GI 1 Flashcards
1
Q
CLEFT LIP AND PALATE
Epidemiology
A
Epidemiology:
Most common congenital disorder of the oral cavity
Cleft lip and palate (50%)
Cleft lip (Cheiloschisis) alone (25%; M>F)
Cleft palate (Palatoschisis) alone (25%; F>M)
White>Black
2
Q
CLEFT LIP AND PALATE
Genetic susceptibility:
A
Genetic susceptibility:
Present in subsequent siblings (3%)
3
Q
CLEFT LIP AND PALATE
Pathogenesis:
A
Pathogenesis:
Failure of fusion of facial processes
4
Q
CLEFT LIP AND PALATE
Clinical features:
A
Clinical features:
Feeding difficulties due to child’s inability to
suck properly (in case of extensive lesions)
5
Q
CLEFT LIP AND PALATE
Complications + treatment
A
. Complications:
Malocclusion
Eustachian tube dysfunction
Chronic Otitis Media
Speech problems
Treatment: Surgical
6
Q
DENTAL CARIES
Synonym: “Tooth decay”
Pathogenetic mechanism:
(Sba)
A
Pathogenetic mechanism:
Streptococcus mutans produces acid from sucrose fermentation => Destruction of enamel by the action of acid, and subsequent exposure of the underlying dentine
Excessive consumption of sugars + Under development of dentine => Development of caries
Destruction of dentine => Bacterial invasion =>
Infection of the pulp (pulpitis)
7
Q
DENTAL CARIES
Prophylaxis
A
Prophylaxis: Oral hygiene and fluoridation of
the drinking water. Fluoride incorporates into
the crystalline structure of enamel, forming
fluoroapatite, and contributes to resistance to
degradation by bacterial acids
8
Q
GINGIVITIS + causes
A
Gingivitis: Inflammation of the mucosa and the
associated soft tissues
Causes: Lack of proper oral hygiene =>
Accumulation of dental plaque and calculus
9
Q
-If plaque not removed => Mineralisation and
formation of calculus (tartar)
- Bacteria in the plaque release acids from sugar-rich
foods, which erode the enamel surface of the tooth -Repeated erosions lead to dental caries
- Plaque build-up beneath the gum-line can cause
gingivitis
A
GINGIVITIS (pathogenesis?)
10
Q
Chronic Gingivitis is characterised by:
A
Chronic Gingivitis is characterised by:
Gingival erythema
Oedema
Changes in contour
Loss of soft-tissue adaptation to the teeth
11
Q
ACUTE NECROTIZING ULCERATIVE GINGIVITIS
Trench mouth, Vincent infection:
Cause
A
-Trench mouth, Vincent infection:
Cause:
- Fusobacterium species, Borrelia
vincentii decreased resistance to
infection
-Patients with decreased resistance to
infection
- Severe necrosis of the free gingival
margin, crest of gingiva and the
interdental papilla with punched out
lesions covered by a grayish pseudo-
membrane
12
Q
PERIODONTITIS + cause
A
Inflammatory process that affects the supporting “
structures of the teeth (periodontal ligaments,
alveolar bone and cementum)
Cause; Association with Actinobacillus actinomycetem-
concomitans, Porphyromonas gingivalis and
Prevotella intermedia
13
Q
Periodontal disease can be:
A
-‘Component of several different systemic diseases
(AIDS, Leukaemia, Mb. Crohn, Sarcoidosis, DM, etc.)
- Aetiologic factor in several important systemic
diseases (Infective Endocarditis, Pulmonary and
Brain Abscesses, etc.)
14
Q
Dentigerous Cyst:
A
Cyst that originates around the crown of
an unerupted tooth
Result of a degeneration of the dental
follicle
Uni-locular lesions
Most often associated with impacted third
molar (wisdom) teeth
15
Q
Microscopic findings:
Cysts lined by a thin layer of stratified
squamous epithelium
Dense chronic inflammatory cell infiltrate
in the stroma
A
Dentigerous Cyst
16
Q
Dentigerous Cyst
Management
A
Management:
Complete surgical excision <=> Curative
Incomplete excision => Recurrence or rarely
neoplastic transformation into an Amelo- blastoma or a Squamous Cell Carcinoma
17
Q
Odontogenic Keratocyst:
Synonym: Keratocytic Odontogenic Tumour
+ Epidemiology
A
locally aggressive and has a high rate of recurrence
Epidemiology:
Appearance at any age, but most often in
patients between 10-40 years
Most commonly in males
18
Q
Odontogenic Keratocyst
Localisation
A
Odontogenic Keratocyst:
Localisation: Within the posterior mandible
19
Q
Odontogenic Keratocyst Imaging studies
A
. Imaging studies: Well-defined uni-locular or
multi-locular radiolucencies
20
Q
Microscopic findings:
Cyst lining with a thin layer of para-
keratinised or ortho-keratinised stratified
squamous epithelium
Prominent basal cell layer
Corrugated appearance of the epithelial surface
A
Odontogenic Keratocyst
21
Q
Important: Evaluation of the patients with
multiple Odontogenic Keratocysts for the
presence of Nevoid Basal Cell Carcinoma
syndrome (Gorlin syndrome); associated
with mutations in the tumour suppressor gene
PTCH
A
Odontogenic Keratocyst
22
Q
Peri-Apical (Radicular) Cyst:
A
‘ Inflammatory in origin
Common lesion localised at
the apex of teeth
23
Q
Peri-Apical (Radicular) Cyst:
Pathogenesis:
A
Pathogenesis:
Result of long-standing pulpitis, caused by ad-
vanced carious lesions or by trauma to the tooth Inflammatory process => Necrosis of the pulpal
tissue => Spreading throughout the length of the
root => Exit the apex of the tooth into the sur-
rounding alveolar bone => Development of a
periapical abscess => Development of granula-
