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MRCP > Oncology > Flashcards

Oncology Flashcards

1
Q

Mechanism of action of anthracycline (e.g., doxorubicin)

A

Stabilises DNA topoisomerase II complex inhibits DNA and RNA synthesis

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2
Q

Side effects of Methotrexate

A

Myelosupression
Mucositis
Liver Fibrosis
Lung Fibrosis

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3
Q

Mechnism of action of 5-Fluorouracil

A

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

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4
Q

Adverse effects of 5-fluorouracil

A

Myelosupression
Mucositis
Dermatitis

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5
Q

Function of mercaptopurine

A

Purine analogue activated by HGPRTase decreasing purine synthesis

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6
Q

Side effect of Mercaptopurine

A

Myelosupression

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7
Q

Mechanism of action of Cytarabine

A

Pyrimidine antagonist - inhibits DNA Polymerase

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8
Q

Side effect of Sytarabine

A

Myelosupression

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9
Q

Mechanism of action of Vincristine

A

Inhibits formation of microtubules

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10
Q

Side effect of vincristine

A

Peripheral neuropathy

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11
Q

Mechanism of atcion of docetaxel

A

Prevents microtubule depolymerisation

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12
Q

Side effect of docetaxel

A

Neutropenia

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13
Q

Name a topoisomerase inhibitor

A

Iriniotecan

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14
Q

Side effects of Irinotecan

A

Myelosupression

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15
Q

Mechanism of action of cisplatin

A

Cross linking in DNA

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16
Q

Side effects of Cisplatin

A

Nephrotoxicity
Ototoxicity
Peripheral Neuropathy
Hypomagenesaemia

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17
Q

Mechanism of action of hydroxyurea

A

Inhibits ribonucleotide reductase

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18
Q

What is Prophase

A

Centrosomes duplicate forming microtubules

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19
Q

What is Metaphase

A

Chromosomes align in the middle of the cells.

The microtubules attach to the centromeres on either side

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20
Q

What is anaphase

A

The chromosomes are separates and moved by centromeres to the other side

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21
Q

What is Telophase

A

The membrane separates to form two cells

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22
Q

Name the three check points in cells

A

G1
G2
M-phase

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23
Q

What happens in the S phase

A

DNA replication - during this Helicase separates the two dna strands

This causes super coils as the process continues.

Topoisomerase II fixes supercoils to reduce tension on the DNA (ie., stop damage).

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24
Q

Role of alkylating agents

A

Bind to nucleotides, form cross links with DNA strands which stops normal replication or cell division - causes cell arrest

Causes apoptosis.

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25
Q

Examples of alkylating agents

A

Cyclophosphamide and Cisplatin

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26
Q

How do anthracyclines function

A

Inhibits Topoisomerase II causing DNA to not relax -> causes it to break!

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27
Q

What is the DVT Well’s score criteria and associated score meanings

A

Active Cancer
Paralysis
Bedridden for 3 days or surgery within 12 weeks
Localised tenderness
Entire leg swollen
Calf 3cm nbigger than the other
Pitting Oedema
COllateral superficial veins
Orevious DVT
An alternative diagnosis has been excluded.

DVT likely if over 2

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28
Q

Management of Wells’ score over 2

A

Proximal leg vein ultrasound within 4 hours.

Positive then anticoagulate

Negative then do d-dimer.

If both negative consider another diagnosis

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29
Q

If Ultrasound is negative but d-dimer is positive, what should be done

A

Stop therapeutic anticoagulation

Offer repeat leg vein ultrasound 6-8 days later

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30
Q

If a DVT is unlikely in Well’s score, what should be done

A

Perform d-dimer test

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31
Q

Management of a VTE

A

DOAC first line then LMWH followed by a DOAC or LMWH followed by Vit K antagonist (ie., warfarin)

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32
Q

What is responsible for the break down of fibrin clots

A

Plasmin

33
Q

How does tissue factor result in DIC

A

Upon extensive trauma, TF is exposed on teh surface of many cells, this binds to coagulation factors activating the extrinsic pathway and intrinsic pathway

34
Q

Blood tests for DIC

A

Low platelets
Low fibrinogen
Increased PT AND ApTT

Schistocytes due to microangiopathic hameolytic anaemia

35
Q

What drugs can induce pancytopaenia

A

Cytotoxics
Antibiotics (trimethoprim and chloramphenicol)
Gold and Penicillamine
Carbimazole
Carbamazapine
Tolbutamide

36
Q

What is an ECOG score

A

Performance status of a patient measure

37
Q

Causes of Eosinophilia

A

Pulmonary:
Asthma
Aspergillosis
Churg-Strauss syndrome
Loffler’s
Eosinophilic penumonias
Hypereosinophilic syndrome

Infective:
Schistosomiasis
Nematoses (TOxocara, Ascaris, Strongyloids)
Echinococcus

Drugs: Sulfsalazine and nitrofurantoin

Psoriasis/Eczema

38
Q

Role of Thrombin (Factor 2)

A

Increases platelet activation
Factors 8, 11, 5, 13

39
Q

Describe the process in which Factor 5 usually gets inactivated

A

AT the end of the formation of a mesh, thrombin binds to thrombomodulin recpetors on the endothelial cells

Protein C then joints the party with Protein S.

