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Rapid review > Haematology and immunology > Flashcards

Haematology and immunology Flashcards

1
Q

ALL - high yield information?

A
  • Most common cancer of childhood
  • Bone pain, CNS involvement and orchidectomy are common + lymphadenopathy
  • B-cell ALL: CD19+
  • T-cell ALL: CD3+
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2
Q

CLL - high yield information?

A
  • Smear cells on microscopy
  • Lymphaedenopathy - often found incidentally
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3
Q

AML - High yield information?

A
  • More common in adults: poor prognosis
  • Gum hypertrophy
  • MPO +ve
  • Auer rods on microscopy
  • May be a result of progression from myelodysplastic syndrome
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4
Q

CML - high yield information?

A
  • Poor prognosis
  • Numerous myeloid cells on microscopy
  • Massive splenomegaly
  • > 80% have philadelphia chromosome (t(9;22) - associated with better prognosis
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5
Q

Hodgkins leukaemia high yield information?

A
  • proliferation of Reed-Sternberh cells (owl-eye nuclei)
  • Young adults and older adults
  • neck mass, pain on alcohol consumption
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6
Q

Non-Hodgkins leukaemia high yield information?

A

All other lymphomas without Reed-sternberg
cells.
* Monomorphic sheets of lymphoma cells on a
slice.
* More likely to experience B-symptoms
* Better prognosis than Hodgkin’s
* Split into high grade and low grade

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7
Q
A

Auer rods -AML

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8
Q
A

Smudge cells (CLL)

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9
Q
A

Popcorn cells - NHSL

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10
Q
A

Classical reed-stern berg cell - HL

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11
Q
A

‘Starry sky’ - Burkett’s lymphoma

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12
Q

Approach to a blood film?

A

1) What is the size
2) What is the shape
3) What is the colour
4) Are there any inclusions

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13
Q
A

Sickle cell anaemia
- Sickle cells
- Aniscytosis
- Polikilocytosis

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14
Q
A

Iron deficiency anaemia

  • Anisopoikilocytosis
  • Poikilocytes (pencil cells)
  • Target cells
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15
Q
A

Thalassaemia
- Mild hypochromic, microcytic anaemia
- Target cells

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16
Q
A

Hyposplenism

Asplenism/hyposplenism leads to different INCLUSIONS.
1) Howell jolly bodies
2) Siderotic granules (also seen in disorders of iron utilization
like sideroblastic anaemias).
3) Heinz bodies

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17
Q
A

Liver Disease
* Macrocytic cells
* Target cells
* Somatocytes (coffee-bean)
* Echinocytes (burr)
* Acanthocytes (spur)

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18
Q
A

Schistocytes (RBC fragment):
* DIC
* Microangiopathic haemolytic anaemia (HUS, TTP),
* Burns,
* Metallic Heart valve

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19
Q
A

Tear drop poikilocytes:
* Myelofibrosis (characteristic!)
* Extramedullary haematopoeisis

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20
Q

Things which cause EPO differences?

A

EPO may be low in CKD or polycythaemia vera
EPO high in EPO-secreting kidney malignancies

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21
Q

Reticulocytosis causes?

A

Acute bleeding

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22
Q

Reticulocytopenia causes

A
  • AOCD
  • CKD (eGFR <60) due to decreased renal synthesis of EPO
  • Parvovirus B19 espeically in sickle cell anaemia
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23
Q

Microcytic anaemia causes?

A
  • iron deficiency
  • Anaemia of chronic disease
  • Sideroblastic anaemia
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24
Q

Normocytic anemia causes?

A

Hyperproliferative:
- Acute blood loss
- haemolytic anaemia

Hypoproliferative
- Anaemia of chronic disease
- Bone marrow failure
- Renal failure

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25
Q

Macrocytic anaemia causes?

