Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MRCP Haematology > MRCP 2 > Flashcards

MRCP 2 Flashcards

1
Q

Warfarin + new necrotic skin?

A

Warfarin induced skin necrosis

Occurs due to protein C deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of warfarin induced skin necrosis ?

A

Deficiency of protein C
Protein C will fall when starting warfarin
WISN –> microthromboi in skin vessels and adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of malignancy is waldenstrom’s?

A

Lymphoplasmacytoid malignancy
Associated IgM
Features of hyperviscocity: Headache, visual disturbances, malaise, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Should you give gentamicin in neutropaenic sepsis?

A

Add in gentamicin if specific microbiology indications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the effect of st John’s wort?

A

Induced of P450

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is normal in alpha thalassaemia ?

A

Protein electrophoresis is normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What receptors are seen on CLL?

A

Circulating clonal B lymphocytes
CD5, CD 29, CD 20, CD23

Immunophenotyping is diagnostic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Prolonged APTT + does not correct on normal plasma + very bleedy?

A

Acquired inhibitor
- May represent an acquired haemophillia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Management of unprovoked DVT?

A
  • Detailed history
  • CXR
  • ECG
  • Routine bloods

Only order tumour markers and scans if there are relevant signs or symptoms (may give false positives)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In HIT should you continue anticoagulation?

A

HIT is hypercoagulable
Require non-heparin anticoagulant

Use a non heparin anticoagulant
e.g. Bivalirudin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are non heparin anticoagulants?

A

Bivalirudin
Fondaparinux
Direct oral anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism of unfractionated heparin ?

A
  • Binds to antithrombin III
  • Activates it
    Binds directly to II, IX X
  • Prevents conversion of prothombin to thrombin
  • Prevent conversion of fibrin to fibringoen

Additionally:
- Binds directly to thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the mechanism of low molecular weight heparin ?

A
  • Binds to antithrombin III
  • Activates it
    Binds directly to II, IX X
  • Prevents conversion of prothombin to thrombin
  • Prevent conversion of fibrin to fibringoen

DOES NOT BIND TO THROMBIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cutaneous manifestation of pseudomonas?

A

Ecythma gangenosum
- Black lesions on skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Factors that make your think its MML?

A

Raised creatinine
Raised blood viscosity
Multiple lytic lesions
Bone pain
Anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Factors that make you think anti-phospholipid?

A

APTT that does not correct on normal plasma
Prone to clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does PT measure?

A

Common + extrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does APTT measure?

A

Intrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does APTT measure?

A

Intrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Factors involved in intrinsic pathway ?

A

12 –> 11–> 9 +8 –> common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Factors involved in common pathway?

A

10 –> 5–> Prothrombin/ thrombin –> fibrinogen/fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Factors invovled in extrinsic pathway?

A

TF + 7 –> common pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Inheritance of haemophillia?

A

X linked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Haemophillia A - what factor?

A

Factor 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Haemophillia B - what factor?

A

Factor 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How to differentiate between intravascular and extravascular?

A

Haemosiderin in intravascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the pathophysiology of paroxysmal nocturnal haemoglobinuria?

A

Glycopeptide deficiency - abscence of red cell membrane proteins

Deficient in CD 55 and CD 59

Prothrombotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Diagnostic tests of PNH?

A

Absence of CD 55 and CD 59
Flow cytometry for abscence of CD 55 and CD 59

Hams test was originally used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Inheritance of G6PD?

A

X linked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

WHO primary polycythaemia criteria?

A

Hb > 16
Haematocrit > .48
BM using hypercellularity
Jak 2 positive

Minor criteria:
EPO below normal range

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Features of Type 1 HIT?

A

Occurs in first 48-72 hours
Count rarely falls below 100
No increase risk of thromboembolism
Count normally returns in 4 days

Can continue dalteparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Features of HIT type 2 ?

A

Occurs day 5-10
Count falls to around 50
Increased risk of thromboembolism
Need to stop dalteparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Smudge cells?

