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159 Cards in this Set
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- Back
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2 main types of polycythemia and their causes |
"* Physiologic polycythemia: eg high altitude
* Polycythemia vera: genetic abnormality in hemocystoblastic cells - don't stop production when RBC count is too high. 1) Usually also see excess WBCs & platelets. 2)Total blood volume increases (up to 2x normal) --> vascular engorgement, capillaries plugged, blood viscosity is 10x water (normal blood is 3x)." |
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"* alpha & beta spectrin chains (defective in spherocytosis)
* ankyrin: anchors chains to transmembrane protein * protein 4.1: anchors ankyrin to actin/tropomysin" |
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AB type |
"A: RBC expresses A antigen; anti-B antibody in plasma
B: v.v. AB: RBC expresses A&B antigens; no Abs, hence universal RBC recipient, universal plasma donor O: no antigen, both antibodies, hence universal blood donor, universal plasma recipient Anti-A & -B antibodies are IgM, thus do not cross placenta" |
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Acute Leukemias: Hallmarks |
"* Blasts predominate in bone marrow and peripheral blood
* Most common malignancy of peds; second incidence after age 60. * Frequent cytogenetic abnormalities (eg Philadelphia chromosome t9;22) * Short precipitous course if untreated: anemia, infection, hemorrhage, death in 6 mos" |
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Adaptive Immunity Process |
"* Process: introduction --> digestion & presentation --> activation --> cloning
1) Introduction: agent enters tissue fluids, usually on a lymphoid surface (GI walls protect gut; tonsils, adenoids protect respiratory tract; nodes protect peripheral tissues; spleen/thymus bone marrow protect blood) 2) Digestion & Presentation: Macrophages lining sinusoids of lymphoid tissue phagocytose & digest invading organism, then present antigenic fragments via cell-to-cell contact to adjoining lymphocytes; macrophages also secrete IL-1, which boosts growth and reproduction of lymphocytes. 3) Activation: B or T lymphocytes activated by a single specific antigen (most antigens activate both types) * Th cells secrete lymphokines (inc IL-2-6; GM-CSF; IFN-gamma) --> activate B lymphocytes (essential for decent Ab response - see HIV/AIDS 4) Cloning: activated lymphocyte reproduces wildly, forming huge numbers of clones (duplicate lymphocytes) Activated B lymphocyte --> lymphoblasts --> plasmablasts (divide rapidly 1x every 10 hours, 500 in 4 days)--> plasma cells: produce insane qty of antibodies (~2000 molecules per second). Memory cells: form new B lymphocytes similar to original clone, circulate through body and populate all lymphoid tissues, but are dormant until antigenically reactivated (bigger 2' response, basis of vaccination) * Activated T lymphocyte clones are specific sensitized T cells, released into lymph & blood and circulated through tissues and back into lymph. * T lymphocyte memory cells also exist; same process & function as B lymphocyte memory cells Activated cells continue their activities until they die, exhausted." |
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Additional sources of lymphocyte receptor diversity |
"1) Combinatorial diversity of heavy & light chains
2) Terminal deoxynucleotidal transferase (Tdt) enzyme - adds random nucleotides to heavy chain btw D-J & V-D joints - affects antigen binding * ALL marker - shuts off early in ALL progression 3) * Allelic exclusion: if bad gene is transcribed, it shuts off (excludes) bad chromosome and pulls other genes from other parental chromosome. * Ensures 1 specificity per cell - lack of specificity is a big problem during selection in bone marrow, thymus * 4 ""chances"" in light chain kappa(mom), kappa (dad), lambda (mom), lambda (dad); only 2 choices in light chain." |
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Algorithm for Anemia Dx |
"1) Decreased Hb/Hct --> get reticulocyte count
2) Reticulocyte count abnormal (>2) = blood loss or hemolytic anemia --> look for hemorrhage (blood loss); check for haptoglobin, LDH, bilirubin (hemolysis) 3) Normal reticulocyte count (<2) --> check MCV 4) Microcytic (MCV < 80) --> check iron studies (Fe & TIBC) DECR Fe, DECR TIBC = anemia of chronic dis DECR Fe, INCR TIBC = iron deficiency NORM Fe, DECR/NORM TIBC = lead poisoning/thalassemia 5) Normocytic (MCV 80-100) --> aplastic anemia, marrow fibrosis, tumor, anemia of chronic dis, renal failure 6) Macrocytic (MCV > 100) --> check B12/folate levels Abnormal B12 /folate = diagnostic Normal = suspect liver disease (altered metabolism of plasma proteins causes huge RBCs)" |
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ALL |
"* Lymphoblasts predominate in bone marrow and peripheral blood:
* Most common malignancy in children * Bone marrow failure & ogran infiltration, neutropenia, DIC, anemia * Most responsive acute leukemia to Tx * Classification and prognosis depend on morphology, cytogenetic changes, cell markers, rearrangement of IG heavy chain or T cell (R) genes: * GOOD prog: B-ALL, women & children, hyperdiploidy, CD10, t(12;21)/TEL-AML1 rearrangement * BAD prog: T-ALL, boys, 70+, hypodiploidy, t(19;22) aka Philadelphia, t(1;19), 11q;23/MLL rearrangement" |
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Alpha-fetoprotein |
Marker for hepatocellular carcinoma
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AML |
"* myeloblasts predominate (note Auer Rods, arrow):
* Clinical presentation similar to ALL * Some differentiation of blasts into granulocytes, monocytes * Responds more poorly to Tx than ALL * Causes: 1' - de novo; 2' - MDS, chemo" |
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Anemias: criteria for microcytic, normocytic, macrocytic |
"Microcytic: MCV < 80 fL
Normocytic: MCV 80-100 fL Macrocytic: MCV > 100 fL" |
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Antibody Production in Neonates vs Fetus |
"* Maternal IgG in Fetus starts at 3 months gest'n, peaks at birth; infant IgG ramps up at birth and is dominant Ab in year 1
* Normal infants get very few infections in first month b/c of maternal IgG * Immunodeficiency in infants doesn't emerge until maternal IgG recedes (almost all gone by 6 months) - so no live vaccines until 12 months - maternal IgG wll likely have Abs to vaccine & gobble it, preventing inoculation * Infant's IgA level at 12 months is 20% of adults - colostrum is important supplement * IgM is only useful isotype in Dx'ing neonatal infection (all cells are naive at birth, also you don't know where their IgG came from) * Note that kid's total Ab level at 12 months is still lower than typical adult's - this is why kids get recurrent infections, esp of mucosa (runny nose, cough, etc.)" |
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Ataxia Telagiectasia |
Deficient kinase involved in cell cycle regulation, telangiectasias are enlarged blood vessel (most apparent in eye - look blood shot)
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B cell |
"Humoral immune response
Originates in Bone marrow; migrates to peripheral lymphoid tissue (lymph node follicles, white pulp of spleen, unencapsulated lymphoid tissue) Antigen --> B cells differentiate into plasma cells and memory cells --> plasma cells express tons of antibodies (immune globulins); memory cells maintain antigen library CD19, CD20 markers" |
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B Cell Receptor |
"* Antibodies can bind to almost any organic molecule & eliminate it
* Antibody molecule is bivalent: 2 identical heavy chains, 2 identical light chains --> 2 sites for identically binding antigen * Hinge molecule allows 1 arm to move and bind even when antigen binds other arm * VL + Vh = variable region - determines idiotype; allows for diversity, specificity * Constant region (CH1, CH2, CH3, CL) determines biological function of molecule region is constant and determines isotype or class (IgG, IgA, etc.) once bound - ie cross placenta, opsonization, Ab-dependent cytotoxicity, activate complement, etc. * If B cell terminally differentiates into a plasma cell - the receptor can be secreted from cell as an ANTIBODY" |
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B Cell Signal Transduction Complex |
CD19, 20, 21 are CORECEPTOR - when activated, lower threshold for antigenic activation. They are also B cell markers.