A

megaloblastic
- Vit B12 deficiency
- Folate deficiency
- Anti-folate drugs

Non megaloblastic
- Hypothyroidism
- Alcohol
- Myelodysplasia

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26
Q

When should patients with IDA be referred to gastroenterology clinic?

A
  • All men and post-menopausal women (unless
    overt non-GI bleeding)
  • All >50 or FH of colorectal carcinoma
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27
Q

When should premenopausal women be referred to gastroenterology clinic for IDA?

A
  • Colonic symptoms, strong FH OR persistent
    despite tx
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28
Q

When should IDA be referred to 2ww endoscopy?

A

Either:
- >60
- <50 + rectal bleeding

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29
Q

Which investigations should be carried out for serious anaemia?

A

Should mention in your answers:
* Coeliac serology screen +/- OGD with a biopsy of the second part
of the duodenum
* Colonoscopy – especially if male and >60y/o
Consider:
* CT – renal, small bowel and pancreas

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30
Q

Summarise ALL the coeliac serology

A
  • Total IgA +IgA anti-TTG + IgA anti-EMA
  • AND IgA anti-DGP
  • AND IgG anti-DGP
    IgG is used to further screen for celiac disease in individuals with
    IgA deficiency
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31
Q

Causes of B12 deficiency

A

Malabsorption:
1) GASTRIC
* Autoimmune (pernicious anaemia – atrophic gastritis)
* Gastrectomy/Bariatric surgery
* Chronic inflammation of gastric mucosa

2) INTESTINAL CAUSES
* Ileal resection or severe Crohn’s disease with terminal ileitis
* Fish tapeworm
* Metformin

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32
Q

Causes of folate deficiency

A
  1. DIETARY !!
  2. MALABSORPTION (coeliac disease)
  3. DRUGS
    * Anticonvulsants: phenytoin, valproate, carbamazepine
    * Methotrexate, trimethoprim (do not co-prescribe) and sulphasalazine
  4. MIXED: liver disease, alcoholism
  5. Excess utilisation
    * Physiological – pregnancy, lactation, prematurity
    * Pathological - haematological eg haemolytic anaemias, malignancy,
    inflammatory disease, psoriasis, rheumatoid
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33
Q
A

Atrophic gastritis mucosa
histology:
* Loss of parietal cells
* Chronic inflammatory infiltrate
* Goblet cell metaplasia
* ECL hyperplasia

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34
Q
A

Classically, coeliac disease has
the triad of:
1. Intraepithelial
lymphocytosis (IEL>30/100
epithelial cells),
2. Lamina propria
inflammation
3. Villous atrophy

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35
Q

Sickle Cell Anaemia – Genetics

A

Genetics:

  • AUTOSOMAL RECESSIVE mutation of the beta-
    globin chain
  • Mutant haemoglobin S (HbS) sickles at low
    PO2/acidic environments.
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36
Q

Sickle Cell Anaemia – Pathology

A
  • Fetal haemoglobin (HbF) is usually replaced by haemoglobin A (HbA) at ~6 weeks of age, and is entirely replaced by 6months.
  • Sickling makes RBCs more fragile, leading to a haemolytic anaemia, microvascular occlusion and other crises
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37
Q

Vaso-occlusive painful crisis

A

PRESENTATION: Symptoms are typically pain, fever and those of the triggering infection.

Areas affected: swollen painful joints, mesenteric ischaemia, CNS infarction, avascular necrosis (especially of femoral head), renal papillary necrosis (loin pain), dactylitis

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38
Q

Vaso-occlusive painful crisis - pathophysiology?

A

Due to microvascular occlusion, causes ischaemia and infarction especially in the bone marrow causing severe pain

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39
Q

Acute chest syndrome

A

Vaso-occlusive crisis in the lungs
Acute chest syndrome is a medical emergency with a high mortality.

