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CSIM2 > Solid organ malignancy 2.61-68 > Flashcards

Solid organ malignancy 2.61-68 Flashcards

1
Q

Extent of surgery in breast cancer?

A

Does not improve survival due to micrometastases; does improve symptoms related to local invasion. Do “lumpectomy” instead if possible.

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2
Q

Transcoelomic spread of ovarian cancer?

A

Spreads up right paracolic gutter, over surface of liver, down omentum.

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3
Q

Why do metastases from gastrointestinal cancers often appear in the liver?

A

Hepatic portal vein!

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4
Q

Lymphatic drainage of ovaries/testes?

A

Paraaortic nodes

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5
Q

Lymphatic drainage of scrotal/vulval/penile cancers?

A

Inguinal nodes

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6
Q

L’dopathy above SCF?

A

ENT!

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7
Q

Axillary and supraclavicular nodes?

A

All of thorax ie stomach, breast, lung.

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8
Q

Clinical presentation of cancer (1): Direct?

A

Mass effect (pressure, pain, palpable), obstruction of conduit (air, blood, bile), ulceration of serosal (organ) or mucosal (epithelial) surfaces e.g. IDA in GI bleed.

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9
Q

Clinical presentation of cancer (2): Other?

A
  1. Metastatic (effusions [microscopic inflammation], organomegaly)
  2. Asymptomatic (screening/Ix)
  3. Non-metastatic effects (fever, weight loss, paraneoplastic).
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10
Q

Two types of paraneoplastic phenomena?

A
  1. Humoral. e.g. ACTH/ADH; actively secreted so will improve once cancer treated.
  2. Immunological e.g. tumour Ag leads to new Ab formed; get cross-reactivity that may persist one cancer treated e.g. Lambert-Eaton syndrome
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11
Q

What is CUP?

A

Unique entity where a primary tumour is able to metastasize before the primary site becomes large enough to be identified

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12
Q

Differences between CUP and known primary tumours?

A

Early disseminsation, unpredictable metastasis, more aggressive, absence of symptoms due to primary.

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13
Q

Most common primary sites in CUP?

A

Lung, pancreas, gynae, GI.

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14
Q

Best approach to CUP?

A

Limited diagnostic approach designed to identify patients with good prognostic features; cheaper, faster, make use of MDT! Communication key!

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15
Q

Assessment in CUP?

A

Thorough exam, basic bloods, FoB, CT thorax/abdomen/pelvis. Only do endoscopy on basis of symptoms/signs. In men, can do serial PSA/AFP/BHCG to exclude treatable/curable cancers, and teste exam. Women need breast exam, mammogram, probably gynae exam. Whole body PET-CT can help with management. do family history!

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16
Q

Median survival in CUP?

A

6-9 months so don’t over investigate! This includes curable GCT/lymphoma so survival is torrid for some patients. Consider cost of time, burden of investigation, what investigation will actually add

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17
Q

Prognostic factors in CUP?

A

LN involvement (except SCF), performance status (key; comorbidity ie renal/hepatic impairment can be overcome; fitness CANNOT), weight loss >10%, serum markers (particularly LDH), males do worse, poorly differentiated cancer

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18
Q

Approach to CUP?

A

Search for primary (exam and image), rule out potentially curable/treatable tumours (GCT/lymphomas etc), characterise specific clinicopathological entity and split into favourable and unfavourable subsets and treat accordingly (curative and palliative INTENT)

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19
Q

Two oddly specific subtypes of patients who can do well with CUP? Do not miss!

A

1) patients with predominantly nodal metastases of poorly differentiated carcinomas
2) women with peritoneal carcinomatosis of a serous type adenocarcinoma

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20
Q

Main lifestyle factor for cancer mortality?

A

Diet (35%) then tobacco, then patterns of reproduction, then alcohol

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21
Q

Main community based factors for cancer mortality?

A

Infections (e.g. HPV), workplace, natural physical exposures, human made pollution, medicines/procedures, consumer products.

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22
Q

Tobacco and carcinogenesis?

A

90% of lung cancer attributable to tobacco. Due to inflammation of bronchial mucosa. Also carcinogens affect oropharynx, oesophagus, pancreas, bladder, RCC, AML.

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23
Q

What does smoking lower the cancer risk for?

A

Endometrial

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24
Q

Asbestos and mesothelioma?

A

Only need low exposure, but higher increases risk. More likely to be right-sided. Eventually obliterates visceral and parietal pleura.

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25
Q

PFTs in mesothelioma?

A

Restrictive

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26
Q

How does ionising radiation cause cancer?

A

High frequency, dislodges electrons, damages tissue. Lower frequencies e.g. electromagnetic radiation, radio waves are not associated with cancer. Spreading dose out over longer duration decreases risk.

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27
Q

Tissues most sensitive to ionising radiation?

A

Bone marrow, thyroid, breast (so be wary in treating mediastinal lymphoma in young women due to high chance of secondary breast malignancy)

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28
Q

What does ionising radiation include?

A

Cosmic rays, X-rays, gamma rays, A/B particles

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29
Q

UV radiation and carcinogenesis?

A

UVC and most of UV-B absorbed in ozone; some UV-B (and tiny proportion of UV-A) can be carcinogenic, but only for skin. Incidence lower in groups with more melanin, higher incidence at warmer latitudes. Heavy and intermittent burning as a child has particular risk.

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30
Q

Xeroderma pigmentosum?

A

AR defect with defective NER enzymes. Get photosensitivity, pigmentation changes, premature skin aging and high incidence of skin cancer (all types) as early as 3-4. Means that every exposure to UV causes lasting DNA damage; normally this is repaired.

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31
Q

What cancer is EBV linked to?

A

Burkitt’s lymphoma

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32
Q

What cancers is HHV-8 linked to?

A

Kaposi’s sarcoma, Castleman’s disease, primary effusion lymphoma

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33
Q

Which HPV strains are linked to cancer?

A

16, 18, 31, 45

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34
Q

Problem with vaccinating against cerival cancer?

A

Any remaining cancers are likely to be extremely aggressive and difficult to treat

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35
Q

Why polcythaemia in HCC?

A

Activation of fetal genes e.g. AFP/epo

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36
Q

Hormones and breast cancer?

A

Early menarche, late menopause, nulliparity, late age at first birth (and breast density) because have heightened exposure. COC does not increase risk directly! HRT does if >55 years old, >10 years

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37
Q

Hormones and endometrial cancer?

A

Post menopausal risk is increased greatly by HRT if it doesn’t contain progesterone too

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38
Q

Ovarian cancer and hormones?

A

Increased risk with nulliparity, early menarche and late menopause; COC protective (reduces number of ovulations)

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39
Q

Parasites and cancer?

A

Schistosoma haematobium can cause bladder cancer; bilharzia can cause bladder cancer, chronic cystitis.

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40
Q

Roughly how much cancer is heritable?

A

10%

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41
Q

Where may mutations be found in familial cancer syndromes?

A

Oncogenes (myc, HER-2, K-ras), TS genes (p52, BRCA1/2), DNA mismatch repair genes, genomic instability genes, dominant transforming genes (MEN2A), polymorphic carcinogen metabolising genes (CYP)

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42
Q

Hereditary breast cancer?

A

Only comprises 5% overall cases. Male beast cancer is mostly due to BRCA-2 mutations

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43
Q

What is Li-Fraumeni syndrome?

A

Rare; germline p53 mutation; AD; penetrance of 50% at 50. Characterised by premenopausal breast cancer, and childhood sarcoma, brain tumours, leukaemia and lymphoma, adrenocortical carcinoma

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44
Q

RR with breast cancer types?

A

First degree relative affected = RR 1.7; first degree relative with bilateral, premenopausal = RR 9

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45
Q

MEN 2b?

A

Mucosal neuromas of tongue, medullary cancer of thyroid, marfanoid, skin pigmented. May get neuromas elsewhere, + phaeo and parathyroid tumours. AD. RET oncogene.

