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163 Cards in this Set
- Front
- Back
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where are high secretions of H confined to in a healthy patient?
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the stomach and the duodenal bulb
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decsribe the pH in the parts of the GIT
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pH is neutral in the oesophagus, very low (1-2) in the stomach and progressively neutralises through the first, second and third part of the duodenum
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what neutralises gastric acid in the duodenum?
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HCO3: lumenal neutralisation is due mostly to exocrine pancreatic bicarbonate secretion into the second part of the duodenum
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what is mucus in the GIT made up of
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85% water and 15% glycoproteins
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what is mucin glycoprotien? i
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it is a densly glycosylated polymer
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what stimulates mucus production?
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PGE2 and epidermal growth factor
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describe the mucus barrier in the stomach?
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is of a gel nature that determined by the mucins ( the glycosylated proteins). it is an active barrier that is constantly replenishing itself when atacked.
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what are stimulants of gastric mucus secretion
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cephalic: vagal stimulaition --> feel hungry --> stimulates a burst of gastric acid --> this stimulates mucus production
cholinergic agonists prostaglandins some bacterial toxins |
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what are some inhibitors of gastric mucus secretion
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NSAIDs
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where are the secretory cells generated in the gastric lining?
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they are generated at the bottom ad migrate up to secrete mucus and bicarbonate
bicarbonate is actively secreted below the mucus layer |
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what regulates bicarbonate secretion?
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luminal acidification
and is controlled by PGs PGE2 increases stomach HCO3 (EP1 Receptor) and increases HCO3 in the duodenum too (EP3 Receptor) |
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what is the second line barrier to gastric acid?
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the tight junction assembly --> regulation of intracellular pH via the Na/H exchanger and the Na/HCO3 co transporter
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what is a main reason it is critical to maintain the gastric mucosa?
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because there is a rich vascular and lymphatic network just beneath which must be kept in good integrity - once blood flow is comprimised --> inhibit PGs and unable to maintain integrity
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what occurs in the event of damaged gastric mucosal cells?
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gastric pits are stimulated to increase activity when damage occurs --> the cells regenerate here and then migrate rapidly.
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what is the result of an imbalance between attack and defense?
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chronic ulceration or erosion of the mucosa
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what are the two major causes of peptic ulcers?
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H pylori and NSAID abuse.
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non-selective NSAIDs and gastro-duodenal damage
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topic effect --> decrease the hydrophobicity of the gastric mucus
systemic effects --> decrease mucosal synthesis and prostaglandins. prostaglandins stimulate mucus defence. we know this because there is no difference in ulceration between the mouth vs the suppository administration |
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what are the release products of H pylori that may mediate local injury to tissue
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urease - basis of the diagnositc test for h pylori
mucinase - dissolves mucus by degrading glycoproteins shape and flagella phospholipase: damages epithelial cells mucus cytokines: causes mucosal injury, influences an inflam response platelet activating factor |
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what is Zollinger-Ellison syndrome
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a rare hypersecretory disorder - causes severe peptic ulcer disease in many patients
non-beta islet cell tumours of the pancreas: uncontrolled secretion of gastrin = gastrinoma |
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what is a common morbidity in Zollinger-Ellison syndrome?
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about 1/4 have multibple endocrine neoplasm syndrome (MENI) - tumours of the parathyroid, pituitary and pancreatic islet cells
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name some anti acid medications for peptic ulcer symptom treatment?
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neutralise H with: H2 blockers, PPI and prostaglandins of E class
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what percentage of people with H pylori infection get active active chronic gastritis
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100%
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what is the neuro-endocrine regulation of acid secretion?
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gastric parietal cells have receptors for:
acetylcholine (incerase) gastrin (increase) histamine (increase) somatostatin (decrease) |
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t/f. NOT ALL gastric acid is secreted by gastric parietal cells.
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false. all gastric acid is secreted by gastric parietal cells. there are no other cells that secrete gastric acid
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what are D cells
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they are cells which are somatostatin secreting cells which act to turn off the gastric acid secretion of parietal cells
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what is an example of an H2R antagonist
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cimitidine, panitidine, famotidine
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what is the role of CN X in gastric acid?
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CN X has parasympathetic signaling that plays a large role in gastric acid secretion
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what is the effect of proton pump inhibitors in the treatment of gastric ulcers?
