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7. Haematology > Haematology COPY > Flashcards

Haematology COPY Flashcards

1
Q

list 4 risk factors of DVT

A

increasing age, pregnancy, synthetic oestrogens (pill, HRT), trauma, surgery, past DVT, cancer, obesity, immobility, thrombophilia

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2
Q

what other disease may a DVT present as?

A

pulmonary embolism

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3
Q

describe the clinical features of a DVT

A

warm, tender calf, with erythema. fever. pitting oedema.

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4
Q

what investigations would you do on a patient with a suspected DVT?

A

D-dimer - -ve result excludes DVT, +ve doesn’t mean it is DVT.
doppler US.

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5
Q

give 4 features included in the Wells score

A

active cancer, immobility, major surgery in last 4 weeks, local tenderness, swollen leg, pitting oedema, collateral superficial veins

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6
Q

how would you manage a patient with a DVT?

A

LMWH or fondaparinux - short term anticoagulation.
warfarin or NOAC - long term anticoagulation.
compression stockings.
mobilise, stop the pill.

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7
Q

what steps can be taken to prevent DVT?

A

stop the pill.
early mobilisation.
compression stockings/leg elevation.
LMWH/fondaparinux.

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8
Q

how does fondaparinux work as an anticoagulant?

A

factor Xa inhibitor - prevents the final coagulation pathway from continuing, preventing formation of fibrin clot.

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9
Q

how do heparins work as anticoagulants?

A

activate antithrombin, which inactivates thrombin and factor Xa.
LMWHs also act to inhibit factor Xa directly.

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10
Q

how would you stop bleeding in an over-anticoagulated patient?

A

IV vitamin K - warfarin ‘antidote’

protamine = heparin antidote

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11
Q

what must you assess before giving anticoagulation therapy? how would you assess this?

A 
bleeding risk.
HAS-BLED.
Hypertension.
Abnormal liver/renal function.
Stroke.
Bleeding.
Labile INR.
Elderly.
Drugs/alcohol.
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12
Q

give a main advantage and disadvantage of NOACs

A

adv - no need for regular INR monitoring - easier for patient.
dis - don’t have an antidote, so patient at risk of massive haemorrhage if injured etc.

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13
Q

what is haemosiderosis?

A

iron deposition at liver, kidney and heart.

this is why you use iron chelation for repeated transfusions etc.

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14
Q

what’s the normal structure of haemaglobin for adults/babies?

A

babies have HbF = 2xalpha + 2xgamma.
adults HbA = 2xalpha + 2xbeta.
HbA2 = 2xalpha + 2xdelta - found normally, but is increased in beta thalassaemia.

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15
Q

what is haemolysis and where can it happen?

A

premature destruction of RBC. can happen in two places:

1) intravascular - trauma (e.g. mechanical heart valve), complement mediated lysis
2) reticuloendothelial system/extravascular - macrophages of liver, spleen, or accelerated due to immune targeting by antibodies.

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16
Q

what does Coombs’ negative/positive mean?

A

direct antiglobulin test.
used in haemolytic anaemia.
positive = immune mediated
negative = non-immune mediated.

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17
Q

what does the bone marrow do? where are biopsies taken?

A

haemopoiesis - at axial skeleton and long bones (vertebrae, sternum, ribs, skull, limbs)

biopsy is at iliac crest

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18
Q

what are megaloblasts?

A
  • large structurally abnormal RBCs
    due to defective DNA synth - leads to leukopaenia + thrombocytopaenia.

causes - B12/folate deficiency, drugs (hydroxyurea).
often asymptomatic as such slow onset means body adjusts.

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19
Q

what are the two main types of haematological malignancies?

A

1) bone marrow origin - myeloid disorders

2) lymphatic origin - lymphoid disorder - B or T cell

20
Q

list the main haematological malignancies and define them

A
  • leukaemias: excess of abnormal white cells in peripheral blood (myeloid or lymphoid)
  • lymphomas: tumour presentation w/ local/scattered lumps in lymphatic system
  • myeloproliferative disorders: involve BM, liver + spleen w/ peripheral blood features
21
Q

which haematological malignancies tend to follow an acute course with rapid progression?

