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Jack Misc List > Haematology list (red and orange) > Flashcards

Haematology list (red and orange) Flashcards

1
Q

Myelodysplasia (red).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. This is a group of acquired bone marrow disorders where there is degeneration of stem cells in the one marrow, affecting one or more cell lineages (RBC/WBC/platelets). Bone marrow failure occurs naturally as we age but this accelerates, as such this is common in over 70s
  2. Chromosomal abnormalities (primary) or secondary to chemotherapy or radiotherapy. RF = ionising radiation, alkylating agents.
  3. Bone marrow fails causing reducition of certain cell lineages, leading to anaemia, infection etc.
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2
Q

Myelodysplasia (red).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Usually asymptomatic, but can present with symptoms of anaemia, leukopenia and thrombocytopenia
  2. Blood film, bone marrow aspirate, FBC, reticulocyte count, serum B12
  3. Aplastic anaemia, HIV, AML
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3
Q

Myelodysplasia (red).

  1. Management
  2. Complications
  3. Prognosis
A
  1. Supportive treatment (red cell and platelet transfusions) is given to elderly patients with symptomatic disease. For younger patients, intensive chemotherapy (as used for acute myeloblastic leukaemia) or allogenic BMT are used.
  2. Infection, bleeding AML
  3. Many patients die from infection in the myelodysplastic syndrome stage of their disease. May progress to AML
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4
Q

Acute Leukaemia (red)

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Malignant neoplasm of haematopoietic stem cells, replacing bone marrow. In acute, there is malignancy of poorly differentiated myeloid (AML) or Lymphoid (ALL) progenitors. Leukaemias are relatively rare.
    ALL - childhood, AML - adults.
  2. Exposure to carcinogens (chemicals, drugs, radiation, viruses, genetics), end point of other bone marrow pathologies
  3. Features are owed to infiltration of bone marrow and other tissues
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5
Q

Acute Leukaemia (red)

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Bone marrow failure - anaemia, bleeding, infection. (AML and ALL present same, immunophenotyping differentiates). Can be lymphadenopathy.
  2. Peripheral blood film (Auer rods indicates AML), bone marrow aspirate, FBC
  3. Other types of leukaemia
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6
Q

Acute Leukaemia (red)

  1. Management
  2. Complications
  3. Prognosis
A
  1. Chemotherapy differs between the two, generally give at intervals for bone marrow to recover and consolidation. AML - Cytarabine/Daunorubicin, ALL - VDAD.
  2. Cause of death usually infection or bleeding (cytopenia).
  3. Both have good prognosis with 80% remission. ALL has worse prognosis in adults.
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7
Q

Chronic leukaemia (red).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Similar to acute leukaemia, but blood cells are almost fully developed. Can be CML (rare) or CLL (the most common form of leukaemia and affects older people)
  2. CML is caused by philadelphia gene, CLL has unknown (carcinogens - viruses, chemicals, drugs etc.)
  3. Similar to acute, symptoms are due to bone marrow infiltration and peripheral infiltration of extra cells. CLL is characterised by uncontrolled proliferation of mature B lymphocytes.
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8
Q

Chronic leukaemia (red).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. CLL has indolent course, generally asymptomatic. Any symptoms are a consequence of BM failure (anaemia, infections and bleeding), lymphadenopathy/ hepatosplenomegaly.
  2. Blood count, bone marrow aspirate, blood film
  3. ALL/AML
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9
Q

Chronic leukaemia (red).

