22 - Gastrointestinal Tract Flashcards
3 gastic secretions
- Describe them and their purpose
Pepsin
- For protein degradation
HCl
- From parietal cells
- Kill bacteria
- Degrade protein
- Convert pepsinogen to pepsin
Mucus
- From superficial mucosal cells
- Create gel-like layer w/ bicarbonate ions to protect stomach lining from acid
- Lubricates food w/ cells
1) What cells secrete HCl?
2) HCl secretion increased by what
3) HCl secretion decreased by what?
1) Gastrin-ECL-parietal cell axis model.
- Acid secreted by parietal cells
2) Increased by
- Histamine from ECL cells
- Gastrin from G cells
- ACh from parasympathetic
3) Decreased by
- PGE2 + PGI2
- Somatostatin from D cells.
What’s Dyspepsia?
Pain/discomfort of GI tract + digestion difficulties.
Peptic ulcers are? Occur when…
3 Causes?
Benign lesion of gastric or duodenal mucosa.
- Due to acid/pepsin presence whilst defense/healing mechanisms disrupted.
Caused by:
- Stress?
- Helicobacter pylori infection (Increased gastrin during chronic inflammation which increases HCl)
- NSAIDs (e.g. Ibuprofen, Diclofenac)
How do NSAIDs cause peptic ulcers?
Inhibit COX-1 which inhibits PGE2 and PGI2 which inhibits it’s protective action. More acid, less mucus, less HCO3- secretion…
4 methods of Tx peptic ulcers?
- Describe them and their mechanism of action
Histamine H2-receptor antagonist:
- Competitively inhibit histamine, gastrin, and ACh stimulated acid secretion. Also reduces pepsin as less is converted from pepsinogen.
Proton-pump inhibitors (PPIs):
- Irreversible inhbition of H+/K+ ATPase. They work only at low pH of stomach.
Gastroprotectants:
- Analogue of PGE1 so inhibits acid production and increases mucus and bicarbonate production.
Antacids:
- Neutralise gastric acid. Usually salts of Mg or Al (often given together since one causes diarrhea whilst other causes constipation which counters each other).
What’s emesis?
- Controlled where?
- Recieves input from what?
Vomitting
- Controlled at vomitting centre
Input from:
- Chemoreceptor trigger zone (CTZ)
- Higher brain centres
- Organs e.g. heart, testes, part of GI
What’s the CTZ?
Chemoreceptor Trigger Zone
- Permeable to circulating substances (not across BBB)
- Blood-borne emtics and 5-HT activate it
- Sends signal to vomiting centre so it can decide if it should vomit
- Stimulated by smells, emotion, pain, motion sick, endocrine disturbance, toxic reactions, radiation, chemo…
List 4 antiemetic drugs
- H1 receptor antagonist
- Muscuranic receptor antagonist
- 5-HT3 receptor antagonist
- Dopamine receptor antagonist
Descrine H1 receptor antagonist in Tx of emesis
Most commonly used antiemtic drug (contraindicated in <6yrs)
- Acts on nucleus of the solitary tract (which integrates info from organs and sends to vomiting centre)
- Effective against motion sickness or irritants in stomach
- Ineffective against subtances at CTZ itself.
- Side effects of drowsiness and sedation.
Descrine muscuranic receptor antagonist in Tx of emesis
Treat motion sickness orally or transdermal patch.
- Acts on vomitting centre and nucleus of the solitary tract
- Adverse effects of dry mouth, blurred vision, and drowsiness.
Descrine 5-HT3 receptor antagonist in Tx of emesis
Prevent/treat, radiation/cytotoxic cause.
- Acts on CTZ
- Oral or injection
- Adverse effects of headache + GI upset
Descrine dopamine receptor antagonist in Tx of emesis
- Treat severe nausea due to cancer, radiation therapy, cytotoxic drugs, opioids, and anaesthetics
- Act on CTZ
- Oral, IV, or supoository
- Adverse effects of sedation. Hypotension, pain in extremities
Describe 2 types of IBDs
1) Ulcerative colitis
- Inflammation + ulcers of colon
- Diarrhoea + blood
- Colon only
- Relapse/remitting
Crohn’s disease
- Immune system attacks GI track (not autoimmune)
- Abdominal pain
- Diarrhoea
- Fever
- Weight loss
- Any part of GI tract affected.
How can IBDs lead to eye problems?
- Uveitis, episcleritis/scleritis
- Vit A deficiency-related keratopaty + retinal damage
- Steroid-related cataract and glaucoma