tion tissue (with or without an epithelial lining)
24
Q
Odontoma
A
Most common Odontogenic Tumour
Hamartoma, derived from odontogenic
epithelium and odontoblastic tissue
Well defined; The internal aspect is very
radiopaque, compared to bone
25
Odontoma
Types
Types:
Complex: Composed of haphazardly arranged
dental hard and soft tissues
Compound: Composed of many small
“denticles” (toothlets)
26
Ameloblastoma + location
Epithelial tumour arising from precursor cells
of the enamel organ
Location: Mandible
27
Ameloblastoma
Imaging
. Imaging: Radiolucency in bone, with a “soap
bubble” appearance
Commonly cystic, slow growing lesion
Indolent course in most cases
Local invasion, but no metastatic potential
28
Papilloma:
Most common benign epithelial tumour of the
oral mucosa
Common sites: Tongue, lips, gingivae, buccal
mucosa
29
Fibrous Epulis:
Benign non-neoplastic growth of the gingivae
Reparative growth rather than a true
neoplasm
30
Irritation Fibroma:
Occurrence in the buccal mucosa, along the
bite line or at the gingivo-dental margin
31
Microscopic findings:
Nodular mass of fibrous tissue
Few inflammatory cells
Covering by squamous mucosa
Irritation Fibroma:
32
Lobular Capillary Haemangioma
(Pyogenic Granuloma)
Epidemiology
Epidemiology
Children, young adults, pregnant women
(pregnancy tumour)
33
Macroscopic features:
Pedunculated masses with red purple colour
and ulceration of the surface
Microscopic findings:
Dense proliferation of
immature vessels (as in granulation tissue)
Lobular Capillary Haemangioma
(Pyogenic Granuloma)
34
Lobular Capillary Haemangioma
(Pyogenic Granuloma)
Progression
'Progression: Either regression, particularly after
pregnancy or fibrous maturation and
development into a Peripheral Ossifying Fibroma
35
Peripheral Ossifying Fibroma:
+ epidemiology
-. Relatively common growth of the gingiva;
considered to be reactive rather than neoplastic
-Epidemiology: Peak incidence in young and
teenage females
36
Peripheral Ossifying Fibroma:
Pathogenesis:
Pathogenesis: Chronic irritation => Reactive
connective tissue hyperplasia
37
Peripheral Ossifying Fibroma:
Sites
Sites: Buccal mucosa along the bite line (trau-
matic fibroma)
38
Macroscopic features: Red, ulcerated, and
nodular lesions of the gingiva
Microscopic findings: Submucosal nodular fibrous
tissue mass with foci of mineralization
Peripheral Ossifying Fibroma:
39
Peripheral Giant Cell Granuloma:
-Relatively common lesion of the gingiva.
-Generally covered by intact gingival mucosa,
but it may be ulcerated
40
Macroscopic features:
Similar to that of Pyogenic Granuloma, but
generally more bluish purple in colour (while
the Pyogenic Granuloma is more bright red)
Not encapsulated, but well delimited
Microscopic findings: Aggregation of multi-
nucleate, foreign-body-like giant cells
separated by a fibro-angiomatous stroma
Peripheral Giant Cell Granuloma:
41
Aphthous Ulcers
Cause + epidemiology
Epidemiology: 40% of population
-Unknown aetiology
-Recurrent Aphthous Ulcers may be
-associated with coeliac disease and inflammatory bowel disease
42
Aphthous Ulcers:
+ Clinical features
Clinical features: Solitary or multiple,
painful, recurrent, erosive oral ulcerations with spontaneous healing after some (7-10) days
43
Macro-/Microscopic features:
Shallow and hyperaemic ulcerations
Covered by a thin exudate
Rimmed by a narrow zone of erythema
Aphthous Ulcers
44
Glossitis
-Term applied to describe the beefy-red
tongue encountered in certain deficiency states (deficiencies of Vitamin B12 [Pernicious Anaemia], Riboflavin, Niacin or Pyridoxine, Sprue and Iron-deficiency Anaemia)
-Result from atrophy of the papillae of the
tongue and thinning of the mucosa, with exposure of the underlying vasculature, leading to inflammation and even shallow ulcerations
45
Glossitis
Plummer-Vinson or Paterson-Kelly syndrome:
Combination of:
Plummer-Vinson or Paterson-Kelly syndrome:
Combination of:
i. Iron-deficiency Anaemia
ii. Glossitis
iii. Oesophageal Dysphagia (usually related
to webs)
46
Glossitis characterised by
Glossitis characterised by ulcerative lesions
may be seen with jagged carious teeth and ill-
fitting dentures (traumatic cause)
47
HERPES SIMPLEX VIRUS INFECTIONS
Synonyms: Fever Blisters, “Cold Sores”
Cause
Cause: Herpes Simplex Virus (HSV), most often
type 1
Primary infections (2-4 years of age): Often
asymptomatic
48
HERPES SIMPLEX VIRUS INFECTIONS
Clinical features:
Clinical features:
Primary infection in form of Acute Herpetic
Gingivo-Stomatitis
Abrupt onset of vesicles and ulcerations through-
out the oral cavity, especially in the gingiva
-Accompanying lymphadenopathy, fever,
anorexia, and irritability
49
HERPES SIMPLEX VIRUS INFECTIONS
Recurrence after activation from:
Recurrence after activation from:
A febrile illness Allergies UV light Trauma
Sunshine Pregnancy and menstruation
50
HERPES SIMPLEX VIRUS INFECTIONS
Locations
Locations: Lips (Herpes labialis), nasal
orifices, buccal mucosa, gingiva, hard palate
51
Microscopic findings:
Intra-cellular oedema => Balooning of the
infected cells
. Inter-cellular oedema (acantholysis) =>
Formation of clefts => Transformation into
