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Clinical > Oncology > Flashcards

Oncology Flashcards

1
Q

How can we define a neutropenic sepsis?

A

Neutrophils <0.5 x 10^9, temperature >38.

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2
Q

Mx for neutropenic sepsis?

A

Once suspected commence on piperacillin and tazobactam.

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3
Q

What causes tumour lysis syndrome?

A

rapid cell breakdown (tumour cells) which release their intracellular contents which causes the symptoms.

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4
Q

What are the electrolyte disturbances of tumour lysis syndrome? How does it affect the kidneys?

A

Elevated uric acid, potassium, and phosphate.
Low calcium.
AKI.

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5
Q

How do you manage tumour lysis syndrome?

A

Give fluids, correct electrolytes, give ruburicase (changes uric acid into allantoin which is more easily excreted by kidneys), can also give allopurinol to help correct hypercalcaemia.

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6
Q

What is Trousseau’s Syndrome?

A

Migratory thrombophlebitis, associated with malignancy.

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7
Q

What is the underlying pathophysiology of multiple myeloma?

A

Plasma cell dyscrasia leasing to abnormal plasma cells which secrete monoclonal antibodies into the serum and urine. You also get a relative loss of functional antibodies (hypogammaglobulinemia).

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8
Q

What symptoms does Multiple Myeloma present with?

A

CRAB: hyperCalcaemia (excessive thirst, loss of appetite, constipation, N+V, abdo pain), Renal disease, Anaemia, Bone disease (lytic lesions).

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9
Q

How do you investigate for multiple myeloma?

A

1) serum protein electrophoresis: identify serum IgG paraprotein and bence jones proteins
2) Immunofixation: identify type of paraprotein
Can also do a bone marrow biopsy which would confirm MM with >10% being plasma cells.

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10
Q

What might you see on blood film for multiple myeloma?

A

Roleuax (stacks of RBCs that form due to the discoid shape and abnormal amounts of proteins).

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11
Q

How is multiple myeloma managed?

A

Stem cell transplant in approperiate pts.
If not appropriate, then MPT (melphalan, prednisolone, thalidomide) therapy.

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12
Q

What are the different types of thyroid cancers from most common to least common?

A

Papillary, follicular adenoma, medullary, anaplastic.

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13
Q

What is seen on aspiration of papillary thyroid cancer?

A

Orphan annie cells.

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14
Q

What are the management strategies for thyroid cancers?

A

Surgery, iodine therapy, neoadjuvant hormonal therapy, targeted therapy (for advanced tumours).

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15
Q

What is the tumour marker for hepatocellular carcinoma? What do you refer for if it is raised?

A

AFP - refer for abdo USS, after this next step would be biopsy.

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16
Q

What are the RFs for hepatocellular carcinoma?

A

Chronic viral hepatitis, cirrhosis, non-alcohlic fatty liver disease, alcoholic liver disease, PBC, inherited metabolic disorders, obesity, T2DM.

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17
Q

What are the signs/sx of hepatocellular carcinoma?

A

Abdo pain, jaundice, ascites, weight loss, hepatomegaly, encephalopathy.

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18
Q

What is the management for hepatocellular carcinoma?

A

Resection, transplantation, radiofrequency ablation.

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19
Q

What signs and sx might someone with gastric cancer present with?

A

ALARMS:
- Anaemia
- Lymphadenopathy (Virchow’s and sister Mary Joseph nodes)/ Loss of weight
- Anorexia
- Recent onset sx
- Malena/haematemesis
- Swallowing difficulty (dysphagia)

+ dyspepsia

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20
Q

What is the most common type of gastric cancer?

A

Adenocarcinoma.

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21
Q

What is the first line investigation for suspected gastric cancer? What is the management?

A

OGD.
Partial/total gastrectomy with adjuvant chemo.

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22
Q

Where are carcinoid tumours most commonly found? What do they secrete and what sx this cause?