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"azole"
they block the final common athway of gastric acid secretion H/K ATPase on gastric parietal cells. They bind to a pore that takes K from the lumen they covalently bind to the proton pump |
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list the common drug combinations for treatment of H. pylori?
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bismuth, amoxicillinn and metronidaloze
PPI, amocicillin and metronidazole PPI, amoxicillin and clarithromycin |
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what is the first line therapy for h pylori as recommended by the therapeutical guidelines
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7 day course of OAC or EAC (O and E are PPI)
in patients who report penecillin allergy OMC or EMC |
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how many people worldwide use NSAIDs every day?
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~30million
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what percentage of NSAIDs are used by people over the age of 60 years
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40%
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GORD?
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very ommon - around 60% of people have had an experience of the symptoms of GORD and around 20% have weekly symptoms
defined as heart burn or acid regurgitation - the degreee of aosphagitis does not correlate to the degree of symptoms |
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what is the best treatment of GORD?
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Ometrazole
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what are some symptoms of Zollinger-Ellison syndrome?
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ulcers extending beyond the first 2 parts of the duodenum
weight loss diarrhoea high serum gastrin |
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what are the broad complications of peptic ulcer?
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bleeding
perforation penetration stenosis (because crhonic disease causes fibrosis - this is so rare!) |
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what is the treatment for a bleeding complication of a peptic ulcer?
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fluid rescusitation and diagnostic endoscopy -
injection of 1/1000 adrenalin or salin around the bleeding point tampenading the vessel with the tissue pressure PPI are used then to prevent a rebleed |
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what is a perforation: as a complication of gastric ulcer?
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erosion through the wall in the duodenum - that means it will be the anterior wall because the duodenum is predominately a retro peritoneal structure.
usually only a small hole 1-2 mm |
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what is the mamnagement of a gastri performation?
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Dx will be CXR seeing gas under the diaphragm on the RIGHT
require braod spectrum antibiotics |
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what is a penetration complication in peptic ulcer?
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erosion to an adjacent organ
pancreas liver colon --> causing a fistula which will reuslt in MASSIVE weight loss like 10kgs over 2 weeks |
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the lower esophageal sphincter receives what innervations?
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excitatory cholinergic innervations
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what occurs during swallowing to the sphincter at the esophagus?
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there is non-adrenergic, non-cholinergic inhibition so that the sphincter relaxes
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when food arrives in the stomach the receptors are stimulated via?
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a vago-vagal reflex - smooth muscle of the proximal stomach relaxes.
and peristaltic comtractions develop in the distal stomach within minutes |
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what can pass the pylorus?
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only liquid and particles <2mm can pass - as they do pass duodenal chemo receptors prompt chime passing
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what can trigger vomitting (emesis)
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stimulation of mechanoreceptors in the mucosa of the stomach wall and duodenum
stimulation of chemo receptors stimulation of mechanoreceptors at the back of the throat by touch stimulatin of the area postrema in the medulla |
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what do chief cells secrete in the stomach?
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pepsinogen I
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what is the effect of h pylori on parietal cell secretions?
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chronic infection --> increase in basal and stimulated acid out [put e.g. the peak acid output after gastrin releasing peptide is up to 3 times
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what is intrinsic factor?
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a glycoprotein assisting in B12 absorption
secreted under the same stimulatory conditions as HCl but response is NOT linked to asic suppresion |
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describe the stimulation and inhibition of gastrin secretion?
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released from G cells by the presence of food in the stomach and release of gastric releasing peptide.
Somatostatin (D cells) inhibits gastrin secretion |
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what is the effect of H pylori on gastrin?
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disinhibition of gastrin production that is secondary to decreased somatostatin release
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what is histamine
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a major paracrine stimulator of acid secretion - in mucosal mast cells and enterchrmaffin like cells (ECL cells)
gastrin is the primary stimulus for histamine release stimuliated ECL cells degranulate and relaese histamine and pancreastatin from the vesicles |
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describe basal acid output?
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it is unstimulated acid secretion that has a cirrcadian variation, increased at night and low in the morning. this varies and does not correlate with serum gastrin weill.
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what are the three phases of food stimulated acid secretion?
