Case 17: oesophageal, pancreatic, prostate, testicle Flashcards

1
Q

2 WW for oesophageal cancer (upper GI endoscopy)

A
  • Dysphagia OR
  • ≥55 with weight loss and upper abdo pain, reflux, dyspepsia
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2
Q

Oesophageal cancer investigations

A
  • FBC (microcytic anaemia)
  • Upper GI endoscopy and biopsy
  • Endoscopic US (EUS): tumour depth, invasion in surrounding structures and regional lymph node involvement (staging)
  • Barium swallow: less sensitive then endoscopy
  • CT: to view local invasion and distant metastases (staging)
  • PET: distant metastases or malignancies
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3
Q

Oesophageal cancer surgery

A
  • In early-stage and localized disease: esophagectomy with or without lymphadenectomy and neoadjuvant chemo
  • Surgical complications: anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
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4
Q

Oesophageal cancer: chemotherapy and radiation therapy

A
  • Neoadjuvant chemoradiation (administered before surgery) can improve survival in locally advanced disease and may increase the likelihood of complete tumour resection.
  • Adjuvant therapy (administered after surgery): in positive surgical margins or advanced nodal disease.
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5
Q

Oesophageal cancer palliative treatment

A

endoscopic stenting, dilation, laser ablation, or chemotherapy can help alleviate symptoms and improve quality of life.

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6
Q

Tylosis and oesophageal cancer treatment time

A

Tylosis: hyperkeratosis of the feet, is associated with oesophageal cancer

Oesophageal cancer treatment time: curative is 12-18 months, palliative is 4 months

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7
Q

Pancreatic cancer

A
  • Most common type: Adenocarcinoma (85%) arising from the ductal epithelium at the head of the pancreas
  • Periampullary tumour: those that arise within 2cm of the ampulla of vater
  • Poor prognosis due to late presentation average is 6 months
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8
Q

Pancreatic cancer risk factors

A
  • increasing age, family history
  • smoking, alcohol
  • diabetes, obesity and consumption of red meats
  • Chronic pancreatitis, H.pylori infection
  • hereditary non-polyposis colorectal carcinoma
  • multiple endocrine neoplasia
  • BRCA2 gene
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9
Q

Pancreatic cancer: clinical feature

A
  • classically painless obstructivejaundice: yellow skin, pale stools, dark urine, generalised itching
  • Courvoisier’s law: painless obstructive jaundice and a palpable gallbladder (epigastric mass) is likely pancreatic cancer
  • Anorexia, weight loss, N+V
  • loss of exocrine function (e.g.steatorrhoea)
  • loss of endocrine function (e.g. diabetes mellitus)
  • epigastric pain radiating to back (relieved n leaning forwards)
  • Trousseau’s sign: recurrent migratory thrombophlebitis, occurs in different locations over time
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10
Q

Pancreatic cancer: 2WW

A
  • Over 40 with jaundice
  • Over 60 with weight loss plus an additional symptom: Diarrhoea, back pain, abdominal pain, Nausea, Vomiting, Constipation, New onset Diabetes
  • Referred for adirect access CT abdomen
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11
Q

Pancreatic cancer: investigations

A
  • CA19-9: used for staging and assessing treatment response
  • US: first line
  • High resolution CT: gold standard
  • CT thorax, abdomen and pelvis (CT TAP): staging CT to look for metastasis and other cancer
  • MRCP: assess assess biliary tract
  • ERCP: to put a stent in and relieve obstruction
  • Biopsy under US or CT
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12
Q

Management pancreatic cancer

A
  • <20% are suitable for surgery at diagnosis
  • Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Resectable means no spread to liver, nodes or vessels
  • adjuvant chemotherapy is given following surgery
  • ERCP with stenting is often used for palliation
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13
Q

Types of surgery for pancreatic cancer

A
  • Total pancreatectomy
  • Distal pancreatectomy
  • Pylorus-preserving pancreaticoduodenectomy(PPPD) (modified Whipple procedure)
  • Radical pancreaticoduodenectomy(Whipple procedure)
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14
Q

Pancreatic cancer: Palliative treatment

A
  • Stents inserted to relieve the biliary obstruction
  • Surgery to improve symptoms (e.g., bypassing the biliary obstruction)
  • Palliative chemotherapy (to improve symptoms and extend life)
  • Palliative radiotherapy (to improve symptoms and extend life)
  • End of life care with symptom control
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15
Q

Pancreatic cancer: Whipple’s procedure

A
  • Removes tumour at the head of the pancreas when its not spread
  • Need good baseline health
  • Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
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16
Q

Management of pancreatic cancer if not resectable

A
  • biliary stent insertion by ERCP to reduce jaundice and pruritus
  • chemo
  • analgesia
  • pancreatic enzymes
  • domperidone/ metoclopramide for N/V
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17
Q

