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How to detect if it is an anaemia is haemolytic? Reticulocyte (adjusted) count is up (>3%)
Non haemolytic normocytic anaemia? Renal disease, Anaemias of Chronic Disease (ACD, not totally sensitive as ACD can progress to microcytic anaemia), and aplastic anaemia
Causes of iron deficiency anaemia and specific symptoms Increased demand: Infants (common), Pregnancy, Decreased GI absorption, Hematuria Increased loss: Menorrhagia (common), GI bleeds VERY poor diet Glossitis, esophogeal webbing
Test results for iron deficiency anaemia MCV<80, hypochromatic, Ferritin low. Ferritin VERY specific, but not sensitive (e.g. inflammation causes it to rise)
Causes of microcytic anaemia Thalessaemia, Anaemias of Chronic Disease (ACD), Iron deficiancy, Lead poisoning, Sideroblastic anaemia (TAILS)
Pathogenesis of microcytic anaemias Defects in heme production:Anaemias of Chronic Disease (ACD), Iron deficiancy, Sideroblastic anaemia Defects to globin production: Lead poisoning, Thalessaemia
Iron digestion and storage sites Gastric acid frees Fe2+ to be absorbed. Vit C reduces Fe3+ to Fe2+ Storage from largest to smallest: Heme, Bone marrow macrophages (can be released rapidly, also present in spleen+liver), myoglobin, cofactor in enzymes
Intravascular Normocytic and Normochromic anaemias and general lab results Autoimmune (cold), Mechanical (valve), GP6D deficiency, HbC, Paroxysmal nocturnal hemoglobinuria, Low haptoglobin, high Lactate dehydrogenase (LDH), damage to vasculature (valves), hemoglobinuria
Extravascular Normocytic and Normochromic anaemias and general lab results Autoimmune (warm), Hereditary spherocytosis) Infection (Malaria), HbC defect, PK and GP6D deficiency, sickle cell RBC phagocytosis in the spleen. (Macrophages attack due to abnormal shape or IgG on the surface), high, UCB billirubin, high LDH
Intravascular Anaemia Pathology Lysis in the blood vessel. Hb released into the blood and immediately bound by haptoglobin for clearance in the liver. LDH also released. If haptoglobin is used up the kidneys will filter. If the kidneys are maxed hb in urine.
Extravascular Anaemia Pathology RBCs attacked prematurely by the liver and spleen phagocytes. Hb is converted into iron for recycling and the globine portion becomes billirubin later. LDH also, but not haptoglobin elevated.
Nonmegaloblastic macrocytic anaemias and pathology DNA synthesis is unimpaired. Cause by bone marrow suppression from liver damage, alcohol abuse, metabolic disorders (purines/pyrimidines), drugs (5-FU, AZY, hydroxyurea) Reticulocytosis
Common pathologies in B12 and folate deficiencies Malnutrition, malabsorbtion, Hypersegmented neutrophils, glossitis, high homocysteine.
Divergent pathologies in B12 and folate deficiencies Folate: causes by impaired metabolism (MTX,Trimethoprim), higher requirements. B12: Malabsorption, tapeworm, high methylmalonic acid. Peripheral neuropathies (dorsal column first), lateral corticospinal spasticity, dementia
Warm autoimmune hemolytic anemia IgG antibodies attach to a red blood cell, leaving their FC portion exposed with reactivity at 37°C. Recognized and grabbed onto by FC receptors found on monocytes and macrophages in the spleen so extravascular HA. Caused by CLL, SLE, RA, Idiopathic.
