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| How to detect if it is an anaemia is haemolytic? | show 🗑
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| show | Renal disease, Anaemias of Chronic Disease (ACD, not totally sensitive as ACD can progress to microcytic anaemia), and aplastic anaemia
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| Causes of iron deficiency anaemia and specific symptoms | show 🗑
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| show | MCV<80, hypochromatic, Ferritin low. Ferritin VERY specific, but not sensitive (e.g. inflammation causes it to rise)
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| Causes of microcytic anaemia | show 🗑
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| Pathogenesis of microcytic anaemias | show 🗑
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| Iron digestion and storage sites | show 🗑
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| Intravascular Normocytic and Normochromic anaemias and general lab results | show 🗑
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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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| show | Folate: causes by impaired metabolism (MTX,Trimethoprim), higher requirements. B12: Malabsorption, tapeworm, high methylmalonic acid. Peripheral neuropathies (dorsal column first), lateral corticospinal spasticity, dementia
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| Warm autoimmune hemolytic anemia | show 🗑
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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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| show | 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)
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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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| show | 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.
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| B12 Metabolism | show 🗑
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| show | Folate is absorbed in the jejunum. The enzyme intestinal conjugase (which is inhibited by phenytoin) is required for absorption.
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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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| Paroxysmal nocturnal hemoglobinuria | show 🗑
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| G6PD deficiency Pathology, Symptoms, and demographics | show 🗑
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| show | 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
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| show | heterozygous HbS, Protective vs Malaria. Very common in africa (1/3?) Largely asymptomatic
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| show | 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
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| Sickle Crisis | show 🗑
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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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| Polycythemia | show 🗑
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| polycythemia vera pathology and treatment | show 🗑
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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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| show | 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
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| Specific ALL pathology, finding, prognosis | show 🗑
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| Specific AML pathology, finding, prognosis | show 🗑
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| Common symptoms/finding in CML and CLL | show 🗑
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| CLL demographics, pathology, findings | show 🗑
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| show | 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
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| Philadelphia chromosome | show 🗑
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| show | 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
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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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| Non-Hodgkin Lymphoma Associated Infections | show 🗑
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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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| show | 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
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| show | Creates any tissue vs just blood tissue + bone?
Embryo vs bone marrow origin
Ethicals concern vs n.p.
No phenotype vs common with CD34+
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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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| EBV | show 🗑
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| General side-effects of cancer therapies | show 🗑
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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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| MGUS | show 🗑
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| show | 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
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| show | Tongue and GI ulcers
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| show | T-cell marker. Appears on B-cells in CLL, mantle C NHL
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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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| Chimeric antigen receptor | show 🗑
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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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| show | 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
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| show | 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
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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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| show | 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
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| show | -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
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| show | Rituximab
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| Ankyrin deficiency in anaemia | show 🗑
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