A 
myeloid = AML
lymphoid = ALL (T or B cell), high grade lymphoma
22
Q

which haematological malignancies tend to follow a slowly progressive course with years between presentation + clinically relevant condition?

A 
myeloid = CML, myeloproliferative neoplasm (e.g. MDS, PRV)
lymphoid = CLL, low grade lymphoma, myeloma
23
Q

what is tumour lysis syndrome

A

Electrolyte and metabolic disturbance due to breakdown of large number of e.g. leukaemic cells

you get: hyperuricaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia,renal impairment

24
Q

what is myelodysplastic syndrome (MDS)?

A

group of malignant haematopoietic disorders characterised by:

1) dysplastic changes in one or more cell lineages
2) ineffective haematopoiesis
3) predilection to develop AML

90% is primary, secondary is due to radio/chemo therapy and has worse prognosis.
usually >70yrs, M, smoker

25
Q

how does myelodysplastic syndrome (MDS) present?

A

1) anaemia - unexplained macrocytic anaemia. usual anaemia symps, worsening angina, CCF.
2) neutropenia - can get granulocyte depletion –> recurrent infections/sepsis
3) thrombocytopenia - bleeding, petechia, bruising, nosebleeds/gums etc

26
Q

how do you diagnose MDS?

A

diagnosis of exclusion:

  • FBC - anaemia (normo/macrocytic), neutropenia, thrombocytopenia, neutrophilia, thrombocytosis.
  • blood film: dimorphic red cells, Pappenheimer bodies, anisocytosis, poikilocytosis.
  • Ferritin + B12 normal
  • BM biopsy - hypercellular with blast cells.
27
Q

how do you manage MDS?

A

supportive blood/plt transfusions + monitoring of iron status - for anaemia/thrombocytopenia.
neutropenia - broad spec abx if sepsis, G-CSF if recurrent infections.

high-intensity chemo!

28
Q

possible complications of MDS?

A
  • Anaemia, thrombocytopenia, low WCC
  • Transfusion related iron overload -> desferrioxamine
  • Transformation to AML
  • Bone marrow failure (leading cause of death)

Median survival - 2 years

29
Q

what is Fanconi anaemia?

A

a mostly autosomal recessive bone marrow failure syndrome.

cells are sensitive to DNA cross-linking.

30
Q

how does Fanconi anaemia present?

A

1) congenital dysmorphic features - triangle face, café au lait + hyperpigmented skin, cardiac and renal malformations, abnormal thumbs
2) pancytopenic BM failure
3) susceptibility to cancer - AML, solid tumours (H&N SCCs, gynae)

presents at <7yrs in similar way to aplastic anaemias, AML, MDS

31
Q

explain how liver disease + vitamin K stuff relates to bleeding problems

A
  • liver is site of coagulation factor and fibrinogen synthesis
  • disease = bleeding + prolonged PT
  • vit K needed to synthesis of 2, 7, 9, 10
  • fat soluble vitamin so deficient in malabsorption esp. obstructive jaundice
  • treat vit K deficiency/liver related bleeding with IV vit K
32
Q

learn coag cascade/platelet physiology if you cba

A

??

33
Q

what drugs influence bleeding?

A

aspirin and clopidogrel = antiplatelets
heparin (factor Xa) and warfarin (factor 2, 7, 9, 10) = affect coag cascade
steroids thin the skin and cause bleeding/bruising

34
Q

what is the mechanism of aspirin?

A

irreversible inhibits COX1

prevents production of thromboxane A2 - TXA2 induces platelet aggregating and vasoconstriction.

35
Q

what is the mechanism of clopidogrel?

A

irreversible P2Y12 antagonist.

P2Y12 is activated by ADP - amplifies platelet activation by activating glycoprotein Gp2b3a.
so clopidogrel inhibits ADP induced platelet aggregation.

