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Haem Flashcards

1
Q

How to replace B12/folate?

A

1mg B12 injections 3 times per week for 2 weeks, then once every 3 months

5mg folate tablets also, but not before B12 as risks SACD

think BeFore - B before F

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2
Q

Causes of high ferritin without iron overload?
With iron overload?
How to tell if there is iron overload?

A

Without (90%):

  • inflammation (acute phase protein)
  • alcohol excess
  • liver disease
  • CKD
  • malignancy

With:

  • Haemochromatosis
  • repeated transfusions

Normal values of transferrin saturation normally excludes iron overload (<45% females and <50% males)

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3
Q

Difference between direct and indirect Coombs test?

A

Direct (DAT):
To test for haemolytic anaemia
Patients RBC are mixed with anti-human Ig (antibodies against human antibodies)
If they are present the cells will agglutinate

Indirect:
Tests for Ig in patient’s plasma (e.g. prenatal for anti-D and before blood transfusion)
Patient’s plasma mixed with donor blood
If Ig present, these will attach to RBC surface
As before, anti-human Ig added, causing agglutination if Ig have attached to RBC surface

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4
Q

If suspected DVT what should you do if:

  • DVT likely?
  • DVT unlikely?
A

2 level wells score

If score 2+ (likely):

  • USS doppler within 4 hours
  • if cannot be done within 4 hours, D-dimer and give anticoagulation; ensure USS within 24 hours
  • if scan negative but D-dimer positive, stop anticoagulation and repeat scan in 6-8 days

If score <2 (unlikely):

  • D-dimer
  • if neg, other diagnosis
  • if pos, doppler USS within 4 hours - again if cannot be done anticoagulate in meantime
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5
Q

Rx for DVT?

If renal failure or anti-phospholipid syndrome?

A

Normally:

  1. DOAC (apixaban/rivaroxaban)
  2. LMWH
  3. Dabigatran
  4. Warfarin

If eGFR<15 or antiphospholipid syndrome:

  1. LMWH
  2. Warfarin
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6
Q

4 most sensitive clinical signs of PE?

A

Tachypnoea (96%)
Crackles (58%)
Tachycardia (44%)
Fever (43%)

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7
Q

If suspected PE what should you do to investigate?

A

PE rule out criteria (PERC)
then 2 PE level Wells score

If >4 points (likely):
- arrange immediate CTPA - if there is a delay then anticoagulate

CTPA +ve - diagnosis
CTPA -ve - leg doppler USS

If <=4 (unlikely):
- D-dimer
+ve then CTPA and anticoagulate
-ve then stop any anticoagulation and consider alternative

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8
Q

Apart from Wells, CTPA etc, what else should be done for suspected PE?

A

ECG:

  • sinus tachycardia
  • S1, Q3, T3 in 20%
  • RBBB or RAD may occur

CXR:

  • Recommended for all patients whilst waiting on CTPA to rule out other pathology
  • Typically normal in PE - may show wedge-shaped opacification
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9
Q

Treatment of PE?
Haemodynamic instability?
Repeat PE?

A

Normally:

  1. DOAC (apixaban, rivaroxaban)
  2. LMWH
  3. Dabigatran
  4. Warfarin

If eGFR <15 or anti-phospholipid syndrome:

  1. LMWH
  2. Warfarin

If haemodynamically unstable:
thrombolysis
OR
thrombectomy (if facilities available)

In repeat PE, IVC filters may be used

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10
Q

Length of anticoagulation in DVT/PE?

A

If provoking factor e.g. immobilisation following surgery, COCP - this transient risk will pass:
3 months

If unprovoked or cancer:
6 months and calculate HASBLED score

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11
Q

Monitoring of unfractioned heparin?

Monitoring of LMWH?

A

aPTT

LMWH - no monitoring

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12
Q

Polycythaemia rubra vera:

  • What is it?
  • features?
  • management?
  • prognosis?
A

Clonal proliferation leading to increased red cells. May also be accompanying increased neutrophils and PLT

Features:

  • itch - worse when hot
  • ‘ruddy complecion’
  • Splenomegaly
  • hyperviscosity
  • JAK2 +ve

Rx:

  • aspirin
  • venesection (keep Hb normal)
  • chemo - hydroxyurea (slight increased risk of secondary leukaemia)

Prognosis:

  • thrombotic events common
  • 10% progress to myelofibrosis
  • 10% progress to acute leukaemia (risk increased with chemo)
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13
Q

Sickle cell crises:

  • thrombotic?
  • sequestration?
  • acute chest?
  • aplastic?
  • haemolytic?
A

Thrombotic: vaso-occlusive, caused by infection/dehydration. Clinically diagnosed from pain. Infarcts occur in various organs including bones (AVN)

Sequestration: pooling in spleen or lungs with worsening anaemia

Acute chest: chest pain, dyspnoea, bilateral infiltrates on CXR, low pO2. Commonest cause of death after childhood.

