GI system → Monogastric and Ruminant stomach (test 1) Flashcards Preview

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Flashcards in GI system → Monogastric and Ruminant stomach (test 1) Deck (58):

what are the 3 critical factors for normal stomach function

  1. Patent pyloric outflow
  2. motility
  3. structural and functional integrity of mucosa



how is gastric motility controlled

Gastric motility is controlled through a balance of stimulatory and inhibitory inputs.


what stimulation and inhibition inputs aides in gastric motility

  • Stimulation:
    • Parasympathetic (vagal nerve)
    • Gastrin
  • Inhibition:
    • Sympathetic nervous system
    • Duodenal conditions
      • <3.5 pH in duodenum
      • peptides and amino acids
      • osmolarity (hypertonicity)
      • fatty acids



What is the function of G cells

G cells:

secrete gastrin→ ↑HCl secretion

↑ pepsinogen



what is the function of parietal cells

H+ and Cl-


what is the function of mucous neck cells

precursor cells for
all the other epithelial types in the stomach


what is the function of enterochromaffin like cells

histamine →  stimulate H2 receptor on parietal cells → ↑HCl


what is the function of chief cells

secrete pepsinogen → autoactivated at acid pH to pepsin, active enzyme


what is the gastric mucosal barrier

“Remarkably, this one cell layer of surface mucus-secreting cells is capable of
maintaining a BARRIER
• that keeps HCl acid and digestive enzymes contained within the lumen
• prevents the loss of abnormal amounts of plasma constituents into the stomach.”


what are the 5 things that make up the gastric mucosal barrier

  1. Mucus (pH gradient)
  2. Bicarbonate secretion
  3. Epithelial barrier (tight junctions)
  4. Mucosal blood flow (subepithelial vasculature)
  5. Prostaglandins (e.g. pGI2)


what role do prostaglandins play in the gastric mucosal barrier

• a general protective effect on gastric mucosa
• stimulate secretion of bicarbonate into mucus layer
• helps maintain mucosal blood flow


what are some general signs of gastric dysfunction

  • abdominal pain
  • vomiting *
  • melena
  • anorexia
  • anemia (bleeding)
  • hematemesis
  • weight loss
  • bruxism (the involuntary or habitual grinding of the teeth, typically during sleep)
  • ptyalism (an excessive flow of saliva)


what are some triggers that stimulate emesis

  • Chemoreceptor trigger zone
    •  toxins, drugs, ketoacidosis, uremia, etc.
  • GI Tract
    • distention / obstruction, mucosal perturbation
  • Outside GI Tract
    • bile duct, peritoneum
  • Extramedullary brain centers
    • certain odors, fears, motion


what are the 3 potential consequences of vomiting

  1. dehydration / hypovolemia
  2. metabolic imbalances
  3. aspiration pneumonia


what are some metabolic imbalances that can stem from chronic emesis

• alkalosis (severe pyloric or high duodenal obstruction)
• hypochloremia
• hypokalemia


what are some clinical signs for gastric outflow obstruction

(a) post-prandial dilation and vomiting
(b) vomiting - poorly digested
(c) vomiting may be chronic & associated with weight loss
(d) horses - reflux when pass stomach tube
(e) full stomach on radiographs – despite Hx


what are the most common / important neoplasms that occur as intraluminal or intramural gastric masses.

  • Adenocarcinoma
    • account for 60-70% of gastric neoplasms in the dog
  • Leiomyoma
    • typically adiscrete solitary intramural lesion (benign)
  • Lymphosarcoma
    • most common gastric malignancy in cats and #2 in dogs
  • SCCa
    • important DfDx for chronic weight loss in horses
  • Polyps
    • benign mucosal lesions occuring in both dogs and cats


what is the most common gastric neoplasm in dogs

Adenocarcinoma → account for 60-70%

followed by lymphosarcoma


what is the most common gastric neoplasm in cats



in the event of chronic weight loss in a horse, what gastric neoplasm should make your DfDx



a GDV (Gastric Dilatation w/ Volvulus is a true surgical emergency in our canine friends.  What are some telltale signs of thie problem?

Signs = rapid gaseous distention of stomach

• abdominal distention & pain
• tachycardia
• restlessness / depression
• shallow breathing
• pale mucous membranes
• weak peripheral pulses
• retching = non-productive vomiting
• inability to pass a stomach tube


Please describe what is shown in the image

this is a simple Gastric Dilatation


Please describe what is shown in the image, and any possible complications that might arise

This is a true Gastric Dilatation w/ Volvulus

• duodenum entwined around esophagus
• spleen carried from left to right side
• vascular compromise → congestion of spleen
ischemic necrosis of stomach wall

This makes it VERY difficult to pass a gastric tube to release the pressure, and is a true surgical emergency.  These patients will die in a matter of hours if not attended to.  The spleen should ALWAYS be examined when venturing to fix this and often times a splenectomy is needed due to the congestion and vascular compromise

The radiograph shows the charactic "revers C" shape that a GDV produces (patient must be in R lateral recumbancy)


You are a small animal veterinarian and you get a phone call from a good friend that says that he got home from some errands and his 2 year old great dane was just laying on the ground and didn't want to get up.  You told him to bring him in and instructed your technicians to take some radiographs upon arrival. 