36
Q

how does warfarin work?

A

vitamin K antagonist, long half life, orally available but super complicated dosing.
prolongs PT.
prevents synthesis of factors 2, 7, 9 and 10.

monitor with INR (derived from PT):
aim 2-3
some may have higher range 3-4.5

37
Q

give examples of NOACs and mechanisms (might need to check if this is up to date)

A

factor Xa inhibitors = apixaban, rivaroxaban
thrombin (factor IIa) inhibitor = dabigatran.

indicated for DVT/PE and AF.
equivalent to warfarin INR 2-3 but no monitoring.
not easily reversible.

38
Q

list some thrombotic disorders you might screen for if someone presents with DVT. what causes DVTs generally?

A
  • protein C or S deficiency (test = assay)
  • factor V Leiden - AD condition, test with PCR
  • antithrombin deficiency
  • prothrombin gene mutation

BUT 95% are due to hypercoagulable state instead - antiphospholipid synd, cancer, obesity, pregnancy, immobility, nephrotic synd, slow blood flow e.g. sickle cell, PRV etc etc

39
Q

try and learn the ABO system for who can give/receive what blood

A 
O = universal donor
AB = universal receiver
40
Q

what are the group and save/screen and cross match blood tests?

A

group and screen - order if any chance pt needs blood. checks group and Rh status. screens for abs to other antigens.

cross match done for most surgery pts. order if 1 in 10 chance of needing blood - checks the specific blood to be given against pt blood by mixing donor RBCs w/pts serum.

41
Q

list some causes of splenomegaly

A

CHINA - MMM

  • Congestion: portal HTN, portal vein thrombosis, Budd-Chiari, HF
  • Haem: haemolytic anaemia, red cell defects, thalassaemia, sickle cell, leukaemias, PRV
  • Infection: malaria, EBV, CMV, HIV, TB
  • Neoplasm: CML, lymphoma, splenic mets/cysts
  • Autoimmune: RA, sarcoidosis, amyloidosis, SLE, Feltys
  • chronic Myeloid leukaemia
  • Myelofibrosis
  • Malaria
42
Q

list some indications for splenectomy

A

1) Spontaneous rupture at massive splenomegaly (infectious mononucleosis) precipitated by trauma
2) Hypersplenism: ITP, hereditary spherocytosis
3) Neoplasia: lymphoma or leukaemic infiltration
4) Splenic cyst or abscess

43
Q

list some possible complications of splenectomy

A

1) thrombocytosis - platelet count peaks at 7-10/7
2) overhwleming infection - esp. encapsulated bacteria

prophylactic abx + vaccine = oral phenoxymethylpenicillin or macrolides; pneumococcal + flu vaccine.
carry health alert card.

44
Q

give some indications for BM transplant

A

malignant - ALL, AML, CML, HL, MM

non-malignant - thalassaemia, sickle cell anaemia, aplastic anaemia, Fanconi anaemia

45
Q

outline the procedure for a haematopoietic stem cell transplant

A
  • chemo/radiotherapy given before transplant
  • harvest: BM removed from pelvis under GA or peripheral blood stem cells removed from blood via apheresis.
  • given GM IV as inpatient
  • engraftment
46
Q

what’s the difference between autologous and allogenic BM transplants?

A

autologous - stem cells harvested from own BM. pt undergoes ablative/reduced treatment. good as rapid immunity, less infection risk, less risk rejection. BUT not suitable for AML due to high relapse.

allogenic - healthy donor and patient. HLA matching to pt HLA at 3 loci. usually sibling/relative match.

47
Q

list possible complications of a BM transplants

A
  • infection
  • veno-occlusive disease
  • mucositis
  • graft vs host disease (immune response launched by graft against host tissue): occurs at <3/12 - maculopapular rash, N&V, cholestatic jaundice.
  • graft v tumour effect can be beneficial - donor T cells react to diseased lymphocytes of recipient - reduces likelihood of relapse.

7. Haematology (15 decks)

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