macroscopic vesicles
Occasionally, presence of eosinophilic intra-
nuclear viral inclusions, within individual
epidermal cells in the margins of the vesicle Fusion of several cells and production of giant
cells (multinucleate polycaryons)
HERPES SIMPLEX VIRUS INFECTIONS
52
HERPES SIMPLEX VIRUS INFECTIONS
Progression:
Progression: Vesicles and shallow ulcers
usually spontaneously clear within 3 to 4
weeks, but the virus treks along the regional
nerves and eventually becomes dormant in the
local ganglia (e.g. the trigeminal)
53
' . Oral Candidiasis:
Synonym + cause + epidemiology
Synonym: Thrush, Moniliasis
Cause: C. albicans
Epidemiology: 'Immuno-compromised individuals (e.g. HIV),diabetic patients, debilitated infants and children
54
Macroscopy: Superficial, curd like, gray to white
membrane with an underlying erythematous base
Microscopy: Membrane composed of matted
organisms enmeshed in a fibrino-suppurative
exudate
Oral Candidiasis
55
, Viral Pharyngitis:
Viral Pharyngitis:
Most common
Cause: Adeno- or Rhinoviruses
Common feature of Common Cold, Influenza,
Measles, Infectious Mononucleosis (Glandular Fever)
56
-Ulcerative Pharyngitis:
Ulcerative Pharyngitis:
Complication of agranulocytosis characterised
by deficiency of polymorphs (in cases of Leu-
kaemia and bone marrow failure)
Cause: Diphtheria (Corynebacterium
diphtheriae), Coxsackie A virus
57
Streptococcal Pharyngitis:
In conjunction with Tonsillitis and Glossitis
(Scarlet Fever)
Development of rash on skin and tongue
(initially white, and then strawberry coloured)
58
Streptococcal Pharyngitis Cause
Cause: Streptococcus pyogenes
59
Streptococcal Pharyngitis:
Complications:
Complications: Acute Proliferative Glomerulo-
nephritis, Rheumatic Fever and Henoch-
Schönlein purpura
60
TONSILLITIS + causes
Definition: Inflammation of the tonsils
Causes: Infection with a common virus (Adeno-
viruses, Influenza Virus, EBV, Parainfluenza
Viruses, Enteroviruses, HSV); bacterial
infections, most commonly with Streptococcus
pyogenes (group A)
61
TONSILLITIS
Epidemiology
Epidemiology:
Children between pre-school ages and the mid-
teenage years
Tonsillitis occurs occasionally or recurs
frequently
62
-TONSILLITIS
Diagnostic procedures:
Diagnostic procedures:
Rapid strep test ([Quick strep]; results in
10 min.)
Throat swab culture (results in 1 to 2 days)
63
TONSILLITIS
' Common Signs and Symptoms:
Red, swollen tonsils
White or yellow coating or patches on the
tonsils
Sore throat
Difficult or painful swallowing
Fever, chills
Enlarged, tender glands (lymph nodes) in
the neck
A scratchy, muffled or throaty voice
Bad breath
Ear pain
Loss of appetite
64
Leukoplakia and Erythroplakia:
Leukoplakia and Erythroplakia:
Leukoplakia: Clinical term describing white
mucosal patches that cannot be scraped off
Erythroplakia: Red patches
65
. Leukoplakia and Erythroplakia:
Causes
Causes: Chronic irritation (e.g. dentures), tobacco
use, alcohol abuse, HPV
66
Microscopy:
Squamous Hyperplasia of the epidermis
Possible progression into Squamous Dysplasia
or invasive SCC
Leukoplakia: 30% rate of progression to SCC Erythroplakia: 60% rate of progression to SCC
Leukoplakia and Erythroplakia:
67
Squamous Cell Carcinoma:
Epidemiology:
90% of head and neck cancers; The
remainder includes: Adeno-CAs (of Sali-
vary gland origin), Melanomas, various
Carcinomas
Sixth most common neoplasm worldwide Middle-aged men
Verrucous Ca: Association with smokeless
tobacco
Basal Cell Carcinoma:
-. Most common Cancer of the upper lip
-. Association with UV light exposure
68
Squamous Cell Carcinoma:
Risk factors
Risk factors: Oncogenic variants of HPV,
tobacco products, alcohol abuse, (actinic
radiation [sunlight] <=> Lower lip cancer)
69
Squamous Cell Carcinoma
-Localisation:
Localisation:
1. Lower lip (vermilion border) 2. Floor of mouth 3. Palate 4. Lateral border of tongue
70
Macroscopic features:
In early stages, presentation either as
raised, firm, pearly plaques or as irregular,
roughened, or verrucous areas of mucosal
thickening
With tumour enlargement, appearance of
ulcerated and protruded masses with
irregular and indurated borders
Squamous Cell Carcinoma:
71
Microscopic findings:
Degree of histologic differentiation: ranging
from well-differentiated keratinising neoplasms
to anaplastic sometimes sarcomatoid tumours
and from slowly to rapidly growing lesions
Degree is not correlated with tumour’s
biological behaviour
Local metastases: Cervical lymph nodes
Distant metastases: Mediastinal lymph nodes,
lungs, liver and bones
Squamous Cell Carcinoma
72
SIALADENITIS + causes
Definition: Inflammation of the salivary glands
Causes: Trauma, viral or bacterial infection,
auto-immune disease
73
Most common form of Viral Sialadenitis
Macroscopic features: Enlargement of all salivary but predominantly of the parotids
Microscopic findings: Interstitial inflammation,
characterised by a mononuclear inflammatory
infiltrate
SIALADENITIS
Mumps:
74
SIALADENITIS Mumps:
Progression:
Children: Self-limited benign condition
Adults: Pancreatitis or Orchitis; latter can
cause infertility
75
SIALADENITIS: Mucocele
CAUSE