You come out of the examination room from another patient and your technician hands your this Radiograph.  Is this acute or chronic in nature? What would you tell your technician to do next?

This is VERY acute.

The technician needs to prepare fore SURGERY

This is a true Gastric Dilatation w/ Volvulus

• duodenum entwined around esophagus
• spleen carried from left to right side
• vascular compromise → congestion of spleen
ischemic necrosis of stomach wall

This makes it VERY difficult to pass a gastric tube to release the pressure, and is a true surgical emergency.  These patients will die in a matter of hours if not attended to.  The spleen should ALWAYS be examined when venturing to fix this and often times a splenectomy is needed due to the congestion and vascular compromise

The radiograph shows the charactic "revers C" shape that a GDV produces (patient must be in R lateral recumbancy)


what are some life threatening metabolic changes that are associated with a GDV?

• Acidosis (due to hypovolemia & necrosis)
• Toxemia (due to necrosis of stomach wall)

•SIRS (Systemic Inflammatory Response Syndrome)

(severe infection-bacteremia/endotoxemia with large areas of devitalized tissue)
• Hypovolemic shock
• Cardiac arrhythmias
(due to toxic myocardial necrosis, electrolyte abnormalities)


what is the pathogenesis of acute gastritis

  1. HCl diffusing back across the GMB (gastric mucosal barrier) stimulates neural plexuses in the submucosa
    • stimulates motility (predisposing to spasm) → Vomiting
    • ↑ secretion of HCl & pepsin 
  2. Back-diffusing chemicals also stimulate cells in sub-mucosa
    • mast cells, endothelial cells, PMN’s (polymorphic nucleated cells), etc.
  3. Leakage of plasma fluid and proteins across damaged mucosa
    • helps decrease gastric acidity
    • provides Ig and antiproteases at site


what is the "key concept" in the pathogenesis of acute gastritis?

Acid & pepsin exacerbate and perpetuate gastric mucosal lesions


what are some cases of primary gastritis, and examples of each

  • Infectious
    • Viruses (e.g. coronavirus in pigs) & bacteria
  • Toxins
    • Bacterial enterotoins
  • Physical
    • Foreign bodies
  • Chemicals
    • Ethanol
  • Drugs
    • NSAIDs
  • Allergens
    • some food allergens


what are some causes of Secondary gastritis, and some examples

Gastric lesions resulting from these disorders are usually due to:
• ↑HCl secretion
• ↓mucosal blood flow
• gastroduodenal reflux
• alterations of the mucus-bicarbonate mucosal barrier
• or some combination of these ...


  • shock & DIC
  • renal failure
  • liver disease
  • hypergastrinemia
  • hypoadrenocorticism
  • hyperhistaminemia (e.g. mast cell tumor)
  • hyperacidity
  • Mast cell tumors


what are 2 key things that need to be in place for the body to recover and heal from a gastric ulcer?

  1. Progression of gastric ulcers involves balance between acid secretion and protective/reparative mechanisms.
  2. Severity of the lesion and associated clinical signs may wax and wane as this balance changes.


what are two potential complications of gastric ulcers?

  1. Erosion into large blood vessels - especially arterioles = BLEEDING ULCER
  2. Perforation of stomach wall (transmural ulceration)


what are some clinical signs that you have erosion into large blood vessels - especially arterioles → BLEEDING ULCER

•weight loss
• melena
• hematemesis
• exsanguination (severe loss of blood)


what are some clinical signs that you have perforation of stomach wall (transmural ulceration)

• peritonitis (may be localized)
• colic
• systemic inflammatory response syndrome
• death


what are the 4 general steps in healing from gastric ulcers?

[1] Ulcer bed fills with granulation tissue –surrounding mucosa actively secretes mucus & bicarbonate, which help protect bed from continued injury
[2] Granulation tissue organizes
[3] Lesion is re-epithelialized from edges
[4] Glandular structures are regenerated by invagination of epithelial surface


what is chronic gastritis

•In small animals, characterized clinically by persistent or intermittent vomiting
•In contrast to acute gastritis, spontaneous recovery is UNUSUAL
•Important to rule out underlying systemic disease (non-GI): e.g. 2o gastritis due to uremia
•Diagnosis: often by endoscopy and/or biopsy


what are the 3 primary effects of chronic gastritis

Chronic gastric inflammation compromises all the major functions of the stomach

  1. Gastric motility is altered and reservoir function is impaired
    • Vomiting
    • Delayed gastric emptying OR “dumping” undigested food into duodenum
  2. Chronic inflammation interferes with secretion functions
    • sometimes causes mucosal proliferation which, if severe, can impede gastric emptying by impeding outflow
  3. Loss of plasma proteins through inflamed, leaky mucosa and into the gastric lumen (barrier function)
    • especially if erosion and ulceration is part of lesion


what is the differences between pathogenesis and pathophysiology?

