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CHAPTER 22 System-Specific Pathology
411
• e commonest malignant ovarian tumour is the serous
carcinoma:
• occurs most frequently between 40 and 60 years
• may be largely cystic (25%), semi-solid (65%) or
entirely solid (10%)
• poor prognosis: 15% 5-year survival.
Germ cell tumours
• May be either benign or malignant.
• Commonest is the benign cystic teratoma (dermoid
cyst).
• Dermoid cysts may present at any age, although usually
in younger patients.
• Dermoid cysts characteristically contain hair, sebaceous
material and teeth, the latter oen being apparent on a
plain abdominal X-ray.
• May undergo torsion.
• Malignant transformation is rare.
Sex-cord stromal tumours
• About 5% of all ovarian tumours.
• Fibromas comprise about half of that 5%.
• Ovarian bromas are not associated with steroid hormone production.
• Other sex-cord stromal tumours are associated with steroid hormone production, e.g. thecoma, granulosa cell
tumour, Sertoli–Leydig tumours.
• Meigs’ syndrome occurs in approximately 1% of patients
with ovarian bromas and includes ascites and pleural
eusions which disappear following removal of the
ovarian broma.
Metastatic tumours
ese arise from:
• stomach (Krukenberg tumours)
• large intestine
• breast.
Clinical presentation of ovarian tumours
• Pain.
• Rupture or torsion of a cyst.
• Abdominal mass.
• Ascites: peritoneal seedlings, pseudomyxoma peritonei,
Meigs’ syndrome.
• Excess hormone production: abnormal uterine bleeding
with oestrogen production; virilization due to androgen
production.
• Pleural eusion: Meigs’ syndrome, lung secondaries,
symptoms of other distant metastases.
Ectopic Pregnancy
• Risk of recurrence aer one ectopic pregnancy is
10–20%.
• Fallopian tube is commonest site.
• May be associated with chronic inammatory disease in the tubes or intrauterine contraceptive devices
(controversial).
• Pain occurs as ectopic pregnancy expands tube.
• Pain and haemorrhage on rupture.
• Pregnancy-associated changes seen in endometrium.
Endometriosis
Endometriosis is the presence of endometrial glands
and stroma in sites other than the body of the uterus.
Endometriosis may be responsible for:
• pelvic inammation
• infertility
• pain.
Sites include:
• ovaries (80%)
• round ligaments
• fallopian tubes
• pelvic peritoneum
• intestinal wall
• umbilicus
• laparotomy scars
• lymph nodes (rare)
• lung and pleura (rare)
• synovium (rare).
Clinical features
• Retrograde menstruation may be important in the aetiology of endometriosis in the peritoneal cavity, but cannot explain spread to distant sites.
• Endometrial tissue retains its sensitivity to hormones,
and bleeding occurs into the lesions at the time of
menstruation.
• Fibrosis may occur at the site of the lesion; in the peritoneal cavity, this may lead to adhesion formation with
subsequent obstruction.
Fibroids
Fibroleiomyoma
• Common tumours of smooth muscle origin.
• Grow during reproductive years; regress aer the menopause but do not completely disappear.
• Firm, white, whorled, well-circumscribed lesions, which
may be submucous, subserosal or intramural.
• Subserosal ones may be pedunculated.
• Aetiology unknown.
• Clinically they may present as follows:
• abdominal mass
• abnormal uterine bleeding
• urinary problems due to pressure on the bladder
• pain due to complications, e.g. red degeneration, tor-
sion of the pedicle of a pedunculated broid.
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SECTION III Pathology
Complications
• Cystic degeneration.
• Necrosis with haemorrhagic infarction (red degeneration).
• Dystrophic calcication (calcied broids may be seen
on a plain abdominal X-ray).
• Sarcomatous change extremely rare.
Endometrial Carcinoma
Two types are recognized:
• First type occurs in young women with polycystic ovary
syndrome or in perimenopausal women.
• It may complicate post-menopausal oestrogen replacement therapy.
• is type is associated with a good prognosis.
• Second type aects elderly post-menopausal women
and is not oestrogen-related.
• It is poorly dierentiated with deep myometrial invasion.
• Poor prognosis.