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46
Q

NF-1?

A

AD. 100% penetrance; variable expression. Axillary freckling, cafe-au-lait macules. Pigmented hamartomas of iris (Lisch nodules in NF1, not NF2); phaeochromocytoma, optic glioma, acoustic neuroma, astrocytoma, meningioma, neurofibrosarcoma.

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47
Q

Acoustic neuromas in NF?

A

Rare in NF-1, but unilateral; uni or bilateral in NF2

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48
Q

Down’s syndrome and cancer?

A

Increased risk of AML

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49
Q

Paget’s disease of the bone?

A

Get bowing of legs, “sabre tibia”. ALP used as marker of disease activity. Get excessive bone breakdown and resorption with abnormal remodelling. Increased risk of osteosarcoma and fractures; must identify if fractures are benign or not.

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50
Q

Considerations in screening programmes?

A

Is it curable if diagnosed early, sensitivity (more important than specificity), is it common, frequency, what demographic, disadvantages of screening e.g. stigma, discomfort, fear.

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51
Q

How does Peutz-Jeghers increase cancer risk?

A

Get entirely benign hamartomous polyps of gut; no malignant potential but increase surface area dramatically so get increased CRC

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52
Q

Evaluating cancer screening programmes?

A

Screening uptake rate, recall rate of screened pop (TP + FP), biopsy rate, cancer detection rate, rate of interval cancers, incidence rate in non-attendees, deaths from cancers

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53
Q

Lead time bias in cancer screening?

A

Detect tumours at earlier stage so survival post-diagnosis seems to improve

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54
Q

Length time bias in cancer screening?

A

At start of screening programme, detect lots of patients with indolent disease (because prevalence of slow growing tumours is higher, even if incidence of faster growing is higher) so get illusory survival benefit in screened cohort

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55
Q

Breast cancer screening?

A

25% reduction in mortality. Women offered are 50-65, three yearly. Most interval cancers are in third year; should it be 2 yearly?

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56
Q

CRC screening?

A

Population testing of over 50s with FOB reduces deaths; sigmoidoscopy also effective. Different in FAP/HNPCC families (need surveillance colonoscopy)

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57
Q

PSA screening?

A

No RCTs have shown survival benefit or optimal therapy for early cancer; low benefit because tend to “die with” it

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58
Q

CIN screening?

A

Works due to clear prodrome. Has reduced SCC incidence; not good for CGIN.

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59
Q

Cancer prevention: vaccines?

A

HBV for HCC; HIV?; HPV for CIN. Social opposition because of fears of sexualising children

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60
Q

Cancer prevention: pharma? Review

A

NSAIDs, tamoxifen, vit A analogies, deltanoids, finasteride??

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61
Q

Why are germ cell tumours so sensitive to chemotherapy?

A

They are rapidly growing i.e. very short doubling

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62
Q

Peak incidence of testicular germ cell tumours?

A

25-35, 55-65.

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63
Q

Why are the adverse effects associated with chemotherapy particularly pertinent in GCC?

A

The survival is so good therefore “less important” factors like fertility must be considered

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64
Q

How do testicular germ cell tumours commonly present?

A

Lump in scrotum (may be detected incidentally after trauma), increase/decrease in teste size, scrotal pain, dragging sensation; can present with hydrocoele or gynaecomastia (if producing sex hormones), or non-specific back ache

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65
Q

Presenting with advanced disease in germ cell tumours?

A

Weight loss, fatigue, dyspnoea (mets/PE), ureteric obstruction (if retroperitoneal), SVC obstruction (mediastinal mass). May only take weeks for this to occur!

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66
Q

Investigating TGCTs?

A

Tumour markers (this is the rare case where they can be diagnostic), scrotal US, CT (thorax/abdomen/pelvis) for staging; may be performed after orchidectomy to assess residual disease.

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67
Q

“Morning sickness” in TGCT?

A

Rate of increase of BHCG

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68
Q

GCTs and tumour markers?

A

Not all germ cell tumours produce tumour markers, and if they are not produced at the start they will probably never be useful

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69
Q

Role of tumour markers in GCT?

A
  1. Can be diagnostic e.g. lump/US findings with raised AFP/BHCG is sufficient often
  2. Prognostic (higher is worse prognosis)
  3. Surveillance; marker relapse can precede clinical relapse by months
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70
Q

B-HCG and thyroid?

A

Very high BHCG can cause thyrotoxicity (acts as “on” switch for metabolism in pregnancy)

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71
Q

GCTs and HCG?

A

Produced by 100% of choriocarcinomas, 15% seminomas, and 75% of NSGCTs

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72
Q

Who may get FP in BHCG?

A

Regular cannabis users

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73
Q

AFP?

A

Physiologically synthesised in foetal yolk sac, liver and intestine

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74
Q

AFP and tumours?

A

Can be diagnostic of HCC along with hypoechoic lesion. 75% of NSGCTs.

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75
Q

Elevations in AFP?

A

Grossly in HCC and GCTs; slightly in other GI cancer and non-malignant liver disease

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76
Q

AFP T1/2?

A

Longer than BHCG, so takes longer to decrease after chemotherapy/surgery

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77
Q

AFP increase paradox?

A

Can be increased just after chemotherapy/necrosis of tumour; patient must be aware of this

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78
Q

LDH?

A

Non-diagnostic; marker of tumour bulk. Associated with necrosis i.e. seen in rapidly growing tumours and therefore is a predictor of TLS

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79
Q

When to do markers in TGCT?

A

Pre-orchidectomy, 24 hours post-surgery, then weekly until normalise. Good to assess residual disease.

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80
Q

Markers indicating no residual disease in GCT?

A

HCG normalises after 24 hours; AFP in 4-6 days.

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81
Q

Pre-op investigations in GCT/

A

Bilateral testicular ultrasound, CT chest/CXR, tumour markers

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82
Q

Differentials of “cannonball mets”?

A

Renal cell carcinoma, melanoma, osteosarcoma, choriocarcinoma, testicular cancer, metastatic adenocarcinoma. Only testicular and choriocarcinoma have a good prognosis.

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83
Q

Differentials for testicular mass?

A

Testicular cancer, benign epididymal mass, epidydimo-orchitis/orchitis, leukaemia/lymphoma infiltrate.

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84
Q

Risk factors for testicular cancer?

A

Genetics, testicular maldescent (orchidolpexy only reduces risk), XXY, trisomy 21

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85
Q

FP in AFP?

A

Alcohol abusers

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86
Q

Two types of TGCTs?

A
  1. Seminoma. Sheets and cord of relatively uniform cells which resemble primitive germ cells.
  2. NSGCTs. Umbrella term; can differentiate along embryonic and extraembryonic lines hence variety of appearances and spread.
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87
Q

NSGCT can be further divided to?

A

Mature teratoma, teratocarcinoma, yolk sac, choriocarcinoma, embryonal

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88
Q

What are the rete testis?

A

Tubules carrying sperm from seminiferous tubules to the efferent ducts

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89
Q

Local spread of seminoma and NSGCT?

A

Both to rete testis; this indicates higher risk of nodal involvement

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90
Q

Lymphatic spread of seminoma and NSGCT?

A
  1. Seminoma is highly predictable; goes to paraaortic, then pelvic, then mediastinal
  2. NSGCT. Less predictable, and may skip nodal junctions
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91
Q

Haematogenous spread of seminoma and NSGCT?

A
  1. This route is uncommon for seminomas.

2. NSGCT often to lungs, rarely to liver/brain/bone. Indicates poorer prognosis.

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92
Q

Poor prognosis for seminoma and NSGCT?

A

No such thing for seminoma! For NSGCT, associated with extrapulmonary visceral metastases, LDH >10* ULN etc.

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93
Q

What differentiates good risk and intermediate risk for seminoma?

A

Presence of extrapulmonary visceral mets.

