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Haematology Flashcards

1
Q

Microcytic anaemia

  1. Causes - TAILS
A 
1. Thalassaemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic anaemia
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2
Q

Normocytic anaemia

  1. Causes - 3 As, 2 Hs
A 
1. Acute blood loss
Anaemia of chronic disease (e.g. renal failure)
Aplastic (marrow failure)
Haemolytic anaemia
Hypothyroidism
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3
Q

Macrocytic anaemia

  1. Two types
  2. Megaloblastic - pathophysiology
  3. Megaloblastic - causes (2)
  4. Normoblastic - causes (5)
A
  1. Megaloblastic, normoblastic
  2. Impaired DNA synthesis prevents normal cell division
  3. B12 deficiency, Folate deficiency
4. Alcohol (+ thiamine deficiency)
Reticulocytosis (haemolytic anaemia or blood loss)
Hypothyroidism
Liver disease (cirrhosis)
Drugs (e.g. azathioprine)
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4
Q

Anaemia - General

  1. Normal Hb levels
  2. Normal MCV
  3. Symptoms
  4. Clinical signs
  5. Signs from specific conditions - IDA
  6. Haemolytic anaemia
  7. Bone deformities
  8. CKD
  9. Blood tests
  10. Further tests
A
  1. 120-165 (F), 130-180 (M)
  2. 80-100 femtolitres
  3. Lethargy, headaches, dizzy, SOB, palpitations, angina
  4. Pale skin/conjunctiva, raised HR, raised RR
  5. Koilonychia, angular stomatitis, glossitis, brittle hair/nails
  6. Jaundice
  7. Thalassaemia
  8. Oedema, HTN, skin excoriations
  9. FBC (Hb), MCV, haematinics (ferritin, B12, folate, EPO), blood film, U+E, LFT, CRP
  10. Marrow biopsy, GI endoscopy (if unexplained IDA)
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5
Q

Iron deficiency anaemia

  1. Iron - absorbed where, in what form
  2. Travels around in blood how
  3. Form when deposited/stored in cells
  4. Causes (4 general)
  5. Specific clinical signs
  6. Specific symptoms from history (2)
  7. Blood results
  8. Iron therapy (ferrous sulphate 3x/day) - side effects
  9. Iron therapy - aim for rise in Hb
  10. Unsuitable when
A
  1. Duodenum, jejunum (in soluble Fe2+ form, needs acidity)
  2. As Fe3+, bound to transferrin
  3. Ferritin
  4. Low dietary intake, malabsorption (coeliac, gastrectomy, PPI), loss (menorrhagia, GI bleed), increased requirements (pregnancy)
  5. Nail spooning (koilonychia), angular stomatitis, glossitis
  6. Pica, hair loss
  7. Microcytic anaemia, high transferrin + TIBC
  8. Black stools, change in bowel habit, abdominal pain, nausea
  9. 10g/L a week
  10. If IDA caused by malabsorption
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6
Q

B12 deficiency anaemia

  1. Causes (2)
  2. B12 normally absorbed how
  3. Pernicious - pathophysiology
  4. Neurological complications
  5. Bloods - 1st line investigation
  6. Management - mild dietary deficiency
  7. Management - if severe dietary, or pernicious
  8. Limitation of this
  9. If folate deficiency too, do what
A
  1. Lack of B12 dietary intake, malabsorption (pernicious anaemia, gastrectomy)
  2. In ileum, with help from intrinsic factor (made in stomach parietal cells)
  3. Autoimmune - antibodies against PCs or IF
  4. Peripheral neuropathy (numbness, paraesthesia), Subacute combined degeneration of the cord dorsal columns (weakness, ataxia and paraplegia), visual impairment, altered mental state
  5. Intrinsic factor antibody
  6. PO replacement - cyanocobalamin
  7. IM hydroxycobalamin 3x a week for 2 weeks, then every 3 months
  8. Will not fix the cord degeneration
  9. Treat B12 deficiency first - giving folic acid when B12 deficient can lead to SCDC
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7
Q

