Kaplan Hematology and Oncology – Flashcards

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Erythrocyte
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Source of energy: glucose (90% anaerobically degraded to lactate, 10% to HMP shunt) membrane contains Cl-/HCO3- antiport important in PHYSIOLOGICAL CHLORIDE SHIFT which allows RBC to transport CO2 from periphery to lungs for elimination 120 day life span
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anisocytosis poikilocytosis reticulocyte
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varying sizes varying shapes (poke it changes the shape) immature erythrocyte
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platelet
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involved in PRIMARY hemostasis activated by endothelial injury, interacts with other platelets and fibrinogen to form hemostatic plug Granules: - dense: ADP and calcium - alpha: vWF and fibrinogen 1/3 of platelets are stored in SPLEEN 8-10 day lifespan Collagen receptor: GpIa vWF receptor: GpIb Fibrinogen receptor: GpIIb/IIIa
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Neutrophils
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acute inflammatory response 40-75% of WBCs Phagocytic azurophilic granules: lysosomes that contain hydrolytic enzymes, lysozymes, myeloperoxidase, and lactoferrin (binds iron and inhibits growth of phagocytosed bacteria and some fungi)
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hypersegmented neutrophils mean?
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B12 and folate deficiency
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monocyte
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2-10% of WBCs large, KIDNEY-SHAPED nucleus extensive "frosted glass" cytoplasm
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macrophage
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phagocytoses bacteria/cell debris/senescent RBCs and scavenges damaged cells and tissues long life in tissues activated by IFN-Y can function as APC via MHC II CD14!!
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eosinophil
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bilobate nucleus large eosinophilic granules HELMINTHIC INFECTIONS using MBP highly phagocytic for ag:ab complexes produces histaminase and arylsulfatase that help LIMIT rxn following mast cell degranulation
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Causes of eosinophilia:
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NAACP neoplastic asthma allergic processes collagen vascular disease parasites (invasive)
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basophil
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mediates allergic rxn bilobate nucleus densely basophilic granules containing heparin, histamine, and other vasoactive amine, and leukotrienes (LTD4)
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mast cell
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mediates allergic rxn degranulation --> histamine, heparin, eosinophil chemotactic factor can bind Fc portion of IgE to membrane TYPE I HYPERSENSITIVITY RXNS Cromolyn Sodium prevents degranulation - (caroline prevented the mass from exploding)
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dendritic cell
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professional APCs always express MHC II and Fc receptor on surface (also B7) MAIN INDUCERS OF PRIMARY ANTIBODY RESPONSE called Langerhans cells in skin
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lymphocyte
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round, densely staining nucleus small amount of pale cytoplasm
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B lymphocyte
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humoral immune response after maturation in bone marrow, it migrates to peripheral lymphoid tissue (lymph node follicles, white pulp of spleen, unencapsulated lymphoid tissue) when Ag is encountered, B cells differentiate into plasma cells and produce Abs can function as APC via MHC II
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Plasma cell
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off-center nucleus, CLOCK-FACE CHROMATIN - abundant RER and well-developed Golgi
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T lymphocyte
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B7-CD28 co-stimulatory signal needed for activation CD3 on both CD4 and CD8 cells majority of lymphocytes are T cells (80%)
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universal donor universal recipient
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- O negative (no antigens on surface of RBC) - AB negative (no antibodies in plasma)
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incompatible blood transfusions cause:
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immunologic response, hemolysis, renal failure, shock, death
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anti-Rh in mother can cause ___ in newborn
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hemolytic disease of newborn (erythroblastosis fetalis) tx: Rhogam (Rho(D) immune globulin)
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Hemophilia A? Hemophilia B?
