GIT 1 Ros' notes

Question 1

What is Xerostomia?

Answer 1

Dry mouth!
Aetiology- lack of salivary secretions (certain drugs including anti-cholinergics) or salivary gland pathology including radiation, autoimmune- Sjorgren syndrome (accompanied by dry eyes and lacrimal gland involvement). Complications include dental caries and candidas, difficulty swallowing and speaking.

Question 2

What are the tumours you can get with Salivary Gland Neoplasms?

Answer 2

Parotid > submandibular > minor + sublingual salivary glands.

MALIGNANT tumours are MORE COMMON in SUBLINGUAL + minor salivary glands > submandibular > parotid.

Question 3

Name some Benign Salivary Gland Tumours

Answer 3

• Pleomorphic adenoma or mixed tumours (50% of all salivary gland tumour)
• Warthin Tumour

Question 4

Describe Pleomorphic adenoma or mixed tumours

Answer 4

50% of all salivary gland tumours.
They are the most common salivary gland tumour. 60% of parotid tumours are pleomorphic adenomas, mixture of ductal (epithelial) and myoepithelial- both epithelial and mesenchymal differentiation.

Ax- Unknown but radiation increases risk.

Macro- round, encapsulated (mostly) demarcated, grey/white/chrondroid cut surface

Micro: heterogenous- epithelial elements ducts/acini/tumours/strands/sheets of cells, loos myxoid tissue, islands of chondroids, foci of bone.

Clinical: 50-70s, slow growing, mobile, painless massess.
Surgery - enucleation of tumour.

CARCINOMA can arise in tumours ie in 2% of tumours present for 15 y and when they occur they can be aggressive

Question 5

Describe the pathology of Warthin Tumour

Answer 5

5-10% of salivary gland tumours

• papillary cystadenoma lymphomatosum

second most common salivary gland benign tumour.

Macro- encapsulated, pale grey with mucous/serous fluid filled clefts.

Micro: Spaces lined with double layer of epithelium resting on a lymphoid stroma, sometimes with germinal centres.

Clinically- usually parotid, M>F, 50s-70s. SMOKERS

Question 6

What are some Malignant Salivary Gland Tumours?

Answer 6

Mucoepithelioid carcinoma (15% of all salivary gland tumours)

Adenocarcinomas (10%)

Acinic Cell Carcinoma (5%)

Adenoid Cystic Carcinoma (5%)

Malignant mixed tumour (3-5%)

Question 7

What is the pathology of Mucoepidermoid Carcinoma?

Answer 7

15% of all salivary gland tumours.
Most common malignant tumour of salivary gland. Mainly in parotids but also in minor salivary glands.

Macro; well circumscribed but lack well defined capsule, gray/white, small mucous containing cysts.

Micro: low, intermediate, high grade. Cords, sheets, cystic, squamous, mucous, intermediate cells.

Clinical: prognosis depends on grade!
Low Grade: 15% may be locally invasive and rarely metastasie: 90% 5 year survival rate
High Grade: recur 25-30% metastasis - 50% 5 year survival rate.

Question 8

What about Adenoid Cystic Carcinoma

Answer 8

5% of malignant tumours- uncommon but troublesome with recurrence following excision. May disseminated widely.
50% cases in minor salivary gland
Slow growing and metastasis

Macro: small poorly encapsulated

Micro: small cells, dark compact nuclei, tubular, solid or cribriform.

Question 9

What are Odonotgenic Cysts? what is the classification?

Answer 9

Epithelial lined cysts common in the jaw bones. Derived from the epithelium from which teeth form. Classification based upon whether developmental or inflammatory

DEVELOPMENTAL
Dentigerous cyst: from the crown of the unerupted tooth. Associate diwht impacted wisdom teeth. Cyst will be lined with stratified squamous epithelium

Odontogenic keratocyst: locally agressive, 10-40yo M>F, posterior mandible.

INFLAMMATORY
-Periapical cyst: inflammatory in origin, common lesions in apex of teeth, develop as a result of long standing pulpitis (advanced caries)

Question 10

What is a leukoplakia?