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94
Q

How to stage in GCT?

A

Have histology, then contrast enhanced CT chest/abdo/pelvis; then have CT within 3 weeks of surgery to identify residual disease. Get CT brain if have multiple lung mets or HCG >10,000!

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95
Q

Complications of disease spread in GCT?

A
  1. Local (get SVC obstruction, pleural effusion, ureteric obstruction)
  2. Metastatic (lung, liver, brain, LNs)
  3. Non-metastatic (TLS, PE)
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96
Q

Biochemical features of TLS?

A

Hyperuricaemia, hyperkalaemia, hyperphosphataemia, hypocalcaemia. Caused by sudden death of tumour cells; can have secondary problems if pre-formed hormones are released e.g. phaeochromocytoma.

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97
Q

Complications of TLS?

A

Acute renal failure (hyperuricaemia and urate nephropathy), cardiac arrest/arrhythmia, DIC (cell death, activation of coag. cascades, intramuscular haemolysis (gives high LDH)

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98
Q

Prevention of TLS?

A

Expected (as usually follow chemotherapy), so can prepare with hydration, allopurinol, alkalinisation of urine.

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99
Q

Drugs to avoid in TLS?

A

ACEI/ARB, K+ sparing diuretics, NSAIDs, high potassium diet (chocolate, bananas)

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100
Q

Predisposing factors to TLS?

A

Large volume, SENSITIVE, tumours (Burkitt’s, NHL, leukaemia, germ cell, neuroblastoma, sarcoma); high LDH is a clue. Renal impairment (be wary of lymphomatous involvement of the kidney), male, <25.

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101
Q

Precipitants for TLS?

A

Cytotoxic chemotherapy, radiotherapy, steroid therapy, immune modifiers, surgery +/- anaesthesia, or DE NOVO argh!!

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102
Q

Managment of TLS?

A

Electrolye control with diet, diuretics, hydration etc., haemodialysis, allopurinol (inhibits uric acid formation by inhibiting xanthine oxidase), recombinant urate oxidase (converts uric acid into allantoins).

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103
Q

Problem with giving allopurinol or other xanthine oxidase inhibitors in TLS?

A

Can get accumulation of xanthine, which is itself nephrotoxic

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104
Q

Definitive management of early GCT?

A

Surgery (orchidectomy), consider biopsy of contralateral testis AFTER SPERM STORAGE. Remember to offer prosthesis! (better psych outcomes)

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105
Q

Options for patients with stage 1 seminoma (i.e. no residual disease after surgery)?

A

17% relapse; best therefore just to do surveillance on all.

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106
Q

Which has higher relapse rate, seminoma or NSGCT?

A

NSGCT, by some way.

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107
Q

How is surveillance done in NSGCT?

A

Monthly clinics for first year, with CXR/markers/exam, and CT @ 3 and 12 months. Then seen bimonthly in second year.

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108
Q

Management of metastatic GCT?

A

Still maintain a good prognosis; treat quickly and aggressively, and monitor Cx. Need to minimise treatment-related toxicity!

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109
Q

Bleomycin for metastatic GCT?

A

Risk of fatal pneumonitis; may wish to avoid in old patients, or those with renal impairment. Need PFTs before every cycle.

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110
Q

Cisplatin for metastatic GCT?

A

Renal impairment common (need to keep hydration), highly emetogenic, severe vascular toxicity (MI/CVA) possibly related to vascular spasm

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111
Q

Detecting residual tumour in GCT?

A

CT/PET-CT

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112
Q

Complications of therapy in GCT?

A

TLS, fertility (also a concern in women as harder to store but more likely to retain function), secondary malignancy! (especially with radiotherapy), pulmonary fibrosis (bleomycin), CVD risk (cisplatin), psychosocial. Need to be hyperaware of secondary malignancy etc. because survival rates are so good; it is not enough to “just survive”.

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113
Q

Fertility issues in GCT?

A

50% of men with testicular tumours will have low sperm count; therefore all who are receiving chemotherapy or radiotherapy should have sperm stored. May also be concern if remove the one working testicle. If sperm count is normal before therapy, 2/3 will be normal after. May be possible to do testicular-saving surgery rather than radical orchidectomy. Women often become amenorrhoeic, though fertility may return before periods do!

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114
Q

Cardiovascular related mortality in GCT?

A

May now begin to decrease as mediastinal radiotherapy less common. Still a problem with HTN after nephrotoxic chemo (particularly cisplatin). Lowest in surveillance, higher in chemo alone, highest if received radiotherapy. Latency period of 5-8 years. Advised not to smoke.

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115
Q

Secondary malignancy in GCT?

A

Risk of haematological cancer (5 years latency) after chemo, and solid organ cancer at/near radiological field. Greatest risk in under 30s. Smoking independently increases risk of 2ndary malignancy.

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116
Q

Psychosexual issues post GCT?

A

Anxiety and depression, sexual dysfunction, body image, relationship issues, gender issues. Mix of chemotherapy damage and psychological trauma of facing cancer.

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117
Q

Which lung cancers are most associated with smoking?

A

SCC and SCLC

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118
Q

Natural history of carcinoma of the bronchus?

A

Spread is circumferential and longitudinal along branch of bronchus, frequently involving regional lymphatics, and can spread in blood to virtually anywhere

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119
Q

LN involvement in Ca bronchus?

A

Peribronchial and hilar nodes ipsilaterally, then mediastinal nodes, then contralateral hilar, and supraclavicular nodes.

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120
Q

Presentation of lung cancer?

A

Some will be asymptomatic and found incidentally.

  1. Intrathoracic sc (cough, SOB, chest pain, haemoptysis, recurrent infections)
  2. Dysphagia from extrnsinc compression, SVC obstruction (mediastinal mass)
  3. Hoarse voice from invastion of RLN; indicates that cancer is inoperable so is significant finding.
  4. Extrathoracic symptoms e.g. anaemia, weight loss, malaise, lethargy
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121
Q

Finger clubbing is most associated with what lung cancer?

A

Squamous

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122
Q

What is Horner’s syndrome?

A

Miosis, enopthalmos, ptosis and anhidrosis (if lesion i pre-ganglionic)

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123
Q

What are most Pancoast’s tumours?

A

SCC or adenocarcinoma

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124
Q

What is Pancoast syndrome?

A

Shoulder pain, radicular pain in T1 distribution, Horner’s syndrome (sympathetic chain begins at T1?). Due to tumour, usually NSCLC in apex of lung invading surrounding soft tissues.

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125
Q

Some non-metastatic manifestations of lung cancer?

A
  1. Haem e.g. anaemia
  2. Neuromuscular e.g. LES
  3. Cutaneous e.g. acanthosis nigricans
  4. Ectopic hormone produciton e.g. PTH-RP causing hypercalcaemia
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126
Q

Signs of SVC obstruction?

A

Facial plethora, distended neck and chest veins (in distribution of SVC drainage) facial swelling, shortness of breath, cough/hoarseness/syncope. 90% have malignant cause; can be compression/invasion/thrombosis. May be aggravated by bending/stooping, improves after standing all day. Elevated JVP with absent waveform! Prognosis depends on cause e.g. may disappear with lymphoma. CXR should help with diagnosis; most common finding is widened mediastinum; may be normal CXR so CT better.

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127
Q

Clinical signs of pleural effusion?

A

Reduced expansion, tachypnoea, dull (stony dull) to percussion, mediastinum away/normal (more prominent with apex than trachea due to gravity), breath sounds absent or diminished, TVF decreased or absent (UNLIKE IN CONSOLIDATION). Bronchial breathing over level of effusion (aegophony), whispering pectoriloquy, may have pleural rub above fluid

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128
Q

Skin deposits in lung cancer?

A

Found in both SCLC and NSCLC. Immediately means stage IV disease. Will respond if site of origin is treated. Can give radiotherapy if uncomfortable.