  1. Management
  2. Complications
  3. Prognosis
A
  1. For CLL give fludarabine (chemo), rituximab (CD20 monoclonal antibody) for remssion if advanced (watchful waiting). CML give imatinib (tyrosine kinase blocker).
  2. infection, anaemia, bleeding
  3. CLL very variable prognosis, depends on disease stage, and cytogenetic monitors. CML has effective treatment.
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10
Q

Hodgkin Lymphoma (red).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Lymphomas are B and T cell malignancies of the lymphoid system and are quite common (»leukaemia). Classified into NHL or HL by histology as present the same. HL is a disease of young adults, indicated by Reed-Sternberg bodies
  2. Idiopathic, may be associated with infection (EBV).
  3. Lymphocytes multiply abnormally and collect in parts of the lymphatic system (lymph nodes). Lymphocytes lose their infection-fighting properties (vulnerable to infection). It can spread, most often to the liver, bone marrow (causing anaemia) or lungs
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11
Q

Hodgkin Lymphoma (red).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Painless lymph node enlargement (lymphadenopathy), systemic B symptoms - fever, drenching night sweats, weight loss, fatigue, anorexia
  2. Blood count, lymph node biopsy showing Reed-Sternberg cells (categorises)
  3. Any other cause of lymphadenopathy (infection, leukaemia etc.)
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12
Q

Hodgkin Lymphoma (red).

  1. Management
  2. Complications
  3. Prognosis
A
  1. Stage 1a, 2a, brief chemotherapy (ABVD) and irradiation at site of bulk disease. More advanced give same but 8 cycles of ABVD chemotherapy.
  2. Weaknened immune system, secondary neoplasms as spreads (BM, lung, liver)
  3. Worse than leukaemia (90% 5yr in stage 1, 60% in stage 4) symptoms = worse prognosis. Still good prognosis and remission rates.
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13
Q

NHL (red)

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Difference between HL and NHL, is in NHL there are no Reed-Sternberg cells. There is clonal expansion of lymphocytes and disease can be described as high or low grade. NHL>HL, presentation <40 is rare.
  2. Same as HL (idiopathic, infection etc.)
  3. Lymphocytes multiply abnormally and collect in parts of the lymphatic system (lymph nodes). Lymphocytes lose their infection-fighting properties (vulnerable to infection). It can spread, most often to the liver, bone marrow (causing anaemia) or lungs
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14
Q

NHL (red)

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Same as HL, Painless lymph node enlargement (lymphadenopathy), systemic B symptoms. More vaired in NHL and extra-nodal involvement is more common.
  2. FBC, lymph node biopsy.
  3. Infection, other neoplasms like leukaemia
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15
Q

NHL (red)

  1. Management
  2. Complications
  3. Prognosis
A
  1. Watch and wait for low grade, chemotherapy (different course of CHOPR for NHL) and radiotherapy for high grade
  2. Weaknened immune system, secondary neoplasms as spreads (BM, lung, liver)
  3. Low grade NHL – median survival is 9-11 years .
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16
Q

Myeloma (red)

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Malignant disease of bone marrow, proliferation of bone marrow plasma cells usually capable of producing paraproteins (IgG or IgA). There are also light chains (FLC).
  2. Aetiology unkown, family history/radiation exposure likely role.
  3. MGUS is pre-myelomatous condition with some paraproteins. Smouldering means enough paraproteins producing to class as myeloma, but no symptoms. THen there is symptomatic myeloma and plasma cell leukaemia, where plasma cells circualte.
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17
Q

Myeloma (red)

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. CRAB
    C - hypercalcaemia from activated osteoclasts
    R - AKI from deposition of light chains
    A - anaemia, BM infilration = infection, bleeding
    B - bone disease - back ache, spinal cord compression
  2. Serum electrophoresis for monoclonal antibodies, Serum free light assay, blood count
  3. MGUS, lymphoma, amyloidosis
18
Q

Myeloma (red)

  1. Management
  2. Complications
  3. Prognosis
A
  1. Incurable, but give chemotherapy (cyclophosphamide)/autologous stem cell transplantation. Correct anaemia (EPO), treat bone disease with bisphosphonates and AKI with hydration.
  2. CRAB
  3. Median survival is 7 years. 10% are dead in 6months due to spinal cord compression.
19
Q

