Upper GI patho Flashcards

1
Q

epithelial tumours of salivary gland (acinar, myoepithelial, ductal cells)

A
  • salivary gland tumours
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2
Q

epithelial tumours of oral cavity and oesophagus
(squamous epithelium-lined
mucosa)

A
  • squamous papilloma
  • squamous cell carcinoma
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3
Q

epithelial tumour of stomach, small bowel, colon
and rectum (Glandular/ Columnar epithelium-lined mucosa)

A
  • adenoma
  • adenocarcinoma
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4
Q

epithelial tumours of anus (squamous epthelium-lined mucosa)

A
  • condyloma acuminatum
  • squamous cell carcinoma
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5
Q

what are ulcers

A
  • local defect of surface of an organ/ tissue caused by sloughing of inflamed necrotic tissue
  • erodes mucosa & muscularis mucosae (reaches SUBMUCOSA as well) -> vs erosion: usually only disrupts mucosa and not any further
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6
Q

causes of ulcers (3)

A
  • aphthous ulcers
  • oral candidiasis
  • HSV infection/ herpetic stomatitis
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7
Q

described aphthous ulcers (canker sores)

A
  • common, usually small, painful shallow ulcer
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8
Q

oral candidiasis presentation

A
  • adherent white, curd-like plaque
  • scrapped to reveal an underlying granular erythematous inflammatory
    base

**infective organism: Candida albicans

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9
Q

what is associated with oral candidiasis

A
  • immunodeficiency - eg AIDS
  • diabetes
  • glucocorticoid therapy
  • antibiotics, chemotherapy
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10
Q

HSV infection presentation

A
  • small vesicles/ blisters containing CLEAR fluid
  • most common on/ around lips
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11
Q

complications of HSV infection in immunocompromised

A
  • more severe, multiple vesicles in oral cavity
  • lymphadenopathy
  • viraemia
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12
Q

mucocutaneous disorders (2)

A
  • lichen planus
  • pemphigus vulgaris
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13
Q

lichen planus presentations

A
  • WICKHAM STRIAE -> lacy web like, white threads; commonly on inside of cheek
  • ulceration
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14
Q

lichen planus cause

A
  • likely autoimmune

*treat with steroids/ immunosuppressant

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15
Q

pemphigus vulgaris presentation

A
  • autoimmune disorder
  • blisters form on mucous membranes (eg mouth)

*treat with steroids, immunosuppressants

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16
Q

types of mucosal change (3)

A

leukoplakia (WHITE patch)
- Whitish, well-defined mucosal patch caused by epidermal thickening/
hyperkeratosis
- cannot be scraped off

erythroplakia (RED patch)
- Thin, friable atrophic mucosa with a red, granular gross appearance

speckled mucosa (red +
white)
- Combined leuko-erythroplakia mucosal changes

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17
Q

what is leukoplakia associated with

A
  • tobacco, chronic friction, alcohol abuse
  • older men
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18
Q

complications of leukoplakia

A
  • mostly benign
  • some transform into INVASIVE CARCINOMA
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19
Q

where is erythroplakia commonly found

A
  • thin squamous mucosal sites
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20
Q

complications of erythroplakia

A
  • epithelial dysplasia
  • carcinoma in situ
  • invasive squamous cell carcinoma
  • absence of keratin production, reduced epithelial cell number
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21
Q

tumours of oral cavity - surface squamous epithelium (2)

A
  • benign: squamous cell papilloma
  • malignant: squamous cell carcinoma
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22
Q

what is squamous cell papilloma associated with

A
  • HPV
  • papilloma on uvula, palate, tongue, gingiva, lower lips, buccal mucosa

*most common benign epithelial neoplasm

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23
Q

squamous cell papilloma morphology

A

macroscopic:
- cauliflower like lesions

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24
Q

what is the majority (95%) of oral cavity cancers

A

squamous cell carcinoma

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25
Q

what is oropharyngeal squamous cell carcinoma (SCC) associated with

A
  • smoking, alcohol, HPV (type 16)
  • men (90%)
  • floor of mouth, tongue, hard palate, base of tongue
26
Q

what decreases risk of SCC in oral cavity

A

fruit & veggie consumption

27
Q

features of SCC in oral cavity

A
  • masses containing NECROSIS, ULCERS, rolled borders
28
Q

diseases of salivary glands

A

Salivary gland neoplasm
- pleomorphic adenoma
- warthin tumour

29
Q

most common tumour of salivary glands

A
  • pleomorphic adenoma
30
Q

where is pleomorphic adenoma found

A
  • most common in PAROTID salivary glands
  • painless, slow-growing mass in front of and below
    the ear (parotid)

*pleomorphic adenomas are benign epithelial tumours

31
Q

2nd most common salivary gland tumour

A
  • warthin tumour
32
Q

what is warthin tumour associated with (3)

A
  • male
  • smoker
  • found in PAROTID GLAND
33
Q

congenital diseases of esophagus (2)

