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Digestive System
  VTT 235/245 Anatomy &
       Pathology Lab
Introduction
 The digestive system consists of:
   **A tube that runs from the mouth to the
    anus.
   Accessory digestive organs that aid in the
    process of digestion and absorption of
    nutrients.
   The accessory organs are:
     Salivary glands
     The liver
     The pancreas
Functions
   Prehension (grasping of food)
   Mastication
   Chemical digestion
   Absorption of nutrients and water
   Elimination of wastes
Oral Cavity
 Mechanical
  digestion- chewing,
  breaking food down
  into smaller particles
  to increase the
  surface area
  available for
  exposure to enzymes
  involved in chemical
  digestion.
Oral Cavity…
 Digestive enzymes are proteins that promote
  (catalyze) the chemical reactions that split
  complex food molecules into simpler
  compounds.
 The addition of saliva helps moisten, soften,
  and shape food into a form that is more easily
  swallowed.
 Salivary amylase breaks down amylose, a
  sugar component of starch.
 Lipase, an enzyme that digests lipids (fats)
  can also be found in the saliva of some
  species.
Oral Cavity…
 The salivary glands are controlled by
  the autonomic nervous system.
 Stimulation of the parasympathetic
  division results in increased salivation.
Peristalsis
 The contents of the digestive tract are
  moved and mixed by two types of
  smooth muscle contractions:
   Peristaltic- move contents along the
    digestive tract.
     They consist of circular muscle contractions
      that propel contents.
   Segmental- cause back-and-forth mixing
    movements.
Esophagus
 A muscular tube that extends from the
  pharynx to the stomach.
 Its function is to conduct swallowed
  material to the stomach.
 The esophagus enters the stomach at
  the cardia.
   Made of smooth muscle,
   Which helps with peristalsis.
Gastroesophageal Reflux &
            Esophagitis
 Inflammation of the
  esophageal wall most often
  associated with contact of
  irritants with the mucosa of
  the esophagus.
 Acids, alkalis, drugs, toxins,
  and hot materials can
  produce lesions of varying
  severity.
 Once inflammatory damage
  occurs, lower esophageal
  sphincter function becomes
  abnormal, perpetuating the
  problem.
Megaesophagus
 Esophageal paralysis or
  hypomotility.
 A dilation of the esophagus
 Due to a vascular ring anomaly or an
  unknown cause
 May be secondary to systemic
  disease (hypothyroidism)
 Primary sign- regurgitation (begins
  at weaning if congenital)
Esophageal Obstruction
 Bones and small toys commonly enlodge
  at the thoracic inlet, cardiac base, or
  distal esophagus.
 The degree of damage to the esophagus
  depends on:
   The size of the object
   The shape
   The time spent in contact with the mucosal
    lining
Spirocera lupi
 Can cause neoplasia
  of the esophagus.
Stomach…
 Divisions-
   Cardia- the area
    immediately surrounding
    the opening from the
    esophagus.
      Associated with the cardiac
       sphincter.
   Fundus- the section that
    forms a blind pouch that
    expands as more food is
    swallowed.
Stomach…
 Divisions-
   Body- also a distensible
    section in the “middle” of the
    stomach.
   ***Pylorus- the distal part of
    the stomach that grinds up
    swallowed food and regulates
    hydrochloric acid (HCl).
      **The glands of the pylorus
       contain endocrine cells called G
       cells which secrete the hormone
       gastrin.
Stomach…
 The body & fundus are both rich in
  glands containing 3 key cells-
   Parietal cells- which produce HCl.
   Chief cells- which produce pepsinogen.
   Mucous cells- which produce protective
    mucus.

 Mucous- adjective      Mucus- noun
Stomach…
 Inside the stomach,
  multiple folds called
  rugae can be
  observed.
Gastric Motility
 Swallowing of food stimulates vigorous mixing,
  grinding, and propulsive contractions that
  move food toward the pylorus.
 The smooth muscle in the wall of the stomach
  responds to several hormones, peptides, and
  nervous system controls.
   Stimulation of the vagus nerve causes the fundus
    to relax (so it can fill), while increasing the
    contractions in the body and pylorus for mixing and
    peristaltic movements.
Gastric Secretions
 Pepsinogen is secreted by chief cells and is a
  precursor for the enzyme pepsin.
 The proteins broken down by pepsin form
  chains of amino acids (polypeptides &
  peptides).
 The presence of peptides in the pylorus
  stimulates the G cells to release more gastrin,
  which stimulates more HCl and pepsinogen
  release.
Gastric Secretions…
 Once the pepsin moves from the acidic pH of
  the stomach to the more alkaline pH of the
  duodenum, it is inactivated by the change in
  pH and stops functioning.
 The mucus produced by the gastric glands
  provides a protective coating of the stomach.
 Mucins are complex molecules produced by
  the goblet cells in the gastric glands and are
  the main constituents of the coating.
 Bicarbonate ion is also secreted onto the
  surface making it more alkaline.
Gastric Secretions…
 The parietal cells in the gastric glands
  secrete hydrogen and chloride ions
  separately into the stomach.
 Once these ions are secreted, they
  combine to produce the HCl that
  accounts for the stomach’s acidic pH.
 The parietal cells have 3 receptors that
  regulate acid production.