Thrombocytopenia - TTP (thrombotic thrombocytopaenic purprua) (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Thrombocytopenia is reduced platelets and so increased bleeding. TTP is a genetic defect in ADAMTS13 which is supposed to breakdown vWF so there is excessive platelet aggregation (they are used up). It is classified by MAHA and purpura. It is rare, effects black and 30-50.
  2. USually genetic defect in ADAMTS13 but can be acquired due to an autoimmune process.
  3. Excess vWF causes excess platelet carrier function forming microthrombi but platelets are used up causing thrombocytopenia. Microvascular thrombi cause pentad: MAHA, purpura, neurological symptoms, fever, renal disease
20
Q

Thrombocytopenia - TTP (thrombotic thrombocytopaenic purprua) (orange).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Neurological symptoms (coma, seizures), fever, bleeding symptoms (purpura)
  2. Platelet count, Hb, ADAMTS-13 activity assay
  3. HUS caused by E.coli
21
Q

Thrombocytopenia - TTP (thrombotic thrombocytopaenic purprua) (orange).

  1. Management
  2. Complications
  3. Prognosis
A
  1. Acute management - plasma exchange (with low vWF), corticosteroids, aspirin. For ongoing give long term aspirin
  2. Ischaemic stroke, renal dysfunction, acute MI
  3. Good with good treatment and many respond well to plasma exchange.
22
Q

Thrombocytopenia - ITP (immune thrombocytopaenic purprua) (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Autoimmune destriction of platelets, idiopathic means no identifiable cause. It is common and common pregnancy.
  2. ITP in children often follows viral infection. In adults it may occur with other autoimmune conditions.
  3. There can be autoantibodies detectable in 60-70% ofcases.
23
Q

Thrombocytopenia - ITP (immune thrombocytopaenic purprua) (orange).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Insidious onset with a fluctuating course - easy bruising, epistaxis, menorrhagia.
  2. FBC, HIV serology
  3. Sepsis MDS
24
Q

Thrombocytopenia - ITP (immune thrombocytopaenic purprua) (orange).

  1. Management
  2. Complications
  3. Prognosis
A
  1. If platelet is >30x10^9 then no treatment. Give corticosteroids (Pred/dexa) for immuno suppression. Can give IVIG. If no response then splenectomy or rituximab.
  2. Life threatening bleeding
  3. Most respond to treatment and have good prognosis.
25
Q

Thrombocytopenia - HIT (Heparin induced thrombocytopenia) (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Drug reaction to heparin causing a decrease in platelet count and hypercoagulability.
  2. Taking heparin
  3. Heparin is anticoagulant which works by binding to PF4 and inhibitng its procoagulant function. Immune system can make IgGs to the H-PF4 complex activating more platelets causing a hypercoagulable state.
26
Q

Thrombocytopenia - HIT (Heparin induced thrombocytopenia) (orange).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Hx of heparin, signs/symptoms of thrombocytopenia - Petechaie, fatigue, purpura etc.
  2. FBC, HIT antigen assay
  3. TTP
27
Q

Thrombocytopenia - HIT (Heparin induced thrombocytopenia) (orange).

  1. Management
  2. Complications
  3. Prognosis
A
  1. stop heparin and alternative anticoagulant (Lepirudin/Danaparoid), consider DOAC.
  2. Life threatening thromboembolism.
  3. Recovery usually 1 week. No long term complications of HIT other than re-exposure to heparin.
28
Q

Polycythaemia (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
  4. Manifestation
  5. Investigation
  6. Management
  7. Complication/prognosis
A
  1. Myeloproliferative disorder where there is too many red blood cells (incr Hb, PCV/Haematocrit, RCC). Rare but common Myeloprol
  2. Usually mutation in PV, secondary = incr EPO to hypoxa or secreting tumours. RF = FH.
  3. JAK2 mutation causes increased EPO switched on.
  4. Signs/symptoms result of hypovolaemia/ hyperviscosity - headache, vertigo, tinnitus, angina, claudication. Hepatosplenomegaly due to extramedullary haematopoiesis.
  5. Hb, Haematocrit, WBC count, platelet count
  6. No cure, venesection to PCV <0.45L/L. Maybe chemo, low dose aspirin, Allopurinol.
  7. Risk of A or V thrombosis. Can become acute leukaemia. Median Px = 13 years.
29
Q

