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Year 6 Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the features of warm AIHA?

A 
37 degree
IgG
extravascular haemolytic
\+ve Coombs test
Blood film - spherocytes
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2
Q

What are the causes of warm AIHA?

A 
Mainly primary idiopathic
Lymphoma
CLL
SLE
Methyldopa
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3
Q

What are the features of cold AIHA?

A 
<37 degrees
IgM
intravascular haemolytic
\+ve Coombs
Often with Raynauds
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4
Q

Causes cold AIHA?

A 
primary idiopathic
lymphoma
infections
EBV
mycoplasma
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5
Q

Management warm AIHA?

A

Steroids
splenectomy
Immunosuppression

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6
Q

Management cold AIHA?

A

Treat underlying condition
avoid the cold
chlorambucil

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7
Q

Causes of inherited haemolytic anaemia?

A

membrane - hereditary spherocytosis
cytoplasm - G6PD deficiency
haemoglobin - SCD or thalassaemia

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8
Q

Causes of acquired haemolytic anaemia?

A

immune mediated:
cold/warm
alloimmune

non immune mediated: 
infection (malaria)
paroxysmal nocturnal haemoglobunuria
prosthetic heart valves
MAHA
- adenocarcinoma
- HUS
- TTP
spherocytosis -ve coombs test
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9
Q

what is the HUS triad?

A

MAHA
thrombocytopenia
AKI
(e.coli toxin 0157)

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10
Q

how does adenocarcinoma cause haemolytic anaemia?

A

releases granules into circulation
pro-coagulant and active coag cascade
platelet activation, fibrin deposition, degranulation
red cell fragmentation due to low grade DIC
bleeding (low platelet and coagulation factor deficiency)

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11
Q

TTP pentad?

A 
MAHA
thrombocytopenia
AKI
neurological impairment
fever
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12
Q

what causes TTP?

A

Deficiency in VWF cleaving protease -> high VWF -> cheese wire in blood vessels
Autoimmune: anti-glycoprotein 2b/3a antibody

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13
Q

Mx TTP?

A

plasma exchange

NOT STEROIDS

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14
Q

Findings on TLS Ix?

A

hyperkalaemia
hyperphosphataemia
hypocalcaemia
+ clinical features

lab
>=2 of: within 7 days chemo or 3 days before
Uric acid >475 umol/l or >25% increase
K>6 mmol/l or 25% increase
PO4 >1.125 or 25% increase
Ca <1.75 or 25% decrease

clinical:
>=1.5x ULN creatinine
cardiac arrhythmia or sudden death
seizure

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15
Q

Mx TLS?

A

prophylaxis:
high risk: IV allopurinol or IV rasburicase
low risk: PO allopurinol

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16
Q

Indications for packed RBC transfusion?

A

no ACS - maintain >70 x10^9/L

ACS - maintain >80

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17
Q

Indications for platelet transfusion?

A

pre-procedure - maintain >50 x10^9
50-75 x 10^9 if high risk of bleeding
>100 if surgery at critical site e.g. the eye

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18
Q

contraindications for platelet transfusion?

A

bone marrow failure (chronic) ITP

heparin induced thrombocytopenia ITP

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19
Q

Inherited thrombophilias?

A 
factor V Leiden (hetero/homo) - hetero most common (activated protein C resistance)
Protein C deficiency
Protein S deficiency
Antithrombin III deficiency
Prothrombin gene mutation
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20
Q

Acquired thrombophilias?

A

APLS

COCP

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21
Q

what is the most common bleeding disorder?

A

VWD

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22
Q

what is heparin induced thrombocytopenia?

A

AB form again PF4 and heparin after 5-10days of treatment with heparin
prothrombotic condition

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23
Q

S/S of HIT?

A

> 50% reduction in platelets
thrombosis
skin allergy

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24
Q

Mx HIT?

A

direct thrombin inhibitor

danaparoid

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25
Q

signs of transfusion reaction?

A 
Fever
low BP
vomiting
headache
chestpain
rigors
dyspneoa
urticaria
collapse
flushing
pain at transfusion site
itching
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26
Q

What are some causes of acute transfusion reactions? <24h

A 
acute haemolytic reactions (ABO incompatibility)
allergic/anaphylactic
infection (bacterial)
febrile non-haemolytic reaction
respiratory (TACO, TRALI)
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27
Q

what are some causes of delayed transfuion reactions >24h?