Gastric Secretions…
 These receptors are for:
   Gastrin
   Acetylcholine
   Histamine
 Stimulation of all receptors results in
  the optimum amount of hydrogen and
  chloride secretion.
Gastric Secretions…
 When the pH of the stomach contents drops
  below 3, gastrin release is inhibited.
 When gastrin is inhibited, hydrogen and
  chloride production is terminated, and HCl
  production declines.
 Selectively blocking any one of these
  receptors decreases the production of
  stomach acid.
   This is the way antacid drugs work.
Mechanism of Vomiting
 Vomiting occurs due to the stimulation
  of the emetic center in the brain.
   Visual, vestibular, toxins…
 Color and content of the vomit can
  assist in a diagnosis.
   Flecks of blood- recent hemorrhage in the
    esophagus or stomach.
   Coffee grounds- digested blood
   Yellow-green- bile
Acute Gastritis
 Causes include:
   Diet- spoiled food, change in diet, food allergy, or
    food intolerance.
   Infection- bacterial, viral, or parasitic.
   Toxins- chemicals, plants, drugs, or organ failure.
 Ingestion of foreign objects may also result
  in gastritis.
 Once the mucosa is damaged, inflammation
  occurs and clinical symptoms develop.
Gastric Ulcers
 Commonly a result of drug therapy.
   NSAID’s
     Aspirin, ibuprofen…
   Disruption of the normal gastric mucosal
    barrier, resulting in ulceration.
GDV
 Diet and exercise have been indicated in
  the development of GDV.
 As the stomach fills with air, food,
  and/or fluid, the outflow tracts become
  occluded.
 Further distension results in a simple
  dilation (air-filled stomach), or the air-
  filled stomach may twist along its
  longitudinal axis (volvulus).
GDV…
 The pylorus usually passes under the
  stomach.
 The enlarged stomach presses against
  the diaphragm, making breathing
  difficult and blocking venous return.
 The spleen may also be involved.
GDV
Pyloric Stenosis
 Hypertrophy of
  circular smooth
  muscle fibers of
  the pyloric
  sphincter
 This causes an
  obstructive
  narrowing and
  projectile vomiting
Pathology…
 Hemorrhagic Gastroenteritis- (HGE)
   Acute onset of bloody diarrhea
 Malabsorption Syndrome- the small intestine
  is unable to deliver nutrients to the
  circulation (EPI)
Small
Intestine

           Function:
   Digestion and absorption
Small Intestine
 Where the majority of nutrients are
  absorbed into the bloodstream.
 Divided into 3 segments-
   Duodenum- first short section leaving the
    stomach.
   Jejunum- longest portion, makes up the
    majority of the small intestine.
   Ileum- enters the colon at the ileocecal
    sphincter.
Small Intestine…
 Ileocecal sphincter- regulates
  movement of materials from the small
  intestine to the colon.
 The parasympathetic nervous system
  provides stimulation for small intestinal
  motility, secretions, & blood flow.
Structure
 The mucosa is adapted to provide a large
  surface area for absorbing nutrients through
  folds in the intestinal wall and millions of villi.
 Each villus contains thousands of microvilli
  called the brush boarder.
 These cells have many digestive enzymes and
  carrier molecules embedded in their cell
  membrane for digestion and absorption of
  nutrients, vitamins, and minerals.
Motility
 Has peristaltic waves, which mix the intestinal
  contents and slow their movement through
  the length of the intestine.
 The churning motion brings digested material
  into contact with the surface for absorption.
 Slowing the movement also allows enough time
  to contact with the intestinal wall long enough
  to be absorbed.
 Peristaltic movements are stimulated by
  reflexes to dilation.
Structure…
 Goblet cells are also present.
 They produce mucus that helps protect
  the intestinal mucosa from the flow of
  ingestion as it passes over the intestinal
  lining.
Digestion
 Electrolytes and vitamins can be
  absorbed intact into the small intestine
  wall while carbohydrates, proteins and
  fats must be chemically digested.
 Chemical digestion has 2 steps-
   By enzymes in the lumen of the intestine.
   By enzymes associated with the brush
    boarder.
Mechanism of Diarrhea
 Osmotic-  or poor absorption of contents.
   Dietary overload, maldigestion or malabsorption
 Secretory- hyper secretion of the valley
  portion of the villi.
   More secretion than absorption.
   Ex. Parvo, bacterial
 Abnormal Motility- abnormal transit time,
  usually a hypomotility.
   Hypomotility allows for bacterial overgrowth and
    rotting ingesta. Yummy!
Small vs. Large Intestine
                Diarrhea
Signs            Small Intestine   Large Intestine
Frequency        Normal to        
Volume           Large             Small
Urgency          Absent            Present
Straining        Absent            Present
Mucus Presence   Absent            Present

Blood Presence   Coffee grounds    Very red
Vomiting         Present           Absent
Weight Loss      Present           Absent
Small Intestine Pathology…
 Enteritis
    Inflammation of the small intestine.
    Can be infectious or inflammatory.
    The diarrhea usually contains digested blood.
 Volvulus-
    Rotation of the bowel.
 Perforations-
    Penetration of the small intestine wall.
    Causes: ulcers, foreign bodies, necrosis IIº to obstruction,
     herniation or external penetration.
    This causes painful peritonitis!
Parvo
 Parvo virus affects the lining of the small
  intestine.
