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| show | Reticulocyte (adjusted) count is up (>3%)
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| Non haemolytic normocytic anaemia? | show 🗑
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| show | Increased demand: Infants (common), Pregnancy, Decreased GI absorption, Hematuria
Increased loss: Menorrhagia (common), GI bleeds
VERY poor diet
Glossitis, esophogeal webbing
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| Test results for iron deficiency anaemia | show 🗑
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| Causes of microcytic anaemia | show 🗑
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| show | Defects in heme production:Anaemias of Chronic Disease (ACD), Iron deficiancy, Sideroblastic anaemia
Defects to globin production: Lead poisoning, Thalessaemia
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| show | 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
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| show | Autoimmune (cold), Mechanical (valve), GP6D deficiency, HbC, Paroxysmal nocturnal hemoglobinuria,
Low haptoglobin, high Lactate dehydrogenase (LDH), damage to vasculature (valves), hemoglobinuria
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| Extravascular Normocytic and Normochromic anaemias and general lab results | show 🗑
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| show | 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.
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| show | 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.
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| show | DNA synthesis is unimpaired. Cause by bone marrow suppression from liver damage, alcohol abuse, metabolic disorders (purines/pyrimidines), drugs (5-FU, AZY, hydroxyurea) Reticulocytosis
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| Common pathologies in B12 and folate deficiencies | show 🗑
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| Divergent pathologies in B12 and folate deficiencies | show 🗑
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| show | 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.
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| show | 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
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| show | 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)
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| Plummer-Vinson Syndrome | show 🗑
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| Hemochromatosis | show 🗑
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| Anaemia of Chronic Disease cause + treatment | show 🗑
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| Thalessaemia beta cause, findings, and diagnostic test | show 🗑
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| Thalessaemia alpha cause, finding, and diagnostic test | show 🗑
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| B12 Metabolism | show 🗑
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| Folate Metabolism | show 🗑
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| show | 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
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| Hereditary spherocytosis/elliptocytosis. Pathology+Findings | show 🗑
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| show | 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
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| G6PD deficiency Pathology, Symptoms, and demographics | show 🗑
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| Pyruvate Kinase deficiency Pathology, Symptoms, findings | show 🗑
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| show | heterozygous HbS, Protective vs Malaria. Very common in africa (1/3?) Largely asymptomatic
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| Sickle cell Anaemia Pathology | show 🗑
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| show | 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.
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| show | 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
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| show | Secondary: Athletes, Hypoxia.
Primary:polycythemia from ectopic EPO production → normal PV, EPO up
polycythemia from polycythemia vera → increased PV, EPO down
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| show | 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
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| show | 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
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| show | Leukopenia → infection risk
Anemia
Thrombocytopenia → hemorrhagic complications
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| Common symptoms/finding in AML and ALL | show 🗑
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| Specific ALL pathology, finding, prognosis | show 🗑
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| show | 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
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| show | 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
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| show | 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
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| CML demographics, pathology, findings, treatment | show 🗑
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| Philadelphia chromosome | show 🗑
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| Hairy cell leukaemia demographics, pathology, findings, treatment | show 🗑
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| show | 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
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| show | 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
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| Non-Hodgkin Lymphoma Types | show 🗑
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| show | 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
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| show | 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+
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| Small lymphocytic lymphoma | show 🗑
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| 5yr survival rates for 4 common leukemias | show 🗑
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| show | 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
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| Splenic dysfunction and asplenia in: | show 🗑
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| Spleen Anatomy/Function | show 🗑
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| Embryonic vs Haematological stem cells | show 🗑
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| GM-CSF | show 🗑
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| show | !Mostly unknown!
Genetics(dna malfunction diseases eg Fanconi's), stem cell disorders, chemicals, radiation, cytotoxic agents (alkylating agents, topoisomerase inhibitors), viruses (HTLV->Tcell NHL)
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| show | 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
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| show | Cytotoxic
Radiotherapy
Endocrine
Immuno
MonoClonal
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| show | 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.
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| show | Monoclonal gammopathy ofundetermined significance (MGUS) is monoclonal plasma cell expansion without the symptoms of multiple myeloma.
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| Bone cancer associated translocations | show 🗑
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| Neutropenia symptoms/signs | show 🗑
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| Methotrexate | show 🗑
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| show |
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| CD5 | show 🗑
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| Monoclonal antibodies | show 🗑
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| Rituximab | show 🗑
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| Imatinib | show 🗑
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| show | aka Trastuzumab. targets Her2, a tyrosine kinase active in breast cancer.
Has cardiotoxicity
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| show | graft IgG to TCR on T cells. Now t-cell attack self cells (according to the IgG antigen e.g. CD19)
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| show | 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
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| Mantle Cell Lymphoma | show 🗑
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| Ann Arbor Staging System | show 🗑
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| show | 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
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| Myelofibrosis | show 🗑
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| Hemoglobin types | show 🗑
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| Internation Prognostic Index | show 🗑
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| show | Rituximab
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| show | 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
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