When protein S binds to Protein C, this leaves a gap in Protein C’s back.

Factor 5 gets caught off guard by this gap and gets cleaved - stopping further fibrin mesh production

40
Q

What is the result of cleaving Factor 5

A

Stops Factor 10 and 9 activation

41
Q

What type of mutation causes Factor V leiden deficiency

A

Singel point mutation where an amino acid is replaced by another

42
Q

How is Factoe V Leiden deficiency inherited

A

Autosomal Dominant

43
Q

WHat type of Factor V Leiden deficiency carry the highest risk of VTEs

A

Factor V Leiden (Heterozygeous)

44
Q

Role of Glutathione

A

Anti-oxidant - neutralises free radicals

Usually are reduced. Can donate H+ to free radicals to produce water instead.

It then gets oxidised in the process.

Glutathione reductase donates a H+ back to Glutathione to reduce it again so it can function.

In the process Glutathiona Reductase recieves another H+ from NADPH

NADP+ as a bbyproduct.

45
Q

Role of G6PD

A

Reduces NADP+ to NADPH from glucose-6-phosphate

46
Q

How is G6PD deficiency inherited

A

X-Linked recessive

Only affects men (not dominant)

47
Q

What happens in G6PD Deficiency

A

Enzymes do not last very long.

48
Q

What does G6PD deficiency provide protetcion against and why

A

Protects against Falciparum Malaria due to reduced half-life of G6PD. Means that erythrocytes are more likey to die from free radicals that are not being swept up by glutathione.

49
Q

Why do we get bite cells in G6PD deficiency

A

RBCs haemo get destroyed by free radicals, leaving heinz bodies.

Splenn macrophages detect they are abnormal and take a bit of the red cells leaving bite cells

50
Q

What happens to Glutathione and NADPH in G6PD deficiency

A

Decreased all of them

51
Q

Causes for G6PD Deficiency causes

A

Food:
Fava Beans
Soy
Red Wine

Infections:
Viral Hepatitis
Pneumonia

Medications:
Primaquine and Chloroquine

NSAIDs + Aspirin
Quinidine
Trimethoprim + Sulphonamides

52
Q

What drugs can cause G6PD Haemolysis

A

Primaquine
Ciprofloxacin
Sulphonamides, Slufonylueras, Sulphsalazine

53
Q

What ethnicity are affected by G6PD Deficiency

A

African and Mediterranean

54
Q

What is G6PD Deficiency diagnosed

A

Measure enzyme activity of G6PD

55
Q

How is Li-Fraumeni syndrome inherited

A

Autosomal Dominant

56
Q

On what chromosome is BRCA1 carried on

A

17

57
Q

On What chromosome is BRCA 2 carried on

A

13

58
Q

What gene mutation is associated with prostate cancer in men

A

BRCA2

59
Q

What is the Amsterdam criteria

A

Three or more family members with a confirmed diagnosis of colorectal cancer (first degree)
Two sucessive affected generations
One or more colon cancers diagnosed under 50

60
Q

What drug can be given to increase neurophil count in neutropenic patients and how do these work

A

Filgrastim - granulocyte-colony stimulating factors

61
Q

What translocation causes mantle cell lymphoma

A

11:14

62
Q

What does 11:14 translocation do to cause mantle cell lymphoma

A

Deregulation of cyclin D1 gene

63
Q

What happens in 14:18 translocation to cause follicular lymphoma

A

Increased BCL-2 transcription

64
Q

What two malignancies are caused by EBV

A

Hodgkin’s and Burkitt’s lymphoma

65
Q

What malignancy is caused by HTLV-1 infection

A

T cell leukaemia/lymphoma

66
Q

What haematological malignancy can be caused by HIV

A

High grade B Cell lymphoma

67
Q

What infection typically results in Burkitt’s lymphoma

A

Malaria

68
Q

Causes of extravascular haemolysis

A

Sickle cell, thalasaaemia
Hereditary Spherocytosis
Haemolytic disease of the newborn
Warm autoimmune haemolytic anaemia

69
Q

Symptoms of hairy cell leukaemia

A

Pancytopaenia
Splenomegaly
Vasculitis (skin)

DRY TAP on bone marrow

TRAP positive

70
Q

Management of Hairy cell leukaemia

A

Chemotherapy - Cladribine and pentostatin

71
Q

How is hereditary angioedema inherited

A

Autosomal Dominant

72
Q

Blood test reuslts in hereditary angiooedema

A

C1-INH levels low during attacks

Low C2 and C4 between attacks

73
Q

Symptoms of hereditary angiooedema

A

Painful macular rash
Painless swelling of tissues

NO URTICARIA

74
Q

Management of Hereditary Angiooedema

A

IV C1-inhibitor concentrate

NB: Does not response to antihistamines or adrenaline

75
Q

Prophylaxis of hereditary angiooedema

A

Danazol

76
Q

Most common type of Hodgkin’s lymphoma

A

Nodular sclerosing (good prognosis)

77
Q

What type of Hodgkin’s lymphoma has the worst prognosis

A

Lymphocyte depleted

the presence of b-symptoms

78
Q

What Hodgkin’s lymphoma carries the best prognosis

A

Lymphocyte predominant

79
Q
A

MRCP (1 decks)

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