Alimentary Ch3-4

• The text discusses malabsorption and maldigestion, which are digestive pathologies related to the ingestion, breakdown, digestion, absorption, and utilization of nutrients, and what happens when parts of the digestive do not work properly.
• Malassimilation occurs when the digestive process doesn't function as expected.
• Maldigestion involves impaired normal digestion and pancreatic function.
• Malabsorption occurs when the body digests normally, but struggles to absorb.
• Malutilisation involves normal digestion and absorption, but abnormal usage or loss of nutrients.

Pancreas and its Functions

• The exocrine pancreas secretes digestive enzymes through the pancreatic duct into the small intestine.
• These enzymes facilitate digestion for all major food types, including lipase, protease, and amylase.
• The epithelial cells of the ductile secrete bicarbonate and water.
• The secretion helps neutralize hydrochloric acid coming from the stomach, creating a suitable environment for pancreatic enzymes.

Nutrient Absorption and Related Factors

• Vitamin A impacts eyesight/retina.
• Vitamin D is involved in calcium metabolism.
• Vitamin E offers protection from toxins, especially in the liver.
• Vitamin K is essential for blood clotting factor activation.

Cobalamin Absorption

• Impaired absorption of cobalamin (vitamin B12) can occur.
• Intrinsic factor, synthesized, by the pancreas and stomach, permits cobalamin absorption.
• Bacterial growth in the upper small intestine can increase.
• Chyme, undigested in the upper gastrointestinal tract, may not be properly broken down which leads to growth media.
• Treatment includes antibiotics and increased cobalamin uptake.

Maldigestion and Pancreatic Insufficiency

• Exocrine pancreatic insufficiency, the most common cause of maldigestion, affects pancreatic enzyme and bicarbonate production and reduces the capacity to neutralize stomach acid.
• Clinical signs appear when 90% of pancreatic function is lost.

Causes and Clinical Signs of Pancreatic Issues

• Pancreatic acinar atrophy can cause this, as well as chronic pancreatitis, pancreatic hypoplasia, and pancreatic neoplasia
• Clinical signs include weight loss, normal or increased appetite, increased fecal volume, abnormal feces, flatulence due to bacterial action on undigested food, and coprophagia.

Diagnosis and Treatment of Maldigestion

• Clinical signs are not pathognomonic.
• Diagnosis involves blood tests for trypsin-like immunoreactivity.
• Fecal tests may reveal fat and starch.
• Treatment varies from fat-restricted diets, enzyme supplements, and antimicrobials.

Further Treatments and Enzyme Deficiencies

• Supplementation of vitamins A, B12, D, E, and K weekly may happen over several weeks or for life.
• Antibiotics may not always be necessary for the patient.
• Secondary enzyme deficiency can be due to non-optimal luminal conditions.
• Bile acid deficiency and brush border enzyme issues can also cause problems.

Pancreatic Acinar Atrophy

• Autoimmune destruction of digestive enzyme-producing cells, without affecting endocrine function.
• Two phases as the disease progresses.
• Subclinical: Inflammation through lymphocyte infiltration.
• Clinical: Severe atrophy.
• Many dog breeds inherit this, which increases the chances of this condition, it's suspected, over-represented, or under-represented.
• It is rare in cats.

Chronic Pancreatitis

• Uncommon in cats, may cause exocrine pancreatic insufficiency for the patient.
• Dogs of middle to older age may get this condition.
• Fibrosis, damages both exocrine and endocrine functions.
• Clinical indications include diabetes and exocrine pancreatic insufficiency.

