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Year 5 > Haematology > Flashcards

Haematology Flashcards

1
Q

Causes of relative polycythaemia

A
  • Dehydration

- Diuretics

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2
Q

Causes of true polycythaemia

A
  • EPO or red cell transfusion
  • Androgens
  • Malignancy - polycythaemia vera
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3
Q

Causes of microcytic anaemia

A
  • Iron deficiency anaemia

- Thalassemia

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4
Q

Causes of normocytic anaemia

A
  • Anaemia of chronic disease
  • Bone marrow failure
  • Haemodilution (IV fluids)
  • EPO insufficiency (renal failure)
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5
Q

Causes of macrocytic anaemia

A
  • Haematinic deficiency (B12 and folate deficiency)
  • Haemolysis
  • Altered lipid content in red cell membrane e.g. alcohol, liver disease, hypothyroidism, drugs
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6
Q

Iron study results in a patient with iron deficiency anaemia

A
  • Low serum iron AND high transferrin

OR

  • Low ferritin
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7
Q

Ferritin levels may be falsely ??? during the acute phase response

A

Raised

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8
Q

Treatment of a patient with iron deficiency anaemia

A

PO ferrous sulphate 200mg tads until FBC normal then continue for 3 months to replenish iron stores

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9
Q

When would you consider looking for causes of iron deficiency anaemia?

A

Iron deficiency in a non-menstruating women - consider upper GI endoscopy and colonoscopy

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10
Q

FBC results in thalassemia

A

MCV much lower than haemoglobin

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11
Q

Most common cause of normocytic anaemia

A

Anaemia of chronic disease

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12
Q

Iron study results in a patient with anaemia of chronic disease

A
  • Normal/high ferritin
  • Low serum iron
  • Low transferrin
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13
Q

Causes of bone marrow failure

A
  • Malignancy e.g. blood cancers
  • Drugs e.g. chemotherapy, cytotoxic, antibiotics
  • Infection e.g. HIV
  • Nutritional
  • Radiation
  • Poisons
  • Congenital
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14
Q

Causes of haematinic deficiency

A
  • Dietary choices e.g. veganism
  • Pernicious anaemia (autoimmune destruction of intrinsic factor)
  • Ileal disease e.g. Crohn’s
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15
Q

Treatment of haematinic deficiency

A
  • Folate: oral replacement

- B12: IM injections

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16
Q

Never replace ??? before checking ??? is normal as this can precipitate subacute combined degeneration of the spinal cord

A
  • Folate

- B12

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17
Q

Causes of haemolysis

A
  • Sickle cell disease
  • Thalassemia
  • GPD6 deficiency
  • Hereditary spherocytosis
  • Autoimmune haemolysis
  • Haemolytic transfusion reaction
  • DIC
  • Eclampsia
  • Malaria
  • Toxins
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18
Q

Clinical features of haemolysis

A
  • Signs of anaemia
  • Jaundice
  • Dark urine/pale stool
  • Splenomegaly (chronic)
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19
Q

Investigations which would indicate haemolysis is occurring

A
  • FBC: macrocytic anaemia, Reticulocyte response, increased LDH
  • LFTs: unconjugated bilirubinaemia
  • Consumption of haptoglobin
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20
Q

Investigations to perform to work out cause of haemolysis

A
  • Blood film

- Coomb’s test

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21
Q

Commonest inherited single gene conditions

A

Haemoglobinopathies

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22
Q

Pathophysiology of sickle cell disease

A

Single nucleic acid substitution (GAG to GTG) in the beta global gene leading to synthesis of structurally abnormal haemoglobin.

This causes HbS to polymerise and form crystals when it becomes deoxygenated at low oxygen tensions, causing haemoglobin to clump and become ‘sickled’ in shape, meaning RBCs are much more easily damaged in the capillaries.

Originally the sickling is reversible but becomes irreversible over time.

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23
Q

Inheritance pattern of sickle cell disease

A

Autosomal recessive

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24
Q

Factors which increase sickling of RBC in sickle cell disease

A
  • Hypoxia
  • Infection
  • Acidosis
  • Cold temperatures
  • Medications e.g. ibuprofen
  • Low levels of HbF (higher levels are protective)
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25
Q

Clinical features & investigation results of a patient with sickle cell TRAIT

A
  • Asymptomatic
  • Normal FBC (no anaemia)
  • Normal blood film
  • Abnormal HbS detected on HPLC (HbA and HbS)
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26
Q

Treatment required in sickle cell trait

A

None - patient’s are asymptomatic and don’t experience anaemia

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27
Q

What are the two main complications of sickle cell disease?

