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FRCPath Histopathology Part 1 > Oesophagus > Flashcards

Oesophagus Flashcards

1
Q

What is the structure of the oesophagus?

A
  • Muscosa- non ketratinising stratified squamous epithelium
  • Submucosa - glands are connected to lumen by squamous lined ducts
  • Muscularis propria - inner circular muscle, outer longitudinal muscle (smooth), myenteric plexus
  • Adventitia
  • Squamocolumnar junction/Z-line
  • Gastrooesophageal junction - marked by rugal folds.
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2
Q

Name some benign incidental findings of the oesophagus

A
  • Gastric inlet patch - heterotopic gastric mucosa (fundic/oxyntic type admixed with mucous glands) in upper 1/3 of oesophagus. Can resemble malignancy radiologically.
  • Pancreatic metaplasia/heterotopia- benign pancreatic acini and ducts
  • Heterotopic sebaceous gland.
  • Glycogenic acanthosis- epithelial hyperplasia, abundent glycogen accumulation in superficial squamous cells. endoscopic appearance: white plaques

extensive glycogenic acanthosis - could be linked to Cowden Syndrome.

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3
Q

Describe Achalasia

A
  • Functional disorder
  • Lack of progressive peristalsis, partial/incomplete relaxation of LES
  • Issue is with circular layer of muscularis propria
  • T Cell mediated destruction, or complete absence of myenteric ganglion cells in lower third of oesophagus
  • Myenteric plexus inflammation/damage -> loss of inhibitory ganglion cells -> neurotransmitter inhibition is decreased (nitric oxide), imbalance of acetylcholine and nitric oxide -> Achalasia
  • bird beak on barium swallow

Risk of:
* Barrett’s
* Candida infection
* GERD
* Lower Oesophageal diverticula
* Pepic ulceration
* Stricture

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4
Q

What are the causes of Achalasia?

A

Primary - idiopathic

Secondary
Diabetes
Malignancy
Chagas Disease
Amyloidosis
Sarcoidosis
Neurofibromatosis
Eosinophilic Gastroenteritis
MEN 2B
Anderson-Fabry Disease
Juvenile Sjogren’s syndrome

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5
Q

What is the treatment of Achalasia?

A
  • Laparoscopic myotomy
  • Pneumatic balloon dilation
  • Botulinum neurotoxin (BOTOX) injection - inhibits contraction promotic cholinergic neurons
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6
Q

Describe Oesophageal Rings

A
  • AKA Schatzki rings
  • Circumferential, thicker
  • Include mucosa, submucosa, occasionally hypertrophic muscularis propria

A RING: distal oesophagus - above GOJ, covered in squamous mucosa

B RING: at squamocolumnar junction of lower oesophagus, may have gastric cardia-type mucosa on under-surface

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7
Q

Describe Oesophageal Webs

A
  • Semi-Circumferential lesions
  • Fibrovascular connective tissue and overlying epithelium

Seen in women >40
May be associated with GERD, graft vs host, blistering skin diseases

Forms part of Plummer-Vinson Syndrome
* Iron deficient anaemia
* Glossitis
* Cheilosis

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8
Q

Plummer-Vinson Syndrome

A
  • AKA Paterson-Brown-Kelly syndrome

TRIAD:
* IDA
* Dysphagia
* Cervical oesophageal web

Premalignant disease

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9
Q

Describe GERD

A
  • Gastro-oesophageal reflux disease
  • Endoscopy: varies - normal to erythema/hyperemia to erosion/ulceration
  • Micro: spongiosis, basal cell hyperplasia, elongation of vascular papilla, scattered inflammatory cells (eosinophils, lymphocytes, neutrophils
  • Usually more prominent in distal aspect near GEJ
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10
Q

Describe Candida Oeophagitis

A
  • Endoscopy: white plaques, scraped off to reveal erythematous/ulcerated underlying mucosa
  • Micro: fungal pseudohyphae and budding yeast, squamous debris, active oesophagitis
  • Stains: GMS (Grocotts), PAS
  • Treat with Fluconazole
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11
Q

Describe HSV Oesophagitis

A
  • Endoscopy: shallow, punched out ulcers, necrotic exudate

Biopsy taken from ulcer edge:
* Acantholysis
* Multinucleated squamous cells - steel blue nuclei, Cowdry type A inclusions (dense, eosinophillic, intranuclear).

