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Sc08 vera's blood vomiting
Sc08 vera's blood vomiting
Sc08 vera's blood vomiting
Sc08 vera's blood vomiting
Sc08 vera's blood vomiting
Sc08 vera's blood vomiting
Sc08 vera's blood vomiting
Sc08 vera's blood vomiting
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Sc08 vera's blood vomiting

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  • 1. Veraʼs Blood VomitingScenario Introduction1. What are haematemesis and melaena?12. What are the most common sites/causes of blood loss in upper GI bleeding?23. What symptoms would you normally try to correct in a patient presenting with an acuteupper GI bleed before endoscopy?3Histology of the GI Tract1. What are the four basic layers of organisation present throughout the entire GI tract?42. What are the main functions of muscularis mucosae and muscularis externa?53. What is the enteric nervous system, name the two main plexuses of this nervoussystem?64. Describe the structure of the oesophagus in terms of layers and glands?75. What are the names for the top part of the stomach (usually full of air) and the bottom?86. What is the function of a gastric pit and the gastric glands within it?97. What are the characteristics of parietal cells in gastric pits?101 Haematemesis = vomiting blood and melaena = passage of black, tarry stools2 gastric ulcer, duodenal ulcer, gastritis, duodentitis, erosions3 tachycardia (high pulse rate) and hypotension by a blood transfusion4 Mucosa (epithelium, lamina propria, muscularis mucosae), Submucosa, Muscularis externa, Adventitia(outermost connective tissue surrounding any organ)5 Muscularis mucosae = local control of the mucosa, Muscularis externa = peristalsis of gut contents6 Enteric nervous system = the intrinsic nervous system which innervates the GI tract. Works of its ownaccord without any direct connection to brain function. Submucosal/Meissnerʼs plexus (control of muscularismucosae) and the Myenteric (Auerbachʼs) plexus which controls peristalsis7 Stratified squamous epithelium (protective), skeletal muscle at top (swallowing) and mixed smooth muscleat bottom, submucosal glands for generating lubricant8 Top = fundus, bottom = pylorus9 Gastric pits house gastric glands whose function is to secrete gastric juice (HCl, pepsinogen and mucus)10 Abundant mitochondria (40% cell volume), intracellular canaliculi (deep foldings which serve to increasethe surface area e.g. for secretion), extensive microvilli, tubulovesicular system
  • 2. 8. How do surface epithelial cells prevent the GI system from ʻdigesting itselfʼ?119. What is the main function of Brunnerʼs glands in the duodenum (first part of smallintestine responsible for digestion and absorption)?1210.What are the three additional features found in the jejunum and ileum (absorbtion partsof the small intestine) which are not found in the duodenum?1311.What are two features other than high surface area which enable villi to absorb food?1412.Why does the epithelium of the small intestine contain ʻcryptsʼ containing with stemcells?1513.What is the main function of the colon?1614.What abrupt histological change occurs at the ano-rectal junction?17Pharmacology of the Gut1. What is a peptic ulcer?182. List the complications of a peptic ulcer193. What substances are secreted by (i) parietal cells, (ii) chief cells2011 Secrete bicarbonate ions to establish a neutral pH in the mucus layer, gastric glands secrete HCl whichwould reach the epithelial lining if not buffered. Below pH4 HCl cannot penetrate the mucus layer at all.12 Production of alkaline mucus in the duodenum13 Plica circulares (large valvular flaps projecting into lumen, slow the passage of food along the intestine andincrease surface area for reabsorbtion), microvilli and Peyerʼs patches (lymphoid nodules which facilitateimmune surveillance and response within the mucosa)14 Richly vascularised for absorbtion, contain lacteals (lymphatics) which take away fat molecules which areto large to freely travel in blood15 Stem cells generate transit amplifying cells which divide very rapidly since cells in the intestine need to bereplenished very frequently due to harsh environment.16 Reabsorbtion of water17 Abrupt transition from simple columnar to stratified squamous epithelium18 Chronic, usually solitary lesion in any area of the GI tract exposed to acid/peptic juices. Although 99% ofthese are in the duodenum or the stomach and are more common in men19 Penetration: ulcer burrows into the pancreas or liver and leads to organ failure. Perforation: ulcer opensinto peritoneal cavity. Upper GI bleeding: ulcer erodes into artery (e.g. in stomach, and bleeding causesblood vomiting (6-10% mortality).20 parietal cells = HCl (gastric acid) & gastrin stimulated by M3 receptor stimulation and histamine which actsby increasing intracellular cAMP. Chief cells = pepsinogen (for protein digestion), chymosin and gastriclipase enzyme (fat digestion)
  • 3. 4. Which cells are found (i) at the top of the gastric pit, (ii) which in the isthmus and neck ofthe oxyntic gland (further down) and (iii) which at the base of the oxyntic gland?215. List the theories of peptic ulcer development/risk factors?226. What is the difference between the main cause of a gastric ulcer vs. a duodenal ulcer?237. Whereabouts in the epithelium does Helicobacter pylori settle?248. How does Helicobacter pylori protect itself from gastric acid?259. What changes occur in the intestinal mucosa in the case of chronic gastritis?2610.What are the ʻ4 layersʼ characteristic of gastric ulceration?2711.What 2 substances directly stimulate mast cells to release histamine, the signal forHCL secretion in the GI tract2812.What is the effect of PGE2 (prostaglandin) on release of substances into the gastriclumen?2913.What pump/channel is ultimately responsible for the secretion of HCl from parietal cellsinto the lumen?3014.Name on example of a proton pump inhibitor and explain its effect on the gastriclumen3121 Gastic pit = surface mucosal cells, Isthmus = mucuous neck cells and parietal cells, Base = chief cells22 Acid hyper-secretion only in Zollinger-Ellison syndrome (gastrin producing tumour), psychosomatic (stressrelated), smoking (interferes with healing/smokers need 2x vitamin C), Non-steroidal anti inflammatory drugs(due to prostaglandins and role in mucosal defence), Helicobactor pylori (main cause)23 Gastric = due to H pylori infection of gastric corpus causing defective mucosa, Duodenal = increasedsecretion of acid or pepsin in pyloris (usually due to H.pylori infection), causes metaplasia (replacement ofone cell type with another) in duodenum which can be infected by H.pylori.24 On surface of epithelial cells beneath the layer of mucus.25 Secretes a urease enzyme which converts urea into ammonia and CO2 thus protecting itself from gastricacid because ammonia is a buffer. H pylori can be measured by drinking urea and then measuring the levelof CO2 in breath, which will be higher if H.pylori is present.26 Atrophy, intestinal metaplasia, lymphoid aggregates, neutrophil inflitrates27 Necrotic debris (lumenal side), inflammatory layer, granulation tissue, fibrous scar (in submucosa?)28 Acetylcholine and gastrin (which both also directly stimulate HCl secretion themselves29 Stimulates HCO3-, mucus and HCl- secretion30 H+/K+ATPase31 Omeprazole (proton pump inhibitor) - inactive at neutral pH so does not affect other areas of the body.Converted to sulfenamide at pH 3 or lower. HCl secretion only happens via H+/K+ ATPase so blocking thisblocks all HCL secretion irreversibly.