A

CLL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Features of hyper-eosinophilic syndrome?

A

Common in men 30-40
Lung invovlement
Cardiac involvement –> restrictive cardiomyopathy
May have angioedema and urticaria

Mnx:
High dose corticosteroids

If had FIP1L1 / PDGFRA mutation –> imatinib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What must be tested for in MALToma?

A

H pylori
If positive - treat with eradication therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

APML translocation?

A

t 15:17
PML - RARA alpha fusion gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Treatment of APML?

A

ATRA - arsenic trioxide treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Side effect of APML?

A

Differentiation syndrome - cytokine storm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment of APML cytokine storm?

A

Dexamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Most common cause of anaphylaxis in blood transfusion?

A

IgA deficiency
Defined as a IgA < 0.05

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Management of a actively bleeding acquire haemophillia?

A

Recombinant factor VII
Support thrombin generation binding to activated platelets and bypasses need for factor VIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

WHat is the mechanism behind tranfusion associated lung injury?

A

anti-hla
anit-neutrophil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the time onset of TRALI?

A

Within 6 hours of transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is desforrioxime given?

A

Subcutaneous
8-10 hours per day for 5-7 days per week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Side effects of desforrioxime?

A

High frequency deafness
Retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Blood findings with CML?

A

Thrombocytosis - different size platelets ( anisothrombia)
Left shifted film
Basophillia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is CML viewed?

A

Myeloproliferative disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Sickle cell: Treatment to reduced admission with pain episodes ?

A

Hydroxyurea
Increases foetal haemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Features of Hodgkin’s?

A

Malignant proliferation of lymphocytes
25% constiutional symptoms
Rarely has alcohol induced pain
Reed Sternberg cells on biopsy
Causes patchy Bone marrow infiltration

Non-hodgkin’s more likely to cause bone marrow infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the mechanism of TTP onset?

A

Acquired disorder
Antibodies to ADAMST13
ADAMST13 cleave vonwilleband
Leads to multimer of von willebrand - platelets clump to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Pentad of TTP?

A

Fever
Micro agiopathic haemolytic anaemia
Thrombocytopaenia
Neuroligcal abnormalities
Kidney disease

In practice:
Schistocytes
Thrombocytopaenia
Elevated LDH sufficent to make diagnosis

Coagulation will be normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Differentiate between TTP and HUS ?

A

Platelet count remains normal on HUS
Massive renal failure in HUS and very uraemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Management of TTP?

A

Plasma exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Loss of protein from kidney, why are they anticoagulable?

A

Antithrombin III deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

TRALI: where are the antibodies?

A

Antibodies are anti HLA or anti granulocyte in the donor blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the only unique factor to the extrinsic pathway?

A

Factor VII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

For APML treatment, what is the derivative of the treatment ?

A

Involved retinoic acid receptor gene
Vitamin A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How to confirm Hodkin’s lymphoma ?

A

PET guided CT for metabolic active lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Atypical lymphocytes with abnormal villous projections ?

A

Hairy cell leukaemia
Abnormal B cell - centric and centrally placed nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How best to treat hair cell luekaemia

A

Responded very well to purine analogues cladribine and pentostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Antibitoic that exacerbates G6PD?

A

Ciprofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Inheritance of G6PD?

A

X linked recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Haemolysis vs liver disease ?

A

Conjugated - liver
Unconjugated - haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What type of antibody of cold agglutinin disease ?

A

IgM - suffer from cold reactive haemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What anitbody is implicated in cold agglutiins ?

A

I antigen (big I)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Vincristine side effect?

A

Painless peripheral neuropathy
Constipation
Jaw pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Mechanism of Cytarabine ?

A

Pyrimidine synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Side effect of cytarabine ?

A

Alopecia
Pancytopaenia
GI upset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Side effect of doxorubicin?

A

Myocardial toxicity
Pancytopaenia
Mucositis
Peripheral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How many blasts in marrow for AML?