A

Appendix, ileum, rectum.
Secrete excess serotonin causing sx of:
- flushing
- diarrhoea
- bronchospasm
- GI symptoms (abdo pain, diarrhoea).

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23
Q

Why can carcinoid tumours lead to decompensated heart failure?

A

Serotonin excess can cause pulmonary fibrosis and tricuspid regurg.

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24
Q

Which vitamin deficiency are carcinoid tumours associated with?

A

B3 - pallagra

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25
Q

How can you diagnose a carcinoid tumour?

A

5-IAA measurement - it is a breakdown product of 5HT so will be raised.
CT/MRI or ocreotide scans.
Biopsy.

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26
Q

How can carcinoid syndrome symptoms be managed?

A

Medical (somatostatin analogues: ocreotide) and surgical (resection, embolisation, etc).

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27
Q

What is the common presentation of cholangiocarcinoma?

A

Jaundice, painless RUQ mass (Courvoisier’s sign), weight loss, anorexia.
Hx of IBD/PSC, smoking/obesity, chronic GB issues.

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28
Q

What are the signs/sx of colorectal cancer?

A

Rectal bleeding, weight loss, change in bowel habit, abdo pain, iron deficiency anaemia, and may present with a bowel obstruction.

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29
Q

What are the RFs for colorectal cancer?

A

IBD, hereditary syndromes (lynch), obesity, age, alcohol excess, smoking, increased intake of processed red meat, and radiation exposure.

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30
Q

How would you investigate someone for colorectal cancer?

A

FIT test.
If this comes back >10micrograms then refer for colonoscopy on 2WW pathway.

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31
Q

What tumour marker can be used for monitoring of colorectal cancer?

A

CEA - monitoring only, not used for diagnosis.

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32
Q

What is the mutation in Lynch syndrome? What cancers is it associated with? what is the risk of non-polyposis colorectal cancer?

A

MLH1 autosomal dominant gene mutation.
Gastric, colorectal, endometrial, breast, and prostate.
NPCC - 80% by 33y/o.

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33
Q

What are the characteristics of osteosarcoma? What age group has a peak in incidence?

A

Prolonged onset of pain and swelling, XR shows new bony growth, periosteal reaction causing ‘sunburnt’ appearance.
2nd decade of life peaks due to rapid bone growth in puberty.

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34
Q

What are the characteristics of chondrosarcoma?

A

progressive pain worse at night, typically in the pelvis, proximal femur, or humerus. More commonly seen in 50-70 y/o age group.
XR shows osteolytic lesion with ‘moth-eaten appearance’.

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35
Q

What symptoms might you see in someone presenting with CLL (chronic lymphocytic leukaemia)? Where is the pathology?

A

Non-tender lymphadenopathy, hepatosplenomegaly, B sx, and possibly features of bone marrow failure.
Pathophysiology: mature B cell neoplasm causing accumulation of monoclonal B lymphocytes.

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36
Q

What age group are most commonly affected by CLL? What is seen on biopsy?

A

> 60s.
Smudge cells.

37
Q

What is the Richter transformation?

A

CLL transforms into high grade B cell lymphoma.
Indicated in a CLL pt with rapidly enlarging nodes.

38
Q

What is the pathophysiology behind CML?

A

BCR-Abl translocation on chromosome 22 (Philadelphia chromosome).
Causes uncontrolled proliferation of myeloid cells (granulocytes: eosinophils, basophils, neutrophils) separated into 3 phases - chronic, accelerated, and blast crisis.

39
Q

How might someone with CML present?

A

Middle aged pts (more common in males), with massive splenomegaly, weight loss, fatigue, B sx, thrombocytopenia, leukocytosis, and gout.

40
Q

What is shown in blood film of CML?

A

Increased levels of mature myeloid cells and leukocytes.

41
Q

How is CML managed in a Philadelphia chromosome +ve pt?

A

Imatinib.

42
Q

What is the pathophysiology of AML?