A

1) Chronic haemolytic anaemia (due to damage and breakdown of RBCs) - Hb 70-90g/l
- leads to jaundice and bilirubinaemia
- leads to reticulocytosis (as bone marrow try to compensate for anaemia)

2) Acute faso-occlusive crisis
- often presents with bony pain

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28
Q

Acute complications of sickle cell disease

A
  • Infection
  • Acute anaemia - splenic/hepatic sequestration, aplastic crisis (associated with parvovirus), haemolytic crisis
  • Chest crisis
  • Stroke
  • Priapism
  • Avascular necrosis of the hip or shoulder
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29
Q

Management of complications in sickle cell disease

A
  • Infection - prophylactic penicillin and vaccinations
  • Stroke - chronic transfusion in high risk patients
  • Avoid precipitating factors e.g. cold, excessive exercise, dehydration
  • Crisis prevention, analgesia and supportive care
  • Transfusion - intermittent top up transfusion or exchange transfusion (to reduce HbS%) OR chronic transfusion and chelation
  • Hydroxycarbamide (increases HbF%)
  • Bone marrow transplant (curative)
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30
Q

Chronic complications of sickle cell disease

A
  • Chronic anaemia
  • End-organ damage e.g. renal failure, pulmonary hypertension, cerebrovascular disease, heart failure, splenic atrophy
  • Immunocompromise and increased risk of infection with encapsulated organisms
  • Transfusion-related complications e.g. iron overload, allo-antibody formation
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31
Q

How would you detect HbS in a patient with suspected sickle cell disease?

A

HPLC

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32
Q

Management of a painful vaso-occlusive episode in a patient with sickle cell disease

A
  • Adequate pain control within 60 mins of presentation e.g. IV morphine
  • Ensure adequate hydration e.g. IV fluids
  • Avoid/treat hypoxia e.g. oxygen
  • Examine/investigate for/treat infection e.g. antibiotics
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33
Q

How are newborns screened for sickle cell disease?

A

Guthrie heel prick test

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34
Q

Current life expectancy in sickle cell disease

A

50-60 years

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35
Q

Pathophysiology of thalassemia

A

Reduced rate of normal beta globin chain synthesis

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36
Q

If a patient has 1 or 2 abnormal alpha globin genes they will have …?

A

Alpha thalassemia trait

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37
Q

If a patient has 3 or 4 abnormal alpha globin genes they will have…?

A

Alpha thalassemia major (not usually compatible with life)

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38
Q

If a patient has 1 abnormal beta globin gene they will have…?

A

Beta thalassemia trait

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39
Q

If a patient has 2 abnormal beta globin genes they will have…?

A

Beta thalassemia major

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40
Q

Risk factors for thalassemia trait

A
  • Family history

- Ethnicity

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41
Q

Investigation results in a patient with alpha thalassemia trait

A
  • Mild anaemia or no anaemia
  • Normal HPLC
  • Normal ferritin

Alpha thalssemia trait is a diagnosis of exclusion.

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42
Q

Investigation results in a patient with beta thalassemia trait

A
  • Anaemia
  • Elevated HbA2
  • Normal ferritin
  • Very low MCV
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43
Q

Clinical features and investigation results in a patient with beta thalassemia major

A
  • Splenomegaly
  • Bony changes (e.g. skull bossing)
  • Failure to thrive
  • Jaundice
  • Gallstones
  • Severe hypochromic microcytic anaemia
  • Increased reticulocytes
  • HPLC: elevated HbA2, HbF and reduced HbA
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44
Q

Management of a patient with beta thalassemia trait

A

None needed if patient asymptomatic (avoid unnecessary iron supplementation)

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45
Q

Management of a patient with beta thalassemia major

A
  • Chronic transfusions + chelation therapy

- Bone marrow transplant

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46
Q

Complications of beta thalassemia major

A
  • Iron overload - leads to cardiac failure, liver failure, endocrine problems e.g. diabetes
  • Allo-antibody formation
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47
Q

Current life expectancy for patients with beta thalassemia major

A

40-50 years

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48
Q

Commonest severe inherited bleeding disorder

A

Haemophilia

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49
Q

Inheritance pattern of haemophilia

A

X-linked recessive - carrier mothers have a 50% chance of each son being affected and each daughter being a carrier

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50
Q

Factor affected in Haemophilia A

A

Factor VIII

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51
Q

Factor affected in Haemophilia B

A

Factor IX

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52
Q

Investigation results in a patient with Haemophilia

A
  • Isolated prolonged APTT (factors VIII and IX both part of intrinsic pathway)
  • Normal PT
  • Normal fibrinogen
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53
Q

Clinical features in a patient with haemophilia

A
  • Family history e.g. carrier mother, history of bleeding problems on haemostatic challenges
  • Birth history of bleeding on delivery
  • Prolonged bleeding, re-bleeding or excess bruising
  • Unusual surgical bleeding
  • Bleeding with IM injections, vaccinations or heel prick test
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54
Q

Categories of haemophilia

A
  • <1% factor VIII/IX = severe
  • 1-5 factor VIII/IX = moderate
  • 6-49% factor VIII/IX = mild

(50-150% = normal)

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55
Q

Symptoms of mild haemophilia

A
  • Bleeding with surgery or dental work

- Bleeding with major trauma

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56
Q

Symptoms of moderate haemophilia

A
  • Bleeding with minor trauma - SC or IM bleeds

- Occasionally spontaneous bleeds

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57
Q

Symptoms of severe haemophilia

A
  • Recurrent spontaneous joint bleeds leading to joint damage

- Spontaneous intra-cranial bleeds

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58
Q

Management of haemophilia

A

Recombinant synthetic factor VIII or IX

Tranexamic acid

Physiotherapy

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59
Q

Commonest inherited bleeding disorder

A

Von Willebrand disease

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60
Q

Clinical features of von Willebrand disease

A
  • Mucosal bleeding
  • Easy bruising
  • Dental bleeding
  • Epistaxis
  • Menorrhagia
  • Surgical and post-traumatic bleeding
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61
Q

Malignant cells in leukaemia are???