129
Q

Horner’s syndrome and apical consolidaiton?

A

Very suggestive of malignancy

130
Q

Investigating lung cancer?

A

Bloods: FBC, U+E, LFT, LDH, calcium. CXR.
Then need sputum cytology (not done very often as not very sensitive), bronchoscopy (definite diagnosis) and possibly transthoracic needle biopsy if can’t do bronchoscopy.

131
Q

SCC?

A

20% lung cancer. Usually central, may cavitate, associated with clubbing. If cavitates, may see fluid level. May see atelectasis, pneumonia, pleural effusion. Has best survival!

132
Q

Large cell carcinoma (lung)?

A

10%. Tends to be around hilum, grow very quickly, once involve lymph nodes then are incurable.

133
Q

Bronchoalveolar carcinoma aka in situ pulmonary adenocarcinoma (AIS)?

A

Diffuse infiltrating disease, frothy pink sputum in huge amounts. Very drug resistant. Get multiple bilateral nodules.

134
Q

SCLC?

A

Very short doubling time. Neuroendocrine. Central mass with hilar or mediastinal lymphadenopathy. 25%. <1% five year survival.

135
Q

Extra imaging in SCLC?

A

Much higher incidence of metastasis; means need imaging probably CT of upper abdomen (liver, adrenals).

136
Q

What investigations might be done for NSCLC if considering radical surgery?

A

PFTs, contrast CT of chest and upper abdo, V/Q, MRI, US, medistinoscopy/laryngoscopy (essentially been replaced by PET-CT), PET-CT. Do more if suspect metastases. Aim is to see if is operable!!! If cannot tolerate bronchscopy (COPD, anxiety) then do virtual.

137
Q

LDH as prognostic factor in lung cancer?

A

IC enzyme; released in necrosis. Only really used as a tumour marker in SCLC! High LDH (indicates burden of cancer, rapid growth (i.e. growth outstrips vascular suppl) and risk of TLS). If it drops after chemo, seen as good thing. Likely to be higher in SCLC, but indicates poorer prognosis if raised in NSCLC.

138
Q

High-scoring predictors of poor survival in lung cancer?

A

Increased LDH, any site metastases, low performance status

139
Q

Medium-scoring predictors of poor survival in lung cancer?

A

Bone mets, liver mets, male gender, >5% weight loss

140
Q

Low-scoring predictors of poor survival in lung cancer?

A

Brain mets, age >65, non squamous, previous radiotherapy.

141
Q

What does very high LDH indicate in pleural effusion?

A

Likely to be empyema, not simple effusion.

142
Q

Staging system for NSCLC and clinical signifiance?

A

I,II,IIIA/B,IV. I-IIIA has surgery indicated. I has good prognosis; all others are 10% or less survival at five years.

143
Q

Adenocarcinoma?

A

40% (most common). 27% survival. Peripheral mass, solitary nodule, pleural effusion.

144
Q

Which lung cancer has highest proportion of non-smokers?

A

Adenocarcinoma. Smokers are most likely to get SCC! SCC patients who are non-smokers are likely to be due to passive smoking.

145
Q

Causes of exudate?

A

Infection, infarction, inflammation, malignancy.

146
Q

Complications of lung cancer?

A
  1. Local = SVC obstruction (thrombosis/obstructioun), pleural effusion.
  2. Distant metastasis = brain, liver, bone.
  3. Non-metastatic (hypercalcaemia, Cushing’s, SIAD, neurological).
147
Q

Primary causes of SVCO?

A

Lung cancer (65%), lymphoma, other malignancies (primary/secondary), non-neoplastic (10%), undiagnosed.

148
Q

Most common cancer causing brain metastasis?

A

Lung (50%), breast, renal cell carcinoma, melanoma, GI. May be CUP! Brain metastasis increasingly diagnosed, and imaging is better. 20% of lung cancers get brain mets.

149
Q

Two CNS mets of lung cancer?

A

Brain (MRI/PET ideal; MRI better for small mets), leptomeningeal (LP).

150
Q

Px of brain mets?

A

80% have headache, 40% cognitive dysfunction, 40% neurological deficit, 15-20% seizures.

151
Q

Why does chemo work in brain mets?

A

Usually do not cross BBB; mets disrupt this and increased the efficacy. Can get very good response!

152
Q

Hypercalcaemia in lung cancer?

A

10% of cancer patients. Often due to bony mets; true paraneoplastic is due to PTH-RP production. 100* more potent than PTH. Will be lost if tumour treated.

153
Q

Hypercalcaemia due to PTH-rP?

A

Cancer types: lung usually SCC, plus renal etc. Rare in breast cancer (calcium changes due to bony mets). See usual calcium symptoms (don’t forget arrhythmias). Treatment is HYDRATION and IV bisphosphonate.

154
Q

Diagnosing hypercalcaemia due to PTH-rP?

A

Ca >2.7, chloride low, hypercalciuria, high urinary phosphate, low or undetectable plasma PTH

155
Q

Ectopic ACTH in lung cancer?

A

Get hyperpigmented mucosa due to high ACTH. Tends to be SCLC (7% of SCLC; causes 50% of ectopic ACTH). Get Cushing’s syndrome.

156
Q

pH in Cushing’s syndrome?

A

Metabolic alkalosis

157
Q

Presentation and diagnosis of ectopic ACTH?

A

Rapid onset, marked weakness secondary to proximal myopathy, hyper-pigmentation, metabolic disturbances e.g. hyperglycaemia, hypokalaemiac alkalosis. High 24 hr urinary cortisol, high plasma ACTH, no response to dex suppression

158
Q

Treating ectopic ACTH?

A

Anti-tumour key! Can decrease actual cortisol secretion surgically or medically (i.e. bilateral adrenalectomy or ketoconazole).

159
Q

SIADH?

A

Most common endocrine paraneoplastic syndrome. SCLC particularly related! As are some chemotherapy drugs. 10% SCLC get it; humoral so treat cancer.

160
Q

Causes of SIADH?

A
  1. CNS (infection, stroke, trauma, vasculitis)
  2. Chest (infectious, tumour, pneumothorax)
  3. Drugs (vincristine, cyclophosphamide, carbamazepine etc.)
161
Q

Presentation and treatment of SIADH?

A

Often asymptomatic. Get fatigue, headaches, altered GCS, confusion, seizures. Diagnosis is to exclude non-malignant causes and then do lab. tests. Treatment is fluid restriction, democlocycline.

162
Q

Lab criteria for SIADH?

A
  1. Hyponatraemia <130
  2. Normal serum albumin and glucose
  3. Hypoosmolar serum (<275)
  4. Urine Osm > serum
  5. urinary sodium >25.
  6. ADH non-suppressed
163
Q

Hypocalcaemia and cancer?

A

Rarer but can be seen in lytic bone lesions e.g. breast, prostate, lung, or occasionally in tumours that secrete calcitonin. Tetani, NM irritability.

164
Q

What condition is calcitonin a useful marker for?

A

Medullary carcinoma of the thyroid!

165
Q

Gonadotrophins and lung cancers?

A

Also produced in germ cell tumours (with lung mets) so be careful! Do not miss. Most common sign of raised BHCG is gynaecomastia in men. Very high BHCG can cause thyrotoxicosis (useful in pregnancy). Do testicular exam, CT/CXR. Can also be hepatoma.

166
Q

Encephalomyopathies?

A

Ab-mediated. See perivascular inflammation and neuronal degeneration at several levels of nervous system. 75% caused by SCLC. Subacute onset; progressive, lose STM, hallucinations, personality changes. Treatment is immunosuppressive and anti-caner.

167
Q

Diagnosing encephalomyopathies?

A
  1. CSF (raised protein/IgG, pleocytosis)
  2. Serum: anti-Hu ab
  3. Imaging - MRI
168
Q

Lambert-Eaton?