Folate deficiency

  1. Causes (4)
  2. Extra tests if suspected (2)
  3. Commonly linked disease
A
  1. Increased requirement (pregnancy), insufficient intake (diet), malabsorption (Crohn’s, coeliac), drugs (methotrexate)
  2. Jejunal biopsy - look for coeliac disease, BM aspirate
  3. B12 deficiency
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8
Q

Haemolytic anaemia

  1. Where are RBC destroyed extravascularly (4)
  2. Inherited causes (cell wall defect)
  3. Immune causes (2)
  4. Non-immune causes (6)
  5. Clinical features (5)
  6. Investigations (FBC, blood film, DC test)
  7. Direct Coomb’s test - what is Coombs reagent
  8. Function
  9. When is it positive
A
  1. Spleen, marrow, liver, phagocytes
  2. Cell membrane (hereditary spherocytosis), Hb dysfunction (thalassaemia, sickle cell), metabolic (G6PD deficiency, pyruvate kinase)
  3. Autoimmune, alloimmune (transfusion reactions, newborn) drug-induced
  4. Heart valves, DIC, drugs, toxins, infection, renal/liver disease
  5. Triad: anaemia, splenomegaly, jaundice
    Other: dark urine, pallor, pigment gallstones
  6. FBC - normocytic anaemia
    Blood film - schistocytes
    DC test - positive in autoimmune haemolytic anaemia
  7. Anti-human globulin
  8. Tests for autoimmune haemolytic anaemia and antibodies/complement attached to RBC surface
  9. Positive if cells agglutinate after being washed in Coombs reagent
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9
Q

Reticulocytosis - 2 classifications

A

Intra-vascular

Extra-vascular

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10
Q

G6PD deficiency

  1. Inheritance
  2. Commonest in which patient cohort
  3. Triggers
  4. Results in
  5. Presentation
  6. Blood film finding
  7. Diagnosis via
A
  1. X-linked recessive
  2. Mediterranean/African patients
  3. Haemolytic anaemia
  4. Infection, antimalarials, fava/broad beans
  5. Neonatal jaundice, gallstones, haemolytic anaemia, splenomegaly
  6. Heinz bodies (Hb fragments)
  7. G6PD enzyme assay
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11
Q

Thalassaemia

  1. Inheritance pattern, what part of Hb affected
  2. Type of anaemia
  3. Clinical features - general
  4. Alpha - chromosome, specific features, management
  5. Blood film finding
  6. Beta - chromosome
  7. B-major - definition
  8. B-intermedia =
  9. B-minor =
  10. Diagnosis
  11. Iron overload - symptoms
  12. Management
  13. Monitoring
  14. What cell may indicate thalassaemia
A
  1. Autosomal recessive; Globin chain - alpha / beta
  2. Microcytic
  3. Delayed growth, congestive HF, splenomegaly, bone deformity, increased risk of infections, iron overload
  4. 16, pronounced forehead, blood/marrow transfusions, splenectomy
  5. Heinz bodies
  6. 11
  7. 2 deletion genes (no B-globin production) - severe microcytic anaemia, splenomegaly, bone deformities. Regular transfusion, chelation, spleen out, BM transplant
  8. 2 defective/deletion genes, occasional transfusions
  9. Carrier of one abnormal, mild microcytic, monitoring
  10. FBC (microcytic anaemia), Hb electrophoresis (globin abnormalities), DNA testing/pregnancy screening
  11. Fatigue, cirrhosis, impotence, HF, arthritis, DM, osteoporosis/joint pain
  12. Limit transfusions, iron chelation
  13. Serum ferritin
  14. Target cells
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12
Q