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40
Q

Aplastic crisis - trigger

A

Usually due to parvovirus B19 infection, often in children

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41
Q

Aplastic crisis - pathophysiology

A

Sudden reduction in marrow production, especially RBCs
* Sudden fall in Hb, low reticulocytes. THIS IS HOW YOU DIFFERENTIATE WITH ACUTE SEQUESTRATION CRISIS

42
Q

Splenic sequestration crisis - pathophysiology

A

sickling of RBCs in the spleen → pooling and sequestration of blood → acute fall in haemoglobin, severe anaemia and potential circulatory collapse (hypovolaemic shock)

Associated with an increased reticulocyte count

43
Q

Splenic
sequestration
crisis - presentation?

A

organomegaly, severe anaemia and shock

44
Q

Splenic
sequestration
crisis - presentation?

A

organomegaly, severe anaemia and shock

45
Q
A

Kidney - Sickle cell crisis

Histology: Classically glomerular
capillary occlusion and extensive
peritubular capillary congestion by
sickled cells

46
Q

‘Special requirements’ on form when requesting blood transfusion

A

Among others
* Severe congenital immunodeficiencies
* Certain types of chemotherapy (lymphoma)
* Hodgkin’s lymphoma
* Females of below and current reproductive age

47
Q

Name the different blood
groups that are ‘grouped’
or ‘screened’

A

Different antigens:
* ABO
* Rh
* Kell
* Several others e.g. Duffy

48
Q

Extrinsic
pathway - test?

A

PT time

49
Q

Intrinsic
pathway - test?

A

aPTT time

50
Q

PT time affected by?

A
  • Warfarin
  • Extrinsic
  • Liver disease
  • K vitamin deficiency (1972 - II, VII, IX, X)
51
Q

aPTT time affected by?

A
  • Antiphospholipid syndrome
  • Haemophilia
  • Von Willebrand disease
  • Heparin
52
Q

Warfarin - MOA?

A

Vitamin K antagonist, hence inhibits clotting factor II, VII, IX and X

53
Q

Warfarin - Side-effects?

A
  • haemorrhage
  • teratogenic, although can be used in breastfeeding mothers
54
Q

Warfarin - clinical use?

A

specific circumstances we use Warfarin over DOACs
* mechanical heart valves
* APLS secondary prophylaxis
* Generally, 2nd line after DOACs
* Severe renal failure where DOACs are not appropriate

55
Q

Warfarin reversal?

A

Exact management depends on urgency of reversal, size of bleed and INR
- Tranexamic acid
- Vitamin K (oral or IV)
- Prothrombin complex concentrate (PCC) - Beriplex

56
Q

Warfarin - bridge?

A

Warfarin preferentially decreases protein C and S first causing a transient increase in thrombosis risk so LMWH bridge is always given when starting Warfarin (usually for at least a few days until INR >2 for 2 consecutive readings)

57
Q

Heparin - MOA?

A

Heparin binds to antithrombin and POTENTIATES its action of inhibiting factor 10a and thrombin

58
Q

Heparin types?

A
  • Low molecular weight: Frequent monitoring needed, can be rapidly reversed
  • Unfractionated heparin: Okay in renal failure
59
Q

Heparin - Contraindications?

A

known hypersensitivity, active bleeding (excluding menstruation), bleeding disorder, severe hepatic impairment

60
Q

Heparin - complications?

A
  • Osteopenia if long-term
  • Heparin-induced thrombocytopenia
    (HIT)
  • Heparin-induced skin necrosis
  • Systemic anaphylactoid reaction
61
Q

Direct Oral Anticoagulants (DOACs/NOACs) - advantages?

A
  • Fixed once or twice daily dosing
  • No routine monitoring required
  • Predictable pharmacology
  • Peak effect occurs in HOURS vs days in Warfarin
62
Q

Direct Oral Anticoagulants (DOACs/NOACs) - caution?

A

NOT METALLIC HEART VALVES (warfarin), in pregnancy, in
severe renal failure or APLS.

