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Digestive II VET 206 Simple stomach Intestines.  Food storage  Start/continue digestion of basic energy formin.

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Presentation on theme: "Digestive II VET 206 Simple stomach Intestines.  Food storage  Start/continue digestion of basic energy formin."— Presentation transcript:

1 Digestive II VET 206 Simple stomach Intestines

2  Food storage  Start/continue digestion of basic energy formin

3 Major Functions of Stomach  Food storage  Start/continue digestion of basic energy forming nutrients

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5 Directional terms/Function  Oral-toward the mouth  Aboral-away from the mouth  Simple Stomach function Protein digestion begins  Formation of chyme Fat emulsification begins

6 Simple Stomach Lesser curvature Greater curvature Rugal Folds Omentum

7 Species variations  Margo plicatus-horses (horses) Line between glandular and nonglandular portions of stomach of the stomach (carnivores don’t have nonglandular portion) Gastrophilus larva attach here!  Ruminants-they get their own lecture!!

8 Cardia  Muscular Thickening-functional sphincter Horses, rats-especially thick!!  Mucus producing cells=Goblet cells Mucin (Alkaline) + Bicarbonate (base) Protect stomach lining from stomach acids (pH 2-3!!)  (mucus-noun; mucous-adj)

9 Fundus and Body  Distend and expand as needed  Glandular area Chief cells-pepsinogen  Inactive precursor to pepsin (proteolytic enzyme) Parietal cells-HCl acid  Activates pepsinogen Mucous cells- mucus Intrinsic Factor-allow absorption of Vitamin B12

10 Fundus and Body

11 Parietal cell -control Gastrin (Parasympathetic neurotransmitter)

12 Antrum  Distal portion of the stomach  Grinds food  Regulates acid production G cells-produce hormone Gastrin Gastrin enters bloodstream, not into lumen Gastrin stimulates production of HCl and pepsinogen  Mucous cells present

13 Pylorus  Sphincter-regulates movement of “chyme” Helps prevent backflow of material from duodenum Remains partially open-liquids move quickly through stomach, solids slower  Enterogastric reflex If: Distended intestines or Increased acidity in intestines Then: decreased stomach emptying

14 Control of motility  PNS Vagus nerve Increases contraction of Body/Antrum for forward motion of chyme  Hormonal control Antrum fills-G cells produce Gastrin Gastrin causes relaxation of Fundus  SNS Decreases motility=“gastric atony” Stress can induce

15 GI hormones  Gastrin Trigger=antrum is stretched Action=relaxes fundus  Secretin Trigger=decreased pH in duodenum Action=decrease peristalsis in body and antrum  CCK Trigger=increased fats and protein in duodenum Action=decrease peristalsis in body and antrum

16 With all this acid, why don’t all animals have ulcers???  Mucus production  pH < 3 G cells stop production of Gastrin  Controls on parietal cells in HCl production  Cells turnover every 3-4 days throughout the gi tract.  Prostaglandins Control HCl production via Gastrin Increase bicarbonate-for mucous layer Maintain blood flow

17 With all this acid, why don’t all animals have ulcers???  Prostaglandins Control HCl production via Gastrin Increase bicarbonate-for mucous layer Maintain blood flow  NSAIDs-block prostaglandins!!! Very hard on the stomach Ulcerogenic

18 Normal Gastric Transit Time?  2-4 hours; longer for high fast foods  What could cause delayed emptying?? Stress Obstruction

19 Intestines  Small Intestines Duodenum (pancreatic and bile duct empties) Jejunum Ileum  Mesentery

20 Layers of the intestines  Mucosa  Submucosa  Muscularis  Serosa Lumen

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22 Function  Most nutrient absorption occurs in the small intestines Microvilli (brush borders)  Digestive enzymes  Nutrients transported via carriers or simple diffusion What are nutrients?  Protein, fats, carbohydrates  Minerals and vitamins  Water (most water absorption in large intestine)

23  Villi: Capillaries Lacteals-vessels where lipids are absorbed  Crypts Replenish cells of villi within 2-3 days (Crypts of Lieberkuhn)  Peyers patches- immune function

24 Peristalsis-antrum

25 SEGMENTAL (MIXING) CONTRACTIONS Mixing action, slows intestinal motility, allows for proper digestion/absorption of nutrients

26 PERISTALTIC (PROPULSIVE WAVE) CONTRACTION Direction of wave

27 Controls of intestinal motility  Stretch controls  Parasympathetic nervous system- maintains normal motility Stress can cause Ileus Post-op, certain antidiarrheals  CCK-action in the intestines-increase motility  Prostaglandins-increase motility and secretions

28 Basic nutrient digestion  Electrolytes, water-absorbed unaltered  Carbohydrates Amylase-enzyme in saliva, pancreas  Complex carbs to dissaccharides (sucrose, maltose, isomaltose, and lactose)  Specific enzymes (sucrase, maltase, isomaltase, lactase)-digest disaccharide to monosaccharide (glucose, galactose and fructose) *** Intestines adapt enzymes to diet, takes time to upregulate proper enzymes!!!!!

29 Basic nutrient digestion-Protein  Pancreatic Proteases (Trypsin, chymotrypsin, carboxypeptidase…) Break proteins (polypeptides) into peptides  All proteases are released as inactive form!! **Trypsinogen activates all protease!! Peptides then absorbed at the brush border

30 Basic nutrient digestion-Fats  Emulsification-starts in the antrum Micelle formed  Bile Acids-release into the duodenum-surrounds micelle-making them water soluble  Pancreatic lipase-breaks down further  Diffuses at brush border

31 Basic nutrient digestion-vitamins  Fat soluble vitamins- Vitamins A, D, E, K  Absorbed with micelles into lacteals  Fat digestion problems can lead to Vitamin deficiencies

32 Large intestine  Cecum (ileocecal junction), colon  Colon terminates in rectum and anal canal  Function-water and electrolyte absorption, lubrication (mucus secreting cells), storage  Microbial action Very simple in carnivores Hindgut fermenters-highly adapted  Control-parasympathetic nervous system  Stretch receptors

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34  Colon Ascending, transverse and descending  Rectum-terminal portion of colon  Rectal valves- Separates gas from solid material L. R.