Beta Thalassaemia (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
  4. Manifestation
  5. Investigation
  6. Management
  7. Complication/prognosis
A
  1. Mutation in one of the chains of haemoglobin. A is generally not compatible with life, B can be minor, intermedia or major.
  2. Homozygous/ heterozygous inheritance. RF - being from Mediterranean/middle east
  3. There is microcytic anaemia as A chains precipitate in RBCs causing damage in BM. There is increased HbF (one gamma) and HbA2 (one delta)
  4. Asympatomatic, symptoms of anaemia (lethargy)
  5. Blood film, PCR + genetic is diagnostic. Also Hb electrophoresis.
  6. In severer forms blood transfusion to keep Hb>100g/L to suppress erythropoesis. Iron chelating agents for iron overload.
  7. Can get thrombotic complications, anaemia, bone deformities. Major is fatal in first years of life. Heart failure is main cause of death.
30
Q

Deep vein thrombosis (red).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Development of a blood clot in major deep vein of the leg. Very common (500,000 per year).
  2. Virchow’s triad. RF: surgery, leg fracture or conditions with thromboembolic risk - cancer, trauma, oral contraceptive pill etc.
  3. Most clots form across valves due to stasis and endothelium dysfunction. Fibrinolytic system begins breaking up clot incr FDPs.
31
Q

Deep vein thrombosis (red).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Unilateral swelling, pain, redness, hot, tenderness (blocked venous return)
  2. Quantitative D-dimer, Well’s score, proximal duplex ultrasound (gold standard)
  3. Cellulitis, Achille’s tendon tear
32
Q

Deep vein thrombosis (red).

  1. Management
  2. Complications
  3. Prognosis
A
  1. LWMH for 5 days, then DOACs (rivaroxaban) + physical activity/stockings. Long term - maintain anticoagulants, physical activity, treat underlying cause.
  2. Pulmonary embolism, HIT.
  3. Survival is 95-97% for DVT, 77-94% for PE. Condition often reoccurs.
33
Q

Pulmonary embolism (red).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Life threatening condition caused from a dislodged thrombi formed in a deep vein, occluding the pulmonary vasculature. Around 50% of venous thrombi will embolise - very common (200,000 case per year UK).
  2. Same as DVT - Virchow’s triad.
  3. The lungs act like a sieve for thrombi due to their capillary network.
34
Q

Pulmonary embolism (red).

  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Dyspnoea, pleuritic chest pain, hypoxaemia, signs of DVT. If massive (rare), haemodynamic effects - hypotension, syncope, tachycardia, right sided heart failure.
  2. Computed tomographic pulmonary angiography (CTPA), echo, D-dimer and FBC. Maybe ABG, ECG.
  3. Unstable angina, MI, pneumonia, bronchitis.
35
Q

Pulmonary embolism (red).

  1. Management
  2. Complications
  3. Prognosis
A
  1. Give unfractionated (fast acting) heparin, oxygen, fluids and thrombolysis (Chemical: Anisterplase, tPA or Mechanical: catheter thrombolysis) or embolectomy but rarerly done. Prevent via mobilisation and hydration, LMWH.
  2. Cardiac arrest/death, pulmonary infarction.
  3. Between 1-11% risk of mortality, mortality owed to cardiogenic shock secondary to right ventricular collapse.
36
Q