  • viral cytopathic effects in epithelial cells - ground glass nuclei
    *** the 3 Ms **- margination of chromatin, multinucleation, and nuclear molding

Tests:
HSV1 and HSV2 IHC stain
PCR for HSV DNA
ISH

Treatment:
Acyclovir in immunosuppressed
Self-limited in immunocompetent individuals

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12
Q

Describe CMV Oesophagitis

A
  • Common in patients with AIDS
  • Endoscopy: erythema, erosions, ulceration - non specific ulcers
  • Viral cytopathic effects in mesenchymal cells - enlarged cells with nucleomegaly and inclusions
  • Owls -eye intranuclear inclusions and granular intracytoplasmic inclusions

Test:
CMV immunostain
ISH

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13
Q

Describe pill/medicine-induced Oesophagitis

A
  • Endoscopy: ulceration
  • Inflammatory exudate (neutrophils), polarisable foreign material/pill filler
  • Microcrystalline cellulose - refractile, transparent
  • Crospovidone - pink/purple
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14
Q

Describe eosinophilic oesophagitis

A
  • Endoscopy: concentric rings/linear furrows - trachealisation/felinization
  • white plaques/exudates
  • micro: intraepithelial eosimophils (>15 per hpf), eosinophilic microabscesses, superficial concentrations of eosinophils with degranulation and surface desquamation
  • basal cell hyperplasia, oedema. elongated papillae, lamina propria fibrosis.

immune/antigen driven - type 2 helper t-cell mediated (Th2)

clinicopathlogical diagnosis:
* clinical features - dysphagia, food impaction, feeding intolerance
* endoscopic appearance
* >15 intraepithelial cells per hpf
* exclusion of other causes of eosinophilia

Association with ectopic triad - allergies, asthma, eczema

Often worse proximally

Treat with PPI for symptoms and corticosteroids

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15
Q

Describe Oesophagitis Dessicans Superficialis

A
  • Sloughing Oesophagitis
  • Endoscopy: white plaques of peeling and sloughing epithelium
  • two tone appearence - superficial hypereosinophilic/necrotic epithelium with parakeratosis and underlying viable uninflamed/minimally inflamed deeper layers

oedema and vacuolisation of interface will eventually cause splitting of squamous epithelium

associated with medications, autoimmune bullous dermatoses, thermal/chemical injury, heavy smoking, alcohol and having multiple comorbidities.

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16
Q

Describe Lymphocytic Oesophagitis

A
  • Endoscopy: may mimic oesinophilic esophagitis - rings/furrows/white plaques
  • increased intraepithelial lymphocytes - concentrated around dermal papillae
  • intracellular oedema, dyskeratotic epithelial vells

associated with:
* GERD
* Crohn’s
* Coeliac
* achalasia and dysmotility
* lichen planus (of oesophagus)
* graft vs host
* common variable immunodeficiency

17
Q

Describe Barrett’s Oesophagus

A
  • extension of salmon-coloured mucosa into the oesophagus extending >1cm prox to the GEJ.
  • Intestinal metaplasia (goblet cells, ACID MUCIN) - seen with Alcian-Blue/PAS
  • True goblet cells - rounded/ovoid, blue tinged cytoplasmic mucin, eccentric nucleus
  • Incomplete IM: only goblet cells with mucin are present
  • Complete IM: goblet cells and brush border present, paneth cells can be seen

British definition doesnt rely on IM, unlike American.
But needs both endoscopic and histological correlation

  • SHORT segment: <3cm
  • LONG segment: >3cm

SEATTLE protocol for biopsies:
* four quadrant biopsies
* taken every 2cm through Barrett’s segment

Dysplasia needs to be double reported

18
Q

What are the risk factors for BE?

