GI Drugs Pt 1

Understand how gastrointestinal (GI) function can be altered by drugs by exploring the mechanisms of action and side effects of various pharmaceuticals.
Identify drugs used to induce and stop vomiting, including mechanisms, indications, contraindications, and side effects.
Recognize drugs used to induce and stop diarrhea, covering classification, dosage, and potential adverse effects.
Learn about drugs used to treat ulcers, including their mechanisms, benefits, and considerations for long-term management.
Know the drugs used to modulate rumen motility, understanding their pharmacodynamics and use in veterinary medicine.

Anatomic Differences:
- Monogastrics: Animals with a single-chambered stomach (e.g., dogs, cats) that primarily rely on enzymatic digestion.
- Ruminants: These animals have a complex, multi-chambered stomach (e.g., cows) to facilitate fermentation and breakdown of fibrous feed.
- Pseudoruminants: Such as camelids, exhibit unique digestive adaptations but do not possess true rumen physiology.
- Nonruminant Herbivores: Animals like horses that have a single stomach but also possess a cecum for fermentation, necessitating different dietary formulations.

Gastric: Pertaining to the stomach; most GI diseases considered at this level stem from gastric disturbances.
Enteric: Related to the duodenum, jejunum, or ileum; crucial for nutrient absorption and digestion.
Colonic: Refers specifically to the colon; disturbances here often relate to water absorption issues leading to diarrhea or constipation.

Nervous System Influence:
- The autonomic nervous system significantly impacts GI motility and secretion, with distinct roles for the sympathetic and parasympathetic divisions.
Hormonal Influence:
- Endocrine hormones such as gastrin, secretin, and cholecystokinin coordinate the various digestive processes and influence appetite and gastric emptying.
Cellular Factors:
- Compounds released by cells, such as histamines or prostaglandins, are vital in modulating GI motility and responses to injury or infection.
Microbial Influence:
- The gut microbiome plays a pivotal role in digestion, synthesizing essential vitamins and metabolites, and influencing immune responses in the gut.

CNS Control:
- Central nervous system encompasses the brain and spinal cord, regulating voluntary actions and reflexes affecting the GI tract.
- Peripheral includes both somatic (voluntary) and autonomic (involuntary) systems, affecting smooth muscle function and secretory activity.
Sympathetic (SNS) vs Parasympathetic (PNS):
- Sympathetic: Increases heart rate and reduces peristalsis, leading to decreased digestive function during stress.
- Parasympathetic: Stimulates peristalsis and secretion, enhancing digestion during restful states.

Parasympathomimetics:
- Drugs that mimic the PNS (e.g., bethanechol) enhance GI activity by increasing muscular contractions and secretions.
Sympathomimetics:
- These drugs mimic the SNS effects (e.g., epinephrine) which often lead to decreased GI activity and potentially prolonged gastric emptying.

Common in veterinary practice, disorders include bloat (gas distension), colic (abdominal pain), ulcers (mucosal damage), diarrhea (increased stool frequency), vomiting (expulsion of gastric content), and constipation (infrequent stools).
General Treatment:
- Non-specific therapy; correction of fluid/electrolyte imbalances; institution of temporary fasting (nothing by mouth for 12-24 hours), and diet modifications tailored to digestive health.

Vomiting:
- Often associated with GI or systemic disease, involves retching and abdominal contractions, and vomitus is typically acidic due to gastric contents.
Regurgitation:
- Related to esophageal conditions; occurs without retching or abdominal contractions; vomitus is generally neutral or alkaline due to the absence of gastric acid.

Emetic Center:
- Located in the medulla (nucleus tractus solitarius); stimulates the vomiting reflex in response to various triggers.
Types of Stimulation:
- Involves direct stimulation (toxins), vagus nerve activation, chemoreceptor trigger zone (CRTZ) activation from chemicals, inner ear nerves (motion sickness connections), and higher brain centers under stress conditions.

Can be due to:
- Opioids (narcotics causing delayed gastric emptying), metabolic toxins (e.g., uremia), GI inflammation (from infections), trauma, or organ diseases impacting GI function.
- Emotional stress and anxiety can also elicit GI reflexes leading to nausea.

Include:
- Serotonin, dopamine, histamine, acetylcholine, norepinephrine, neurokinin-1, substance P—integral to the emetic response.
- Receptors show species variations; cats exhibit greater sensitivity to specific sympathetic stimuli compared to dogs, impacting veterinary treatment approaches.

When to Induce:
- Detoxification; indicated when the poison has yet to exit the stomach (typically within 2 hours for liquids, up to 4 hours for solids).
When NOT to Induce:
- In cases involving comatose, convulsing patients, or animals with severe bloat or suspected gastric torsion where risks outweigh benefits.

Potential risks include:
- Aspiration pneumonia from inhalation of vomitus, irritation or burns from corrosive substances, and inadequate gag reflex with certain toxins posing significant health risks.

Centrally Acting Emetics:
- Apomorphine: Directly stimulates D2 receptors; highly effective and fast-acting in dogs, less so in cats, necessitating careful usage.
- Xylazine: Induces vomiting through α2 receptor stimulation and is more effective in certain species like cats and dogs.
Locally Acting Emetics:
- Options include hydrogen peroxide (one-time use), warm salt water, mustard solution, manual techniques for dogs, and syrup of Ipecac (use with caution and only as a single dose).