63
Q

DOAC reversal agents:

A
  • Xa inhibitors = PCC
  • Dabigatran = Idarucizumab
    (Praxbind)
  • Rivaroxaban = Andexanet Alfa
64
Q

Investigations you should do in NAI

A

Initial blood tests:
* FBC and blood film
* Clotting screen (PT, aPTT, fibrinogen and
thrombin time)

Further bloods:
* Discuss with haematology about the need for 2nd line investigations:
* VWF
* Factor assays (especially factor VIII),
* platelet aggregation and

Rarer causes of bleeding/clotting disorders:
* Vitamin C deficiency
* Connective tissue disorders e.g. Ehlers Danlos
* Copper deficiency
* Zinc deficiency

Imaging:
* Skeletal survey
* CT head scan
* Bone profile
* Rule out leukaemia, ITP etc.
* Fundoscopy (retinal haemorrhages)

65
Q

Thrombin time (TT)- Measures?

A

measures the common pathway
measures fibrinogen to fibrin
Beware of heparin contamination

66
Q

Reptilase time?

A

To get around the heparin contamination

If TT is prolonged, but Reptilase time is normal, there is heparin contamination

67
Q

Causes of thrombocytopenia – Framework

A

1) Reduced production -> congenital or Aquired
2) Increased consumption -> Immune or Non-immune

68
Q

CONGENITAL causes of thombocytopaenia?

A
  • Bone marrow failure syndromes -Fanconi anaemia
  • Rare inherited platelet disorders e.g. Wiscott Aldrich
69
Q

ACQUIRED causes of thrombocytopenia

A
  • Aplastic anaemia
  • Infection: CMV, HIV,
    parvovirus
  • Liver disease
  • Bone marrow infiltration in
    cancer
70
Q

IMMUNE causes of thrombocytopenia?

A
  • ITP (diagnosis of
    exclusion)
  • Drug-induced
  • Other autoimmune
    disease e.g. SLE
71
Q

NON-IMMUNE causes of thrombocytopenia

A
  • DIC
  • Thrombotic microangiopathies
    e.g. TTP, HUS
  • Mechanical loss e.g. dialysis,
    ECMO
72
Q

Haemophilia - definition?

A

Inherited deficiency of a clotting
factors 8/9/11
* Usually INHERITED X-LINKED
* aPTT!!

73
Q

Haemophillia 3 subtypes?

A
  • Haemophilia A: factor 8 deficiency
  • Haemophilia B: factor 9 deficiency
  • Haemophilia C: RARE - factor 11 deficiency
74
Q

Haemophillia presentation?

A

Symptoms usually begin in neonates or early childhood
* Typically very DEEP bleeding (unlike e.g. vWD
which presents with platelet-bleeding i.e. Epistaxis,
menorrhagia etc)
* Untreated haemoarthroses lead to joint contractures.

75
Q

Haemophillia - management?

A

IV factor infusions +/- desmopressin
Emicizumab (Hemlibra)

76
Q

Complications of donor clotting factors in the
management of haemophilia

A

Production of recipient antibody against factor VIII or IX - Results in treatment becoming ineffective

Blood born viruses - HIV and Hep C

77
Q

Von Willebrand Disease - definition?

A

Defects in either the
amount, structure or function of vWF.
Inherited AUTOSOMALLY (both
recessive and dominant).

78
Q

Von Willebrand Disease = Pathophysiology

A

vWF produced in endothelial cells and megakaryocytes.
* Role of von Willebrand factor
1. Cofactor for platelet adhesion to damaged endothelium (vWF in the multimeric form is required)
2. Carrier protein for factor 8 (vWF stabilises factor VIII).

79
Q

THREE subtypes of von Willebrand disease:

A

o Type 1 (80%) - low levels of normal vWF - AUTOSOMAL
DOMINANT
o Type 2 - normal levels of vWF but abnormal function -
AUTOSOMAL DOMINANT
o Type 3 - there is NO von Willebrand factor and low/no
Factor VIII - AUTOSOMAL RECESSIVE, most severe form

80
Q

Von Willebrand Disease - Diagnosis?