A
  • Chronic GERD
  • Male
  • Caucasian
  • Central obesity
  • Smoking
  • Age >50
  • Lack of nonsteroidal anti inflammatory agent use
  • Lack of PPI use
  • Lack of statin use
19
Q

Describe the pathgenesis of BE

A
  • Chronic GERD induces tissue damage
  • Upregulation of columnar transcription factors (SOX9)
  • Induces columnar differentiation
  • Upregulation of intestinal differentiation factors (CDX2)
  • Intestinal metplasia
  • Molecular alterations
  • Low-grade dysplasia
  • TP53, DNA aneuploidy
  • High-grade dysplasia and carcinoma
20
Q

Negative for dysplasia

A

Polarity seen in 4 lines:
* apical neutral mucin cap
* base of mucin cap
* eosinophilic cytoplasm below the mucin
* row of nuclei

Endoscopic surveillance interval:** 3-5 years**

21
Q

Indefinite for dysplasia

A

Used if unsure if reactive vs neoplastic
ie - inflammation/ulceration/technical artifacts/diathermy

Treat for GERD and repeat biopsy in 3-6 months

22
Q

Low grade dysplasia

A
  • Adenoma-like or intestinal type
  • Cytological abnormality, little/no architectural complexity
  • Nuclear enlargement
  • Hyperchromasia
  • Retained nuclear polarity
  • Both strong or absent (null phenotype) p53 staining considered significant
  • AMACR and **IMP3 **sometimes useful

Findings extend to surface and often show abrupt transition point from non-dyplastic to dysplastic area

  • Manage with endoscopic mucosal ablation
  • endoscopic surveillance every 12 months an acceptable alternative
23
Q

High grade dysplasia

A
  • greater degree of cytological atypia
  • Often with architectural abnormalities
  • No surface maturation
  • Crowded crypts with variable size and shape
24
Q

What are endoscopy timelines in Barretts?

A
  • Just Squamous epithelium - ?sampling error - Repeat

Barretts
* <3cm, gastric metaplasia –> repeat –> if same, consider discharge
* <3cm, IM –> repeat OGD every 3 to 5 years
* >3cm –> repeat OGD every 2 to 3 years

Dysplasia
* Indefinite –> repeat OGD in 6 months with max acide suppression
* Low grade –> OGD every 6 months until 2 consecutive non-dysplastic –> follow Barratts flowchart
* High grade –> MDT discussion –> Therapeutic intervention

25
Q

What underlying conditions can lead to oesophageal Ca?

A

1) **Barrett’s Oesophagus **
Effects 1-6% people
10% go on to develop ADENOCARCINOMA
Familial Barretts Oesophagus - gene MSR1

2) Achalasia
1 in 100,000 people
x50 higher risk of SCC and ADENOCARCINOMA

3) Tylosis
‘Howel-Evans Syndrome’
Rare hereditary disease - autosomal dominant
Gene RHBDF2
High risk (25-95%) of SCC

4) Fanconi anaemia
gene FANCA

5) Bloom Syndrome
gene BLM

26
Q

Adenocarcinoma patterns

A
  • TUBULAR: most common, irregular single or anastomosing glandular structures
  • PAPILLARY: form papillae or micropapillae
  • MUCINOUS: tumour cells float in abundant extracellular mucin
  • SIGNET-RING: worse prognosis
27
Q

What are adverse features of Oesophageal AdenoCa?

A
  • Submucosal invasion (pT1b) over 500 microns
  • Poor differentiation
  • LVI
  • Positive margins
28
Q

What is the treatment of Oesophageal AdenoCa?

A
  • pT1 adenos with NO adverse features - endoscopic resection +/- radiofrequency ablation
  • Advanced Ca - oesophagectomy +/- chemoradiation

HER2 testing is done routinely - if amplified, Trastuzumab

Pembrolizumab - promising early results.