 It invades/wipes out the simple columnar
  tissue which exposes blood vessels causing
  “bloody diarrhea”.
 The intestinal response is to become
  inflamed-
   Increased peristaltic activity- cramps
   Propels chyme through rapidly- diarrhea!
Intussusception
 The cause is usually idiopathic but can
  be the result of:
     Parasite infection
     Foreign bodies
     Infections
     Neoplasia
Intussusception…
 The telescoping of the
  proximal intestine into the
  distal intestine.
 It produces a partial to
  complete blockage and
  compromises blood supply
  to the segments causing
  bowel necrosis.
Mesentery
 Mesentery-
 Clear, suspends the intestines from the roof
  of the abdomen.
   Prevents intestine entanglement
   Supplies blood to the intestines (small & large)
 Omentum-
   Part of the mesentery.
   Helps prevent a torsion.
   Attached at the greater curvature of the stomach.
Large Intestine

Water absorption and bacterial
          digestion
Anatomy Review
 “Colon”
   Ascending
   Transverse
   Descending
Colitis
 Acute-                           Chronic-
    Sudden onset of
                                     Long-term, non-specific
     inflammation of the colon.
    Often in dogs.                   inflammation of the colon.
    Frequent defecation,            Causes include: idiopathic,
     small amounts.                   FIV+, FIP+
    Causes: garbage ingestion,      Signs include: diarrhea
     stress, parasites:
       Trichuris, Coccidia
                                      with slow, progressive
       Bacteria: Salmonella          weight loss.
 All cause a change in
  motility!
Megacolon
 An abnormally dilated colon or segment of the
  colon.
 Seen frequently in cats.
 The presenting symptom is straining to
  defecate.
 These cats are usually dehydrated and may be
  vomiting.
 The cause of this disorder has been thought
  to involve a defect in the neurostimulation
  mechanism that promotes colon evacuation.
Megacolon…
 Other causes include:
   Hypothyroidism
   Pelvic deformities
 Severe prolonged colon distension for
  any reason can disrupt normal motility
  and result in megacolon.
Constipation
 True constipation is uncommon.
 The presence of foreign objects,
  tumors, pelvic injury, anal sac
  abscesses, urinary obstruction, and
  dehydration can result in the failure to
  pass feces.
Inflammatory Bowel Disease (IBD)-

 A group of GI diseases characterized by
  similar signs with unknown causes.
 Diagnosis is made when an excessive number
  of inflammatory cells are found in mucosal
  samples of the GI system.
 Colonic inflammation disrupts mucosal
  integrity and results in decreased absorption
  of sodium and water.
 Inflammation also results in hypermotility,
  resulting in more frequent defecation.
Inflammatory Bowel Disease
            (IBD)…
 Signs include:
   Diarrhea with little weight loss.
    frequency of defecation and  fecal
    volume.
Rectum & Anus
 Rectum- the part of the colon running
  through the anal cavity.
 Anus-
   Anal sphincter- a muscular ring that
    controls the passage of feces out of the
    body.
   What type of muscle?
     Smooth!
Anatomy
 Perianal Glands- sebacous glands
  located in the skin, encircling the anus.
 Anal Glands- located in the submucosa,
  at the anocutaneous junction.
   Where are the ducts?
Anal Gland Impaction
 Retention of anal sac secretions
 If left untreated, they may abscess
 Anal sac rupture is secondary to
  obstructions
Perianal Adenoma
 Usually in intact male dogs.
 Bengin, hormone dependant tumor that
  arises from the perianal gland.
   Which hormone?
   Testosterone
Perianal Fistulae
 Multiple ulcerative, smelly draining
  tracts surrounding the anus
 Caused by dogs with a low tail carriage
  and/or a broad tail base (which retains
  fecal film) ex. GSD
Hepatic Anatomy
The Liver
 The largest gland in the body.
 A digestive gland of substantial
  importance in metabolism.
The Liver…
 Functions:
     Detoxification of drugs and toxins.
     Formation and secretion of bile.
     Metabolism of carbohydrates and fats.
     Plasma protein production.
     Urea formation.
Anatomy
 The liver consists of six lobes.
   HEPATOCYTES.
Blood Supply
 The liver has a unique venous system referred
  to as the Hepatic Portal System, which
  receives both oxygenated and deoxygenated
  blood.
 All products of digestion are filtered through
  the liver and approximately 80% of the blood
  that flows into the liver enters through the
  portal vein and originates from the stomach
  and intestines.
Blood Supply…
 The hepatocytes are nourished by this
  blood which is rich in nutrients but not
  in oxygen.
 As blood enters the lobules, it flows
  across the hepatocytes and filters into
  the central vein.
 The blood then travels from the central
  vein into the hepatic vein and
  eventually the caudal vena cava.
Blood Supply…
 As the blood is filtered through the
  liver, it passes through Kupffer cells,
  which help remove bacteria.
 The hepatic artery supplies the
  remaining 20% of blood to the liver.
   This blood, which is rich in both oxygen and
    nutrients, supports the high metabolic
    activity of the hepatocytes.
Hepatocytes
 The hepatocytes also secrete hormones
  and bile, a green digestive hormone
  liquid.
 The bile is carried through channels to
  the gallbladder where it is stored and
  the common bile duct, which leads to
  the duodenum, where bile is released.
Physiology
Bile
 Bile plays an important role in digestion, and
  bile production is one of the main functions of
  the liver.