Sickle cell

  1. Inheritance
  2. Crisis - types(4)
  3. Blood tests (6)
  4. Bedside tests (3)
  5. Further test
  6. Acute management
  7. Acute chest syndrome - definition
  8. Prevention (3)
  9. Complications
A
  1. Autosomal recessive
  2. Vaso-occlusive (pain), sequestration (spleen pain, hypovolaemia), aplastic (from parvovirus B19), haemolytic (jaundice, commoner with G6PD defiency)
  3. FBC, U+E, LFTs, bilirubin, LDH, ABG
  4. Urine analysis, sputum analysis, blood culture
  5. Blood film, CXR
  6. ABCDE, fluids, analgesia, ABX if infection, maybe blood transfusion
  7. Fever/respiratory symptoms + new infiltrates on CXR
  8. Vaccinations, penicillin V prophylaxis, avoid triggers, hydroxycarbamide (stimulates HbF production)
  9. Avascular necrosis, pulmonary HTN, priapism, CKD
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13
Q

Indirect Coombs test

  1. Who for
  2. Function
  3. When is it positive
A
  1. Pregnant women/ pre-blood transfusion
  2. Detects antibodies against foreign red blood cells
  3. Positive if serum from patient sample agglutinates after being incubated with antigenetic RBCs and added to Coombs reagent
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14
Q

Haemophilia

  1. Inheritance
  2. A - deficiency + management
  3. Complication
  4. B (Christmas disease) - deficiency + management
  5. Features
  6. Bleeding sign in neonates
  7. Blood result
A
  1. X-linked recessive
  2. Factor 8; give desmopressin (stimulates vWF release) + factor 8 IV infusion
  3. 10-15% develop antibodies to factor VIII treatment
  4. Factor 9; treat with factor 9 IV infusion
  5. Haemoarthroses, haematomas, prolonged bleeding
  6. Cord bleeding
  7. Prolonged APTT, normal PT/vWF
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15
Q

von Willebrand Disease (vWD)

  1. Types (3)
  2. Presentation
  3. Blood result
  4. Management (4)
A
  1. Partial vWF reduction (commonest, AD), abnormal form, total absence (AR)
  2. Behaves like platelet disorder (epistaxis, menorrhagia, gums when brushing teeth), family history of bleeding
  3. Prolonged bleeding/APTT, normal PT, low F8/vWF
  4. TXA (mild), desmopressin, vWF concentrate, factor 8
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16
Q

DIC

  1. Pathophysiology
  2. Effect
  3. Causes (5)
  4. Blood results
A
  1. Pathological activation of coagulation, so depletion of platelets + clotting factors
  2. Bleeding and microvascular thrombosis
  3. Infection, malignancy, obstetrics, anaphylaxis, liver disease
  4. Prolonged APTT / PT / TT, low fibrinogen
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17
Q

Thrombophilia

  1. Primary causes (3)
  2. Secondary causes (7)
  3. Hepatic vein blood clot - name of syndrome
  4. Symptoms (triad)
  5. Factor V leiden - what it is
A
  1. Antiphospholipid syndrome protein S/ C deficiency, antithrombin III deficiency, Factor V leiden
  2. Malignancy, immobility, major surgery, OCP, smoking, pregnancy, APS
  3. Budd-Chiari
  4. Abdominal pain, hepatomegaly, ascites
  5. Commonest inherited thrombophilia - ‘activated protein c resistance’ so Factor V is inactivated much more slowly
18
Q