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Cephalic phase - thought sight and smell
Gastric phase - when the food reaches the stomach intestinal phase - entry of chime into small intestines |
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tolerance and acid rebound?
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tolerance to H2Rantagonists develops after as few as 7 days and may contribute to poor clinical response in some patients with ulcer or GORD
Rebound acid hypersecretion occurs after cessation of 1-9months of therapy - this is more common in patients who do not have H pyroli |
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causes of upper GI bleeding?
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duodenal/gastric ulcer
varices mallory-weiss tear |
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what are the two enzymes produced in the mouth that may be relevant to digestion?
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salivary amylase
salivary lipase |
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what are the types of fat in our diet?
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triglycerides (95%)
phospholipids cholesterol |
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what happens to a triglyceride in the duodenum?
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the hydrophosphate part of bile acids come into contact with the TG so that lipase can not get in ocntact with the TG. Co-lipase is a smaller molcuse that can interdigitate between the bile acids and attracts lipase.
another molecule interfering with the process is phosphatidyl choline which repels co-lipase --> so PLA2 is added to make the phospholipid soluble allowing co-lipase back in. |
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what are the two important molecules in mycelles and the two important enzymes
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hydrophosphate of bile salts. and phosphatidyl choline
and lipase and co-lipase. |
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what is the definition of fat malabsorption
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in a 3-5day fat balance study the measured faecal fat is >7% of fat digestion.
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what is main mechanisms of fat malabsorption?
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pancreatic insufficiency causing problems with the hydrolysis of fat
a bile acid defficiency such as in cholestatic liver disease --> inadequate mcelle solubilisation of impaired mucosal absorption of fat e.g. coeliac disease |
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what is the percentage of fat malbsorption in coeliac disease?
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10-40%
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in coeliac disease what will you see in the stools?
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microscopically there will be fatty acid crystals
there will not be oil droplets because the pancrease works and does digest the lipids |
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what are some classic signs of coeliac disease?
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distended abdomen
creases on inner thigh gluteus muscles will be flat and wasting |
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what do you see in the intestines of coeliac disease?
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there is villous atrophy and crypt cells are hyperplastic to replace the destroyed villi between the epithelial cells and so called intraepithelial lymphocytes
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what is anderson's disease?
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autosomal recessive due to a mutation in SARA2 which encodes sas1b protein ribosylation factiof family of small guanosine triphosphates - role in IC traficking of fat through the golgi apparatus
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consequences of fat malabsorption?
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diarrhoae
colonic fermetation bile acid malabsorption decreased secretion of bile acid - gall stones decrease in enrgy --> wasting and stunting vitamin A, D, E, K deficiencies Vitamin A def --> impaired adaptation to dark and xeophthalmia D --> rickets K --> coagulopathies E -> haemolytic anaemia in infants |
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what is Colycystekinin
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CCK stinulates enzyme secretion from the pancrease.
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what is secretin
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it causes HCO3 production form the pancreas to neutralise the acidfrom the stomach
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what is trypsinogen?
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released into the duodenum --> has to be activated here by an enzyme that comes from the brush border call "enteropeptidase" which cleaves off the terminal part of the trypsinogen to form the active trypsin which then hydrolyses itself.
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what is a primary protein losing enteropathy?
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it is gut related if it is primary; examples include
hypertrophic gastritis H pylori coeliac disease IBD eosinophilic gastroenteritis |
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what is a secondary protein losing enteropathy?
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an example might be cardia - constrictive pericarditis, TB or autoimmune
also couls be caused by liver disease or lymphatic obstruction and lymphoma |
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what is the consequence of failure to absorb lactose?
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osmotic diarrhoea
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what is the commonest cause of am osmotic diarrhoea?
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rotavirus
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if this osmotic gap is >100 what does this imply?
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that Na is <50 and this will causes an osmotic diarrhoea
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if the osmotic gap is < 100 what does this imply?
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that Na is >70 and this causes a secretory diarrhoea
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failure to digest and absorb carbohydrates causes what kind of diarroea?
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osmotic
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what is the result of colonic fermentation of the unabsorbed carbohydrates
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production of H2 CH4, gaseous distension and flatulence
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what is osmotic diarrhoea?
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a diarrhoea that drags fluid into the lumen of the gut: causes incude malabsorption, lactose intolerance and laxatives
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what is secretory diarrhoea?