A

> 20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Total protein high + albumin low

A

Think of reason - ? myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Prognostic scoring for Waldenstroms?

A

Age < 65 - 0 points
age 66-75 - 1 point
age > 75 - 2 points
Beta 2 microglobulin > 4mg (1 point)
LDH > 250 ( 1 point)
Serum albumin < 35 ( 1 point)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Gum infiltration, organomegally, lymphadenopathy, monocytoid blasts, raised lysozyme levels?

A

AML subtype M4
Translocation 8:21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Beta thalassaemia minor - explain haemoglobins?

A

Reduced HbA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Mutations of Hb B ?

A

Hb C
HbD
HbE
Hb O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How many genes for HbA ?

A

4 genes

HbH disease if 3 deletion
Hydrops in 4 gene deletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How many genes for Hb B?

A

2 genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Increased HbA2 ?

A

Think Beta thal trait

HbA will not show on ratios - as there is more gene redundancy. Requires genetic testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How to test for alpha thal?

A

Genetic testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Best imaging for myeloma?

A

Whole body MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are high risk features for tumour lysis syndrome?

A

High tumour burden
High grade tumours with rapid cell turnover
Pre-existing renal impairment or renal involvement by the tumour
Increased age
Treatment with highly active, cell-cycle specific agents
Concomitant use of drugs that increase uric acid levels (the list is available on the guidance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is considered low risk for tumour lysis ?

A

When there are no high risk features?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Management of low risk tumour lysis ?

A

Adequate hydration (consider IV fluids and allopurinol prophylaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Management of medium risk tumour lysis?

A

7 day allopurinol + IVF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Management for high risk tumour lysis ?

A

Rasburicase and IV fluids (consider low dose chemotherapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are these?

A

Acanthocytes - they all just different shapes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is Zieve syndrome

A

Jaundice
Hyper-triglyceridaemia
Coomb’s negative haemolytic anaemia
Alcoholism and recent binge.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Causes of acquire Coomb’s positive haemolysis?

A

autoimmune: warm/cold antibody type
alloimmune: transfusion reaction, haemolytic disease newborn
drug: methyldopa, penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Causes of acquire Coomb’s negative haemolysis?

A

Microangiopathic haemolytic anaemia (MAHA): TTP/HUS, DIC, malignancy, pre-eclampsia
Prosthetic heart valves
Paroxysmal nocturnal haemoglobinuria
Infections: malaria
Drug: dapsone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is used in treatment of hereditary angioedema?

A
  1. IV CI inhibitor
  2. FFP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is used as a prophylaxis in hereditary angioedema?

A

Danazol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is danazol?

A

A synthetic androgen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is cryoglbulinaemia ?

A

Immunoglobulins which undergo reversible precipitation at 4 deg C, dissolve when warmed to 37 deg C. One-third of cases are idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the causes and features of cryoglobulinaemia type 1?

A

monoclonal - IgG or IgM
associations: multiple myeloma, Waldenstrom macroglobulinaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the causes and features of cryoglobulinaemia type 2?

A

mixed monoclonal and polyclonal: usually with rheumatoid factor

associations: hepatitis C, rheumatoid arthritis, Sjogren’s, lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the causes of features of cryoglbouninaemia type 3?

A

polyclonal: usually with rheumatoid factor

associations: rheumatoid arthritis, Sjogren’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Features of type 1 cryoglobulinaemia?

A

Raynaud’s only seen in type I
cutaneous
- vascular purpura
- distal ulceration
- ulceration
arthralgia
renal involvement
diffuse glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How to manage cryoglbulinaemia?

A

treatment of underlying condition e.g. hepatitis C
immunosuppression
plasmapheresis

99
Q

What is the cause of methaemoglobinaemia?

A

Drugs - nitric drugs

reduction of Fe3+ (ferric) to Fe2+ (ferrous)

100
Q

Management of 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

101
Q

Presentation of acute intermittent porphyria?