Lymphoma

  1. Hodgkin’s lymphoma - cells found
  2. Associated conditions
  3. Types (3)
  4. Blood test commonly raised
  5. Symptoms
  6. Management (+ risks)
  7. Non-Hodgkin’s lymphoma - main presentation
  8. Lymphadenopathy - locations
  9. Burkitt’s - types (2)
  10. Microscopy findings
  11. MALT (mucosa-associated lymphoid tissue)
  12. Diffuse large B cell lymphoma - presentation
  13. Both - diagnosis
  14. Both - staging system
  15. Both - complication
A
  1. Reed-Sternberg cells (very big B cells with multiple nuclei, + nucleoli inside those)
  2. EBV, HIV, autoimmune (RA, sarcoid)
  3. Nodular sclerosing - commonest, has “fibrotic bands”
    Lymphocyte rich - RS cells + small lymphocytes
    Mixed cellularity - RS cells, mixed infiltrate
  4. LDH
  5. Painless (pain if alcohol), rubbery nodes, B symptoms
  6. Chemotherapy (leukaemia, infertility), radiotherapy (other malignancy)
  7. Painless lymphadenopathy
  8. Cervical, axilla, inguinal
  9. Endemic (African, EBV), sporadic (ileo-caecal, HIV)
  10. ‘Starry sky’ - lymphocyte sheets + macrophages with dead apoptotic tumour cells
  11. In stomach, associated with H.pylori
  12. > 65yo, rapidly growing painless mass
  13. Lymph node biopsy (also do FBC, blood film, CXR)
  14. Ann-Arbor (1 local nodes, 2 node spread, 3 nodes above / below diaphragm, 4 organs e.g. lungs/liver)
  15. Autoimmune haemolytic anaemia
19
Q

Leukaemia - general

  1. Pathophysiology
  2. Action of leukaemia cells on bone marrow
  3. Symptoms due to bone marrow suppression
  4. Blood test - what commonly raised
A
  1. Increase non functional haemopoietic blood cells produced by bone marrow
  2. Suppress production of normal cells
  3. Anaemia, bruising, bleeding, susceptible to infections
  4. LDH
20
Q

Acute lymphoblastic leukaemia (ALL)

  1. Commonest patient cohort (2)
  2. Associated syndrome
  3. Pathophysiology
  4. Blood film - predominant cell type
  5. Associated with which translocations
A
  1. Children, >65
  2. Down’s
  3. Acute proliferation of a single lymphocyte, (usually B)
  4. Blast cells
5. t(15:17) (30% of children with ALL)
Ph chromosome (t(9:22) (30% of adults with ALL)
21
Q

Philadelphia chromosomal defect

  1. Which chromosome on the leukaemia cell
  2. Which leukaemias is it associated with
A
  1. Chromosome 22

2. CML (90%) on p210; ALL on p190

22
Q

Chronic lymphocytic leukaemia (CLL)

  1. Pathology
  2. WBC type raised
  3. Commonest age group
  4. Blood film - cell seen
  5. Can cause what autoimmune condition
  6. Can transform into what
A
  1. Uncontrolled proliferation and accumulation of mature non-functional lymphocytes (usually B lymphocytes)
  2. Lymphocytes
  3. > 55
  4. Smudge/smear cells (mature fragile lymphocytes)
  5. Warm autoimmune haemolytic anaemia
  6. High-grade lymphoma (Richter’s transformation)
23
Q

Acute myeloid leukaemia (AML)

  1. What do the blasts infiltrate (5)
  2. Main causes (5)
  3. Presentation (4)
  4. Blood test results (FBC, urate, LDH, Ca2+)
  5. Non-blood tests (3)
  6. Blood film - findings
  7. Commonest age group
A
  1. Mainly bone marrow, then liver, spleen, skin and gums
  2. Myelodysplastic syndromes (PRV, myelofibrosis)
    Chemotherapy, radiotherapy
  3. Hepatosplenomegaly, lymphadenopathy, bone pain
  4. Pancytopaenia (normocytic, normochromic anaemia), Urate/LDH/Ca2+ and young white cell blasts up
  5. Blood film, bone marrow, cytogenic/molecular analysis
  6. High blast cells, auer rods in cytoplasm
  7. > 75
24
Q

Chronic myeloid leukaemia

  1. Pathophysiology
  2. Phases (3)
  3. Transforms into (2)
  4. Blood tests (RBC, WBC, platelet, urate, LDH, B12)
  5. Associated chromosomal defect
  6. Commonest age group
  7. Management - lifelong
A
  1. Chronic accumulation of basophils, eosinophils and neutrophils (granulocytes, metamyelocytes)
  2. Chronic (5 years, asymptomatic), accelerated (10-20% blasts), blast (>30% blasts)
  3. Blast transformation - AML (80%), ALL (20%)
  4. RBC down, WBC/platelet/urate/LDH/B12 up
  5. Philadelaphia chromosome
  6. > 65
  7. Imatinib
25
Q