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Bacterial Vaccines |
"* DTP: C. diphtheriae = toxoid
* DTP, DtAP: B. pertussis = toxoid & hemaggluten * DTP: C. tetani = toxoid * Hib: H. influenzae = capsule & protein * PCV (ped): S. pneumoniae = capsular serotypes & protein * PPV (adult): S. pneumoniase = capsular serotypes * MCV: N. meningitidis = capsular serotypes" |
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Basophil |
"* Type I hypersensitivity (IgE) allergic response: release pharmacologically active substances very rapid response
* Attachment of antigen to specific IgE antibody to basophil / mast cell causes rupture and release of granules * Granules: heparin (sim to mast cells), histamine, bradykinin, serotonin * Nucleus: bilobed - can barely be seen b/c of dark staining granules * Cytoplasm: LARGE BLUE granules * Note: neutrophils, basophils, eosinophils are also known as ""polymorphic ___phils"" or ""polys""" |
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B-cell: main fxn & specific cell markers |
"produce antibodies
CD19, 20, 21" |
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Beta-HCG |
Marker for choriocarcinoma of the ovary, testis, placenta
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Breakdown of Adaptive Immunity Cells & Rel % of Each |
"* 55-60% Granulocytes: 55% Neutrophils: chief phagocyte for early inflammation; 1-4% Eosinophils: IgE-mediated response to parasites & allergens; <1% Basophils: mediate vasoactivity & anticoagulation. Mast Cells: Initiate inflammation & release mediators
* 40-45% Agranulocytes: 35% Lymphocytes = T Cells and B Cells, 5-10% NK Cells: kill tumors and virus-infected cells * Phagocytes: monocytes: migrate to site of inflammation and become macrophages; macrophages: eat antigens, activate processes" |
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Bruton's X-linked Hypogamma Globulinemia |
"* ONLY humoral defect with NO B CELLS
* Defect is in Bruton's tyrosine kinase (BTK) needed to go from precursor B cell to immature B cell; pre-B cells develop but can't get out." |
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C1 esterase |
"Breaks down C1 --> INCR production & activation of C2, 3, 4.
Deficiency in C1 esterase inhibitor can cause hereditary angioedema." |
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CA 19-9 |
Marker for pancreatic cancer
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CA-125 |
Marker for ovarian cancer
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Catalase (+) Bacteria |
Staph aureus, Ecoli, Salmonella, Shigella, Pseudomonas, Aspergillus
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Chronic Granulomatous Disease |
"* Granules can't fuse, can't phagycytose so they just swell and get really large
* X-linked * ***PATIENTS ARE ALSO ALBINOS***" |
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Chronic Leukemias: Hallmarks |
"* Proliferating cells (lymphoid or hematopoietic) are more mature than acute leukemias
* Less devastating clinical course, but also less responsive to treatment" |
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CLL |
"* Monoclonal proliferation of mature but defective lymphocytes (can't differentiate into Ab-manufacturing plasma cells)
* Most common leukemia in Western world * Usu older adults 60+ * Gen'ly least aggressive, with better survival than CML * Sx: USUALLY ASX; painless lymphadenopathy, splenomegaly; resp/skin infxns; LATE: anemia Sx * Anemia, thrombocytopenia, neutropenia * Smudge cells * Tx: Ptts usually observed until Sx. Chemo doesn't chg survival, but provides some Sx relief." |
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CML |
"* myeloid stem cells (RBC, granulocyte, monocyte, platelet precursor) proliferate - note blast cells, promyelocytes, myelocytes, and bands:
* usu men, usu age 35-50 * t(9;22) Philadelphia is tell-tale marker; 95% have it (path.: c-abl proto-oncogene is transposed from 9 to 22, adjacent to bcr (breakpoint cluster region). Fusion gene is bcr-abl, which codes for p210 protein, a tyrosine kinase whose activity is crucial to pathogenesis of CML.) * Sx: SOB, weight loss, fever, fatigue, freq infxn, easy bruising & bleeding, splenomegaly, hepatomegaly, lymphadenopathy * Chars: marked leukocytosis, basophilia, leukemic cells in peripheral blood and bone marrow, mainly mid-to-late myeloid (granulocytic) precursors, marked reduction in leukocyte alkaline phosphatase (LAP) in luekemic leukocytes. * Prog: blast crisis = INCR primitive blast cells and promyelocytes" |
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Coagulation pathways |
"Intrinsic (collagen, bsmt membrane, activ's platelets): 12-11-9-10-2-1 Long line; determines PTT
Intrinsic (tissue damage): 7-10-2-1 - short line; determines PT 2/7/9/10 are Vit K/ Ca++ dependent factors" |
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Common Features of Leukemia Tx |
"1) Induction: chemo for bone marrow remission
* Prednisone, vincristine, anthracycline - poss. cyclophosphamide, L-asparaginase 2) Consolidation: chemo eliminates remaining leukemic cells * MTX, G-MP * High doses, multiple drugs, lasts for months 3) CNS met prophy: usu radiation to head/spine * Alternative: BMT" |
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Complement Deficiencies |
"* C5/6/7/8 (MAC) deficiency --> chronic Neisseria infxns
* C1-INH defic - > hereditary angioedema; complement turned on, but without C1-inhibitor, it can't turn off --> SEVERE INFLAMMATION (eg giant ballooning lips; doesnt stop until complement proteins exhausted) * C3 is most profound deficiency - affects both pathways" |
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Course of HIV Infection |
"1) Multiplication in activated lymphocytes and macrophages --> Reproduces virus |
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Cytotoxic T lymphocytes (CTLs): markers, functions, external stimuli, killing process |
"* Fxns: Lyse & kill altered cells; transform cells; effect anti-tumor activity, transplant rejection, etc. Killing Process: * Fas ligand recognition >> CTL releases TNF --> binds TNF-(R) on target cell --> target cell apoptosis |
