Cancer Flashcards

1
Q

Define gastric cancer

A

Gastric malignancy, most commonly adenocarcinoma, more rarely lymphoma, leiomyosarcoma.

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2
Q

Explain the aetiology / risk factors of gastric cancer

A

Most cases are probably caused by environmental insults in genetically predisposed individuals that lead to mutation and subsequent unregulated cell growth.

Risk factors include: Helicobacter pylori infection; atrophic gastritis; diet high in smoked, processed foods and nitrosamines; smoking; alcohol.

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3
Q

Summarise the epidemiology of gastric cancer

A

Common cause of cancer death worldwide, with highest incidence in Asia, especially Japan. Sixth most common cancer in UK (annual incidence is 15 in 100 000).

Male:female is around 2:1. Age>50

Cancer of the antrum/body is becoming less common, while that of the cardia and gastrooesophageal junction is increasing.

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4
Q

Recognise the presenting symptoms of gastric cancer

A

In the early phases, it is often asymptomatic.

Early satiety or epigastric discomfort.

Weight loss, anorexia, nausea and vomiting.

Haematemesis, melaena, symptoms of anaemia.

Dysphagia (tumours of the cardia).

Symptoms of metastases, particularly abdominal swelling (ascites) or jaundice (liver involvement).

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5
Q

Recognise the signs of gastric cancer on physical examination

A

Physical examination may be normal.

Epigastric mass. Abdominal tenderness. Ascites. Signs of anaemia.

Many eponymous signs: Virchow’s node/Troisier’s sign: Lymphadenopathy in left supraclavicular fossa.

Sister Mary Joseph node: Metastatic nodule on umbilicus.

Krukenberg’s tumour : Ovarian metastases. (metastasis from primary site, classically in the GI tract, most commonly from gastric adenocarcinoma, particularly at the pylorus)

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6
Q

Identify appropriate investigations for gastric cancer and interpret the results

A

Upper GI endoscopy (+multiquadrant biopsy of all gastric ulcers)

Blood: FBC (anaemia) and LFTs

CT/MRI: staging of tumour and planning surgery

USS liver: staging of tumour

Bone scan: staging of tumour

Endoscopic ultrasound: Assesses depth of invasion and lymph node spread.

Laparoscopy: May be needed to determine if tumour is resectable.

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7
Q

Define prostate cancer

Outline the structure of the prostate gland.

Where does BPH (i.e. not prostate cancer) commonly occur

A

Prostate cancer, usually refers to prostate adenocarcinoma, where adeno- means gland and carcinoma refers to uncontrolled growth of cells - so prostate cancer is a tumor or growth that originates in the prostate gland.

The prostate is covered by a capsule of tough connective tissue and smooth muscle.
Beneath this layer, the prostate can be divided into a few zones.

The peripheral zone, which is the outermost posterior section, is the largest of the zone and contain about 70% of the prostate’s glandular tissue.
Moving inward, the next section is the central zone which contains about 25% of the glandular tissue as well as the ejaculatory ducts that join with the prostatic urethra.
Last, is the transitional zone, which contains around 5% of the glandular tissue as well as a portion of the prostatic urethra.

The transitional zone undergoes hyperplasia, or an increase in the number of cells, in a large percentage of older men, and that often leads to compression of the urethra.
This is called benign prostatic hyperplasia and is often considered a normal part of aging.

At microscopic level: each of glands covered by BM (mostly collagen, then a ring of cube-shaped basal cells and neuroendocrine cells, and finally an inner ring of luminal columnar cells which are within the lumen or centre of the gland.

Luminal cells secrete substances into prostatic fluid including PSA.

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8
Q

Explain the aetiology / risk factors of prostate cancer

A

Prostate adenocarcinoma most often results from a genetic mutation in a luminal cell, but can also be a basal cell, and it results in that cell dividing uncontrollably.

Some risk factors for a genetic mutation include old age, obesity, and a high fat-low fiber diet.

Mutations in two genes that have been linked specifically to prostate cancer are breast cancer gene 1 and breast cancer gene 2, also known as BRCA1 and BRCA2 - both of which also cause breast cancer.

Early on, prostate cancer cells depend heavily on androgens for survival, but eventually, the cancer cells mutate and find a way to keep multiplying without relying on androgens.

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9
Q

Summarise the epidemiology of prostate cancer

A

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10
Q

Recognise the presenting symptoms of prostate cancer

A

Early on, prostate cancer typically causes no symptoms.
That’s because the majority of prostate cancers arise in the posterior peripheral zone, which is far away from the urethra.

As a result, these tumors can grow quite large before they cause problems with urination.

Over time, if the cancer does compress or invade the urethra or bladder, it can cause difficulty urinating, bleeding, and pain with urination and ejaculation.