A 
delayed type haemolytic transfusion reactions
infection (viral, malaria, vCJD)
TA-GvHD (1-2w after transfusion)
post transfusion purpura
iron overload
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28
Q

Aetiology of febrile non-haemolytic transfusion reaction (FNHTR)?

A

release of cytokines from white cells during storage

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29
Q

S/S of FNHTR?

A

mild to mod reaction
small rise in temperature
chills, rigors

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30
Q

Mx FNHTR?

A

stop/slow transfusion

paracetamol

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31
Q

Aetiology allergic/anaphylactic transfusion reactions?

A

more common with FFP (proteins in plasma)

worst reaction if IgA deficient as anti-IgA abs in recipient attack the donor

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32
Q

S/S allergic/anaphylactic transfusion reactions?

A

mild itchy rash

anaphylaxis

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33
Q

Mx allergic/anaphylactic transfusion reactions?

A

stop/slow transfusion
mild (IV antihistamine)
anaphylaxis (adrenaline, ABC)

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34
Q

Aetiology ABO incompatibility/wrong blood?

A

IgM mediated intravascular haemolysis

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35
Q

S/S (acute haemolytic transfusion) ABO incompatibility/wrong blood?

A 
septic looking
restless
chest/loin pain 
fever
vomiting
flushing
haemoglobinuria
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36
Q

Ix ABO incompatibility/wrong blood?

A

FBC, XM, DAT

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37
Q

Mx ABO incompatibility/wrong blood?

A

stop transfusion

fluid resuscitation

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38
Q

Aetiology bacterial contamination transfusion reaction?

A

bacterial endotoxin build up in bag

platelets>RBC> FFP

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39
Q

S/S bacterial contamination transfusion reaction?

A 
septic looking
restless
chest/loin pain 
fever
vomiting
flushing
haemoglobinuria
40
Q

S/S TACO?

A 
Transfusion associated circulatory overload
VERY COMMON
SOB
raised HR
raised BP 
low O2 sats
clinical fluid overload
41
Q

Mx TACO?

A

Slow/stop transfusion

IV furosemide O2

42
Q

TRALI presentation?

A

similar presentation to ARDS
FFP/plts>RBCs
mostly after infusion of plasma components

43
Q

Aetiology TRALI?

A

anti-WBC AB in donor clump recipient WBCs

occurs within 6 hours of transfusion

44
Q

S/S TRALI?

A 
SOB
Raised HR
Raised BP
low O2
fever
normal CVP (0-6)
45
Q

Ix TRALI?

A

CXR - bilateral pulmonary infiltrates

normal pulmonary arterial wedge pressure (PAWP)

46
Q

Mx TRALI?

A

STOP transfusion

supportive

47
Q

causes of prolonged PT?

A

Inherited: factor VII defieincy
acquired: vit K def, liver disease, warfarin, DIC

48
Q

Causes of a prolonged APTT?

A

inherited: deficiency of VIII, IX, XI, XII, VWD
acquired: heparin, dabigatran, DOAC, acquired inhibitor of VIII, IX, XI or XII, acquired VWD, lupus anticoagulant

49
Q

Causes of prolonged PT and APTT together?

A

inherited: prothrombin, fibrinogen, factor V/X deficiency
acquired: liver disease, DIC, severe vitamin K deficiency, anticoagulants ie combined warfarin and heparin, direct thrombin inhibitors
amyloidosis associated factor X deficiency

50
Q

S/S G6PDD?

A

neonatal jaundice (<3/7 of life - most common requiring transfusion)
acute intravascular haemolytic precipitated by:
- infection
- drugs
- fava/broad beans

fever
abdo pain
malaise
dark urine

51
Q

Ix G6PDD?

A

1st line ix = G6PDD levels now and in a month

nothing abnormal between acute episodes
raised G6PD during an acute episode - higher enzyme concentration in reticulocytes
reduced G6PD after the acute episode
blood film (acute) - heinz bodies, bite cells

52
Q

Mx G6PDD?

A

Aware of signs of acute haemolysis (jaundice, pallor, dark urine)
avoidance of specific drugs, chemicals and foods
acute haemolysis: supportive care + folic acid
blood transfusion rarely required

53
Q

Causes of neutropenia?