Answer 10

A white patch or plaque that cannot be scraped off and cannot be given a specific diagnosis (ie. not candidas etc).

3% of world population
5-25% are pre-malignant and need histologic evaluation.

Ax: multifocal, tobacco mainly

Macro: varied appearance, multiple or solitary, fissured thickened, smooth/corrugated

Micro: hyperkeratosis/markedly dysplastic/carcinoma in situ

Question 11

What is an Erythroplakia

Answer 11

Red velvety sometimes eroded into oral cavity. Mucossa is markedly atypical, higher risk of malignant transformation

Clinically: both leukoplakia and erythroplakia seen in adults (40-70, 2M:1F), Lesions can occur anywhere in oral cavity, often buccal mucosa, floor of mouth, ventral surface of tongue, palate, gingiva.

Question 12

What is a hairy leukoplakia

Answer 12

Oral lesion seen in IMMUNOCOMPROMISED PATIENTS (80% of patients with HIV+)

Macro: White, confluent patches of fluffy (hairy) hyperkeratotic thickenings, almost always on the lateral border of the tongue.
Symtoms of AIDS follow in 2-3 years.

Micro: hyperparakeratosis, acanthosis with balloon cells in upper spinour layer. Cells contain Epstein Barr Virus (EBV)

Question 13

Squamous Cell Carcinoma

Answer 13

95% of the cancers of the head and neck are squamous cell carcinomas (HNSCC)

Ax: In the oral cavity: The S’s (Smoking, Spirits, Sepsis (act as promotors), Sunlight for the lower lip, HPV (HPV vvaccine), ‘betel nut’ (india and Asia), family hx.

Macro: Variable appearance, may be multiple tumours, increased risk of developing new lesions (field cancerisation) 3-7% per year, be wary, may not arise anywhere in oral cavity, floor of mouth, ventral surface of tongue, lower lip, soft palate, gingiva are favoured locations. May have evidence of premalignant lesion. Local invasion, mastastasis to cervical, mediastinal, LN, Lungs, liver, bone.

clinical: oral lesion- may be multiple and have evidence of premalignant lesion.

Tratment: surgery, radiation, chemo, 5 yr survival rate is 80-90%, late stage 19%.
Poor long term survival, need to diagnose early and monitor for subsequent tumous.

Question 14

Describe a differential diagnosis for Lump in the necl!

Answer 14

can arise from: skin, subcutaneous fat, lymph nodes (check lymphatic drainage area for infection/malignancy) and organs in that region.

Congenital:

• Branchial cyst: anterolateral neck, remnant branchial arches, 2-5 cm lind by stratified squamous epithelium or pseudostratified columnar often lymphocytic infiltrate
• Thyroglossal tract cyst: anterior neck, can have thyroid tissue involvement

Acquired:

• Lymphadenopathy
• Thyroid: enlargement/tumour
• Salivary gland: enlargement/tmour
• Zenker diverticulum
• Paraganglioma - carotid body tumour- tumour of neuroendocrine cells associated with ANS.

Question 15

What is an oesophageal mucosal web

Answer 15

semi-circumferential fibrovascular CT Protruding into (most commonly) the upper oesophagus lumen. Clinically: uncommon

Females >40 yo, dysphagia, not pain.
If upper oesophageal weba are accompanied by iron deficient anaemia, glossitis, cheiloisis- Patterson-Brown- Kelly or Plummer-Vinson Syndrome

Question 16

Oesophageal Ridges

Answer 16

(Schatzki rings)

Similar to webs but are circumferential and thicker

Question 17

Oesophageal stenosis

Answer 17

Occasionally congenital

Severe GORD, Radiation, caustic injury, schleroderma

Question 18

Explain MOTOR DYSFUNCTION 1 degree

Answer 18

Achalasia (failure to relax): has 3 characteristics:

1. ) Oesophageal Aperistalsis
2. ) Partial/incomplete lower oesophageal sphincter (LOS) relaxation
3. ) Increase rest tone LOS

1 degree motor dysfunction has unknown cause. Usually young adults. Progressive dysphagia.

