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Qual v.s Quant
| Question | Answer |
|---|---|
| Total white blood cells | 6,000-10,000/mm3 |
| Segmented neutrophils | 1800-7800 (56 %) |
| Bands | 0-700 (1-3 %) |
| Lymphocytes infant | 1000-9000 |
| Lymphocytes children | 1000-7000 |
| Lymphocytes adults | 1000-4500 (34 %) |
| Monocytes | 0-800 (4 %) |
| Eosinophils | 0-450 (1-33 %) |
| Basophils | 0-200 (0.3 %) |
| African americans have a lower white blood count | 5,000 |
| Normal hemtocrit | 39-46 |
| Lower than 1500 of neutrophils (Neutropenia) | more prone to infections, Bone marrow replacement (leukemia, metastatic tumor, granulomas ,Myelodysplasia , Bone marrow aplasia (drugs, toxins, virus), Hypersplenism ,Autoimmune, Cyclic neutropenia |
| Congenital neutropenia (Kostmann syndrome) | Autosomal recessive, 60-80% point mutation in neutrophil elastase gene with abnormal protein folding and apoptosis, Respond to rG-CSF,Risk of transformation to myelodysplasia/ acute myeloblastic leukemia |
| Schwachman-Diamond syndrome | autosomal recessive marrow failure w/ predominant neutropenia, ½ anemia, increase fetal Hb 10-44%, 10-25% pancytopenia, Impaired Chemotaxis, Pancreatic Insuff w/ steatorrhea &failure to thrive, hepatic steatosis, 46% metaphyseal dysostosis, Risk of MDS/A |
| Fanconi anemia | Congenital bone marrow failure, Apoptosis of stem & progenitor cells, High Risk of MDS/AML, Wilm’s Tumor, Brain tumors & solid tumors, squamous cell carcinoma of head and neck, esophagus and vulva |
| Dose-related drug induced neutropenia | Alkylating Agents, Phenothiazine, Clozapine, Chloramphenicol, Propylthiouracil-hyperactive Thyroid |
| Idiosyncratic (specific to each patient)drug-induced neutropenia (NOT dose-related)- | NSAIDS, Antibiotics,Anticonvulsants, Psychopharmaceuticals,Diuretics,Antimalarial, Cardiac Meds, H2 Blockers |
| Immune neutropenia | Neonatal alloimmune , Systemic lupus erythematosus (antibodies against own bod) , Rheumatoid arthritis with Felty syndrome, Sjögren's syndrome (attack salivary & lacrimal glands) |
| Cyclic Neutropenia | Mutation of neutrophil elastase gene (ELA 2) , Apparent G-CSF cycling with 21 day cycles; 30% of cases cycle 14-36 days, AD; apparent in infancy, Bone marrow: lack of maturation beyond myelocyte stage, Clinical: gingivitis, stomatitis, cellulitis, clostr |
| Causes of Consistent FEVER in NEUTROPENIA | Resistant, Bacterial Infection, Bacterial Infection cuz of Necrosis/Mucositis, Nonculturable cell wall-deficient bacteria,Nonbacterial Infection, Malignancy-related fever, Superinfection w/ fungi, Drug or Transfusion Fever |
| Causes of Death in Adult Acute Leukemia | Infection Alone Main Cause – 66%, Hemorrhage, Infection + Hemorrhage, Organ Failure, etc |
| Neutropenic Enterocolitis | cecum-distention and thickened amplifying ischemia incident due to bacterial enterotoxins, potential perforation-fatal, terminal ileum & ascending colon involved, after high dose chemo w/ bone marrow rescue, Pseudomonas, Clostridium species, coliform b |
| Invasive aspergillosis (FUNGI) | cuz neutropenia –asthma (very low WBC-~500) |
| Necrotizing invasive aspergillosis | chemotherapy-induced neutropenia |
| Congenital neutropenia (Kostmann syndrome) | Autosomal recessive, 60-80% point mutation in neutrophil elastase gene with abnormal protein folding and apoptosis, Respond to rG-CSF,Risk of transformation to myelodysplasia/ acute myeloblastic leukemia |
| Schwachman-Diamond syndrome | autosomal recessive marrow failure w/ predominant neutropenia, ½ anemia, increase fetal Hb 10-44%, 10-25% pancytopenia, Impaired Chemotaxis, Pancreatic Insuff w/ steatorrhea &failure to thrive, hepatic steatosis, 46% metaphyseal dysostosis, Risk of MDS/A |
| Fanconi anemia | Congenital bone marrow failure, Apoptosis of stem & progenitor cells, High Risk of MDS/AML, Wilm’s Tumor, Brain tumors & solid tumors, squamous cell carcinoma of head and neck, esophagus and vulva |
