brain cancers Nitrosureas (carmustine, lomustine, semustine, streptozocin), brain tumor, dizziness, ataxia
10. What type of lymphoma has the histological appearance of a “starry-sky” pattern? What virus is associated with this type of lymphoma? (FA p352) Burkitt's Lymphoma, adolescents and young adults, t(8;14) c-myc, EBV assocition, jaw lesion endemic in Africa
10. Where would you expect to find B cells in a lymph node? Where would you find T cells, plasma cells, and macrophages? (FA p198) B-cells are in the Follicle T-cells are in the paracortex Plasma Cells are in the medullary chords Macrophages - Medullary sinus
14. What lab findings are indicative of disseminated intravascular coagulation (DIC)? (FA p350) consumptive coagulation, Platelet Count decreased, Bleed Time increase, PT and PTT increased. Labs - schistocytes, increased fibrin split products (D-dimers), decreased fibrinogen, decreased factor V and VIII.
Causes of DIC STOP Making New Thrombi - Sepsis, trauma, OB, acute pancreatitis, Malignancy, Nephrotic syndrome, Transfusion.
14. What is the underlying cause of hereditary spherocytosis? What microscopic findings and lab values would you suspect in a pt with hereditary spherocytosis? (FA p346) defect in RBC membrane skeleton by ankyrin or spectrin. Pathogenesis - no central pallor. Increased MCHC and RDW causes spleen removal. Findings - splenomegaly, B19 aplastic crisis, Howell-Jolly Bodies.
Howell-Jolly Bodies Always present after splenectomy
anticancer agent given for estrogen sensitive breast cancers, how is Raloxifen different Tamoxifen - prevent breast cancer, increase endometrial cancer,prevent osteoporosis, Raloxifen does not cause cancer.
anticancer agent S-phase antimetabolite; myelosuppression reversible with leucovorin Methotrexate - Folic acid analogue, inhibits dihydrofolate reductase and dTMP,
anticancer agent S-phase antimetabolite; myelosuppression not reversible with leucovorin 5-fluroouracil, pyrimidine analog, inhibits thymidylate synthase, rescue with thymidine
anticancer agent ototoxic and nephrotoxic (much like aminoglycosides and loop diuretics) Cisplatin and carboplatin, crosslink DNA
anticancer agent 2 agents known for causing pulmonary fibrosis Busulfan, alkylating agent, hyperpigmentation
anticancer agent inhibits topoisomerase II Etoposide, Small cell carcinoma, GI irritant, alopecia
12. What is the life span of an RBC? Define the following terms: polycythemia, anisocytosis, poikilocytosis, reticuloctye (FA p336) life span - 3 months polycythemia - increased number of RBC Reticulocyte - immature erythrocyte Anisocytosis - varying sizes Poikilocytosis - varying shapes
7. What are the causes of aplastic anemia? What is the treatment for aplastic anemia? (FA p345) pancytopenia, caused by radiation and drugs (benzene, chloramphenicol, alkylating agents, antimetabolites), viral (B19, EBV), Fanconi's anemia. Tx - withdrawl of agent, immunosuppressive (cyclosporine), allogenic BM transplant, RBC and Pt, G-CSF, GM-CSF
8. A smear of your patient’s blood reveals target cells. What diseases do you immediately suspect? (FA p342) HALT - HbC, Asplenia, Liver Disease, Thalassemias
4. Which types of cancer are associated with the following chromosomal translocations? (FA p355) t (9;22) t (8;14) t (14;18) t (15;17) t (11;22) t (11;14) 9;22 - philadelphia - CML 8;14 - Burkitt's Lymphoma (c-myc) 14;18 - Follicular Lymphoma (bcl-2) 15;17 - M3 type AML (responds to ATRA) 11;22 - Ewing sarcoma 11;14 - mantle cell lymphoma
most common malignancy in children (FA p354); ALL - mediastinal mass, Bone marrow replaced by many lymphoblasts, TdT +, very responsive to tx, 12;21 is good prognosis.