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Dendritic |
"* Antigen-presenting
* Mostly in tissues & epithelia * Long cytoplasmic arms * Follicular dendritic cells (less comon) are cell memory: trap antigen and hold it for a long time, and continually re-present it to keep memory * APC dendritic cell: most important in antigen processing & presentation" |
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Dendritic cell |
"Highly phagocytic APC - links innate & adaptive immunity
MHC II & Fc (R) expressed In skin, called Langerhans cells" |
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Diff btw intra- and extravascular hemolysis |
"* Intravascular hemolysis = RBCs destroyed in vascular compartment
* Extravascular hemolysis (more common) = RBCs destroyed in reticuloendothelial (mononuclear phagocyte) system - ie spleen & liver. 2 main results: 1) Alterations in deformability make RBCs unable to clear narrow passageways of spleen (also lyse in tight capillaries) 2) INCR bilirubin --> jaundice & ""pigment"" gallstones" |
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DiGeorge Syndrome |
"* Failure during embryonic development of 3rd/4th phayngeal pouch (thymus & parathyroid)
* NO T Cells (no TH, no CTLs, nada) * Sx: craniofacial abnormalities (fish lip, heightened forehead), HypoPTH (affects heart b/c of Ca++) * Only Ab you can find is IgM (need T cells for IgG, IgA, IgE; IgD is negligible)" |
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Direct Actions of Antibodies |
"* Note: most of their protective effect comes from #1
1) Amplifying effects of complement (Ag-Ab complex formation uncovers a reactive site on Ab, which binds C1 and activates classic pathway) 2) Agglutination: bind large antigenic particles in a clump 3) Precipitation: Ab-Ag complex gets so large it's rendered insoluble and precipitates 4) Neutralization: Abs cover toxic sites of antigenic agent 5) Lysis: antibodies attack and rupture cellular membrane" |
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Dominant Hematopoietic Organs During Gestation and Lifespan |
"* Gestation - 8 weeks: yolk sac
* 8-28 weeks gestation: hemangioblasts in liver, spleen dominate * 20-23 weeks: bone marrow appears (clavicle first) and starts production; clavicle * 32-36 weeks gestation: bone marrow becomes dominant * Birth: all marrow is red, then becomes mostly yellow with aging (~70% yellow by age 70) * Infant marrow is all red * Adulthood: axial skeletal bones & proximal femur ends (note above) * Blood loss can ""pressure"" yellow marrow to go back to being red to produce more blood cells (extramedullary hematopoiesis)" |
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Draw the Barone Coagulation Diagram |
"1) Draw #s from 12 --> 1 in a line
2) 3, 4 & 6 don't exist 3) 5 & 8 are cofactors - go above the line 4) 7 is lucky 7 - put it below the line 5) 10 is special - gets to cut in line before 9, & everyone wants to be around it (7 below, 5 & 8 above) 6) Draw a long line from 12-1 = intrinsic 7) Draw a short right angle line from 7-10-2-1; extrinsic 8) Draw a triangle around 9, 2, and 7: Vi K. Ca++ dep factors |
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Effects of EPO |
"* In the absence of EPO, few RBCs are formed in the marrow.
* Stimulate maximal RBC production within 24 hours; new cells don't appear for 5 days b/c it stimulates production of proerythroblasts, takes time to appear as new cells * EPO also causes newly-created cells to pass more quickly through the maturation stages." |
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Eosinophil |
"Parasitic infections (major basic protein)
Bilobed nucleus Packed with granules " |
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Eosinophil |
"* Fxns: parasitic infection & Type I (IgE-mediated) hypersensitivity response
* Poor phagocytic ability, some chemotaxis (neither) on par with a neutrophil * ANNIHILATE PARASITES - attach with special surface molecules, bomb them with lysosome granules, ROS & major basic protein (polypeptide - highly toxic to larva) * Makes histaminase, arylsulfatase to detoxify inflammatory substances release by mast cells & basophils, phagocytose allergen-antibody complexes - limit rxn post-mast cell degranulation, prevent spread * Allergy: Mast cells & basophils release eosinophil chemotactic factor that draws them to inflamed allergic tissue. * Nucleus: bilobed * Cytoplasm: LARGE PINK granules * Rare in bloodstream: 0-450/uL * Eosinophilia causes: Neoplasm, Athma, Allergy, Collagen Dis, Parasites (""NAACP"")" |
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EPO |
"* Released by kidneys if there is DECR Po2 (hemorrhage, anemia or DECR # RBCs)
* Effect: INCR # of progenitor cells committed to erythropoiesis * 90% produced by kidneys, 10% by liver" |
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Erthyrocytes (RBCs) |
"Carries O2 to tissues, CO2 to lungs
No nucleus. 120 day lifespan. Membrane contains Cl-/HCO3- antiporter; allows sequestration of HCO3- and transport CO2 from periphery to lungs for elimination. Erythrocytosis = polycythemia = INCR HCt Reticulocyte = immature erythrocyte, marker of erythroid proliferation" |
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ESR |
"* Erythrocyte Sedimentation Rate (""sed rate"")
* Non-specific marker of inflammation * # is mm of clear fluid (plasma) at top of tube after 1 hour (newer test uses 4 mins centirfugation) * Can be useful to monitor inflammation in RA, Kawasaki * CRP is a more sensitive and responsive measure" |
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Ewing Sarcoma |
"Presents like osteomyelitis
X-Ray: ""onion-skin"" layering of periosteum t(11; 22) translocation Most common in males under 15. Aggressive, but responds well to treatment." |
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G6PD Deficiency |
important biochemically, but same immune profile as CGD, b/c G6PD is precursor for NADPH oxidase
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Hallmarks of Hodgkin Lymphomas |
"Malignant with features resembling inflammatory disorder: fever, infiltrates, etc.