| Dose-related drug induced neutropenia | Alkylating Agents, Phenothiazine, Clozapine, Chloramphenicol, Propylthiouracil-hyperactive Thyroid |
| Idiosyncratic (specific to each patient)drug-induced neutropenia (NOT dose-related)- | NSAIDS, Antibiotics,Anticonvulsants, Psychopharmaceuticals,Diuretics,Antimalarial, Cardiac Meds, H2 Blockers |
| Immune neutropenia | Neonatal alloimmune , Systemic lupus erythematosus (antibodies against own bod) , Rheumatoid arthritis with Felty syndrome, Sjögren's syndrome (attack salivary & lacrimal glands) |
| Cyclic Neutropenia | Mutation of neutrophil elastase gene (ELA 2) , Apparent G-CSF cycling with 21 day cycles; 30% of cases cycle 14-36 days, AD; apparent in infancy, Bone marrow: lack of maturation beyond myelocyte stage, Clinical: gingivitis, stomatitis, cellulitis, clostr |
| Causes of Consistent FEVER in NEUTROPENIA | Resistant, Bacterial Infection, Bacterial Infection cuz of Necrosis/Mucositis, Nonculturable cell wall-deficient bacteria,Nonbacterial Infection, Malignancy-related fever, Superinfection w/ fungi, Drug or Transfusion Fever |
| Causes of Death in Adult Acute Leukemia | Infection Alone Main Cause – 66%, Hemorrhage, Infection + Hemorrhage, Organ Failure, etc |
| Neutropenic Enterocolitis | cecum-distention and thickened amplifying ischemia incident due to bacterial enterotoxins, potential perforation-fatal, terminal ileum & ascending colon involved, after high dose chemo w/ bone marrow rescue, Pseudomonas, Clostridium species, coliform b |
| Invasive aspergillosis (FUNGI) | cuz neutropenia –asthma (very low WBC-~500) |
| Necrotizing invasive aspergillosis | chemotherapy-induced neutropenia |
| Signs of PMN Dysfunction | Recurrent acute bacterial infections, Low PMN count in infected body fluids, Cold abscesses, Granulomatous response to non-granuloma producing organism, Inappropriate (limited) response to infections, Early periodontitis , Spherical pneumonias |
| Non-neutropenic fever directly associated with neoplastic disease | Non-Hodgkin’s Lymphoma (release cytokines), Hodgkin’s Lymphoma (release cytokines), Adenocarcinomaof kidney (tumor necrosis) |
| Leukocyte Adhesion Deficiency (LAD) –TYPE 1 | Rare-Autosomal Recessive –BETA 2 INTEGRIN problem (needed so PMN’s can stick), Delayed separation of umbilical cord, severe periodontitis, recurring infections of skin and mucous membranes, lungs and intestinal tract, 75% mortality by age 10 yrs |
| Leukocyte Adhesion Deficiency (LAD) –TYPE 2 | Rare-Defect of CARB FUCOSYLATION—sialyl Lewis, ligand for SELECTIN ,Associated growth retardation, abnormal facies and neurologic impairment |
| Job Syndrome | Rare-Leukopenia &Poor Chemotaxis (Hyper IgE recurrent infection) wide set eyes (hypertelorism), big jaw (macroganthia); Recurrent sino-pulmonary infections: S. aureus, H. influenza, P. aeruginosa, Aspergillus |
| Chediak Higashi Syndrome | Defective giant lysosome granules in PMNs, L, M, melanocytes, Schwann cells, endocrine cells, renal tubular cells, Neutropenia & poor chemotaxis; Albinism |
| Neutrophil-specific granule deficiency | Absent Neutrophil granules |
| Chronic Granulomatous disease (CGD) | Deficient NADPH oxidase, w/ absent H2O2 production (bacteriocidal); Mostly X-linked, PMNs not wrkin-so mostly macrophages present; Treatment: T-cell-depleted stem cell allograft |
| Myeloperoxidase Deficiency | Deficient HOCl production (bacteriocidal) |
| Specific Granule Deficiency | Rare -PMN Appearance: Pelger-Huet nuclei with ground glass cytoplasm; Deficiency: lactoferrin, transcobalamin, procollagenase; Impaired chemotaxis ; Clinical: Bacterial infections skin, subcutaneous fat, sinuses, and lungs |
| If bacteria is Catalase + (CGD) | destroys hydrogen peroxide which is a source of superoxides (staph, gram neg, fungus-candida, aspergillus) à destroys itself |