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36 Anus  Internal and external anal sphincter Internal  Parasympathetic-relax internal anal sphincter  Sympathetic-tighten internal anal sphincter External  Voluntary control  Perianal surgery Risk of nerve damage-incontinence  Avulsion of tail Spinal cord injury

37 Anal Glands  Scent glands  Normally expressed with normal BM

38 Avian Digestive System  Esophagus-right side of the neck Mucous glands-lubricates  Crop-expansion of esophagus-storage Larger crop-need less meals per day Mucosal lining  crop milk (pigeons, doves) Protection for insectivores

39 Avian Digestive System  Stomach Glandular Stomach =Proventriculus  Chemical digestion Muscular Stomach =Gizzard  Striated muscles to grind food (bone, scales, nuts)  Produces pellets to be regurgitated (owls, hawks, herons, etc)

40 Avian Digestive System  Cloaca-termination of tracts Coprodeum-from intestines Urodeum-from kidneys and genitals Proctodeum-site of sperm storage prior to “cloacal kiss”, stores other excrement. Mute= waste product  Dark fecal center with ring of urates

41 Related Organs-Liver (Hepatic)  Largest organ (skin?)  Hepatocytes  Hepatic portal system Intestinal capillaries to hepatic sinusoids Lining sinusoids=phagocytic cells  Infectious agents, toxins, old RBCs  Hepatic Triad: 1) A hepatic artery 2) A branch of the hepatic portal vein 3) A bile duct

42 Liver  Storage-excess glucose stored as glycogen Glycogenesis= production of glycogen Glycogenolysis= release of glucose by breakdown of glycogen  Gluconeogenesis AA broken down to then form into Glucose Liver can perform if needed

43 Liver Function  Blood-storage and Filtration Recycles RBC’s, macrophages Clotting Iron Storage  Metabolic Nutrients Drug Metabolism  Excretory/Secretory Bile

44 Liver-Metabolic functions  Carbohydrates Store Glycogen Gluconeogenesis- (Amino acids to glucose) Converts Galactose and Fructose to Glucose Why do we need glucose???

45 Liver-Metabolic Functions  Fats Forms Ketone Bodies for an alternate energy source when Carbohydrates are not available Form Lipoproteins-LDL and HDL Form Cholesterol and Phospholipids Where do we need phospholipids?? Fat Synthesis-Convert CHO and proteins to Fat

46 Liver-Metabolic Functions  Protein- Synthesize nonessential Amino Acids Nitrogen Removal-Converts Ammonia to Urea Forms All Plasma Proteins (Except Globulins- who produces globulins??)  ALBUMIN!!!!!!  Clotting Factors!!!!!

47 Liver-Storage functions  Storage/metabolism –glucose, amino acids, some vitamins (fat soluble), Iron and minerals (Copper)

48 Liver-Bile  Fat digestion with bile acids  Bile Bile acids, cholesterol, bilirubin (breakdown product of hemoglobin in RBCs) Bile is secreted into canaliculi, come together to form bile ducts  Hepatic duct, cystic duct and common bile duct  Horses and Rats- No gallbladder

49 Liver-RBC recycling chem/images/bilirubin%20metabolism.jpg

50 Liver Disease-What do we look for Blood work  Liver enzymes  Albumin  Bilirubin levels  Bile Acid Trials  Clotting Factors  Ammonia levels Ultrasound Biopsy

51 Liver Disease-What do we look for Liver disease-Ascites!  Fluid that has left the capillaries in attempt to maintain oncotic pressure

52 Liver Disease-What do we look for Improper bilirubin metabolism= Jaundice (clinical sign) or Icterus (appearance of serum)

53 Liver-What do we look for??  Hepatoencephalopathy-clinical sign of excess ammonia in the blood Portosystemic shunts

54 Pancreas  Exocrine gland=empties product via pancreatic duct Pancreatic amylase Proteases (trypsin) Lipase Bicarbonate-neutralize stomach acids  Endocrine function Production of insulin and glucagon

55 Pancreas-exocrine function  Hormonal control is most important. Secretin-released by response to HCL in intestine CCK - released by presence of protein & fats

56 Pancreas  Insulin  Produced by beta cells in the islets of Langerhans  Stimulated by increase in blood glucose (after a meal)  Drives glucose from blood into cells Feed the cells  Glucagon  Alpha cells produce  Released when blood glucose is low (between meals)  Stimulates glycogenolysis and gluconeogenesis

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58 This workforce solution was funded by a grant awarded under the Workforce Innovation in Regional Development (WIRED) as implemented by the U.S. Department of Labor’s Employment and Training Administration working in partnership with the Colorado Department of Labor and Employment, the Metro Denver Economic Development Corporation, and the City and County of Denver's Office of Economic Development. The solution was created by the grantee and does not necessarily reflect the official position of the U.S. Department of Labor. The Department of Labor makes no guarantees, warranties, or assurances of any kind, express or implied, with respect to such information, including any information on linked sites and including, but not limited to, accuracy of the information or its completeness, timeliness, usefulness, adequacy, continued availability, or ownership. This solution is copyrighted by the institution that created it. Internal use by an organization and/or personal use by an individual for non-commercial purposes is permissible. All other uses require the prior authorization of the copyright owner.


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