most common solid tumor location in children (FA p425); brain
2 most common brain tumors in children (FA p425); craniopharyngioma, pilocytic astrocytoma
most common supratentorial brain tumor in children (FA p425); craniopharyngioma - benign, can cause bitemporal hemianopia, derived from Rathke's pouch, calcification is common - tooth enamel.
most common extracranial solid tumor in children (FA p292); neuroblastoma - most common in the adrenal medulla or along sympathetic chain
most common malignant bone tumor in children (FA p377); Ewings sarcoma - anaplastic blue malignant cells, boys, agressive but responsive, onion skinning, diaphysis and flat bones, 11;22 translocation
most common tumor of adrenal medulla in children (FA p292); Neruoblastoma
most common renal tumor in children (FA p468); Wilms Tumor - huge flank mass and hematuria, assd with hemihypertrophy syndromes, deletion of WT1 on chromosome 11, part of WAGR complex: Wilm's tumor, Aniridia, Genitourinary malformation, mental motor retardation
most common primary cardiac tumor in kids and what association do they have (FA p273); rhabdomyoma, assd with tuberous sclerosis
2. What are the clinical findings in a pt with lead poisoning? (FA p349) LEAD - lead lines (burton's lines), Encephalopathy and Erythrocyte basophilic stippling, Abdominal colic and sideroblastic Anemia, Drop (wrist and foot), tx is Dimercaprol and EDTA.
14. What effects do prostaglandins, prostacyclines, and thromboxane have on platelet aggregation? (FA p387) thromboxane - increase plateley aggregation and vasoconstriction Prostaglandins - decrease vascular tone, increase pain, incresase uterine tone, increase temperature Prostacyclin - decrease Pt aggregation, decrease uterine tone
6. What is the structure of HbH? What disease results in HbH production? What is the structure of Hb Barts? What disease results in Hb Barts production? (FA p343) deletion of 3 genes in alpha thalassemia causes congregation of B4 or HbH HbBarts is gamma-4 which is caused by deletion of 4 alpha genes, not compatible with life, causes hydrops fetalis
7. What are the causes of normocytic, normochromic anemia? (FA p344) non-hemolytic-AOCD, aplastic anemia, kidney disease. intrinsic hemolysis - hereditary spherocytosis, G6PD def, pyruvate kinase deficiency, sickle cell, HbC, paroxysmal nocturnal hemoglobinuria.
7. What are the causes of normocytic, normochromic anemia? (FA p344) Extrinsic Hemolytic - autoimmune, microangiopathies (DIC, TTP-HUS), infection
intravascular hemolysis paroxysmal nocturnal hemoglobinuria, autoimmune (cold agglutination), mechanical destruction (stenosis or prosthetic valve),
extravascular hemolysis spherocytosis, G6PD, pyruvate kinase def, sickle cell, HbC, autoimmune (warm agglut), microangiopathies (DIC, TTP-HUS)
7. What lab findings allow you to distinguish iron deficiency anemia from a microcytic, hypochromic anemia resulting from thalassemia? (FA p347) thalassemia will have normal iron studies while iron deficiency will have derceased serum iron and ferratin, increased TIBC and and transferrin
4. What is the typical presentation of a pt with Hodgkin’s disease? (FA p351) Reed-Sternberg cells (poor prognosis), localized and single group of continguous nodes, B symptoms -low grade fever, night sweats, weight loss, mediastinal lymphadenopathy (nontender), EBV, incidence <20 or >60
and with non-hodgkins - HIV and immunosuppression, not continuous nodes, extranodal, few B symptoms, incidence 20-40
12. What lab findings indicate hemolysis as a cause of anemia? (FA p344) Bite cells - G6PD, Schistocytes - DIC, TTP-HUS, trauma, Sickle Cells, Spherocytes,
8. What test is used to confirm the diagnosis of hereditary spherocytosis? What findings are a/w hereditary spherocytosis? (FA p346) positive osmotic fragility test, look for increased MCHC and RDW
