RACP Divisional Written Exam · FRACP

Oncology for the written exam

Everything Physify has for Oncology: short lessons written to Australian guidance, exam-style questions with a worked explanation for each, and Bedside, our AI tutor, under every one. Try a question below, no sign-up.

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34courses
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152lessons
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723exam-style questions
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19figures in the lessons

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Oncology

A 63 year old woman in Adelaide had a negative iFOBT through the National Bowel Cancer Screening Program 12 months ago. She has no symptoms, no family history of colorectal cancer and a normal haemoglobin. A friend does a stool test every year, and she asks whether she should do another kit now. What is the most appropriate advice?

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What's covered

34 courses, each a set of lessons with a quiz after them. The bar shows how many questions each has. Open a course to see its lesson outline.

From the lessons

19 figures sit in the Oncology lessons: ECGs, diagrams, films and clinical images, each with what to look for. Here are 4. Tap one to enlarge it.

Schematic of the cell cycle as a ring (phase lengths not to scale): G1, S, G2 and M, with quiescent G0 outside it and mitogens pushing cells back into G1. The cyclin-CDK pairs are listed in the centre: cyclin D with CDK4/6 in early G1, cyclin E with CDK2 at G1 to S, cyclin A with CDK2 in S, cyclin A with CDK1 in G2 and cyclin B with CDK1 into M. Four numbered checkpoints are marked. 1, the restriction point in late G1: cyclin D with CDK4/6 and then cyclin E with CDK2 phosphorylate RB, which releases E2F and commits the cell to S phase; p16INK4A brakes CDK4/6 and p21 brakes CDK2; palbociclib, ribociclib and abemaciclib block CDK4/6 and cause G1 arrest, which needs functional RB. 2, the G1 to S DNA damage checkpoint: ATM activates CHK2 and p53, and p21 holds the cell in G1; it is lost with p53, so the tumour leans on the S and G2 checkpoints. 3, the S and G2 checkpoints: ATR activates CHK1, which inhibits CDC25, and WEE1 phosphorylates CDK1 to hold the cell in G2 (ATR and WEE1 inhibitors are investigational). 4, the spindle assembly checkpoint in M: MAD2, BUB1 and BUBR1 hold APC/C with CDC20 inactive until every kinetochore is attached. Below, where chemotherapy acts: antimetabolites (methotrexate, fluorouracil, cytarabine) in S phase; bleomycin in G2; taxanes, which stabilise microtubules, and vinca alkaloids and eribulin, which prevent polymerisation, in M phase, causing mitotic arrest and neuropathy; CDK4/6 inhibitors in G1, cytostatic rather than cytotoxic; and alkylating agents and platinum compounds as phase non-specific, with a steeper dose-response. Phase-specific drugs kill more with prolonged exposure, hence infusional schedules.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “The Cell Cycle, p53, Checkpoints and DNA Repair” in Cell, Molecular and Cancer Biology

Schematic in two panels. Panel 1, priming in the lymph node: a dendritic cell presents antigen on MHC to the T cell receptor, and CD80/86 engages CD28 (go); CTLA-4 on the T cell takes CD80/86 from CD28 and stops priming, and an anti-CTLA-4 antibody frees the brake. Panel 2, the effector phase in the tumour: PD-L1 on the tumour engages PD-1 on the T cell and switches it off; an anti-PD-1 or anti-PD-L1 antibody frees the brake. The antibodies: anti-CTLA-4 ipilimumab and tremelimumab; anti-PD-1 nivolumab and pembrolizumab; anti-PD-L1 atezolizumab, durvalumab and avelumab; anti-LAG-3 relatlimab with nivolumab. Below, the immune related adverse events: colitis and hypophysitis (low ACTH, TSH and gonadotrophins) more often with anti-CTLA-4; thyroiditis (thyrotoxic, then hypothyroid), pneumonitis and type 1 diabetes more often with anti-PD-1; and hepatitis, nephritis, skin, arthritis, myositis, myocarditis and myasthenia with any checkpoint inhibitor, since any organ can be inflamed. Most occur within the first months but can appear late, even after stopping; infection, disease progression and other drugs must be excluded first.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Immune Related Adverse Events, CRS & ICANS” in Systemic Therapy, Immunotherapy Toxicity & Cardio-Oncology

Dermoscopic close-up of an irregular, asymmetric pigmented skin lesion in several shades of dark brown, red-brown and blue-grey, with a ragged edge; a white circle marks finger-like dark projections at the upper right border.
Dermoscopy of a superficial spreading melanoma (Breslow thickness 0.79 mm): asymmetry of shape and colour, a blue-grey centre, and pseudopods (bulbous projections at the edge, in the circle, which marks the biopsy site), which, when irregular and focal as here, points to melanoma rather than a naevus (symmetrical pseudopods all round the edge suggest a Reed naevus). Image: Braga JCT, Macedo MP, Pinto C and colleagues, PLoS One 2013 (figure 5A), CC BY 4.0, via PubMed Central; cropped. Original. Tap the image to zoom.

From the lesson “Epidemiology, Subtypes & Molecular” in Melanoma

Small dark brown-black flat spots scattered over the lips, the corner of the mouth and the inside of the cheek of an open mouth.
Peutz-Jeghers syndrome in a boy: mucocutaneous melanotic macules on the lips and buccal mucosa, which appear in childhood and may fade from the lips in adulthood but persist inside the mouth. The hamartomatous polyps cause small bowel intussusception and bleeding, and the syndrome (STK11) carries raised risks of small bowel, colorectal, gastric, pancreatic, breast and gonadal cancers. Image: Abdullah Sarhan, CC BY-SA 4.0, via Wikimedia Commons; resized. Original. Tap the image to zoom.

From the lesson “Small Bowel & Appendiceal Tumours” in Anal, Small Bowel & Appendiceal Cancers

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Oncology in the clinical exam

1 long case for the RACP Divisional Clinical Exam: you examine, present and are marked on the five RACP domains.

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