Most common lesion of the salivary glands
Cause: Blockage or rupture of a salivary gland
duct => Leakage of saliva into the surrounding connective tissue stroma
76
SIALADENITIS Epidemiology + localisation
Epidemiology: Occurence in toddlers, young
adults and geriatric population as a result of trauma
Localisation: Lower lip
77
SIALADENITIS Mucocele
Clinical features:
Clinical features:
Fluctuant swellings of the lower lip, with a
blue translucent hue
78
Microscopic findings:
Cyst-like space, filled with mucin and
inflammatory cells (particularly macrophages) Lining of the cyst-wall: Either by
inflammatory granulation tissue or by fibrous
connective tissue
SIALADENITIS
Mucocele:
79
SIALADENITIS
Ranula: LOCALISATION
Mucocele that arises when the duct of the
sublingual gland has been damaged
Localisation: Floor of the mouth
80
SIALADENITIS
Ranula: CLINICAL FEATURES
. Clinical features: Potential to reach extremely
large size and develop into a “Plunging
Ranula”, when it dissects its way through the
connective tissue stroma connecting the two
bellies of the mylohyoid muscle
Histologically identical to Mucocele
81
Sialolithiasis
Ductal obstruction caused by stones
Stone formation sometimes related to obstruction of the orifices of the salivary glands i. by impacted food debrisor ii. by oedema about the orifice after some injury
82
Non-specific bacterial Sialadenitis:
Common condition secondary to Sialolithiasis
Most often involvement of the major salivary glands, particularly the submandibular glands
83
Non-specific bacterial Sialadenitis:
Causes:
Causes: Staphylococcus aureus and Streptococcus
viridans
84
When staphylococcal or other pyogens are the
causative organisms => Overt suppurative
necrosis and abscess formation
SIALOLITHIASIS & NON-SPECIFIC BACTERIAL SIALADENITIS
85
Clinical features:
SIALOLITHIASIS & NON-SPECIFIC BACTERIAL SIALADENITIS
Clinical features:
Unilateral involvement of a single gland
Affected gland: Painful, enlarged and
sometimes with a purulent ductal discharge
86
SIALOLITHIASIS & NON-SPECIFIC BACTERIAL SIALADENITIS
Dehydration and decreased secretory function
may:
Dehydration and decreased secretory function
may:
Predispose to secondary bacterial invasion,
as sometimes occurs in patients receiving
long-term Phenothiazines (drugs
suppressing salivary secretion)
Lead to the development of Bacterial
Suppurative Parotitis in elderly patients
with a recent history of major thoracic or
abdominal surgery
87
Sjögren Syndrome:
Cause:
Cause: Autoimmune origin
88
Sjögren Syndrome:
Diagnostic criteria for primary Sjögren Syn
Diagnostic criteria for primary Sjögren Syn:
Keratoconjunctivitis sicca
Xerostomia
Extensive lymphocytic infiltrate on minor
salivary gland biopsy
Laboratory evidence of a systemic autoimmune
disorder
Specific exclusions are pre-existing Lymphoma,
graft-versus-host disease, AIDS & Sarcoidosis
Increased incidence of Malignant Lymphoma
89
Pleomorphic Adenoma:
Synonym: Mixed tumour (myxoid, cartilage-
like components and epithelial cells) .
Epidemiology
Epidemiology:
Most common salivary gland tumour
Women, 20-40 years
Benign neoplasm that frequently recurs Increased risk after radiation exposure
90
Pleomorphic Adenoma:
Localisation
Localisation: Parotid gland (90%); often
proximity to facial nerve
91
Macroscopic features:
Size: Most often, less than 6cm in diameter
Firm, non-tender, multi-lobulated, well-
demarcated and mostly encapsulated
Cut surface: Gray-white with myxoid and blue
translucent areas of chondroid
Microscopic findings:
Irregular masses of anastomosing strands of
stellate or fusiform epithelial cells partly in ducts or tubules, embedded in myxoid stroma with fibrous, cartilage-like or hyalinised areas
'Pleomorphic Adenoma:
92
Pleomorphic Adenoma
Clinical features:
Clinical features:
Painless, slow-growing, mobile discrete mass
93
Pleomorphic Adenoma
Microscopic picture:
Microscopic picture: Adenocarcinoma or
Undifferentiated Carcinoma with coexistence of Pleomorphic Adenoma traces
94
Warthin Tumour:
Synonym: Papillary Cystadenoma
Lymphomatosum
Benign neoplasm that arises almost exclusively
in the parotid gland
95
Warthin Tumour:
Epidemiology
Epidemiology:
Second most common salivary gland neoplasm More commonly in males than in females
Age: 5th-6th decade of life
10% multifocal; 10% bilateral
Risk: Smokers 8x more compared to non-smokers
96
Macroscopic features:
Round to oval, encapsulated mass
Size: 2-5 cm in diameter
Cut surface: Pale gray, punctuated by narrow
cystic or cleft like spaces filled with mucinous
or serous secretion
“Motor oil” quality of the cyst fluid
Warthin Tumour:
97
Microscopic findings:
Cystic spaces lined by a double layer of neoplastic
epithelial cells, resting on dense lymphoid stroma Spaces are frequently narrowed by polypoid
projections of the lympho-epithelial elements
The double layer of lining cells consists of:
-A surface palisade of columnar cells (with an
abundant, finely granular, eosinoph. cytoplasm)
-A layer of cuboidal to polygonal cells
Secretory cells: Dispersed btw columnar cells Occasionally, foci of squamous metaplasia
Warthin Tumour
98