9. Which type of lymphoma has a presentation that is very similar to CLL? (FA p351) CLL - smudge cells, and peripheral blook lymphocytosis, over 60 yo
1. Compare the clinical findings of platelet disorders to those of coagulation factor defects. (FA p349) platelet disorders - increased bleeding time, mucous membrane bleeding, epistaxis, petechiae, purpura coagulation - PTT tests VII and XII are intrinsics PT tests I, II, V, VII, X and extrinsics
1. Three days ago you hospitalized a 40-year-old male for myocardial infarction. He has been given all of the usual medications. Today you notice that his platelet count is 30,000. What do you suspect is the cause of his low platelets? (FA p356) HIT due to autoimmune attack of platelets
1. Compare the age distribution of those affected by Hodgkin’s lymphoma to those affected by non-Hodgkin’s lymphoma. (FA p351) bimodal vs. unimodal
2. What might you see under a light microscope that would lead you to suspect lead poisoning as a cause of microcytic, hypochromic anemia? (FA p343, FA p349) lead poisoning - basophilic stippling from sideroblastic anemia,
2. What long-term complication is associated with having to receive multiple blood transfusions? (FA p343) you can get 2ndary hemochromatosis
Bernard-Soulier disease decreased PC, increased BT, defect in platelet plug and decrease in GpIb causing a defect in platelet-collagen aggregation
Glanzmanns thrombasthenia no change in PC and increased BT, GpIIb/IIIa - defect in platelet to platelet aggregation
ITP decreased PC and increased BT, decreased survival of Pt, similar to Glanzmanns, anti GpIIb/IIIa, increased megakaryocytes
TTP decreased PC and increased BT, ADAMTS 13 - degredation of vWF multimers that increase platelet aggregation. Labs show schistocytes and increased LDH, PENTAD - neuro, renal, fever, thrombocytopenia, MAHA.
hemophilia A or B increased PTT only - A is factor VIII and B is IX, macrohemorrage, hemarthroses
Vit K def increases PT and PTT while decreasing II, VII, IX, and X, protein C and S.
von Willebrand's disease increase BT only, vWF carries/protects factor VIII, defect in platelet to collagen adhesion
basophilic stippling thalassemia, AOCD, iron def, lead poisoning
MCV < 80 microcytic anemia - area of central pallor is decreased because Hb is not being produced, iron deficiency, AOCD, Thalassemia, Sideroblastic Anemia
MCV > 100 B12 and Folate deficiency
Normocytic with low corrected reticulocyte count aplastic anemia and renal disease
Normocytic with high corrected reticulocyte hemolytic - spherocytosis, sickle cell, G6PD, MAHA
Where is iron absorbed duodenum
Where is Folate absorbed jejunum
Where is B12 absorbed Terminal Ileum
RBC hyperplasia found in the bone marrow marrow compensates for the anemia
increased reticulocytes found in the blood bone marrow is compensating for an anemia
how to determine the corrected reticulocyte count Hemoglobin/45 * reticulocyte count == 3% or greater is good and if young RBCs are present, which are darker, then you must divide the reticulocyte count by 2
Hemoglobin Rule of 3 Hb x 3 = hematocrit
Pac Unit Blood rule of three Hb up by 1 point for each pac unit and Hct up by 3%
Most common cause of anemia Iron Deficiency
Most common cause of iron def GI bleed
Celiac disease affects what Duodenum, jejunum
Microcytic anemia with increased RDW iron defiency because the Hg is normal and micro
Who gets target cells alcoholics, thal, sickle cell anemia
TIBC same thing as transferrin, total binding by transferrin, if iron stores in the bone marrow go down then TIBC goes up as is the case with Iron Deficiency
Ferratin Soluble circulating form of iron, soluble and equivalent to how much iron is in the Bone Marrow
% saturation serum iron/TIBC normally equals 100/300 or about 33%
Created by: burkill
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