 Bile consists primarily of bile salts, water, and
  bile pigments such as bilirubin.
 One of the most important functions of bile is
  to emulsify fat so it can be broken down by
  digestive enzymes in the gut.
Carbohydrate Metabolism
 In a process called glycolysis, the liver
  metabolizes carbs by converting excess
  glucose into glycogen for storage.
 The process is reversed when energy is
  needed.
 The entire cycle is known as
  glycogenolysis and is under the
  influence of the hormone glucagon.
Deamination
 Amino acids are broken down by the
  removal of an amino group.
 The discarded amino group is converted
  into ammonia and then into urea or uric
  acid, which is excreted through renal
  filtration.
   Animals with liver failure may have
    increased levels of ammonia.
Synthesis
 The liver synthesizes both alpha and
  beta globulins, which transport lipids
  and fat-soluble vitamins throughout the
  body.
 Prothrombin is one of the most
  important alpha globulins produced by
  the liver.
Pathology
 Cirrhosis- scarring of the liver, which is
  replaced with connective tissue. 70% of the
  liver can be destroyed before problems occur.
 Jaundice- A build-up of bilirubin in the body.
 Hepatitis- inflammation of the liver causing
  damage to the hepatocytes.
 Cholecystitis- inflammation of the
  gallbladder.
Infectious Canine Hepatitis
 Caused by Canine Adenovirus I and has
  long been recognized as a cause of
  hepatic necrosis in dogs.
 Infection occurs via the oronasal route.
 Viral replication occurs in the tonsils
  and lymph nodes.
Infectious Canine Hepatitis…
 Signs include:
     Petechial hemorrhages
     Lethargy
     Fever >103°F
     Depression
     Pale MM
     Abdominal pain
     Anorexia
     Bloody diarrhea
     Hepatomegaly
Feline Hepatic Lipidosis
 “Fatty Liver Disease”
 Severe accumulation of fat in the liver
 Secondary to diabetes mellitus in obese cats,
  malnutrition, drugs, toxins, or idiopathic.
 Complete anorexia in obese cats
 CBC- non-regenerative anemia, stress
  neutrophilia, lymphopenia.
 ↑ALP (20x normal), ↑ALT (10x normal),
  hyperbilirubinemia, hypoalbuminemia,  bile
  acids.
Hepatic Lipidosis
 Signs-
     Hepatoencephalopathy
     V/D
     Icterus
     Sporadic vomiting
     Anorexia
     Obesity
     Melena (black, tarry stools)
Portosystemic Shunts
 Portal Systemic Shunts
 The blood by-passes the
  liver due to a congenital
  defect or acquired by
  chronic hepatitis.
 This leaves the blood
  unfiltered as it returns
  to the heart.
 Ammonium biurate
  crystals in the urine can
  be an indicator.
Shunts
 Causes:
    Congenital- a vascular
     anomaly
    Acquired- IIº to chronic
     active hepatitis or
     serosis, (portal vein non-
     functional)
 Signs:
    CNS-
     hepatoencephalopathy d/t
     ammonia build-up in the
     brain.
Shunts

 Signs-
   Anorexia
   Depression
   Ataxia
   Head-pressing
   Circling, pacing,
    blindness
   Seizures
   Hypersalivation
Pancreas: Anatomy Review
Pancreatic Function
 An endocrine and exocrine gland.
 The primary organ supplying digestive
  enzymes.
 Helps regulate glucose levels.
 4 Secretions-
     Sodium bicarbonate
     Trypsin
     Amylase
     Lipase
Pancreatic Function
 No secretion: starvation due to
  nutrients not digested.
 Oversecretion: over digestion,
  autodigestion of the pancreas.
Anatomy
 Located along the greater curvature of
  the stomach.
 Venous drainage of the pancreas to the
  portal vein, (filtered by the liver), and
  then returned to circulation.
   Hepatitis is common with acute
    pancreatitis.
Pancreatic Anatomy…
 Pancreatic secretions
  pass from secreting
  cells in the pancreas
  into small ducts.
 The small ducts
  ultimately unite to form
  the ducts that carry
  secretions to the small
  intestine.
 The pancreas is made up
  of small clusters of
  glandular epithelial cells.
Pancreatic Anatomy…
 About 99% of the cells are arranged in
  clusters called acini and constitute the
  exocrine portion of the organ.
 The cells within the acini secrete a mixture of
  fluid and digestive enzymes called pancreatic
  juice.
 The remaining 1% of cells are organized into
  clusters called pancreatic islets.
 They form the endocrine portion of the
  pancreas that secrete the hormones insulin
  and glucagon.
Pancreatitis
 Inflammation of the pancreas.
 May be acute or chronic.
 Develops when digestive enzymes are
  activated within the gland, resulting in
  autodigestion.
 Once autodigestion develops, the gland
  becomes inflamed, resulting in tissue damage,
  multisystemic involvement, and often death.
 More prevalent in obese animals.
Pancreatitis…
 Diets high in fat may predispose animals
  to the disease.
 Most commonly a post-holiday disease.
   Feeding scraps from turkey, ham, or roast
    drastically increases an animal’s dietary fat,
    resulting in acute signs of the disease.
