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Pathology 1 > GI 1 > Flashcards

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

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2
Q

CLEFT LIP AND PALATE
Genetic susceptibility:

A

Genetic susceptibility:
 Present in subsequent siblings (3%)

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3
Q

CLEFT LIP AND PALATE

Pathogenesis:

A

Pathogenesis:
 Failure of fusion of facial processes

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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)

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5
Q

CLEFT LIP AND PALATE

Complications + treatment

A

. Complications:
 Malocclusion
 Eustachian tube dysfunction
 Chronic Otitis Media
 Speech problems

Treatment: Surgical

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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)

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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

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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

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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?)

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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

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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

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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

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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.)

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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

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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

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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

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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

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18
Q

Odontogenic Keratocyst
Localisation

A

Odontogenic Keratocyst:
Localisation: Within the posterior mandible

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19
Q

Odontogenic Keratocyst Imaging studies

A

. Imaging studies: Well-defined uni-locular or
multi-locular radiolucencies

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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

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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

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22
Q

Peri-Apical (Radicular) Cyst:

A

‘ Inflammatory in origin
 Common lesion localised at
the apex of teeth

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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)

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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

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25
Q

Odontoma
Types

A

Types:
Complex: Composed of haphazardly arranged
dental hard and soft tissues
Compound: Composed of many small
“denticles” (toothlets)

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26
Q

Ameloblastoma + location

A

Epithelial tumour arising from precursor cells
of the enamel organ
Location: Mandible

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27
Q

Ameloblastoma
Imaging

A

. 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

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28
Q

Papilloma:

A

Most common benign epithelial tumour of the
oral mucosa
Common sites: Tongue, lips, gingivae, buccal
mucosa

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29
Q

Fibrous Epulis:

A

 Benign non-neoplastic growth of the gingivae
 Reparative growth rather than a true
neoplasm

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30
Q

Irritation Fibroma:

A

Occurrence in the buccal mucosa, along the
bite line or at the gingivo-dental margin

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31
Q

Microscopic findings:
Nodular mass of fibrous tissue
Few inflammatory cells
Covering by squamous mucosa

A

Irritation Fibroma:

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32
Q

Lobular Capillary Haemangioma
(Pyogenic Granuloma)
Epidemiology

A

Epidemiology
Children, young adults, pregnant women
(pregnancy tumour)

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33
Q

Macroscopic features:
Pedunculated masses with red purple colour
and ulceration of the surface

Microscopic findings:
Dense proliferation of
immature vessels (as in granulation tissue)

A

Lobular Capillary Haemangioma
(Pyogenic Granuloma)

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34
Q

Lobular Capillary Haemangioma
(Pyogenic Granuloma)

Progression

A

‘Progression: Either regression, particularly after
pregnancy or fibrous maturation and
development into a Peripheral Ossifying Fibroma

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35
Q

Peripheral Ossifying Fibroma:
+ epidemiology

A

-. Relatively common growth of the gingiva;
considered to be reactive rather than neoplastic
-Epidemiology: Peak incidence in young and
teenage females

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36
Q

Peripheral Ossifying Fibroma:

Pathogenesis:

A

Pathogenesis: Chronic irritation => Reactive
connective tissue hyperplasia

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37
Q

Peripheral Ossifying Fibroma:

Sites

A

Sites: Buccal mucosa along the bite line (trau-
matic fibroma)

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38
Q

 Macroscopic features: Red, ulcerated, and
nodular lesions of the gingiva

 Microscopic findings: Submucosal nodular fibrous
tissue mass with foci of mineralization

A

Peripheral Ossifying Fibroma:

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39
Q

Peripheral Giant Cell Granuloma:

A

-Relatively common lesion of the gingiva.
-Generally covered by intact gingival mucosa,
but it may be ulcerated

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40
Q

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

A

Peripheral Giant Cell Granuloma:

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41
Q

Aphthous Ulcers
Cause + epidemiology

A

Epidemiology: 40% of population
-Unknown aetiology
-Recurrent Aphthous Ulcers may be
-associated with coeliac disease and inflammatory bowel disease

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42
Q

Aphthous Ulcers:
+ Clinical features

A

Clinical features: Solitary or multiple,
painful, recurrent, erosive oral ulcerations with spontaneous healing after some (7-10) days

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43
Q

Macro-/Microscopic features:
Shallow and hyperaemic ulcerations
Covered by a thin exudate
Rimmed by a narrow zone of erythema