If the cancer becomes metastatic, it most commonly spreads to the bones, like the vertebrae or pelvis, resulting in hip or lower back pain.

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11
Q

Recognise the signs of prostate cancer on physical examination

A

Prostate cancer can be detected by a digital rectal examination, which is where a finger, is inserted into the rectum to feel against the anterior wall of the rectum which lies along the posterior part of the prostate.
A tumor located here would feel like an irregularly hard lump.
But if the tumor arises elsewhere, like in the anterior peripheral zone, then the tumor would be out of reach during the digital rectal exam.

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12
Q

Identify appropriate investigations for prostate cancer and interpret the results

A

Another approach is to use a transrectal ultrasound or MRI to image the prostate.

Prostate cancer can also cause an elevation in the prostate specific antigen.

But ultimately, the diagnosis of prostate cancer requires a biopsy, so that the cells can be scored using the Gleason grading system.

The Gleason scale identifies the two most common cell patterns within the prostate tissue and assigns a score between one and five to both of them:

SCORES:
1- normal, well differentiated cells
5- highly abnormal cells barely resembling normal prostate tissue

Once the primary and secondary patterns have each received a score from one to five, these two numbers are added together, resulting in a total Gleason score between two and 10 with two representing low-grade tumors and 10 representing high-grade, dangerous tumors.

Treatment:
In terms of treatment, when the tumor is confined to the prostate, and hasn’t metastasized, active surveillance is usually done.

This includes routine tumor marker measurement as well as imaging, to ensure that the prostate cancer remains confined to the prostate.
If the tumor spreads beyond that point, treatment options include surgery, radiation therapy, chemotherapy, and hormonal therapy.

Treatment may include chemotherapy, radiation therapy, surgery, and hormonal therapy, but active surveillance is also an option in many cases where it’s localized to the prostate.

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13
Q

Define tumour lysis syndrome

A

Rapid cell death with initiation of chemotherapy resulting in:

  • hyperkalaemia,
  • hyperphosphataemia,
  • hyperuricaemia (–> gout)
  • secondary hypocalcaemia,
  • acute renal failure.

It damages the kindeys and may cause potentially life-threatening renal failure.

Note, it’s called secondary hypocalcaemia because it occurs SECONDARY to hyperphosphataemia.

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14
Q

Explain the aetiology / risk factors of tumour lysis syndrome

How to prevent?

Risk factors

How does it cause damage to the kidneys?

A

High levels of potassium, phosphate, and urate, and low levels of calcium can lead to clinical manifestations of:

Kidney injury and failure
Abnormal heart rhythms
Muscle cramps and weakness
Seizures

See high risk tumours below.

Risk factors:

  • Dehydrated patients
  • Those with existing kidney dysfunction

Renal dysfunction:
Calcium phosphate crystals obstruct renal tubules –> AKI

Nucleic acid –> uric acid –> hyperuricaemia –> urate nephropathy and risk of AKI

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15
Q

Summarise the epidemiology of tumour lysis syndrome

Who is most likely to develop TLS

A

Not all cancer patients are at equal risk of developing TLS

High risk tumours following chemo include those that have rapidly dividing cells:

  • Acute leukaemia (myeloid OR lymphoid)
  • High grade lymphoma

Can occur spontaneously before cancer treatment, but is more common within a week of starting treatment.

Not just in patients with traditional chemo, also in patients receiving steroids, hormonal therapy targeted therapy, or radiation therapy.

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16
Q

Recognise the presenting signs and symptoms of tumour lysis syndrome

A

Nausea +/- vomiting

Haematuria

Lack of appetite/fatigue

Dark urine, reduced urine output

(LOW CALCIUM:) Numbness, seizures, hallucinations

(LOW CALCIUM:) Muscle cramps and spasm

(HIGH POTASSIUM:) Heart palpitation and muscle weakness

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17
Q

Identify appropriate investigations for tumour lysis syndrome and interpret the results

A

TLS is diagnosed based on blood tests, along with signs and symptoms. Its onset may be subtle, with only a few abnormal laboratory values, but it can also present with frank kidney and organ failure.

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18
Q

What are the B symptoms of lymphoma

A

Weight loss, fever and night sweats

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19
Q

What are the types of bladder cancer, which is most common of these

A

Bladder cancer can either be a

transitional cell carcinoma (most common) or a squamous cell carcinoma.

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20
Q

How would you differentiate haematuria between bladder cancer and glomerulonephritis

What about ureteric stone

A

Bladder cancer causes macroscopic haematuria.

Glomerulonephritis causes micrcoscopy usually.

Ureteric stone usually microscopic

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21
Q

Define thyroid cancer, what are the subtypes

A

GOOD (90%):
Papillary(80%),
follicular, (10%)
These originate from thyroxine producing stroma and commonly present as solitary lump in a euthyroid patient. Infiltrative symptoms like hoarseness/dysphagia may be seen
Papillary tumours are slow growing and have excellent survical rates.

