Mouth and oesophagus Flashcards

1
Q

what are the 3 salivary glands?

A

parotoid, submandibular and sublingual

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2
Q

List 5 functions of saliva

A

lubrication, hydration, cytoprotection, immune protection and digestion (mainly for detection by taste cells)

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3
Q

what cells produce saliva?

A

Acinar

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4
Q

What is the role of duct cells?

A

Modify saliva’s composition
uptake NaCL secrete HCO3 and K +
makes saliva hypotonic and alkaline

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5
Q

what is mumps?

A

viral infection, saliva glands swollen (particularly parotid glands) orchitis also a symptom in mean

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5
Q

what is the average amount of saliva produced every 24 hours?

A

1.5L

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5
Q

what is Sjogren’s syndrome?

A

autoimmune attack of saliva and tear glands resulting in dry mouth and eyes. Commonly associated with rheumatoid arthritis and more common in women

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6
Q

how is saliva secretion controlled?

A

autonomic nervous system, primarily the parasympathetic nervous system

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7
Q

list the and explain the 4 stages of swallowing

A
  • Mouth phase - chewed to increase surface area to volume ratio aid swallowing / digestion
    • Oral phase- tongue propels food posteriorly until the pharyngeal swallow is activated
    • Pharyngeal phase - once pharyngeal is activated the bolus is transported through the pharynx, this occurs at the same time as closing of the glottis via the epiglottis movement, cessation of breathing and relaxation of the upper oesophageal sphincter (UOS)
    • Oesophageal phase - oesophageal peristalsis carries the bolus from the UOS to the lower oesophageal sphincter
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8
Q

list the causes of GORD

A

dysfunction of LOS- can be due to drugs that relax it (e.g. anticholinergic drugs)
can be due to hiatus hernia
increase in intra-abdominal pressure -
obesity, pregnancy, hiatus hernia

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8
Q

what are the symptoms of GORD?

A

heart burn and retrosternal discomfort, following eating / eating down etc
dysphagia (difficulty swallowing)
Laryngopharyngeal reflux - chronic cough, horse voice secondary to reflux into the pharynx

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8
Q

what is the definition of metaplasia?

A

change of epithelial tissue in response to environmental stress

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9
Q

what is Barret’s Metaplasia?

A

A pre-malignant condition, where the normal squamous epithelial lining is replaced by intestinal metaplasia epithelium, often due to repeated irritation from GORD
increases risk of oesophageal adenocarcinoma

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9
Q

how can GORD be diagnosed?

A

24-hour PH monitoring- a probe down oesophagus
contrast swallow - barium meal to see the areas of damage

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9
Q

How can GORD be managed / treated?

A

conservative measures include, weight loss, decreasing alcohol and avoiding alcohol/ food close to bed time
medical treatments = PPI’s e.g. omeprazole, H2 blockers, antiacids (Gaviscon)
surgical - repairing hernias, or fundoplication (anti-reflux surgery, rarely used has side effects)

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9
Q

what is achalasia?

A

motor disorder - failure to relax LOS, sphincter too tight for food to enter
symptoms include dysphagia solids and liquids, regurgitation, chest discomfort halitosis

10
Q

what are the stages of acid secretion in the stomach

A
  • Basal phase - low acid levels follows a circadian rhythm acid levels low in the pm high in the am
    • Cephalic phase - smell, sight, taste, swallowing of food initiates this phase, which is mediated by the vagus nerve. 30% of acid made before food enters stomach
    • Gastric phase - food entered stomach all other mechanisms mentioned earlier activated 50-60% acid secretion made here
    • Intestinal phase - partially digested peptides / amino acids in proximal part of small intestine trigger some gastrin to be produced by duodenal G cells 5-10% stomach secretion produced
11
Q

what is mutated in cystic fibrosis?

A

CFTR channel, cystic fibrosis transmembrane regulator

12
Q

how does cystic fibrosis effect the pancreas? what symptoms does it cause?

A

Cl- cannot be efficiently recycled through CFTR as its prematurely degraded
this reduces water levels in pancreatic duct, also causes deficiencies in HCO3 secretion (due to lack of Cl for HCO3 / Cl exchanger)
this results in thick mucus can cause blockages and pancreatitis
increases risk of diabetes
this lack of secretions reaching the duodenum leads to malnutrition

13
Q

explain the phases of pancreatic secretion?

A
  • Cephalic phase - sight, smell , taste etc. = 25% total secretion. Mediated by only Ach primary focus on the acinar cells not duct cells
    • Gastric phase - 10-20% Gastrin release - weak CCK agonist some production, neural pathways stimulated by stomach distention through a vagovagal gastropancreaitc reflex
    • Intestinal phase - 50-80% via all pathways Ach, lipids-CCK, neural pathways
14
Q

what does H.Pylori cause in the corpus?

A

Hypochloridria and gastritis, causes ILB release which inhibits gastrin release, leading to reduced acid secretion and stomach ulcers

15
Q

What does H.Pylori cause in the antrum?

A

Lead to G cells to hyper secrete gastrin, hypergastrinemia excess acid production, peptic ulcers

16
Q

Explain the role of Chief Cells in the stomach?

A

secrete inactive proteases such as pepsinogen, which is converted to pepsin at PH 3, and inactivated at PH 7.2

17
Q

when is somatostatin produced?

A

Low PH in the antrum causes D cells to produce somatostatin

18
Q

what promotes gastrin secretion in G cells?

A

GRP from branch of vagus nerve and amino acids / digested protein in the antrum

19
Q

what is the treatment for H.Pylori?

A

triple therapy - PPI and 2 antibiotics, amoxicillin and clarithromycin

20
Q
A