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the net secretion or loss is greater than the absorption - this is caused by infection or IBD
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what genetic factors are involved in coeliac disease?
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HLA DQ 2 and 8
2 is present in 90% and 8 accounts for the other 10% however DQ2 is popular in the population and only 1/30 who is positive for it has coeliac disease |
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t/f. 5% of coeliacs presents with IgA deficiency
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true
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what is Ulcerative colitis
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in the colon only; the rectum is always involved
it is a superficial inflammation - mucosa ONLY affecting the vasculature of the colon |
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what is IBD
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is ulcerative colitis and crohn's disease
may be due to an inappropriate immune response to intestinal bacteria in a genetically susceptible host. |
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what is Crohn's disease
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any part of the GIT may be affected but mostly in the ileum and colon
is a transmural inflammation - cobblestone appearance of deep linear ulcers |
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what are some management options for crohn's disease
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5-aminosalicyclic acid --> sulphasaline, musalazine
imunosuppresants -> methotrxate surgery - resection |
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what is the expcrine component of the pancreas?
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95% of it is and consists of ducts of acini and droduces 2L of pancreatic juices a day
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how much pancreatic juice is produced each day?
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2L
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what is Acinar secretion from the pancreas?
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it is an isotonic NaCl rich fluid with a wide range of proteins
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what is the mechanism of secretion of acini ducts
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relies upon uptake of Cl from the blood into cytoplasm driven by Na dependancy transporters at the basolateral membrane
na flows passively through tight junction sand paracellular spaces |
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what precursors do acini cells secrete
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trypsinogen
chymotrypsinogen protease E proelestase kallikreinogen |
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what are the enzymes secreted by the acini cells
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exopeptidase - procarboxypeptidase A/B
lypolitic enzyme precursors - pro-pancreatic phospholipase A(2) lipolytic enzymes - pancreatic lipase and non-specific carboxypeptidase |
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where are the precursors released by the pancrease activated?
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in the gut lumen
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what do duct cells secrete?
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NaHCO3 rich fluid and low amounts of micro proteins - the mechanism is probably due to HCO3 concentration in the cytosol due to NaH exchanger
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how much pancrease function must be lost before there is clinical evidence of dysfunction
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up to 90% can be resected with normal function preserved
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what are some congenital conditions causing pancreatic insufficiency
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cystic fibrosis
schwachman syndrome congenital tryipsinogen deficiency |
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what will a patient with pancreatic insufficiency present with?
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diarrhoea and fatty stools --> will have undigested triglycerides confirmed with a fat soluble dye.
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how are carbohydrates digested?
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pancreatic amylase digests starch --> to maltose, maltorose and alpha-limit dexrins which contain alpha-1, 6 bonds that cannot be attacked by amylase
further digestion requires brush border enzymes dietary fibres can not be digested they reach the large bowel in tact where they are fermented by the colon muco-flora releasing short fatty chain acids |
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how is protein digested?
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intiially by endo-peptidase pepsin secreted by duct cells of the gastric mucosa
pepsinogen is converted to pepsin in low pH and small intestine protein is degraded |
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how are carbohydrate absorbed?
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Na glucose transporter SGLT1 transports glucose and galactose across the apical membrane of the small intestine villous cells.
fructose transported by the glucose transporter GLUT5 - this is passive and not coupled with an ion or sing ATP |
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how s protein absorbed in the gut
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there are lots of transporters moving amino acids across the apical membrane
inside the cell peptides are broken down by cytosolic hydrolase to aa's the basolateral membrane of the cell contains ~5 amino acid transfer systems 2 are Na dependent |
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t/f. a gluten free diet is <1mg of gluten a day.
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false. a gluten free diet is around 30 mg/day compared with a normal diet which is 1000-1400 mg
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what is the treatment for pancreatic disease?
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in the pancreatic enzyme is replaced - the dosage must be individual and adjusted to fat intake
a PPI may also help reduce enzyme destruction there may be some malabsorption of minerals (Ca, Zn, Mg) which need replacing. |
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t/f. if greater than 100cm of ileum is removed malabsorption is expected.
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true. B12 is required in ileal supplementation
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what is lactose
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a disaccharide in nearly all mammalian milks
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what is necessary for lactose to be absorbed by the gut?