A

viral

  • HIV
  • Epstein-Barr virus
  • hepatitis

drugs: cytotoxics,carbimazole, clozapine

benign ethnic neutropaenia:
common in people of black African and Afro-Caribbean ethnicity
requires no treatment

haematological malignancy: myelodysplastic malignancies
aplastic anemia
rheumatological conditions
systemic lupus erythematosus: mechanisms include circulating antineutrophil antibodies
rheumatoid arthritis: e.g. hypersplenism as in Felty’s syndrome
severe sepsis
haemodialysis

54
Q

How does acute porphyria present?

A

abdominal pain, neurological symptoms such as motor neuropathy or paresis, and paranoid/delusional psychiatric disturbance

55
Q

Diagnosis of porphyria?

A

classically urine turns deep red on standing
raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)
assay of red cells for porphobilinogen deaminase
raised serum levels of delta aminolaevulinic acid and porphobilinogen

56
Q

Mx porphyria?

A

avoiding triggers
acute attacks
- IV haematin/haem arginate
- IV glucose should be used if haematin/haem arginate is not immediately available

57
Q

What are the complications of CLL?

A

anaemia
hypogammaglobulinaemia leading to recurrent infections
warm autoimmune haemolytic anaemia in 10-15% of patients
transformation to high-grade lymphoma (Richter’s transformation)

58
Q

What is Ritcher’s transformation?

A

Ritcher’s transformation occurs when leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma. Patients often become unwell very suddenly.

59
Q

What symptoms are seen in Ritcher’s transformation?

A 
lymph node swelling
fever without infection
weight loss
night sweats
nausea
abdominal pain
60
Q

What are some causes of DIC?

A

sepsis
trauma
obstetric complications e.g. aminiotic fluid embolism or hemolysis, elevated liver function tests, and low platelets (HELLP syndrome)
malignancy

61
Q

What are tear drop poikilocytes associated with?

A

thalassaemia, megaloblastic anaemia and myelofibrosis

62
Q

What is myelofibrosis?

A

a myeloproliferative disorder
thought to be caused by hyperplasia of abnormal megakaryocytes
the resultant release of platelet derived growth factor is thought to stimulate fibroblasts
haematopoiesis develops in the liver and spleen

63
Q

features of myelofibrosis?

A

symptoms of anaemia e.g. fatigue (the most common presenting symptom)
massive splenomegaly
hypermetabolic symptoms: weight loss, night sweats etc

64
Q

lab findings of myelofibrosis?

A

anaemia
high WBC and platelet count early in the disease
‘tear-drop’ poikilocytes on blood film
unobtainable bone marrow biopsy - ‘dry tap’ therefore trephine biopsy needed
high urate and LDH (reflect increased cell turnover)

65
Q

what do you give for antiphospholipid syndrome in pregnancy

A 
aspirin (low dose)
and enoxaparin (discontinued at 34 w gestation)
66
Q

What is ITP?

A

is an immune-mediated reduction in the platelet count. Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex.

67
Q

S/S ITP?

A

Symptomatic patients may present with:
petichae, purpura
bleeding (e.g. epistaxis)
catastrophic bleeding (e.g. intracranial) is not a common presentation

68
Q

Mx ITP?

A

first-line treatment for ITP is oral prednisolone
pooled normal human immunoglobulin (IVIG) may also be used
it raises the platelet count quicker than steroids, therefore may be used if active bleeding or an urgent invasive procedure is required
splenectomy is now less commonly used

69
Q

What is Evans syndrome?

A

ITP in association with autoimmune haemolytic anaemia (AIHA)

70
Q

Presentation CML?

A

anaemia: lethargy
weight loss and sweating are common
splenomegaly may be marked → abdo discomfort
an increase in granulocytes at different stages of maturation +/- thrombocytosis
decreased leukocyte alkaline phosphatase
may undergo blast transformation (AML in 80%, ALL in 20%)

71
Q

management CML?

A

imatinib is now considered first-line treatment
inhibitor of the tyrosine kinase associated with the BCR-ABL defect
very high response rate in chronic phase CML
hydroxyurea
interferon-alpha
allogenic bone marrow transplant

72
Q

what bleeding time results would you expect to see in VWD?