A

Blasts/haematopoetic stem cells/early progenitor cells (acute leukaemia) or myeloid cells or lymphocytes (chronic leukaemia)

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62
Q

Clinical features of acute leukaemia

A
  • Symptoms onset over days-weeks
  • Bone marrow failure symptoms e.g. anaemia, bleeding, infection
  • Hepatomegaly
  • Splenomegaly
  • Lymphadenopathy
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63
Q

Investigation results in acute leukaemia

A
  • Blasts seen in blood
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64
Q

Clinical features of chronic leukaemia

A
  • Symptoms onset over months-year
  • Hepatomegaly
  • Splenomegaly
  • Lymphadenopathy
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65
Q

Investigation results in chronic leukaemia

A
  • Leucocytosis
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66
Q

Laboratory definition of leukaemia

A

> 20% blasts seen in bone marrow

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67
Q

Pathological hallmark of AML

A

Auer rods

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68
Q

Clinical features of AML

A
  • Most common acute leukaemia in adults
  • Middle-aged to elderly patients
  • Short clinical history
  • Bone marrow failure symptoms
  • Infiltrates in liver, spleen and other tissue
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69
Q

Investigation results in AML

A
  • WCC elevated or reduced

- Coagulation disorders

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70
Q

Clinical features of ALL

A
  • Most common childhood malignancy
  • Children affected
  • Short clinical history
  • Bone marrow failure symptoms
  • Infiltrates in lymph nodes, bone, liver, spleen and CNS
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71
Q

Investigation results in ALL

A
  • WCC elevated or reduced
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72
Q

Investigations to consider in a patient with suspected leukaemia

A
  • Urgent FBC - will be abnormal
    AML/ALL: pancytopenia +/- circulating blasts
    CML: neutrophils and myeloid precursors
    CLL: lymphocytes
  • Blood film to look for circulating malignant cells
  • Urgent coagulation screen
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73
Q

Diagnostic test for leukaemia

A

Bone marrow aspirate and trephine from the posterior iliac crest

Can also do bone marrow examination under the microscope

Can do immunophenotyping to determine antigens on cell surface

Can do cytogenetic analysis to determine any genetic causes e.g. trisomy 8 (only present in blood cells)

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74
Q

Management of leukaemia

A
  • Chemotherapy - intensive regimes with multiple drugs, oral, IV or IT
  • Stem cell transplantation - allogenic transplant from sibling or unrelated donor
  • Monoclonal antibodies - Imatinib targeted at Philadelphia chromosome in CML
- Supportive care e.g.
Infection prophylaxis and treatment
Blood transfusion - red cells or platelets
Coagulopathy management
Central venous access
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75
Q

Clinical features and investigation results for a patient with CML

A
  • Age 40-60
  • Abdominal discomfort
  • Splenomegaly
  • Very high WCC - mostly neutrophils and precursors
  • Hyperviscosity - mucosal bleeding, shortness of breath, visual changes, neurological symptoms
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76
Q

Definitions of lymphomas

A

Malignancy of lymphocytes (T or B cells) in the lymph glands and other tissues

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77
Q

Pathological hallmark of Hodgkin’s lymphoma

A

Reed-Sternberg cells

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78
Q

Most common haematological malignancy

A

Non-Hodgkin’s lymphoma

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79
Q

Clinical features of Hodgkin’s lymphoma

A
  • Young adults and >50s
  • More common in men
  • Very aggressive symptoms
  • Asymmetrical painless superficial lymphadenopathy (usually cervical)
  • Organomegaly
  • Constitutional symptoms e.g. drenching night sweats, fever, weight loss, itch
  • Alcohol induced nodal pain
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80
Q

Clinical features of Non-Hodgkin’s lymphoma

A
  • 55-60 year olds
  • Varying clinical course
  • Lymphadenopathy
  • Organomegaly
  • Constitutional symptoms e.g. drenching night sweats, weight loss, fever, itch
  • Extra-nodal involvement more common
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81
Q

Features of pathological lymphadenopathy

A
  • > 1cm in size
  • Persistant
  • Painless
  • No reactive cause
  • Rubbery/matted texture
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82
Q

FBC results in lymphoma

A

May be NORMAL - will only be abnormal if bone marrow is involved

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83
Q

Diagnostic test for lymphoma

A

Lymph gland biopsy

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84
Q

Lymphoma management

A
  • Watchful waiting
  • Chemotherapy e.g. CHOP therapy
  • Targeted therapies e.g. Rituximab
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85
Q

Pathophysiology of multiple myeloma

A

Malignant proliferation of plasma cells within the bone marrow - these plasma cells secrete antibodies (para-proteins)