Young adults (esp men) Sx: pruritus, fever, diaphoresis, leukocytosis (resembles acute infection) Reed-Sternberg giant cells" |
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Hematopoietic Growth Factors in Hematopoiesis |
"* Hematopoietic growth factors (glycoprotein growth hormones)
* Fxn: proliferation, differentiation, anti-apoptotic, maturation, activation * Net effect: maintain pool of stem/ progenitor cells * Act locally, circulate and can adhere to ECM and form niches where stem cells/ progenitors can adhere * Sources: stromal cells (except EPO - from kidneys, TPO - from liver) * Synergy: 2 factors can combine effects on cell * 1 factor can stimulate release of another" |
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Hemophilias: deficient factors |
Hemophilia A: Factor VIII deficient/ B: Factor IX ("A rhymes with Eight; B is one more than A")/ C: XI deficit
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Hereditary Spherocytosis |
"Auto-dom
Path: spectrin defic --> weaker cytoskeleton --> RBCs become spherical --> sequester in spleen Sx: triad - Hemolytic anemia, jaundice, splenomeg" |
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HIV Virus |
"* D-type retrovirus
* Binds CD4 (R) on host cells via gp120 glycoprotein * Early in infection, virus uses CCR5 chemokine (R) on macrophage as coreceptor * Late in infection, virus uses CXCR4 chemokine (R) on T lymphocytes as coreceptor * Nef is the virulence gene of HIV - strains without Nef are harmless (ie they are still susceptible to NK cells) * Mutates frequently due to absence of proofreading" |
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IgA |
"* Functions: inhibits binding to mucosal surfaces; key component in breast milk - protects infant in period between when maternal IgG diminishes and when baby's immune system develops
* Secreted as dimer with J chain * Primarily produced in mucosa" |
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IgE |
"* Fights parasites, but also mediates atopy / allergic (Type I) immediate response
* Binds via Fc region to mast cells and basophils" |
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IgG |
"* Functions: ONLY Ab that can opsonize; activates complement; mediates ADCC (antibody dependent cell-mediated cytotoxicity)
* Major Ab produced post-IgM * Major Ab in serum (~75% of antibodies) * 2 identical heavy chains, 2 identical light chains " |
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IgM |
"* Functions: trap free antigen, activate complement (along with IgG)
* IgM is always first antibody made in response to any antigen * Secreted as pentamer, each monomer held together by joining chain (J chain) * Valence = 10; can bind 10 antigens (but all the same antigen)" |
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Innate Immunity Barriers |
"* Skin
* Mucosa (thick mucosy, lots of degradative enzymes) * Chemicals (eg lysozyme, finger proteases) * pH (stomach acid, skin is slightly acid) * Temperature (fever)" |
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Innate Immunity Blood Proteins |
Complement
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Innate Immunity Cellular Components |
phagocytes (PMNs, macros, NKs)
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Intracellular Killing Mechanisms |
"2 types: oxygen dependent & oxygen independent
1) O2 dependent: * NADPH oxidase is crucial for creating superoxide radicals that are so good at killing pathogens * Myeloperoxidase turns H2O2 into hypochlorite 2) Oxygen Independent: lysosome (lysozyme, defensins, lactoferrin, hydrolytic enzymes)" |
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Job Syndrome |
"TH1s can't make IFN-gamma, INCR IgE (comes from TH2 not being suppressed by absence of IFN-gamma)
Eczema" |
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Key Calculation of Anemia |
(Circulating Hb) / (Plasma Volume)
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Kinin cascade |
"Factor XIIa --(+)--> Prekallikrein --> Kallikrein --(+)--> HWMK --> Bradykinin --> Kinin Cascade
Kinin Cascade effects: INCR vasodilation/permeability/ pain ACE inactivates bradykinin" |
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Leukocyte Adhesion Deficiency |
"* CD18 needed to mediate tight binding to get into tissue, cells approach inflammation site, but can't adhere & thus can't enter tissue.
* No pus. * Cheilitis, gum infections (gingivostomatitis)" |
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Leukocytes (white cells) |
"2 categories:
1) granulocytes (neutrophil, eosinophil, basophil - ""the phils are filled with granules"") 2) mononuclear cells (monocytes, lymphocytes)" |
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Lymph Node: anatomic features & role in immunity |
"* Afferent lymphatic = antigen site of entry
* Cortex: site of first contact * Primary follicle is B-cell rich; also contains macrophages and dendritic cells * Paracortex is T-cell rich region; * As antigen enters cortex and starts activating, the cortex enlarges and becomes a secondary follicle, then becomes germinal center with ightly packed rings of activating cells * Medulla = where differentiation into plasma cells occurs * Memory cells exit via efferent lymphatics & start dumping antibody all over" |
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Lymphocytes (gen'l) |
"* Mediate adaptive/acquired immunity
* Found in bloodstream, lymph nodes, spleen, submucosa and epithelia * Constantly cycling from lymphoid tissue --> bloodstream --> lymphoid; mostly via diapedesis (allows large cells to pass through smaller holes in tissues) * #2 most common behind neutrophils * 2 cell types: B and T cells * Big round cell * Nucleus: large round and dark/densely-staining * Cytoplasm: small ring * Lifespans of weeks to months" |
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MAC Complex is made of which complement proteins? |
C5b-C9
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Macrocytic anemia classification & examples |
"* Megaloblastic: folate defic, B12 defic, orotic aciduria
* Non-Megaloblastic: liver disease, alcoholism, reticulocytosis" |
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Macrophage |
"* Key in phagocytosis, antigen processing & presentation, cytokine secretion (""Tissue macrophage is first line of defense against infection"")
* Line the lymph nodes extensively can catch infectious agents before they are disseminated generally. * Can phagocytose much larger and numerous bacteria than neutrophils (up to 100 bacteria before cell dies) * Can engulf much larger particles & after digesting particles, can extrude residual contents and keep living for some time. * Activate by presence of products of infection or inflammation (eg IFN-gamma) * Live for months in tissues * DETACH FROM TISSUE AND BREAK LOOSE INTO CIRCULATION * Ruffled membrane, cytoplasm stuffed with vacuoles and vesicles (important for phagocytosis) * APC via MHC II * Marker: CD-14+" |
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Examples of Tissue Macrophages |
"* Alveolar macrophages phagocytose particles caught in alveoli
* Kupffer cells in liver sinusoids stop foodborne bacteria that has passed through GI mucosa into bloodstream. * Spleen / bone marrow macrophages protect general circulation in reticular meshwork * Histiocytes in skin * Microglia in brain" |
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Major Effects of Leukemias |
"* Metastasis - almost all invade spleen, lymph nodes, liver, regardless of origin
* Normal blood cells displaced by non-fxnl leukemic cells: infection, severe anemia, bleeding tendency (due to absence of platelets) * Nutrient deficits: rapidly dividing cells soak up resources, esp amino acids and vitamins. Patient energy rapidly depleted, tissues experience protein depletion." |
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Major opsonization proteins |
C3b, IgG
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Major Sx of Anemia - General and 4 major types |
"* General Sx: SOB, weakness/lethargy, palpitations, headaches (often seen in elderly because of angina, claudication, etc.