A
  • esophageal atresia, tracheo-esophageal fistula
  • diaphragmatic hernia
34
Q

esophageal atresia/ tracheo-esophageal fistula presentations & complications

A

presentation
- regurgitation during feeding

complications
- aspiration pneumonia, suffocation

*requires prompt surgical repair

35
Q

diaphragmatic hernia pathogenesis

A
  • incomplete formation of diaphragm allowing abdominal viscera to herniate into the thoracic cavity
  • more common on left side
  • can lead to PULMONARY HYPOPLASIA (severe)
36
Q

motility disorders of esophagus (3)

A
  • nutcracker esophagus
  • corkscrew esophagus (diffuse esophageal spasm)
  • achalasia
37
Q

motility disorders presentation

A
  • heartburn, dysphagia, frequent coughing/ choking
38
Q

nutcracker esophagus pathogenesis

A
  • High amplitude, uncoordinated contractions of inner circular and outer longitudinal smooth muscle
  • normal barium swallow, diagnosis by manometry
39
Q

corkscrew esophagus pathogenesis

A
  • Uncoordinated peristalsis with repetitive, simultaneous contractions (normal amplitude) of the distal oesophageal smooth muscle
40
Q

achalasia pathogenesis

A

TRIAD
- incomplete LES (lower esophageal sphincter) relaxation
- increased LES tone
- aperistalsis of esophagus

treatment
- balloon dilation, botox injection

41
Q

laceration injuries to esophagus (2)

A
  • mallory-weiss tears
  • boerhaave syndrome
42
Q

mallory-weiss tears pathogenesis

A
  • longitudinal superficial mucosal tears near the GEJ
  • often associated with severe retching/ vomiting secondary to acute alcohol intoxication
  • usually do not require surgical intervention
43
Q

mallory-weiss tears presentation

A
  • haematemesis (vomit blood)
44
Q

boerhaave syndrome pathogenesis

A
  • barogenic injury from sharp increase in intraluminal pressure -> transmural tearing and rupture of the distal oesophagus
  • cause severe mediastinitis
  • require surgery
45
Q

boerhaave syndrome presentation

A
  • severe chest pain
  • tachypnea
  • shock
46
Q

pathogenesis of esophageal varices

A
  • dilated vessels (usually submucosal), within lower esophagus & proximal stomach
  • due to PORTAL HYPERTENSION in liver cirrhosis -> form collateral channels at sites where portal & caval system communicate (eg esophagus) -> congestion & dilation
47
Q

complications of esophageal varices

A
  • variceal rupture -> haematemesis, maelena (upper GI bleeding)
48
Q

common symptoms of esophageal MUCOSAL injury (eg ulceration, tears, inflammation)

A
  • heartburn, chest pain, haematemesis
49
Q

types of inflammation in esophagus (5)

A
  • reflux esophagitis
  • chemical esophagitis -> alcohol, corrosive acid/alkali
  • infectious esophagitis -> HSV, CMV, candida
  • eosinophilic esophagitis -> eosinophil dominated
  • iatrogenic injury -> radiation, chemotherapy
50
Q

reflux esophagitis pathogenesis

A
  • most common cause of esophagitis
  • reflux of gastric contents into lower esophagus (transient LES relaxations)
51
Q

what is reflux esophagitis associated with

A
  • abrupt increase in abdominal pressure (cough, bending)
  • alcohol
  • obesity/ pregnancy
52
Q

complications of reflux esophagitis

A
  • chronic GORD
53
Q

presentation of reflux esophagitis

A
  • heartburn, dysphagia, postprandial regurgitation of sour-tasting gastric contents, sore throat/cough
54
Q

barrett esophagus pathogenesis

A
  • complication of chronic GORD
  • intestinal metaplasia within esophageal squamous mucosa
55
Q

what can barrett esophagus develop into

A
  • increase risk of dysplasia and ADENOCARCINOMA
56
Q

most common esophageal neoplasia

A
  • squamous cell carcinoma

*men > women

57
Q

presentations of esophageal SCC & adenocarcinoma(3)

A
  • mass -> dysphagia (difficulty swallowing), odynophagia (pain swallowing), obstruction
  • ulceration
  • systemic weight loss
58
Q

where is esophageal SCC usually found

A

upper 2/3 of esophagus

59
Q

how does esophageal SCC spread

A

Circumferential and longitudinal spread

Local invasion into adjacent structures:
- Respiratory tree (tracheo-oesophageal fistula) → aspiration pneumonia
- Aorta → catastrophic exsanguination
- Mediastinum → mediastinitis

Lymph node metastasis
- Upper third → cervical lymph nodes
- Middle third → mediastinal, paratracheal and tracheobronchial nodes
- Lower third → gastric and coeliac nodes

Distant metastasis

60
Q

what is esophageal adenocarcinoma associated with

A
  • long standing GORD
  • men > women
61
Q

where is esophagus adenocarcinoma found

A
  • lower 1/3 of esophagus
  • may invade adjacent gastric cardia