Aetiological factors for endometrial carcinoma include:
• obesity
• hypertension
• diabetes mellitus
• nulliparity
• long-term tamoxifen therapy.
Spread
is occurs:
• by direct extension into pelvis and adjacent viscera
• to the iliac and para-aortic nodes
• via the bloodstream to the liver and lungs.
• Urate (5%):
• arise in acid urine
• hard, smooth, faceted and light brown in colour
• radiolucent.
• Cystine (2%):
• usually multiple
• arise in acid urine
• are of metabolic origin, owing to decreased reabsorption of cystine from the renal tubules
• white and translucent
• radio-opaque because of their sulfur content.
• Xanthine and pyruvate stones:
• rare
• due to inborn error of metabolism.
Precipitating Factors
ese include:
• diet
• dehydration
• stasis
• infection
• hyperparathyroidism
• idiopathic hypercalciuria
• milk-alkali syndrome
• hypervitaminosis D
• cystinuria
• inborn errors of purine metabolism
• gout
• chemotherapy (excess uric acid following treatment of
leukaemia or polycythaemia).
Urinary Tract Calculi
Urinary calculi occur in 1–5% of the population in the UK.
Stones may form in the kidney or bladder. Ureteric calculi
are in transit from the kidney to bladder. 90% of calculi are
radio-opaque.
Types of Calculi
Calculi are classied according to their composition. e
types are:
• Calcium oxalate (75%):
• ‘mulberry’ stones covered with sharp projections
• occur in alkaline urine
• cause bleeding and are oen black owing to altered
blood on their surface
• because of their sharp surface they give symptoms
when comparatively small.
• Magnesium ammonium phosphate (struvite) stones (15%):
• smooth and dirty white
• may enlarge rapidly and ll the calyces, taking on
their shape, i.e. staghorn calculus
• occur in strongly alkaline urine.
Sites
Renal pelvis
• Solitary or multiple.
• Unilateral or bilateral.
• Small stones are commonest, but large-branched ‘staghorn’
calculi may occur and completely ll the pelvis and calyces.
Bladder
• Bladder stones may originate in the kidney with subsequent enlargement in the bladder due to phosphate
encrustation.
• Formed primarily in the bladder, usually of phosphates.
Ureteric and urethral stones
• Ureteric stones in transit from kidney to bladder.
• Urethral stones in transit from bladder to outside.
Clinical Effects
ese are:
• Obstruction:
• at the pelviureteric junction
• in the ureter
CHAPTER 22 System-Specific Pathology
413
• at the bladder neck
• rarely at the external urethral meatus.
• Ulceration:
• of calyces, pelvic mucosa or bladder, causing
haematuria.
• Chronic infection, e.g. pyelonephritis, pyonephrosis.
Urinary Tract Infections (UTIs)
ese may be divided into those aecting the kidney
(pyelonephritis) and those aecting the bladder (cystitis).
UTIs are more common in women and the majority of
women will have had a UTI at some time during their life.
Risk factors include:
• pregnancy
• urinary tract malformations
• urinary tract obstruction
• calculi
• prostatic obstruction
• bladder diverticulum
• spinal injury
• trauma
• urinary tract tumour
• diabetes mellitus
• immunosuppression.
Acute Pyelonephritis
Infection of the kidney by pyogenic organisms.
Pathogenesis
• Haematogenous spread.
• Retrograde ureteric spread.
• Organisms include E. coli, Proteus, Enterobacter, Klebsiella,
Pseudomonas and faecal streptococci.
Clinical features
ese include:
• malaise
• fever
• dysuria
• urgency of micturition
• pain and tenderness in the loin.
Complications
ese include:
• renal papillary necrosis
• pyonephrosis
• perinephric abscess.
Chronic Pyelonephritis
Chronic pyelonephritis occurs in association with:
• vesicoureteric reux, either due to congenital lesions or
occurring in early life
• obstruction developing during childhood.
Clinical features
• Vesicoureteric reux is associated with abnormal entry
of the ureter into the bladder.
• Reux of urine into the kidney during micturition raises
intrapelvic and intracalyceal pressure.
• e presence of infection accelerates scarring, due to
reux.
• End result is scarring of the kidney with interstitial
brosis.