Muco-Epidermoid Carcinoma:
+ epidemiology
Neoplasm composed of variable mixtures of
squamous cells, mucus-secreting cells, and intermediate cells
Epidemiology:
~15% of salivary gland tumours
Most common malign. tumour of salivary glands
99
Muco-Epidermoid Carcinoma:
Genetics
Genetics: >50% of cases associated with a
balanced (11;19) (q21;p13) chromosomal trans- location => Fusion gene, composed of portions of the MECT1 and MAML2 genes
100
'Macroscopic features:
Size: 8cm in diameter
Circumscribed lesion
Lack of well-defined capsule; infiltrative
growth at the margins
Cut surface: Pale and gray-white, with
presence of small, mucin-containing cysts
Muco-Epidermoid Carcinoma '
101
-Microscopic findings:
Histologic picture dominated by cords, sheets,
or cystic configurations of squamous, mucous,
or intermediate cells
The hybrid cell types often have squamous
features, with small to large mucus-filled
vacuoles (demonstrable with mucin stains)
Tumour cells with variable cytologic features:
-Regular and benign appearing or
- Highly anaplastic and malignant
, Muco-Epidermoid Carcinoma '
102
Muco-Epidermoid Carcinoma
Prognosis (depending on tumour’s grade):
Prognosis (depending on tumour’s grade):
Low grade Tm: Local invasion, and recurrence
in 15% of cases; 5yrs survival: 90%
High grade Tm: Marked invasion with difficulty
in excision; Recurrence rate of 25-30%;
Metastases to distant sites; 5yrs survival: 50%
103
Adenoid Cystic Carcinoma:
Localisation
Relatively uncommon tumour
, Localisation: Minor salivary glands (in particular
the palate) in about 50% of cases
. Similar neoplasms present in the nose, sinuses,
and upper airway
104
Macroscopic features:
Small gray-pink lesions
Rarely circumscribed
Almost never encapsulated
Infiltrative growth
Adenoid Cystic Carcinoma:
105
Microscopic findings:
Small cells
Dark, compact nuclei
Scant cytoplasm
Arrangement of cells in tubular, solid or cribri-
form patterns, reminiscent of Cylindromas of
the skin adnexa
Presence of cystic spaces, filled with either
granular basophilic material or PAS-positive
eosinophilic material
Neural invasion <=> Hallmark of this entity
Adenoid Cystic Carcinoma
106
Adenoid Cystic Carcinoma
Progression and Prognosis:
Progression and Prognosis:
Generally, slow growing tumours
Tendency for invasion of peri-neural spaces High recurrence rate
50% wide dissemination to distant sites
(bone, liver and brain)
5yr survival rate: 60-70%
10yr survival rate: 30%
15yr survival rate: 15%
107
Acinic Cell Carcinoma:
Epidemiology:
Epidemiology:
Uncommon malignant tumour; 2-3% of
salivary gland tumours
Young men
108
Acinic Cell Carcinoma:
Localisation
Localisation:
Mostly in the parotids; the remainder arise
in the submandibular glands
Sometimes, bilateral or multi-centric (like
Warthin tumour)
109
Macroscopic features:
Small discrete lesion that appears encapsulated
Microscopic findings:
Variable architecture and cell morphology
Cells with clear cytoplasm; but alternating
appearance between solid and vacuolated Arrangement of cells in sheets or microcystic,
glandular, follicular, or papillary patterns
Usually, little anaplasia
Few mitotic figures
Acinic Cell Carcinoma
110
Acinic Cell Carcinoma
Progression and Prognosis:
Progression and Prognosis:
Clinical course dependent on the level of
pleomorphism
Recurrence after resection, uncommon
Lymph node metastasis: 10-15% of cases Survival rate:
90% at 5 years 60% at 20 years
111
TRACHEO-OESOPHAGEAL FISTULA
+ risk factors
Most common congenital anomaly
Risk factors: Advanced maternal age, smoking,
obesity
112
TRACHEO-OESOPHAGEAL FISTULA
Clinical findings:
Clinical findings:
Maternal Poly-Hydramnios
Abdominal distention in newborn
Frothing and bubbling around the mouth, at birth Difficulty with feeding
VATER syndrome: Vertebral anomaly, Anorectal
(anal atresia), TE fistula, Renal disease and
absent radius
113
TRACHEO-OESOPHAGEAL FISTULA
Three distinct variants:
Most common (90%):
Lower portion of oesophagus communicates
with the trachea near tracheal bifurcation
Upper oesophagus ends in a blind pouch
(Oesophageal Atresia)
Association with maternal Poly-Hydramnios
Second most common:
Fistulous connection between the upper oeso-
phagus and the trachea; the lower oesophageal segment no connection to the upper part
Third variant:
Fistulous connection between the trachea and
a completely patent oesophagus
114
OESOPHAGEAL DIVERTICULA
Pouches lined by one or more layers of the
oesophageal wall
115
OESOPHAGEAL DIVERTICULA
Types of Diverticula:
Types of Diverticula:
False (pulsion):
- Weakness in underlying muscle wall
- Out-pouching of mucosa and submucosa
True (traction):
- Result from peri-oesophageal inflammation
and scarring
116
'OESOPHAGEAL DIVERTICULA
Locations
Locations:
Above upper oesophageal sphincter (Zenker)
Near midpoint of oesophagus
Above lower oesophageal sphincter (epi-phrenic)
117
ZENKER DIVERTICULUM
Synonym: Pharyngo-Oesophageal diverticulum
“Pulsion” type
Area of weakness of crico-pharyngeous muscle
118
ZENKER DIVERTICULUM
Clinical findings + Treatment
, Clinical findings:
Painful swallowing
Food regurgitation
Halitosis (due to entrapped food)
