Pathology - oesophagus + mouth

Question 1

causes of esopagitis

When we discuss infectious esophagitis, three common pathogens come into play. these are:

Answer 1

Candida
HSV - Herpes Simplex Virus
CMB - Cytomegalovirus

Question 2

most commone form of infectious esophagitis + MANAGEMENT

Answer 2

Candida esophagitis

Antifungal therapy e.g. FLUCONAZOLE

Overgrowth occurs when local or systemic immunity is compromised
* in patients with HIV/AIDS,
* those on inhaled or systemic corticosteroids,
* or in individuals who have undergone chemotherapy.

Question 3

painful swallowing is called

Answer 3

odynophagia

Question 4

difficulty swallowing is called

Answer 4

dysphagia

Question 5

oral thrush - what is it

Answer 5

white plaques on the oral mucosa

Question 6

Herpes esophagitis is cause by a virus (HSV). yes?

Answer 6

yes

Question 7

endoscopic findings of herpes esophagitis

Answer 7

well-circumscribed “volcano-like” ulcers typically seen in the mid-to-distal esophagus.

Question 8

CMV - Cytomegalovirus

endoscopic findings of CMV esophagitis

Answer 8

Large, linear, and deep ulcerations typically located in the distal esophagus.

Question 9

compare the immune status of Candida, CMV, Herpes

Answer 9

While Candida esophagitis can occur in both mildly and severely immunocompromised individuals (and even in those using inhaled steroids), herpes and CMV esophagitis are more strongly associated with significant immunosuppression.

Question 10

describe and compare ulcer characteristics of Candida, CMV, Herpes

Answer 10

Candida: Presents with plaques rather than ulcers.

Herpes: Causes small, well-circumscribed ulcers.

CMV: Leads to larger, linear ulcerations.

Question 11

Risk factors for reflux oesophagitis

Answer 11

1. Increased intra-abdominal pressure i.e. pregnancy
2. Abnormal oesophageal motility “dysmotility”
3. Defective lower oesophageal sphincter +/- hiatus hernia

Question 12

management for eosinophilic oesophagitis

Answer 12

1. Drugs: PPI, steroids
2. Diet: avoidance of allergens
3. Dilatation of strictures/stenosis

Question 13

Barrett’s oesophagus
features

Answer 13

• Due to persistent reflux of acid or bile
• Metaplasia: transformation of one cell type into another
• Aims to be protective

Oesophageal **squamous epithelium transforms into columnar epithelium +/- goblet cells **(which secrete mucin) to try and protect against acid.

Alternatively, there is expansion of columnar epithelium from usual gastric glands up the oesophagus, or normal submucosal glands transform to try and recapitulate glands seen in the stomach/intestine.

Question 14

macrosocpic feature of eosinophilic oesophagitis

Answer 14

Increased eosinophils in squamous mucosa
+/-
Extreme basal zone hyperplasia
Eosinophilic micro-abscesses
Eosinophil degranulation
Surface desquamation
Lamina propria fibrosis

Question 15

squamous cell carcinoma is benign. True or false

Answer 15

false
it is MALIGNANT

Normal
severe dysplasia
carcinoma

Question 16

adenocarcinoma is a malignant tumour. True or false?

Answer 16

True

Question 17

Risk factors for oesophageal squamous cell carcinoma

Answer 17

Tobacco
Alcohol
Lower socioeconomic status
Radiation
Vitamin A/zinc deficiency
Hot foods – thermal injury
Pickled foods
HPV
Inflammation – oesophagitis
Genetic

Question 18

squamous papilloma is benign. true or false

Answer 18

true

associated with HPV. asymptomatic

Question 19

macroscopic features of oesophageal squamous cell carcinoma

Answer 19

Exophytic/polypoid/fungating lesion
Ulceration
Stenosis
Stricture

causing dysphagia

Question 20

describe th pathogenesis of oesophageal adenocarcinoma

Answer 20

Pathogenesis:
Genetic factors, reflux disease
Chronic reflux oesophagitis
Barrett’s oesophagus (metaplasia)
Low grade dysplasia
High grade dysplasia
Adenocarcinoma

Question 21

oesophageal adenocarcinoma
macroscopic features

Answer 21

Lower oesophagus
Often seen at advanced stage
Strictures
Polypoidal/fungating tumour
Ulceration
Diffuse infiltration

causes dysphagia - obstruction of the oesophageal lumen

Question 22

describe the 3 mechanisms of oesopageal cancer metastasis

Answer 22

Direct invasion: nearby organs e.g. trachea/bronchi/pericardium/chest wall/diaphragm
Lymphatic invasion
Vascular invasion - haematogenous metastasis

Question 23

clinical presentation of oesophageal cancer

Answer 23

Dysphagia
Persistent indigestion/heartburn
Vomiting/regurgitation of food
Loss of appetite
Weight loss
Epigastric/chest/back pain
Anaemia
Lethargy
Malaise

Question 24

name a common cause of acute upper GI bleeding

Answer 24

Mallory Weiss Tear

Tear in oesophagus with resulting haemorrhage
Longitudinal, superficial mucosal tear
Usually at gastro-oesophageal junction

Question 25

what can cause massive GI haemorrhage

Answer 25

rupture of oesophageal varices

Question 26

name 2 common infections of the mouth

Answer 26

HSV Candidiasis

Question 27

describe the oral cavity HSV

Answer 27

Children = gingivostomatitis Adults = pharyngitis Immunocompromised = chronic mucocutaneous infection Most orofacial infections are cause by HSV-1 Blisters/bullae filled with clear serous fluid Rupture to become painful, shallow ulcers After primary infection virus become latent in epithelial cells/ganglia Reactivation of latent HSV = recurrent herpes labialis (cold sores)/herpes gingivostomatitis

Question 28

commonest fungal infection in oral cavity

Answer 28

Candidiasis

Question 29

name 2 Pre-Malignant Lesions of the Oral Cavity

Answer 29

Leukoplakia - strong association with tomacco/alcohol use erythroplakia

Question 30

Leukoplakia description

Answer 30

Smooth, thin white coloured patch with well demarcated borders Biopsy showing severe dysplasia (squamous cell carcinoma in-situ)

Question 31

risk factors for H+N ssc

Answer 31

High-risk HPV Smoking Alcohol Chewing of betel quid & paan Pipe smoking & sun exposure – lower lip SCC

Question 32

head + neck SCC could be 2 things

Answer 32

”Classic” HPV-negative keratinising SCC HPV-associated SCC

Question 33

features of ketatinising SCC - common seen in - location - typically preceded by - common sites of local metastasis - distal metastasis sites - how it seems

Answer 33

Ventral tongue, floor of mouth, lower lip, soft palate, gingiva Tobacco, alcohol Typically preceded by pre-malignant lesions (dysplasia) Tend to invade locally before metastasizing Cervical lymph nodes are common sites of local metastasis Distant mets: mediastinal nodes, lungs, liver, bones Ulceration and induration of oral mucosa

Question 34

HPV associated SCC - location - typically preceded by - description of their growth

Answer 34

Associated with high-risk HPV infection Tonsil, base of tongue, soft palate, pharynx Tend to develop without a readily identifiable dysplastic component Bulky cervical lymphadenopathy Proliferation of nests and lobules of non-keratinising/basaloid cells growing within sheets of lymphocytes

Question 35

immunohistochemistry test for HPV- associaated SCC

Answer 35

p16 demonstrating positive staining of tumour cells – p16 can be used as a surrogate marker for HPV-associated tumours