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VIII IX
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___ activates bradykinin, ___ inactivates bradykinin
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kallikrein (activated by XIIa) - also activates plasmin (which activates C3 --> C3a) ACE inactivates bradykinin bradykinin --> increased vasodilation, increased permeability, and increased pain
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vit K -->
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epoxide reductase --> activated vit K which acts as a cofactor for 2, 7, 9, 10, C and S (warfarin inhibits epoxide reductase, glutamyl carbosylase activity)
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Antithrombin inactivates
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factors 2, 7, 9, 10, 11, 12
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vWF carries/protects ___
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factor VIII
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protein C -->
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activated protein C -- (Protein S) --> cleaves and inactivates Va and VIIIa ("helping" factors) - Factor V Leiden --> a factor V that is resistant to activated protein C's inhibition
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platelet plug formation:
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Injury: vWF binds to exposed collagen on endothelium Adhesion: platelets bind vWF through GpIb at site of injury only (specific) Platelets release ADP and Ca2+ (dense granules) necessary to coag cascade - ADP helps platelets adhere to endothelium - ADP binding to receptor induces GpIIb/IIIa expression on platelet surface Fibrinogen binds GpIIb/IIIa and links platelets together Balance between: Pro-aggregation factors = TXA2 (released by platelets) --> decreased blood flow and increased platelet aggregation Anti-aggregation factors = PGI2 and NO (released from endothelial cells) --> increased blood flow and decreased platelet aggregation
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ESR
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acute-phase rxns in plasma (e.g. fibrinogen) can cause RBC aggregation, thereby increasing ESR Increased ESR: infections, inflammatory disease (temporal arteritis, polymyalgia rheumatica), malignant neoplasms, GI disease (UC), pregnancy Decreased ESR: polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia
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Acanthocyte Echinocyte Basophilic stippling Bite cell Elliptocyte Macro-ovalocyte Ringed sideroblasts Schistocyte, helmet cell Sickle cell Spherocyte Teardrop cell Target cell
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- (spur cell), liver disease, abetalipoproteinemia - renal disease (decreased EPO) - thalassemias, anemia of chronic disease, iron deficiency, lead poisoning (BASte the ox TAIL) - G6PD deficiency - hereditary elliptocytosis - megaloblastic anemia (also hypersegmented PMNs), marrow failure - sideroblastic anemia - DIC, TTP/HUS, traumatic hemolysis - sickle cell anemia - hereditary spherocytosis, autoimmune hemolysis (warm) - bone marrow infiltration (e.g. myelofibrosis) - HbC disease, Asplenia, Liver disease, Thalassemia (HALT, said the hunter to the target)
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Heinz bodies Howell-Jolly bodies
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- oxidation of iron from ferrous to ferric --> denatured HEMOGLOBIN precipitation and damage to RBC membrane --> formation of bite cells (seen with alpha-thals and G6PD deficiency) --- (HEINZ ketchup is RED like blood = hemoglobin) - basophilic nuclear remnants in RBCs (seen in pts with functional hyposplenia or asplenia) --- (the JOLLY man had a large CENTER = nucleus)
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Plummer Vinson syndrome
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triad of iron deficiency anemia, esophageal webs, and atrophic glossitis
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Alpha-thalassemia
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DELETIONS Defect: alpha-globin gene mutation --> decreased alpha-globin synthesis (no change in electrophoresis because alpha is in every combination and they are all decreased similarly) ASIANS and AFRICANS 1-2 gene deletion: no significant disease 3 gene deletion: HbH disease (4 Betas) 4 gene deletion: Hb Barts (4 gamma) = HYDROPS FETALIS (incompatible with life)
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Beta-thalassemia
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DEFECTIVE GENES Defect: point mutations in splice sites and promoter sequences --> decreased B synthesis MEDITERRANEAN and BLACKS B-thal minor: heterozygous - B chain in underproduced, usually asymptomatic - diagnosis confirmed by increased HbA2 on electrophoresis (a2d2) B-thal major: homozygous - no B chain --> severe anemia requiring blood transfusions (--> secondary hemochromatosis) - marrow expansion (crew cut on skull x-ray) --> skeletal deformities (chipmunk facies) BOTH major and minor: increased HbF (a1y2) HbS/B-thal heterozygous: mild to moderate sickle cell disease depending on amount of B production