A

Aphthous Ulcers

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44
Q

Glossitis

A

-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

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45
Q

Glossitis
Plummer-Vinson or Paterson-Kelly syndrome:
Combination of:

A

Plummer-Vinson or Paterson-Kelly syndrome:
Combination of:
i. Iron-deficiency Anaemia
ii. Glossitis
iii. Oesophageal Dysphagia (usually related
to webs)

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46
Q

Glossitis characterised by

A

Glossitis characterised by ulcerative lesions
may be seen with jagged carious teeth and ill-
fitting dentures (traumatic cause)

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47
Q

HERPES SIMPLEX VIRUS INFECTIONS
Synonyms: Fever Blisters, “Cold Sores”

Cause

A

Cause: Herpes Simplex Virus (HSV), most often
type 1

Primary infections (2-4 years of age): Often
asymptomatic

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48
Q

HERPES SIMPLEX VIRUS INFECTIONS

Clinical features:

A

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

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49
Q

HERPES SIMPLEX VIRUS INFECTIONS
Recurrence after activation from:

A

Recurrence after activation from:
 A febrile illness  Allergies  UV light  Trauma
 Sunshine  Pregnancy and menstruation

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50
Q

HERPES SIMPLEX VIRUS INFECTIONS
Locations

A

Locations: Lips (Herpes labialis), nasal
orifices, buccal mucosa, gingiva, hard palate

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51
Q

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)

A

HERPES SIMPLEX VIRUS INFECTIONS

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52
Q

HERPES SIMPLEX VIRUS INFECTIONS
Progression:

A

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)

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53
Q

’ . Oral Candidiasis:
Synonym + cause + epidemiology

A

Synonym: Thrush, Moniliasis
Cause: C. albicans

Epidemiology: ‘Immuno-compromised individuals (e.g. HIV),diabetic patients, debilitated infants and children

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54
Q

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

A

Oral Candidiasis

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55
Q

, Viral Pharyngitis:

A

Viral Pharyngitis:
 Most common
 Cause: Adeno- or Rhinoviruses
 Common feature of Common Cold, Influenza,
Measles, Infectious Mononucleosis (Glandular Fever)

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56
Q

-Ulcerative Pharyngitis:

A

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

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57
Q

Streptococcal Pharyngitis:

A

In conjunction with Tonsillitis and Glossitis
(Scarlet Fever)
 Development of rash on skin and tongue
(initially white, and then strawberry coloured)

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58
Q

Streptococcal Pharyngitis Cause

A

Cause: Streptococcus pyogenes

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59
Q

Streptococcal Pharyngitis:

Complications:

A

Complications: Acute Proliferative Glomerulo-
nephritis, Rheumatic Fever and Henoch-
Schönlein purpura

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60
Q

TONSILLITIS + causes

A

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)

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61
Q

TONSILLITIS

Epidemiology

A

Epidemiology:
 Children between pre-school ages and the mid-
teenage years
 Tonsillitis occurs occasionally or recurs
frequently

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62
Q

-TONSILLITIS
 Diagnostic procedures:

A

Diagnostic procedures:

 Rapid strep test ([Quick strep]; results in
10 min.)
 Throat swab culture (results in 1 to 2 days)

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63
Q

TONSILLITIS
‘ Common Signs and Symptoms:

A

 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

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64
Q

Leukoplakia and Erythroplakia:

A

Leukoplakia and Erythroplakia:
 Leukoplakia: Clinical term describing white
mucosal patches that cannot be scraped off
 Erythroplakia: Red patches

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65
Q

. Leukoplakia and Erythroplakia:
Causes

A

Causes: Chronic irritation (e.g. dentures), tobacco
use, alcohol abuse, HPV

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66
Q

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

A

Leukoplakia and Erythroplakia:

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67
Q

Squamous Cell Carcinoma:
 Epidemiology:

A

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

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68
Q

Squamous Cell Carcinoma:
Risk factors

A

Risk factors: Oncogenic variants of HPV,
tobacco products, alcohol abuse, (actinic
radiation [sunlight] <=> Lower lip cancer)

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69
Q

Squamous Cell Carcinoma
-Localisation:

A

Localisation:
1. Lower lip (vermilion border) 2. Floor of mouth 3. Palate 4. Lateral border of tongue

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70
Q

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

A

Squamous Cell Carcinoma:

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71
Q

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

A

Squamous Cell Carcinoma

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72
Q

SIALADENITIS + causes

A

Definition: Inflammation of the salivary glands
Causes: Trauma, viral or bacterial infection,
auto-immune disease

