What does each pertain to?

1. Gastrin
2. Enteric
3. Colonic
4. Foregut Fermentor
5. Rumination
6. Hind-gut Fermentor

1. Stomach
2. Intestines
3. Colon
4. Ruminants (Sheep, Goats)
5. Esophagus expands to mix food
6. Large Colon (Horse, rat)

List four stomachs of ruminants:

( which is the "true" Stomach?)

Rumen, reticulum, omasum, abomasum

(Abomasum)

Which branch of the ANS controls the GI tract?

And which nerve in particular?

Parasympathetic Nervous System

Vagas Nerve (10th cranial nerve)

1. What is Gastrin?
2. Where does it come from?
3. What causes its release?
4. What does it do?

1. Stomach hormone
2. Secreted by stomach lining
3. Stimulation of the Vagas nerve
4. Causes release of HCl, relaxes stomach, and signals motion of stuff through colon

1. Gastrin- Antril stomach
2. Histamine-Mast cells/basophils
3. Acetylcholine-Vagas nerve

Are nerve endings in the blood & cerebral spinal fluid that detect chemical/bacteria toxins, azotemia, ketones, opiates...so they monitor for toxins.

ps. species variability in CRTZ receptors makes emetic drugs more/less effective (Cat:seratonin/alpha receptors) (Dog:histamine/dopamine receptors)

Misoprostal/Cytotec©

(H² antagonists)

What is it and list some side effects (4 total).

Anti-ulcer drug (synthetic prstaglandin E), protects gastric mucosa by ↑mucus production, ↑blood supply to mucosa, ↑ mucosal turnover, inhibits acid secretion.

side effects: diarrhea, abd. discomfort, cramping (abd. & uterine contractions), colic (gas)

expensive

Antacid that binds to luminal surface of stomach (proton pump inhibitor) to inhibit secretion of H+ into the stomach lumen.

ex. Prilosec©, Losec©, gastogard©

Sucralfate (anti-ulcer)

~5 facts~

1. Binds to ilcerated areas & protects it.
2. Stimulates PgE production.
3. Not absorbed systemically, acts locally.
4. Must seperate from other drugs bc it binds to them.
5. Works best in an acidic environment.

Antacids (nonsystemic)

ex. Tums, Amphogel, Rolaids, Maalox (aka.buffers)

~3 facts~

Neutalize gastric acid w salts of Ca,Al,Mg.

 problems:

1. Ca & Al cause constipation, Mg causes diarrhea
2. Acid rebound (CaCO³ causes gastrin release ~HCl secretion, which starts the whole cycle again)
3. Interferes w absorbtion of other drugs (tetracyclines, digoxin, acepromazine, corticosteroids.

Where are H¹ receptors found (5 places)?

What happens during the stimulation of these receptors?

Skin, respiratory tract, vascular tissue, smooth muscle, brain.

Histamine is released by basophils/mast cells which results in allergic reaction/inflammation

Where are H² receptors found?

What does stimulation of the receptors cause?

Stomach Parietal Cells

Release of HCl into GI lumen

Prostaglandins (GI tract)

4 facts

Protective (PgE & Pgl²) prostaglandins:

1. ↑GI mucus production
2. ↑intestinal mobility
3. ↑local blood flow
4. ↑HCO³- buffers in mucus

Systemic Antacids:

1. What are they?
2. What do they do?
3. Routes of administration (4)
4. Where are they metabolized?
5. List 3

1. Competitive inhibition of H² receptors
2. Block secretion of HCl
3. IV, IM, SQ, PO
4. Metabolized by the liver
5. Cimetidine(tagament©), Ranitidine(Zantac©), famotidine(pepsid©) (all OTC)

*stagger doses w other drugs that rely on acidity

1. Regurgitation: Passive process, usually facilitated by gravity, as the head/neck become lower than the contents in the stomach.
2. Vomit: Coordinated process in vomiting center of brain caused by input from Vagus nerve stimulatation, CRTZ, Vest. apparatus, or cerebrum , where glottis closes, abd. muscles contract, reverse peristalsis (SNS Stimulation) 

1. A parasympethetic nerve, "The Wanderer," bc it is everywhere
2. Coordinates vomiting
3. Innervates GI tract, peritoneum, larynx, pharynx, and more
4. Stimulated by distention/ irritation of the pharynx, stomach, duodenum, peritoneum, kidney, gall bladder, uterus 

Vomiting Center

~3 facts~

1. Alpha receptors and seratonin receptors
2. Stimulation causes vomiting
3. Cats esp. sensitive to SNS stimulation of alpha receptors (stress vomiting, dexmedetomidine, etc)

Located in the inner ear, it has CaCO³ crystals suspended in a gelatonous coat and the movement of that coat stimulates hair that are connected to nerve fibers, one of which is the Vestibulocochlear Nerve, which goes to the vomiting center/CRTZ.

*Antihistamines block CRTZ that are stimulated by Vestibular apparatus.

Do not induce vomiting if :

~7 things~

1. Ingestion of corrosive materials
2. Oils/petroleum products (aspiration)
3. Unconscious/comatose
4. Seizuring
5. Bloat (esophageal damage, rupture)
6. If already vomiting
7. Timing too late(liquids<2hrs & solids <4hrs)

1. Central-acting (Affect CNS-usually the CRTZ) ex. Apomorphine, xylazine
2. Local-acting (gastric irritants-usually stimulate the Vagus) ex. hydrogen peroxide

• Central-acting emetic that stimulates dopamine receptors in the CRTZ (opioid)
• Can be given IV, IM, conjuctival sac
• More effective in dogs than cats
• causes respiratory depression & sedation
• Side effects can be reversed w naloxone
• prolonged vomiting can be reversed w phenothiazines (dopamine antagonists) 

• Alpha² agonist
• stimulates alpha receptors in CRTZ & vomiting center
• reverse w yohimbine
• effects 50% of dogs/90% of cats
• use w caution bc of adverse cardiovascular effects.

• Ipecac-no longer made, irritant to intestinal mucosa, won't cause emesis but cardiotoxic
• Hydrogen Peroxide-household 3% (must be fresh), Risk of aspiration from froth, ½-1ml/lb, but less than 45ml total, May repeat once after 10-15 min
• Salt-throw into pharynx, stimulates Vagus nerve, observe hydration

• Vomiting is usually self-limiting, so withold food for 12-24 hours after vomiting stops.
• Begin with water then bland diet, in small quantities.
• Drug intervention is usually not necessary. 

1. Phenothiazines
2. Antihistamines
3. Anticholinergics
4. Prokenetic Drugs
5. Serotonin antagonists
6. Neurokinin-1 receptor antagonists