• Atrophic and dilated tubules containing eosinophilic
casts, giving the appearance of ‘thyroidization’ of the
kidney.
• Unless vesicoureteric reux is successfully corrected,
the condition may proceed to chronic renal failure and
need for dialysis and transplantation.
Cystitis
Inammation of the bladder (cystitis) is a common occurrence as part of a urinary tract infection.
Aetiology
• Causative organism usually derived from patient’s faecal
ora, e.g. E. coli, Proteus and Klebsiella.
• Mostly due to retrograde spread of the organisms along
urethra.
• 20–30% of women will have bacterial cystitis at some
time during their lives.
• Predisposing factors in females:
• short urethra
• urethral trauma during sexual intercourse
• preg nan cy.
• Instrumentation of the urinary tract in both sexes increases
both the incidence and variety of infecting organisms.
• Other organisms include Candida in immunosuppressed patients or patients on prolonged antibiotic
therapy; tuberculous cystitis always reects tuberculosis
elsewhere in the urinary tract.
• Irradiation, trauma due to instrumentation and drugs
(e.g. cyclophosphamide) may cause cystitis, which is
oen sterile.
Clinical features
ese include:
• frequency
• lower abdominal pain
• dysuria
• occasionally haematuria
• general malaise and pyrexia in some patients.
Sterile Pyuria
Pus cells are apparent on microscopy but there is no growth
on culture. Causes include:
• inadequately treated UTI
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SECTION III Pathology
• tuberculosis
• tumour
• stone
• prostatitis
• polycystic kidneys
• appendicitis (appendix adheres to and ‘irritates’ the
bladder)
• diverticulitis (adheres to bladder)
• analgesic abuse.
Urinary Tract Tuberculosis
is has shown a decline in the past 30 years but remains a
problem in the ird World and in immigrant populations
in the UK. Features include:
• always secondary to TB elsewhere
• urinary tract is involved by haematogenous spread
• kidney is aected most frequently
• lower urinary tract secondarily infected by descending
infection, giving rise to cystitis or infection of the epididymis or seminal vesicles.
Clinical features
• Oen silent.
• Repeated UTIs with frequency, dysuria, haematuria.
• Occasionally dull loin pain.
• Weight loss, fever, night sweats.
• Symptoms of uraemia.
• Epididymitis.
• Scrotal sinuses.
Tumours of the Urinary Tract
Kidney
Tumours of the kidney include:
• benign:
• adenoma
• angiomyolipoma
• malignant:
• Wilms’ tumour (nephroblastoma)
• renal cell carcinoma (hypernephroma)
• transitional cell carcinoma of renal pelvis.
Benign Neoplasms
Cortical adenoma
• Commonest benign tumour of kidney.
• Usually small, <2 cm in diameter.
• Distinction from well-dierentiated adenocarcinoma
no t easy.
• Lesions <3 cm are classied as adenoma.
• ose >3 cm are classied as carcinoma.
• Malignancy may develop in cortical adenomas.
Angiomyolipoma
• Intrarenal mass composed of mixture of blood vessels,
muscle and mature fat.
• Best regarded as hamartoma.
• 40% associated with tuberous sclerosis.
• May be painful if there is intralesional haemorrhage.
Malignant Renal Tumours
Wilms’ tumour
• Commonest renal tumour of childhood.
• Peak incidence 1–4 years.
• Commonest clinical presentation is with an abdominal
mass.
• Other presentations include haematuria, hypertension,
abdominal pain and intestinal obstruction.
• Aggressive tumour – rapidly growing, spread to lungs
oen present at time of diagnosis.
• Spread occurs as follows:
• into renal parenchyma and perinephric tissues
• lymphatic to regional lymph nodes
• blood: commonly to lung, less frequently to liver,
peritoneum, and rarely to bone.
• Prognosis: over 90% survival due to aggressive therapy
involving radiotherapy, chemotherapy and surgery.
Renal cell carcinoma (hypernephroma, Grawitz tumour)
is is the commonest primary kidney tumour in adults.
Aetiology
• Smoking
• Genetic predisposition in von Hippel–Lindau disease.
Clinical presentation
is includes:
• Haematuria.
• Loin pain.
• Loin mass.