BAD:
Medullary and anaplastic tumours

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22
Q

Aetiology and RFs for thyroid cancer

A

CHILDHOOD EXPOSURE TO RADIATION (for papillary tumours)

MEN syndrome IIa and IIb associated with medullary thyroid cancers.

Lymphoma associated with hashimoto’s thyroiditis

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23
Q

Hx for thyroid cancer

A

Slow growing thyroid neck lump/nodule

Discomfort on swallowing or hoarse voice

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24
Q

Examination for thyroid cancer

A

Palpable nodule or diffuse enlargement of thyroid gland

If cervical nodes enlarged, suspect malignancy

Usually patient is euthyroid

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25
Q

Are thyroid cancers usually hyper/hyp/eu thyroid?

A

Euthyroid

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26
Q

Investigations for thyroid cancer

A

BLOOD:
TFTs. If hyperthyroid, less likely to be malignant. Bone profile. See tumour markers.

FNA cytology/US guided core needle biopsy:
Histological diagnosis.

Imaging: USS, isotope scanning, CT/MRI, bone scan

1st investigations: TSH, USS neck, FNA, laryngoscopy (paralysed vocal cord highly suggestive of malignancy)

see for histological diagnosis

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27
Q

What is the tumour marker for papillary and follucular vs medullar cancers

A

Serum thyroglobulin (only for papillary and follicular tumours)

Serum calcitonin (for medullar thyroid cancer)

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28
Q

What thyroid cancer type does this describe:

-Well differentiated, derived from parafollicular calcitonin secreting C cells

A

Medullary adenocarcinomas

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29
Q

What thyroid cancer type does this describe:

-tend to be multifocal, “orphan Annie”, pale, empty and grooved nuclei

A

Papillary adenocarcinomas

30
Q

T/F you cannot diagnose folluclar adenocarcinoma on FNAC

A

T. The malignancy is based on vascular and/or capsular invasion

31
Q

What would you see if you did a thyroid uptake scan

A

Hyperfunctioning hot nodule is almost always benign.

Most nodules are hypofunctioning (cold), most of these are benign. BUT malignant nodules are also hypofunctioning

32
Q

When would you do a core biopsy with thyroid cancer

A

If the FNA suggests lymphoma

33
Q

What gene may be changed in medullar thyroid cancer

A

Mutations in RET proto-oncogene (MEN type II)

34
Q

Kaposi’s sarcoma is associated with which virus

A

HHV8

this condition is most often associated with
HIV positive
men and
immunosuppressed
individuals (transplant patients), elderly men of Mediterranean, or Sub-Saharan African descent.

35
Q

What cell type is found with kaposis sarcoma

A
he presence of 
lymphocytes
 in biopsy, as well as the proliferation of endothelial cells (
spindle cells
), leads to a diagnosis of 
Kaposi sarcoma
36
Q

How is HHV-8 transmitted

A
This condition is caused by infection with 
human herpes virus
 8 (HHV-8), a member of the 
herpes family
. It is transmitted via 
sexual contact
.
37
Q

How to differntiate between kaposis sarcoma and bartonella henselae

A

kaposis sarcoma- lymphocyte

bartonella henselae- neutrophils

38
Q

What is Irish node

A

Node in the left axilla gastric cancer

39
Q

What % of pancreatic cancers arise in the head

A

60% arise in the pancreatic head, 15% the tail and 25% the body

40
Q

T/F pancreatic cancer can present as acute pancreatitis

A

Occasionally

41
Q

What are the known risk factors for pancreatic cancer

A

Known risk factors include smoking, alcohol and diabetes.

42
Q

What is bladder cancer

A

Malignancy of bladder urothelium

Majority are transitional cell carcinoma

Squamous cell carcinoma with chronic inflammation e.g. schistosomiasis

43
Q

Genetic abnormalities in bladder cancer

A

p15, p16 mutations, p53, p21, ras, c-myc, c-jun

44
Q

Risk factors for bladder cancer

A

Tobacco, exposure to napthylamines and benzidine in dye, rubber and leather industries

Cyclophosphamide treatment, pelvic irradiation, chronic UTIs, schistosomiasis, early menopause increases risk by 50%

45
Q

Patent urachus is associated with which type of bladder cancer

A

Adenocarcinoma

46
Q

T/F menopause has nothing to do with bladder cancer

A

F

early menopause increases risk by 50%

47
Q

Hx of bladder cancer

A

Painless macroscopic haemiaturia
Urinary frquency, urgency, nocutria, recurrent UTIs.