  • 4. 15.Name on example of an H2 receptor blocker and explain its effect on the gastriclumen3216.What is the effect of bismuth chelate?3317.What are the effects of sucrafate?3418.Give one example of an antacid?3519.What are the potential side effects of antacids?3620.Why would you give misoprostil?3721.What would you give to someone:(i) with H.pylori 38(ii) with a non steroidal anti inflammatory drug induced peptic ulcer 3922. What antimicrobial treatment (to kill H pylori) would typically be given with:(i) Clarithromycin40(ii)Bismuth (as 2nd line treatment)41Motility of the Gut1.Is GI muscle single unit or multi unit smooth muscle?4232 Cimetidine, ranitidine or famotidine - reduces acid secretion by blocking parietal cell H2 receptors. Sideeffect: can slow the metabolism of some drugs such as warfarin33 This is a treatment used to enhance mucosal protection, coats the ulcer and stimulates secretion ofmucus, prostaglandins and HCO3-. Adverse effects are nausea & vomiting and can cause impaired renalfunction if accumulates. Generally more effective treatment than cimetidine.34 Main use is for stress ulcers. -ve Sulphated sucrose binds to hydrochloric acid and forms a viscousadhesive which binds to +ve groups in the ulcer crater. Buffers acid and stimulates secretion of mucus,prostaglandins and bicarbonate. Reduces number and adherence of H.pylori.35 Sodium Bicarbonate, Magnesium Carbonate, Aluminium Hydroxide36 Constipation (Aluminium Salts), diarrhoea (Magnesium Salts) so are combined to offset these37 Taken with non-steroidal anti inflammatory drugs to reduce their negative effect on prostaglandins andmucosa. Adverse effects: diarrhoea and abdominal cramps so avoid in pregnancy.38 Antibacterial (to kill the H.pylori) plus proton pump or H2 receptor antagonists to reduce acid secretion39 Change the type of NSAID (e.g. cyclo-oxygenase 2-selective NSAID) and give misoprostil (increasePGE2), maintain treatment with proton pump inhibitor40 Amoxicillin or metronidazole and PPI41 Metronidazole AND tetracycline and PPI42 Single - the visceral smooth muscle has gap junctions that couple the cells and act as a single unit.
  • 5. 2. What mechanism operates in smooth muscle to reduce the use of ATP?433. How are actin and myosin arrangements structured differently in smooth musclecompared to striated?444. What does it mean to have a ʻpacemakerʼ of the GI tract?455. Which cells act as pacemakers in the GI tract?466. What are the 3 layers of muscle in the stomach?477. In which part of the stomach does the most vigorous peristalsis occur?488. What substances stimulate (i) excitatory (ii) inhibitory fibres of the GI smooth muscle?499. What is the term used to describe smooth muscle when it is able to function over a widerange of lengths (e.g. stomach maintaining same pressure with varying volume of foodingested)?5010.Which part of the GI tract has the fastest rate of spontaneous activity?5111.What would the relative speed of digestion differ for (i) fat-laden chyme (ii)carbohydrate rich chyme?5212.What are the immediate effects of: (i) Secretin (ii) Cholecystokinin (iii) Gastric inhibitorypeptide (iv) Motilin5313.What is the difference between ʻshort reflexesʻ and ʻlong reflexesʻ in terms of gastricactivity?5443 The latch bridge mechanism44 Not arranged in rows like striated muscle45 Bioelectrical slow wave potential that leads to contraction of the smooth muscle down the GI tract to churnand move boluses of chyme. Dependent on hormone activity, enteric nervous system, autonomic nervoussystem.46 Interstitial cells of Cajal47 Longitudinal muscle layer, circular muscle layer, oblique muscle layer overlying mucosa48 The pyloric antrum and pyloric canal49 Excitatory fibres (acetylcholine), Inhibitory (vasoactive intestinal peptide, ADP, noradrenaline)50 plasticity51 Duodenum (about 13 contractions per minute)52 Fat rich chyme is digested slower causing food to remain in the stomach for longer53 1/ Secretin = stimulates HCO3- secretion and inhibits stomach activity, 2/ CCK - stimulates gallbladder tosecrete bile, inhibits stomach activity, 3/ Gastric inhibitory peptide = inhibits gastric contractions, 4/Motilinincreases gastric and intestinal motility54 Short reflexes = Enteric nervous system, Long reflexes = Autonomic nervous activity