A

abdominal: abdominal pain, vomiting
neurological: motor neuropathy
psychiatric: e.g. depression
hypertension and tachycardia common

102
Q

Diagnosis of acute intermittent porphyria?

A

Urinary screen for ALA and Prophybilinogen

103
Q

General management for sickle cell crisis?

A

analgesia e.g. opiates
rehydrate
oxygen
consider antibiotics if evidence of infection
blood transfusion

104
Q

When should exchange transfusion be used in sickle cell?

A

acute vaso-occlusive crisis (stroke, acute chest syndrome, multiorgan failure, splenic sequestration crisis
rapidly reduce the percentage of Hb S containing cells

105
Q

DVT + Cancer: Duration of anticoagulation?

A

6 months

106
Q

Why can G6PD levels be normal in a haemolytic episode?

A

Haemolysis

check levels in a couple of weeks time

107
Q

Indications to treat in CLL?

A

Progressive marrow failure: the development or worsening of anaemia and/or thrombocytopenia

Massive (>10 cm) or progressive lymphadenopathy

Massive (>6 cm) or progressive splenomegaly

Progressive lymphocytosis: > 50% increase over 2 months or lymphocyte doubling time < 6 months

Systemic symptoms: weight loss > 10% in previous 6 months, fever >38ºC for > 2 weeks, extreme fatigue, night sweats

Autoimmune cytopaenias e.g. ITP

108
Q

Treatment of CLL?

A

fludarabine, cyclophosphamide and rituximab (FCR) has now emerged as the initial treatment of choice for the majority of patients

Ibrutinib - for consolidation, or if FRC fails

109
Q

What is a mimic for gastric cancer?

A

Myelfibrosis

massive spleen, vomiting, early satiety

110
Q

Causes of TTP?

A

post-infection e.g. urinary, gastrointestinal
pregnancy
drugs: ciclosporin, oral contraceptive pill, penicillin, clopidogrel, aciclovir
tumours
SLE
HIV

111
Q

What can eculizmab be used to treat? What is it?

A

Terminal complement protein C5
Used to treat paroxysmal nocturnal haemoglobinurea

112
Q

What vaccine should patients with PNH and on eculizumab be given?

A

Nessira meningitis

Patients with C5 deficiency are at elevated risk of serious meningococcal infections and all patients being treated with eculizumab should receive a quadrivalent vaccine against the meningococcal strains A, C, W, and Y.

113
Q

What is the management of JAK2 positive erythrocytosis?

A

Aspirin
Venesection < 0.45

114
Q

Mechanism of dabigitran?

A

Direct thrombin inhibitor

115
Q

Excretion of dabigitran?

A

Renal

116
Q

Reversal of dabigitran?

A

Idarucizumab

117
Q

Mechanism of rivaroxiabn?

A

Direct factor Xa inhibitor

118
Q

Reversal of rivaroxiban?

A

Adexonate

119
Q

Excretion of rivaroxiban?

A

Majority liver

120
Q

Mechanism of apixaban?

A

Direct factor Xa inhibitor

121
Q

Excretion of apixaban?

A

Mostly faecal

122
Q

Reversal of apixaban?

A

Adexonate

123
Q

Poor prognosis of CLL?

A

male sex
age > 70 years
lymphocyte count > 50
prolymphocytes comprising more than 10% of blood lymphocytes
lymphocyte doubling time < 12 months
raised LDH
CD38 expression positive
TP53 mutation

deletions of part of the short arm of chromosome 17 (del 17p) are seen in around 5-10% of patients and are associated with a poor prognosis

124
Q

Good prognosis of CLL?

A

deletion of the long arm of chromosome 13 (del 13q) is the most common abnormality, being seen in around 50% of patients. It is associated with a good prognosis

125
Q

If DVT less than 7 days before surgery, what should be done?

A

IVC filter + LMWH

126
Q

What is the first line management of myelofibrosis?

A

Hydroxycarbamide

127
Q

Features of porphyria cutanea tarda?