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73
Q

 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

A

SIALADENITIS
Mumps:

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74
Q

SIALADENITIS Mumps:

Progression:

A

Children: Self-limited benign condition
Adults: Pancreatitis or Orchitis; latter can
cause infertility

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75
Q

SIALADENITIS: Mucocele
CAUSE

A

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

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76
Q

SIALADENITIS Epidemiology + localisation

A

 Epidemiology: Occurence in toddlers, young
adults and geriatric population as a result of trauma
 Localisation: Lower lip

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77
Q

SIALADENITIS Mucocele
Clinical features:

A

Clinical features:
Fluctuant swellings of the lower lip, with a
blue translucent hue

78
Q

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

A

SIALADENITIS
Mucocele:

79
Q

SIALADENITIS
Ranula: LOCALISATION

A

Mucocele that arises when the duct of the
sublingual gland has been damaged
 Localisation: Floor of the mouth

80
Q

SIALADENITIS
Ranula: CLINICAL FEATURES

A

. 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
Q

Sialolithiasis

A

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
Q

Non-specific bacterial Sialadenitis:

A

 Common condition secondary to Sialolithiasis
 Most often involvement of the major salivary glands, particularly the submandibular glands

83
Q

Non-specific bacterial Sialadenitis:

Causes:

A

Causes: Staphylococcus aureus and Streptococcus
viridans

84
Q

When staphylococcal or other pyogens are the
causative organisms => Overt suppurative
necrosis and abscess formation

A

SIALOLITHIASIS & NON-SPECIFIC BACTERIAL SIALADENITIS

85
Q

Clinical features:
SIALOLITHIASIS & NON-SPECIFIC BACTERIAL SIALADENITIS

A

Clinical features:
 Unilateral involvement of a single gland
 Affected gland: Painful, enlarged and
sometimes with a purulent ductal discharge

86
Q

SIALOLITHIASIS & NON-SPECIFIC BACTERIAL SIALADENITIS

Dehydration and decreased secretory function
may:

A

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
Q

Sjögren Syndrome:

Cause:

A

Cause: Autoimmune origin

88
Q

Sjögren Syndrome:
Diagnostic criteria for primary Sjögren Syn

A

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
Q

Pleomorphic Adenoma:
Synonym: Mixed tumour (myxoid, cartilage-
like components and epithelial cells) .
Epidemiology

A

Epidemiology:
Most common salivary gland tumour
Women, 20-40 years
Benign neoplasm that frequently recurs Increased risk after radiation exposure

90
Q

Pleomorphic Adenoma:

Localisation

A

Localisation: Parotid gland (90%); often
proximity to facial nerve

91
Q

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

A

‘Pleomorphic Adenoma:

92
Q

Pleomorphic Adenoma
Clinical features:

A

Clinical features:
Painless, slow-growing, mobile discrete mass

93
Q

Pleomorphic Adenoma
Microscopic picture:

A

Microscopic picture: Adenocarcinoma or
Undifferentiated Carcinoma with coexistence of Pleomorphic Adenoma traces

94
Q

Warthin Tumour:
Synonym: Papillary Cystadenoma
Lymphomatosum

A

Benign neoplasm that arises almost exclusively
in the parotid gland

95
Q

Warthin Tumour:
Epidemiology

A

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
Q

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

A

Warthin Tumour:

97
Q

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

A

Warthin Tumour

98
Q

Muco-Epidermoid Carcinoma:
+ epidemiology

A

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
Q

Muco-Epidermoid Carcinoma:

Genetics

A

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
Q

‘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

A

Muco-Epidermoid Carcinoma ‘

101
Q

-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

A

, Muco-Epidermoid Carcinoma ‘

102
Q

Muco-Epidermoid Carcinoma
Prognosis (depending on tumour’s grade):

A

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
Q

Adenoid Cystic Carcinoma:

Localisation

A

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
Q

Macroscopic features:
Small gray-pink lesions
Rarely circumscribed
Almost never encapsulated
Infiltrative growth

A

Adenoid Cystic Carcinoma:

105
Q

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

A

Adenoid Cystic Carcinoma

106
Q

Adenoid Cystic Carcinoma
Progression and Prognosis:

A

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
Q

Acinic Cell Carcinoma:
Epidemiology:

A

Epidemiology:
Uncommon malignant tumour; 2-3% of
salivary gland tumours
Young men

108
Q

Acinic Cell Carcinoma:
Localisation

A

Localisation:
Mostly in the parotids; the remainder arise
in the submandibular glands
Sometimes, bilateral or multi-centric (like
Warthin tumour)