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Lead poisoning
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inhibits FERROCHELATASE and ALA DEHYDRATASE --> decreased heme synthesis - also inhibits rRNA degradation LEAD: Lead Lines on gingivae (Burton's lines) and on epiphyses of long bones Encephalopathy and Erythrocyte basophilic stippling (ribosome aggregation) Abdominal colic and sideroblastic Anemia Drops (foot and wrist), Dimercaprol and eDta are first line tx
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Sideroblastic anemia
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Defect in heme synthesis Hereditary: X-linked defect in delta-ALA synthase gene (1st enzyme in heme synthesis) Reversible etiologies: alcohol, lead Ringed sideroblasts with iron-laden mitochondria (the iron goes in but can't get out) Labs: increased iron, normal TIBC, increased ferritin Tx: pyridoxine (B6) therapy
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Megaloblastic anemia caused by folate deficiency
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Etiologies: malnutrition, malabsorption, impaired metabolism (methotrexate, trimethoprim), increased requirement Hypersegmented neutrophils, glossitis, decreased folate, INCREASED HOMOCYSTEINE but NORMAL METHYLMALONIC ACID
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Megaloblastic anemia caused by B12 deficiency
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Etiologies: insufficient intake (VEGANS), malabsorption, pernicious anemia, Diphylloborthrium latum Hypersegmented neutrophils, glossitis, decreased B12, INCREASED HOMOCYSTEINE and INCREASED METHYLMALONIC ACID Neurological symptoms: subacute combined degeneration (DCs and lateral CS, dementia) INCREASED RISK FOR GASTRIC ADENOCARCINOMA
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Nonmegaloblastic macrocytic anemia
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macrocytic anemia with unimpaired DNA synthesis Causes: liver disease, alcoholism, reticulocytosis --> increased MCV, metabolic disorder (orotic aciduria or other congenital deficiences of purine/pyrimidine synthesis), drugs (5-FU, AZT, hydroxyurea)
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Normocytic, normochromic anemias are classified as ___ or ___ -- then ___ further by ___
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hemolytic or non-hemolytic -- hemolytics: cause of hemolysis (intrinsic or extrinsic to the RBC) and by the location of the hemolysis (intravascular vs. extravascular)
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Intravascular vs. Extravascular hemolysis
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Intra: decreased haptoglobin, increased LDH, hemoglobin in the urine (e.g. paroxysmal nocturnal hemoglobinuria, mechanical destruction) Extra: macrophage in spleen clears RBC - increased LDH and UCB --> JAUNDICE (e.g. hereditary spherocytosis, G6PD defiency, sickle cell anemia)
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bottom line for hemolytic anemias:
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increased red cell destruction --> increased red cell production destruction: • Increased serum bilirubin • Increased LDH (enzyme found in red cells) • Decreased haptoglobin (carrier molecule for hemoglobin) because it is saturated with hemoglobin • Hemoglobinemia/uria production: • Reticulocytosis • Nucleated red cells in the blood
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Anemia of chronic disease
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nonhemolytic, normocytic inflammation --> INCREASED HEPCIDIN (released by liver, binds to ferroportin on intestinal mucosa and macrophages inhibition iron transport) --> DECREASED RELEASE OF IRON FROM MACROPHAGES Labs: decreased serum iron, DECREASED TIBC (because storage of iron is high), and INCREASED FERRITIN (because of increased storage of iron)
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Aplastic anemia
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nonhemolytic, normocytic Causes: failure or destruction of myeloid stem cells due to radiation and drugs (benzene, chloramphenicol, alkylating agents), viral agents (parvo, EBV, HIV, HCV), Fanconi's anemia (DNA repair defect), Idiopathic (immune mediated, may follow acute hepatitis) PANCYTOPENIA: anemia, neutropenia, and thrombocytopenia - normal cell morphology but hypocellular bone marrow with fatty infiltrate Symptoms: fatigue, pallor, purpura, petechiae, infection Treatment: withdrawal offending agent, immunosuppressive regimen, bone marrow transplant, transfusion, G-CSF OR GM-CSF
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- List- Intrinsic Hemolytic Anemias Extrinsic Hemolytic Anemias