• Paraneoplastic manifestations:
• pyrexia of unknown origin
• polycythaemia from erythropoietin production
• hypercalcaemia
• hypertension.
• Le-sided tumour may present with varicocele due to
invasion of the le renal vein with tumour and obstruction of the le testicular vein.
Spread
• Direct into renal parenchyma, renal pelvis and perinephric tissues.
• Lymphatic: 30% have tumour in para-aortic nodes at
presentation.
• Blood: lungs (cannon-ball metastases), bone.
Prognosis
• Depends on staging and dierentiation.
• If tumour is localized to kidney, nephrectomy oers a
5-year survival rate of 70%.
CHAPTER 22 System-Specific Pathology
415
Transitional cell carcinoma of renal pelvis
ese form 5–10% of renal tumours and arise from the
urothelium of the renal pelvis.
Aetiology
• Analgesic abuse.
• Exposure to aniline dyes used in the dye, rubber, plastics
and gas industries.
Clinicopathological features
• May present with:
• haematuria
• infection secondary to hydronephrosis
• ureteric colic due to obstruction or clot.
• In presence of pelvic stones, urothelium may undergo
squamous metaplasia. Squamous cell carcinoma may
subsequently develop, and is known to be associated
with calculi and chronic infection.
• Tumours may seed down the ureter and involve the
bladder.
Bladder Tumours
Epithelial tumours of the bladder are common. e majority are transitional cell carcinomas but a small proportion are squamous. Adenocarcinoma of the bladder is
uncommon.
Aetiology
• Chemical substances – seen particularly in aniline dye
and synthetic rubber workers; chemical substances
implicated include β-naphthylamine and benzadine;
dyes used in textiles, printing, rubber, and cable and
plastic industries.
• Smoking.
• Schistosomiasis.
• Leucoplakia: associated with squamous cell carcinoma.
• Bladder diverticulum: tumour complicates about 2% of
diverticulae.
• Ectopia vesicae: adenocarcinoma may complicate this
condition.
Transitional Cell Carcinoma
Transitional cell carcinomas arise from the urothelium and
are frequently multiple. Carcinoma is oen preceded by
dysplasia.
Clinical features
• Painless haematuria commonest presenting feature.
• Dysuria.
• Frequency and urgency.
• Obstruction with unilateral pyelonephritis or hydronephrosis if tumour obstructs ureteric orice.
• Urethral obstruction: retention of urine.
• Extension to other organs: stula formation; vesicocolic
stula with pneumaturia; vesico-vaginal stula with
incontinence.
Staging and grading
• Transitional cell carcinomas are graded I–III according
to degree of cytological atypia.
• Grading is a guide to prognosis.
• TNM staging is also used to judge prognosis.
• Good correlation between grade and stage.
• Majority of papillary growth are grade I and
non-invasive.
• Grade III lesions are usually at, ulcerated, invasive and
carry a poor prognosis.
Squamous Cell Carcinoma
ese arise from metaplastic squamous epithelium. Metaplasia occurs most oen in association with:
• calculi
• schistosomiasis.
Clinicopathological features
• Solid invasive tumours.
• Prognosis is not as good as for transitional carcinoma.
Conditions of the Urethra
Urethral obstruction
• Extrinsic compression by prostate gland enlargement.
• Intrinsic lesions include:
• congenital valves
• rupture
• stricture.
Urethritis
May be associated with:
• More proximal infection in the urinary tract.
• Adjacent to a local urethral lesion, e.g. calculus.
• Indwelling urinary catheter.
• Sexually transmitted infection:
• gonococcal urethritis
• non-gonococcal (non-specic) urethritis.
Gonococcal urethritis
• A purulent infection due to Neisseria gonorrhoeae.
• Bacteria multiply on urethral mucosa and invade periurethral glands in male and endocervix and Bartholin’s
glands in female.
• Yellow, purulent discharge 3–8 days aer initial
infection.
• Organisms may be seen as Gram-negative intracellular
diplococci in Gram stain of smears.
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SECTION III Pathology
Course and complications
• May resolve in 2–4 weeks, either spontaneously or following treatment.
• May progress to chronic infection with abscesses and
brosis, leading to urethral stricture in males.