Pancreatitis…

 Clinical signs-
      Depression
      Anorexia
      Vomiting
      Dehydration
      Abdominal pain
Exocrine Pancreatic Insufficiency
              (EPI)
 Develops with a progressive loss of acinar
  cells followed by inadequate production of
  digestive enzymes.
 Clinical signs may not develop until 85%-90%
  of the secretory ability has been lost.
 Lack of normal secretions affects the mucosal
  lining of the small intestine and decreases its
  absorptive power.
 Disruption of the normal acinar structure may
  affect insulin production, leading to glucose
  intolerance.
Exocrine Pancreatic Insufficiency
             & EPI…
 Clinical signs-
     Mild to marked weight loss
     Polyphagia, copraphagia
     Diarrhea, fatty stool
     Flatulence
Lp 14 digestive system 2009
Lp 14 digestive system 2009

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Lp 14 digestive system 2009

  • 1. Digestive System VTT 235/245 Anatomy & Pathology Lab
  • 2. Introduction  The digestive system consists of:  **A tube that runs from the mouth to the anus.  Accessory digestive organs that aid in the process of digestion and absorption of nutrients.  The accessory organs are:  Salivary glands  The liver  The pancreas
  • 3. Functions  Prehension (grasping of food)  Mastication  Chemical digestion  Absorption of nutrients and water  Elimination of wastes
  • 4. Oral Cavity  Mechanical digestion- chewing, breaking food down into smaller particles to increase the surface area available for exposure to enzymes involved in chemical digestion.
  • 5. Oral Cavity…  Digestive enzymes are proteins that promote (catalyze) the chemical reactions that split complex food molecules into simpler compounds.  The addition of saliva helps moisten, soften, and shape food into a form that is more easily swallowed.  Salivary amylase breaks down amylose, a sugar component of starch.  Lipase, an enzyme that digests lipids (fats) can also be found in the saliva of some species.
  • 6. Oral Cavity…  The salivary glands are controlled by the autonomic nervous system.  Stimulation of the parasympathetic division results in increased salivation.
  • 7. Peristalsis  The contents of the digestive tract are moved and mixed by two types of smooth muscle contractions:  Peristaltic- move contents along the digestive tract.  They consist of circular muscle contractions that propel contents.  Segmental- cause back-and-forth mixing movements.
  • 8.
  • 9. Esophagus  A muscular tube that extends from the pharynx to the stomach.  Its function is to conduct swallowed material to the stomach.  The esophagus enters the stomach at the cardia.  Made of smooth muscle,  Which helps with peristalsis.
  • 10. Gastroesophageal Reflux & Esophagitis  Inflammation of the esophageal wall most often associated with contact of irritants with the mucosa of the esophagus.  Acids, alkalis, drugs, toxins, and hot materials can produce lesions of varying severity.  Once inflammatory damage occurs, lower esophageal sphincter function becomes abnormal, perpetuating the problem.
  • 11. Megaesophagus  Esophageal paralysis or hypomotility.  A dilation of the esophagus  Due to a vascular ring anomaly or an unknown cause  May be secondary to systemic disease (hypothyroidism)  Primary sign- regurgitation (begins at weaning if congenital)
  • 12. Esophageal Obstruction  Bones and small toys commonly enlodge at the thoracic inlet, cardiac base, or distal esophagus.  The degree of damage to the esophagus depends on:  The size of the object  The shape  The time spent in contact with the mucosal lining
  • 13. Spirocera lupi  Can cause neoplasia of the esophagus.
  • 14. Stomach…  Divisions-  Cardia- the area immediately surrounding the opening from the esophagus.  Associated with the cardiac sphincter.  Fundus- the section that forms a blind pouch that expands as more food is swallowed.
  • 15. Stomach…  Divisions-  Body- also a distensible section in the “middle” of the stomach.  ***Pylorus- the distal part of the stomach that grinds up swallowed food and regulates hydrochloric acid (HCl).  **The glands of the pylorus contain endocrine cells called G cells which secrete the hormone gastrin.
  • 16. Stomach…  The body & fundus are both rich in glands containing 3 key cells-  Parietal cells- which produce HCl.  Chief cells- which produce pepsinogen.  Mucous cells- which produce protective mucus.  Mucous- adjective Mucus- noun
  • 17. Stomach…  Inside the stomach, multiple folds called rugae can be observed.
  • 18. Gastric Motility  Swallowing of food stimulates vigorous mixing, grinding, and propulsive contractions that move food toward the pylorus.  The smooth muscle in the wall of the stomach responds to several hormones, peptides, and nervous system controls.  Stimulation of the vagus nerve causes the fundus to relax (so it can fill), while increasing the contractions in the body and pylorus for mixing and peristaltic movements.
  • 19. Gastric Secretions  Pepsinogen is secreted by chief cells and is a precursor for the enzyme pepsin.  The proteins broken down by pepsin form chains of amino acids (polypeptides & peptides).  The presence of peptides in the pylorus stimulates the G cells to release more gastrin, which stimulates more HCl and pepsinogen release.
  • 20. Gastric Secretions…  Once the pepsin moves from the acidic pH of the stomach to the more alkaline pH of the duodenum, it is inactivated by the change in pH and stops functioning.  The mucus produced by the gastric glands provides a protective coating of the stomach.  Mucins are complex molecules produced by the goblet cells in the gastric glands and are the main constituents of the coating.  Bicarbonate ion is also secreted onto the surface making it more alkaline.