A
  1. Stress releases vWF into the blood stream → masking low levels
  2. Differences with blood group O (naturally lower levels)
81
Q

Von Willebrand Disease - Management?

A
  • Avoid anti-platelet drugs
  • Antifibrinolytics e.g. tranexamic acid (TXA)
  • Desmopressin (DDAVP)
82
Q

Primary haemostasis - what is it?

A

Think of this as a problem with the initial
platelet plug forming (and therefore presenting
broadly like a platelet issue).

83
Q

Secondary haemostasis = what is it?

A

Think of this as a problem with the secondary
coagulation cascade (and presenting like a
‘coagulation’ issue).

84
Q

Primary haemostasis presentation?

A

PRESENTATION: superficial bruises/petechiae,
bleeding of mucosal membranes, epistaxis,
menorrhagia.

85
Q

Secondary haemostasis presentation?

A

bruising in deeper tissues,
muscles, joints (haemarthroses).

86
Q

Primary haemostasis - causes?

A

vWD, ITP, Glanzmans

87
Q

Secondary haemostasis - causes?

A

Deficiency of factor VIII, IX, factor XIII
(Haemophilia)
Liver problems

88
Q

Neutrophils - pathogens?

A

Bacteria: especially Staph. aureus

Fungi: invasive fungal species e.g. aspergillus, disseminated candida

89
Q

Signs of Immunodeficiency?

A

“SPUR”
- Serious infections
- Persistent infections
- Unusal infections
- Recurrent infections

90
Q

SCID - what is it?

A

a group of rare disorders
caused by mutations in genes involved in
the development and function of B and T
cells.

91
Q

SCID - genetics?

A

Most SCID is an autosomal recessive
Some are X linked

92
Q

SCID - treatment?

A

HSC transplant, ideally from a
sibling who is a close tissue match. Transplants
from matched siblings lead to the best
restoration of immune function,

93
Q

BTK deficiency - also known as?

A

(X-linked
agammaglobulinemia)

94
Q

BTK deficiency presentation?

A

BTK deficiency leads to an absolute deficiency of mature B cells (and hypogammaglobulinaemia).

Symptoms present as soon as the protective effect of maternal
immunoglobulins wanes at around six months of age.

95
Q

BTK deficiency - PATHOPHYSIOLOGY?

A
  • Bruton’s tyrosine kinase is expressed during the pre-B cell stage.
  • Signalling through it is ESSENTIAL for B-cell survival and differentiation.
96
Q

Flow cytometry in BTK deficiency?

A

If flow cytometry shows no mature B cells (CD19+), and there is a hypogammaglobulinaemia, think BTK.

97
Q

Chronic granulomatous disease - definition?

A

Primary immunodeficiency caused by X-linked recessive mutation in NADPH oxidase gene.

Remember that this effectively leads to lack of neutrophils → this means that you are unable to clear bacterial infections, and form lots of chronic granulomas (hence the name)!

98
Q

Chronic granulomatous disease - pathophysiology

A
  • NADPH is required to produce the oxidative
    burst in neutrophils that usually kills and lyses
    ingested bacteria.
  • Deficiency results in an inability to form the
    oxidative burst in neutrophils = inability to clear
    infections
99
Q

Chronic granulomatous
disease presentation?

A

NEUTROPHIL deficiency so especially
susceptible to Catalase positive organisms
(Staphylococci, Listeria, Corynebacterium diphtheriae).

Presents with abscesses, periodontal disease
INVARIABLY CAUSED BY STAPH AUREUS → fibrosis of
viscera.

100
Q

Chronic granulomatous
disease - diagnosis?

A

Diagnosis can occur by either nitroblue tetrazolium test
negativity or dihydrorhodamine flow cytometry

Rapid review (7 decks)

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