A

AI destruction of VGCC limits ACh release. 60% have cancer. SCLC! Presents with proximal weakness; doesn’t affect bulbar muscles unlike MG.

169
Q

Diagnosing and treating Lambert-Eaton?

A

Diagnose with EMG; can do serum Ab against VGCC. Treatment is anti-tumour and immunosuppression; treating cancer usually leads to resolution. Can do plasma exchange!

170
Q

Humoral vs antibody mediated paraneoplastic syndromes?

A

Humoral should immediately resolve once cancer treated; antibody mediated may persist.

171
Q

Complications of lung cancer therapy?

A 
Chemo = anaemia, neutropenic sepsis (!)
Radiation = pneumonitis, toxicity to normal tissue e.g. spinal cord.
Surgery = reduced exercise tolerance.
172
Q

Defining neutropenic sepsis?

A

Neutrophil count <1
with pyrexia >38 (1 reading) or >37.5 on two readings over two hours, rigor, hypothermia, unexplained hypotension or tachycardia. Usually secondary to chemo but can be due to radiotherapy. Leading cause of chemo-related death. Hard to evaluate because IR abnormal e.g. CXR often normal/

173
Q

Risk of infection in neutropenic sepsis?

A

Risk depends on degree of neutropenia and its duration + patient factors e.g. Hickman line.

174
Q

Managing neutropenic sepsis?

A

Blood cultures (central and from Hickman), MSU, CXR, swabs for culture (throat, Hickman site).
+ empirical antibiotics (taz/gent) and keep platelets over 20.
Time to antibiotics key!
Stabilise, careful history and exam, don’t do PR/PV, avoid paracetamol until have established cause.

175
Q

Bad prognosis in neutropenic sepsis?

A

Diarrhoea, hypotension, coagulopathy, 1+ organ failure

176
Q

Radiation pneumonitis?

A

Hyperaemia and oedematous mucosa. 2-3 weeks latency, then degenerative phase and regenerative phase, causing epithelial proliferation and sclerosis.

177
Q

Risk factors for breast cancer?

A

Previous benign breast diseases, age, early menarche and late menopause, nulliparity/first pregnancy >35, oestrogen therapy (HRT over 55, for >10 years), obesity, FHx (of any cacner), radiation e.g. for medistinal lymphoma. COC not a cause, but could lead to pregnancy being pushed back.

178
Q

Epidemiology of breast cancer?

A

Higher in Caucasian women, higher in higher NS-SEC. Left breast more than right, particularly UO quadrant and retroalveolar.

179
Q

Features of familial (breast) cancers?

A

AD pattern, younger age, multiple affected relatives, multiple primary cancers, male breast cancers, bilateral breast cancers, ovarian cancers.

180
Q

Breast cancer genes?

A

BRCA1/2, p53 (Li-Fraumeni), Cowden syndrome, Peutz-Jeghers, ataxia telangectasia.

181
Q

Characteristics of BRCA-associated cancer?

A

Younger age of onset, frequently bilateral, worse histology (more aneuploidy, higher grade at presentation, higher proliferation indices, higher hormone receptor negative therefore tamixofen less useful).

182
Q

Presentation of breast cancer?

A
  1. Asymptomatic and found @ screening/incidentally.
  2. Lump found. If abates cyclically then less worrying.
  3. Paget’s disease
  4. Other local symptoms (pain, breast enlargment, skin/nipple retraction, nipple discharge/crusting/erosion.
183
Q

Paget’s disease of the nipple?

A

Associated with intraductal carcinoma invading terminal ducts; get eczematoid (erythematous keratotic patches) change in nipple/breast mass/bloody discharge. 50% malignant.

184
Q

Clinical signs of breast cancer presentation?

A
  1. L’dopathy (axilla, supraclavicular fossa)
  2. Nipple discharge or retraction (due to fibrosis pulling)
  3. Breast: discolouration, oedema, p’eau d’orange (infiltration of subcutaneous lymphatics), erythema, skin thickening, lack of symmetry (if new), nodules.
  4. Chest: consolidation, skin nodules
  5. Abdomen (hepatomegaly)
  6. MSK (focal tenderness in axial and peripheral skeleton could be mets?)
  7. Distant metastases (bone, lung, liver, pleura, adrenals, skin, brain (decreased order of likelihood)).
185
Q

Erythema in breast?

A

Can be inflammatory infiltrate in inflammatory breast cancer; mistaken for cellulitis.

186
Q

Lymphatic spread of breast cancer?

A

Medial goes to internal mammary nodes (impalpable); lateral to axillary and supraclavicular nodes.

187
Q

Extent of surgery in breast cancer?

A

Has no impact on survival due to presence of micrometastasis; may improve burden of local symptoms.

188
Q

Impact of self exam?

A

More likely to have smaller tumours, less likely to have axillary node metastasis, but rarely done well

189
Q

Evaluating cystic mass (breast)?

A

Ultrasound should show if solid or cystic, and if cyst is complex or simple. Then do FNA; if cystic should no non-bloody and lesion should completely resolve. If there is blood, or it doesn’t completely resolve, or if recurs after repeated aspiration, do biopsy. Cystic carcinoma = <1% of all breast cancer, but is a possibility.

190
Q

Evaluating solid mass (breast)?

A

Have to be extremely thorough before opting just to observe a solid mass. Mammogram assesses mass and rest of breast and contralateral breast. FNA done for easy cytology; high FN rate. Core biopsy gives architecture too. Excisional biopsy (lumpectomy) definitively establishes diagnosis.

191
Q

Evaluation of non-palpable mass?

A

Wire excision biopsy, stereotactic-guided core biopsy, ultrasound-guided core biopsy, breast MRI.

192
Q

CA 15.3?

A

No value in screening (low sensitivity for early disease). False positives in gynae cancers, and possibly lung/gastric. However, does increase with increasing stage of disease, highest in metastatic disease, and can be used to predict relapse fairly accurately, 2-9 months before clinical relapse. Not accurate enough alone to define response.

193
Q

Histological types of breast cancer?

A

Invasive ductal carcinoma (70%); the commonest type with or without DCIS. Invasive lobular accounts for most of remainder.

194
Q

DCIS?

A

20% of screen-detected cancers. High risk of becoming invasive. Needs treatment. Mulitfocal in 1/3 of cases.

195
Q

LCIS?

A

A predisposing risk factor for developing cancer in either breast (7% at 10 years); loess so than DCIS.

196
Q

Rules for screening BRCA relatives?

A

Start screening (with triple assessment) from 5 years below youngest (BRCA-associated) cancer in family. MRI preferable in young women to avoid serial radiation dose.

197
Q

Features suggestive of malignancy on mammogram?

A

Asymmetry, microcalcification, mass, architectural distortion

198
Q

What is breast ultrasound good for?

A

Differentiating fibroadenoma from cysts

199
Q

Cytology in breast cancer?

A

C1-5; 5 is definitely malignant. 1 is no cells. 2 normal, 3 abnormal, 4 suspicious. Tells you nothing about origin! Need to find something to biopsy, probably under US/CT guidance. This will rule out treatable i.e. lymphoma/GCT. Check clotting first!

200
Q

Two ways of detecting HER-2 status?

A

FISH, histology w/ immunohistochemistry. Remember, HER-2 has no naturally occuring ligand, and forms heterodimers with high proliferation index

201
Q

Complications of breast cancer?

A
  1. Local invasion: lymphoedema, pleural effusion, ascites
  2. Distant mets (bone, liver, lung, brain. Cord compression.
  3. Non-metastatic: hypercalcaemia (mets, or rarely PTH-rP
202
Q

Bony mets in breast cancer?

A

Most people who die of cancer have mets. Bone is third most common (behind lung and liver), and second most common site of spread in breast (after lymph nodes?). Average 2 year survival. Early detection and aggressive management key.

203
Q

Four main goals in managing patients with bony mets?