A

Uncontrolled proliferation of myeloid precursors in bone marrow, leading to BM failure and accumulation of blasts (immature WBCs) in peripheral blood.
May begin as myelodysplasia which a premalignant disease of myeloid cells (30% of AMLs).

43
Q

How does AML present?

A

Presents in adults with bone marrow failure (anaemia, thrombocytopenia, leukopenia) and signs of infiltration (hepatosplenomegaly and gum hypertrophy).

44
Q

What is seen on bone marrow biopsy for AML?

A

Hypocellular marrow, auer rods, ring sideroblasts.

45
Q

Myelodysplastic syndrome increases your risk of which blood cancer?

A

AML

46
Q

What is PML (promyelocytic leukaemia)?

A

A form of AML where there is a t(15;17) translocation which is a block in differentiation at a precursor stage causing a build up of promyelocytes (immature platelets).
This prevents clotting and causes excessive bleeding/bruising.
Accounts for about 8% of AMLs.

47
Q

What is the pathophysiology of ALL?

A

Uncontrolled proliferation of lymphoid precursors (lymphoblast).

48
Q

How does ALL present?

A

In children with anaemia (fatigue, pallor), thrombocytopenia (bleeding/bruising), and neutropenia (recurrent infection).
Other signs include painless lymphadenopathy, hepatosplenomegaly, CNS involvement (meningism, CN palsies), and testicular enlargement in boys.

49
Q

What chromosomal abnormality is associated with ALL?

A

Down’s.

50
Q

What is shown on bone marrow biopsy of ALL?

A

Leucocytosis and blast cells.

51
Q

Burkitt’s Lymphoma is is what type of lymphoma? What virus is it associated with?

A

Non-Hodgkin B cell Lymphoma.
Pts almost always test +ve for EBV.

52
Q

How does Hodgkin’s Lymphoma present? How is it diagnosed?

A

Often in young adults with non-tender lymphadenopathy (cervical/supra-clavicular), B sx (<30% of cases), pain on drinking alcohol, or with sx of obstruction of surrounding structures (e.g., SVC).
Biopsy - Reed-Sternberg cells

53
Q

What is the Ann-Arbour staging of Hodgkin’s Lymphomas?

A

1) Single nodal group
2) 2 or more nodal groups on the same side of the diaphragm
3) Nodal group on both sides of the diaphragm
4) disseminated disease with extra-lymphatic organ involvement.
Additionals:
A - asymptomatic
B - B sx
X - bulky nodes
S - splenic involvement
E - extra-nodal disease

54
Q

How is Hodgkin’s Lymphoma managed?

A

Stage 1 can be managed with radiotherapy. More advanced stages include ABVD chemotherapy (Adriamycin [doxorubicin], bleomycin, vinblastine, dacarbazine).

55
Q

How does Non-Hodgkin’s Lymphoma present? How is it diagnosed?

A

Painless, symmetrical lymphadenopathy (cervical, axillary, inguinal)and B sx (more common B sx than in Hodgkin’s).
Biopsy: no Reed-Sternberg cells, and confirm subtype.

56
Q

How do you categorise NHL?

A
  • B or T cell
  • High (aggressive) or low grade (indolent)
57
Q

What are the most common forms of NHL?

A

Diffuse large B cell lymphoma and follicular lymphoma.

58
Q

How is NHL managed?

A

Low grade: watch/wait, localised radiotherapy, potentially some immunotherapy/chemo.
High grade: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone).

59
Q

What is Polycythaemia Vera? What is the initial management?

A

Blood cancer causing excessive production of RCs making thicker blood, more likely to clot.
Associated with JAK2 mutation.
Venesection and 7 mg PO aspirin.

60
Q

What is essential thrombocythemia?

A

Blood cancer causing excessive platelet production, associated with JAK2, MPL, and CALR mutations.

61
Q

What is the most common type of mouth cancer? How does it present?