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(I) = intravascular, (E) = extravascular Intrinsic: - Hereditary Spherocytosis (E) - G6PD Deficiency (I) - Pyruvate Kinase Deficiency (E) - HbC defect - Paroxysmal Nocturnal Hemoglobinuria (I) - Sickle Cell Anemia (E) Extrinsic: - Autoimmune Hemolytic Anemia (Warm and Cold) - Microangiopathic Anemia (I) - Macroangiopathic Anemia - Infections
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Hereditary Spherocytosis
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Intrinsic, Extravascular Defect in proteins interacting with RBC membrane skeleton and plasma membrane (ankyrin, spectrin) Less membrane --> spherocyte (increased MCHC and RDW) --> premature removal of RBCs by spleen Findings: splenomegaly, aplastic crisis (B19 infection) Labs: positive osmotic fragility test Treatment: Splenectomy (Howell-Jolly bodies present after)
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G6PD Deficency
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Intrinsic, Intravascular X-linked Defect in G6PD --> decreased glutathione --> increased RBC susceptibility to oxidant stress (sulfa drugs, fava beans, infection) Findings: back pain, hemoglobinuria a few days later Labs: blood smear shows RBCs with Heinz bodies and bite cells
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Pyruvate Kinase Deficiency
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Extravascular Autosomal recessive Defect in pyruvate kinase --> decreased ATP --> rigid RBCs hemolytic anemia in a NEWBORN
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HbC deficiency
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glutamic acid-to-lysine mutation at position 6 in chain mutation (not valine like HbS) Pts with HbSC (1 of each gene) have milder disease than do HbSS pts
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Paroxysmal Noctural Hemoglobinuria
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Intravascular Increased complement-mediated RBC lysis (impaired synthesis of GPI anchor/DAF in RBC membrane) Labs: Increased urine hemosiderin Complication: thrombosis CD59!!
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Sickle cell anemia
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Extravascular, intrinsic HbS mutation: single amino acid replacement in B chain of glutamic acid to VALINE at position 6 Pathogenesis: low O2 or dehydration --> sickling (HbS polymerizes) --> anemia and veno-occlusion NEWBORNS are initially asymptomatic b/c of increased HbF and decreased HbS HETEROZYGOTES are resistant to malaria Findings: crew-cut skull on x-ray (also in thalassemias) Complications in homozygotes: - aplastic crisis (parvo), autosplenectomy, splenic sequestration crisis, SALMONELLA OSTEOMYELITIS, painful crisis, renal papillary necrosis and microhematuria Treatment: HYDROXYUREA (increases HbF) and bone marrow transplant
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Autoimmune hemolytic anemia
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Extrinsic Warm (IgG) = chronic anemia seen with SLE, CLL, or certain drugs (a-methyldopa) Cold (IgM) = acute anemia triggered by cold; seen in CLL, MYCOPLASMA pneumonia, or infectious mono Findings: erythroblastosis fetalis (newborns due to Rh or other blood Ag incompatibilities) Coombs positive: - direct = pts RBCs + anti-IgG Ab - indirect = pts serum + normal RBCs
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Microangiopathic anemia
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RBCs are damaged when passing through obstructed or narrowed vessel lumin Seen in DIC, TPP/HUS, SLE, malignant HTN SCHISTOCYTES
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Macroangiopathic anemia
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Prosthetic heart valves and aortic stenosis SCHISTOCYTES and triangulocytes
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Infections and extrinsic anemia
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cause increased destruction of RBCs - malaria (schizont) - Babesia (maltese cross)
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Transferrin Ferritin
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transports iron in the blood (increases when STORAGE of iron is low) --- increased in iron deficiency anemia, decreased in anemia of chronic disease even though both have decreased serum iron
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lead poisoning
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ferrochelatase and ALA dehydratase protoporphyrin accumulates in blood symptoms: microcytic anemia, GI and kidney disease - children: mental deterioration - adults: HA, memory loss, demyelination Tx: EDTA
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Acute intermittent porphyria
