AS Lecture 1/2 - Burden of GI disease & Oesophagus and Stomach Flashcards
<p><p>What is digestion?</p></p>
<p><p>Process of breaking down macromolecules to allow absorption</p></p>
<p><p>What is absorption?</p></p>
<p><p>Process of moving nutrients and water across a membrane</p></p>
<p><p>How can digestion take place?</p></p>
<p><p>Mechanically: Chewing, gastric churning, peristalsis OR enzymatically</p></p>
<p><p>What happens after ingestion?</p></p>
<p><p>Either direct excretion/absorption OR digestion</p></p>
<p><p>What are the components of the GIS?</p></p>
<p><p>Parotid gland, sublingual gland, submandibular gland, oesophagus, liver, stomach, gall bladder, pancreas, duodenum, jejenum, ileum, appendix, ascending colon, descending colon, sigmoid colon, rectum, anus</p></p>
<p><p>What are some diseases specific to each part of the GI system?</p>
</p>
<p><p>Main: LIVER - hence hepatology</p>
</p>
<p><p>What is disease burden - the checklist?</p>
</p>
<p><p>Burden to the patient, economy, population, society</p>
</p>
<p><p>What are the different classes of symptoms that can be caused by GIT diseases?</p>
</p>
<p><p>General, Upper GI, hepatobiliary, mid GI, lower GI</p>
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<p>What are some general symptoms of GIT diseases?</p>
<p>Anorexia, weight loss, anaemia</p>
<p>What are some UGI symptoms?</p>
<p>Haematemesis, melaena, N and V, Dysphagia, odynophagia, heartburn, Acid regurgitation, belching, chest pain, epigastric pain</p>
<p>What are some hepatobiliary symptoms?</p>
<p>RUQ pain, Biliary colic, Jaundice, Dark urine, pale stool, abdominal distention</p>
<p>What are some mid GI symptoms?</p>
<p>Abdominal pain, steatorrhea, diarrhoea, abdominal distention</p>
<p>What are some lower GI symptoms?</p>
<p>Abdominal pain, bleeding, constipation, diarrhoea, incontinence</p>
<p>Why is incontinence important?</p>
<p>A patient won't want to share that they are incontinent - embarrassing</p>
<p>What are the 4 places that show signs due to GIS disease?</p>
<p>General, hands, abdomen, anus and rectum</p>
<p>What signs are generally visible?</p>
<p>Cachexia, obesity, lymphadenopathy, anaemia, jaundice</p>
<p>What are some signs on the hands?</p>
<p>Koilinychia, leuconychia, clubbing, dupytrens contracture, tachycardia, tremor</p>
<p>What are some signs of the abdomen?</p>
<p>Organ enlargement, mass, tenderness, distension</p>
<p>What are some signs of the anus and rectum?</p>
<p>Haemorrhoids, fistula, fissure, rectal masses or proctitis</p>
<p>What investigations can be used for the GI systems?</p>
<p>History, Basic physical examination, Haematology/biochem/microbio (blood test, tumour markers, urea, etc), procedures (x-ray, mri, colonoscopy)</p>
<p>What is the biggest specific killer of people in UK, wrt GID?</p>
<p>Liver cirrhosis</p>
<p>What is the biggest portion of systemic cancers in the UK?</p>
<p>Gastrointestinal</p>
<p>What position is GI most likely to cause problems and lead to death?</p>
<p>4th (don't need to know but to appreciate)</p>
<p>What is happening to the trend of alcoholic liver disease vs. liver cancer?</p>
<p>Alcoholic liver disease is high among younger populations, and decreases with age BUT liver cancer increases with age, affecting the older generations</p>
<p>In which sex, is alcoholic liver disease and liver cancer more common?</p>
<p>Males</p>
<p>Which GI cancers are common?</p>
<p>Colorectal (2nd), Prostate(3rd), Oesophagus, pancreas, stomach (6th), liver (13th) [oral cancer commonish]</p>
<p>What are some prevalent inflammatory conditions that are burden?</p>
<p>Ulcerative colitis (1/500)
Crohn's disease (1/1000)
Coeliac disease (1/87)
Gastro-oesophageal reflux disease</p>
<p>How is ulcerative colitis treated and what causes it?</p>
<p>Treated: colectomy, Cause: thought to be autoimmune</p>
<p>What causes coeliac disease?</p>
<p>Gluten sensitivity</p>
<p>What are some pancreatic conditions?</p>
<p>Acute/chronic pancreatitis</p>
<p>What is acute pancreatitis?</p>
<p>Blockage of the pancreatic duct causes back up of pancreatic enzymes, causing severe inflammation - mild->life-threatening</p>
<p>What is chronic pancreatitis?</p>
<p>Permanent damage to pancreas, alcohol excess is the main cause and can greatly impair quality of life</p>
<p>What kind of infections can occur in the GIS?</p>
<p>Bacterial - Helicobacter pylori (nausea, bloating, weight loss), E. coli (Nausea, diarrhoea, cramps)
Virus - Norovirus (N, V, D)</p>
<p>How does H. pylori affect people globally?</p>
<p>Infects around 60% of people - 85% have no problems, 14% peptic ulcers, 1% gastric adenocarcinoma/lymphoma</p>
<p>What are GI disease risks based on?</p>
<p>Mainly on environment - energy intake, staple foods</p>
<p>What are the different effects on the economy from GID?</p>
<p>Mortality and lost years, absence from work, morbidity, NHS prescription costs, QALY, DALY</p>
<p>What do QALY and DALY mean?</p>
<p>Quality and Disability adjusted life years</p>
<p>What kind of healthcare costs are there (GI burden)?</p>
<p>In-patients, out-patients, primary care, community health and social care</p>
<p>What kind of other costs are there (GI burden)?</p>
<p>NHS costs and non-working costs</p>
<p>What are the costs of dyspepsia?</p>
<p>Only 2% consult GPs and 40% of adults suffer from it - OTC drugs</p>
<p>What is a cost effective screening programme in the UK - to do with GID?</p>
<p>Bowel cancer screening</p>
<p>What are the 4 detrimental social aspects of GID?</p>
<p>Dietary limitation (intolerances), flatulence (sound and smell), treatment (smell/slight), incontinence (soiling)</p>
<p>Which GI cancer has the poorest survival rate?</p>
<p>Pancreatic</p>
<p>What is the most common cause of GI-related death in a 75 year old man?</p>
<p>Cancer</p>
<p>What is the layer plan of the gut wall?</p>
<p>Mucosa (epithelium, lamina propria, muscularis mucosae), Submucosa (connective tissue w/nerve plexus), Muscularis (smooth muscle w/nerve plexus), serosa/adventitia (connective tissue +/- epithelium)</p>
<p>What is the structure of the oesophagus?</p>
<p>Starts at C5, passes through the thorax into the abdomen, close to the heart, laryngeal nerves</p>
<p>What is the purpose of the oesophagus?</p>
<p>Conduit for food, drink and swallowed secretions from pharynx to stomach</p>
<p>What are some complications of the place where the oesophagus is placed?</p>
<p>Close to the pericardium, so a rupture could lead to acidic contents/bacteria entering into the thorax and causing infections; also close to the recurrent laryngeal nerves, which could be damaged during surgery</p>
<p>What is the structure/function relationship of the oesophagus' epithelium?</p>
<p>It is non-keratinising, stratified squamous - very robust, as needs to protect underlying structures and deal with wear and tear - secrete mucous to help with bolus lubrication</p>
<p>What is the structure/function relationship of the oesophageal sphincters?</p>
<p>Upper/lower oesophageal sphincters - tonically active (need swallowing to open)
LOS needed to stop negative pressure drawing up the acid from stomach and UOS needed to close so breathing can occur</p>
<p>What is the structure of the oesophagus muscles?</p>
<p>Skeletal, transition between skeletal/smooth and then smooth - there is NO VOLUNTARY CONTROL</p>
<p>What is the process of swallowing and how is it controlled?</p>
<p>The swallowing centre in the brain sends a signal to open both sphincters, and when the bolus passes the UOS, it closes. The LOS stays open until the bolus has entered the stomach</p>
<p>How does peristalsis occur?</p>
<p>Smooth muscle - particularly circular muscle - immediately above bolus is contracted, below bolus is relaxed - longitudinal helps, but mainly circular</p>
<p>What are secondary peristaltic waves?</p>
<p>If the bolus hasn't reached the stomach and it is detected by the oesophagus, another wave of contraction is sent down the oesophagus, so the bolus can reach the stomach</p>
<p>What is the gastro-oesophageal junction?</p>
<p>Joining of oesophagus with stomach - where the LOS is to prevent reflux (prevented by diaphragm)</p>
<p>What is the LOS?</p>
<p>It is the diaphragm, assisting circular muscle at lower end of oesophagus</p>
<p>How does the level of the GOJ help to prevent reflux?</p>
<p>Negative pressure in thorax vs positive pressure in stomach would lead to acid being drawn up the oesophagus</p>
<p>What is a histological feature that can be seen at the GOJ?</p>
<p>Epithelial transition from stratified squamous to simple columnar AND gastric folds (rugae) are present in the stomach</p>
<p>What is the purpose of the epithelial transition in the GOJ?</p>
<p>Change in function as in stomach it has to be more secretory rather than protective</p>
<p>Why are the gastric folds present in the stomach?</p>
<p>Allows for huge changes of surface area - to expand and contract as required</p>
<p>How does belching work?</p>
<p>The OS are both opened and the pressure in the oesophagus causes the air to be pushed out - not pushing out by the stomach</p>
<p>What is the function of the stomach?</p>
<p>Break down food into smaller particles; holds food and releases at steady rate into duodenum; kills parasites and certain bacteria</p>
<p>What are the types of cell in the stomach lining?</p>
<p>Simple columnar, which invaginate into mucosa - tubular glands</p>
<p>What are the regions in the stomach and what do they produce?</p>
<p>Cardia and Pyloric regions - Mucus</p>
<p>Body and fundus - Mucus, HCl, pepsinogen</p>
<p>Antrum - Gastrin</p>
What are the different cell types in the stomach?
Mucus secreting cells - secrete mucus high in carbonates, acting as a protective barrier for the lining of the stomach from the acid
Chief cells - secrete pepsinogen
Parietal cell - secrete H+ into the stomach
How much acid does the stomach produce in a day? (+some other facts)
2L/day
150mM H+ - very acidic!!
How do the mucus secreting cells protect the stomach lining?
They secrete mucins (gel coating) and pump out HCO3- which gets trapped in the mucus gel - this means that it can act as a buffer, neutralising the stomach acid
What is the pH at the stomach lining compared to the centre?
Mucus lining/epithelial surface - 6-7
Lumen - 1-2
How are chief cells adapted for their function in the stomach?
Protein secreting epithelial cell, abundant RER, golgi packaging and modifying for transport, masses of apical secretion granules
How are parietal cells adapted for their function in the stomach?
Many mitochondria, cytoplasmic tubulovesicles (contain H+/K+ ATPase, merge with cannaliculi when cell activated), internal cannaliculi (reservoirs near the apical membrane)
How is the acid produced in the parietal cell?
Carbonic anhydrase catalyses CO2 + H2O into H+ and HCO3-, then Na+/K+ pumps, bring K+ in which then diffuses into the cannaliculi. The HCO3- are moved out of the cell via pump which brings Cl- in which diffuse into the cannaliculi. The K+/H+ ATPase causes H+ to enter cannaliculi and K+ into the cell
How would inhibition of carbonic anhydrase influence acid secretion in the stomach?
Decreases acid secretion
How does pepsinogen work?
Produced by chief cell - is an acidic precursor which needs the acidic pH of the stomach (HCl) to enzymatically cleave each other, to produce pepsin (which is needed to break down proteins)
What is gastrin?
Released in pyloric antrum - to stimulate acid secretion.
What is the mechanism of gastrin release?
Ingested proteins increase the pH of the stomach contents, removing inhibition of gastrin, which causes more acid production to decrease the pH.
What does gastrin act on?
Gastrin acts on parietal cells to increase acid secretions and can stimulate histamine release as well
What are the 3 phases of gastric secretion?
Cephalic phase, gastric phase, intestinal phase
What is the cephalic phase and where does it take place?
Occurs in brain - when thought/sight/smell of food occurs, brain activates vagus nerve to release ACh and react with parietal cells, or cause histamine release to increase acid production
What is the gastric phase and where does it take place?
Once food reaches stomach - stomach reacts to distension (stretch receptors), sends signal up to brain saying there is food present (reflex - to send signal to increase acid secretion)
Also chemoreceptors present to trigger gastrin secretion
What does the enteric nervous system do?
It reacts to the distension as well, and increased acid secretion
What is the intestinal phase and where does it take place?
Mainly inhibition phase - as stomach contents pass to intestine, sends signal to brain if pH is low, to switch off gastrin secretion OR low pH in chyme causes 3 hormones to be secreted, so they can be reabsorbed into stomach to reduce gastrin/acid/other stomach secretions
What are the 3 hormones (enterogastrones) secreted in response to low pH in the chyme (enterogastric reflex)?
Gastric inhibitory peptide, cholecystokinin, secretin
What is the counter intestinal cycle - the excitatory version?
If the protein concentration in the duodenum is too high, gastrin secretion is stimulated, and acid is increased
What part of acid secretion would you inhibit to reduce acid secretion?
Histamine receptor antagonist (Ranitidine)
K+/H+ ATPase inhibitor (Omeprazole)
Which of the following stimuli would be most likely to decrease acid secretion in the stomach? A. Chyme fatty acid content B. Increased acetylcholine secretion C. Increased gastrin secretion D. Protein content of the meal E. Stomach distension
Chyme fatty acid content
Which of the following structures within the
parietal cell contains the most H+/K+ ATPase?
A. Canaliculi
B. Carbonic anhydrase
C. Golgi body
D. Mitochondria
E. Tubulovesicles
Tubulovesicles