Paraproteins

  1. Variations (3)
  2. Light chains - found in
  3. Paraproteinaemia - definition
A
  1. Whole immunoglobulins, heavy chains, light chains (bence jones)
  2. Urine (filtered out by the kidneys)
  3. Presence of monoclonal immunoglobulins in the blood
26
Q

Multiple myeloma

  1. Type of malignancy
  2. What is released, + consequence of this
  3. Presentation
  4. Investigations - initial (‘BLIP’)
  5. Diagnostic investigation
  6. Blood film - finding
  7. Blood test - result
  8. Bone assessment - whole body MRI findings
  9. Name for finding in skull
  10. Management - supportive
  11. Management - hyperviscosity
  12. Complications (2)
A
  1. Plasma cell (type of B lymphocyte in marrow)
  2. Large number of one monoclonal antibody/paraprotein (IgG normally) so normal IG function down (infections)
  3. High Ca2+, renal failure, anaemia, bone pain/fracture, regular infections
  4. Bence–Jones protein (monoclonal light chain from abundant antibody) (request urine electrophoresis)
    Serum: Light‑chain assay
    Immunoglobulins
    Protein electrophoresis (monoclonal paraprotein band)
  5. Bone marrow biopsy (specifies paraprotein)
  6. Rouleaux formation
  7. Low RBC (normocytic normochromic anaemia) + WCC, High Ca2+, ESR, plasma viscosity
    Low RBC/platelets/neutrophils (if marrow infiltration)
  8. Punched out, lytic lesions - common locations are skull, spine, long bones and ribs (increased osteoclast/decreased osteoblast activity)
  9. ‘Pepper pot’ / ‘raindrop’ skull
  10. Bisphosphonates, ABX, analgesia, chemotherapy, radiotherapy for bone pain
  11. Plasmaphoresis
  12. Spinal cord compression
    Renal disease
    Hyperviscocity syndrome - epistaxis, visual disturbance, headaches, confusion
27
Q

Myeloproliferative disorders - general

  1. Definition
  2. Types (3) + proliferation of which cells
  3. Progress into

Myelofibrosis

  1. AKA
  2. Cause
  3. Consequence
  4. Blood results
  5. Bone marrow aspirate - result
  6. Management - primary
A
  1. Overproduction of one or more of the early cell lines in the bone marrow
  2. Primary myelofibrosis (haematopoietic stem cells)
    Polycythaemia vera (erythroid cell)
    Essential thrombocytosis (megakaryocyte)
  3. Acute myeloid leukaemia
  4. Marrow fibrosis
  5. Primary, or secondary to PC / ET
  6. Marrow failure, so extramedullary haematopoiesis, so hepatosplenomegaly, so portal HTN + maybe cord compression
  7. Anisocytosis, poikilocytosis (teardrop shape), blasts
  8. ‘Dry’ aspiration
  9. Allogeneic stem cell transplant, chemo, supportive
28
Q

Thrombocytosis

  1. Essential thrombocytosis - definition
  2. Clinical features
  3. Management
  4. Secondary thrombocytosis - causes (4)
A
  1. High platelets (often abnormal so don’t work properly)
  2. Aysymptomatic, but then:
    VTE, GI bleeds, bruising, CV symptoms, weight loss, pruritis, sweats
  3. Aspirin, chemo to control
  4. Iron deficiency, chronic bleed, trauma, inflammation
29
Q