109
Q

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

A

Acinic Cell Carcinoma

110
Q

Acinic Cell Carcinoma
Progression and Prognosis:

A

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
Q

TRACHEO-OESOPHAGEAL FISTULA
+ risk factors

A

Most common congenital anomaly
Risk factors: Advanced maternal age, smoking,
obesity

112
Q

TRACHEO-OESOPHAGEAL FISTULA
Clinical findings:

A

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
Q

TRACHEO-OESOPHAGEAL FISTULA
Three distinct variants:

A

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
Q

OESOPHAGEAL DIVERTICULA

A

Pouches lined by one or more layers of the
oesophageal wall

115
Q

OESOPHAGEAL DIVERTICULA
Types of Diverticula:

A

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
Q

‘OESOPHAGEAL DIVERTICULA
Locations

A

Locations:
 Above upper oesophageal sphincter (Zenker)
 Near midpoint of oesophagus
 Above lower oesophageal sphincter (epi-phrenic)

117
Q

ZENKER DIVERTICULUM

A

Synonym: Pharyngo-Oesophageal diverticulum
 “Pulsion” type
 Area of weakness of crico-pharyngeous muscle

118
Q

ZENKER DIVERTICULUM
Clinical findings + Treatment

A

, Clinical findings:
 Painful swallowing
 Food regurgitation
 Halitosis (due to entrapped food)
 Possible diverticulitis

Treatment: Surgery

119
Q

‘OESOPHAGEAL MUCOSAL WEBS
+ Pathogenesis

A

. Uncommon ledge-like protrusions of mucosa that
may cause obstruction

Pathogenesis: Unknown

120
Q

OESOPHAGEAL MUCOSAL WEBS
Epidemiology

A

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
Q

OESOPHAGEAL MUCOSAL WEBS
Localisation + Clinical features

A

Localisation: Most common in the upper oesophagus
Clinical features: Dysphagia associated with
incompletely chewed food

122
Q

Macroscopic features:
 Semi-circumferential, eccentric lesions
 Protrusion of less than 5mm
 Thickness of 2-4mm

Microscopic findings:
 Fibro-vascular connective tissue and
 Overlying epithelium

A

OESOPHAGEAL MUCOSAL WEBS

123
Q

OESOPHAGEAL RINGS
( Schatzki Rings )

A
  • Similar to webs, but circumferential and thicker
  • Rings include mucosa, submucosa, and in some
    cases, hypertrophic muscularis propria
124
Q

OESOPHAGEAL RINGS
Types

A

 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
Q

ACHALASIA

A

Increased tone of the lower oesophageal sphincter,
as a result of impaired smooth muscle relaxation

126
Q

ACHALASIA
Characterised by the triad of:

A
  1. Incomplete LES relaxation
  2. Increased LES tone
  3. Aperistalsis of the oesophagus
127
Q

Primary Achalasia:

A

 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
Q

‘Secondary Achalasia:

A

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
Q

Achalasia-like disease may be caused by:

A

 Diabetic Autonomic Neuropathy
 Infiltrative disorders (e.g. Malignancy, Amyloidosis, or Sarcoidosis)
 Lesions of dorsal motor nuclei (e.g. polio or
surgical ablation)

130
Q

ACHALASIA
Epidemiology + Clinical features:

A

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
Q

ACHALASIA
Diagnosis

A

Diagnosis:
 Dilated aperistaltic oesophagus with a beak-like
tapering at distal end (barium enema)
 Detectable aperistalsis (oesophageal manometry)

132
Q

‘ACHALASIA
. Treatment

A

Treatment:
Non-pharmacologic:
Pneumatic balloon dilatation
Oesophago-myotomy

Pharmacologic:
Long-acting nitrates
Calcium channel blockers
Injection of Botulinum neurotoxin (Botox)

133
Q

HIATAL HERNIA
Epidemiology:

A

 Women > Men
 Association with: i. Sigmoid Diverticulosis (25%),
ii. Oesophagitis (25%), iii. Duodenal Ulcers (20%), iv. Gallstones (18%)

134
Q

Para-Oesophageal (Rolling) Hernia:

A

 Gastro-Oesophageal junction at diaphragm’s level  Part of stomach bulges into the thoracic cavity

135
Q

Pleuro-Peritoneal Diaphragmatic (Bochdalek)
Hernia:

A

-70% of cases, in newborns
-Loops of bowel in the left pleural cavity, through
the postero-lateral part of diaphragm on the left