Aplastic: caused by parvovirus B19, sudden fall in Hb

haemolytic: rare, increased rate of haemolysis

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14
Q

Features of G6PD deficiency?
What is seen on film of G6PD deficiency?
Diagnosis?
Inheritance?

A

Features: intravascular haemolysis, gallstones, splenomegaly (neonatal jaundice common)

Heinz bodies
Bite cells
Blister cells

Diagnosis: G6PD enzyme assay - check levels 3 months after acute haemolysis

X-linked recessive

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15
Q

Hereditary spherocytosis inheritance?
features?
Diagnosis?
Management acute and long-term?

A

AD

Failure to thrive, jaundice, gallstones, splenomegaly, MCHC elevated
Parvovirus causes aplastic crisis
spherocytes on film

Diagnosis: EMA binding test

Management:
acute - supportive, transfusion
long term - splenectomy, folate supplements

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16
Q

What is seen in hyposplenism on film?

A

Howell-Jolly bodies
Pappenheimer bodies
Target cells

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17
Q

Can LMWH cause heparin-induced thrombocytopaenia?

How can it cause a PE?

A

Yes

Heparin/LMWH binds to a platelet factor on the surface and causes an immune response. Some people form IgG which bind to the heparin-PF4 complex, which can actually activate the platelet, causing a clot

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18
Q

Primary haemostasis?

A

Vessel wall damage exposes collagen which platelets bind to via vWF

Platelets activated and change shape, release ADP and TXA2 which stimulate aggregation,

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19
Q

Extrinsic pathway?

Measurement?

A

Most important

Tissue factor (factor 3) is released from damaged vessel walls and binds to factor 7

TF/7 converges on common pathway and activates factor 10

Measure: PTT

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20
Q

Intrinsic pathway?

Measurement?

A

Amplification of response

Exposed collaged activates factor 12
12-11-9

9a binds and activates 8

9a/8a converge on common pathway

Measure: aPTT

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21
Q

Common pathway?

A

TF/7 or 9/8 activate 10

10a binds 5a to activate prothrombin (2) to thrombin (2a)

This converts fibrinogen to fibrin

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22
Q

Control of haemostasis?

A

ATIII - protease that blocks all pathways of the cascade

Protein C/S - proteins that are on the surface of platelets and inhibit factor 5/8

Fibrinolysis - breakdown of fibrin by plasmin, which is activated from plasminogen by tissue plasminogen factor

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23
Q

ITP?

A

Autoimmune condition against platelets in adults or children

Isolated low platelets

Kids: aged 2-6, self-limiting post-infection

Adults: variable and fluctuating course
1st line - steroids
2nd - pooled IVIG

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24
Q

TTP:

  • what is it?
  • what gene?
  • features?
  • bloods?
  • film?
  • management?
A

Emergency characterised by thrombocytopaenia + MAHA - widespread micro-thrombi and intravascular haemolysis, caused by a trigger

ADAMTS-13

Fever, bleeding, AKI (haematuria + proteinuria), fluctuating CNS signs (drowsy, confusion, seizures)

Bloods:
profound thrombocytopaenia
MAHA: low Hb, high LDH, high bili, low haptoglobin
NORMAL COAGULATION

Film: schistocytes

Management: Plasmapheresis

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25
Q

Management of HUS?

A

Supportive - no role for abx

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26
Q

Causes of severe thrombocytopaenia?

Mild?

A

ITP
TTP
DIC
Malignancy

Mild:

  • heparin-induced
  • drugs - diuretics, aspirin, thiazides
  • alcohol, liver disease
  • hypersplenism
  • pregnancy
  • SLE/APS
  • B12 def
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27
Q

Causes of thrombocytosis?

A

Reactive - acute phase reactant
Malignancy
Hyposplenism
Essential thrombocytosis

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28
Q

What is essential thrombocytosis?
Features?
Mutation?
Management?