Bleeding disorders - vWD (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
  4. Manifestation
  5. Investigation
  6. Management
  7. Complication /prognosis
A
  1. Deficiency in vWF which causes defective platelet function and bleeding. See doc for types. VWD is the most common inherited bleeding disorder.
  2. Mainly genetic, if acquired - autoantibodies. RF: FH.
  3. vWF helps platelets aggregate and protects factor 8 from degradation, hence lack = bleeding.
  4. Prolonged bleeding time Mucutaneous bleeding - Ecchymoses, GI bleeding.
  5. PT (normal), APTT (prolonged), FBC
  6. Factor replacement (8+vWF) in concentrates, platelet/ cyroprecipitate transfusion. DDAVP, desmopressin
  7. Excess bleeding. Most patients require acute treatment throughout life but respond well to treatment.
37
Q

Bleeding disorders - Haemophilia A (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
  4. Manifestation
  5. Investigation
  6. Management
  7. Complication /prognosis
A
  1. Mutation of gene encoding factor 8 on X chromosome. Affects males, 1 in 5000.
  2. X-linked recessive inheritance. Rarely acquired due to AID. RF: Fh, male.
  3. Bleeding is impaired so clotting time is prolonged.
  4. Bleed into muscles and joints (haemarthropathy) causing inflammation and bone deformities. depending on severity - spontaneous frequent bleeding.
  5. APTT (prolonged), factor 8/9 assay, FBC
  6. Recombinant factors in episodes/ prophylaxis (3x a week in severe). Give NovoSeven or FEIBA if patient has inhibitors (autoantibodies 30%). Can give immune tolerance therapy.
  7. Cerebral haemorrahage, deformity from joint bleeding, infection from transfusion. Can give near normal lifestyle/length with new treatments.
38
Q

Bleeding disorders - DIC (orange).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
  4. Manifestation
  5. Investigation
  6. Management
  7. Complication /prognosis
A
  1. Widespread generation of fibrin in blood vessels due to initiation of coagulation pathway (microthrombi). Consumption of platelets and factors causes secondary bleeding. Difficult to estimate DIC.
  2. Acquired, major initiator is release of tissue factor (TF) due to sepsis, trauma, tissue destruction, cancer, APML.
  3. Thrombi lead to vascular occlusion. TF is a cofactor for factor 7 and initates coagulation.
  4. None to complete haemostatic failure - excessive bleeding (epistaxis etc.), and clots (dyspnoea, delirium, coma)
  5. Prolonged PT, APTT, TT, elevated D-dimer, blood film.
  6. Acute - treat underlying conditon, give platelet concnetrates, FFP, cyroprecipitate and antithrombin 3. Chronic - give heparin + antifibrinolytic agents.
  7. life threatening haemorrhage, AKI, gangrene. Mortality can be high (59%) in certain cases.
39
Q

Anaemia (red).

  1. Define/epidemiology
  2. Aetiology/risk factors
  3. Pathophysiology
A
  1. Lack of Haemoglobin causing less oxygen transport. Common(33% global population), Iron deficiency is the most common cause
  2. Many - Microcytic RBCs: Iron deficinecy, thalassaemia. Normal RBCs: blood loss, Combined Iron (bleeding, pregnancy) and folate deficiency, marrow infiltration, haemolytic anaemias
    Macrocytic RBCs - vitamin B12/folate deficinecy, liver disease etc.
  3. Depends on cause.
40
Q
  1. Clinical manifestations
  2. Investigations
  3. Differentials
A
  1. Depends on severity and onset as can adjust if slow. Non-specific symptoms: fatigue, faintness, breathlessness, exacerbation of comorbdities (angina, claudication, CHF etc.). Haemolytic anaemia - jaundice, splenomegaly
  2. Hb, Haematocrit, platelet count, MCV and MCH, blood count and film, serrum ferritin, iron, serum folate/B12 (parietal cell autoantibodies)
  3. Any cause of anaemia
41
Q
  1. Management
  2. Complications
  3. Prognosis
A
  1. Treat underlying cause. Depends on anaemia (Oral/parenteral iron/folic acid/B12).
  2. Cognitive impairment, renal failure, impaired muscular performance
  3. Depends on underlying cause (pregnancy = good prognosis, GI cancer = bad)

Jack Misc List (9 decks)

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