A

Hepatic porphyria
Blisters on sun exposure skin
elevated plasma porphyrins and elevated uroporphyrin I in the urine, and isocoproporphyrin in the faeces

subepidermal blisters with minimal inflammation, marked solar elastosis, thickening of the vessel wall in the papillary dermis and ‘caterpillar bodies’ in the roof of the blister.

classically photosensitive rash with bullae, skin fragility on face and dorsal aspect of hands
urine: elevated uroporphyrinogen and pink fluorescence of urine under Wood’s lamp

128
Q

Where is the defect in porphyria cutanea tarda?

A

defect in uroporphyrinogen decarboxylase

129
Q

How do you manage porphyria cutanea tarda?

A

Chloroquine

130
Q

How do you manage ITP when you need to raise platelets quickly?

A

Intravneous immunoglbulin

131
Q

Consequences of gastrectomy ?

A

Vitamin B 12 deficiency

132
Q

Management of congenital methahaemoglbin?

A

NADH methaemoglobin reductase deficiency

Management: Ascorbic acid

133
Q

Ziev’s syndrome ?

A

rare clinical syndrome of Coombs-negative haemolysis, cholestatic jaundice, and transient hyperlipidaemia

134
Q

When should mast cell try-take be taken?

A

Immediately
Then one to two hours later

135
Q

Anterior mediastinal mass + symptoms of myasthenia

A

thymoma

136
Q

Abdominal pain, constipation, neuropsychiatric features, basophilic stippling?

A

Lead poisoning

Also:
dimorphic picture, significant reticulocytosis and high basophil numbers with cytoplasmic stippling.

Bilateral radial nerve palsies

137
Q

When should neutropenic sepsis antibiotics be reviewed?

A

48 hours

138
Q

What are the photosensitive porphyria ?

A

1) Neurovisceral - neuropathy, epilepsy, psychiatric disorders, abdominal, vomiting, constipation
2) Photosensitive - bullous eruption in sun exposed areas
3) Haemolytic

139
Q

Mutation associated with myelofibrosis?

A

JAK2

140
Q

Mutations seen in DLBCL?

A

BCL2 and TP53 mutations are seen in diffuse large B cell lymphoma.

141
Q

What mutation is. seen in Burrito’s lymphoma?

A

C MYC

142
Q

What is Hyper IgM syndrome?

A

Hyper IgM syndrome is a heterogeneous group of disorders characterised by defective class-switch recombination leading to raised serum IgM with low levels of IgG and IgA

X linked

Hyper IgM syndrome characteristically presents with infections e.g. Pneumocystis pneumonia, hepatitis, diarrhoea

143
Q

How does ATRA work?

A

Treatment is with all-trans retinoic acid (ATRA) to force immature granulocytes into maturation to resolve a blast crisis prior to more definitive chemotherapy

144
Q

Anaphylaxis in blood products?

A

IgA deficiency

145
Q

Management of hereditary spherocytosis/?

A

Splenectomy

146
Q

What food shoulder neutropenic patients avoid?

A

Soft cheese

147
Q

What is post thrombotic syndrome?

A

painful, heavy calves
pruritus
swelling
varicose veins
venous ulceration

148
Q

Positive combs test at 37>0?

A

Warm haemolytic anaemia

149
Q

Indications for irradiated blood?

A
150
Q

Criteria for MGUS?

A

A monoclonal paraprotein band lesser than 30 g/L (< 3g/dL)
Plasma cells less than 10% on bone marrow examination
No evidence of bone lesions,anemia, hypercalcemia, or renal insufficiency related to the paraprotein
No evidence of another B-cell proliferative disorder

151
Q

What supportive medication must be started in FRC?§

A

Co- trimoxazole

152
Q

Deranged clotting in DIC + Emergent bleeding. How best to manage?

A

Fresh frozen plasma

153
Q

Score above what in two level wells should support a doppler diagnosis?

A

Score of 2

154
Q

CLL + New fevers + no signs of infection?

A

Richter transformation

155
Q

Innate glycoprotein IIb/IIIa deficiency?