Cold autoimmune hemolytic anemia (Cold agglutinin disease) At body temperatures of 28-31°C, such as those encountered during winter months in the periphery IgM bind to RBC and initiates the classical complement pathway leading to intravascular HA. Caused by Idiopathic, Lymphoma, CLL
Coombs direct and indirect Direct: Anti-Human antibody to patient RBC (tests for antibodies present on RBCs) Indirect: Add potential donor RBC to patients serum. Then add Anti-Human antibody. (If there is coagulation then serum antibodies attached to donor RBC. Not suitable)
Plummer-Vinson Syndrome Triad of anemia, glossitis and esophageal webs. Iron deficiency
Hemochromatosis Too much Iron. Appear bronze coloured and symptom overlap with anaemia + low libido and joint pain. Primary caused my high absorption due to genetic disorders. Secondary cause by abnormal heme production from other pathologies (e.g. thalesseamia)
Anaemia of Chronic Disease cause + treatment Infective/Inflammatory process -> body sequesters iron. DO NOT supplement iron. Treat the underlying problem.
Thalessaemia beta cause, findings, and diagnostic test B+ allele=reduced synthesis beta globin. Bo allele=no synthesis. CoDom (Single abnormal=T minor). Microcytosis, hypochromia, target cells , poikilocytosis, EPO+ (bone scan). Minor=TC and MC sometimes Use Hb electrophoresis. Excess HbF(gamma), Hbdelta
Thalessaemia alpha cause, finding, and diagnostic test 2 gene, 4 alleles. 1 delete=silent carrier. 2 deletion (cis or trans). MC and clinically similar to BT minor. 3 deletion=excess beta chains->EV hemolysis, Heinz bodies and clinically similar to BT major. Episodic pallor/anaemia. Use Hb electrophoresis.
B12 Metabolism B12 is bound by R-factor which protects it from gastric acidity. In the duodenum, pancreatic enzymes hydrolyze the R-factor bond and B12 is bound by IF (which is synthesized by gastric parietal cells). The B12-IF complex is absorbed in the terminal ileum.
Folate Metabolism Folate is absorbed in the jejunum. The enzyme intestinal conjugase (which is inhibited by phenytoin) is required for absorption.
Aplastic anaemia cause and pathology Bone marrow failure Toxins,rarely can be due to NSAIDs, methimazole, propylthiouracil) → hypocellular bone marrow → pancytopenia Bone marrow->hypocellularity. Severe (rare): Siderosis, Macrocytic Viral: pvB19, HIV, EBV, HCV Fanconi's, radiation
Hereditary spherocytosis/elliptocytosis. Pathology+Findings spherocytes, Autosomal dominant. EV HL. Normocytic with higher MCHC. Hereditary elliptocytosis: same deal but with ellipsoidal RBS.
Paroxysmal nocturnal hemoglobinuria spontaneous somatic mutation of the GPI anchor necessary for CD55 and CD59 attachment. Gene on the X chromosome. GPI anchor deficiency leads to complement mediated hemolysis. IV (at night?) Sx: anemia, thrombosis, pancytopenia, hypercoagulable state
G6PD deficiency Pathology, Symptoms, and demographics African+Mediterranean, X linked recessive. IV HL from increased sensitivity to oxidative stresses (no glucothione regen). Heinz bodies and Bite cells
Pyruvate Kinase deficiency Pathology, Symptoms, findings autosomal recessive. Since RBCs can only produce ATP via glycolysis, this deficiency severely effects the ability of RBCs to produce energy. Decreased ATP production in the RBC → altered membrane integrity → EV HL (Splenomegaly, Jaundice) Spur cells
Sickle cell trait heterozygous HbS, Protective vs Malaria. Very common in africa (1/3?) Largely asymptomatic
Sickle cell Anaemia Pathology β-globin point mutation valine for glutamic acid (codon 6). Low O2 tension (higher hydrophobia interactions) → RBCs sickle and cell membranes stiffen, becoming more likely to hemolyze (EV). Treat: hydroxyurea (causes increased HbF synthesis) in severe
Sickle Crisis Transportation of RBCs through inflamed tissue can also lead to occlusion of microvasculature. Then more inflammationI mediators → ↑ adhesion molecules → sickling and occlusion. and the cycle continues. Manage:NSAIDs then opiates. Spleen is special case.