  • 21. Gastric Secretions…  The parietal cells in the gastric glands secrete hydrogen and chloride ions separately into the stomach.  Once these ions are secreted, they combine to produce the HCl that accounts for the stomach’s acidic pH.  The parietal cells have 3 receptors that regulate acid production.
  • 22. Gastric Secretions…  These receptors are for:  Gastrin  Acetylcholine  Histamine  Stimulation of all receptors results in the optimum amount of hydrogen and chloride secretion.
  • 23. Gastric Secretions…  When the pH of the stomach contents drops below 3, gastrin release is inhibited.  When gastrin is inhibited, hydrogen and chloride production is terminated, and HCl production declines.  Selectively blocking any one of these receptors decreases the production of stomach acid.  This is the way antacid drugs work.
  • 24. Mechanism of Vomiting  Vomiting occurs due to the stimulation of the emetic center in the brain.  Visual, vestibular, toxins…  Color and content of the vomit can assist in a diagnosis.  Flecks of blood- recent hemorrhage in the esophagus or stomach.  Coffee grounds- digested blood  Yellow-green- bile
  • 25. Acute Gastritis  Causes include:  Diet- spoiled food, change in diet, food allergy, or food intolerance.  Infection- bacterial, viral, or parasitic.  Toxins- chemicals, plants, drugs, or organ failure.  Ingestion of foreign objects may also result in gastritis.  Once the mucosa is damaged, inflammation occurs and clinical symptoms develop.
  • 26. Gastric Ulcers  Commonly a result of drug therapy.  NSAID’s  Aspirin, ibuprofen…  Disruption of the normal gastric mucosal barrier, resulting in ulceration.
  • 27. GDV  Diet and exercise have been indicated in the development of GDV.  As the stomach fills with air, food, and/or fluid, the outflow tracts become occluded.  Further distension results in a simple dilation (air-filled stomach), or the air- filled stomach may twist along its longitudinal axis (volvulus).
  • 28. GDV…  The pylorus usually passes under the stomach.  The enlarged stomach presses against the diaphragm, making breathing difficult and blocking venous return.  The spleen may also be involved.
  • 29. GDV
  • 30. Pyloric Stenosis  Hypertrophy of circular smooth muscle fibers of the pyloric sphincter  This causes an obstructive narrowing and projectile vomiting
  • 31. Pathology…  Hemorrhagic Gastroenteritis- (HGE)  Acute onset of bloody diarrhea  Malabsorption Syndrome- the small intestine is unable to deliver nutrients to the circulation (EPI)
  • 32. Small Intestine Function: Digestion and absorption
  • 33. Small Intestine  Where the majority of nutrients are absorbed into the bloodstream.  Divided into 3 segments-  Duodenum- first short section leaving the stomach.  Jejunum- longest portion, makes up the majority of the small intestine.  Ileum- enters the colon at the ileocecal sphincter.
  • 34. Small Intestine…  Ileocecal sphincter- regulates movement of materials from the small intestine to the colon.  The parasympathetic nervous system provides stimulation for small intestinal motility, secretions, & blood flow.
  • 35. Structure  The mucosa is adapted to provide a large surface area for absorbing nutrients through folds in the intestinal wall and millions of villi.  Each villus contains thousands of microvilli called the brush boarder.  These cells have many digestive enzymes and carrier molecules embedded in their cell membrane for digestion and absorption of nutrients, vitamins, and minerals.
  • 36.
  • 37.
  • 38. Motility  Has peristaltic waves, which mix the intestinal contents and slow their movement through the length of the intestine.  The churning motion brings digested material into contact with the surface for absorption.  Slowing the movement also allows enough time to contact with the intestinal wall long enough to be absorbed.  Peristaltic movements are stimulated by reflexes to dilation.
  • 39. Structure…  Goblet cells are also present.  They produce mucus that helps protect the intestinal mucosa from the flow of ingestion as it passes over the intestinal lining.
  • 40. Digestion  Electrolytes and vitamins can be absorbed intact into the small intestine wall while carbohydrates, proteins and fats must be chemically digested.  Chemical digestion has 2 steps-  By enzymes in the lumen of the intestine.  By enzymes associated with the brush boarder.
  • 41. Mechanism of Diarrhea  Osmotic-  or poor absorption of contents.  Dietary overload, maldigestion or malabsorption  Secretory- hyper secretion of the valley portion of the villi.  More secretion than absorption.  Ex. Parvo, bacterial  Abnormal Motility- abnormal transit time, usually a hypomotility.  Hypomotility allows for bacterial overgrowth and rotting ingesta. Yummy!
  • 42. Small vs. Large Intestine Diarrhea Signs Small Intestine Large Intestine Frequency Normal to   Volume Large Small Urgency Absent Present Straining Absent Present Mucus Presence Absent Present Blood Presence Coffee grounds Very red Vomiting Present Absent Weight Loss Present Absent
  • 43. Small Intestine Pathology…  Enteritis  Inflammation of the small intestine.  Can be infectious or inflammatory.  The diarrhea usually contains digested blood.  Volvulus-  Rotation of the bowel.  Perforations-  Penetration of the small intestine wall.  Causes: ulcers, foreign bodies, necrosis IIº to obstruction, herniation or external penetration.  This causes painful peritonitis!