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affected enzyme: porphobilinogen deaminase (aka uroporphyrinogen-I-synthase) accumulation: porphobilinogen, delta-ALA, uroporphyrin (urine) symptoms: painful abdomen, red wine colored urine, polyneuropathy, PSYCH DISTURBANCES, precipitated by drugs treatment: glucose and heme (inhibit ALA synthase) A CUTE PORker was INTERMITTENTly BILIgerent to DEAnna, he looked CRAZY, so we gave him a lot of SUGAR (glucose) to stop him
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Porphyria Cutanea Tarda
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enzyme: uroporphyrinogen decarboxylase accumulation: uroporphyrin (tea colored urine) symptoms: BLISTERING CUTANEOUS PHOTOSENSITIVITY most common porphyria
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substances needed for heme metabolism:
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glycine and succinyl CoA (with B6) --> delta-ALA -- enzyme required for this step is delta-ALA synthase which requires B6, is inhibited by heme and glucose, and is defective in inherited sideroblastic anemia (tx = B6) This step occurs in the mitochondria and so does ferrochelatase rxn, the rest occur in the cytoplasm
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PT tests ___ PTT tests ___
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extrinsic pathway (I, II, V, VII, X) intrinsic pathway (all except VII AND XIII)
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Hemophilia A or B
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VIII or IX no change in PT, increased PTT Macrohemorrhage X-linked! (IX is also called Christmas Disease)
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Bernard-Soulier Disease
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decreased platelet count, increased bleeding time defect in platelet plug formation due to decreased GpIb (platelet-to-collagen adhesion) Bernard = IB deficiency
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Glanzmann thrombasthenia
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no change in platelet count, increased bleeding time decreased GpIIb/IIIa --> decreased platelet-to-platelet aggregation (no fibrinogen holding platelets together) blood smear shows NO PLATELET CLUMPING
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ITP
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decreased platelets and increased BT decreased platelet survival due to anti-GpIIb/IIIa Abs --> peripheral platelet destruction Labs: increased megakaryocytes Increased Targeting of Platelets --> decreased platelets
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TTP
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decreased platelets and increased BT decreased platelet survival due to deficiency of ADAMTS 13 (vWF metalloprotease) --> decreased degradation of vWF multimers Pathogenesis: increased large vWF multimers --> increased platelets aggregation and thrombosis Labs: increased SCHISTOCYTES, increased LDH Symptoms: PENTAD = neurological symptoms, renal symptoms, fever, thrombocytopenia, MAHA (neuro and fever not in HUS)
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C3b C3a and C5a Hereditary Angioedema
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encapsulated bacteria anaphylactic shock (C5a also PMN chemotaxis) C1 esterase inhibitor deficiency --> uncontrolled complement activation
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HUS
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Shiga or Shiga-like toxin (Shigella or E.coli) Triad: MAHA, renal failure, thrombocytopenia
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vWF disease
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increased BT, PTT may or may not be increased CARRIES VIII Intrinsic pathway coag defect: protects/carries VIII Platelet plug defect: binds collagen-to-platelet Mild but most common inherited bleeding disorder, autosomal dominant Treatment: DDAVP (desmopressin) --> release of vWF stored in endothelium
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DIC
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widespread activation of clotting --> deficiency in clotting factors --> bleeding state Causes: Sepsis (gram -), Trauma, OB, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion (STOp Making New Thrombi) Labs: schistocytes, increased fibrin split productes (d-dimers), DECREASED FIBRINOGEN, decreased factors V and VIII
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Factor V Leiden Prothrombin gene mutation Antithrombin deficiency Protein C or S deficiency
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- mutant Factor V that cannot be degraded by protein C (most common inherited hypercoagulopathy) - mutation in 3' untranslated region associated with VENOUS CLOTS - inherited deficiency of antithrombin, reduced increased in PTT after admin of heparin - decreased ability to inactivate factors V and VIII, INCREASED RISK OF THROMBOTIC SKIN NECROSIS WITH HEMORRHAGE FOLLOWING ADMIN OF WARFARIN
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Component: Clinical use - packed RBCs - platelets - fresh frozen plasma - cryoprecipitate Blood transfusion risks include:
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- increased Hb and O2 carrying capacity for acute blood loss or severe anemia - increase platelet count to stop significant bleeding (thrombocytopenia, qualitative platelet defects) - increase coag factor levels by 20% in DIC, cirrhosis, warfarin over-anticoag - contains fibrinogen, factor VIII and factor XIII to treat coag factor deficiencies involving fibrinogen and factor VIII infection transmission, transfusion rxns, iron overload, hypocalcemia (citrate is a Ca2+ chelator), hyperkalemia (RBCs may lyse in old blood units)
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leukemoid rxn vs. leukemia
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increased leukocyte alkaline phosphatase (increased WBC count with L shift, 80% bands) decreased leukocyte alkaline phosphatase
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Hodgkin vs. Non-Hodgkin Lymphoma
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Hodgkin: - Reed Sternberg cells - localized, single group of nodes (extranodal is rare), contiguous spread - B signs/symptoms - mediastinal lymphadenopathy - 50% associated with EBV - good prognosis = increased lymphocytes, decreased RS Non-Hodgkin: - may be associated with HIV or immunocompromise - multiple, peripheral nodes, extranodal involvement common, non-contiguous spread - majority involve B CELLS (except those of lymphoblastic T-cell origin) - fewer B signs - peak incidence: 20-40
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Reed Sternberg Cells
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CD30+ and CD15+ B cell origin Necessary but not sufficient for dx Variants include lacunar cells in nodular sclerosis SOMATIC HYPERMUTATION (increased variability of Abs)
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Types of Hodgkin Lymphoma
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Nodular Sclerosing (65-75%): more lymphocytes, excellent prognosis, collagen banding, LACUNAR CELLS, primarily young adults (W>M) Mixed Cellularity (25%): large increase in both lymphocytes and RS, intermediate prognosis, lots of RS cells, associated with EBV Lymphocyte Predominant (6%): lots of lymphocytes, excellent prognosis, <35 yr old males Lymphocyte Depleted (rare): more RS, poor prognosis, older males with disseminated disease, associated with EBV (LLMN)
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Types of Non-Hodgkin Lymphoma
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B cells: (Big Flunking MDs Asked for Mercy) - Burkitt's Lymphoma - Diffuse Large B-cell Lymphoma - Mantle Cell Lymphoma - Follicular Lymphoma T cells: - Adult T-cell Lymphoma - Mycosis Fungoides / Sezary Syndrome
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Burkitt Lymphoma
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Non-Hodgkin, mature B cell neoplasm t(8;14) c-myc moves next to heavy-chain Ig gene (chromosome 14) "Starry sky" appearance, sheets of lymphocytes interspersed with macrophages Associated with EBV Jaw lesion in endemic form in Africa, pelvis/abdomen in sporadic form
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Diffuse B-cell Lymphoma Mantle Cell Lymphoma Follicular Lymphoma
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- usually older adults, most common adult NHL, may be mature T cell in origin (20%), aggressive but responsive to tx - older males, t(11;14) --> deactivation of cyclin D regulatory gene, poor prognosis, CD5+ - adults, t(14;18) --> bcl-2 expression, difficult to cure but with an indolent course (bcl-2 inhibits apoptosis)
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Adult T-cell Lymphoma Mycosis fungoides / Sezary syndrome
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- adults, caused by HTVL-1 (retrovirus), adults present with CUTANEOUS LESIONS, esp in Japan/West Africa/Caribbean, AGGRESSIVE - (cutaneous T cell lymphoma) adults, present with cutaneous patches/nodules, indolent CD4+ --- becomes Sezary syndrome once mycosis gets into the blood stream
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Multiple Myeloma
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think CRAB: hyperCalcemia, Renal insufficiency, Anemia, Bone lytic lesions/Back pain Associated with: - increased susceptibility to infection - primary amyloidosis (AL) - punched-out lytic bone lesions - M spike on electrophoresis - Ig light chains in urine (Bence-Jones protein, usually kappa) --> nephropathy - rouleaux formation of RBCs Numerous plasma cells with "clock-face" chromatin and intracytoplasmic inclusions containing Ig (or IgA)
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How to distinguish MM from Waldenstrom's Macroglobulinemia
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M spike in MM = IgG or less commonly IgA M spike in WM = IgM! --> hyperviscosity syndrome and no lytic bone lesions
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MGUS