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it must be hydrolysed to galatose and glucose by the enzyme lactase.
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where is lactose expressed
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in the brush border villous epithelial cells
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what are hepatocytes?
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epithelial cells with basolateral and apical membranes, they have a avariety of secretory and metabolic functions
60% of the liver |
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what are kupfer cells
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make up 25% of the liver - are the reticuloendothelial cells and they phagocytose particles, organisms, cell debris, tumours cells all coming from the GIT
they also endocytose immune complexes and endotoxins they are involved in antigen processing and presentation so they have immune functions - they produce REDOX species used in defence of the ody against tumour cells/ microorganisms and other |
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describe the endothelial cells of the liver
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tey make up 10% of the liver cells.
they do NOT form a continueous endotelium they are fenestrated, leaving gaps between the end cells - the reason being the fenestrations allow albumin and large proteins to move between the cells and the blood stream they also synthesize factor VII |
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t/f. unlike most capillaries of the body, the liver is permeable to protein.
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true
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describe the fat storage cells of the liver
|
ITO cells or pit cells, they make up around 5% - they are the rpincile store of vitamin A
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what is the response of ITO cells in the liver to tissue damage?
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they become contracilie and secrete collagen and play a key role in the processes that lead to cirrhosis
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what role does the liver play in protein synthesis?
|
it produces albumin.
also produces all proteins involved in clotting except VIII and produces transport proteins transferrin, TH-binding globulin and sex steroid binding globulins |
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what is vitamin A
|
retinol
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what is the role of the liver in carboydrate metabolism?
|
the liver is the regulator of glucose levels.
glucose is taken up into the hepatocyte via GLUT2 - inside the cell glucokinase and gluco-G-phosylase convert glucose to glucose-6-phositate which is membrane impermeable so that glucose concentration inside the cell actually depends in the balance of the two reactions |
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what happens to the hepatocyte when there is a large load of nutrients and and energy from the gut?
|
the hepatocyte swells
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once glucose is trapped in the cell there are three places it can go?
|
converted to pyruvate --> Ach A which can become energy in the TCA cycle or can become fatty acids
or Ach A can become acetoacetate which geerates ketone bodies or converted to aa's |
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t/f. in the presence of increasein circulating glucose the predominant pathway end in glycogon, AAs, pyruvate
|
true
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what does the liver convert ammonium to?
|
urea
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in a case of acidosis what does the liver do to compensate?
|
switches off urea production to save HCO3
and produces glutamine from glutamate and ammoninum |
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what does the liver do wit cholesterol?
|
secretes it into the bile
bile salts are produced from cholestero |
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describe the histology of the liver
|
there is a central venule and then the triad consisting of the hepatic arteriole, bile duct and portal vein that arranged haxagonally around the central venule
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describe the acinar zone 1?
|
it is highly oxygenated and is involved in
amino acid catabolism gluconeogenesis cholesterol synthesis urea produciton bile salt secretion oxidative metabolism |
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describe the zone 3 in the liver?
|
it is close to the central venule and this is very oxygen depleted
it is involved in: glycolysis glycogen synthesis liponeogenesis bile salt production ketogenesis bile acid independent bile production biotransformation of drugs. |
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describe ketoneogenesis?
|
when glucose levels are limited. high levels of glucagon result to rpoduce glucose from amino acids, and from muscle protein.
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what is bile
|
essentially isotonic NA-bicarbonate
|
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what are the consitituents of bile
|
salts
bilirubin cholesterol phospholipisd Cu |
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what is the function of bile
|
it has a detergent function critical for the digestion of fats
|
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what are the primary bile acids
|
cholic acid
chenodeoxycholic acid |
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what are the secondary bile acids
|
they are transformations of the primary acids
deoxycholic acid lithocholic acid |
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how much bile acid do hepatocytes make a day?
|
600mg
|
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how much bile acid do we use a day?
|
2-3grams for a meal = 12-15 across the day.
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how does the body reuse bile saits?
|
via the entrohepatic recirculation mechanism
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what is the pat of bile salts
|
secreted by hepatocytes into canaliculi
from down the bile duct into the duodenum they move thorugh the gut to the ileum where they are reabsorbed in the ileum by a specific transported called Na bile salt protein |
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what is Na bile salt protein
|
the transporter in the ileum that reabsorbes bile salts in the entrhepatic circulation.