• Important cause of pelvic inammatory disease in
females.
• Systemic spread is rare, but may produce suppurative
arthritis, tenosynovitis, skin rashes and endocarditis.
Non-gonococcal (non-specific urethritis)
• Commonest sexually transmitted disease.
• Mucopurulent urethral discharge and dysuria develop
within a few days of infection in males.
• Discharge contains pus cells but gonococci cannot be
identied.
• Commonest organisms are Chlamydia, Trachomatosis
and Ureaplasma urealyticum.
Tumours
Tumours of the urethra include:
• viral condyloma
• transitional cell carcinoma.
Viral condyloma
• Viral warts in penile urethra.
• Caused by human papillomavirus.
• Relation to neoplasia uncertain.
Transitional cell carcinoma
• Papillary transitional cell carcinoma may rarely develop
in urethra.
• Oen in association with similar tumour in bladder.
• May develop as a result of tumour implantation in the
urethra following instrumentation of the bladder.
Conditions of the Penis
ese include:
• congenital malformations
• tumours
• infections.
Congenital Lesions
ese include:
• hypospadias
• epispadias.
Hypospadias
• Due to failure of fusion of urethral folds over urogenital
sinus.
• Urethra does not reach tip of penis but opens on inferior
aspect.
• Commonest site of meatus is on inferior aspect of glans.
Epispadias
• Much less common than hypospadias.
• Urethra opens onto dorsum of penis.
• Results in urinary incontinence and infections.
• Sometimes associated with extrophy of the bladder.
Inflammation and Infections
Balanoposthitis
• Inammation of the prepuce is posthitis.
• Inammation of the glans is balanitis.
• Balanoposthitis oen associated with tight prepuce
(phimosis).
• Bacteria include staphylococci, coliforms or gonococci.
• In diabetic and immunosuppressed patients, Candida
infection is a further risk.
• Redness and swelling of prepuce and glans associated
with purulent exudate.
• Scarring may occur with formation of preputial adhesions or severe phimosis.
Phimosis
• Prepuce cannot be retracted over glans penis.
• In most cases it is an acquired lesion as a late sequel of
ammoniacal preputial dermatitis in infancy.
• Prepuce may ‘balloon’ on micturition.
• Indication for circumcision.
Paraphimosis
• Tight prepuce retracted behind glans may not be reducible, and causes obstruction of venous return from glans
and prepuce.
• Oedematous swelling of glans and prepuce.
• Requires circumcision.
Balanitis xerotica obliterans
• Aects 30–50-year age group.
• Uncommon.
• ickened white plaques and ssures on glans and prepuce.
• Non-retractile prepuce or preputial discharge.
• Requires circumcision.
Genital herpes
• Acute infectious disease caused by herpes simplex virus
(HSV).
• Usually HSV type II as sexually transmitted disease.
• Acute vesicular eruption on glans penis or in coronal
sulcus.
• Vesicles produce shallow, painful ulcers.
Genital warts
• Prevalence increasing.
• Caused by human papillomavirus (HPV6, HPV11).
• Warts (condylomata acuminata) occur usually on glans
but may occur in urethra, penile sha, perineum and
around anus.
• Clinical diagnosis is usually obvious.
• High incidence of recurrence.
CHAPTER 22 System-Specific Pathology
417
Tumours of the Penis
ese include:
• Intraepidermal carcinoma:
• Bowen’s disease on the foreskin
• erythroplasia of Queyrat (on the glans).
• Invasive squamous carcinoma.
Invasive squamous carcinoma
• Rare in UK.
• Only occurs in uncircumcised men.
• May follow premalignant conditions described above.
• Presents clinically as an indurated nodule or plaque
which later ulcerates.
• May be hidden under the foreskin and eventually produces an oensive purulent discharge.
• Spread:
• direct: through prepuce and proximally along sha
of penis
• lymphatic: to inguinal nodes
• blood spread is uncommon.
• Prognosis:
• if lymph nodes free of tumour, 80–90% 5-year sur-
vival occurs following amputation
• prognosis poor with node involvement.
Conditions of the Prostate
Prostatitis
is may be:
• acute suppurative prostatitis: caused by coliforms,
gonococcus, Staphylococcus
• chronic non-specic prostatitis
• granulomatous prostatitis: idiopathic, tuberculous; following transurethral resection.