Pathogenesis = the manner of development of a disease.

Pathophysiology = the disordered physiological processes associated with disease or injury


what is the function of each of the 4 ruminant stomachs


Ruminal fermentation is a complex interaction bewteen what 2 things?

  1. Motility of forestomachs
  2. Microbial populations

Given this thearpy is often times aimed at restorying normal rumen flora (transfaunation) and or stimulating rumen motility


what is transfaunation

Transfaunation is the process of transferring rumen microbes from one cow to another. Generally, transfaunation is used to re-inoculate the rumen of a sick cow with a healthy microbial population.


the forestomachs have no intrinsic contractile power, as such the movment of the walls depends on these 3 things.

  1. the integrity of the afferent and efferent nerves
  2. the medullary motor center (gastric center in the brain)
  3. and input signals (exciatory and inhibitory)


what are the 4 general mechanisms that produce ↓ rumenal motility

  1. Gastric center depression
  2. ↑ in inhibitory inputs
  3. decreased excitatory imputs
  4. motor pathway dysfunction


what is vagal indigestion

= Dysfunction of the vagusnerve → rumen and reticulum motility disrupted → outflow of ingestaimpaired → ruminal distention


what is the pathogenesis to ruminal acidosis

Ingestion of highly fermentable carbohydrate (CHO)- usually grains → Gm+ streptococcus bovis multiply rapidly, utilizing CHO to produce lactic acid and long chaing VFAs → buffering mechanisms in rumen are over come → ruminal pH falls below 5 → protozoal, cellulolytic, and lactate using organisms are destroyed → at a pH of 4-4.5 Strep. bovis are rapidly over grown by Gm+ Lactobacilli


Results in

  • Metabolic acidosis
  • Decreased rumen motility
  • Dehydration
  • Toxemia
  • Diarrhea
  • Possible death
  • Founder(laminitis)



what is ruminal tympany

Bloat = distention of the rumen with the gases produced by fermentation due to a failure of eructation



what are the 2 types of tympany

1.Free gas bloat
2.Frothy bloat


what is primary and secondary bloat?

Primary bloat = frothy bloat

Secondary bloat = Free-gass bloat


what are some causes of free gass bloat?

  • Mechanical obstruction
    • Esophageal foreign body
  • Occlusion of the lower esophageal orifice
    • Rumen fluid during lateral recumbency–POSTURAL
  • Deficits in eructation reflex
    • Hypocalcemia, anesthesia


what is the pathogenesis of Primary bloat

Frothy bloat

A stable foamprevents the normal process of gas bubble formation → coalescence → expansion → bursting to form the normal rumen gas cap → Gas bubbles remain within rumen contents and do not rise to the top


there are 2 types of primary bloat.... what are they?

1.Legume/pasture bloat
•Plant proteins adsorbed onto bubble surfaces → stable foam
2.Feedlot bloat
•Microbial products → stable foam
•Lack of fiber → decreased rumen motility


regaurdless of the type of bloat, what are some common consequences

•Decreased rumen motility (severe distention)
•Increased intra-abdominal pressure → inhibition of respiration and cardiac function
•Compression of caudal vena cava → venous return inhibited
•Compression of abdominal viscera → blanching
•Increased mucosal permeability of rumen due to distention


what is traumatic reticuloperitonitis? and what are some of the signs?

Hardware Dz

perforation of the wall of the reticulum by sharp foreign body produces an acute local peritonitis, lesions my remain localized or may spread to produce an acute diffuse peritonitis

Signs (may or may not be present)

  • sdden onset of anorexia
  • pain on palpation and movement
  • expiratory grunt
  • constipation
  • fever
  • ↓ rumen motility
  • humped back
  • abducted elbows



what is Ostertagias, and how is it presented?

  • a disease of ruminants caused by invasion of the abomasum by Ostertagia spp (a worm). Two forms occur.
  • Type I is in lambs or calves in their first summer at pasture and is characterized by the presence of large numbers of adult worms in the abomasum, profuse watery diarrhea, depressed appetite and a high morbidity rate.
  • Type II occurs in cattle in the late winter after that first summer and sometimes in adults. It is characterized by emergence of large numbers of inhibited larvae from the abomasal mucosa, by chronic diarrhea, emaciation, a high death rate and a greatly thickened and edematous abomasal mucosa, subcutaneous edema and high plasma pepsinogen levels. The timing of the two forms varies between countries.
  • The disease is more properly referred to as ostertagiosis but common usage is ostertagiasis.



what are the 4 types of abosmal ulcers

I) non-perforating → subclinical or vague indigestion

II) Ulcer with sever blood loss → anemia, melena, death

III) Perforation with localized peritonitis → fever, anorexia, +/- diarrhea

IV) Peforation with diffusep eritonitis → shock, toxemia