Lecture 8 Flashcards
What is the role of the GI System?
- break down large molecules in food = proteins, fats, carbs into simpler molecules to be used by body = digestion
- MATABOLISM breaks down molecules => energy
- undigested material will pass through GI tract and is excreted as faeces
*What are the major disease states associated with the GI tract
- GORD = lower oesophageal sphincter malfunction => leaked gastric acid
- Peptic Ulcer Disease = break in tissue lining of stomach mc caused by H. Pylori virus
- Gastroenteritis = Inflammation of the lining of the stomach/intestine as a result of infection(viral or bacterial) or parasitic infestation
- Inflammatory Bowel Disease (IBD) = (autoimmune disorder) involves chronic inflammation of all or part of your digestive tract. IBD primarily includes ulcerative colitis and Crohn’s disease. Both usually involve severe diarrhoea, pain, fatigue and weight loss.
- Haemorrhoids = Damage to the lining of the rectum and anus causing painful irritation, anal fissures and enlarged veins
- Gastrointestinal complaints occurring as a result of disruption of food passing through the GI tract (constipation, diarrhoea, irritable bowel syndrome).
- Zollinger-Ellison syndrome = hyper secretion of HCl caused by a gastrin-producing tumour.
*Outline the process of GASTRIC ACID PRODUCTION and it control by hormones
NEED MORE INFO!!!!!
Gastric acid production by the parietal cells is under the control of a variety of cellular hormones.
These include acetylcholine, histamine (through H2 receptors), PGI2 and PGE2 and gastrin.
Gastrin is secreted by cells in the gastric gland.
*Describe the pathophysiology of GERD
Reflux of stomach and duodenal contents into oesophagus inflaming eosophageal mucosa (OESOPHAGITIS) from ineffective leaky lower oesophageal sphincter. Chronic oesophagitis leads to a condition called BARRETT’S METAPLASIA which is a premalignant condition leading to OESOPHAGEAL ADENOCARCINOMA.
GERD affects 1 in 10 people (heartburn)
*Describe the pathophysiology of Peptic Ulcer Disease PUD
- Includes: gastric, duodenal, and esophageal ulcers, with common etiologies of Helicobacter pylori infection, NSAID use, and stress-related mucosal damage
- Cause: hypersecretion of HCL acid and pepsin. Mucosal defenses include mucus, secretion of bicarbonate, mucosal blood flow, and epithelial cell defense.
- When acid and pepsin invade a weakened area of the mucosal barrier, HIATAMINE is released. => stimulate parietal cells to secrete more acid. This cycle => erosion and ulcer fromation
*What is the mode of action of ANTACIDS? + examples
The wall of the stomach is protected from gastric acid by a layer of mucous continuously secreted by the stomach lining. Excess acid secretion can result in damage to the mucous layer resulting in pain and inflammation.
Antacids NEUTRALISE stomach acids thus reducing acidity relieving symptoms and allowing the mucous layer to repair itself.
E.g. 1. ALUMINIUM HYDROXIDE = Al(OH)3 Gaviscon, Alu-tab, Kaomagma 2. CALCIUM CARBONATE = CaCO3 Andrews Tums, Gaviscon, Mylanta 3. MAGNESIUM HYDROXIDE = Mg(OH)2 Gastrogel, Mylanta, Mucaine 4. SODIUM BICARBONATE = NaHCO3 Sodibic, Alka Seltzer, Gaviscon
*What are some adverse effects associated with ANTACIDS?
SODIUM BICARBONATE =
Bloating, belching, metabolic acidosis, fluid retention (CHF and hypertension)
CALCIUM CARBONATE =
Bloating, belching, metabolic acidosis, hypercalcaemia
MAGNESUIM HYDROXIDE =
Osmotic diarrhoea caused by unabsorbed magnesium
ALUMINIUM HYDROXIDE =
Constipation caused by unabsorbed aluminium
What are the 4 classes of ulcer healing drugs
- Histamine H2 receptor antagonists
- Muscarinic M1 receptor antagonists
- Proton pump inhibitors
- Prostaglandins
*Describe the adverse effects associated with Ulcer Healing Drugs
- H2 RECEPTOR ANTAGONISTS =
Mild diarrhoea or constipation headache, myalgia, confusion, hallucinations, excitement, particularly cimetidine when administered IV to elderly or patients with renal or liver disease.
M1 RECEPTOR ANTAGONISTS
PPI =
Small increase in the incidence of diarrhoea and headache
PROSTYGLANDINS =
Diarrhoea and abdominal discomfort. Contraindicated in women unless proved negative for pregnancy.
*What is the mode of action of Mucosal Strengtheners? + examples
These are poorly soluble molecules that polymerise in the acid environment of the stomach. The polymer then binds to the injured tissue and forms a protective coating over the ulcer beds. Sucralfate Carafate Ulcyte Bismuth chelate Pylorid KA
*Describe the Physiology of the Digestive system
- Mouth = oral cavity
- Pharynx
- Larynx
- Oesophagus
- Stomach
small intestine=
- Duodenum
- Jejunum
large intestine=
- Cecum
- Ascending colon
- Transverse Colon
- Descending colon
- Sigmoid colon
- Rectum
- Anal canal => Anus
Anciliary Organs = Salivary glands of mouth + Liver + Pancreas + Gallbladder
IBD - Define Ulcerative Colitis ; Chron’s Disease
Ulcerative Colitis = inflammatory bowel disease that characteristically involves the rectum and extends proximally to affect a variable length of the colon
Chron’s Disease = transmural inflammation of the GI tract, involve any or all parts of the entire GI tract, usually seen in the terminal ileal and perianal locations.
Describe the structure of the lining of the stomach
The wall of the stomach is lined with millions of gastric glands, which together secrete 400–800 ml of gastric juice at each meal.
3 types of cells found within gastric glands: (From bottom to top)
CHIEF CELLS which synthesize and secrete pepsinogen, the precursor to the proteolytic enzyme pepsin.
PARIETAL CELLS which secrete HCl
Mucus-secreting cells (GOBLET CELLS) which secrete the protective mucus lining.
DRUGS to treat GORD
Antacids, PPIs and H2 antagonists to reduce acid production as for peptic ulcers
Alginates to form a protective raft on the stomach
Prokinetics to increase gastric emptying