* Iron deficiency: spoon nails * Sickle: leg ulcers * Hemolytic: jaundice * Thalassemia major: bone deformities" |
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Mast cell |
"* Allergic reaction in local tissues. Type I rxns
embedded in tissues, mucosa & epithelia * Nucleus: small * Cytoplasm: LARGE BLUE granules * Granules: histamine, heparin, eosinophil chemotactic factors * Can bind Fc portion of IgE to membrane; IgE crosslinks on antigen binding --> degranulation * Cromolyn sodium prevents mast cell degranulation." |
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Mature T Cell Receptor |
"* ""Cut one arm off a Beta-cell receptor and plop it onto a cell""
* Binding is much more selective; can only bind peptide which has been processed and presented by other cells mounted on MHC * Alpha and Beta chains - analogous to light chain & heavy chain, respectively * Monovalent - only one 1 site to bind * No hinge region - doesn't need flexibility * Key difference with B cells: always cell bound - can't be secreted. Antibodies made by B cells can be released into blood stream, and can bind free antigen. T cell receptors can only bind antigen from APCs, ie that is digested & mounted on MHC, and T cell receptors are bound to cell membrane." |
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MHC Deficiencies |
"Affects antigen presentation, but also selection: T cells will never make it out of thymus
1) MHC I deficiency --> DECR CD-8+ T cells, recurrent viral infxns, normal CD-4+, Abs and DTH. Typically a TAP deficiency (can't transport), or aberrant MC molecule 2) MHC II (aka Bare Lymphocyte Syndrome) --> (more severe - mimics AIDS) DECR CD-4+ T cells, DECR Ab response (IgM only), DECR DTH, NO GVHD" |
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Microcytic anemia classification & examples |
small TAILS: Thalassemias, ACD (starts as normocytic), Iron deficiency, Lead poisoning, Sideroblastic
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Microcytic hypochromic anemias: iron deficiency |
* Iron deficiency: [bleed, malnutrition, malabsorption, INCR demand] --> DECR final step in heme synth. DECR Iron & ferritin; INCR TIBC. Plummer-Vinson Syn = triad of iron defic anemia, esophageal webs, atrophic glossitis.
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Microcytic hypochromic anemias: lead poisoning |
"Lead --(-)--> ferrochelatase & ALA dehydratase --> DECR heme synthesis. Also inhibits RNA degradation --> RBCs retain rRNA aggregates (hence basophilic stipppling).
Signs: LEAD lead lines on gingiva (Burton's lines) & long bones on X-ray; encephalopathy; erythrocyte basophilic stippling, abdominal colic, sideroblastic anemia; drop wrist & foot. Tx: Dimercaprol, EDTA, succimer chelation" |
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Microcytic hypochromic anemias: thalassemias |
"* alpha-thalassemia: alpha-globin gene mutation --> DECR alpha globin. Asians & Africans. 1-2 deletions: clin insig; 3: Hbh Disease = excess beta-globin (HbH); microcytic, hypochromic. 4 deletion: hydrops fetalis, incompatible with life.
* beta-thalassemia: beta-globin gene mutation --> DECR beta globin. Mediterraneans. 3 forms: 1) minor (heterozygote); INCR HbA2. ASx. 2) major (homozygote) - no beta; INCR HbF; severe anemia; micro+hypo+poikilocytes, schistocytes; requires transfusion, marrow expands --> skeletal deformities, ""chipmunk"" facies." |
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Monocyte |
"* ""baby macrophage"" just released from bone marrow, has yet to become tissue macrophage (only takes about 10-20 hours in blood before transformation into macrophages occurs).
* Has very little ability to destroy infectious agents while circulating in blood * Nucleus: Kidney or horseshoe shape * Marker: CD-14+ * Phagocytic: differentiate in tissue * Mononucleosis: labs show monocytes predominate" |
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Myeloid & Lymphoid Stem Cell Products |
"Lymphoid: Lymphocytes
Myeloid: everything else: dendritic, macro, neutro, eosino, mast cell, baso, platelet, RBC" |
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Myeloid:Erythroid Ratio: Normal range |
= 2.5:1 - 12:1
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Myeloperoxidase (MPO) Deficiency |
"Cell unable to generate hypochlorite -
Generally Asx" |
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Myultiple Myeloma |
"* Plasma cells proliferate, often infiltrate bone marrow; secrete tons of 1 kind of antibody
1) Usu older adults 2) Lytic bone lesions: neoplastic plasma cells secrete osteoclast activating factor: lucid on X-ray (""punch out"" lesions); esp prominent on skull, skeleton; severe bone pain 3) Prominent urine & serum abnormalities * Clones produce tons of usu IgM or IgA antibodies; synthesis of normal Ig is often impaired * First shows up as spike in serum protein, hyperglobulinemia * Urine: Bence-Jones protein (free Ig kappa/lamda light chains) * Kidney: myeloma nephrosis b/c of Bence-Jones protein: tubular casts, giant cells (derived from macros), met calcifications. * Blood: rouleaux (consequence of hyperglobulinemia), INCR ESR 4) Sx: anemia, INCR susceptibility to infxn (impaired normal Ig production), hypercalcemia (2' to osteoclastic activity - note: AP does not INCR unlike normal hyperCa++), renal insufficiency with azotemia, amyloidosis (1' type)" |
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Naïve B Cell Surface Molecules |
"IgM and IgD on cell surface - serve as antigen receptor.