Complications: Oesophageal SCC

Question 19

Explain MOTOR DYSFUNCTION 2 degrees

Answer 19

Rarer causes- to CHAGAS disease (Trypanosoma cruzi), polio, diabetic autonomic neuropathy, amyloid, sarcoid.

Question 20

What is a hiatus hernia? What are the two types?

Answer 20

Separation of the diaphragmatic crura and widening of the space betwene the cura and the oesophageal wall.

TWO TYPES:

1. Sliding: 95% oesophagus and stomach moves up
2. Paraoesophageal: a portion of the stomach moves up along side the oesophagus.

Question 21

What is a mallory-weiss tear?

Answer 21

Longitudinal tears in the oesophagus at the oesophago-gastric junction or gastric cardia.

Ax: Severe/prolonged retching/vomiting often associated with alcohol intoxication.

5-10% upper GIT bleeds (can be profuse) .

Question 22

Boerhaave Syndrome

Answer 22

Rare rupture of the oesophagus, results in mediastinitis, high mortality.

Question 23

What are oesophageal varices?

Answer 23

Collateral bypass channels (veins) where the portal and caval circulation meet.

Ax: Portal hypertension: Cx 90% of cirrhotic patients most often associated with alcoholic cirrhosis- cause of death 50% of these patients (note Schistosomiasis Ax of varices also)

Macro: Tortuous, dilated veins with submucosa of the distal oesophagus.

Micro: May see dilated veins beneath mucosa. Associated with mucosal inflammations.

No symptoms untill RUPTURE/haematemesis. High mortality

Question 24

Oesophagitis

Answer 24

Inflammation of oesopahgeal mucosa

GORD common; other: toxic, hot beverages, heavy smoking etc etc.

Question 25

GORD

Answer 25

Oesophagitis is secondary to reflux of gastric contents into lower oesophagus

Ax: impaired lower oesophageal sphincter tone or increased abdominal pressure: sliding hiatal hernia, slowed oesophageal clearance of reflux material, delayed gastric emptying, obesity, smoking, pregnancy. Poor healing secondary to ongoing exposure to acid

Macro: Hyperemia (redness)
Micro: Inflammatory cells: eosinophils, neutrophils, lymphocytes in mucosal epithelium.
Basal zone hyperplasia. Elongation of lamina propria papillae, capillary congestion.

Clinically: 40+ yo, occasionally also infants/children. Dysphagia, heartburn, regurgitated acid.

Complications: Bleeding, ulceration, stricture, Barretts oesophagus.

Question 26

Barrets Oesophagus

Answer 26

Distal squamous epithelium are replaced by metaplastic columnar epithelium and goblet cells (intestinal metaplasia) as a response to prolonged injury.

Ax: Up to 10% of patients with long standing symptomatic GORD (risk factors for GORD) likely result of altered differentiation of mucosal stem cells.

Macro: tongues, patches or circumferential red, velvety mucosa extending upward from the gastro-oesophageal junction, between smooth pale pink and lush light brown gastric mucosa distally

Micro: Squamous epithelium replaced with metaplastic columnar epithelium containing intestinal goblet cells. DYSPLASIA: Recognised by cytological and architectural abnormalities in columnar epithelium; enlarged crowded and stratified hyperchromatic nuclei, crowded glands with lack of intervening stroma. Low (basal nuclei) or high grade (high stratified nnuclei)

Barrett’s oesophagus is a pre-malignant condition, most individuals do not develop ADENOCARCINOMA but have a greatly increased risk and therefore must be monitored.

Clinically: 40-60yo, M>F, increased risk of oesophageal adenocarcinoma with >3cm Barrett Mucosa

Diagnosis requires:
1. Endoscopic evidence of columnar epithelium above G-O junction. 2. Histological evidence of ‘intestinal metaplasia’ (goblet cells) in columnar epithelial biopsies. Long >3cm or short <3cm segment.