Malabsorption Issues

• Absorption impairment in the patient's small intestine.
• Primary: structural causes of malabsorption, most commonly.
• The wall's disease or gut, like parasites, inflammatory bowel diseases, lymphangiectasia, GI lymphoma.
• Feline infectious peritonitis (FIP) can also cause this (it is contagious).
• Deep mycosis can be a factor, in the US is endemic.
• Secondary: non-structural, and it makes the diagnosis harder in the diagnosis stages.
• Luminal issues with digestion: the cause of it, can be from hyperthyroidism or acid hypersecretion. Fat Malabsorption:
• A lack of pancreatic enzymes.
• Problems with the liver or ileum. Mucosal Enterocyte Defect
• With an intestinal or inflammatory bowel disease.
• A possible brush border issue.

Causes of Malabsorption

• Congenital: lactose intolerance.
• Acquired: deficiency of intrinsic factors in the small intestine.

Transport and Clinical Signs of Malabsorption

• Lymphatic obstruction might be the issue: primary or secondary lymphangiectasia.
• Vascular compromise, or vasculitis, may lead to the condition.

Clinical Signs

Weight loss, diarrhea, and coprophagia can be signs.

Treatment:

• Treatment depends on the underlying cause, ranging from diet and immunosuppressants for inflammatory conditions to antimicrobials for bacterial infections, antifungals for fungal infections, antiparasitics, or chemotherapy for neoplastic conditions.
• Treatment depends on the pathology of the disease.

Liver Function Overview

• Metabolism: Carbohydrate storage and breakdown, fat breakdown for energy, protein processing.
• Conversion of amino acids, fats, and carbs for energy, and detoxification of ammonia.
• Synthesis: Production of albumin, globulin, clotting factors, and bile.
• Storage: Nutrient release and assimilation, including vitamins/minerals and glycogen.
• Detoxification: Removal of drugs and toxins.

Reticuloendothelial System

• Kupffer cells: resident macrophages, destroy damaged blood cells, metabolize hemoglobin into bilirubin.
• Contribute to inflammation, immunity, influence neuroendocrine & lymphoid development.

Liver Disease Causes and Clinical Signs

• Infection: by viral agents, bacteria and fungi.
• Parasites: liver flukes.
• Vascular issues: portal systemic shunts.
• Toxicity from plants, drugs or aflatoxins.
• Neoplasia, degeneration, fibrosis, and even being genetic can be factors when determining what happens.

The Clinical Signs of Disease

• Clinical: Inappetence, anorexia, vomiting, diarrhea, jaundice due to high bilirubin, depression, lethargy, polydipsia, and neurological encephalopathy.
• May cause coagulopathy.
• GI ulceration with blood in feces, and photosensitization.

Pathology

• Increase in liver enzymes, bilirubin, bile acids, blood ammonia, and globulin.
• Decrease in blood glucose, albumin, and clotting factors.
• Possible regulation issues: increase or decrease.
• Platelet dysfunction.

Case Studies of Liver Disease

• Fred: 6-month-old cat, depressed, lethargic, with jaundice and dehydration.
• Bertie: 18 y/o horse, head pressing, ataxia, central blindness after tetanus vaccination. Diagnosed with Theiler's disease (acute equine serum hepatitis).
• Jessie: 15 y/o cat, intermittent weakness, pinpoint pupils, diagnosed with hepatocellular carcinoma.
• Blossom: 15 y/o horse, yellow mucus membranes, liver biopsy showed pyrrolizidine alkaloid toxicity.
• Bruce: 10 m/o dog, intermittent vomiting, normal water intake, hyperthermia and normal abdominal palpation.
• Roger: 12 y/o dog, watery diarrhea, vomiting, gallon bladder mucocoele.
• Rocky: 2 y/o, Rottweiler dog, weight loss, variable appetite, and liver changes show it's not as healthy.

Diagnosis

• Feline infectious peritonitis (FIP): viral, treatable now.
• Look at the organs after the patient dies: jaundiced tissues, white plaques on abdominal organs, liver changes, lymph node necrosis. Histopathology reveals arteritis.
• Bertie: Theiler's disease (acute equine serum hepatitis).
• Hypertonic saline treatment.