IgM and IgD look the same in terms of binding, but have different constant region." |
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Neutrophil |
"FIRST & MOST NUMEROUS CELL TO ARRIVE ON SITE OF INFLAMMATION
Acute inflammatory response, bacterial infections, phagocytic 2 types of granules: Small granules (AP, collagenase, lysozyme, lactoferrin); Lg granules (lysosomes: acid phosphatase, peroxidase, beta-glucuronidase). * Can migrate into tissue via diapedesis (squeeze through narrow opening) or ameboid motion (very fast - 1 cell diam/min) * 1 neutrophil can phagocytose ~3-20 bacteria before it dies. * Nucleus: multilobed * Cytoplasm: small pink granules * Predominant in blood: 1,800-7,800/uL * INCR bands (immature neutrophils) = INCR myeloid proliferation (bacterial infxn, CML) *Hypersegmented polys = B12/folate defic" |
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NK cell |
"* surveys body for transformed tumor/virus cell targets (which it doesn't kill) or antibody-coated target cells (which it does kill); in bloodstream
* ~10% of lymphocytes * Cytoplasm: LARGE granules * CD16, 56" |
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"Normal Platelet Levels Severity & Sx ass'd with reduced levels" |
"Normal: 150-400k
< 100k: abnormal bleeding unusual, even after trauma/surgery 20k-70k: INCR bleeding hemorrhage during trauma/ surgery <20k: minor spontaneous bleeding - easy bruising, petechiae, menorrhagia, epistaxis, bleeding gums <5k: Major spontaneous bleeding (intracranial, heavy GI bleed)" |
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Normocytic anemia classification & examples |
"* Non-hemolytic: ACD (progresses to microcytic), aplastic, chronic kidney dis
* Hemolytic - Intrinsic: RBC membrane defects (eg sphero), RBC enzyme defic (G6PD, PK), HbC, sickle, paroxysmal nocturnal hemoglobinuria * Hemolytic - Extrinsic: autoimmune, microangiopathic, macroangiopathic, infections" |
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Notable Component Vaccines |
HBV, HPV
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Notable Killed Vaccines |
"""R.I.P. - Always""
Rabies, Influenza, Polio (Salk), A (Hep)" |
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Notable Live Vaccines |
"Adenovirus
MMR Polio (Sabin - not used in US) Rotavirus Shingles Smallpox Varicella Zoster Yellow Fever" |
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Omenn Syndrome |
"
rag missense mutation - enzyme is is less-functional - absent B-cells & decreased T-cells" |
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Pathology of aplastic anemia |
bone marrow aplasia (absence of functioning marrow eg rad/X-ray exposure)
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Pathology of Blood Loss Anemia |
Body can replace plasma portion of blood loss in 1-3 days, but RBC replacement takes 3-6 weeks.
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Pathology of hemolytic anemia |
Fragile RBCs. eg hereditary spherocytosis, sickle cell, erythroblastosis fetalis.
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Pathology of megaloblastic anemia |
dysfxn of intrinsic factor/B12/folate --> slow RBC synthesis. Resulting cells have large, fragile, bizarrely-shaped membranes and rupture easily
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Pathology of Microcytic hypochromic anemia |
chronic blood loss + inadequate absorption of dietary iron --> RBCs are small & low in Hb
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Physiologic effects of anemia |
"* DECR blood viscosity (blood is more plasma) --> DECR TPR --> INCR blood flow & INCR hypoxia
* Hemo: RIGHT SHIFT of Hb dissociation curve (INCR 2,3 DPG synthesis) * Vascular: hypoxia --> vasodilation --> INCR venous return * Cardiac: INCR CO (up to 4x normal), INCR workload * Note: response can be effective at normal levels of activity. However, heart cannot pump much additional capacity, so exercise presents major strain acute heart failure)." |
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Physiologic Effects of Polycythemia |
"* INCR blood viscosity --> INCR TPR --> DECR blood flow through peripheral vessels
* Normal cardiac output: INCR viscosity but DECR venous return; strain balances out * Normal arterial pressure in most cases; 1/3 are elevated - normal mechanisms of regulating peripheral resistance / BP can handle it most of the time. * Complexion: ruddy (more blood in venous plexuses) with bluish tint (sluggish blood flow so more deoxygenated blood present)" |
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Plasma Cell Disorders: characterization |
well-differentiated Ig-producing cells proliferate
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Plasma cells: fxns, marker, cytology, notable disease(s)) |
"Express tons of antibody specific to 1 antigen; endpoint of B-cell differentiation;
Found in lymph nodes, spleen, MALT, bone marrow * Large cells * Nucleus: small, dark, off center, ""clock face"" chromatin * Cytoplasm: well-developed Golgi stains intensely, abundant RER * Once B-cell is given signal to differentiate into plasma cell, it secretes huge quantities of antibody for ~2 weeks, then dies. Multiple myeloma is a plasma cell cancer" |
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Platelet Disorders: main classifications & subcategories, causes of each |
"* 2 main classifications: * Autonomous thrombocytosis: myeloproliferative dis (eg polycythemia vera), essential thrombocytosis, CML |
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Plummer-Vinson Syn |
"Sx: spoon nails (koilonychia), iron-defic anemia, dysphagia (esophageal webs). Cheilities, atrophic glossitis, stomatitis, pallor. Hypochromic microcytic anemia.