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monoclonal gammopathy of undetermined significance monoclonal plasma cell expansion without symptoms of MM may increase risk of MM
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Oncogenic Microbes
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HTLV-1 = Adult T-cell Lymphoma / Leukemia HBV, HCV = HCC EBV = Burkitt Lymphoma, Hodgkin Lymphoma, Nasopharyngeal Carcinoma HPV = Cervical Carcinoma (16 and 18) HHV-8 = Kaposi Sarcoma HIV = Primary CNS Lymphoma (CD4 < 50) H pylori = Gastric Adenocarcinoma and PUD Schistosoma = SCC of bladder
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Leukemias
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unregulated growth of leukocytes in bone marrow --> increased or decreased # of circulating leukocytes --> anemia, infections, hemorrhage
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Acute Lymphoblastic Leukemia/Lymphoma
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<15 years of age!! presentation: bone marrow mass in childhood, mediastinal mass in adolescent male Super high increase of lymphoBLASTS in bone marrow TdT+ (marker of pre-T and pre-B cells) usually responsive to therapy may spread to CNS and/or testes t(12;21) is a BETTER PROGNOSIS
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Chronic Lymphocytic Leukemia / Small Lymphocytic Lymphoma
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> 60 years of age Often asymptomatic SMUDGE CELLS Warm Ab autoimmune hemolytic anemia (SLL same as CLL except CLL has increased peripheral blood lymphocytosis)
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Hairy Cell Leukemia
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Adults Mature B cell tumor in elderly cells have filamentous, hair-like projections TRAP+!!
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AML
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median age of onset is 60 years AUER RODS which if released can cause DIC Super high increase of myeloBLASTS on peripheral smear t(15;17) = M3 AML subtype, responds to VIT A (all-trans retinoic acid) = acute promyelocytic leukemia
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CML
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30-60 years Philadelphia chromosome: t[9;22], bcr-abl --> myeloid stem cell proliferation Presents with increased neutrophils, metamyelocytes, basophils, splenomegaly May accelerate and transform to AML or ALL ("blast crisis") Very low LAP due to immature granulocytes (vs. leukemoid rxn which are mature cells) Responds to imantinib (bcr-abl tyrosine kinase inhibitor)
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chromosomal translocations t(9;22) t(8;14) t(14;18) t(15;17) t(11;22) t(11;14) t(12;21)
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- CML (Philadelphia chromosome, bcr-abl hybrid) - Burkitt's Lymphoma (c-myc activation) - Follicular Lymphoma (bcl-2 activation) - AML: M3 Promyelocytic (responsive to all-trans retinoic acid) - Ewing's Sarcoma - Mantle Cell Lymphoma - ALL (better prognosis)
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Langerhan cell histiocytosis
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proliferative disorder of dendritic cells etiology is unknown cells are functionally immature and do not efficiently stimulate T lymphocytes via antigen presentation cells express S-100 and CD1a Birbeck granules (tennis rackets on EM) are characteristic!!!
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Chronic Myeloproliferative Disorders
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Polycythemia Vera: increased RBC/WBC/platelets, no Phil chr, JAK2 mutation - abnormal clone of hematopoietic stem cells that are increasingly sensitive to growth factors Essential Thrombocytosis: only increased platelets, no Phil chr, 30-50% + for JAK2 - similar to polycytemia but specific for megakaryocytes Myelofibrosis: decreased RBC/WBC/platelets, no Phil chr, 30-50% + for JAK2 - fibrotic obliteration of bone marrow, TEAR DROP CELLS, pancytopenia CML: decreased RBCs, increased WBC and platelets, + for Phil chr, negative for JAK2
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Polycythemias: plasma volume, RBC mass, O2 sat, EPO associated diseases Relative Appropriate Absolute Inappropriate Absolute PCV
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decreased, no change, no change, no change, dehydrated no change, increased, decreased, increased, lung disease/congenital heart disease, high altitude no change, increased, no change, increased, RCC/Wilm's tumor/cyst/HCC/hydronephrosis (due to ectopic erythropoietin) increased, very much increased, no change, decreased
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megestrol acetate -->
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increased appetite in chemo patients a steroidal progestin and progesterone derivative
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