Diarrhea and Small Intestine Structure

• Diarrhea is discussed.
• Small intestines include villi.
• Jejunum long, Ileum shorter: Increase surface area through villi and microvilli.
• Villi tips shed, develop with absorptive brush border.
• Continuous cell division from formation inward from the crypts.

Intestinal Pathology and Absorption

• Brush border enzymes aid carb and protein digestion.
• ATP for absorption.
• Fat uptake with diffusion, can be disrupted by villi widening.
• Fluid balance maintained.

Intestinal Dynamics and Mechanisms of Diarrhea

• Small intestinal dynamics include villus function for absorption with tight junctions and crypt base function for secretion with leaky junctions.
• Secretory diarrhea occurs from increased fluid secretion due to altered epithelial cell transport, often caused by bacterial infections.
• It is self-limiting.

Fluid Content and Villus Structure

• Increased fluid content is related to adherent bacteria.
• Altered villus mucosal structure affects permeability due to bacterial Cytotoxins damage.
• Can produce cell death.

Neoplastic and Immune Disorders

• Neoplastic: Intestinal lymphoma with "cobblestone gut", inflammation.
• Immune-mediated disorders: inflammatory bowel disease with inappropriate immune response, bacteria, cell issues.

Infectious Diseases

• Infectious diseases: Johne's disease in cows, causing thickened mucosa.
• Microscopic: Villus distortion, macrophage, infiltrations.

Viral Infections

• Viral: Lytic infections target specific cells, for example coronavirus in piglets, feline, and EDIM. It includes damage..
• Collapse of mucosa.
• Discoloration.

Osmotic Diarrhea and Motility

• Osmotic diarrhea occurs when the gut is drawing more water into the intestine.
• Altered motility affects what will happen.
• Intestinal transit time: hypermotility reduces, while hypomotility increases bacterial overgrowth.

GI Histopathology

• Equine gastric ulcer syndrome, involves specific regions of the stomach.
• Region with protective mechanisms affects the clinical signs.
• Gastric reflux damages the non-glandular.
• Vomiting/pain causes weight loss.

Parvovirus and Paratuberculosis

• Canine parvovirus: virus that has an affinity for dividing quickly. Clinical signs include diarrhea and death.
• Paratuberculosis and Johns: mycobacterial infection accumulate in cell then lamina, which will lead to reduced function.
• Clinical signs: low nutrients, low energy.
• Less milk production from the patient.

Liver Homeostasis

• Types 1, 2 can be present for patient diagnosis.
• Gestational can be.
• Test the diabetes.

Pearl

• Cat has glucose issues.
• Injection needed, must get better.

Ruminant Anatomy

• It involves the anatomy and physiology of the ruminant digestive system, particularly focusing on the structure and function of the stomach.
• The stomach develops from a single tube into a multi-compartment organ.
• Histology: Ruminal papillae structures provide fermentation.
• Structures contract. It helps move what the patient.
• Caudal area has important pillars which are going to separate the area.

Reticulum Contraction

• Food is filtered, antiperistaltic contractions, and relaxation help movement.
• Damage can result.
• Distention and consistency affect it.
• Chemoreceptors monitor various concentrations.

Stomach Anatomy

• Omasum: Ventral and epithelial.
• Abomasum: A true stomach that resembles carnivores and digests milk.
• Blood supply via the celiac artery.

Newborn Digestion

• Small stomachs digest the right food well.
• Diarrhea and malabsorption has to be avoided.
• It involves the anatomy and physiology of the equine and swine digestive systems, covering aspects like stomach structure, sphincter function, intestinal features, caecum details, and ileocaecocolic junction characteristics. Other key topics are the components and topography or relevant regions.. Stomach:
• Most of these organs/animals have a small stomach.
• They have a sphincter as well.

Canine Abdomen Dissection

• Study abdominal points here.
• Aponeurosis is a sheet.
• Visceral etc. is what the patient will get.

Nerve

• Supply what is necessary, in the GI tract.
• Cisternal/4 regions.
• Liver is here.