Risk factors for prostate cancer

A
  • Increasing age
  • Family history
  • Black African or Caribbean origin
  • Tall stature
  • Anabolic steroids

Most prostate cancers are adenocarcinomas

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18
Q

Where can prostate cancer spread and how do you rate severity

A
  • seminal vesicles, bladder and rectum via lymphatics
  • bone via bloodstream

What is used to rate severity of prostate cancer: IPSS

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19
Q

Prostate cancer: presentation

A
  • Asymptomatic- lower urinary tract symptoms
  • Haematuria, haematospermia
  • Erectile dysfunction
  • tenesmus
  • Pain: back, perianal or testicular
  • Bladder outlet obstruction: hesitancy, urinary retention
  • Symptoms of advanced disease or metastasis (e.g., weight loss, bone pain or cauda equina syndrome)
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20
Q

Consider a PSA and sigital rectal exam if

A
  • Any lower urinary tract symptoms, such asnocturia, urinary frequency, hesitancy, urgency or retention or
  • erectile dysfunction or
  • visible haematuria.
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21
Q

Prostate exam investigations

A
  • PSA
  • Urinalysis
  • FBC, U&E, LFT
  • Digital rectal exam: hard, firm, asymmetrical, craggy or irregular
  • Prostate biopsy: do if Likert 3 or above. Can be false negative if miss the cancerous zone. Types of prostate biopsies: Transrectal ultrasound guided biopsy (TRUS), Transperineal biopsy
  • Multiparametric MRI: reported on a Likert scale
  • Isotope bone scan: to look for boney metastasis
  • Transrectal ultrasound guided (TRUS) biopsy
22
Q

Prostate cancer management

A
  • Surveillanceorwatchful waitingin early prostate cancer
  • External beam radiotherapydirected at the prostate: side effect is proctitis
  • Brachytherapy: implanting radioactive seeds into the prostate
  • Hormone therapy: Androgen receptor blocker (bicalutamide) or GnRH agonists such as goserelin or 17a hydroxylase inhibitors. Bilateral orchidectomy to remove testicles
  • Surgery: radical prostatectomy with removal of seminal vesicles
  • Alternative to surgery: radical radiotherapy (external beam, possibly with brachytherapy) with adjunct androgen deprivation therapy
23
Q

PSA levels may be raised by

A
  • Benign Prostatic Hyperplasia (BPH)
  • prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 1 month after treatment)
  • ejaculation (ideally not in the previous 48 hours)
  • vigorous exercise (ideally not in the previous 48 hours)
  • Urinary retention
  • instrumentation of the urinary tract
24
Q

Surveilance for early prostate cancer

A
  • active surveillance with: 6 monthly PSA, 12 monthly DRE
  • repeat multiparametric MRI at 1 year

Side effects of prostate cancer treatment: erectile dysfunction, urinary incontinence

25
Q

Testicular cancer

A
  • Relatively rare
  • Two main subtypes: Seminomas (40-60%) and non-seminomatous germ cell tumours (NSGCT 30-50%) also known as Teratoma. These are both Germ cell tumours
  • Non germ cell tumours: Leydig cell tumour and sarcoma
  • Commonly affects young Caucasian men (15-35)
  • Very good prognosis even in metastatic disease
  • Prognosis: 95% survival
26
Q

Male germ cell cancer

A
  • Seminomas: No reliable tumour marker but beta-HCG in 20%. Any tumour that produces AFP is considered mixed even if the pathology suggests pure seminoma. 50% of germ cell tumours. Slow growth. Responds better to radiation and chemo
  • Non-seminomas: disease spreads earlier so more likely to present with advanced disease. AFP and hCG markers are elevated in majority. More prone to early metastasis
  • Mixed: Beta-hCG and AFP
  • Intratubular germ cell neoplasia is the precursor to germ cell tumours
27
Q

Testicular cancer: risk factors

A
  • Infertility
  • <45
  • Caucasian
  • HIV
  • Cryptorchidism: undescended testis
  • Family history
  • Klinefelter’s syndrome, Down syndrome
  • History of testicular torsion
  • Mumps orchitis
  • 80% of testicular cancer express 12p gain
  • Family history
28
Q

Testicular cancer: clinical features

A
  • A painless lump is the most common presenting symptom
  • Lump: Hard, irregular, not fluctuant, no transillumination. Can cause enlargement of testicle
  • Can have scrotal pain or back pain
  • Pain is present in a minority of men
  • Other possible features include hydrocele, gynaecomastia (Leydig cell tumour)
  • Weight loss, fatigue
  • Can present similar to epididymo-orchitis but persists after antibiotics
29
Q