Acute suppurative prostatitis
• Usually from spread of infection along prostatic ducts
secondary to urethritis or cystitis.
• Common causative organisms include coliforms, staphylococci and gonococci.
• May follow urethral catheterization or endoscopy.
• May be blood-borne.
• Clinically characterized by fever, rigors, low back pain,
dysuria, perineal pain. Prostate palpably enlarged, oen
tender.
• Prostatic abscess may occur with discharge into urethra.
Chronic non-specific prostatitis
• May develop from recurrent episodes of acute infective
prostatitis. Organisms include E. coli, Chlamydia and
Ureaplasma.
• Clinical features include:
• symptoms of UTI, dull perineal ache, normal or
indurated irregular prostate
• bacterial infections can be diagnosed by culture of
urine following prostatic massage.
Benign prostatic hypertrophy
• A common non-neoplastic lesion of the prostate.
• Involves periurethral zone.
• Nodular hyperplasia of glands and stroma.
• Not premalignant.
• Aects most men over the age of 50, but only 10% present with symptoms.
• Severity of symptoms depends on degree of encroachment on prostatic urethra.
• Clinical features include:
• cardinal symptoms are diculty in starting micturi-
tion and a poor stream of urine
• nocturia
• frequency
• dribbling
• incontinence
• acute retention
• haematuria from ruptured dilated bladder neck veins
• occasionally, palpable bladder.
• Examination reveals smooth enlarged prostate, midline
sulcus, enlarged lateral lobes.
Complications
ese include:
• hypertrophy of bladder muscle with trabeculation
• hydroureter with reux of urine
• hydronephrosis
• pyonephrosis
• pyelonephritis and impaired renal function.
Carcinoma of the Prostate
is is one of the commonest forms of malignant disease
and is the second leading cause of male deaths from malignancy in Europe and the USA. e tumour is rare below
the age of 50 years, the peak incidence being between 60
and 85 years.
Aetiology
• Largely unknown.
• Possibly related to changes in circulating androgen
levels.
• Family history: 2- to 3-fold risk of tumour developing in
men with rst-degree relatives in whom prostatic carcinoma was diagnosed under the age of 50 years.
• Rare in eunuchs.
Clinicopathological types
Two clinicopathological types are recognized, which dier
in their behaviour:
• clinical (symptomatic) carcinoma
• latent (incidental) carcinoma.
Clinical (symptomatic) carcinoma
• Arises in posterior subcapsular area of gland.
• Adenocarcinoma.
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SECTION III Pathology
• Invades stroma.
• Asymmetrical, hard, irregular enlargement of prostate
palpable per rectum.
• Metastasizes, especially to bone.
Latent (incidental) carcinoma
• Microscopic focus of tumour found incidentally, e.g. at
histological examination of prostatectomy specimens
removed for benign hyperplasia or at autopsy.
• Common; incidence high in old age.
• Dormant lesions; metastases in 30% aer 10 years.
Spread
Spread of prostatic carcinoma may be:
• direct: stromal invasion through the prostatic capsule,
urethra, bladder base, seminal vesicles
• via lymphatics to sacral, iliac and para-aortic nodes
• via blood to bone (pelvis, lumbosacral spine, femur),
lungs, liver.
Clinical presentation and features
Clinical presentation and features of prostatic carcinoma
include:
• urinary symptoms: dysuria, haematuria, hesitancy,
dribbling, retention, incontinence
• bone metastases: pain, pathological fractures, anaemia
• rectal examination revealing hard, craggy prostate.
Prognosis
• Variabl e .
• Dependent on stage at presentation.
• Patients with clinically localized tumours treated radically may expect normal life expectancy.
• ose with metastatic disease at presentation have a
median 3-year survival.
GASTROINTESTINAL SYSTEM
Carcinoma of the Oesophagus
Carcinoma of the oesophagus accounts for about 2% of
all malignant disease in the UK. Incidence is increasing
worldwide. ere is considerable geographical variation in
its incidence, being 300 times higher around the Caspian
Sea than in the UK.
Causes
ese include:
• High dietary intake of tannic acid, e.g. in strong tea.
