Brainscape's Knowledge GenomeTM

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


See full index

Clinical > Oncology > Flashcards

Oncology Flashcards

1
Q

How can we define a neutropenic sepsis?

A

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

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

Mx for neutropenic sepsis?

A

Once suspected commence on piperacillin and tazobactam.

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

What causes tumour lysis syndrome?

A

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

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

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

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

What is Trousseau’s Syndrome?

A

Migratory thrombophlebitis, associated with malignancy.

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

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

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

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

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

How is multiple myeloma managed?

A

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

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

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

A

Papillary, follicular adenoma, medullary, anaplastic.

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

What is seen on aspiration of papillary thyroid cancer?

A

Orphan annie cells.

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

What are the management strategies for thyroid cancers?

A

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

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

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

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

What are the signs/sx of hepatocellular carcinoma?

A

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

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

What is the management for hepatocellular carcinoma?

A

Resection, transplantation, radiofrequency ablation.

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

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

What is the most common type of gastric cancer?

A

Adenocarcinoma.

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

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

A

OGD.
Partial/total gastrectomy with adjuvant chemo.

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

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

Why can carcinoid tumours lead to decompensated heart failure?

A

Serotonin excess can cause pulmonary fibrosis and tricuspid regurg.

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

Which vitamin deficiency are carcinoid tumours associated with?

A

B3 - pallagra

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

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

How can carcinoid syndrome symptoms be managed?

A

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

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

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

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

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

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

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

A

CEA - monitoring only, not used for diagnosis.

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

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

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

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

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
A

Clinical (27 decks)

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