Question 27

Describe some benign oesopahgeal tumours

Answer 27

BENIGN: mesenchymal in origin, within oesophageal wall
- Leiomyoma (smooth muscle)
- Lipoma (adipose)
- Haemangioma
- Neurofibroma
etc etc

Question 28

Describe some malignant Oesopahgeal Tumours

Answer 28

Cx asymptomatic until Late DYSPHAGIA

90% of oesophageal cancer world wide is SQUAMOUS CELL CARCINOMA but adenocarcinoma is increasing.

Question 29

Adenocarcinoma

Answer 29

NB: Malignant tumour arising from epithelial lining of glands or ducts.

Ax: Majority arise from Barrett Mucosa

Risk Factors: Smoking, obesity, tobacco, diet poor in fresh frut and veges. Some serotypes of H.pylori are associated with a reduced risk of adenocarcinoma, potentially by causing gastric atrophy and therefore reducing acid reflux.

Macro: Distal third of the oesophagus ; flat /raised patches early to large nodular masses or deeply infiltrative/ulcerative in distal oesopahgus

Micro: mucin producing glandular tumours exhibiting intestinal-type features. Multiple foci of dysplastic mucosa are frequently adjacent to the tumour

Clinically: 40 + yo, M>F. Dysphagia, weight loss, haematemesis, chest pain. Poor prognosis if advanced. If limited to the mucosa and submucosa- 80% 5 yr survival.

Question 30

Squamous Cell Carcinoma of Oesophagus

Answer 30

Ax: SMOKING + Alcohol, HPV. Diet: Carcinogens, vitamin deficiencies, fungus contaminated foods, frequent very hot drinks; previous mediastinal radiation, poverty, achalasia

Macro: 20% upper (metastasis to vervical lymph node) , 50% middle (metastases to mediastinal, paratracheal, tracheobronchial LN), 30% lower thirds of oesophagus (met. to gastric and coeliac LN). Early small plaque through to protruded (60%) polypoid exophytic lesion or flat (15%), diffuse infiltrateive forma nd necrotic ulcerated, excavates into surrounding structures (25%)

Micro: Evidence of carcinoma in situ /over malignancy, lymphatic network in submucosa promotes spread

Clinically: 50+, M>F, dysphagia, weight loss, change of diet to semi solid, liquid.
75% 5 year survival with superficial oesophageal carcinoma

Question 31

What initiates acid secretion?

Answer 31

Vagal stimulation (cholinergic) and gastrin (G cells in the antral/pyloric regions) stimulate ECL HISTAMINE release that stimulates parietal cell proton pump

Question 32

What inhibits acid secretion?

Answer 32

On parietal cells include somatostatin (released from D cells, also reduces ECL histamine release), (octreotide: somatostatin agonist (mimic) greatly reduces acid), prostaglandins E series (NSAIDs, aspirin inhibit), epidermal growth factor.

Question 33

What protects the mucosa?

Answer 33

Mucous, bicarbonate, epithelial barrier-tight junction, mucosal blood flow, prostaglandin synthesis by the mucosal cells (reducing parietal acid secretion and promoting mucous secretion)

Question 34

What is congenital hypertrophic pyloric stenosis?

Answer 34

3M, 1f
1/300-900 births

Ax: Multifactorial- familial, associated with turners syndrome (XO) and trisomy 18.

Clinically:regurgitation, persistant projectile vomiting, presenting in the 2-3 weeks of life, visible peristalsis (wont have bil)

Treatment: Surgical splitting

• adults can aquire pyloric stenosis or gastric outlet obstruction secondary to peptic ulcer close the pyloris, carcinoma, lymphoma, carcinoma of the pancreas

Question 35

Acute Gastritis

Answer 35

Transient inflammation of the gastric mucosa

Ax: Loss of mucosal protection- NSAID, excessive alcohol, chemical ingestion, chemo, systemic infection, severe stress (trauma, burns, surgery), ischaemia and shock

Macro: Oesema and vascular congestion through to erosiions and haemorrhage predominantly neutrophils (especially if intraepithelial) +- haemorrhage. Mucosal erosions (loss of superficial epithelium, no breach in muscularis mucosae) may also occur.

clinically: Asymptomatic or variable pain, nausea, omiting, to server ulceration, haemorrhage, haemetemesis and malaena.