• Dietary deciency of vitamin A.
• Dietary deciency of riboavin.
• Dietary deciency of zinc.
• Fungal contamination of food.
• Opium ingestion.
• ermal injury.
• Possible association with cigarette smoking and drinking spirits.
• Higher incidence in patients with Barrett’s oesophagus.
• Oesophageal stasis may increase risk of carcinoma:
• 22-fold increase with lye strictures
• 9-fold increase with oesophageal webs
• 7-fold increase in achalasia
• 6-fold increase with peptic strictures
• post-cricoid carcinoma usually occurs in females
and is part of the Plummer–Vinson syndrome.
Types
• Most are squamous cell carcinomas.
• In the lower third, adenocarcinomas are the predominant type.
• Squamous cell carcinoma usually commences as an
ulcer, spreading to become annular and constricting,
causing dysphagia.
• Dysplasia usually precedes malignant change.
Spread
• Lymphatic spread occurs within submucosa beyond
the recognizable margins of the tumour viewed
endoscopically.
• Lymphatic metastases occur early to local lymph nodes.
• Local spread within the mediastinum may result in
tracheo-oesophageal stula, pleural eusion, superior
vena caval obstruction.
• Haematogenous spread occurs to lung and liver.
Prognosis
• At time of presentation, spread has usually occurred to
adjacent organs.
• Surgical resection possible in only 30–40%.
• Prognosis extremely poor: most patients survive less
than 6 months.
• 5-year survival only 5%.
Peptic Ulcer Disease
A peptic ulcer is a breach of the epithelial surface of the gastrointestinal tract due to attack by acid and pepsin. Peptic
ulcers may occur in the:
• stomach (common on lesser curve)
• duodenum (anterior or posterior aspect of rst part of
duodenum)
• lower oesophagus
• gastrojejunal anastomosis, following past surgery for
duodenal ulcer
• Meckel’s diverticulum (containing gastric mucosa).
Peptic ulcers may be acute or chronic.
Acute Peptic Ulceration
• Part of acute gastritis as a response to severe stress.
CHAPTER 22 System-Specific Pathology
419
• Due to severe hyperacidity such as Zollinger–Ellison
syndrome.
• Acute ulcers arising following acute gastritis are usually
a consequence of:
• steroids
• non-steroidal anti-inammatory drugs
• alcohol.
• Stress-induced ulcers may follow:
• severe sepsis
• acute pancreatitis
• major trauma
• head injury (Cushing’s ulcer)
• burns (Curling’s ulcer).
Chronic Peptic Ulceration
Chronic peptic ulceration occurs when the action of acid
and pepsin is not opposed by adequate mucosal protection mechanisms. e mucosal defences against acid attack
consist of a mucus–bicarbonate barrier and the surface
epithelium. Several factors show an association with peptic
ulceration:
• acid hypersecretion
• Helicobacter-associated gastroduodenitis
• non-steroidal anti-inammatory drugs
• steroids
• smoking
• alcohol
• diet
• stress.
An increased incidence of peptic ulceration, especially
duodenal ulceration, has been associated with:
• uraemia
• hyperparathyroidism
• hypercalcaemia
• chronic obstructive pulmonary disease
• alcoholic cirrhosis.
Complications of peptic ulcer
ese include:
• perforation, resulting in peritonitis
• bleeding, due to erosion of vessel in the base of an ulcer
• penetration into underlying structures, e.g. pancreas,
liver
• scarring: this may result in pyloric stenosis
• malignant change: this may occur rarely in gastric ulcers
but never in duodenal ulcers.
Carcinoma of the Stomach
Gastric cancer is the second most common fatal malignancy (aer lung cancer) in the world. ere is a high incidence in Japan, China, Colombia and Finland, but in these
countries as elsewhere in the world, the incidence of carcinoma of the stomach is declining.
Aetiology
• Nitrosamines: possible relationship between high levels
of nitrates in the diet and carcinoma. Nitrates converted
to nitrites, which ultimately lead to potential carcinogenic N-nitroso compounds.
• High-salt diet.
• High vegetable content in diet: vegetables contain antioxidants such as vitamin C and vitamin E.
• High intake of animal fat and proteins.