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86
Q

Main risk factor for multiple myeloma

A

Age

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87
Q

Clinical features of multiple myeloma

A
  • Bone pain and pathological fractures
  • Anaemia
  • Recurrent infections
  • Renal failure/AKI
  • Hypercalcemia
  • Hyperviscosity
  • Hyperuricaemia
  • Spinal cord compression
88
Q

Screening tests for multiple myeloma

A

1) Serum protein electrophoresis
2) Bence-Jones proteinuria

BOTH must be tested as some patients will have one and not the other

89
Q

Diagnostic test for multiple myeloma

A

Bone marrow aspirate and trephine

90
Q

Laboratory definition of multiple myeloma

A

> 10% clonal plasma cells on bone marrow aspiration

91
Q

Investigation results in multiple myeloma

A
  • Raised serum protein electrophoresis
  • Raised Bence-Jones proteinuria
  • Anaemia on FBC
  • AKI on U&Es
  • Hypercalcemia
  • Raised ALP
  • Raised ESR
92
Q

Definition of multiple myeloma

A

Evidence of multiple myeloma-related tissue impairment

93
Q

Definition of smouldering myeloma

A

Confirmed diagnosis of multiple myeloma but no evidence of multiple myeloma-related tissue impairment

94
Q

Management of multiple myeloma

A
  • Chemotherapy - usually intensive therapy and autologous stem cell transplant
  • Radiotherapy (bone pain and spinal cord compression)
  • Bisphosphonates e.g. monthly IV Zolendronate (for hypercalcemia and bone protection)
  • Adequate hydration e.g. 3l of 0.9% NaCl over 24 hours (to prevent renal failure)
  • Haematopoetic stem cell transplantation
95
Q

PT assesses the ??? pathway of the coagulation cascade

96
Q

APTT assesses the ??? pathway of the coagulation cascade

97
Q

A raised APTT and raised PT indicates a problem in the ??? pathway of the coagulation cascade

98
Q

A raised PT and normal APTT indicates a problem in the ??? pathway of the coagulation cascade

99
Q

A raised APTT and normal PT indicates a problem in the ??? pathway of the coagulation cascade

100
Q

Causes of a prolonged PT

A
  • Deficiency/inhibition of factors II, V, VII, X or fibrinogen
  • Warfarin use
  • Vitamin K deficiency
  • Liver disease (+++)
  • DIC
101
Q

Causes of a prolonged APTT

A
  • Deficiency/inhibition of factor II, V, VIII, IX, X, XII or fibrinogen (e.g. Haemophilia A or B)
  • Heparin therapy
  • Lupus anticoagulant/antiphospholipid disease
  • Liver disease (+)
  • DIC
102
Q

Causes of a raised fibrinogen

A
  • Acute phase response
103
Q

Causes of a lowered fibrinogen

A
  • Severe sepsis
  • DIC
  • Rare congenital states
104
Q

Risk factors for venous thromboembolism

A
  • Personal history of VTE
  • Pregnancy and puerperium
  • Oestrogen-containing medication e.g. Tamoxifen, COCP
  • Antiphospholipid antibodies (rare)
  • Prolonged immobility e.g. surgery, travel
  • Smoking
  • Obesity
  • Malignancy
  • Recent surgery
  • Family history
  • IVDU
  • Inherited thrombophilia
105
Q

Mechanism of action of heparins

A

Binds to antithrombin causing a conformational change and potentiating the action of antithrombin which inhibits factor Xa and thrombin (factor IIa)

106
Q

Administration method of unfractionated heparin

A

Continuous IV infusion

107
Q

Indications for use of unfractionated heparin over other anti-coagulants

A

Rapid reversibility required e.g. high bleeding risk, severe hepatic/renal failure

108
Q

Risk of heparins

A
  • Bleeding
  • Heparin-induced thrombocytopenia (risk lower in LMWH)
  • Heparin-induced osteoporosis (risk lower in LMWH)
109
Q

Monitoring of unfractionated hepatin

A

APTT ratio (compared to normal APTT) every 4-6 hours initially then daily once stable

110
Q

Reversal of heparin can be achieved with ??

111
Q

Administration method of LMWH

A

Once daily SC injection

112
Q

Indications for LMWH

A
  • DVT
  • Thromboprophylaxis
  • Pregnancy
113
Q

Contra-indications for LMWH

114
Q

When is monitoring indicated whilst using LMWH?

A
  • Pregnancy
  • Renal failure
  • In Children
115
Q

How would you monitor LMWH?

A
  • Anti-Xa assay
116
Q

Mechanism of action of warfarin

A

Prevents vitamin K ‘recycling’ by inhibiting vitamin K reductase and vitamin K epoxide reductase so reduces the rate of synthesis of vitamin K dependent clotting factors

117
Q

Drugs which interact with warfarin

A
  • Antibiotics e.g. erythromycin, clarithromycin, ciprofloxacin
  • NSAIDs
  • Amiodarone
  • Anti-epileptics
  • Azole anti-fungals
  • Statins
  • H2 receptor antagonists and PPIs
118
Q

How would you monitor a patient on warfarin?