Pre-malignant - rish of hypopharyngeal & esophageal squamos cell CA. Women in 5th decade." |
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Polycythemia |
"* Sx: marked erythrocytosis, INCR circulating granulocytes & platelets, HIGH Hct
* Sludging high HCt blood * Dx: DECR EPO * Late phase: anemia, bone marrow fibrosis, extramedullary hematopoiesis" |
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RBC Synthesis Events |
"* Proerythroblasts are first cells identifiable as RBC precursors; divide several times in subsequent stages
* Basophil erythroblasts have very little hemoglobin * As stages progress: cells fill with hemoglobin up to about 34%, nucleus condenses, and final nuclear remnant (and ER) is absorbed/extruded from cell. * Reticulocyte still has small amount of Golgi, mitochondria & other organelles. * Reticulocytes pass out of bone marrow via diapedesis through pores of capillary membrane. * Remaining basophilic material disappears in 1-2 days. * Cell is now a mature erythrocyte" |
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RBC: Key Metabolic Pathways |
"* Glucose is major fuel, enters cells via facilitated transfer
* Lactate: Glycolysis via Embden-Meyerhof-Parnas (EMP) pathway - most common one * +2 ATP: fuels 3 Na+/2 K+-ATPase pump * NADH fuels MetHb reductase recycling of oxidized Hb * 2,3-BPG: via Rapoport-Luebering shunt (takes 1,3-BPG from glycolysis pathway and converts to 2,3-BPG, sacrificing 1 ATP) * Hexose Monophosphate Pathway: generates NADPH, used to maintain glutathione (prevents oxidative damage) and reduce MetHb" |
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Reactive Leukocytoses: what are they, what causes them |
"Leukemoid reactions - mimic leukemia:
Typically due to reactive inflammatory state from microbial / non-microbial stimuli - correponds roughly to what you'd expect * Neutrophilic: acute bacterial infxn; sterile inflammation (eg tissue necrosis, MI, burns) * Eosinophilic: allergic disorders (asthma, hay fever, allergic skin diseases); parasitic infestations; drug reactions; certain malignancies (e.g., Hodgkin, some NHLs); collagen vascular disorders; atheroembolic disease (transient) * Basophilic Leukocytosis (Basophilia): rare, often indicative of a myeloproliferative disease (e.g., chronic myelogenous leukemia) * Monocytosis: chronic infections (e.g., tuberculosis), bacterial endocarditis, rickettsiosis, and malaria; collagen vascular diseases (e.g., systemic lupus erythematosus); and inflammatory bowel diseases (e.g., ulcerative colitis) * Lymphocytosis: Accompanies monocytosis in many disorders associated with chronic immunologic stimulation (e.g., tuberculosis, brucellosis); viral infections (e.g., hepatitis A, cytomegalovirus, Epstein-Barr virus); Bordetella pertussis infection" |
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Receptor Diversity Generation |
"RAG1/RAG2 are genes of recombinase (found only in B and T cells).
V-D-J-C regions: Variable-Diversity-Joining-Constant Constant determines isotype (eg Cmu --> IgM) IgM and IgD are first types expressed when cell is naïve Heavy chain first: D& J joined; then desired V segments (with intervening segments excised) V-D/J. Light chain: V-J joining only Heavy& Light Chains joined & escorted to cell surface" |
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Regulation of Hematopoiesis |
"Starts with division of stem cell into…
--> (1) replacement stem cell and --> (2) differentiating cell (progenitor) Effected by transcription factors, hematopoietic growth factors, and adhesion molecules" |
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Relationship of Intracellular Killing Mechanisms to Chronic Granulomatous Disease |
"* H2O2 is a byproduct of normal bacterial metabolism
* Chronic granulomatous disease = no NADPH oxidase * Hallmarks are chronic infection with catalase+ bacteria & granulomas: O2 cannot be converted into superoxide radicals--> H2O2 accumulates as bacterial metabolism byproduct --> Bacteria which are catalase + (turns H2O2 into water) convert H2O2 & can't be killed because other killing mechanism (hypochlorite via myeloperoxidase) is neutralized. Catalase (-) bacteria give off H2O2, which myeloperoxidase converts to hypochlorite & it kills the bacteria. * Granuloma = macrophages ""seal off"" infxn they can't resolve" |
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Rh type |
"Antigen on RBC surface. Anti-Rh antibodies are IgG & can cross placenta.
Hemolytic disease of newborn = Rh-NEG mom exposed to Rh+POS fetal blood, develop antibodies which affect next Rh+POS fetus. Tx: Rhogam = Rho(D) immune globulin given to mom at first deliver to prevent sensitization to Rh antigen." |
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Role of Adhesion Molecules in Hematopoiesis |
"* Adhesion molecules (glycoproteins)
* 1) Immune globulins: TCRs, Ig, antigen-independent, ADH molecule * 2) Selectins: leukocyte/ platelet adhesion in inflammation/ coagulation * 3) Integrins: cell adhesion to ECM * Modified buy cytokines (IL-1, TNF, IFN-gamma), events * Pattern of adhesion molecule expresison on tumor cells may determine localization and spread" |
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SCID |
nonsense Rag mutation - no recombinase protein - B & T cells absent
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SCIDs |
"* Rag1/2 mutations: no recombinase --> can't rearrange immunoglubulin genes & T cell (R) genes --> NO B OR T CELLS
* Absence of cytokines means you lose effects, but still have some response * Hallmark: infant can't respond to bacteria or viruses or fungi (eg very bad diaper rash = think SCID) * ADA deficiency is classic SCID (""bubble boy""); ADA needed to generate nucleotides --> rapidly dividing cells most affected (B & T cells are most rapidly dividing in body)" |
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Selective IgA Deficiency |
"* Most common immunodeficiency
* Hallmark: patient with repeated mucosal surface infections (eg salmonella, influenza, respiratory) * Tx: antibiotics, but NOT gammaglobulins (risk of IgE response --> anaphylaxis) Seen in infancy" |
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Signs of Ineffective Erythropoiesis |
"* INCR unconjugated bilirubin
* INCR LDH (cell breakdown product)" |
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Skin CA with best prognosis |
Basal cell (one of the 'laziest' cancers in humans)
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Spleen |
"* Splenic artery (top right) enters
* Periarteriolar Lymphoid Sheath (PALS) surrounds artery & is T-cell region of spleen * Marginal zone & corona are the B cell region of the spleen * Germinal center = B & T come together = (concentric rings of activating & differentiated cells)" |
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Steps in Hb Synthesis |
"1. 2 succinyl CoA + 2 glycine --> pyrrole
2. 4 pyrrole --> 1 protoporphyrin IX 3. 1 protoporphyrin IX + Fe++ --> heme 4. heme + polypeptide --> alpha or beta Hb chain 5. 2 alpha chains and 2 beta chains --> HbA" |
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Subtypes of Th Cells |
"TH0 Cell: Jack of All Trades, master of none: can dabble in many activities: cell-mediated immunity, humoral immunity etc but is not great at any. Differentiates into Th1, Th2, Treg and T17:
Th1: promotes cell-mediated (intracellular) immunity Th2 cells: promote humoral immunity - making antibodies, class switching, etc. TH1 and TH2 INHIBIT EACH OTHER's RESPONSES Regulatory T cells (Treg): tamp down T-cell response from being overactive, also prevent autoimmune disease - differentiation caused by IL-10 TH17: play role in damage caused by autoimmunity; differentiation caused by T17" |
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Suppressor T Cells |
little is known - suppress fxn of CTLs & Th lymphocytes
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T Cell Signal Transduction Complex |
CD3 is coreceptor - yields cellular proliferation and cytokine secretion marker. Also a marker for Th & CTLs
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T cells |
"Cellular immune response - majority of circulating lymphocytes
Originates in bone marrow; matures in thymus 3 types 1) Cytotoxic Tc (CD8, recognize MHC I) 2) Helper Th (CD4, recognize MHC II) 3) Regulatory T cells CD 28 req;d for T cell activation." |
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T-Cell Maturation Selection |
"* Progenitor T cells express nothing when they leave bone marrow & go to thymus
* Once inside thymus, becomes precursor, starts expressing all markers: CD3/4/8, T-cell (R). 1) Positive Selection ensures T-Cell can recognize / bind MHC - if not recog'd --> apoptosis 2) Negative selection is the safety net: keeps ""too excited"" T-cells that overly bind MHC (high potential to be autoreactive) from being activated --> apoptosis * Low affinity cells are the 5% allowed to escape thymus" |
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Test for Chronic Granulomatous Disease |
"Nitroblue tetrazolium reduction = incubate WBCs with bacteria and nitroblue tetrazolium
(+) = functional NADPH oxidase (=NO CGD), turns purple (-) = NADPH oxidase can't convert, turns yellow" |
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Th cells |
"#1 T cell: 3/4ths of all T cells
* Regulate cell-mediated response: command B cells and & CTLs via: * Stimulate growth & proliferation of CTLs (esp via IL-2) * Stimulate B cell growth and differentiation (esp via IL4-6) - as mentioned above, the normal B cell response to antigen is negligible without lymphokine input * Activate macrophages: slow/stop macrophage migration (so they stay at site of chemotactic attraction), and boost phagocytotic ability * Self-feedback; lymphokines can help activate more Th cells" |
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Thrombocytes (platelets) |
"1' hemostasis.