• High intake of rened carbohydrate.
• Cigarette smoking.
• Blood group A.
• Only 4% of patients with gastric cancers have a family
history of the disease.
Conditions associated with an increased risk of gastric cancer are:
• Achlorhydria
• due to chronic gastritis
• autoimmune
• Helicobacter-associated.
• Following partial gastrectomy, risk is increased 3- to
6-fold, with peak 20–30 years aer surgery.
• Intestinal metaplasia.
• Epithelial dysplasia.
• Ménétrier’s disease.
Pathogenesis
Gastric cancer is believed to develop by a sequence of pathological changes:
Normal mucosa → chronic gastritis → intestinal
metaplasia → dysplasia → intramucosal carcinoma →
invasive gastric carcinoma
Classification
Gastric cancers are classied on the basis of their direct
spread through the stomach wall as:
• early
• advanced.
Early
• Conned to either mucosa or submucosa.
• Increased diagnosis at this stage due to routine endoscopies and introduction of screening, e.g. in Japan,
where the number of early cases has increased from
4% to 30%.
• Early gastric cancer has a 5-year survival of 80–100%.
Advanced
• Cancer extending beyond muscularis propria.
• More than 80% of gastric cancers in the UK are in this
categ ory.
• Mainly in prepyloric region, pyloric antrum and lesser
curve.
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SECTION III Pathology
• Macroscopically, three types are recognized:
• ulcerating
• nodular or fungating
• inltrating.
• Spread:
• direct to adjacent organs, e.g. pancreas
• lymphatic: initially to local lymph nodes along the
right and le gastric artery, then to coeliac glands;
retrograde spread to nodes at the porta hepatis
(obstructive jaundice); distal nodes, e.g. to le supraclavicular fossa (Virchow’s node, Troisier’s sign)
• blood: usually via portal vein to liver
• transcoelomic, e.g. to ovaries (Krukenberg tumours).
Prognosis: overall 5-year survival 10%.
BOX 22.5 Causes of jaundice
Prehepatic (unconjugated hyperbilirubinaemia)
Congenital defects
Gilbert’s disease
Crigler–Najjar syndrome
Haemolysis
Congenital red cell defects
Hereditary spherocytosis (congenital acholuric jaundice)
Sickle cell disease
G6PD deficiency
Thalassaemia
Acquired red cell defects
Malaria
Incompatible blood transfusion
Autoimmune
Haemolytic disease of the newborn
Absorbing large haematoma
Hypersplenism
Hepatobiliary Disorders
Jaundice
Jaundice is yellow discoloration of the tissues, noticed
especially in the skin and sclera due to the accumulation
of bilirubin. Jaundice is clinically apparent when the circulating level of bilirubin is in excess of 35 µmol/L. Jaundice
may be:
• prehepatic (due to haemolysis)
• hepatic (due to intrinsic liver disease)
• cholestatic (due to either intrahepatic cholestasis or
posthepatic biliary obstruction). e causes of jaundice
are shown in Box 22.5.
Chronic autoimmune hepatitis
End-stage liver disease
Alcohol
Cirrhosis
Haemochromatosis
Wilson’s disease
Cholestatic
Intrahepatic
Drugs, e.g. chlorpromazine
Total parenteral nutrition (TPN)
Primary biliary cirrhosis
Viral hepatitis
Pregnancy
Extrahepatic (obstructive)
In the lumen
Gallstones
Infestation: clonorchiasis (liver fluke); schistosomiasis
Hepatic
Acute hepatocellular disease
Viral hepatitis
Hepatitis A, B, C
Epstein–Barr virus
CMV
Other infections
Leptospirosis
Drugs, e.g. paracetamol, halothane
Toxins, e.g. carbon tetrachloride
Autoimmune
Chronic hepatocellular disease
Chronic viral hepatitis
In the wall
Congenital biliary atresia
Cholangiocarcinoma
Stricture, e.g. inflammatory, post-operative
Cholangitis
Sclerosing cholangitis
Choledochal cyst
Outside the wall
Carcinoma of the head of the pancreas
Carcinoma of the ampulla of Vater
Malignant nodes in the porta hepatis
Chronic pancreatitis
Mirizzi syndrome
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