A
  1. Pain relief
  2. Preservation and restoration of function
  3. Skeletal stabilisation
  4. Local tumour control e.g. relief of tumour impingement on normal structure, prevention of release of chemical mediators that have local and systemic effects!
204
Q

Bisphosphonates in bony mets?

A

Reduce bony mets incidence, and apparently visceral mets (in breast cancer).

205
Q

Survival and number on axillary nodes involvement (Ca breast)?

A

Inversely proportional!

206
Q

Spinal cord compression?

A

Clinical diagnosis, but can only be confirmed radiologically. MRI is best. Mostly thoracic. Findings include bilateral UMN signs, are key. Any neoplasm capable of metastasis or local invasion can produce MSCC! If below L1/2, get LMN signs i.e. CES. Must be keenly aware of symptoms e.g. new back pain!

207
Q

Key predictor of outcome in MSCC?

A

Degree of pre-treatment neuro dysfunction! Histology of primary tumour also affects response to non-surgical therapy.

208
Q

Tumours most likely to cause MSCC?

A

Breast, lung, prostate, myeloma, renal, lymphoma, sarcoma.

209
Q

LN surgery and sentinel nodes? (breast)

A

Sentinel found with radioisotope; if clear then others probably clear. Do “sample” by taking 4-6 nodes from lower axilla. 99% of cancers have orderly lymphatic spread; occasionally skip a level

210
Q

Risk factors for distant mets in breast cancer?

A

> 3 involved LNs, T3/4 tumour.

211
Q

Who is recommended to get staged in breast cancer?

A

Tumour >5cm, >3 nodes clinically palpable, clinical suspicion (get CXR, US (liver), bone scan; then CT/MRI if suspicious. Tumour markers not used, although Ca15.3 is often raised in metastatic disease.

212
Q

Radiotherapy in breast cancer?

A

Used as adjuvant. Mandatory for conserved breast; less important in complete mastectomy, but still advised if tumour >5cm, tumours deep in the breast with clearance <3mm, all patients with 4+ LN mets.
Radiotherapy to chest wall/axilla reduces local recurrence rate in patients who have had heavy LN infiltration, and radiotherapy to LN areas improve cause-specific survival

213
Q

Adjuvant and neoadjuvant therapy in breast cancer?

A

Adjuvant is designed to treat micrometastatic disease, or cells that have escaped locally but not yet established a metastasis. Goes after surgery primary treatment). Treats a “risk”, not actual disease.
Neoadjuvant goes before primary treatments; shrinks tumour e.g. hormonal, chemotherapy.

214
Q

Options for adjuvant therapy in breast cancer?

A

Chemotherapy, radiotherapy and endocrine.

215
Q

Adjuvant taxanes and contralateral breast cancer?

A

Taxanes e.g. tamoxifen decrease incidence of contralateral breast cancer

216
Q

Role of chemotherapy in breast cancer?

A

Only as adjuvant; gives incremental reductions in death/recurrence with combination serial strategies.

217
Q

When is neoadjuvant treatment used in breast cancer?

A

Give before surgery, particularly if large or aggressive.

218
Q

Breast cancer prevention?

A
  1. Mastectomy reduces risk in BRCA patients to 1% (because volume of tissue reduced).
  2. Surgical oopherectomy in BRCA-1 carriers reduces oestrogen, and incidence of breast cancer
  3. Tamoxifen decreases incidence of breast cancer in high risk women BUT no survival benefit because of increased rates of endometrial cancer; also get DVT/PE risk, and only prevents ER+ tumours.
  4. Aromatase inhibitors for secondary prevention; probably effective in post-menopausal women.
  5. Surveillance; evidence that combo of mammography and MRI better to either alone. US has no value as screening.
219
Q

Ovarian cancer epidemiology?

A

Median age 63. Primarily a disease of post-menopausal women. Highest rates in European born Jews (BRCA carriage).

220
Q

Aetiology of ovarian cancer?

A

An accumulation of multiple, variable discrete mutations. 5-10% due to inherited disease e.g. BRCA2/1, HNPCC (i.e. Lynch; endometrium and ovarian).

221
Q

Hormonal risk factors for ovarian cancer?

A

Nulliparity, low parity (1-2), infertility, HRT (weak; >55, >10 years), ovulation-inducing drugs (IVF, PCOS), early and late menopause. COC protective (fewer ovulations).

222
Q

Other risk factors for ovarian cancer?

A

Talc, ionising radiation, higher animal fat consumption, obesity.

223
Q

BRCA and ovarian cancer?

A

AD, increased risk, variable penetrance. Much more prevalent in European jews. However, BRCA-associated ovarian cancers tend to be less aggressive. Mainly BRCA1 for ovarian. BRCA mutations do not usually feature in sporadic ovarian cancer, but much higher de novo rates than expected (no FHx, but germline so have implications for future family).

224
Q

Strongest risk factor for ovarian cancer?

A

Family history! Next is nulliparity.

225
Q

Criteria for COC reducing ovarian cancer risk?

A

Must be combined, must be at least 10 years!

226
Q

Spread of ovarian cancer?

A

Up right paracolic gutter, over surface of liver (not parenchyma), shedding on underside of diaphragm then on omentum; must sample these areas when staging.

227
Q

Signs and symptoms of early ovarian cancer?

A

Early is very insidious. May be detected on VE as mass incidentally. Bloating often first symptom. Can grow to ~10cm before impinging on ureter/bowel and causing symptoms (urinary frequency, rectal pressure). Key is CHANGE (no specific symptoms).

228
Q

Signs and symptoms of advanced ovarian cancer?

A

Even when advanced, have few symptoms. May have bloating, swelling, bladder or rectal symptoms.Rarely, can get abnormal PV bleeds.DD IBS! Eventually, get ascites, indigestion, back ache, anorexia, weight gain.

229
Q

Advanced ovarian cancer and ovary size?

A

Can have advanced stage but essentially normal size ovaries, hence confusion re CUP.

230
Q

Specific signs and symptoms of advanced ovarian cancer?

A

Fatigue, anorexia.
Bowel: get bloating, distention, anorexia, n+v, altered bowel habit (particularly constipation), abdo pain, obstruction,
Kidney: ureteric obstruction and hydronephrosis, haematuria, recurrent UTI, loin pain, renal failure.
Pleural effusion: usual stuff.
Also, can be extremely prothrombotic, particularly clear cell so get pulmonary embolism/DVT.

231
Q

Pleural effusion in ovarian cancer?

A

Tends to be on the right!

232
Q

Investigating potential Ca ovary?

A

FBC, biochem, LFTs, TFTs (can be relevant re BHCG), bone profile, and tumour markers. First imaging is ultrasound. CT and MRI not used for diagnosis; may be useful preoperatively but need to do laparotomy to be certain. Staging is with laparotomy. Can do endometrial sampling (if have PV bleed); coexistent endometrial cancer is possible (Lynch).

233
Q

Tumour markers to do for Ca ovary?

A

CA-125, CEA; younger women do hCG, AFP, LDH (i.e. germ cell tumours). CEA not terribly helpful for diagnosis; goes up in many forms of adenocarcinoma. Some will have no marker production.

234
Q

Staging of ovarian cancer?

A

Done SURGICALLY with exploratory median laparotomy, then pathology. Aim is to debulk tumour; >1cm remaining is suboptimal and has no survival benefit. Can also be optimal (<1cm) or complete. If open them up and apparent that is inoperable, get chemotherapy first (becomes neoadjuvant or PRIMARY MEDICAL THERAPY)

235
Q

Doing cytology/histology before ovarian cancer laparotomy?

A

Can do preoperative cytology/histology (of effusions, masses); however, paracentesis (ascites) or needle biopsy only delay definitive management and may lead to seeding; skin disease immediately makes them C4. Therefore only drain ascites first if very symptomatic.

236
Q

RMI?

A

UMCa-125. Menopausal status (1 or 3), US appearance (up to 3). If >200, see special gynae surgeon; if lower then can have routine gynaecologist.