A

raised APTT
increased bleed time
normal INR and platelets

73
Q

VWD inheritance?

A

autosomal dominant

74
Q

Types of VWD?

A

type 1: partial reduction in vWF (80% of patients)
type 2*: abnormal form of vWF
type 3**: total lack of vWF (autosomal recessive)

75
Q

Mx VWD?

A

tranexamic acid for mild bleeding
desmopressin (DDAVP): raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
factor VIII concentrate

76
Q

what is polycythaemia vera associated with?

A

JAK2 mutation (95%)

77
Q

what is polycythaemia vera?

A

Polycythaemia vera is a myeloproliferative disorder caused by clonal proliferation of a marrow stem cell leading to an increase in red cell volume, often accompanied by overproduction of neutrophils and platelets

78
Q

what are the typical features of polycytheamie?

A

hyperviscosity, pruritus and splenomegaly

79
Q

what is the management of polycythaemia?

A

aspirin -reduces the risk of thrombotic events
venesection - first-line treatment to keep the haemoglobin in the normal range

chemotherapy
hydroxyurea - slight increased risk of secondary leukaemia
phosphorus-32 therapy

80
Q

What is acute sickle chest syndrome?

A

dyspnoea, chest pain, pulmonary infiltrates, low pO2

the most common cause of death after childhood

81
Q

what are the types of crisis associated with sickle cell?

A 
thrombotic, 'painful crises'
sequestration
acute chest syndrome
aplastic
haemolytic
82
Q

what is the management of lead poisoning?

A

dimercaptosuccinic acid (DMSA)
D-penicillamine
EDTA
dimercaprol

83
Q

features of lead poisoning?

A 
abdominal pain
peripheral neuropathy (mainly motor)
fatigue
constipation
blue lines on gum margin (only 20% of adult patients, very rare in children)
84
Q

Ix lead poisoning?

A

blood lead level (>10 = significant)
full blood count: microcytic anaemia.
Blood film: basophilic stippling and clover-leaf morphology
raised serum and urine levels of delta aminolaevulinic acid
urinary coproporphyrin is also increased (urinary porphobilinogen and uroporphyrin levels are normal to slightly increased)

85
Q

What is in cryoprecipitate?

A

factor VIII, fibrinogen, von Willebrand factor and factor XIII

86
Q

Management of CLL?

A

Fludarabine and cyclophosphamide

87
Q

Presentation of CML?

A

Often 60-70 years
anaemia: lethargy
weight loss and sweating are common
splenomegaly may be marked → abdo discomfort
an increase in granulocytes at different stages of maturation +/- thrombocytosis
decreased leukocyte alkaline phosphatase
may undergo blast transformation (AML in 80%, ALL in 20%)

88
Q

Management of CML?

A

imatinib is now considered first-line treatment
inhibitor of the tyrosine kinase associated with the BCR-ABL defect
very high response rate in chronic phase CML
hydroxyurea
interferon-alpha
allogenic bone marrow transplant

89
Q

prognosis of PRV?

A

thrombotic events are a significant cause of morbidity and mortality
5-15% of patients progress to myelofibrosis
5-15% of patients progress to acute leukaemia (risk increased with chemotherapy treatment)

90
Q

What is the reversal agent for apixaban and rivaroxaban?

A

andexanet alfa

91
Q

How is von willebrand inherited?

A

AD

92
Q

Symptoms of VWD?

A

common: epistaxis and menorrhagia
rare: haemoarthroses and muscle haematomas

93
Q

Types of VWD?

A

type 1: partial reduction in vWF (80% of patients)
type 2*: abnormal form of vWF
type 3**: total lack of vWF (autosomal recessive)

94
Q

investigation of VWD?

A

prolonged bleeding time
APTT may be prolonged
factor VIII levels may be moderately reduced
defective platelet aggregation with ristocetin

95
Q

Management of VWD?

A

tranexamic acid for mild bleeding
desmopressin (DDAVP): raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
factor VIII concentrate

96
Q

What are the symptoms of digoxin toxicity?

A

gastrointestinal disturbance (nausea, vomiting, abdominal pain), dizziness, confusion, blurry or yellow vision, and arrhythmias.

Year 6 Medicine (18 decks)

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