A

Glanzmann’s thombasthenia

156
Q

What does a PFA- 100 assay show?

A

The ability of platelets to coagulate

157
Q

What are glycoprotein IIb/IIIa receptors?

A

Fibrinogen receptors

158
Q

Rivaroxiabn, how long before procedure?

A

24 hours

159
Q

Dabigatran , how long before procedure?

A

24-48 hours

160
Q

Apixaban, how long before procedure?

A

24-48 hours

161
Q

Fondaparinux, how long before prodecure?

A

36-48 hours

162
Q

LMWH, how long before procedure?

A

12 hours prophylaxis,
24 hours treatment disease

163
Q

Features of graft vs host skins disease?

A

Salary rash
14 days after transplant

164
Q

Translocation of Burrito’s lymphoma?

A

t(8:14)

165
Q

Acutely elevated WCC in AML + stroke like symptoms?

A

Leukaphoresis

166
Q

When should CMV seronegative blood be used ?

A

The use of CMV-seronegative blood products is reserved for CMV-seronegative individuals that are likely to proceed to haematopoietic stem cell transplant, or neonates

or if pregnant

167
Q

Dapsone + dyspnoea?

A

methaemoglobinaemia

168
Q

What is gaucher”s disease?

A

hepatomegaly and massive splenomegaly along with anaemia and thrombocytopenia. While all of the options listed can cause splenomegaly, only Gaucher’s disease is associated with constriction of the diaphysis and flaring of the metaphysis of the femur, resulting in a deformity known as the Erlenmeyer flask deformity (named because it resembles the conical flask used by chemists).

169
Q

Platelets not incrementing with MDS, what investigation?

A

HLA-matched platelets and single-donor platelets are used for individuals that are refractory to platelet transfusions and have developed anti-HLA or antiplatelet antibodies

170
Q

What is the dose for adrenaline in anaphylaxis?

A

0.5ml of 1:1000

171
Q

What antibiotic can cause eosinophillia?

A

Nitrofurantoin

172
Q

Mutation in hairy cell leukaemia?

A

BRAF mutation

173
Q

What informs surgical management for Breast cancer?

A

If presence of auxiliary lymphadenopathy

174
Q

Breast cancer + no auxiliary lymphadenopathy?

A

Auxiliary ultrasound

175
Q

Breast cancer + clinical auxiliary lymphadenopathy ?

A

Auxiliary lymph node

176
Q

When is a mastectomy indicated in breast cancer?

A

Multifocal tumour
Central tumour
Large lesion in the breast
Ductal carcinoma in situ > 4 cm

177
Q

When is a wide local excision indicated in breast cancer?

A

Solitary lesion
Peripheral tumour
Small lesion in the breast
Ductal carcinoma in situ < 4 cm

178
Q

When is radiotherapy offered in breast cancer?

A

Stage T3-T4 in women who have had a mastectomy
Or women with 4 or more lymph nodes

179
Q

When is hormone therapy indicated in breast cancer?

A

Positive for hormone receptors

Use tamoxifen for 5 years post diagnosis

180
Q

What hormone drug should be used and when?

A

Tamoxifen –> pre and post menopsaul
Anastrozle –> post menopausal women

181
Q

When is Neo-adjuvant chemotherapy used?

A

Downgrade tumours

182
Q

Risk factors for breast cancer?

A

BRCA1, BRCA2 genes - 40% lifetime risk of breast/ovarian cancer
1st degree relative premenopausal relative with breast cancer (e.g. mother)
nulliparity, 1st pregnancy > 30 yrs (twice risk of women having 1st child < 25 yrs)
early menarche, late menopause
combined hormone replacement therapy (relative risk increase * 1.023/year of use), combined oral contraceptive use
past breast cancer
not breastfeeding
ionising radiation
p53 gene mutations
obesity
previous surgery for benign disease (?more follow-up, scar hides lump)

183
Q

What is the mechanism of cyclophosphamide?