119
Q

How would you reverse the effects of warfarin?

A

Oral/IV vitamin K (takes 6-12 hours to have an effect)
Or
Prothrombin concentrate complex (mix of vitamin K dependent factors made from donor blood)
Or
Fresh frozen plasma

120
Q

Contra-indications for warfarin

A

Pregnancy - warfarin is teratogenic

121
Q

Complications of warfarin

A
  • Bleeding
  • Thrombotic complications if dose is sub-therapeutic
  • Fetal toxicity
  • Interactions with medication and alcohol
  • Poor INR control in liver dysfunction
  • Itchy maculopapular rash
  • Alopecia
122
Q

Mechanism of action of DOACs

A

Directly inhibit coagulation factors - either thrombin (Dabigatran) or factor Xa (Apixaban, Rivoroxaban, Edoxaban)

123
Q

Advantages of DOACs compared to warfarin

A
  • Rapid onset and offset of action
  • Fewer drug interactions, no dietary interactions
  • Fixed dosing
  • No monitoring requirements
  • Overall lower risk of major bleeding, particularly intra-cranial haemorrhage
124
Q

Contra-indications to DOAC use

A
  • Pregnancy
  • End-stage cirrhosis
  • Caution should be used in renal disease
125
Q

Side effects of DOACs

A
  • Bleeding complications
  • GI upset
  • Alopecia
126
Q

Which anticoagulant should you use in a pregnant woman?

127
Q

Features of pseudomonas aeruginosa

A
  • Small gram negative bacilli
  • Aerobic
  • Oxidase positive
  • Produces diffusible pigments and appear green-blue colour on culture or when colonising wounds
  • ‘Freshly cut grass’ odour
  • Widespread in moist environments e.g. soil
  • Colonises moist sites on humans e.g. groin, axilla, ear, perineum
128
Q

Risk factors for pseudomonas infection

A
  • Immunocompromise/ neutropenia

- ITU admission

129
Q

Potential infections caused by pseudomonas aeruginosa

A
  • Line infection leading to bacteraemia
  • Catheter-associated UTI
  • Hospital/Ventilator acquired pneumonia
  • Surgical site infections
130
Q

Management of pseudomonas infection in Lothian

A

Vancomycin + Tazocin

131
Q

Features of strenotrophomonas maltophilia

A
  • Aerobic
  • Gram negative bacilli
  • Oxidase negative
  • Pale yellow colour on culture
  • Ammonia-like odour
132
Q

Risk factors for infection with Strenotrophomonas

A
  • Haematological malignancy
  • Immunocompromise/prolonged neutropenia
  • Prolonged treatment with carbapenems/Cephalosporins/Fluoroquinolone
  • Lines/intravascular devices or catheters
133
Q

Potential infections caused by strenotrophomonas

A
  • Bacteraemia (often secondary to line infection)
  • Respiratory infections
  • UTIs
134
Q

Antibiotics which strenotrophomonas is resistant to

A
  • Beta-lactams
  • Fluoroquinolones
  • Aminoglycosides
  • Carbapenems
    (- Disinfectants)
135
Q

Treatment of infection with strenotrophomonas in Lothian

A

Co-trimoxazole

136
Q

Features of pneumocystis

A
  • Unicelluar fungus

- Lacks ergosterol in it’s cell wall - so is resistant to many anti-fungals

137
Q

Risk factors for pneumocystis

A

Immunocompromise:

  • HIV patients
  • Haematological and other malignancies
  • Solid organ and bone marrow transplant recipients
  • Collagen vascular disorders on immunomodulator therapy
138
Q

Most common clinical presentation of pneumocystis infection

A

Pneumocystis pneumonia (from inhalation of cyst form of pneumocystis jirovecii:

  • Progressive dyspnoea
  • Fever
  • Non-productive cough
  • Tachycardia
  • Tachypnoea
  • Fine end inspiratory crackles
139
Q

An immunocompromised patient has bilateral diffuse interstitial infiltrates extending from the peri-hilar region on CXR. What is the most likely causative organism?

A

Pneumocystis jirovecii

140
Q

An immunocompromised patient has ‘ground glass’ changes in their lungs on high resolution CT scanning. What is the most likely cause of their pneumonia?

A

Pneumocystis jirovecii

141
Q

What is the diagnostic test for pneumocystis pneumonia?

A

Induced sputum or bronchoscopic alveolar lavage for immunofluorescent antibody staining

142
Q

Pneumocystis is easily cultured in the laboratory (true/false)?

A

False - pneumocystis can not be cultured in the lab

143
Q

First line management of pneumocystis pneumonia in Lothian

A

High-dose Co-trimoxazole (+ prednisolone if pO2 <9.3 kPa) for 14-21 days in immunocompromised patients (21 days in HIV patients).