A

SCC - presents with a painful slowly progressing mouth ulcer that may be fungating. Associated with painless lymphadenopathy of the head/neck

62
Q

What are the common signs/sx of prostate cancer?

A

Urinary changes, haematospermia, pelvic discomfort, ED, bone pain (if metastatic).

63
Q

How do we score prostate cancer?

A

Biopsy to do a gleason score (1-5)

64
Q

When would you refer someone on 2WW for prostate cancer?

A
  • Prostate feels malignant on DRE
  • Suspicious sx
  • PSA above threshold for age
65
Q

How is metastatic prostate cancer most commonly managed?

A

Hormonal therapy with GnRH analogues.

66
Q

What cancers does BRAC2 increase the risk of?

A

pancreatic, prostate, gastric, breast.

67
Q

What are possible signs/sx of breast cancer?

A

Unexplained breast lump, nipple discharge, retraction, and skin changes.

68
Q

What is the most common type of breast cancer?

A

Invasive ductal carcinoma.

69
Q

What treatment can be used for pre or post-menopausal women with oestrogen receptor +ve breast cancer?

A

Pre: tamoxifen (blocks oestrogen receptors but allows continued production of oestrogen in uterus and bone)
Post: Letrozole or anastrozole (aromatase inhibitors)

70
Q

What therapy is given for HER2+ve breast cancer?

A

Trastuzumab/neratinib/pertuzumab

71
Q

What are the signs/sx of ovarian cancer?

A

bloating, early satiety, urinary changes, and ascites in advanced disease.

72
Q

What are the RFs for ovarian cancer?

A

older age, smoking, obesity, HRT, BRCA genes, numerous ovulations (early menarche, late menopause, nulliparity)

73
Q

What is the tumour marker for ovarian cancer?

A

Ca125

74
Q

What are the types of ovarian cancers? Which is most common?

A

Epithelial cell tumours (cystic), germ cell tumours, sex-cord stromal tumours.
Epithelial cell is most common.

75
Q

What are the signs/sx of endometrial cancer?

A

Postmenopausal bleeding, abnormal vaginal bleeding, dyspareunia, pelvic pain, weight loss, anaemia, and abdominal discomfort.

76
Q

What are the RFs for endometrial cancer?

A

More cycles (Nulliparity, early menarche, late menopause), obesity, unopposed oestrogen, PCOS, obesity.

77
Q

What are the signs/sx of vulvar cancer?

A

Unexplained lump, itching, non-healing ulceration, pain, skin changes, and bleeding.

78
Q

What is the most common type of vulvar cancer?

A

SCC on the labia majora.

79
Q

Burkitt’s Lymphoma is associated with what appearance on biopsy? What translocation is it associated with?

A
  • Starry sky
  • between chromosomes 8 and 14
80
Q

How does bladder cancer present?

A

Haematuria, bladder outflow obstruction +/-hydronephrosis/hydroureters.

81
Q

What is the 2WW criteria for bladder cancer?

A

> 45 years old and:
- unexplained visible haematuria with no UTI
- persistent visible haematuria after successful treatment of UTI

82
Q

What stage is muscle invasive bladder cancer?

A

T2-4

83
Q

What is the 2WW criteria for testicular cancer?

A

Painless enlargement or change in shape/texture of testes

84
Q

What is the 2WW criteria for Penile cancer?

A

Penile mass/ulcerated lesion without STI
Persistent penile lesion despite successful treatment of STI
Unexplained/persistent sx of the foreskin or glans

85
Q

What is the most common cytogenic abnormality associated with ALL?

A

t(12:22) translocation.

86
Q

What is the triad associated with Hyperviscosity syndrome?

A
  • Neurological deficits
  • Visual changes
  • Mucosal bleeding
87
Q

What is hyperviscosity syndrome most commonly associated with?

A

Waldenstrom’s macroglobulinemia

88
Q
A

Clinical (27 decks)

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