A

Akylinating agent
causing cross-linking of DNA

184
Q

Adverse effects of cyclophosphamide?

A

haemorrhagic cystitis: incidence reduced by the use of hydration and mesna
myelosuppression
transitional cell carcinoma

185
Q

Treatment for haemorrhgaic cystitis?

A

2-mercaptoethane sulfonate Na
a metabolite of cyclophosphamide called acrolein is toxic to urothelium
mesna binds to and inactivates acrolein helping to prevent haemorrhagic cystitis

186
Q

Mechanism of bleomycin?

A

Degrades preformed DNA

187
Q

Adverse effect for bleomycin?

A

Lung fibrosis

188
Q

Mechanism of antracyclines?

A

Stabilizes DNA-topoisomerase II complex inhibits DNA & RNA synthesis

189
Q

Adverse effect of anthracyclines?

A

Cardiomyopathy

190
Q

Mechanism of methotrexate?

A

Inhibits dihydrofolate reductase and thymidylate synthesis

191
Q

Mechanism of 5-FU?

A

Pyrimidine analogue inducing cell cycle arrest and apoptosis by blocking thymidylate synthase (works during S phase)

192
Q

Mechanism of 6 mercaptourine?

A

Purine analogue that is activated by HGPRTase, decreasing purine synthesis

193
Q

Mechanism of cytaarbne?

A

Pyrimidine antagonist. Interferes with DNA synthesis specifically at the S-phase of the cell cycle and inhibits DNA polymerase

194
Q

Mechanism of vincristine?

A

Inhibits formation of microtubules

195
Q

Mechanism of docetaxil?

A

Prevents microtubule depolymerisation & disassembly, decreasing free tubulin

196
Q

Mechanism of irinotecan?

A

Inhibits topoisomerase I which prevents relaxation of supercoiled DNA

197
Q

Mechanism of cisplatin?

A

Causes cross-linking in DNA

198
Q

Mechanism of hydoxyurea/

A

Inhibits ribonucleotide reductase, decreasing DNA synthesis

199
Q

What is the mechanism of checkpoint inhibitors?

A

Checkpoint inhibitors block inactivation of T cells and reactivate and increase the body’s own T-cell population, enhancing the immune systems own ability to recognise and fight cancer cells.

200
Q

Mechanism of Ipilimumab and its use?

A

Melanoma

checkpoint inhibitor that blocks CTLA-4 (cytotoxic T lymphocyte-associated protein 4)

201
Q

Mechanism of Nivolumab and its use?

A

pembrolizumab (Keytruda) blocks PD-1 (programmed cell death protein 1)

melanoma, Hodgkin’s lymphoma, non-small cell lung cancer and urological cancers.

202
Q

Side effects of immune checkpoint inhibitors?

A

Dry, itchy skin and rashes (most commonly)
Nausea and vomiting
Decreased appetite
Diarrhoea
Tiredness and fatigue
Shortness of breath and a dry cough.

203
Q

Investigating cancer of unknown primary?

A

FBC, U&E, LFT, calcium, urinalysis, LDH
Chest X-ray
CT of chest, abdomen and pelvis
AFP and hCG

Myeloma screen (if lytic bone lesions)
Endoscopy (directed towards symptoms)
PSA (men)
CA 125 (women with peritoneal malignancy or ascites)
Testicular US (in men with germ cell tumours)
Mammography (in women with clinical or pathological features compatible with breast cancer)

204
Q

Most common lung cancer in non-smokers?

A

Adenocarcinoma

205
Q

Most common lung cancer in smokers?

A

squamous

206
Q

Features of large cell lung cancer?

A

typically peripheral
anaplastic, poorly differentiated tumours with a poor prognosis
may secrete β-hCG

207
Q

Causes of lymphoedema?

A

primary: inherited

secondary e.g. surgery, radiation, infection (classically filariasis) or injury resulting in damage to the lymphatic system

208
Q

Management of spinal cord compression

A

High dose dexamethasone

209
Q

Options of agitation in palliative care?