144
Q

Methods for preventing infection with pneumocystis pneumonia

A
  • Primary or secondary chemoprophylaxis with co-trimoazole for as long as the patient is immunocompromised
  • Prevention of transmission/exposure e.g. isolate patient in side room with respiratory precautions
145
Q

Features of candida

A
  • Yeasts
  • Normal human commensal in skin, GI tract and GU tract
  • Gram positive
  • Small, thin-walled ovoid cells
  • Appear smooth creamy-white glistening colonies on blood agar
  • 5 species which most commonly cause invasive disease
    1) Candida albicans
    2) Candida glabrata
    3) Candida tropicalis
    4) Candida parapsilosis
    5) Candida krusei
146
Q

Risk factors for candidaemia

A
  • Exposure to broad-spectrum antibiotics
  • Presene of indwelling IV catheters
  • Neutropenia
  • Solid organ transplant recipients on immunosuppression
  • TPN
  • GI or thoracic surgery
147
Q

How would you confirm a diagnosis of candidaemia?

A

Blood cultures (from central and peripheral venous access if possible)

148
Q

Management of candidaemia

A
  • Anti-fungal treatment (Fluconazole or Caspofungin) for a minimum of 14 days from the first set of negative blood cultures
  • Repetition of blood cultures every 48 hours until cultures are negative
  • Removal of all indwelling catheters
  • Cardiology review and echocardiogram
  • Ophthalmology review and dilated eye examination within 1 week of diagnosis
  • Review potential sources of candidaemia e.g. GI and GU imaging
  • Identification and management of risk factors e.g. stop or narrow spectrum of antibiotics
149
Q

Complications of candidaemia

A
  • Endocarditis

- Endopthalmos and blindness

150
Q

Features of VRE

A
  • Gram positive cocci
  • Enterococci resistant to Vancomycin

(Usually E. faecium or E. faceless)

151
Q

Risk factors for VRE infection

A
  • Broad spectrum antibiotic treatment
  • IV lines/urinary catheter
  • Haematological malignancy
  • Increased age
  • Diabetes
  • Transplant recipient
  • Surgery
  • Long inpatient stay
  • ICU stay
152
Q

Potential infections caused by VRE

A
  • UTI
  • Bacteraemia
  • Endocarditis
  • Skin and soft tissue infections
  • Intra-abdominal/pelvic infections

(VRE can be carried in the gut without symptoms)

153
Q

Which antibiotics are VRE resistant to?

A
  • Aminoglycosides
  • Carbapenems
  • Cephalosporins
  • Macrolides
  • Penicillins
  • Quinolones
  • Tetracyclines
154
Q

Management options for VRE infections

A
  • Linezolid

- Daptomycin

155
Q

VRE infection control and prevention measures

A
  • Antimicrobial stewardship
  • Patient isolation
  • Contact precautions
  • Dedicated single patient equipment
  • Staff PPE and hand washing
  • Daily and terminal decontamination of patient bed area, room and sanitary facilities
156
Q

Main risk factors for line infections

A

Immunocompromise

157
Q

Management of a line associated infection

A
  • Blood cultures from line and peripheral sites
  • Line removal
  • Antibiotics (duration depends on organism cultured)
  • Daily review of all exit sites
158
Q

Interventions which reduce the infective complications of CVCs

A
  • Removal of catheters discussed daily
  • Early removal of unnecessary catheters
  • Check list for CVC insertion and maintenance bundle
  • Documentation of time and date of catheter insertion
  • Hand washing, aseptic technique and PPE use during insertion
  • Education
159
Q

Features of Staph Aureus

A
  • Coagulase positive
  • Gram positive cocci
  • Virulent - produces toxins
  • Commensal which colonises 30% of the population - found in nose, respiratory tract and on skin
  • Transmitted from person to person via contact
160
Q

Which antibiotic is MRSA resistant to?

A

Flucloxacillin

161
Q

Management of S. Aureus bacteraemia

A

At least 2 weeks IV Flucloxacillin

Vancomycin in patients with penicillin allergy or MRSA

162
Q

Most common cause of line infections in patients with haematological malignancies

A

S. epidermidis (60% of line infections are coagulase negative Staphs)

163
Q

Features of S. epidermidis

A
  • Coagulase negative
  • Gram positive cocci
  • Less virulent than S. Aureus
  • Forms biofilms on plastic devices
  • Normal skin flora
  • Can be pathogenic in immunocompromised hosts
164
Q

Functions of the spleen

A
  • Filtration of damaged cellular material, RBCs, antibodies, bacteria and parasites
  • Regulation of inflammation
  • Immunity - maturation of T and B-cells
  • Haemostasis
165
Q

Causes of asplenia

A
  • Congenital
  • Surgery
  • Splenic infarction
166
Q

Causes of acquired hyposplenia

A
  • Sickle cell anaemia
  • Graft vs Host disease
  • Coeliac disease
  • HIV
  • ALD
  • IBD (mainly UC)
  • Primary amyloidosis
  • SLE
167
Q

Bacterial organisms most associated with post-splenectomy sepsis

A

Encapsulated bacteria e.g. Streptococcus Pneumoniae, Haemophilus influenzae type B and Neisseria meingitidis

168
Q

Which of the following is LEAST likely to cause sepsis in a patient following a splenectomy?

a) S. Aureus
b) Streptococcus pneumoniae
c) Haemophilus influenzae type B
d) Neisseria meningitidis