Polycythaemia

  1. Definition
  2. Primary - aka
  3. Cause
  4. Mutation in 92%
  5. Clinical findings
  6. Abnormal bloods
  7. Non-blood tests
  8. Management (3)
  9. Secondary polycythaemia - causes
A
  1. High RBCs
  2. Polycythaemia rubra vera
  3. Malignant myelopoliferative disorder
  4. JAK2
  5. Erythema, facial plethora, fatigue, gout, vascular occlusive event, hyperviscosity symptoms
  6. High: Hb, packed cell volume, RBC, WBC, platelets
  7. FBC, ABG, CXR, renal USS
  8. Venesection, aspirin, reduce vaso-occlusive RFs, chemo to control
  9. Increased EPO production, either:
    Inappropriately, from renal/lung disease
    Chronic hypoxia, from heart/lung disease or high altitude
30
Q

Blood transfusion

  1. Hb level for transfusion in most patients
  2. For ACS patients
  3. MHP 1st pack contents (+ product ratio)
  4. Non-urgent blood transfusion - given over
  5. When to take observations during transfusion
A
  1. < 70 g/L - aim (70 - 90)
  2. < 80 - aim (80 - 100)
  3. 4x blood, 4x FFP (1:1 ratio)
  4. 2-3 hours
  5. 0, 15 mins and 30 mins
31
Q

Venous disease

  1. Valve reflux disease - risk factors (4)
  2. Management
  3. Varicose veins - definition
  4. Saphina varix - definition
  5. Lipodermatosclerosis - cause
A
  1. FH, pregnancy, obesity, occupation
  2. Compression stockings, ligation + stripping
  3. Dilated subcutaneous vein with reversed blood flow
  4. Dilation of saphenous vein at its junction with the femoral vein in the groin
  5. Chronic venous hypertension leading to subcutaneous fat becoming fibrotic
32
Q

Heparin/LMWH

  1. Heparin - activates what, inhibits what
  2. LMWH - examples
  3. Activates what, inhibits what
  4. Monitoring - heparin
  5. Monitoring - LMWH
A
  1. Activates antithrombin III, inhibits thrombin + factors 9/10/11/12a
  2. Enoxaparin, dalteparin
  3. Activates antithrombin III, inhibits factor Xa only
  4. Activated partial thromboplastin time (APTT)
  5. Anti-Factor Xa (routine monitoring not required)
33
Q

Blood transfusions - reactions

  1. Urticaria - cause
  2. Management
  3. Anaphylaxis - management
  4. Acute haemolytic reaction - cause
  5. Management
A
  1. IgE reacting with foreign material
  2. Slow transfusion rate, give antihistamine
  3. ABCDE, stop infusion, oxygen, IM adrenaline, IV hydrocortisone, IV fluids
  4. ABO incompatibility
  5. STOP transfusion
34
Q

Blood transfusions - product indications

  1. Whole blood
  2. Platelets
  3. FFP
  4. Cryoprecipitate
A
  1. Bleeding
  2. Active bleeding + thrombocytopaenia < 30 x10(9)/ L
  3. Clotting problem
  4. Clotting including fibrinogen
35
Q

Blood film findings

  1. Anisocytosis (varied RBC sizes)
  2. Target cells (central pigment, pale outer)
  3. Heinz bodies (denatured globin blobs in RBCs)
  4. Howell-Jolly bodies (DNA material blobs in RBCs)
  5. Reticulocytosis (large immature RBCs)
  6. Schistocytes (RBC damaged fragments)
  7. Sideroblasts (immature RBCs, contain iron)
  8. Smudge cells (ruptured WBCs)
  9. Spherocytes (RBC without biconcave disc space)
  10. Reed-Sternberg cells
  11. Auer rods
  12. Rouleaux formation
A
  1. Myelodisplastic syndromes, some anaemia
  2. Iron deficiency anaemia, thalassaemia, post-splenectomy
  3. G6PD deficiency, alpha-thalassaemia
  4. Post-splenectomy, severe anaemia
  5. Haemolytic anaemia, blood loss
  6. HUS, DIC, TTP (metallic valves, haemolytic anaemia)
  7. Myelodysplasic syndrome
  8. Chronic lymphocytic leukaemia
  9. Autoimmune haemolytic anaemia, hereditary spherocytosis
  10. Hodgkin’s lymphoma
  11. Acute myeloid leukaemia
  12. Multiple myeloma
36
Q