A

Myeloproliferative disorder which overlaps with CML and polycythaemia rubs vera and myelofibrosis. Megakaryocyte overproduction causing increased PLT

Both arterial or venous thrombus or haemorrhage can be seen
Characteristic symptom - burning sensation in hands

JAK2 mutation

Management - hydroxyurea
aspirin
interferon a in younger people

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29
Q

What is seen on coag of vWD?

A

increased aPTT and bleeding time

low vWF and factor 8

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30
Q

Haemophilia A and B?

Seen on coag?

A 
A = factor 8 def
B = factor 9 def

Coag: increased aPTT

Factor infusions

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31
Q

Seen on coag of liver disease?

A

Increased PTT/aPTT

May be increased TT if production of prothrombin reduced

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32
Q

Causes of abnormal platelets?

A

Drugs: NSAIDs, aspirin, anti-platelets
Systemic: renal/liver disease
Haem: paraprotein/myeloproliferative disease

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33
Q

Bloods for DIC?

Management?

A 
D dimers - high
PLT - low
Bleeding - high
PTT, aPTT, TT - long
Fibrin degradation products - high
Film: schistocytes

Management:

  • Treat underlying cause
  • PLT transfusion
  • FFP
  • Cryoprecipitate
  • RBC infusion
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34
Q

General what causes an increase in:

  • PTT?
  • aPTT?
  • TT?
  • Everything?
A

PTT - liver disease, warfarin

aPTT - haemophilia, vWD, heparin

TT - heparin, advanced liver disease

everything - DIC

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35
Q

Coag for ITP?

A

low PLT

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36
Q

Coag for TTP?

A

low PLT

low Hb, high LDH, low haptoglobin, schistocytes

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37
Q

Coag for vWD?

A

increased aPTT

low factor 8

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38
Q

Coag for haemophilia?

A

increased aPTT

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39
Q

Coag for liver disease?

A

Increased PTT, aPTT, late on increased TT as well

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40
Q

Coag for vitK def/warfarin?

A

Very high PTT, high aPTT

41
Q

Coag for heparin?

A

high PTT, very high aPTT and TT

42
Q 
MOA heparin?
Excretion?
Coag?
Monitoring?
When to stop before surgery?
A

potentiates ATIII, inhibits factor Xa

(LMWH Xa only, unfractioned also 2, 9, 11 and 12)

Renal

Coag - increased PTT, very high aPTT and TT

Monitor - aPTT

Before surgery - stop the day before

43
Q

Fondaparinux MOA?

A

Also potentiates ATIII to inhibit factor Xa

44
Q

Warfarin change in coag?
When starting warfarin?
Monitoring?
When to stop before surgery?

A

Very high PTT, high aPTT

Cover with heparin for a couple of days

INR - modified PTT compared to international normal
2-3 = DVT, PE, AF
3-4 = VET on warfarin, APS, metallic valve
- check INR daily until within range 2 days in a row, then check twice weekly then weekly. Once stable check every 6-12 weeks

5 days before surgery

45
Q

What can potentiate warfarin?

A

Liver disease
Cranberry juice
P450 inhibitors (cipro, amiodarone, valproate)
NSAIDs

46
Q

Management of warfarin if:

  • major bleeding?
  • INR 5+, minor bleeding?
  • INR >8, no bleeding?
  • INR 5-8, no bleeding?
A

Major: stop warfarin, IV vit K and prothrombin complex concentrate

INR 5+, minor bleed: Stop warfarin, IV vit K, restart when INR <5

INR >8, no bleeding: stop warfarin, oral VitK using IV preparation, restart when INR <5

INR 5-8, no bleeding: withhold 1-2 doses of warfarin, reduce maintenance dose

47
Q

MOA Dabigatran?

A

2a inhibitor

48
Q

Causes of inherited thrombophilia?

A

Factor V leiden (protein C resistance) - most common

Prothrombin mutation - 2nd commonest

Others:
- ATIII, protein C or protein S deficiency

49
Q

Causes of acquired thrombophilia?

A

APS

COCP

50
Q

when to consider thrombophilia?

A

Recurrent VTE or miscarriage
VTE <40y/o
VTE in unusual place e.g. mesenteric/cerebral veins

51
Q

Common lymphoid precursor produces?
Common myeloid precursor?
Common erythroid precursor?