A

a) S. Aureus - the others are all encapsulated organisms

169
Q

Parasites most commonly associated with post-splenectomy sepsis

A

Red cell parasites:

  • Babesia microtia
  • Plasmodium falciparum

Anasplama/human granulocytic ehrlichiosis

170
Q

Pathological hallmark of Babesia microtia infection

A

Maltese cross sign on histology

171
Q

Risk factors for post-splenectomy sepsis

A
  • Extremes of age
  • Recent splenectomy (0-90 days)
  • Indication for splenectomy (immune cytosine is higher risk than trauma)
  • Haemoglobinopathies
  • Lack of appropriate vaccinations pre-splenectomy
  • Immunosuppressant treatment
  • HIV
    Amyloidosis/sarcoidosis
  • Autoimmune disease
  • Splenic radiation
172
Q

Methods for prevention of post-splenectomy infection

A

1) Prophylactic antibiotics
- Penicillin V 250-500mg BD, lifelong OR
- Clarithromycin 250mg OD, life long
(Can consider rescue therapy instead in low risk patients)

2) Vaccinations
- Pneumococcal - ideally 4-6 weeks before splenectomy or 2 weeks after, repeated every 5 years
- Meningococcal
- Influenza (as soon as practicable pre- or post-splenectomy, repeated annually

3) Avoidance of parasite vectors in endemic regions
4) Avoidance of dog bites/scratches

173
Q

Clinical features of an acute haemolytic transfusion reaction

A
  • Collapse within a few minutes of starting transfusion
  • Dark urine
  • Renal failure
  • DIC
174
Q

Clinical features of delayed haemolytic transfusion reaction

A
  • Occurs several days after transfusion
  • Haemoglobin fails to rise after transfusion
  • Patient becomes jaundices
  • Dark urine
  • Direct anti-globulin test
175
Q

Clinical features of a minor allergic reaction

A
  • Urticarial or itchy rash
  • Respiratory wheeze
  • More common after plasma or platelet transfusion
  • History of other allergies or atopy
176
Q

Clinical features of a minor febrile reaction

A
  • Mild rise in temperature
  • Rigors
  • More common after RBC or platelet transfusion

(Much rarer now transfused blood is leucodepleted)

177
Q

Clinical features of anaphylaxis after transfusion

A
  • Presents suddenly immediately after transfusion
  • Hypotensive shock
  • Breathlessness
  • Wheeze
  • Laryngeal and facial oedema
178
Q

Commonest cause of death related to transfusion

A

Transfusion associated circulatory overload

179
Q

Risk factors for TACO

A
  • Extremes of age
  • Renal impairment
  • Heart failure
180
Q

Management of TACO

181
Q

Clinical features of TRALI

A
  • Severe breathlessness
  • Hypoxia
  • Occurs with 6 hours
182
Q

Typical CXR appearance of TRALI

A

Bilateral pulmonary infiltrates

183
Q

Biggest risk factor for TRALI

A

Donor platelets from a women

184
Q

Risk factors for TA GvHD

A
  • Immunosuppression

- HLA-matched/HLA similar

185
Q

Investigations results which would indicate haemolysis is occurring

A
  • Decreased haemoglobin
  • Increased unconjugated bilirubin
  • Increased LDH
  • Increased reticulocytes
  • Increased urinary urobilinogen
  • Folate deficiency
  • Thrombocytosis
  • Neutrophilia
  • Immature granulocytes
186
Q

Differentials for spherocytes seen on blood film

A
  • Autoimmune haemolysis

- Hereditary spherocytosis

187
Q

Differential for schistocytes seen on blood film

A
  • Micro-angiopathic haemolysis
188
Q

Causes of intra-vascular haemolysis

A
  • ABO transfusion reactions
  • Paroxysmal nocturnal haemolgobinuria
  • Infections e.g. malaria, C. perfringens
  • Heart valves
  • DIC
  • Enzymopathies e.g. G6PD deficiency
189
Q

Intra-vascular haemolysis causes a ??? in haptoglobin

190
Q

Pathophysiology of inherited spherocytosis

A

Red cell membrane defect, meaning each time these cells pass through the spleen they lose some elasticity and lost membrane relative to cell volume, causing increased MCHC, abnormal cell shape and haemolysis

191
Q

Inheritance pattern of inherited spherocytosis

A

Autosomal dominant

192
Q

Investigation results seen in inherited spherocytosis

A

Mostly asymptomatic patients with compensated chronic haemolytic state:

  • Spherocytes seen on blood film but Coomb’s test NEGATIVE
  • Reticulocytosis
  • Mild hyperbilirubinaemia
  • Pigmented gallstones
193
Q

3 potential crises of inherited spherocytosis

A

1) Haemolytic crisis - severity of haemolysis increases, usually associated with infection
2) Megaloblastic crisis - follows development of folate deficiency, usually during pregnancy
3) Aplastic crisis - occurs with parvovirus - patients present with anaemia and low reticulocytes