136
Q

(Hiatal hernia) Sliding Hernia:

A

.  Most common type (99% of cases)
 Herniation of proximal stomach into thoracic
cavity through the diaphragmatic Oesophageal hiatus

137
Q

Sliding Hernia
Clinical findings:

A

-Heartburn
-Nocturnal epigastric distress from acid reflux -Haematemesis
-Ulceration
-Stricture

138
Q

OESOPHAGEAL ATRESIA

A

‘Incomplete formation of the Oesophagus, frequently
associated with Tracheo-Oesophageal Fistula

139
Q

OESOPHAGEAL ATRESIA
Epidemiology:

A

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
Q

OESOPHAGEAL ATRESIA
. Diagnosis

A

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
Q

‘OESOPHAGEAL ATRESIA
Treatment

A

‘Treatment:
 Extra-pleural surgical repair
 Occasionally, interposing of a segment of colon
between the oesophageal segments

142
Q

MALLORY-WEISS SYNDROME
+ cause

A

‘Definition: Mucosal tear in the proximal stomach
and distal oesophagus
Cause: Severe retching, associated with alcoholism
or bulimia

143
Q

MALLORY-WEISS SYNDROME
Clinical feature:

A

. Clinical features: Haematemesis, upper GI
bleeding (5% of cases)

144
Q

. MALLORY-WEISS SYNDROME
Treatment

A

-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
Q

GASTRO-OESOPHAGEAL REFLUX DISEASE (GOERD)
, Definition:

A

Definition: Reflux of the gastric contents into
the lower oesophagus

146
Q

GASTRO-OESOPHAGEAL REFLUX DISEASE (GOERD)
Epidemiology + Risk Factors

A

‘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
Q

‘GASTRO-OESOPHAGEAL REFLUX DISEASE (GOERD)
Pathogenesis

A

 Transient relaxation of lower oesophageal
sphincter => Reflux of acid and bile into the
distal oesophagus

148
Q

GOERD , Histological findings:

A

‘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
Q

GOERD
Clinical manifestations:

A

‘Clinical manifestations:
 Heartburn
 Indigestion
 Nocturnal cough, nocturnal asthma
 Early satiety, abdominal fullness

150
Q

GOERD Complications

A

Complications: Oesophagitis, strictures,
ulceration, haematemesis, intestinal metaplasia of oesophagus (Barrett Oesophagus)

151
Q

GOERD Treatment

A

‘Proton pump inhibitors or H2 . Histamine receptor antagonists

152
Q

OESOPHAGEAL STRICTURE & STENOSIS
+Oesophageal Strictures

A

‘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
Q

OESOPHAGEAL STRICTURE & STENOSIS
Locus:

A

Squamo-columnar junction; Length: 1-4cm

154
Q

‘OESOPHAGEAL STRICTURE & STENOSIS
Progressive process:

A

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
Q

OESOPHAGEAL STRICTURE & STENOSIS
Predictors (risk factors) of stricture formation:

A

Elderly patients with GOERD that show:
Lower esophageal tone of less than 8mmHg Impaired oesophageal motility
Duodeno-Gastric Reflux

156
Q

OESOPHAGEAL STRICTURE & STENOSIS
Diagnostic tests:

A

Diagnostic tests: Barium oesophagogram, endoscopy,
oesophageal manometry (measurement of LES tone),
24 hour pH monitoring

157
Q

OESOPHAGEAL STRICTURE & STENOSIS
.. Management:

A

Management:
 Stricture dilatation
 Proton pump inhibitors
 Surgery

158
Q

PERFORATION/RUPTURE OF OESOPHAGUS
Synonym: Boerhaave Syndrome

Causes

A

Causes:
 Endoscopy (75% of cases)
 Retching, bulimia

159
Q

PERFORATION/RUPTURE OF OESOPHAGUS

Complications:

A

Complications: Bacteria and acids => Mediastinum
=> Mediastinitis and sepsis => Multi-organ failure and death

160
Q

PERFORATION/RUPTURE OF OESOPHAGUS

Clinical features

A

Clinical features: Chest pain, fever, subcutaneous
emphysema, pneumothorax

161
Q

PERFORATION/RUPTURE OF OESOPHAGUS
Diagnosis

A

i. Oesophagogram with water soluble
contrast agent in supine position; ii. CT (extra-
luminal air or contrast, peri-oesophageal fluid, etc.)