A

Lymphoid: T, B and NK cells

Myeloid: granulocytes - neutrophils, basophils, eosinophils, macrophages

Erythroid: PLT, RBC

52
Q

What drug can cause neutrophilia?

A

Steroids (due to reduced marginisation)

53
Q

What are atypical lymphocytes in glandular fever?

A

Increase in cytoplasm and wrapping around the cell

54
Q

What causes conversion to Fe3+?

A

Oxidative stress

55
Q

What controls iron absorption via down regulation of ferroportin in response to iron load and inflammation?

A

Hepcidin

56
Q

Iron, ferritin and TIBC in:

  • haemochromatosis?
  • iron deficiency anaemia?
  • AOCD?
  • thalassaemia?
A

Haem: iron and ferritin raised, TIBC low

Iron def: iron and ferritin low, TIBC high

AOCD: iron low, ferritin high, TIBC low

Thalassaemia: iron normal or high, ferritin normal or high, TIBC normal

57
Q

Main 3 causes of microcytic anaemia

A

Iron def
Thalassaemia
AOCD

58
Q

Iron replacement if uncomplicated?

A

200mg ferrous fumarate/sulfate TDS for a minimum of 3 months

59
Q

What is seen on film with a thalassaemia trait?

A

Heinz bodies - accumulations of B globin tetramers

60
Q

What is seen on film in HbH?
On HPLC?
Management?

A

Heinz bodies, target cells

HPLC - low HbA, HbA2 and HbF
High HbH - with B globin tetramers

Folic acid
Intermittent transfusions
May need splenectomy

61
Q

Physical features of B thalassaemia major?
CXR?
HPLC?
Management?

A

Severe anaemia
Extramedullary haematopoiesis - hepatosplenomegaly, skull bossing
CXR - hair on end sign

HPLC - High HbF, HbA2, low HbA

Regular transfusions and iron chelators (desferrioxamine)

62
Q

Where are folate and B12 absorbed in bowel?

A

Folate - duodenum

B12 - ileum

63
Q

In pernicious anaemia which Ig’s are sensitive and specific?

A

Anti-parietal cell - sensitive, not specific

Anti-IF - specific, not sensitive

64
Q

What is seen on film of B12 deficiency anaemia?

A

Hypersegmented neutrophils

Howel Jolly bodies

65
Q

Causes of non-megaloblastic macrocytosis (may not have anaemia)?

A

Alcohol
Pregnancy
Hypothyroidism
Liver disease - TARGET CELLS

Marrow failure - myelodysplasia/aplastic anaemia
- unlike the others this will always cause anaemia

66
Q

What causes spurious macrocytosis?

A

Reticulocytosis
Cold agglutination

(reticulocytosis - haemolysis, haemorrhage, treatment of anaemia, thalassaemia)

67
Q

3 hallmarks of extravascular haemolysis?

A

Hepatosplenomegaly

Protoporphyrin release (converted to unconjugated bilirubin, causing jaundice and pigment gall stones)

Urobilinogen (normal products in excess)

68
Q

Hallmarks of intravascular haemolysis?

A

Schistocytes
Increased LDH
Low haptoglobin
Haemoglobinaemia

69
Q

Causes of extravascular haemolysis?

A

Thalassaemia
Sickle cell
Hereditary spherocytosis
Autoimmune haemolytic anaemia

70
Q

Woman returns from Haiti 25 days ago and has fever/chills on alternating days, headache and myalgia. O/E temp 39, hepatomegaly - what is it?

A

Malaria

71
Q

Platelet transfusion limit in active bleeding?

A

30 in most cases

Can be up to 100 if bleeding at critical site such as CNS

72
Q

Platelet transfusion limit for pre-invasive procedure?

A

50 for most

50-75 if risk of bleeding

100 if surgery at a critical site

73
Q

Platelet transfusion threshold if no bleeding or planned invasive procedure?
Contraindications for platelet transfusion? (4)

A

10

Contra:

  • Chronic bone marrow failure
  • ITP
  • Heparin-induced thrombocytopaenia
  • TTP
74
Q

Atypical blood cells seen on film with hyposplenism?

A

Howell-Jolly bodies
Target cells
Pappemheimer bodies

75
Q

Seen on film with iron-deficiency anaemia?

If combined iron deficiency/B12 deficiency?