Sickle cell secondary pathogies AREAS Autosplenectomy, acute pain crisis Renal papillary necrosis Encapsulated organism infection (S. pneumo, Haemophilus, Salmonella etc) Aplastic anemia from Parvovirus B19 Salmonella osteomyelitis, Splenic sequestration
Polycythemia Secondary: Athletes, Hypoxia. Primary:polycythemia from ectopic EPO production → normal PV, EPO up polycythemia from polycythemia vera → increased PV, EPO down
polycythemia vera pathology and treatment mutation on JAK2 on chromosome 9 (myelofibrosis, myeloid metaplasia, essential thrombocythemia). Clonal expansion of myeloid stem cells (high cell count in all their lineage). hyperviscosity/phlebotomy or hydroxyurea. prognosis :6 – 18 months. ++B12
Symptoms due to hyperviscosity and vessel congestion. Hepatosplenomegaly: ++RBCs Burning pain in hands Red face Thrombosis CNS involvement Headache,Blurred vision,Retinal vein engorgement,Vertigo, ischemic attacks,Stroke ++histamine: Peptic ulcers/itching after bathing. Gout: ++cell turnover ++nucleic
Common Leukaemia issues Leukopenia → infection risk Anemia Thrombocytopenia → hemorrhagic complications
Common symptoms/finding in AML and ALL ACUTE onset Fever, bleeding and fatigue common Thrombocytopenia Hypercellular bone marrow, >20% blasts elevated WBC count common children and >60 years of age Without intervention, often fatal within 6 to 12 months Treat: Chemo,more rarely stem cel
Specific ALL pathology, finding, prognosis Most common malignancy children. Lymphoblasts predominate B-ALL: common metastasize CNS CD10, CD19, CD20 and CD22 t(12;21) common= good T-ALL: common as ant. mediastinal mass CD1,2,3,4,7+CD10- PoorProg: Age < 2 or >12,blasts > 100K,phila chromoso
Specific AML pathology, finding, prognosis 20s→early 60s as well Blasts on film APML: t(15;17) →protein w/ retinoic acid receptor and promyelocytic leuk. protein. Auer rods-> DIC t(15;17) treat w/ all-trans retinoic A, binds RARα protein, antagonist → differ. of promyelo→ neutrophils
Common symptoms/finding in CML and CLL Insidious onset generalized, painless lymphadenopathy. Sometimes Hepatosplenomegaly Lab findings similar to ALs, except for blasts which are <10% in chronic leukemia. Clinical course is less devastating, but also less responsive to therapy
CLL demographics, pathology, findings Most common leukemia (adults). Commonly male, > 60, Mean survival 3 to 7 years. Infiltration of marrow/hepatosplenomegaly. WBC 50-200K, warm AIHA Malignant B-cs → decreased plasma cs → hypogammaglobulinemia → ↑ infections CD5,23,19,20 translocations
CML demographics, pathology, findings, treatment Peak incidence: 35-50 age Differentiated stem cs predominate Phila chrom: t(9;22) WBC 50-200K low leukocyte alkaline phosphatase activity (given WBC count) Results in blast crisis: number of blast forms ↑↑ like AML (short survival Treat: imatinib me
Philadelphia chromosome ABL on c9 moves to BCR on c22 creating bcr-abl, with tyrosine kinase activity Imatinib (Gleevec) is a tyrosine kinase inhibitor specific for BCR-ABL Defines CLL, sometimes found in ALL, rarely in AML
Hairy cell leukaemia demographics, pathology, findings, treatment chronic B-cell leukemia, (avg age: 55) Infiltration (marrow, etc) → Splenomegaly is more common than hepatomegaly. Pancytopenia → infections Cells stain TRAP (tartrate-resistant acid phosphatase) Responds well to therapy. Tx: 2-chlorodeoxyadenosine
Hodgkin's Lymphoma General Info Young male,Reed-Sternberg (RS) cells required 4 diagnosis. Diaphoresis, pruritus, leukocytosis and localised!! nontender lymphadenopathy. ("B") signs/symptoms low-grade fever, night sweats, weight loss Disease severity = RS/Lymphocyte ratio correlated