  • 6. 14.What are the key differences between the myenteric and submucosal plexuses of theenteric nervous system?5515.List the peptide, amino acid and biogenic amine substances that could be described asenteric nervous system neurotransmitters?5616.What are the effects of gastrin and cholecystokinin on motility of different parts of thestomach?5717.What is the migrating motor complex?5818.Are enteric nervous ganglia myelinated or unmyelinated?59Salivary, Gastric and Pancreatic Secretions1. What causes the activation of pancreatic enzymes such as pepsinogen?602. What is the main danger when a peptic ulcer penetrates the pancreas?613. What is the function of bile salts?624. List all 3 salivary glands in the buccal cavity635. What is the effect of parasympathetic stimulation to the salivary glands6455 Myenteric = regulation of smooth muscle contraction (either acetylcholine/excitatory or vasoactiveintestinal peptide/inhibitory). Submucosal = regulation of endocrine and exocrine secretion (both Ach andVIP are excitatory).56 Substance P, CCK, VIP, gastrin, somatostatin, GABA, adrenaline, serotonin, histamine, serotonin, Ach,dopamine57 Gastrin and cholesystokinin act to relax the proximal stomach (fundus, cardia) and enhance contraction inthe distal stomach (pyloris), this has the net effect of decreasing the rate of stomach emptying.58 ʻHousekeepingʼ current of motor activity that propagates through GI tract between meals to removeresidual undigested material.59 Unmyelinated - they do not originate in the CNS60 Acid environment (lower than pH3) on entry into the lumen61 Pancreatic enzymes get activated by acid from the peptic ulcer and are activated en-masse and begin todigest the bodyʼs own tissues.62 Allow emulsification of fats, meaning fats can be absorbed into the intestinal wall and lymph/blood63 parotid, sublingual, submandibular64 Increased blood flow resulting in increased saliva secretion (fluid and electrolyte flux) across fenestratedepithelium into salivary ducts
  • 7. 6. What is ʻatropine resistant vasodilationʼ?657. What starch degrading enzyme does saliva contain?668. What is the name of the cells that secrete saliva?679. What happens to saliva to change its chemical makeup as it travels down the salivaryduct?6810.What is blood plasma concentration of sodium?6911.As the rate of saliva flow increases, what happens to the chemical change in (9)?7012.What is intrinsic factor?7113.Out of gastrin and pepsinogen which is exocrine and which is endocrine?7214.Describe the HCO3- buffering mechanism in the small intestine7315.What is the histological difference between an active parietal cell and a passive one?7416.What substances activate parietal cells directly (to secrete HCl)?7517.Which cells produce gastrin?7665 Atropine usually inhibits parasympathetic function. Atropine resistant vasodilation is where an area of thebody resists the effect of atropine, continuing to vasodilate at all times, this is true of the salivary glands. Sowhilst the secretion of saliva may be inhibited by atropine, the increased blood flow may not be.66 Amylase67 Acinar cells68 It is isotonic when secreted in the acinar cells, however at it travels down the duct sodium and electrolytesare reabsorbed back into the bloodstream, so the end product is hypotonic saliva69 143mmol70 As saliva flow increases, less electrolytes can be reabsorbed by the salivary duct so the electrolyteconcentration in the saliva (end product) goes up, although it is still hypotonic.71 A glycoprotein produced by the parietal cells which is necesscary for the absorbtion of vitamin B1272 Pepsinogen = secreted into lumen of intestine/stomach (exocrine), gastrin = secreted into blood(endocrine) to stimulate release histamine which acts on H2 receptors to stimulate release of HCL fromparietal cells.73 HCO3- pumped out of parietal cells and into bloodstream after being formed by the H+/K+ ATPase fromcarbonic acid. HCO3- exits bloodstream (via fenestrated capillaries) into gut lumen where it buffers the acidicsolution74 At rest parietal cells have underdeveloped tubular vesicles, when activated these vesicles become muchmore prominent and developed.75 gastrin, acetylcholine or histamine76 G-cells (endocrine cells) in gastric glands.
  • 8. 18.Describe the mechanism by which gastrin acts to stimulate release of HCl?7719.What does omeprazole do?7820.What stimulates the release of somatostatin and what does it do?7921.Why are increased circulating levels of gastrin undesirable?8022.Why does omeprazole act irreversibly?8177 Gastrin produced in endocrine cells, secreted into the bloodstream, releases CCK, which acts on ECLcells to release histamine, histamine picked up by H2 receptors on parietal cells which release gastrin. CCKcan also stimulate parietal cells directly78 Irreversibly blocks H+ pump in parietal cells (so they do not secrete HCl). This does not however stop thebuildup of gastrin.79 A negative feedback mechanism. Release is stimulated by acid in the lumen and somatostatin acts toprevent G-cells releasing any more gastrin so inhibiting HCl release.80 Can cause damage to the brain and carcinoma81 Forms a disulphide link with H+/K+ ATPase (H+ going out, K+ going in).

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