Question 36

Chronic Gastritis- H.pylori infection

Answer 36

H. pylori: flagella, gram negative. Urease produces ammonia from endogenous urea and elevates local gastric pH
Increases acid secretion

Bacteria lives in superficial mucous layer among microvili. Oral Faecal; oral-oral spread.

Macro: Antral+- body/fundic erythema. Predominantly antral gastritis with high acid production (H.pylori present in 90% of cases of patients with antral gastritis).

Micro: Inflammatory infiltrate: lymphocytes, plasma cells, with or without ‘active inflammation’ neutrophils in glandular and surface epithelium.
Regenerative change is seen, with metaplasia- metaplastic columnar absorptive cells and goblet cells of intestinal morphology. Atrophy (loss of glandular structures); and dysplasia (cytologic features variation size, shape, orientation of epithelial cells, nuclear enlargement and atypia severe carcinoma in situ.

Question 37

Autoimmune Gastritis

Answer 37

<10% cases of chronic gastritis. Typically in body of stomach. Characterised by

1. Autoantibodies against parietal cell proton pump, intrinsic factor (therefore a lack of B12 absorption- only B12 deficiency related anaemia in this setting is known as pernicious anaemia).
2. Reduced pepsinogen 1 concentration - secondary to chief cell destruction
3. Antral endocrine hyperplasia
4. Defective gastric acid secretion - achlorhydria.

Autoimmune gastritis is associated with other autoimmune diseases- associated with an increased risk of gastric carcinoma and carcinoid tumour.

Macro: diffuse mucosal ivolvement, may become flattened.
Micro: atrophy: marked loss of glandular structures.

Clinically: chronic gastritis: symptoms of nausea, upper abdo discomfort, sometimes with vomiting. Pain less severe but more persistant than acute gastric ulceration.
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Question 38

Peptic Ulcer Disease

Answer 38

Ulcer = a breach in the mucosa that extends through the MUSCULARIS MUCOSA into the submucosa or deeper

Occur most FREQUENTLY first part of the duodenum; antrum; G-O junction!

Duodenum, stomach +- jejunum ulcers are seen in ollinger Ellison syndrome (gastrin producing tumour most commonly in the small intestine and pancreas)

Peptic ulcers can occur in ANY part of the GIT tract exposed to acid/peptic juices: therefore peptic ulcers can also occur in Meckel diverticulum that contains ectopic gastric mucosa

Ax: Generally the same as chronic gastritis: largely NSAID and or HPYLORI infection that leads to an IMBALANCE BETWEEN MUCOSAL DEFENCE AND DAMAGING FORCES OF GASTRIC ACID AND PEPSIN. Smoking and alcohol also contribute.

H.pylori is present in nearly all duodenal and 65% gastric ulcers, but only 10-20% infected develop peptic ulcer disease. H.pylori increases gastric acid secretion. High dose corticosteroid use that reduces prostaglandin synthesis. Hypercalcaemia- stimulates gastrin production. Psychological stress can also increase gastric acid secretion.

Macro: 98% peptic ulcers are located in the first part of the duodenum- anterior >posterior wall. Gastric ulcers located along the lesser curvature, border of body and antrum. 10-20% of patients may have gastric and duodenal ulcer.

Classically: round to oval punched-out defect with relatively straight walls, margins level or only slightly elevated (heaping out of margins is more characterisstic of malignant lesions), base is smooth and clean, blood vessels may be present, surrounding scarring with mucosal distortion.

Micro: active necrosis, chronic inflammation, scarring, healing
Active ulcers: 4 zones present
1. Base and margins thin layer of NECROTIC FIBRINOID DEBRIS
2. Non specific acute inflammation
3. active GRANULATION TISSUE infiltrated with mononuclear leukocytes, associated with features of chronic gastritis in surrounding mucosa especially in duodenal ulcer (85-100%) and also in gastric ulcer (65%).