A

Fe def:

  • target cells
  • pencil poikilocytes
  • microcytic hypochromic

Mixed:
- microcytic and macrocytic (dimorphic) film - so MCV often normal

76
Q

What to prescribe to people with heart failure who are receiving packed red cells?

A

Furosemide dose STAT - even if already on it

77
Q

What can polycythaemia rub vera progress to?

A

AML

Myelofibrosis

78
Q

Management of vWD in mild bleeding?
What can raise levels of vWF?
What else can be given if severe?

A

Mild - tranexamic acid

Desmopressin can raise levels of vWF by inducing release of vWF from endothelial cells

Factor VIII concentrate

79
Q

Commonest ages of Hodgkin’s?

A

Bimodal peak - 30’s and 70’s

80
Q

Types of Hodgkin’s?

Typical symptoms?

A
  • Nodular sclerosing - most common - good prognosis
  • Mixed cellularity
  • lymphocyte predominant - best prognosis
  • lymphocyte depleted - rare, worst prognosis

‘B’ symptoms - weight loss, fever, night sweats

Presence of B symptoms are assoc w a poor prognosis

81
Q

How is tranexamic acid given in major haemorrhage?

A

IV bolus followed by slow infusion

82
Q

Features of Waldenstrom’s Macroglobulinaemia?

A

Lymphoplasmacytoid malignancy characterised by secretion of monoclonal IgM paraprotein

Weight loss, lethargy
Hyperviscosity - visual disturbance, stroke etc
Hepatosplenomegaly
Cryoglobulinaemia e.g. Raynaud’s

Renal function fine
No bone lesions on skeletal survey

83
Q

What is generally given 1st line in DIC after resus measures?

A

FFP or cryoprecipitate

84
Q

Over how long is a unit of RBC transfused in non-urgent cases?

A

90-120 mins

85
Q

What malignancy might EBV cause?

A

Non-hodgkins lymphoma (specifically Burkitt’s)

86
Q

Apart from biopsy, what in Hx can help differentiate hodgkin’s from non-hodgkin’s?

A

Hodgkins get alcohol-induced pain

B symptoms typically occur later in non-hodgkins

Extra nodal disease is commoner in non-hodgkins (marrow failure, bone pain, gastric, CNS, testicular)

87
Q

Ix for lymphoma?

What are good prognostic indicators?

A
  1. biopsy
  2. CTCAP - staging
  3. FBC - rule out leukaemia

Offer HIV - RF for non-hodgkin’s

LDH and ESR - prognostic indicator

88
Q

Staging of lymphoma?

A
  1. one node
  2. more than one node on same side of diaphragm
  3. nodes on both sides of diaphragm
  4. extra-nodal disease
89
Q

Commonest type of non-hodgkin’s lymphoma?
Specifically associated with immunosuppressed?
Rarest?
Other types?

A

Commonest - diffuse large B cell (40%) - high grade but these typically respond better to chemo

Burkitt’s - immunosuppressed, young, ‘starry-sky’, c-myc mutation

Rarest - Mantle cell

Others - follicular - low grade
Cutaneous T cell - quite rare

90
Q

What DOAC should be avoided in kidney failure?

What one should be used?

A

Dabigatran - renally excreted

Use Apixaban - faecally excreted

(Rivaroxaban is hepatic ally excreted)

91
Q

How long should cancer patients get VTE prophylaxis after DVT/PE?

A

6 months

Exception to the rule

92
Q

Indications for cryoprecipitate use?

What is its major constituent?

A

Major haemorrhage and haemophilia

Major constituent = factor VIII

93
Q

What leukaemia can cause raised platelets?

A

CML

94
Q

Management of APS in pregnancy?

A

Aspirin as soon as pregnancy confirmed

LMWH once foetal heart is seen (around 6-7 weeks) and discontinued at 34 weeks

95
Q

Are any Ix needed to be performed in sickle cell crises?

A

No, clinical diagnosis

96
Q

What is seen on film with sickle cell disease?

A

Howell-Jolly bodies
Target cells

(due to hyposplenism)

97
Q

How often should sickle cell patients be given the pneumococcal vaccine?

A

Every 5 years

98
Q

Common presentation of sickle cell in late infancy?

A

Hand-foot syndrome - both hands and feet get swollen

99
Q

Management of post-thrombotic syndrome?

A

Stockings

Finals Revision (29 decks)

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