237
Q

Borderline ovarian tumour?

A

Not benign but not yet invasive so not technically malignant. Should be removed.

238
Q

RMI ratings?

A

<25 low, 25-250 mod, >250 high. >200 need specialist surgeon.

239
Q

MRI in ovarian cancer?

A

Can be useful for surveillance of cysts; not particularly for diagnosis.

240
Q

Ca-125?

A

Produced by coelomic epithelium, so any inflammation of peritoneal surface (pleuritis, peritonitis, pancreatitis, appendicitis) will cause, as will several tumours including lymphomas. 50% of early stage ovarian cancers will have elevated Ca-125; increased in ascites (ASCITES ALONE CAN RAISED CA-125). High levels before surgery in stage 1 has poorer prognosis (prognostic not diagnostic). Also, serial rise of >25% is most accurate predictor of progression. So if elevated at diagnosis, then returns to normal after surgery, monitoring it IN THAT INDIVIDUAL is very sensitive. But not diagnostic on population level.

241
Q

CA-125 marker relapse?

A

Confirmed DOUBLING from ULN during follow up predicts clinical relapse with almost 100% specificity.

242
Q

Problem with Ca-125 marker relapse?

A

Patients latch on to it; means that rise even when have no symptoms can be very anxiety-provoking.

243
Q

Pathology of ovarian cancers?

A

Can be epithelial (90%) or other (sex cord stromal, sarcoma, germ cell). Epithelial are mostly serous (fallopian tube epithelium). Mucinous is near-identical to GI epithelium; can lead to further CUP confusion. Clear cell is rare, aggressive, with Ca-125 often normal.

244
Q

Serous ovarian cancer and BRCA?

A

Prevalence of BRCA almost 20%; de novo rather than somatic. Means do gene testing at diagnosis because has implications for treatment! Even if no FHx!

245
Q

Significance of staging for ovarian cancer?

A

5YS 90% for 1a. 10% for IV.

246
Q

Complications of ovarian cancer?

A
  1. Locally get lymphoedema, vaginal discharge, bowel obstruction (GI primary DD), ascites, pleural effusion.
  2. Distant metastasis (liver, lung, bone, brain). Not common at diagnosis. May be GCT. Seeing more because living longer.
  3. Non-metastatic (PE, dermatomyositis).
247
Q

Meig’s syndrome?

A

Ovarian fibroma + transudative ascites/pleural effusion.

248
Q

Ovarian cancer and Trousseau syndrome?

A

Syndrome more associated with lung/pancreatic/gastriuc cancer, but get recurrent thrombophlebitis; tumour causing hypercoagulable state.

249
Q

Significance of malignant ascites?

A

Likely to be due to serosal implants in peritoneum. May have prognostic significance, but doesn’t really alter management and curative may still be possible. Just drain it. Should be investigated for malignant cells.

250
Q

Cause of (malignant) ascites?

A

If just presents with ascites, rather than merely being present at diagnosis, need to find cause (HF/LF/RF, infectious etc.) 10% have malignancy. If have advanced cancer likely to be malignant ascites but do not assume, so do cytology; larger sample better.

251
Q

Ascites and CUP?

A

If it turns out to be ovarian, actually have a pretty good prognosis, so ascites of unknown origin in female patient needs thorough investigation.

252
Q

Treating malignant ascites?

A

Treatment is usually paracentesis; if recurring very quikcly can use indwelling Pleurx catheter. Not much point using loop diuretics/Na+ restriction/aldosterone antagonists because pathology is not due to Na+ retention. Albumin i.e. colloid does not help either! Unless have concurrent liver problems.

253
Q

Heliotrope rash and Gottron’s papules?

A

Dermatomyositis. Most likely cancer is upper GI, can be ovarian.

254
Q

Dermatomyositis?

A

Cancer underlying in 10-40%. GI, SCLC, NSCLC, breast, ovary. Proximal myopathy, skin changes, and systemic feautres including cardiopulmonary conditions, arthralgias, retinopathy. Often present prior to cancer diagnosis

255
Q

Diagnosing dermatomyositis?

A

High CK, LDH, aldolase; muscle biopsy shows myositis; can do EMG (show fibrillation and insertion irritability).

256
Q

Treating dermatomyositis?

A

Find and treat tumour! May be independent of tumour and not get better. Steroids etc.

257
Q

Principles of treatment in ovarian cancer?

A

(Preventative), adjuvant (chemotherapy after surgery to mop up remaining cells); neoadjuvant/primary medical therapy is where are unfit for surgery. Vast majority of chemotherapy given with palliative intent; means aim to improve quality of life. Must record intent. Once cancer has relapsed, all treatment is palliative, but can still have years of remission.

258
Q

Surgery in ovarian cancer?

A

More tumour removed has better outcome; may be confounded by better-behaving cancers being easier to remove, or has surgeon “fixed” them. Essentially, selection process vs disease modification. >1cm left is suboptimal.

259
Q

Bevacizumab in ovarian cancer?

A

VEG-F inhibitor; relies on tumours being unable to grow beyond 1mm3 without own blood supply. Has had significant effect on survival. Very expensive. Used in poor prognosis patients. Potentially may need to be on it for life?

260
Q

Intraperitoneal chemotherapy in ovarian cancer?

A

Can give huge doses of chemo; used for microscopic seeding on peritoneum. However, get “chemical burn” so uncomfortable.

261
Q

Best way to think about ovarian cancer?

A

A chronic disease, with multiple relapses. May not cure, but can get remission again and again, chemotherapy, hormonal therapy etc.

262
Q

Median lead time between CA-125 marker relapse and clinical relapse?

A

5 months or so. Should we treat at marker relapse? However, once have relapsed, treatment becomes palliative, so no point giving chemotherapy before have symptoms. Confers no survival benefit.

263
Q

Determinants of response to treatment with relapse in Ca ovary?

A

Longer interval since first line treatment has much better response rate, and higher survival. (called “platinum-free interval”). Relates back to finding favourable subsets! (and treating accordingly)

264
Q

Other response determinants in ovarian cancer (in patients who have already had platinum treatment) to platinum?

A

Serous histology (serous do better, probably due to high prevalence of BRCA mutations), no. of disease sites and tumour size are independent predictors of prognosis. p53 etc. too!

265
Q

Mutant p53/p21 and response to platinum in ovarian cancer?

A

Mutants in p53 or downstream pathway elements means virtually no response to carboplatin (as cannot arrest cell cycle) so probably should not be treated with it. Conversely, BRCA mutations do well because cannot repair damage by chemotherapy. BRCA carriers get more ovarian cancer but there prognosis is better!

266
Q

When should relapse be treated in ovarian cancer?

A
  1. Aggressive says treat while burden low and PS good, particularly as symptoms may be due to bowel obstruction (bad for chemo).
  2. Conservative says, as not curative, and chemo has adverse effects, wait till symptomatic then treat. This is better and has no negative impact on survival! So don’t intervene early! However, surgery the second time round may be effective early.
267
Q

Radiotherapy in ovarian cancer?

A

Good for spot therapy to relieve symptoms, particularly PV/PR bleeding. Not good for whole abdomen.

268
Q

Endocrine therapy in ovarian cancer?

A

Oestrogen receptors often found on ovarian tumours (predictably); low response rates to tamoxifen but remains a viable option if have failed chemo or cannot tolerate it!

269
Q

Patients who relapse within six months with ovarian cancer?

A

Very poor prognosis subset (platinum resistant). Independent adverse prognostic factor. Goal of treatment is symptoms control and QOL. Offer them new clinical trials if they want, but be realistic about disease and be aware of risk-benefit of chemotherapy. Constantly re-evaluate this!

270
Q

Aims of chemotherapy at relapse?