Possible diverticulitis
Treatment: Surgery
119
'OESOPHAGEAL MUCOSAL WEBS
+ Pathogenesis
. Uncommon ledge-like protrusions of mucosa that
may cause obstruction
Pathogenesis: Unknown
120
OESOPHAGEAL MUCOSAL WEBS
Epidemiology
Epidemiology:
Most frequently in women over age 40
Often associated with: i. Gastro-OEsophageal
Reflux Disease, ii. Chronic-Graft-versus-Host
Disease, or iii. Blistering skin diseases
Upper oesophageal webs accompanied by Iron-
Deficiency Anaemia, Glossitis and Cheilosis <=>
Part of the Peterson-Brown-Kelly or Plummer-
Vinson syndrome
121
OESOPHAGEAL MUCOSAL WEBS
Localisation + Clinical features
Localisation: Most common in the upper oesophagus
Clinical features: Dysphagia associated with
incompletely chewed food
122
Macroscopic features:
Semi-circumferential, eccentric lesions
Protrusion of less than 5mm
Thickness of 2-4mm
Microscopic findings:
Fibro-vascular connective tissue and
Overlying epithelium
OESOPHAGEAL MUCOSAL WEBS
123
OESOPHAGEAL RINGS
( Schatzki Rings )
- Similar to webs, but circumferential and thicker
- Rings include mucosa, submucosa, and in some
cases, hypertrophic muscularis propria
124
OESOPHAGEAL RINGS
Types
A Rings: Located in the distal oesophagus,
above the gastro-oesophageal junction; covered
by squamous mucosa
B Rings: Located at the squamo-columnar
junction of the lower oesophagus; may have
gastric cardia-type mucosa on their under-
surface
125
ACHALASIA
Increased tone of the lower oesophageal sphincter,
as a result of impaired smooth muscle relaxation
126
ACHALASIA
Characterised by the triad of:
1. Incomplete LES relaxation
2. Increased LES tone
3. Aperistalsis of the oesophagus
127
Primary Achalasia:
Caused by failure of distal oesophageal inhibitory
neurons
Degenerative changes in neural innervation,
either intrinsic to the oesophagus or within the
extra-oesophageal vagus nerve or the dorsal
motor nucleus of the vagus
128
'Secondary Achalasia:
Secondary Achalasia:
May arise in Chagas disease
Trypanosoma cruzi infection causes:
1.Destruction of the myenteric (Auerbach’s) plexus
2.Failure of peristalsis
3.Oesophageal dilatation
129
Achalasia-like disease may be caused by:
Diabetic Autonomic Neuropathy
Infiltrative disorders (e.g. Malignancy, Amyloidosis, or Sarcoidosis)
Lesions of dorsal motor nuclei (e.g. polio or
surgical ablation)
130
ACHALASIA
Epidemiology + Clinical features:
Epidemiology: Bimodal age distribution:
20-40yrs and >60yrs
Clinical features:
Nocturnal regurgitation of food rest
Dysphagia for solids and liquids
Chest pain and heartburn
Frequent hiccups
Nocturnal cough from aspiration
131
ACHALASIA
Diagnosis
Diagnosis:
Dilated aperistaltic oesophagus with a beak-like
tapering at distal end (barium enema)
Detectable aperistalsis (oesophageal manometry)
132
'ACHALASIA
. Treatment
Treatment:
Non-pharmacologic:
Pneumatic balloon dilatation
Oesophago-myotomy
Pharmacologic:
Long-acting nitrates
Calcium channel blockers
Injection of Botulinum neurotoxin (Botox)
133
HIATAL HERNIA
Epidemiology:
Women > Men
Association with: i. Sigmoid Diverticulosis (25%),
ii. Oesophagitis (25%), iii. Duodenal Ulcers (20%), iv. Gallstones (18%)
134
Para-Oesophageal (Rolling) Hernia:
Gastro-Oesophageal junction at diaphragm’s level Part of stomach bulges into the thoracic cavity
135
Pleuro-Peritoneal Diaphragmatic (Bochdalek)
Hernia:
-70% of cases, in newborns
-Loops of bowel in the left pleural cavity, through
the postero-lateral part of diaphragm on the left
136
(Hiatal hernia) Sliding Hernia:
. Most common type (99% of cases)
Herniation of proximal stomach into thoracic
cavity through the diaphragmatic Oesophageal hiatus
137
Sliding Hernia
Clinical findings:
-Heartburn
-Nocturnal epigastric distress from acid reflux -Haematemesis
-Ulceration
-Stricture
138
OESOPHAGEAL ATRESIA
'Incomplete formation of the Oesophagus, frequently
associated with Tracheo-Oesophageal Fistula
139
OESOPHAGEAL ATRESIA
Epidemiology:
Epidemiology:
Most common GI atresia
Syndromes associated with atresia:
. VACTERL: Vertebral anomalies, Anal atresia,
Cardiac malformations, Tracheo-Esophageal fistula, Renal anomalies, Radial aplasia and Limb anomalies
CHARGE: Coloboma, Heart defects, Atresia of
the choanae, Retardation of mental and/or physical development, Genital hypoplasia, Ear abnormalities
Five major types of Oesophageal Atresia
140
OESOPHAGEAL ATRESIA
. Diagnosis
Diagnosis:
Prenatal: Ultrasonography (absence of foetal
stomach bubble [<50% of cases])
Postnatal:
X-ray: Radiopaque catheter for determining the
location of atresia
Fluoroscopy: Water-soluble contrast material
(quick aspiration to avoid chemical pneumonitis) Failure to pass a nasogastric tube
141
'OESOPHAGEAL ATRESIA
Treatment
'Treatment:
Extra-pleural surgical repair
Occasionally, interposing of a segment of colon
between the oesophageal segments
142
MALLORY-WEISS SYNDROME
+ cause
'Definition: Mucosal tear in the proximal stomach
and distal oesophagus
Cause: Severe retching, associated with alcoholism
or bulimia
143
MALLORY-WEISS SYNDROME
Clinical feature:
. Clinical features: Haematemesis, upper GI
bleeding (5% of cases)
144
. MALLORY-WEISS SYNDROME