Hodgkin's Lymphoma types, pathology, demographics, Prognosis Nodular sclerosing: 65-70% male=female, fibrous bands and lacunar cps Mixed cell: 20-25% Older:Strongly associated w/ EBV LymphoC rich: 5%: 40% EBV, great pro <50males LymphoC low: 5%: HIV association, bad prog Nonclassical LymphoC rich: CD20+, CD15,3
Non-Hodgkin Lymphoma Types Periaortic nodes common Noncontiguous spread B-cells originate from germinal follicle: Burkitt's Lymphoma Diffuse large B-cell Follicular Small lymphocytic (SLL) MALToma t(1;14) T-cell lymphoma: Mycosis fungoides and Sezary syndrome
Non-Hodgkin Lymphoma Associated Infections Bacterial -H. pylori: MALToma Viral Infections -HTLV-1 (Human T-cell leukemia virus type I): adult T-cell lymphoma -EBV: Burkitt's lymphoma, DLBCL, CNS lymphoma -HCV: B-cell lymphoma Hashimoto's thyroiditis predisposes to thyroid lymphoma
Diffuse large cell lymphoma pathology, demographics, Prognosis most common NHL 80% B-cell in origin, 20% T-cell in origin can be present anywhere in the body. Can be found in nodal or extranodal tissue. Associated with an aggressive, widespread dissemination → rapidly fatal if untreated. CD 19,20+
Small lymphocytic lymphoma Related to CLL Older persons, indolent course B-cell origin, but most commonly express CD5 (normally a T-cell marker) and CD23. Because these are B-cells, they are also CD19 and CD20 positive Widespread nodal + liver/spleen/bone marrow also involved
5yr survival rates for 4 common leukemias ALL: 90% AML: 20% CLL: 75% CML: 90%
Common lymph nodes for metastatic (and primary) cancer spread. Submental or tonsillar:SSC mouth Cervical: HeadNeck,HL L Supracla: Abdo C. R Supracla:Lung+esophageal, HL Axillary:Breast Epitrochlear:NHL, Sarcoidosis bilat) Hilar:Lung Mediastin:Lung,HL,NHL(TC) P-aortic:testicular or Burkitt Inguinal:genital
Splenic dysfunction and asplenia in: - IgM, less complement activation, less C3b opsonization, more encapsulated organisms. SSHiN Salmonella, S. pnewnoniae, H. influenzae, N. meningitidis. Howell-Jolly bodies (nuclear remnants), Target cells, Thrombocytosis
Spleen Anatomy/Function Long, vascular channels in red pulp with fenestrated basement membrane: filtration of RBCs. Reserve of monocytes White Pulp at centre: B cs in follicles here T cs found in tperiarterial lymphatic sheath (PALS) and white pulp Only efferent Lymphatics
Embryonic vs Haematological stem cells Creates any tissue vs just blood tissue + bone? Embryo vs bone marrow origin Ethicals concern vs n.p. No phenotype vs common with CD34+
GM-CSF Granulocyte macrophage colony-stimulating factor stimulates stem cells to produce granulocytes. associated with IL4,5,13 Used to replace WBC post chemo. Also found in RA joints
Acute leukaemia aetiology !Mostly unknown! Genetics(dna malfunction diseases eg Fanconi's), stem cell disorders, chemicals, radiation, cytotoxic agents (alkylating agents, topoisomerase inhibitors), viruses (HTLV->Tcell NHL)
EBV Causes Infectious mononucleosis aka mono aka glandular fever. 90% of adults exposed to it Associated with HL, Burkitt's NHL, nasopharyngeal carcinoma. autoimmune diseases (dermatomyositis, SLE, RA, Sjögren's, MS
General side-effects of cancer therapies Cytotoxic Radiotherapy Endocrine Immuno MonoClonal
Aplastic anaemia symptoms and treatment Anaemia symptoms + purpura, mucosal bleeding, petechiae, infection Treatment: withdrawal of offending agent, immunosuppressive regimens (antithymocyte globulin, cyclosporine), bone marrow transplantation, RBC and platelet transfusion, G-CSF, or GM-CSF.
