Session 6: Group Work Flashcards

1
Q

What are the three main salivary glands.

A

Submandibular
Sublingual
Parotid gland

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2
Q

List the main contents of saliva.

A
Water
Bicarbonate
Amylase
Antibodies
Lingual lipase
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3
Q

What clinical sign might you expect in a patient with poor saliva production?

A

Dry mouth
Mouth ulcers
Poor dental health

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4
Q

What broad class of drugs can reduce saliva production and why?

A

Anti-cholinergics as they inhibit the parasympathetic system which stimulates the saliva prod.

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5
Q

During which phase of swallowing is the airway at risk from aspiration?

A

Pharyngeal phase

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6
Q

Describe the mechanisms that exist in the upper GI tract to prevent food and fluid being aspirated in the lungs?

A

Vocal cords adduct
Closure of epiglottis by the elevation of the larynx
Oesophageal sphincter opens

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7
Q

Given that epithelia lining the oesophagus are stratified squamous epithelia, briefly explain how an adenocarcinoma has developed.

A

Persisten inflammation leading to SS metaplasia to columnar epithelium. In columnar epithelium glands can found. The columnar epithelium is more prone to become malignant as it has undergone metaplasia.

This is called Barrett’s oesophagus

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8
Q

A 70 yr old man present to his GP with difficulty swallowing solid foods. He is able to initiate the swallow but then regurgitates the food bolus back up. This has been getting progressively worse over the last six weeks. He reports that he is still able to swallow liquids. He has lost weight and is feeling constantly tired.

Adenocarcinoma in oesophagus is found.

Why is this man’s dysphagia to solids progressively getting worse?

A

The tumour is growing.

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9
Q

Why is he able to swallow liquids but not solids.

A

Liquids can more easily move past

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10
Q

The man reports constant tiredness. Apart from lethargy caused from decreased calorific intake, can you suggest another possible reason for his tiredness?

A

Cancers are highly metabolically active.

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11
Q

A 45 y old man presents to this GP with epigastric pain that comes on 2-3 hours after meal times. The pain is a gnawing and burning pain in character and occasionally wakes him up at night. The GP examines the man and elicits mild epigastric tenderness. The GP suspects a peptic ulcer.

Briefly describe how Gastrin secretion is stimulated and what effects it has after it is released.

A

Stimulated by peptides and amino acids + vagal stimulation by ACh as well as GRP.

Gastrin stimulates the release of pepsinogen from chief cells and H+ secretion from parietal cells.

Gastrin also stimulates enterochromaffin cells to release histamina which stimulates the parietal cells to secrete H+ as well.

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12
Q

In broad terms describe how gastric acid secretion is inhibited.

A

Somatostatin produced by D cells which are stimulated by the presence of acid/low pH

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13
Q

Define peptic ulcer.

A

Defects in gastric/duodenal mucosa and must extend through muscularis mucosae.

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14
Q

State two locations in the upper GI tract where peptic ulceration is common.

A

Lesser curve/antrum

First part of duodenum

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15
Q

From an embryological PoV, why is the pain of peptic ulceration felt in the epigastric area of the abdomen?

A

Visceral innervation by grater splanchnic nerve. Feeding back to the T5-T9 roots. They supply the dermatomes of the T5-T9

It is also bilateral.

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16
Q

From the history the GP suspects that the location of this peptic ulcer is in the duodenum. Which parts of the history suggests this and why?

A

Because it is delayed by 2-3 hours. If it was in the stomach it would be faster.

17
Q

State two common precipitants of peptic ulceration and briefly describe how they promote ulceration.

A

H. pylori producing urease leading to inflammation and cytotoxin release. Also metabolise stomach to increase ammonia.

NSAIDs inhibiting prostaglandin which reduces the blood flow to the stomach. This promotes peptic ulceration.

18
Q

Given that the GP suspects this man to have a peptic ulcer. What investigations are appropriate?

A
Medical history
Blood test
Urease test
Endoscopy
Stool antigen test
19
Q

State two pharmacological treatments that exist for peptic ulcer disease that reduce acid production in the stomach.

A

PPi (can cause hyponatraemia)

H2 receptors antagonists

20
Q

State on other pharmacological treatment that exists for peptic ulcers and describe how it reduces peptic ulceration.

A

Antacids to increase pH

Antibiotics vs the H. pylori

21
Q

Briefly describe how the pancreas helps to raise the pH in the duodenum.

A

Pancreatic duct cells secrete HCO3- in response to secretin. This raises pH as a buffer.

Secretin also inhibits gastric juice secretion.

22
Q

With reference to the constituents of chyme, what stimulates the release of CCK and what are the effects of its release?

A

Fats and proteins.
Digestion of fats, proteins and carbs by stimulating pancreatic cells. It also stops gastric juice secretion and contracts the gallbladder.

23
Q

What is the role of bile salts in the duodenum?

A

Emulsification of fat to increase surface area of the fat droplets to make lipase more efficient.

Also creates micelles to transport the fat droplets to the enterocytes. The bile salts are then recycled.

Made by cholesterol so indirectly lower cholesterol.

24
Q

Briefly describe the stages of fat absorption.

A

Emulsification -> Digestion -> Micelles -> transport to enterocytes -> Fat picked up by golgi to make triglycerides again and make chylomicrons for further transport -> into lymph -> thoracic duct -> left subclavian vein.