Iron overload (haemochromatosis)

  1. Blood results
  2. Other causes of bloods suggesting iron overload (2)
A
  1. High serum ferritin / iron / transferrin saturation
    Low TIBC / serum transferrin
  2. Iron supplementation
    Acute liver damage (lots of iron is stored in the liver)
37
Q

Hereditary spherocytosis

  1. Inheritance
  2. Presentation
  3. Blood results
  4. Management
  5. Hereditary eliptocytosis (AD) - blood film
A
  1. Autosomal dominant
  2. Jaundice (intermittent), gallstones, failure to thrive, hepatosplenomegaly, aplastic crisis (parvovirus)
  3. Spherocytes, reticulocytosis, raised mean corpuscular Hb concentration (MCHC)
  4. Folate supplements, splenectomy, ? cholecystectomy
  5. Ellipse not sphere-shaped - same signs/treatment
38
Q

Autoimmune haemolytic anaemia

  1. Pathophysiology
  2. Classified by
  3. Commonest type
  4. Haemolysis location
  5. Causes
  6. Other type - aka, what happens
  7. Haemolysis location
  8. Causes
  9. Management
A
  1. Antibodies against RBCs
  2. Temperature at which auto-antibodies destroy RBCs
  3. Warm type
  4. Extravascular (e.g. spleen)
  5. SLE, CLL, lymphoma, methyldopa, idiopathic
  6. Cold type (-10 C), cold agglutinin disease; antibodies agglutinate RBCs (complement mediated)
  7. Intravascular
  8. Lymphoma, mycoplasma, EBV, CMV, HIV
  9. Blood transfusions, prednisolone, rituximab (anti-B cell), splenectomy
39
Q

Thrombocytopaenia (low platelets)

  1. Causes - production problems
  2. Excessive destruction
  3. Purpura - typical cause
  4. Differentials to rule out in children (2)
  5. Immune thrombocytopaenic purpura (ITP) - features
  6. Clinical features (4)
  7. Platelet level at which it should be treated
  8. Treatment (2)
  9. Thrombotic thrombocytopaenia purpura (TTP) - features
  10. Protein with problem
  11. Management
  12. Heparin induced thrombocytopenia - cause
  13. Effect
  14. Management
A
  1. Sepsis, low B12/folate, leukaemia, liver failure (reduced thrombopoietin production), myelodysplastic syndrome
  2. Medications (valproate, methotrexate, isotretinoin, PPI), alcohol, ITP, TTP, heparin-induced, HUS
  3. Low platelets
  4. Meningococcal septicaemia, acute lymphoblastic leukaemia
  5. Epistaxis, bruising under skin, menorrhagia, gingivitis
  6. Antigens on platelet surface
  7. <30
  8. Prednisolone, IV IG
  9. Small vessel clots use platelets (thrombocytopaenia), then break up (haemolytic anaemia)
  10. ADAMTS13
  11. Plasma exchange, steroids, rituximab
  12. Anti-PF4/heparin (HIT) antibodies (post-heparin use)
  13. Antibodies bind to platelets, activate clotting mechanisms, so hypercoagulable state + thrombosis. Platelets then break down, so thrombocytopenia
  14. Stop heparin
40
Q

Myelodysplastic syndrome

  1. Types (3)
  2. Commonest patient cohort
  3. Symptoms (if not asymptomatic)
A
  1. Single lineage - refractory anaemia
    Multilineage - refractory anaemia, neutropaenia, thrombocytopaenia
    Excess blasts - higher risk of developing AML
  2. > 60, previous chemo/radiotherapy
  3. Anaemia (pale, fatigue, SOB)
    Neutropaenia (frequent/severe infections)
    Thrombocytopaenia (purpura, bleeding)

Medical School (28 decks)

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