Rarely, pain due to clot retention, ureteral obstruction of extension to pelvis

48
Q

Examination of bladder cancer

A

Often no signs, mass or lymphadenopathy may be palpable if advanced

49
Q

Investigations of bladder cancer

A

Urine: cytology microscopy culture. RBCs may be seen (but may already be macroscopic haemuturia)

CYSTOSCOPY: visualisation of tumour and biopsy/removal

USS, IVU: to assess upper and lower urinary tract as tumours can be mutlifocal

CT/MRI for staging

TNM staging

Grading G1, 2 and 3. 3 is poorly differentiated

50
Q

What is cholangiocarcinoma

A

Epithelial cancer arising from bile ducts

51
Q

What are the risk factors for cholangiocarcinoma

A

Associated with chronic inflammation and cholestasis

PSC, choledochal cysts, parasitic infections (liver flukes), hepatolithiasis, lynch syndrome II, biliary papillomatosis

52
Q

What is the most common cause of death due to a primary liver tumour in the UK

A

Cholangiocarcinoma (greater than HCC!)

53
Q

Hx of cholangiocarcinoma

A

Obstructive jaundice (yellow skin, pale stools, dark urine, pruritis)

Abdominal fullness or pain

Symptoms of malignancy (weight loss, fatigue, etc)

54
Q

Examination of cholangiocarcinoma

A

Jaundice

Palpable gallbladder (Courvoisier’s law- in presence of jaundice, enlarged gallbladder is unlikely to be due to gallstones)

Epigastric or RUQ mass in advanced cases

55
Q

Location of cholangiocarcinoma

A

Intrahepatic (10%)

Extrahepatic (90%)

  • Hilar (Klatskin)
  • Mid-duct
  • Distal
  • Diffuse
56
Q

What are the 3 types of growth patterns from cholangiocarcinoma

A

Mass forming, periductal infiltrating and intraductal growing

57
Q

What type of cancers are cholangiocarcinoma

A

More than 95% are adenocarcinomas.

58
Q

Distinguishing between cholangiocarcinoma and pancreatic carcinoma?

A

A characteristic feature of pancreatic carcinoma is significant weight loss. Patients may also experience epigastric or back pain, which is not commonly seen with cholangiocarcinoma.

59
Q

Investigations to order for cholangiocarcinoma

A

Serum bilirubin, alk phos and GGT (ALL elevated)

AST/ALT may be minimally elevated or highly elevated in intrahepatic cholangiocarcinoma

Increased PTT (reduction of fat soluble vitamin absorption)

Serum CA19-9 (elevated, but not specific as also elevated in pancreatic or gastric malignancy and severe hepatic injury from any cause)

CEA elevated (also in IBD, other tumours and severe liver injury)

INITIAL IMAGING: USS

Then abdominal CT/MRI, CT angio (staging), ercp/mrcp

60
Q

Which kind of dye involved in bladder cancer

A

Aniline dyes

61
Q

Risk factor for prostate cancer

A

cadmium

62
Q

Burkitt’s lymphoma which chromosomal translocation

A

chromosome 8 on the c-myc gene with chromosome 14.

63
Q

CA 15-3 is tumour marker for which type of cancer

A

High Ca 15-3 levels suggest metastatic breast disease. However, it has poor sensitivity and is therefore not used as a screening procedure to detect breast carcinoma.

This tumour marker has recently been superseded by Ca 27-29, which is claimed to be more sensitive and specific. However, CA 27-29 lacks predictive value in the earliest stages of breast cancer and thus has no role in screening for or diagnosing the malignancy.

64
Q

Most common cause of SVC obstruction

A

This occurs when the SVC is subjected to pressure from a tumour in the superior mediastinum or from thrombosis. The most common cause is lymph node metastases from bronchial carcinoma.

65
Q

Massive splenomegaly is characteristic of which cancer

A

Massive splenomegaly is characteristic of chronic myeloid leukaemia (CML).

66
Q

T/F Abelson-BCR is a poor prognostic factor

A

F

Up to 90% of patients have the Abelson-BCR gene (the molecular equivalent of the Philadephia chromosome you may have heard of). Patient’s without the Philadelphia chromosome tend to have a worse prognosis than those with it.

67
Q

Which rash is characteritic of glucagonoma

A

Necrolytic migratory erythema

It is characterised by the spread of erythematous blisters across the lower abdomen, buttocks, perineum and groin.

68
Q

Medullary thyroid cancers arise from which cells?

A

Medullary thyroid carcinoma are uncommon and arise from the parafollicular cells of the thyroid.

69
Q

Which tumour marker for medullary thyroid cancer?

A

These tumours produce calctionin and elevated levels are diagnostic. They may occasionally present with hypocalcaemia and tetany as a result of this.

70
Q

Polycythaemia vera linked with

A

Budd chiari syndrome (before diagnosis)

myelofibrosis (after)