29
Q

IHC for Oesophageal Adeno vs Squamous

A
  • Can be difficult to distinguish poorly diff adeno from poorly diff squamous

CK7: positive in adeno, negative in SCC
CK5/6, p63, p40: negative in adeno, positive in SCC
PAS, Mucin: positive in adeno, negative in SCC

30
Q

Describe HER2 IHC

A
  • IHC 3+: strong, complete lateral or basolateral membranous reactivity in >10% tumour cells
  • IHC 2+/Equivocal: weak to moderate complete lateral or basolateral membranous reactivity in >10% tumour cells - perform ISH testing
  • IHC 1+: faint membranous reactivity in >10% tumour cells
  • IHC 0: no reactivity, or membranous reactivity in <10% tumour cells
31
Q

Describe Squamous Papilloma

A
  • Small polypoid lesions, warty surface
  • Benign papillary proliferation of squamous epithelium
  • Fibrovascular core of lamina propria
  • Vacuolated cells can be seen (look like koilocytes, without atypical nuclear features
  • Usually exophytic, but can be flat/endophytic

Caused by mucosal irritation- hyper-regenterative response:
* GERD
* Trauma
* HPV infection

US populations - distal oesophagus
Asian populations - mid oesophagus

32
Q

Describe Squamous Dysplasia

A
  • Flat lesions are better highlighted by Lugol iodine solution
  • needs BOTH cytological and architectural atypia
  • LOW GRADE: involves lower half of the epithelium only, with mild atypia
  • HIGH GRADE: involves more than half of the epithelium OR severe cytological atypia is present regardless of the extent of epithelial involvement.

Risk factors are similar to those of SCC

Accumulting genetic abnormalities result in normal -> low grade dysplasia -> high grade dysplasia -> invasive carcinoma

TP53 mutation is key early driver mutation

33
Q

What are the genetic mutations in Oesophageal SCC?

A
  • TP53 mutation found in 59 - 93% of all cases
  • NOTCH1 and **NOTCH3 **mutations detected in up to 28% of cases
  • **EGFR **overexpression reported in 59.6 - 76% of cases
  • Mutations or amplification in RAS and **AKT **family seen in at least 75% of cases
34
Q

SCC Subtypes

A

VERRUCOUS:
* well-differentiated, minimal cytological atypia, minimal mitotic activity
* invasive front - broad bulbous pushing projections

SPINDLE CELL:
* polypoid growth pattern
* biphasic pattern - squamous epithelium and spindle cells
* squamous - well to moderately differentiated or carcinoma in situ alone
* spindle - high grade malignancy, may have osseus, cartilaginous or skeletal muscle diff

BASALOID:
* Solid or nested growth pattern of basaloid cells - sometimes comedo necrosis, pseudoglandular/cribriform formations.
* Unlike in oropharynx… NO association with HPV infection

35
Q

What are the risk factors for Oesophageal SCC?

A
  • Tobacco
  • Alcohol
  • Hot Beverages
  • Plummer-Vinson syndrome
  • Achalasia
  • Tylosis
  • Radiotherapy
  • Caustic Ingestion
36
Q

What is Tylosis?

A
  • Autosomal dominant keratosis disorder
  • Missense mutation in RHBDF2, 17q25.3
  • Associated with familial early onset oesophgeal SCC
37
Q

Describe Granular Cell Tumour

A
  • Second most common benign mesenchymal tumour behind leiomyomas
  • Soft tissue tumour
  • Neuroectodermal differentiation (schwannian origin)
  • Common 30-50 year olds
  • Mostly asymptomatic with slow, indolent growth
  • Associated with Noonan (Leopard) syndrome

macro:
yellow, finely granular

micro:
poorly defined mass - sheets or nests separated by thin collagenous bands
Round/polygonal to slightly spindled cells
Mild to mod nuclear atypia
Abundant eosinophillic cytoplasm
Overlying squamous epithelium - pseudoepitheliomatous hyperplasia

38
Q

How do you diagnosis granular cell tumour?

A

** Fanburg-Smith Criteria** - 6 features
* Necrosis
* Spindling
* Vesicular nuclei with large nucleoli
* >2 mitoses/10 high-power fields
* High NC ratio
* Pleomorphism

3 or more: malignant
1-2: Atypical
0/focal pleomorphism: Benign

IHC:
S100+
SOX10+
CD68+
NSE+
EMA+

Treatment:
Benign - surgical excision, excellent prognosis
Malignant - Wider surgical resection

FRCPath Histopathology Part 1 (39 decks)

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