A

Halloperidol
other options: chlorpromazine, levomepromazine

210
Q

Management of hiccups in palliative care?

A

chlorpromazine is licensed for the treatment of intractable hiccups
haloperidol, gabapentin are also used
dexamethasone is also used, particularly if there are hepatic lesions

Hiccups + nausea –> metoclopramide

211
Q

How to convert beteen codine –> oral morphine?

A

divide by 10

212
Q

How to convert between tramadol –> oral morphine ?

A

Divide by 10

213
Q

How to convert oral morphine –> Oxycodone ?

A

Divide by 1.5 - 2

214
Q

Convert between oral morpine –> subcut morphine/?

A

Divide by 2

215
Q

Convert between oral morphine and subcut diamorphine?

A

Divide by 3

216
Q

Convert between oral oxycodone –> subcut diamorphine

A

Divide 1.5

217
Q

When increasing opiods, how much of an increase should you increase by?

A

30-50 %

218
Q

How are people fed if radiotherapy mucositis expected?

A

PEG tube

219
Q

Symptoms of spinal mets?

A

Unrelenting lumbar back pain
Any thoracic or cervical back pain
Worse with sneezing, coughing or straining
Nocturnal
Associated with tenderness

220
Q

Features of SVC obstruction?

A

dyspnoea is the most common symptom
swelling of the face, neck and arms - conjunctival and periorbital oedema may be seen
headache: often worse in the mornings
visual disturbance
pulseless jugular venous distension

221
Q

Common malignancies that cause SVC obstruction?

A

common malignancies: small cell lung cancer, lymphoma
other malignancies: metastatic seminoma, Kaposi’s sarcoma, breast cancer
aortic aneurysm
mediastinal fibrosis
goitre
SVC thrombosis

222
Q

Treatment of SVC obstruction?

A

Endovascular stenting

223
Q

Ca 125?

A

Ovarian cancer

224
Q

Ca 19-9

A

Pancreas

225
Q

Ca 15-3

A

Ca 15-3

226
Q

AFP?

A

Hepatocellular carcinoma, teratoma

227
Q

CEA

A

Carcinoembryonic antigen (CEA)

228
Q

S-100

A

Melanoma, schwannomas

229
Q

Bombesin

A

Small cell lung carcinoma, gastric cancer, neuroblastoma

230
Q

What can be used as a third line opiod in difficult to control pain ?

A

Methadone

231
Q

What pain killer works through NMDA antagonism?

A

Methadone

232
Q

Conversion of fentanyl to morphine?

A

100 micrograms fentanyl to 15 morphine

233
Q

Prefered method of antiemetic if metabolic cause of vomiting?

A

Levomepromazine

234
Q

Chance of acquiring cancer if BRCA 1 postivie?

A

55-60%

235
Q

Imaging for SVC obstruction

A

CT chest

236
Q

Transdermal fentanyl absorption is increased by heat (e.g. hot water bottle) or pyrexia, potentially leading to opioid toxicity

A

Transdermal fentanyl absorption is increased by heat (e.g. hot water bottle) or pyrexia, potentially leading to opioid toxicity

237
Q

Complications of ketamine?

A

Can increase intracranial pressure

Monitor: headache, papilloedema, and vomiting

238
Q

Vertebral collapse?

A

neurosurgery

239
Q

Treatment for delayed phase vomiting from chemo?

A

Dexamethasone

240
Q

Onset of immediate release morphine?

A

30 minutes

241
Q

How can fentanyl lead to opiod toxicity?

A

Pyrexia increases transdermal absorption

242
Q

TTF stain + adenocarcinoma histology

A

Non small cell lung cancer

243
Q

Just know the fact : Causes for Non-Pitting Edema
1. Lymphedema
2. Myxedema
3. Lipedema
4. Angioedema

A

Just know the fact : Causes for Non-Pitting Edema
1. Lymphedema
2. Myxedema
3. Lipedema
4. Angioedema

MRCP Haematology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions