GI Flashcards
Give 9 functions of the stomach.
- Store and mix food.
- Regulate emptying into the duodenum.
- Secrete proteases.
- Dissolve and continue digestion.
- Kill microbes.
- Secrete intrinsic factor.
- Activate proteases.
- Lubrication.
- Mucosal protection.
What are the 4 key cell types in the stomach?
- Mucous cells.
- Parietal cells.
- Chief cells.
- Enteroendocrine cells.
What is gastric acid? How much do we make a day?
Hydrochloric acid. We make ~2 litres/day.
Which 3 ions are needed for gastric acid secretion?
H+, Cl-, and K+.
Describe the cephalic phase of activating gastric acid secretion.
- Stimulated by sight, smell, taste of food and chewing.
- Parasympathetic nervous system.
- Acetylcholine is released.
- ACh acts directly on parietal cells, triggering gastrin and histamine release.
- Gastrin and histamine stimulate parietal cells.
- Therefore, increases acid production .
Describe the gastric phase of activating gastric acid secretion.
- Gastric distension.
- Presence of peptides and amino acids.
- Gastrin released, acts on parietal cells, triggers histamine release.
- Histamine then acts directly on parietal cells.
- Therefore, increases acid production.
Describe how protein in the stomach has a role in activating gastric acid secretion.
- Directly stimulates gastrin release.
- Luminal proteins act as a buffer, mopping up H+, causing pH to rise.
- Decreases somatostatin secretion.
- Allows more parietal cell activity due to lack of inhibition.
- Therefore, increases acid production.
Describe the gastric phase of deactivating gastric acid secretion.
- Low luminal pH from high H+.
- Low pH inhibits gastrin secretion.
- Therefore, indirectly inhibits histamine release (via gastrin).
- Low pH also stimulates somatostatin release, which inhibits parietal cell activity.
- Therefore, decreases acid production.
Describe the intestinal phase of deactivating gastric acid secretion.
- Duodenum has higher pH than the stomach at rest.
- Gastric contents entering causes duodenum distension, lower luminal pH, hypertonic contents, and presence of amino acids and fatty acids.
- This triggers the release of enterogastrones: secretin and cholecystokinin (CCK).
- Secretin inhibits gastrin release, and promotes somatostatin release.
- Short and long neural pathways which reduce ACh release.
- Therefore, decreases acid production.
Give a simple list of facts about the regulation of gastric acid secretion.
- Controlled by the brain, stomach, and duodenum.
- 1 parasympathetic neurotransmitter (ACh = + acid).
- 1 hormone (gastrin = + acid).
- 2 paracrine factors (histamine = + acid, somatostatin = - acid).
- 2 key enterogastrones (secretin and cholecystokinin = - acid).
What is an ulcer?
A breach in a mucosal surface.
Give 4 causes of an ulcer.
- Helicobacter pylori infection.
- Drugs (NSAIDs).
- Chemical irritants (alcohol, bile salts, diet).
- Gastrinoma (tumours of gastrin producing cells).
Where can peptic ulcers occur?
In the stomach, duodenum, and oesophagus.
Describe the two ways an ulcer can occur in terms of the mucosal attack/defences.
Increased mucosal attack, or decreased mucosal defences.
How does the gastric mucosa defend itself? Give 4 ways.
- Alkaline bicarbonate-rich mucus, which forms a barrier between acid and epithelial cells.
- Tight junctions between epithelial cells, prevent acid passing between cells to tissue below.
- Replacement of damaged cells, occurs via stem cells in gastric pits.
- Feedback loops, irritation causes surface mucous cells to produce more.
What is the purpose of intrinsic factor?
To bind to Vitamin B12 taken in in the diet, helping it to be absorbed in the terminal ileum.
What is the role of parietal cells?
Produce intrinsic factor and gastric acid.
What is the role of enteroendocrine cells?
Produce gastrin.
Describe how helicobacter pylori cause peptic ulcers.
- Bacteria lives in gastric mucus.
- Secretes urease, splitting urea into CO2 and ammonia.
- Ammonia and H+ = ammonium.
- Ammonium damages gastric epithelium.
- Inflammatory response.
- Reduced mucosal defence.
How do you treat patients with peptic ulcers from helicobacter pylori?
- Eradicate the organism
- Proton pump inhibitor.
- 2 antibiotics from: clarithomycin, amoxicillin, tetracycline, and metronidazole.
Describe how NSAIDs cause peptic ulcers.
- Non-steroidal anti-inflammatory drugs.
- Cyclo-oxygenase 1 needed to synthesise prostoglandins.
- NSAIDs inhibit COX-1, reducing prostoglandin synthesis.
- Mucus secretion stimulated by prostoglandins.
- Inhibits mucus secretion, and reduces mucosal defence.
How do you treat patients with peptic ulcers from NSAIDs?
- Prostoglandin analogues e.g. misoprostol, to stimulate mucus secretion.
- Reduce acid secretion.
Describe how bile salts can cause peptic ulcers.
- Duodenal-gastric reflux.
- Regurgitated bile strips away mucus layer.
- Reduce mucosal defence.
What is the role of chief cells?
Produce pepsinogen (inactive form of pepsin).
Why is pepsinogen synthesised rather than pepsin?
Synthesised as a zymogen (in its inactive form), as proteases break down proteins, so if the cell made an active protease it would digest itself.
How is pepsinogen mediated?
By input from the enteric nervous system (acetycholine).
Describe the protease activation of pepsinogen -> pepsin.
- Positive feedback loop.
- Secretion parallel to HCl secretion.
- HCl cleaves pepsinogen -> pepsin.
- This pepsin breaks down pepsinogen -> more pepsin.
- Most efficient at pH <2.
Describe the inactivation of pepsin.
Irreversible inactivation in duodenum by HCO3-.
Describe the role of pepsin in protein digestion.
- Not essential, protein digestion can occur if the stomach is removed.
- Accelerates protein digestion, and normally accounts for ~20% of total.
- Breaks down collagen in meat, helps shred into smaller pieces = greater SA for digestion.
What is the volume of an empty stomach?
~ 50mL.
When eating, how much can the stomach accommodate with little increase in luminal pressure?
~ 1.5 L.
Give the 3 steps of gastric peristalsis.
- Waves begin in gastric body (weak contractions, little mixing).
- More powerful contractions in gastric antrum, pyloric sphincter closes as peristaltic wave reaches it.
- Little chyme enters the duodenum, antral contents forced back towards the body -> mixing.
What is the normal frequency of peristaltic waves?
3/minute.
What determines the basic electrical rhythm of the peristaltic waves?
Pacemaker cells in the muscularis propria, called interstitial cells of cajal.
Describe the basic electrical rhythm of peristaltic waves, and what happens in an empty stomach.
- Undergo slow depolarisation-repolarisation cycles.
- Waves of depolarisation transmit through gap junctions to adjacent smooth muscle cells.
- Do not cause significant contraction in an empty stomach.
Give 2 factors that increase the strength of peristaltic contractions.
- Gastrin.
- Gastric distension (mediated by mechanoreceptors).
Give 1 factor that decreases the strength of peristaltic contractions.
- Duodenal distension.
Which has a larger capacity, the stomach or the duodenum?
The stomach.
What causes dumping syndrome?
Overfilling of the duodenum by a hypertonic solution.
Give 8 symptoms of dumping syndrome.
- Vomiting.
- Bloating.
- Cramps.
- Diarrhoea.
- Dizziness.
- Fatigue.
- Weakness.
- Sweating.
What is gastroparesis?
Delayed gastric emptying.
Give 9 causes of gastroparesis.
- Idiopathic.
- Autonomic neuropathies (e.g. in diabetes mellitus).
- Drugs.
- Abdominal surgery.
- Parkinson’s disease.
- Multiple sclerosis.
- Scleroderma.
- Amyloidosis.
- Female gender.
Give 7 symptoms of gastroparesis.
- Nausea.
- Early satiety.
- Vomiting undigested food.
- GORD.
- Abdominal pain.
- Abdominal bloating.
- Anorexia.
What is receptive relaxation?
Presence of food in stomach makes it relax, then it can stretch without increasing the pressure.
Which type of muscle in which parts of the stomach undergo receptive relaxation?
Smooth muscle in the body and the fundus.
How is receptive relaxation mediated/coordinated?
- Mediated by parasympathetic nervous system, acting on enteric nerve plexuses.
- Acetylcholine released, triggers nitric oxide and serotonin release by enteric nerves, which mediates relaxation.
- Coordination controlled via the vagus nerve (CN X).
What are the 3 pairs of major salivary glands called?
- Parotid.
- Submandibular.
- Sublingual.
What % of salivary flow are the major salivary glands responsible for?
80%.
Where can the minor salivary glands be found?
In the submucosa of oral mucosa e.g. lips, cheeks, hard and soft palate, tongue.
What % of salivary flow are the minor salivary glands responsible for?
20%.
Describe the general structure of salivary glands.
Composed of 2 epithelial tissues.
- Acinar cells, which sit around…
- Ducts
Have channels and transporters in the apical and basolateral membranes to enable fluid and electrolyte transport.
What are the 2 types of acini?
Serous acinus, and mucous acinus.
Describe serous acini.
- Dark staining nucleus in basal 1/3.
- Small central duct.
- Secrete water and alpha amylase.
- Tightly packed.
Describe mucous acini.
- Pale staining (foamy).
- Nucleus at base/edge of cell.
- Large central duct.
- Secrete mucous (water and glycoproteins).
Which type of acini are present in each of the 3 major pairs of salivary glands?
Parotid = serous acini.
Submandibular = mixed, aka seromucous acini.
Sublingual = mixed, but more mucous acini.
Describe the structure of ducts in the salivary glands.
Intralobular ducts -> main excretory duct.
Intralobular ducts = intercalated ducts and striated ducts.
Describe intercalated ducts.
Short, narrow duct segments, cuboidal cells that connect acini to larger, striated ducts.
Describe striated ducts.
Striped, major site for NaCl reabsorption, basal membrane folded into microvilli (for active transport of HCO3- against conc gradient), microvilli filled with mitochondria for energy to facilitate active transport.
What do ducts secrete, and reabsorb?
Secrete: K+ and HCO3-.
Reabsorb: Na+ and Cl-.
Describe the process from primary saliva to final saliva.
Primary = NaCl rich, isotonic plasma-like fluid, secreted by acini.
Epithelium of duct does not allow water movement.
Therefore, final saliva = hypotonic.
Describe the location of Stenson’s duct, and which of the major salivary glands it comes from.
Comes from the parotid gland.
Crosses the masseter, pierces the buccinator, and enters the oral cavity near the second upper molar.
Describe the parotid capsule.
Very tough.
Give 3 structures that pass through the parotid.
- External carotid and its terminal branches.
- Retromandibular vein.
- Facial nerve and branches to muscles of facial expression.
Where can you find the parotid gland on physical examination?
Palpate a finger’s breadth below the zygomatic arch.
Describe the structure/location of the submandibular glands.
Two lobes separated by the mylohyoid muscle:
- Larger, superficial lobe
- Smaller, deep lobe (in floor of the mouth)
Describe the location of Wharton’s duct, and which of the major salivary glands it comes from.
Comes from the submandibular glands.
Empties into the oral cavity underneath the tongue.
Describe the location of the sublingual glands.
Between the mylohyoid muscle and the oral mucosa of the floor of the mouth.
Describe the duct system of the sublingual glands.
Has no large duct, instead drains into Wharton’s duct, and has small ducts that pierce the oral mucosa on floor of the mouth.
Describe the duct system of the minor salivary glands.
Lacks a branching network of draining ducts, each unit has its own simple duct.
Describe the locations in which the minor salivary glands are concentrated.
The buccal, labial, palatal, and lingual regions.
Give 3 other locations of minor salivary glands.
- Superior pole of tonsils (Weber’s glands).
- Tonsillar pillars.
- Base of the tongue (von Ebner’s glands).
What is the flow rate of saliva?
0.3 -> 7ml per minute.
What is the daily salivary secretion in adults?
Between 800 -> 1500ml per day.
Give the pH range of saliva.
6.20 -> 7.40.
Give 8 factors that can affect the composition and amount of saliva produced.
- Flow rate.
- Circadian rhythm.
- Type and size of gland.
- Duration and type of stimulus.
- Diet.
- Medications/drugs.
- Age.
- Gender.
Give 4 functions of saliva.
- Lubrication for mastication, swallowing, and speech.
- Oral hygiene.
- Maintenance of oral pH ~ 7.20, to prevent damage of tissues or teeth.
- Digestive enzyme, dilutes food to allow taste.
Describe saliva’s role in oral hygiene/health.
Lubrication, mechanical cleaning, buffering salts, remineralisation, defensive and digestive function.
How does saliva maintain oral pH?
Bicarbonate/carbonate buffer system rapidly neutralises acids.
Describe oral defence and saliva’s role in it.
The mucosa = the physical barrier.
Palatine tonsils = immune surveillance and resistance to infection.
Salivary glands = wash away food particles that bacteria or viruses may use for metabolic support.
Which salivary glands are continuously active?
Submandibular, sublingual, and minor salivary glands.
Describe the composition of unstimulated saliva.
Dominated by submandibular components.
Describe the composition of stimulated saliva.
Resembles parotid secretion, the main component of this.
What is contained in ‘whole’ saliva?
Salivary gland secretions, blood, oral tissues, microorganisms, and food remnants.
What happens if salivary output falls? How much does it have to fall for this to occur?
Xerostomia (dry mouth).
Has to fall below 50% of normal flow.
What are some problems with xerostomia?
Low lubrication -> oral function becomes difficult.
Low (natural) oral hygiene -> poor pH control -> plaque accumulation, opportunistic infection (especially fungal e.g. candida = thrush).
What are the most common causes of xerostomia?
Medication, and irradiation for head/neck cancers.
Which 2 conditions may cause xerostomia?
Cystic fibrosis, or Sjorgens syndrome.
Describe how obstructive salivary gland diseases occur.
Saliva contains calcium and phosphate ions, these can form salivary calculi (stones) that can cause obstructions.
Where is obstructive salivary gland disease most often found?
In submandibular glands (80% cases).
Blocking duct at bend around mylohyoid, or at the exit of the sublingual papillae.
Describe how inflammatory salivary gland diseases occur.
Infection secondary to a blockage.
Which type of disease/illness/infection is mumps?
A viral infection.
Give 4 symptoms of mumps.
- Fever.
- Malaise.
- Swelling of glands (especially parotid).
- Pain especially over the parotid, as the tough capsule does not allow much enlargement.
What is the most common type/cause of salivary gland dysfunction to encounter?
Drug side effects. About 500 prescription drugs have a sympathomimetic effect (reduce salivary flow massively, or completely).
What % of salivary gland tumours (SGTs) are benign? What is the most common benign SGT?
80%. 65% of these are pleomorphic adenomas.
Describe the distribution of SGTs across the different salivary glands?
Parotid = 70% SGTs.
Submandibular = 10%.
Sublingual = less than 1%.
Minor glands = around 20%.
Are sublingual tumours almost always benign or malignant?
Malignant.
Describe the malignancy %s of SGTs in major vs minor glands.
In major glands, 20% = malignant.
In minor glands, 50% = malignant.
What can degenerative salivary gland diseases be a complication of?
Radiotherapy to the head/neck.
Name a degenerative salivary gland disease.
Sjogren’s syndrome.
Which group of people are mainly effected by Sjogren’s syndrome?
Post-menopausal women.
What other condition may be present alongside Sjogren’s syndrome?
Rheumatoid athritis.
Give 5 diseases/problems associated with metabolic problems.
- Diabetes.
- Increased BMI.
- High cholesterol.
- Malnutrition.
- Absorption problems.
How is glucose produced and where in the body?
Breaking down carbohydrates = glucose, occurs in the intestines.
Where and how is glucose transported in the body?
Absorbed into the bloodstream after production, is transported to the liver and various other places such as muscle, the brain, RBCs and adipocytes.
Which hormone takes up glucose into the liver?
Insulin.
What can glucose be stored as in the liver?
Glycogen.
Explain the uses of glucose in the liver.
- Some feeds into Acetyl CoA and Krebs’ cycle, makes energy (ATP).
- Acetyl CoA can also be converted into triglycerides.
- Triglycerides combine with proteins = VLDL (very low density lipoproteins).
Which hormone takes up glucose into muscle?
Insulin.
What can glucose be stored as in muscle?
Glycogen.
Describe the brain’s relationship with glucose.
Needs a constant supply of glucose from the bloodstream in order to have a constant supply of energy.
How is glucose stored in the brain?
It is not, the brain cannot store glucose.
How can glucose produce energy for the brain?
Glucose -> Acetyl CoA -> Krebs’ Cycle -> ATP.
How do RBCs utilise glucose?
To create a source energy, can’t make their own ATP as they have no mitochondria.
Instead, convert glucose -> pyruvate and lactate, which can be used as sources of energy.
Which hormone takes up glucose into adipocytes?
Insulin.
How is glucose utilised in adipocytes?
To produce ATP, or to be converted into triglycerides.
How are amino acids formed and when?
Proteins are digested, then broken down into amino acids, which can then go into the bloodstream.
There is constant backwards/forwards of protein and amino acid production.
What can amino acids be used for?
- Make various compounds.
- Can feed into Kreb’s cycle, and therefore ATP production.
How are triglycerides formed?
Fats taken in through the diet are broken down into triglycerides, which are transported through the bloodstream.
What can triglycerides be used for?
- They are insoluble, so can combine with proteins.
- Different combinations = different molecules, e.g. chylomicron (in the lymphatic system).
Describe what happens to the products of macronutrients during fed state.
Food and macronutrients digested are used as fuels, and oxidised into ATP. Any excess is stored as triglycerides in adipose tissue, or glycogen in the liver and muscle.
When we are not eating, what level needs to be maintained?
Blood glucose level.
How does our body respond to a short fast?
Glycogenolysis.
- If the body needs more glucose, glycogen is broken down back to it, and released into the bloodstream to maintain blood glucose level.
- Glucose mainly goes -> brain and RBCs, which need a constant supply, but also the rest of the body.
- Hormone that does this is glucagon.
How does our body respond to a longer fast?
Gluconeogenesis.
- When glycogen stores are used up, alternative source of glucose is needed.
- Amino acids, lactate fro RBCs, and glycerol from adipose tissue are used. These go to the liver, which uses them to create glucose to release into the bloodstream.
- Mainly for brain and RBCs.
Describe what happens to fats/triglycerides during fasting.
Lipolysis.
- Triglycerides in adipocytes can be broken down -> glycerol.
- Glycerol goes to the liver and is used to make glucose.
- Triglycerides also broken down to fatty acids, which are used by kidneys and muscle.
- Fatty acids can also go to the liver and make ketones, an alternative energy source to glucose.
- Glucagon is the hormone that promotes this process.
How does our body respond to prolonged fasting?
Ketogenesis.
- After 4/5 days = ‘starvation’ state.
- Gluconeogenesis decreased, as do not want to overuse amino acids, or necessary muscles will be broken down.
- Fatty acids still creating ketones, so decreased use of glucose necessary, as there is an alternative energy source for the brain.
- Brain uses ketones, keeps glucose available for RBCs which cannot used ketones.
- Muscle will use less ketones.
Name the 2 main hormones regulating fuel metabolism from the pancreas.
Insulin.
Glucagon.