8-10 d lifespane. Aggregates with other platelets & fibrin to form platelet plug. Contains dense granules (ADP, calcium), and alpha granules (vWF, fibrinogen). ~1/3 of platelet pool is in spleen. Thrombocytopenia / platelet dyfxn --> petechiae vWF (R): GpIb Fibirinogen (R): GpIIb/IIa" |
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Tolerance |
"= deletion of auto-reactive cells
1) clonal deletion of immature cells in primary lymphoid tissue - thymus is harsher enviro, usually catches all autoreactive cells prior to release 2) clonal anergy in periphery = shutting off autoreactive B cells in periphery - more of a B cell process" |
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Transcription Factors in Hematopoiesis |
"* Transcription factors commit progenitors to a specific cell lineage
* Regulate gene expression; have 2 domains 1) DNA-binding domain binds specific sequence 2) Activation domain: helps assemble transcription complex" |
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Types of Hypersensitivity Reactions, MoA, Examples of Each |
"Type I immediate IgE-mediated: allergy (hay fever, anaphylaxis)
Type II tissue specific cytotoxic autoAbs: Goodpasture, HDN Type II noncytotoxic: Graves Type III immune complexes circulate and activate complement wherever they land: SLE, RA, serum sickness Type IV delayed-type via Th1 cells: TB (normal response), Guillain-Barre, Celiac" |
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Viral Vaccine Types: LAV Pro & Cons |
* LAVs: have best immunogenicity but also riskier: can possibly revert to pathogenic form or cause infection in immunocompromised. Also require special storage, have contamination risk
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von Willebrand Factor |
"* aka Factor VIII-Related Antigenic Protein
* Enhances platelet aggregation & adhesion (first steps in clot formation) * Synthesized in endothelial cells and megakaryocytes * Binds Factor VIII and protects it from degradation" |
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Warfarin vs Heparin monitoring |
"WEPT vs HIPPT" Wafarin = Extrinsic PT; Hep = Intrinsic PTT
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WBC Proportion, largest to smallest |
"Neutrophils (54-62%)
Lymphocytes (25-33%) Monocytes (3-7%) Eosinophils (1-3%) Basophils (0.075%) ""Nurses Like Making Everything Better""" |
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What are Reed-Sternberg Cells |
"Hodgkin Lymphoma Hallmark
B cell derivatives with multiple nuclei and brightly eosinophilic nucleoli. CD15, CD30 - NO CD45" |
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What are the 4 major measures of coagulation cascade function, what do they mean, and what major drugs affect them? |
"* PT: extrinsic pathway; prolonged by warfarin
* PTT: intrinsic pathway; prolonged by heparin * Thrombin time: fibrinogen concentration * Bleeding time: platelet function" |
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Which complement proteins attract neutrophils? |
C3a, C5a
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Why do RBCs die? What happens to them & their parts afterward |
"* RBCs have enzymes that metabolize glucose, produce ATP, maintain membrane, keep iron as Fe++ not Fe+++, prevent oxidation of cell proteins.
* Enzymes eventually wear out * Cell ruptures when it passes through a narrow part of circulation, often the spleen's red pulp (3 um wide vs 8 um average RBC width) * Hb recycled by monocytes/macrophages * Porphyrin converted by macrophages into bilirubin * Bilirubin released into blood and removed by the liver via bile" |
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Wiskott-Aldrich |
"Defect in cytoskeletal glycoprotein
""triad"" immunodeficiency, thrombocytopenia, eczema X-linked" |
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X-linked Hyper-IgM |
"mutation is actually on T cell
pathology is due to absence of class switching Seen in young adults" |
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Acanthocytes (spur cells) |
liver dis, abetalipoproteinemia
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Basophilic stippling |
thalassemias, anemia of chronic dis, lead poisoning
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Bite cells |
G6PD defic
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Elliptocyte |
hereditary elliptocytosis
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Heinz Bodies |
G6PD - iron oxidation to ferric form denatures & precipitates Hb, damages RBC membrane ("Heinz Baked Beans in an iron can")
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Howell-Jolly Bodies |
asplenia / fxnl hyposplenia --> basophilic nuclear remnants normally removed by spleen remain in RBCs. also occurs with naphthalate (mothball) toxicity. (Holly Jolly Christmas sweater in mothballs)
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Macro-ovalocyte |
megaloblastic anemia, marrow failure
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Ringed sideroblasts |
sideroblastic anemia (excess iron in mitochrondria; pathologic)
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Schistocyte helmet |
DIC, TTP/HUS, traumatic hemolysis (eg metal heart valve)
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Sickle cell |
self expl
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Spherocyte |
hereditary spherocytosis, autoimmune hemolysis
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Teardrop cell |
bone marrow infiltration (eg myelofibrosis)
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Target cell |
HbC, asplenia, liver dis, thalassemia ("HALT")
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