Testicular cancer: presentation of metastatic disease

A
  • Lung cancer or PE: dyspnoea, cough
  • Mediastinal mass: SVC obstruction
  • Retroperitoneal disease: Ureteric obstruction, abdo mass, abdo or back pain
  • CNS symptoms
  • Liver capsular pain
  • Advanced disease: weight loss, fatigue
  • Where might testicular cancer spread to: lymphatics, lungs, liver, brain
30
Q

Testicular cancer: investigations

A
  • Scrotal US: confirms diagnosis
  • Staging CT chest/abdomen/pelvis: look for areas of spread and stage the cancer. Performed after orchidectomy
  • AFP, hCG and LDH (elevated in germ cell tumour)
  • CXR: bilateral hilar lymphadenopathy, cannonball mets
  • CT brain if multiple lung metastases and/or serum hCG >10,000
  • Genetic analysis if appropriate: Trisomy 8 and Kleinefelter’s syndrome
  • Biopsy tumour and histology
31
Q

Testicular cancer monitoring

A
  • Serum tumour markers (AFP, hCG, LDH): are measured pre-orchidectomy, 24hrs post orchidectomy and weekly until normal.
  • Suggests absence of residual disease if hCG normalises in 24hrs and AFP in 4-6 days
  • In non-seminomas increased tumour markers suggest worse prognosis
  • Beta-hCG tends to be elevated in metastatic seminoma, testicular choriocarcinoma and non-seminomas (can falsely elevate due to marijuana)
  • LDH raised in seminomas and non-seminomas, associated with growth rate
  • AFP rises in teratomas (not seminomas)
32
Q

Testicular cancer: factors associated with poor prognosis

A
  • Metastasis: distant nodes and non pulmonary organs
  • Non-seminomas: how much serum tumour markers are elevated
  • Tumours originating in the mediastinum and not the testis
  • Histology: Non-seminoma have worse outcomes
  • Even patients with widespread metastasis including the brain can have curable disease and should be treated with intent
33
Q

Staging of testicular cancer

A
  • Stage 1: no evidence of metastasis, isolated to testicle
  • Stage 2: infradiaphragmatic nodal involvement
  • Stage 3: supradiaphragmatic nodal involvement
  • Stage 4: extralymphatic involvement, spread to other organs
34
Q

Testicular cancer differentials

A
  • Benign epididymal masses are relatively common
  • Epididymo-orchitis or orchitis (if not resolving within 3 weeks should be referred for urological assessment)
  • Lymphoma/leukaemic infiltrate
35
Q

Testicular cancer 2ww

A
  • Non painful enlargement or change in shape or texture of the testis
  • US
36
Q

Testicular cancer management

A
  • Treatment depends on whether the tumour is a seminoma or a non-seminoma
  • Orchidectomy: prosthesis can be inserted
  • Sperm banking: to save sperm
  • Chemotherapy and radiotherapy
  • Seminoma’s tend to respond well to radiation and chemotherapy, have better prognosis
  • Non-seminomas can have teratomatous elements which are resistant to chemo and may need surgery for cure.
37
Q

Testicular cancer: when do markers return to normal after surgery

A
  • Beta hCG: within 24 hours
  • AFP: within 5 days
  • Follow up with monitoring of tumour markers and imaging
38
Q

Treatment of testicular cancer by stage

A
  • Stage 1: radical inguinal orchiectomy with clamping of the spermatic cord to prevent inguinal seeding. Dont need pre-op biopsy. Just monitor cancer markers. In seminoma adjuvant radiotherapy is used in the lymph nodes. In non seminoma 2 cycles of BEB chemotherapy can reduce relapse
  • Stage 2A and B seminoma: radiotherapy to the lymph nodes. After orchiectomy you dissect their lymph node to confirm staging. They may then receive adjuvent chemo
  • For stage 3 and above you delay orchiectomy as chemo is the mainstay of treatment. You perform orchiectomy post chemo once tumour markers are stabilised
  • Chemo: cycles of bleomycin, etopside and cisplatin (BEP)
39
Q

Non seminomatous testicular tumours include

A
  • Embryonal carcinomas
  • Yolk sac tumours
  • Choriocarcinomas
  • Teratomas
  • Mixed germ cell tumours
40
Q

Side effects of testicular cancer management

A
  • Infertility: should be offered sperm storage but many can still conceive naturally. Recommended wait at least 3 months post chemo to conceive naturally
  • Secondary leukaemia: non-lymphocytic, especially with platinum based chemo and radiotherapy
  • Restrictive lung disease: with cisplatin based chemo, rarely causes toxic pulmonary effects, if this happens stop the drug
  • Hypogonadism (testosterone replacement may be required)
  • Peripheral neuropathy
  • Hearing loss
  • Lasting kidney, liver or heart damage
  • Increased risk of cancer in the future
  • Psycho-sexual: anxiety, depression, body image issues
41
Q