A
  1. To help the individual patient (palliate symptoms [&prolong survival]).
  2. To define activity of new drugs, and non-cross resistance with standard therapy. (Assess with response rate, progression-free survival, overall survival, quality of life, economic analysis).
271
Q

Notes on BRCA inheritance?

A

Homozygotes not compatible with life usually. Has recessive cellular function i.e. need loss of both alleles to lose tumour suppressor effect, but behaves in dominant inheritance because having one mutation makes you very likely to get another. Can get sporadic, but unlikely to get two hits in same cell lineage.

272
Q

IHC in GI/ovarian cancer?

A

Can be identical; means metastatic pancreatic/gastric cancer can be impossible to differentiate from ovary. Can also have tumour anatomically completely encasing the ovary, but IHC says gastric origin and OGD normal! Don’t get carried away with puzzle.

273
Q

Three ways to find primary site in CUP?

A

Imaging, scope, sometimes even exploratory laparotomy.

274
Q

Metoclopramide in bowel obstruction?

A

Good in subacute; moves things along and anti-emetic. In acute, increases pain and exacerbates things. Use haloperidol instead.

275
Q

Epithelial site gives rise to?

A

Carcinoma (i.e. from ORGANS). Glandular = adenocarcinoma, sarcoma = connective tissue. (+ haem).

276
Q

Signs to look for if have effusion?

A

Cancer: clubbing, l’dopathy
HF: JVP
LF: leuconychia, spidar naevi, gynaecomastia
RF: vascular access grafts, AV fistuale
RA, DVT (PE can cause effusion if is peripheral)

277
Q

Significance of pleural effusion without mediastinal shift?

A

Suggests an associated collapse, and need bronchoscopy to rule out obstructing lesion

278
Q

Investigating pleural fluid?

A

Microscopy, glucose (low in empyema, RA), pH <7.2 in empyema (usually post-pneumonia), amylase raised in pancreatitis/oesophageal rupture, triglycerides (milky, fatty fluid in chylothorax),protein (SAAG) for exudate vs transudate.

279
Q

Investigating pleural exudate?

A

Effusion albumin/plasma albumin >0.5 (Light’s), LDH >200 and ELDH/plasmaLDH >0.6; very high LDH, low glucose and pH <7.2 may be empyema rather than true exudate. Cytology 60% diagnostic, CT-guided biopsy 70%, thoracoscopy 90%.

280
Q

Unexplained nausea?

A

Hypercalcaemia, occult brain mets, hypomagnasaemia, other metabolic disturbance.

281
Q

What is corrected calcium?

A

Accomodates for low albumin levels.

282
Q

Which cancers are most likely to give hypercalcaemia?

A

Myeloma, breast, lung, kidney, head and neck, lymphoma.

283
Q

Mass at porta hepatis?

A

Gastric and pancreatic cancer?

284
Q

Masses in liver parenchyma?

A

Lung, gastric, pancreatic, breast, CRC; ovarian less likely.

285
Q

Widespread peritoneal involvement?

A

More common in peritoneal or ovarian cancer, less gastric

286
Q

Ovaries normal size?

A

Can still have normal ovaries but their metastases are causing the problem! I.e. pelvic exam not the be-all

287
Q

Microcytic anaemia? (M/F)

A

F think menorrhagia; M think GI bleed; if post-menopausal or bowel habit change consider GI bleed in women. Increases suspicion of GI primary!

288
Q

Most sensitive liver function test?

A

Clotting?

289
Q

What could artifically elevate CA-125?

A

Ascites/effusion! Has no role in diagnosis. Epithelial origin so heart failure etc. can raise it; ECF space ie pleural effusion is reservoir for the antigen, even without having actual inflammation.

290
Q

Biopsy showing focal mucinous change?

A

GI, maybe ovarian. Indicates probably less favourable response to chemo.

291
Q

What is TTF1 for?

A

SCLC vs NSCLC

292
Q

Primary goal in palliative treatment?

A

QOL! Duration of life is secondary

293
Q

Factors affecting treatment choice?

A

Age (not really), organ impairment might alter specific drug etc but not nature of treatment, patient priorities, FITNESS

294
Q

Most important thing when deciding on type of palliative treatment?

A

Taking time to make correct choice; once not curative, actually not that much urgency always.

295
Q

Something to consider when choosing a test?

A

What would identify emergency or treatable cause e.g. Ca2+

296
Q

Which serum markers can be diagnostic in ANY patient with CUP?

A

AFP/HCG could be HCC; testicular with AFP/HCC could be GCT. PSA slightly raised may just be BPH; PSA if 600 can only be disseminated prostate cancer therefore sensitivity and specificity altered by level/patient. C- (CHO) Ag never really diagnostic but may have a role in surveillance.

297
Q

Most important consideration in CUP?

A

Exclude curable cancers

298
Q

Some things that can cause raised Ca-125?

A

Cervical adenocarcinoma, endometrial carcinoma, fallopian tube carcinoma, HF, hypothyroid, liver cirrhosis with severe necrosis, NHL, non-mucinous epithelial ovarian cancer, pleural effusion (not exhaustive)

299
Q

CRC screening?

A

60-74 get FOB; starting to do one-off flexi sig @ 55.

300
Q

Problems with hormonal treatments in aggressive cancer?

A

Fairly low response rates and takes a few months to start working

301
Q

When is it appropriate to give clinical trial agent?

A

Must have exhausted standard therapy or is unethical!

302
Q

What actually is cachexia?

A

Reduction in carcass weight; constellation of events involving anorexia, weight loss, muscle wasting, anaemic and lack of energy. In cancer patients likely to be due to anorexia + metabolic derangement.

303
Q

Causes of pruritis in suspected cancer patients?

A

Hodgkin’s, obstructive jaundice, uraemia, allergy, dermatitis, neuropathy, drug reaction (OFTEN WITH OPIATES)

304
Q

How can haematological malignancy cause ascites?

A

Prone to extra-hepatic portal vein thrombosis, or by infiltrating liver and spleen, or by obstructing lymphatic duct drainage.

305
Q

Causes of jaundice in cancer patient?

A

Widespread parenchymal liver mets, solitary liver mets near porta hepatis, lymph node mass at porta hepatis, pancreatic cancer, cholangiocarcinoma, drug reaction or viral infection

306
Q

How do peritoneal seedlings arise?

A

Transcoeolomic spread; can cause bowel obstruction

307
Q

Hydronephrosis with thin renal cortex?

A

Suggests chronic kidney problem. Means must be wary for drug therapy.

308
Q

Key thing for serum and fluid gradient for albumin?

A

Must be sent on the same day!

309
Q

Why is viral serology important in cancer?

A

Can cause cancers and means can be reactivated once chemotherapy started

310
Q

Use of TTF1?

A

Lung adenocarcinoma usually +ve; squamous usually -ve. Small cell tumours, of any origin, are usually +ve. Also differentiates between primary pulmonary adenocarcinomas (+ve) and metastatic pulmonary adenocarcinomas (-ve)

311
Q

Most valuable application of tumour markers?

A

The detection of recurrence of malignant disease after recurrence.

312
Q

What does prostatic acid phosphatase indicate?

A

Spread of prostatic cancer

313
Q

What does bone alkaline phosphatase indicate (Alk phos)?

A

Primary and secondary osteoblastic tumours e.g. osteogenic sarcoma; NOT MULTIPLE MYELOMA

314
Q

What does liver alk phos indicate?

A

Primary and secondary liver tumours, associated with localised intra-hepatic biliary obstruction. May also see rise in GGT?

315
Q

What does neuorne specific enolase indicate?

A

SCLC; raised in 70% untreated patients

316
Q

CEA use?

A

Post-op CRC; lacks sens and spec to establish diagnosis.

317
Q

AFP use?

A

HCC, teratoma

318
Q

Ca 199 elevated in?

A

Pancreatic, gastric, hepatobiliary

319
Q

Ca 15 3 elevated in?

A

Breast cancer

CSIM2 (21 decks)

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