  • 44. Parvo  Parvo virus affects the lining of the small intestine.  It invades/wipes out the simple columnar tissue which exposes blood vessels causing “bloody diarrhea”.  The intestinal response is to become inflamed-  Increased peristaltic activity- cramps  Propels chyme through rapidly- diarrhea!
  • 45. Intussusception  The cause is usually idiopathic but can be the result of:  Parasite infection  Foreign bodies  Infections  Neoplasia
  • 46. Intussusception…  The telescoping of the proximal intestine into the distal intestine.  It produces a partial to complete blockage and compromises blood supply to the segments causing bowel necrosis.
  • 47. Mesentery  Mesentery-  Clear, suspends the intestines from the roof of the abdomen.  Prevents intestine entanglement  Supplies blood to the intestines (small & large)  Omentum-  Part of the mesentery.  Helps prevent a torsion.  Attached at the greater curvature of the stomach.
  • 48. Large Intestine Water absorption and bacterial digestion
  • 49. Anatomy Review  “Colon”  Ascending  Transverse  Descending
  • 50. Colitis  Acute-  Chronic-  Sudden onset of  Long-term, non-specific inflammation of the colon.  Often in dogs. inflammation of the colon.  Frequent defecation,  Causes include: idiopathic, small amounts. FIV+, FIP+  Causes: garbage ingestion,  Signs include: diarrhea stress, parasites:  Trichuris, Coccidia with slow, progressive  Bacteria: Salmonella weight loss.  All cause a change in motility!
  • 51. Megacolon  An abnormally dilated colon or segment of the colon.  Seen frequently in cats.  The presenting symptom is straining to defecate.  These cats are usually dehydrated and may be vomiting.  The cause of this disorder has been thought to involve a defect in the neurostimulation mechanism that promotes colon evacuation.
  • 52. Megacolon…  Other causes include:  Hypothyroidism  Pelvic deformities  Severe prolonged colon distension for any reason can disrupt normal motility and result in megacolon.
  • 53. Constipation  True constipation is uncommon.  The presence of foreign objects, tumors, pelvic injury, anal sac abscesses, urinary obstruction, and dehydration can result in the failure to pass feces.
  • 54. Inflammatory Bowel Disease (IBD)-  A group of GI diseases characterized by similar signs with unknown causes.  Diagnosis is made when an excessive number of inflammatory cells are found in mucosal samples of the GI system.  Colonic inflammation disrupts mucosal integrity and results in decreased absorption of sodium and water.  Inflammation also results in hypermotility, resulting in more frequent defecation.
  • 55. Inflammatory Bowel Disease (IBD)…  Signs include:  Diarrhea with little weight loss.   frequency of defecation and  fecal volume.
  • 56. Rectum & Anus  Rectum- the part of the colon running through the anal cavity.  Anus-  Anal sphincter- a muscular ring that controls the passage of feces out of the body.  What type of muscle?  Smooth!
  • 57. Anatomy  Perianal Glands- sebacous glands located in the skin, encircling the anus.  Anal Glands- located in the submucosa, at the anocutaneous junction.  Where are the ducts?
  • 58. Anal Gland Impaction  Retention of anal sac secretions  If left untreated, they may abscess  Anal sac rupture is secondary to obstructions
  • 59. Perianal Adenoma  Usually in intact male dogs.  Bengin, hormone dependant tumor that arises from the perianal gland.  Which hormone?  Testosterone
  • 60. Perianal Fistulae  Multiple ulcerative, smelly draining tracts surrounding the anus  Caused by dogs with a low tail carriage and/or a broad tail base (which retains fecal film) ex. GSD
  • 62. The Liver  The largest gland in the body.  A digestive gland of substantial importance in metabolism.
  • 63. The Liver…  Functions:  Detoxification of drugs and toxins.  Formation and secretion of bile.  Metabolism of carbohydrates and fats.  Plasma protein production.  Urea formation.
  • 64. Anatomy  The liver consists of six lobes.  HEPATOCYTES.
  • 65.
  • 66. Blood Supply  The liver has a unique venous system referred to as the Hepatic Portal System, which receives both oxygenated and deoxygenated blood.  All products of digestion are filtered through the liver and approximately 80% of the blood that flows into the liver enters through the portal vein and originates from the stomach and intestines.
  • 67. Blood Supply…  The hepatocytes are nourished by this blood which is rich in nutrients but not in oxygen.  As blood enters the lobules, it flows across the hepatocytes and filters into the central vein.  The blood then travels from the central vein into the hepatic vein and eventually the caudal vena cava.
  • 68. Blood Supply…  As the blood is filtered through the liver, it passes through Kupffer cells, which help remove bacteria.  The hepatic artery supplies the remaining 20% of blood to the liver.  This blood, which is rich in both oxygen and nutrients, supports the high metabolic activity of the hepatocytes.
  • 69.
  • 70. Hepatocytes  The hepatocytes also secrete hormones and bile, a green digestive hormone liquid.  The bile is carried through channels to the gallbladder where it is stored and the common bile duct, which leads to the duodenum, where bile is released.
  • 72. Bile  Bile plays an important role in digestion, and bile production is one of the main functions of the liver.  Bile consists primarily of bile salts, water, and bile pigments such as bilirubin.  One of the most important functions of bile is to emulsify fat so it can be broken down by digestive enzymes in the gut.