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bile salt indendent production involves what?
|
the break down product, bilirubin which when conjugated becomes water soluble and is a good detergent
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what are the 3 phases of xenobiotic transformation
|
phase 1: usually redox involving p450
phase 2 conjugation phase 3 secretion |
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what are some mechanisms that protect the liver from toxic injury?
|
richly endowed with enzymes concermed with biotransformation
cytochrome p450 is a key component --> very adaptable system |
|
|
what is the histological progression of liver injury
|
enzyme abnormalities --> necrosis -> steatohepatitis --> fibrosis --> cirrhosis --> vascular sinusoidal injury
|
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what do sulphonamides do to the liver
|
they can cause severe drug induced liver disease - although this is very rare.
|
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what is the most common toxic liver injury
|
drug induced hepatitis
accounts for ~5% of hepatitis in the community |
|
|
which drugs can cause injury to the liver?
|
Anti-TB
chlorpromazine valproic acid NSAIDs flucoxicyllin/arethromycin |
|
|
what are some dose dependent toxins to the liver?
|
EtOH
paracetamol metals cytotoxic drugs like radiotherapy carbon tetrachloride ciflatoxin |
|
|
what is the mechanism of alcohol injury to the liver
|
alcohol induces CYP2E1 which causes oxidative stress which is also relevant to paracetamol
|
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paracetamol toxicity
|
no more than 16 tablets in a day is the new recomendation
risk factor fo OD are: chronic alcohol, dilantin fasting male the two CYP enzymes involved in the pathway are 2E1 and 3A4 so note 2E1 in an alcoholic 4 tablets can be toxic! |
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t/f. the OCP induces cholestasis
|
true; but require a genetic predisposition
|
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|
pathology of cirrhosis
|
characterised by fibrous bands of tissue surrounding nodules of preserved hapatocytes
the hepatocytes lose their relationship with the surrounding extracellular matrix there is loss of acinar zonation and the nodules no longer possess a central venule |
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alcoholic liver diseased is associated with which inflammatory inflitrate?
|
with a neutrophilic inflammatory infiltrate and pericellular fibrosis
|
|
|
describe the virology of the Hep B
|
the virus is 40nm with an outer surface and an inner core
it is double stranded DNA replication occurs in the hepatocyte but also in salivary glands, pacreas and teses |
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how does hep B act in the cell
|
DNA P is activated and completes a circularisation of the genomic DNA which becomes like a mini-chromosome beside the host chromosomes
|
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|
what does the presence of Hep B antigen in the serum indicate?
|
that there is active virus synthesis occuring in the liver - however ~25% of HBV strains have a mutuation preventing HBe
|
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|
how is HBV transmitted?
|
via maternal and parenteral methods very efficiently
sexual transmission is also efficient - saliva is LOW |
|
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t/f. hep B is is 50-100 times more infectious than HIV
|
true
|
|
|
is there a vaccination for HBV
|
yes. recombinant HBs antigen is VERY effective
|
|
|
what are the 4 distinct phases of the HBV infection
|
1. immune tolerance phase
2. immune clearance phase (may spontaneously convert from HBeAg+ to HBeAg- with the develpment of antibodies 3. immune control phase: normal with normal liver enzymes 4. some patients progress to the immune escape phase with chronic hep --> liver disease |
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|
what is the aim of treatment in hepB?
|
prolongued suppression of the viral replication
|
|
|
serum ALT
|
greater than 10 x normal indicates hepatocellular necrosis
ALT>AST but an exception is alcoholic liver disease and cirrhosis |
|
|
GGT
|
present on the hepatocyte plasma membrane
is a biliary enzyme because cholestasis is a common cause for it to be raised |
|
|
serum bilirubin concentrations indicate?
|
may be raised due to increased production, impaired hepatic uptake and conjugation or impaired bile secretion
|
|
|
If the bilirubin is unconjugated?
|
this implies liver disease cause as the liver is unable to conjugate
|
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What is Gilbert's syndrome?
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commonest cause of mild unconjugated hyperbilirubinaemia and is confirmed by genetic testing
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Injury in the liver activates what?
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hepatic stellate cells which increase the extracellular matrix and cause tissue re-modelling
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