194
Q

Management of hereditary spherocytosis

A
  • Lifelong folic acid 5mg
  • Consider splenectomy in severe haemolysis with complications
  • Management of acute, severe haemolytic crisis with blood transfusion
195
Q

Most common human enzymopathy

A

G6PD deficiency

196
Q

Inheritance pattern of G6PD deficiency

A

X-linked - usually affects males

197
Q

Clinical features of G6PD deficiency

A
  • Acute drug induced haemolysis (aspirin, anti-malarials, antibiotics, quinidine, probenecid, vitamin K, dapsone)
  • Chronic compensated haemolysis
  • Infection or acute illness
  • Neonatal jaundice
  • Favism (acute haemolysis after eating broad beans)
198
Q

Blood film features of G6PD deficiency

A
  • Bite cells
  • Blister cells
  • Irregularly shaped small cells
  • Polychromasia (reflecting reticulocytosis)
  • Heinz bodies
199
Q

Management of G6PD deficiency

A
  • Avoid precipitants

- Treat underlying infection

200
Q

Pathophysiology of autoimmune haemolytic anaemia

A

Increased red cell destruction due to red cell autoantibodies - IgM or IgG, causing intravascular or extravascular haemolysis

201
Q

Investigation results in autoimmune haemolytic anaemia

A

Blood film:

  • Haemolysis
  • Spherocytes
  • Polychromasia

Direct Coomb’s test:
- POSTIVE

202
Q

Management of warm autoimmune haemolysis

A
  • Treat underlying causes
  • Stop implicated drugs
  • Management of haemolysis
    1) PO prednisolone then taper dose
    2) Immunomodulation/suppression e.g. rituximab
    3) Splenectomy
    4) Transfusion in life-threatening problems
203
Q

Pathophysiology of ITP

A

Immune-mediated disorder with autoantibodies directed against platelet membrane proteins IIb or IIIa which sensitise the platelet and result in it’s premature removal from the circulation

204
Q

Conditions associated with ITP

A
  • Connective tissue disease
  • HIV infection
  • B-cell malignancies
  • Pregnancy
  • Drug therapy
205
Q

Clinical features of ITP

A
  • Spontaneous bleeding
  • Easy bruising
  • Epistaxis
  • Menorrhagia
  • Asymptomatic
206
Q

Investigation results in ITP

A
  • Normal FBC except thrombocytopenia
  • Increased megakarocytes on bone marrow aspiration
  • Autoantibodies (present in connective tissue disease)
207
Q

Features which indicate no treatment is required in ITP

A
  • Stable, compensated disease

- Platelets >30

208
Q

Management of ITP patients with spontaneous bleeding

A

1) High dose glucocorticoids
2) Plus IV immunoglobulins (in severe haemostatic failure, evidence of significant mucosal bleeding or slow response to steroids alone)
3) Plus platelet transfusion (in life-threatening bleeding)

209
Q

Management of ITP relapses

A

1) Glucocorticoids
2) Thrombopoietin receptor agonists, splenectomy or immunosuppression (if >2 relapses or primary refractory disease present)

210
Q

Pathophysiology of haemolytic disease of the newborn

A

IgG antibodies from the mother cross the placenta and attack the foetal red blood cells, causing haemolysis

211
Q

Clinical features of haemolytic disease of the newborn

A
  • Anaemia - heart failure, pallor, hepatosplenomegaly, oedema, respiratory distress
  • Jaundice within 24 hours of birth
  • Kernicterus
212
Q

Investigations and potential results in haemolytic disease of the newborn

A
  • Blood film: reticulocytosis, erythroblasts
  • Positive direct Coomb’s test
  • LFTs: elevated cord bilirubin
  • FBC: neutropenia, neonatal alloimmune thrombocytopenia

(Mother will have positive indirect Coomb’s test)

213
Q

Management options for haemolytic disease of the newborn (after birth)

A
  • Temperature stabilisation
  • Phototherapy
  • IV immunoglobulin
  • Transfusion with compatible packed red cells
  • Exchange transfusion with blood type compatible with mother and infant
  • Sodium bicarbonate to correct acidosis
214
Q

Pathophysiology of DIC

A

Generalised activation of the clotting pathways, resulting in the formation of intra-vascular fibbing and thrombotic occlusion of small and medium vessels and end-organ damage

215
Q

Causes of DIC

A
  • Infection e.g. sepsis, Rocky Mountain spotted fever, malaria
  • Obstetric complications e.g. miscarriage, amniotic fluid embolism, eclampsia
  • Tissue trauma e.g. burns
  • Malignancy
  • Drugs e.g. quinine, cocaine
  • Liver failure
  • Acute pancreatitis
  • Transfusion reactions
  • Respiratory distress syndrome
216
Q

Investigation results seen in DIC

A
  • Prolonged APTT and PT
  • Increased fibrin
  • Decreased antithrombin or protein C
  • Decreased fibrinogen
  • Thrombocytopenia
  • Schistocytes on blood film
217
Q

Management options for DIC

A
  • Treat underlying cause
  • FFP and platelets
  • Cryoprecipitate
  • Antithrombin treatment
  • Unfractionated heparin

Year 5 (9 decks)

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