Treatment
-Treatment:
•Often, spontaneous cessation of haemorrhage
• Severe bleeding (10% of patients) => Requirement
of significant intervention (e.g. transfusion or
endoscopic haemostasis [by injection of Ethanol,
Polidocanol, or Epinephrine or by Electrocautery])
or therapeutic Embolisation into the left gastric
artery during angiography
145
GASTRO-OESOPHAGEAL REFLUX DISEASE (GOERD)
, Definition:
Definition: Reflux of the gastric contents into
the lower oesophagus
146
GASTRO-OESOPHAGEAL REFLUX DISEASE (GOERD)
Epidemiology + Risk Factors
'Epidemiology: '
Approximately 80% of pregnant women Presence of hiatal hernia in 70% of people with
GOERD
Risk factors: Smoking, alcohol, caffeine,
chocolate, pregnancy, obesity, hiatal hernia
147
'GASTRO-OESOPHAGEAL REFLUX DISEASE (GOERD)
Pathogenesis
Transient relaxation of lower oesophageal
sphincter => Reflux of acid and bile into the
distal oesophagus
148
GOERD , Histological findings:
'Histological findings:
Hyperaemia with congested vessels
Presence of eosinophils in the squamous
mucosa, followed by neutrophils; latter associated with more severe injury
Basal zone hyperplasia, exceeding 20% of the
total epithelial thickness
Elongation of lamina propria papillae, with
extension into the upper third of the
epithelium
149
GOERD
Clinical manifestations:
'Clinical manifestations:
Heartburn
Indigestion
Nocturnal cough, nocturnal asthma
Early satiety, abdominal fullness
150
GOERD Complications
Complications: Oesophagitis, strictures,
ulceration, haematemesis, intestinal metaplasia of oesophagus (Barrett Oesophagus)
151
GOERD Treatment
'Proton pump inhibitors or H2 . Histamine receptor antagonists
152
OESOPHAGEAL STRICTURE & STENOSIS
+Oesophageal Strictures
'Oesophageal narrowing (<13mm; normal: 30mm
diameter), causing dysphagia
.
Oesophageal Strictures: End stage result of
chronic reflux oesophagitis due to exposure to acid-
peptic content of stomach
153
OESOPHAGEAL STRICTURE & STENOSIS
Locus:
Squamo-columnar junction; Length: 1-4cm
154
'OESOPHAGEAL STRICTURE & STENOSIS
Progressive process:
Progressive process:
At the beginning, mucosal oedema and inflam-
matory cell infiltrates of lamina propria
Trans-mural progression of Chronic Oesophagitis
even into peri-oesophageal tissues => Subsequent
fibrosis and scarring => Luminal compromise
and oesophageal foreshortening
155
OESOPHAGEAL STRICTURE & STENOSIS
Predictors (risk factors) of stricture formation:
Elderly patients with GOERD that show:
Lower esophageal tone of less than 8mmHg Impaired oesophageal motility
Duodeno-Gastric Reflux
156
OESOPHAGEAL STRICTURE & STENOSIS
Diagnostic tests:
Diagnostic tests: Barium oesophagogram, endoscopy,
oesophageal manometry (measurement of LES tone),
24 hour pH monitoring
157
OESOPHAGEAL STRICTURE & STENOSIS
.. Management:
Management:
Stricture dilatation
Proton pump inhibitors
Surgery
158
PERFORATION/RUPTURE OF OESOPHAGUS
Synonym: Boerhaave Syndrome
Causes
Causes:
Endoscopy (75% of cases)
Retching, bulimia
159
PERFORATION/RUPTURE OF OESOPHAGUS
Complications:
Complications: Bacteria and acids => Mediastinum
=> Mediastinitis and sepsis => Multi-organ failure and death
160
PERFORATION/RUPTURE OF OESOPHAGUS
Clinical features
Clinical features: Chest pain, fever, subcutaneous
emphysema, pneumothorax
161
PERFORATION/RUPTURE OF OESOPHAGUS
Diagnosis
i. Oesophagogram with water soluble
contrast agent in supine position; ii. CT (extra-
luminal air or contrast, peri-oesophageal fluid, etc.)
162
EOSINOPHILIC OESOPHAGITIS
Association+ Clinical symptoms
Association with: Atopic Dermatitis, Allergic
Rhinitis, Asthma, peripheral eosinophilia
Clinical symptoms:
Food impaction and dysphagia (adults)
Feeding intolerance or GOERD-like symptoms
(children)
163
Microscopic findings: Numerous intraepithelial
eosinophils, at sites far from the GOE junction
EOSINOPHILIC OESOPHAGITIS
164
'EOSINOPHILIC OESOPHAGITIS
Treatment
'Treatment: Dietary restrictions (avoidance of
food allergens), topical or systemic corticosteroids
165
INFECTIOUS OESOPHAGITIS
+ causes
Debilitated or immunosuppressed individuals
Causes: Viruses (CMV, HSV), Fungi (C. albicans,
Mucormycosis, Aspergillus)
166
'Herpes Virus Oesophagitis (INFECTIOUS OESOPHAGITIS)
Clinical Features:
'Clinical Features: Difficult, painful swallowing
167
Macroscopy: Punched-out ulcers
Microscopy: Nuclear viral inclusions within
multinucleated squamous cells, at ulcer edge
Herpes Virus Oesophagitis:
, INFECTIOUS OESOPHAGITIS
168
' Macroscopy: Shallow ulcerations
Microscopy: Nuclear and cytoplasmic inclusions
within capillary endothelium and stromal cells
INFECTIOUS OESOPHAGITIS
Cytomegalovirus Oesophagitis:
169
Candida albicans Oesophagitis:
, Synonym + Causes
Synonym: Moniliasis
Causes: Antibiotic use, DM, malignant disease
170
Candida albicans Oesophagitis:
Clinical features
-'Clinical features: Painful, difficult swallowing
171
Macroscopy: Adherent, gray-white pseudo-
membranes (mucosal patches)
Microscopy: Densely matted fungal hyphae
and inflammatory cells over the oesophageal
mucosa
Candida albicans Oesophagitis:
172
BARRETT OESOPHAGUS
Complication of long-standing Gastro-