  • 73. Carbohydrate Metabolism  In a process called glycolysis, the liver metabolizes carbs by converting excess glucose into glycogen for storage.  The process is reversed when energy is needed.  The entire cycle is known as glycogenolysis and is under the influence of the hormone glucagon.
  • 74. Deamination  Amino acids are broken down by the removal of an amino group.  The discarded amino group is converted into ammonia and then into urea or uric acid, which is excreted through renal filtration.  Animals with liver failure may have increased levels of ammonia.
  • 75. Synthesis  The liver synthesizes both alpha and beta globulins, which transport lipids and fat-soluble vitamins throughout the body.  Prothrombin is one of the most important alpha globulins produced by the liver.
  • 76. Pathology  Cirrhosis- scarring of the liver, which is replaced with connective tissue. 70% of the liver can be destroyed before problems occur.  Jaundice- A build-up of bilirubin in the body.  Hepatitis- inflammation of the liver causing damage to the hepatocytes.  Cholecystitis- inflammation of the gallbladder.
  • 77. Infectious Canine Hepatitis  Caused by Canine Adenovirus I and has long been recognized as a cause of hepatic necrosis in dogs.  Infection occurs via the oronasal route.  Viral replication occurs in the tonsils and lymph nodes.
  • 78. Infectious Canine Hepatitis…  Signs include:  Petechial hemorrhages  Lethargy  Fever >103°F  Depression  Pale MM  Abdominal pain  Anorexia  Bloody diarrhea  Hepatomegaly
  • 79. Feline Hepatic Lipidosis  “Fatty Liver Disease”  Severe accumulation of fat in the liver  Secondary to diabetes mellitus in obese cats, malnutrition, drugs, toxins, or idiopathic.  Complete anorexia in obese cats  CBC- non-regenerative anemia, stress neutrophilia, lymphopenia.  ↑ALP (20x normal), ↑ALT (10x normal), hyperbilirubinemia, hypoalbuminemia,  bile acids.
  • 80. Hepatic Lipidosis  Signs-  Hepatoencephalopathy  V/D  Icterus  Sporadic vomiting  Anorexia  Obesity  Melena (black, tarry stools)
  • 81. Portosystemic Shunts  Portal Systemic Shunts  The blood by-passes the liver due to a congenital defect or acquired by chronic hepatitis.  This leaves the blood unfiltered as it returns to the heart.  Ammonium biurate crystals in the urine can be an indicator.
  • 82. Shunts  Causes:  Congenital- a vascular anomaly  Acquired- IIº to chronic active hepatitis or serosis, (portal vein non- functional)  Signs:  CNS- hepatoencephalopathy d/t ammonia build-up in the brain.
  • 83. Shunts  Signs-  Anorexia  Depression  Ataxia  Head-pressing  Circling, pacing, blindness  Seizures  Hypersalivation
  • 85. Pancreatic Function  An endocrine and exocrine gland.  The primary organ supplying digestive enzymes.  Helps regulate glucose levels.  4 Secretions-  Sodium bicarbonate  Trypsin  Amylase  Lipase
  • 86. Pancreatic Function  No secretion: starvation due to nutrients not digested.  Oversecretion: over digestion, autodigestion of the pancreas.
  • 87. Anatomy  Located along the greater curvature of the stomach.  Venous drainage of the pancreas to the portal vein, (filtered by the liver), and then returned to circulation.  Hepatitis is common with acute pancreatitis.
  • 88.
  • 89. Pancreatic Anatomy…  Pancreatic secretions pass from secreting cells in the pancreas into small ducts.  The small ducts ultimately unite to form the ducts that carry secretions to the small intestine.  The pancreas is made up of small clusters of glandular epithelial cells.
  • 90. Pancreatic Anatomy…  About 99% of the cells are arranged in clusters called acini and constitute the exocrine portion of the organ.  The cells within the acini secrete a mixture of fluid and digestive enzymes called pancreatic juice.  The remaining 1% of cells are organized into clusters called pancreatic islets.  They form the endocrine portion of the pancreas that secrete the hormones insulin and glucagon.
  • 91. Pancreatitis  Inflammation of the pancreas.  May be acute or chronic.  Develops when digestive enzymes are activated within the gland, resulting in autodigestion.  Once autodigestion develops, the gland becomes inflamed, resulting in tissue damage, multisystemic involvement, and often death.  More prevalent in obese animals.
  • 92. Pancreatitis…  Diets high in fat may predispose animals to the disease.  Most commonly a post-holiday disease.  Feeding scraps from turkey, ham, or roast drastically increases an animal’s dietary fat, resulting in acute signs of the disease.
  • 93. Pancreatitis…  Clinical signs-  Depression  Anorexia  Vomiting  Dehydration  Abdominal pain
  • 94. Exocrine Pancreatic Insufficiency (EPI)  Develops with a progressive loss of acinar cells followed by inadequate production of digestive enzymes.  Clinical signs may not develop until 85%-90% of the secretory ability has been lost.  Lack of normal secretions affects the mucosal lining of the small intestine and decreases its absorptive power.  Disruption of the normal acinar structure may affect insulin production, leading to glucose intolerance.
  • 95. Exocrine Pancreatic Insufficiency & EPI…  Clinical signs-  Mild to marked weight loss  Polyphagia, copraphagia  Diarrhea, fatty stool  Flatulence