Adverse effects of tumour lysis syndrome

A
  • Cardiac arrest/arrhythmia’s: hypocalcaemia, hyperkalaemia, hyperphosphataemia
  • Acute renal failure: urate nephropathy, hyperuricaemia
  • DIC: cell death, activation of coagulation cascade, intravascular haemolysis (high LDH)
42
Q

Prevention and management of tumour lysis syndrome

A
  • Prevention: adequate hydration and urine output. Allopurinol or rasburicase as urate oxidase inhibitors
  • Management: Requires adequate hydration and strict management of electrolytes but using a low K+ diet, oral and rectal resonium, IV calcium gluconate, IV bicarbonate, insulin/glucose, furosemide, forced hydration and in some cases haemodialysis.
43
Q

Ovarian germ cell cancers

A
  • 3% of ovarian cancers are germ cell tumours
  • Affects young women and adolescent girls
  • Monitor with AFP and hCG, CA!”% is often normal
44
Q

Extragonadal germ cell tumours

A
  • mediastinal: chest pain, SOB, cough, SVC obstruction, dysphagia, hoarseness. Presents in 30’s
  • retroperitoneal: few symptoms until advand
  • pineal region (brain): raised ICP, neurological symptos, endocrine dysfunction
  • sacrococcygeal
  • Associated with Klinefelter’s (especially mediastinal)
45
Q

How to investigate extra-gonadal germ cell tumours and treatment

A
  • gonadal examination and ultrasound to look for a hidden primary
  • CT chest abdo pelvis
  • biopsy of tumour
  • Placental ALP
  • Treatment: chemo and radiation
46
Q

The 4 main types of ovarian tumours

A
  • Surface derived tumours
  • Germ cell tumours
  • Sex cord stromal tumours
  • Metastasis
47
Q

Surface derived tumours (65% of ovarian tumours)

A
  • Serous cystadenoma: most common benign ovarian tumour, often bilateral. Cyst lined by ciliated cells
  • Serous cystadenocarcinoma: malignant, often bilateral. Psammoma bodies seen (collection of calcium). Most common ovarian cancer
  • Mucinous cystadenoma: benign, cyst lined by mucus secreting epithelium
  • Mucinous cystadenocarcinoma: malignant. May be associated with pseudomyxoma peritonei
  • Brenner tumour: benign, Contain Walthard cell rests (benign cluster of epithelial cells), similar to transitional cell epithelium. Typically have ‘coffee bean’ nuclei.
  • Epithelial origin
48
Q

Where do surface derived ovarian tumours (Epithelial) originate from

A
  • Serous (46%): Fallopian tube epithelium – majority of tumours
  • Mucinous (35%): GI tract or endocervical epithelium
  • Endometrioid (8%): Proliferative endometrium
  • Clear cell (3%): Gestational endometrium – relatively rare, aggressive, CA-125 often not raised in this type
  • Squamous cell (<1%)
  • Transitional cell (Brenner): Urinary tract epithelium (rare)
49
Q

Germ cell tumours ovarian cancer

A
  • Most common in adolescent girls and account for 15-20% of tumours
  • Teratoma- the mature teratoma (dermoid cyst) is the most common and is benign. Immature teratoma is malignant. Account for 90% of germ cell tumours, contain a combination of ectodermal i.e. hair, mesodermal i.e. bone and endodermal tissue
  • Dysgerminoma- most common malignant germ cell tumour. Histological appearance similar to a testicular seminoma. Associated with turners syndrome. Typically secretes hCG and LDH
  • Yolk sac tumour: typically secretes AFP, schiller-duval bodies on histology
  • Choriocarcinoma- malignant. Rare tumour that is part of the spectrum of gestational trophoblastic disease. Typically, have increased hCG levels. Characterised by early haematogenous spread to the lungs
50
Q

Sex cord stromal tumours- ovarian cancer

A
  • Around 3-5% of ovarian tumours, often produce hormones
  • Granulosa cell tumour: malignant, produces oestrogen, leading to precocious puberty if in children or endometrial hyperplasia in adults. Contains Call-Exner bodies (small eosinophilic fluid filled spaces between granulosa cells)
  • Sertoli-Leydig cell tumour: benign, produces androgens causing a masculinizing effect. Associated with Peutz-Jegher syndrome
  • Fibroma- benign. Associated with Meigs syndrome (ascites, pleural effusion). Solid tumour consisting of bundles of spindle shaped fibroblasts. Typically occur around the menopause, classically causing a pulling sensation in the pelvis.