MGUS Monoclonal gammopathy ofundetermined significance (MGUS) is monoclonal plasma cell expansion without the symptoms of multiple myeloma.
Bone cancer associated translocations t(15;17) APML aka M3 AML. t(8;21) M2 AML inv(16) M4 AML t(4;11) ALL t(9;22) BCRABL Philadelphia chr. CLL, sometimes ALL t(11;22) Ewing's IgH Hijackers: t(8;14) Burkitts NHL c-myc t(11;14) Mantle NHL bcl-1 t(14;18) Folicular NHL bcl-2
Neutropenia symptoms/signs Tongue and GI ulcers
Chemo to test and CNS
CD5 T-cell marker. Appears on B-cells in CLL, mantle C NHL
Monoclonal antibodies Highly targeting and specific antibodies. Usually end in imab
Rituximab MA vs CD20. targets B-cells. Used in NHL and RA (w/ methotrexate)
Imatinib aka Gleevac targets BRCABL tyrosine kinase for CML, GI tumors
Herceptin aka Trastuzumab. targets Her2, a tyrosine kinase active in breast cancer. Has cardiotoxicity
Chimeric antigen receptor graft IgG to TCR on T cells. Now t-cell attack self cells (according to the IgG antigen e.g. CD19)
Follicular Lymphoma 25% go NHL t(14;18)→ (oncogene: inhibits apoptosis) . Overexpression of BCL2 → ↓ apoptosis. CD10,19, CD20,BCL2+,BCL6+ Lymph nodes obliterated by nodules (uniform,round,isolated) Comprised of B-cs in germinal centers of lymphoid follicles
Mantle Cell Lymphoma Morphology like CLL (both CD5,19,20+) t(11;14) → bcl-1 (cyclin D1) overexertion → ↑ cell cycle → high grade; terrible prognosis avg survival 3 years
Ann Arbor Staging System I: Single Lymphoid structure II: 2 or more on one side of diaphragm III: On both sides IV Extranodal involvement Also hematological involve (liver, marrow) Classically seen on PET scans
Langerhans cell histiocytosis Proliferative disorder (dendritic). Dont stim T-cells with antigen presentation. S-100,CD1a,Birbeck granules 2 types: eosinophilic granuloma->pathologic fractures in adolescent HSChristianson disease->lytic lesion
Myelofibrosis Fibrotic Obliteration of bone marrow. teardrop cell. in compensation Huge splenomegaly
Hemoglobin types HbA: 2alpha, 2 beta HbA2: 2alpha, 2delta HbF: 2alpha2gamma Pathological Hb HbH 4 betas (severe thalassemia alpha) HbS: 2 alpha 2 betaS (SCD) HbBarts: 4 gamma (hydrops fetalis) HbC: 2 alpha 2 betaC (HbC) HbSC: HbS,SCD HBAS: 1gene SCD, 1gene SCT
Internation Prognostic Index -Age > 60 -Stage 3 or 4 - 2 or more extra nodal sites - ECOG 2 or higher - LDH high 0,1 low 2 low/inter 3 inter/high 4,5 high
R-CHOP Rituximab
Ankyrin deficiency in anaemia Ankyrin binds CDs (55), called GPIs, -> prevent complement lysis in RBCs+platelets. ->Paroxysmal Nocturnal Hemoglobinuria. Can test CD55-. platelet lysis=thrombosis Ankyrin+spectrin, Band 3, Protein 4.2 give RBCs their shape. Def=HS 10% get AML
Created by: BillBillson