| Molecular effects of corticosteroid Tx | Blocks phospholipase induced arachidonic acid sequence; Upregulates gene expression:NFkB, IL-4, IL-10, IL-13, TGF-b; Downregulates gene expression: inflammatory =IL-1, IL-2, TNFa, COX-1, MMP-1, NOS |
| Features of Chronic Inflammatory Response | 1.Injury persists in tissue for weeks, months, years; 2. Cellular Response- Macrophages & Lymphocytes; 3. Granuloma formation cuz prolonged macrophage stimulus; 4.Tissue Necrosis w/ granulation – scar formation (persistent suppuration may also be seen |
| Lymph nodes-Germinal centers | produce B lymphocytes become plasma cells & make immunoglobulins (IgA, IgD, IgE, IgG & IgM |
| Lymph nodes- Area between germinal centers | T cells produced in Thymus |
| B & T Lymphocyte cell pathway- Start w/ stem cell | Terminal deoxynuclear transferase |
| CD20 (T cell) | late mature characteristic of b cells; To treat lymphomas |
| CD4 (T cell) | helper –help kill (MHC2) |
| CD8 (T cell) | cytotoxic -will kill lymphocytes in liver (MHC1) |
| TH1 (T cell) | activates monocytes (helper) |
| TH2 (T cell) | release cytokines which regulate IGE’s & parasites |
| ADCC (T cell) | Antibody Dependent Cell Cytotoxicity |
| CD4-Th0 (T cell) | uncommited |
| CD4-Th1 (T cell ) | macrophage & lymphocyte induced - granuloma formation via release of IL2 (helper cytokines) & INF gamma |
| CD4-Th2 (T cell ) | IL 5 (eosinophils), IL4 & IL10 (Supress macrophage activation), IL4 only (Produce IgG and IgE)IL13 IL3, (attracts antibodies, inhibit TH1 cells) |
| Neutralization | Antibody prevents bacterial adherence |
| Opsonization | Antibody promotes phagocytosis |
| Complement Activation | Antibody activates complement, enhances opsonization and lyses some bacteria |
| Perforin | CD8 cell & NK cells kill by drilling holes into cells they are attacking…the holes are made by the release of perforin |
| IFN -alpha and IFN-beta | 1. Induce resistance to viral replication, 2.Increase MHC-1 expression & antigen presentation, 3. Activate NK cells to kill virus infected cells |
| How does a macrophage get activated? | First monocyte, then tissue macrophage, then activation by microbes, dead cells etc. as well as cytokine & IFN-gamma (as an immune response from activated T cell) to become activated macrophage. |
| Activated macrophage needed for | Tissue Injury & Inflammation & Fibrosis |
| Structural and Functional Changes Associated with Macrophage Activation | Morphological Changes= Membrane ruffling, Spreading, Increased pinocytosis , Increased mitochondria, Expanded lysosomes & phagolysosomes ; Metabolic Changes= Accelerated oxidative metabolism, Superoxide (O2-) generation, H2O2 production, Lysosomal enzyme |
| When macrophages become huge | become EPITHELIOD CELLS and then MULTINUCLEATED GIANT CELLS (LAN-HANS) |
| GRANULOMA | Spherical collection of activated macrophages surrounded by Th1 lymphoctes |
| CASEATION | product of cell wall –dead macrophages inside and activated macrophages in the outside keeping it intact…release TNF, then activation of fibroblast = scar |
| Pink color of macrophages due to | Lots of Cytoplasm |
| Granulation tissue | proliferating fibroblasts and angiogenesis, representing the early reparative phase of injury |
| SARCOIDOSIS | Granuloma disease - increased in african americans, unknown ideology (Blurring of vision and photophobia); Treatment - steroids but not too much cuz may develop diabetes or osteoporosis, try to reduce inflammation |
| Non caseating granulomas | enormous lymph nodes |
| Asteroid body | can be seen in fungal infection or sarcoid |
| Caseation Necrosis | Eosniphiles surrounded by lymphocytes (Pink- so much cytoplasm) |
| Immune reconstitution syndrome | Exuberant inflammatory reaction and worsening of clinical manifestations of opportunistic infections; Criteria: New appearance or worsening of opportunistic infectious diseases,Negative results of cultures or bio-markers |
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