Oesophageal Reflux Disease (GOERD) that is
characterised by intestinal metaplasia within
the oesophageal squamous mucosa
Represents a pre-malignant condition
173
BARRETT OESOPHAGUS
. Epidemiology
Epidemiology: '
10% of individuals with symptomatic GOERD
White males; 40-60 years
Epithelial dysplasia (pre-invasive lesion) in
0.2% to 2.0% of individuals with Barrett
Oesophagus
174
BARRETT OESOPHAGUS
. Diagnosis:
i. Endoscopic evidence of abnormal
mucosa above GOES junction and ii. Histologically
documented intestinal metaplasia
175
Macroscopic features:
One or several tongues or patches of red, velvety
mucosa extending upward from the GOES junction
This metaplastic mucosa alternates with residual
smooth, pale squamous (oesophageal) mucosa and
interfaces with light-brown columnar (gastric)
mucosa distally
Microscopic findings:
Gastric type of columnar cells and small intestine
type of cells (Goblet cells) [defined as intestinal metaplasia]
'BARRETT OESOPHAGUS
176
Microscopic findings
Dysplasia: Low and High Grade
Cyto- and Histomorphological characteristics of
Dysplasia
Atypical mitoses
Nuclear hyperchromasia and stratification
Irregularly clumped chromatin
Increased Nuclear-to-Cytoplasmic (N:C) ratio
Failure of epithelial cells to maturate as they
migrate to the oesophageal surface
Abnormal gland architecture (budding, irregu-
lar shapes of gland and cellular crowding)
High-grade Dysplasia exhibits more severe
cytologic and architectural changes (e.g. gland- within-gland, or cribriform profiles)
Intramucosal Carcinoma is characterised by
invasion of neoplastic epithelial cells into the lamina propria
. BARRETT OESOPHAGUS
177
BARRETT OESOPHAGUS
Complications
Ulceration with stricture formation
Glandular Dysplasia =>Progression to distal
Adenocarcinoma
178
'Adenocarcinoma + risk factors
Typically arises in a background of Barrett
Oesophagus and long-standing GOERD
Risk factors: Documented dysplasia, tobacco
use, obesity, and prior radiation therapy
179
Adenocarcinoma Epidemiology + pathogenesis
Epidemiology: Most frequent in Caucasians;
M:F = 7:1
Pathogenesis: Progression of Barrett
Oesophagus to Adenocarcinoma occurs over
an extended period through the stepwise
acquisition of genetic and epigenetic changes
180
'Adenocarcinoma (:
Genetic changes:
Chromosome abnormalities and TP53 mutation
present at early stages of oesophageal Adeno-CA Amplification of c-ERB-B2, Cyclin-D1 and Cyclin
E genes
Mutation of the Rb tumour suppressor gene Allelic loss of the Cyclin dependent Kinase inhi-
bitor p16/INK4a or epigenetic silencing of
p16/INK4a by hypermethylation
Increased epithelial expression of Tumour
Necrosis Factor (TNF)- and Nuclear Factor
(NF)-κΒ-dependent genes
181
. Adenocarcinoma
Clinical features:
Clinical features:
Pain or difficulty in swallowing
Progressive weight loss
Haematemesis
Chest pain
Vomiting
182
Adenocarcinoma Prognosis
Prognosis:
Widespread tumours: 5-year survival <=> 25% Adenocarcinomas limited to the mucosa or
submucosa: 5-year survival <=> About 80%
183
Squamous Cell Carcinoma:
Epidemiology. + Risk factors
Epidemiology: Adults, >45 years; M:F = 4:1
. Risk factors: Alcohol, tobacco use, poverty,
caustic oesophageal injury, achalasia, Plummer- Vinson syndrome, consumption of very hot beverages
184
Squamous Cell Carcinoma
Genetic changes:
Loss of several tumour
suppressor genes, including p53 and p16/INK4a
185
Squamous Cell Carcinoma:
. Localisation
Localisation: Half of Squamous Cell Carcinomas
occur in the middle third of the oesophagus
186
Macroscopic features:
Early lesions: Small, gray-white, plaque-like
thickenings
Over months to years, development of tumour
masses that may be polypoid or exophytic with
protrusion and obstruction of the lumen
Other tumours are either ulcerated or diffusely
infiltrative lesions; the latter spread within the
oesophageal wall and cause thickening, rigidity,
and luminal narrowing as well as invasion of
surrounding structures (respiratory tree, aorta,
mediastinum or pericardium)
'Squamous Cell Carcinoma
187
Microscopic findings:
Most Squamous Cell Carcinomas are
moderately to well-differentiated
Less common histologic variants include:
-Verrucous Squamous Cell Carcinoma
-Spindle Cell Carcinoma
- Basaloid Squamous Cell Carcinoma
Squamous Cell Carcinoma
188
Squamous Cell Carcinoma :
Sites of lymph node metastases dependent
on tumour location; Cancers in:
Sites of lymph node metastases dependent
on tumour location; Cancers in:
Upper third of the oesophagus => Cervical
lymph nodes
Middle third of the oesophagus =>
Mediastinal, para-tracheal, and tracheo-
bronchial lymph nodes
Lower third of the oesophagus => Gastric
and coeliac lymph nodes
189
Squamous Cell Carcinoma):
Clinical features:
Clinical features: '
Insidious onset
Ultimately, development of dysphagia,
odynophagia and obstruction
Extreme weight loss and debilitation Haemorrhage and sepsis (in cases of tumour
ulceration)
190
Squamous Cell Carcinoma
Prognosis
5-year survival rates: 75% in individuals with
superficial Oesophageal Carcinoma
LN metastases: Association with poor prognosis Overall 5-year survival: Only 9%