162
Q

EOSINOPHILIC OESOPHAGITIS

Association+ Clinical symptoms

A

Association with: Atopic Dermatitis, Allergic
Rhinitis, Asthma, peripheral eosinophilia

Clinical symptoms:
 Food impaction and dysphagia (adults)
 Feeding intolerance or GOERD-like symptoms
(children)

163
Q

Microscopic findings: Numerous intraepithelial
eosinophils, at sites far from the GOE junction

A

EOSINOPHILIC OESOPHAGITIS

164
Q

‘EOSINOPHILIC OESOPHAGITIS
Treatment

A

‘Treatment: Dietary restrictions (avoidance of
food allergens), topical or systemic corticosteroids

165
Q

INFECTIOUS OESOPHAGITIS
+ causes

A

 Debilitated or immunosuppressed individuals
 Causes: Viruses (CMV, HSV), Fungi (C. albicans,
Mucormycosis, Aspergillus)

166
Q

‘Herpes Virus Oesophagitis (INFECTIOUS OESOPHAGITIS)

Clinical Features:

A

‘Clinical Features: Difficult, painful swallowing

167
Q

Macroscopy: Punched-out ulcers

Microscopy: Nuclear viral inclusions within
multinucleated squamous cells, at ulcer edge

A

Herpes Virus Oesophagitis:
, INFECTIOUS OESOPHAGITIS

168
Q

‘ Macroscopy: Shallow ulcerations
 Microscopy: Nuclear and cytoplasmic inclusions
within capillary endothelium and stromal cells

A

INFECTIOUS OESOPHAGITIS
Cytomegalovirus Oesophagitis:

169
Q

Candida albicans Oesophagitis:
, Synonym + Causes

A

Synonym: Moniliasis
Causes: Antibiotic use, DM, malignant disease

170
Q

Candida albicans Oesophagitis:
Clinical features

A

-‘Clinical features: Painful, difficult swallowing

171
Q

 Macroscopy: Adherent, gray-white pseudo-
membranes (mucosal patches)

 Microscopy: Densely matted fungal hyphae
and inflammatory cells over the oesophageal
mucosa

A

Candida albicans Oesophagitis:

172
Q

BARRETT OESOPHAGUS

A

 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
Q

BARRETT OESOPHAGUS
. Epidemiology

A

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
Q

BARRETT OESOPHAGUS
. Diagnosis:

A

i. Endoscopic evidence of abnormal
mucosa above GOES junction and ii. Histologically
documented intestinal metaplasia

175
Q

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]

A

‘BARRETT OESOPHAGUS

176
Q

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

A

. BARRETT OESOPHAGUS

177
Q

BARRETT OESOPHAGUS
Complications

A

Ulceration with stricture formation
 Glandular Dysplasia =>Progression to distal
Adenocarcinoma

178
Q

‘Adenocarcinoma + risk factors

A

Typically arises in a background of Barrett
Oesophagus and long-standing GOERD

Risk factors: Documented dysplasia, tobacco
use, obesity, and prior radiation therapy

179
Q

Adenocarcinoma Epidemiology + pathogenesis

A

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
Q

‘Adenocarcinoma (:
Genetic changes:

A

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
Q

. Adenocarcinoma
Clinical features:

A

Clinical features:
Pain or difficulty in swallowing
Progressive weight loss
Haematemesis
Chest pain
Vomiting

182
Q

Adenocarcinoma Prognosis

A

Prognosis:
Widespread tumours: 5-year survival <=> 25% Adenocarcinomas limited to the mucosa or
submucosa: 5-year survival <=> About 80%

183
Q

Squamous Cell Carcinoma:
Epidemiology. + Risk factors

A

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
Q

Squamous Cell Carcinoma
Genetic changes:

A

Loss of several tumour
suppressor genes, including p53 and p16/INK4a

185
Q

Squamous Cell Carcinoma:
. Localisation

A

Localisation: Half of Squamous Cell Carcinomas
occur in the middle third of the oesophagus

186
Q

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)

A

‘Squamous Cell Carcinoma

187
Q

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

A

Squamous Cell Carcinoma

188
Q

Squamous Cell Carcinoma :
Sites of lymph node metastases dependent
on tumour location; Cancers in:

A

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
Q

Squamous Cell Carcinoma):
Clinical features:

A

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
Q

Squamous Cell Carcinoma
Prognosis

A

5-year survival rates: 75% in individuals with
superficial Oesophageal Carcinoma
LN metastases: Association with poor prognosis Overall 5-year survival: Only 9%

Pathology 1 (4 decks)

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