Oesophageal and gastric pathology left over Flashcards

1
Q

Define an ulcer

A

An ulcer is a local defect of the mucous membrane or the skin due to gradual disintegration of the surface epithelial cells

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2
Q

What is the mechanism of action of a PPI?

A

-Binds irreversibly to H+/ATPase enzyme (proton pump) on gastric parietal cells and blocks secretion of H+, which combine in the stomach with Cl- to form HCL

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3
Q

What is the action of HCL in the stomach?

A

-Activates pepsinogen to pepsin which helps in proteolysis
-Antimicrobial

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4
Q

How can NSAIDs cause PUD?

A

-Prostaglandins are important for gastric mucosal protection: NSAIDS suppress their production (cyclooxygenase inhibitors)
-Topical irritant effect on epithelim
-Reduced gastric mucosal blood flow

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5
Q

Why can hypercalcaemia cause peptic ulcer?

A

Hypercalcaemia –> increased gastrin release –> increased HCL production

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6
Q

What are the common causes of hypercalcamiea?

A

-Hyperparathyroidism
-Malignancy
-Renal failure

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7
Q

How can you localise parathyroid glands?

A

-Sestamibi scan (pre operative)
-Frozen section (intra operative)

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8
Q

What is the epithelium of gastric mucosa in the antrum?

A

-Simple columnar with mucosal and goblet cells

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9
Q

What immune endocrine diseases and malignancy associated with helicobacter infections?

A

-Hashimoto’s thyroiditis
-MALT
-Adenocarcinoma

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10
Q

What is the histology of a parathyroid adenoma?

A

-Uniform, polygonal chief cells with small, centrally placed nuclei
-A few nests of larger oxyphil cells are present as well. Uncommonly, adenomas are composed entirely of this cell type (oxyphil adenomas)
-A rim of compressed, non-neoplastic parathyroid tissue, generally separated by a fibrous capsule, is often visible at the edge of the adenoma

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11
Q

Where can you find the parathyroid gland if you do not see them in the normal position?

A

-The superior mediastinum: the thymus originates from the third branchial arch, so it occasionally drags the inferior glands down to the mediastinum

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12
Q

How would you treat a parathyroid adenoma?

A

Excision

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13
Q

What is the treatement of hypercalcaemia?

A

-Hydration
-Forced diuresis
-Bisphosphonates: IV pamidronate
-Calcitonin

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14
Q

What is the normal lining of the oesophagus?

A

-Non keratinised stratified squamous

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15
Q

What would be the cause of a pleural effusion in a pateitn with oesophageal adenocarcinoma

A

-Spread of cancer cells to pleura
-Lung mets
-Obstruction of thoracic duct

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16
Q

In pt with pleural effusion and oesophageal carcinoma, what pathological test would you want to do?

A

Effusion cytology

17
Q

How can you treat such a pleural effusion

A

Palliative treatments
-Thoracocentesis
-Indwelling pleural catheters
-Pleurodesis
-Pleuroperitoneal shunting

18
Q

What is troponin?

A

A complex of three regulatory proteins (Troponin C, I and T) that is integral to muscle contraction

19
Q

Where is troponin found?

A

Cardiac muscle and skeletal muscle

20
Q

What is the pathogenesis of gastric carcinoma?

A

-Believed to develop by a sequence of pathological changes
-Normal mucosa –> chronic gastritis –> intestinal metaplasia –> dysplasia –> intramucosal carcinoma –> invasive gastric carcinoma

21
Q

Patient with LIF pain and gastric cancer. Surgery was done (gastrectomy with splenectomy) pathology report inside

On entering you are given a histopath report showing:
–> signet ring carcinoma
–> positive lymph nodes
–> margin positive
–> spleen involved

Discuss the report with the family

A

Discuss the pathology report with the family
–> cancer of the stomach
–> incomplete resection
–> high possibility of recurrence
–> patient will require further resection and chemotherapy

22
Q

Describe the classification of gastric cancer

A

WHO classification

–> Tubular adenocarcinoma: made up of different sized small branching tubules

–> Papillary adenocarcinoma: this tumour grows outward from stomach wall and contains finger-like growths that stick out into stomach cavity.

–> Mucinous addenomacrcinoma: lots of mucin (main substance in mucus) outside the cancer cells

–> Poorly cohesive carcinomas (including signet ring cell carcinoma and others): these are arranged into clumps of cancerous cells

–> mixed carcinoma: mix of types of adenocarcinoma of the stomach

23
Q

Describe the lauren classification

A

-Intestinal type: tumours are well differentiated, slow growing and tend to form glands. Found more often in men than women and occurs more in older people

-Diffuse type: tumour cells are poorly differentiated, behave aggressively and scatter throughout stomach (ratbher than form gladns). Metastasises much quicker than intestinal type

24
Q

7-10 days later after gastric ca the patient had axillary vein thrombosis, what predisposes to that?

A

-Hypercoagulable state in malignancy
-Venous stasis from virchow LN

25
Q

6 months later the patient came with ascites, deranged LFT, hepatic metastasis. What 2 pasthagolical tests would you do?

A

-Ascitic tap and cytology
-Liver biopsy from metastasis
-FNA from left supraclavicular lymph node

26
Q

How would you treat the patient with metastatic gastric ca with hepatic mets and ascies?

A

-Feeding jejunostomy
-Palliation of ascites by repeated tapping
-Anticipatory medications for symptom control
-Palliative chemotherapy

27
Q

What is the mechanism of malignant ascites in cirrhotic liver?

A

-Hypoalbuminaemia leading to raised oncoting pressure
-Portal hypertension leading to ascites

28
Q

What is the borrmann classification of gastric ca?

A

-Polypoid growth
-Fungating growth
-Ulcerating growth
-Diffusely infiltrating growth (linitis plastica)

29
Q

Which para-neoplastic syndromes are associated with gastric ca?

A

-acanthosis nigricans
-Dermatomyositis

30
Q

What are the procedure specific complications of total gastrectomy?

A

Early:
–> anastamotic leak
–> pancreatitis
–> cholecystitis
–> haemorrhage
–> infection

Late
–> dumping syndrome
–> vitamin B12 defiency (lack of intrinsic factor)
–> metabolic bone disease
–> recurrence of malignancy

31
Q

What is dumping syndrome?

A

-Loss of the resevoir function of the stomach (e.g. following gastrectomy) results in rapid transit of highly osmotically active substances into the duodenum following meals and may cause ‘dumping syndrome’

-Early dumping: 30-60 minutes following meal, rapid transit of hyperosmolar gastric contents into the small bowel results in a fluid shift from the intravascular compartment to the gastric luman and small bowel distension, colicky abdominal pain, diarrhoea and vasomotor symptoms, such as tachycardia and postural hypotension

-Late dumping: 1-3 hours following meals. Rapid transit of carbohydrate into the small bowel results in sudden absorption of high levels of glucose and compensatory hyperinsulinaemia resulting in subsequent hypoglycaemia