Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/141

Click to flip

141 Cards in this Set

  • Front
  • Back
What are the normal functions of the colon? (5)
1) to act as a reservoir for storage, allowing complete absorption of fluids and electrolytes. (Major function)

2) Motor function has both propulsive (peristaltic) movements and mixing (segmental) contractions. Luminal distension is the main stimulus for motility. Distension also stimulates evacuation of the colon.

3)Mucus provides for lubrication and acts as a buffer due to high HCO3 content. (Main secretory component)

4) Osmosis - water follows Na+ and Cl- absorption.

5) Highest concentration of bacterina in the GI tract (10^11 or ^12 bacter/gram) Enterobacteriaceae most common.
What is the major function of the colon?
act as a storage vessel which allows for reabsorption of electrolytes and fluids.
What is the motor function of the colon?
Has both peristaltic movements and segmental contractions.

Main stimulus for motility is luminal distension which also stimulates evacuation.
What is the main secretory component of the colon?
Mucus which lubricates and buffers the HCO3 content (which is high).
Where, and how many, are the most bacteria in the gut found?
colon with 10^11 or 10^12 bacteria per gram of feces are found. Enterobacteriaceae are the most common.
What types of inflammatory disease can you have of the large intestine? (5)
1) parasitic
2) fungal
3) Bacterial
4) Idiopathic Bowel Disease
5) Variants of IBD
What are two types of parasitic infammatory large intestine diseases?
1) Trichuriasis (Whipworms)
2) Giardiasis (Giardia)
What are two types of fungal inflammatory large intestine diseases?
1) Histoplasma colitis
2) Protothecal colitis
What are 3 types of bacterial inflammatory large intesting diseases?
1) Campylobacter jejuni
2) Pseudomembranous colitis caused by enterotoxins of Clostridium difficile
3) Clostridium perfringens
What are the most common forms of IBD affecting the large intestine?
1)lymphocytic-plasmacytic colitis
2) eosinophilic colitis
3) suppurative colitis
4) histiocytic colitis
Diagnosis of Trichuriasis is by?
identification of ova on fecal flotation

multiple fecal specimens may be needed.
Where do the Trichuris vulpis (whipworms) reside?
In the cecum and proximal colon
What physiological effect do whipworms have?
Cause:
1) severe mucosal hyperplasia
2) chronic inflammatory cell infiltrates
Whipworms (Trichuris vulpis) are the common cause of ?
1) acute, chronic, or intermittent large intestinal diarrhea in the dog
Treatment of whipworms (Trichuris vulpis) consists of?
Fenbendazole (Panacur) daily for 3 days (22mg/lb). Repeat fecals in 3 months.
Diagnosis of Giardiasis is by?
1)Fresh fecal smears looking for trophozoites
2) Zinc sulfate concetration looking for cysts
Treatment of Giardiasis consists of?
1) Fenbendazole (Panacur)
2) Albendazole also works
Giardia is most commonly found?
1) in the small intestine,
2) may also cause colonic inflammation
Pathogenic mechanism by which Giardia causes colonic disease?
unknown
What is the pathogen that causes Protothecal colitis?
Prototheca spp, a blue green algae.
1.)How does Prototheca spp enter the GI tract?

2.)How does it spread?
1) enters the GI tract probably via the colon

2) Dissemination occurs by blood or lymphatic movement. Can go to other organs including the eyes and CNS
1) What is the most common sign of Protothecal colitis?

2) What are other signs of Protothecal colitis?
1) Intermittent or chronic bloody diarrhea.

2) Weight loss and debilitation in the advanced disease. Ocular disease in about 1/2 the cases.
How is Protothecal colitis diagnosed?
by organism identification in biopsy specimens.
What is the prognosis of disseminated protothecal colitis?
Poor prognosis
What is the treatment of disseminated protothecal colitis?
There is no treatment!
What is the definition of diarrhea?
A change in frequency, fluidity, or volume of bowel movement.
Clinical signs of colitis?
Diarrhea, tenesmus, hematochezia, mucoid stools.

Multiple attempts to defecate small volumes of feces.
Campylobacter jejuni is?
a curved, microaerophilic, gram negative rod.

It has zoonotic potential.
What are the types of esophageal peristaltic waves?
Primary and secondary
What is the significance of the different types of esophageal peristaltic waves?
The primary peristaltic wave is what initially moves the food bolus. The bolus itself is a stimulus for the peristaltic wave whose strength is determined by the size, pressure, and location of the bolus within the esophagus.

The secondary wave is initiated only if the bolus remains in the esophagus after the primary peristaltic wave has passed. The secondary wave is initiated by the luminal distension by relaying info to the motor center of the brain.
What are the two most common causes of esophagitis?
The most common cause is Gastroesophageal reflux associated with anesthesia, hiatal hernia, or use of anticholinergic drugs.
The second most common cause is foreign bodies such as bones, fish hooks, or needles.

Lesser causes are: ingestion of chemical irritants, acute or persistent vomiting,or infectious causes.
What is a rational therapy for esophagitis?
Diagnose with endoscopy.
1. identify and remove the underlying cause.
2. withhold food and water for 1-2 days.
3. Increase LES tone by feeding a low fat, high protein diet. This directly affects GI motility (empties faster)
4. H2 blockers if reflux is present (Cimetidine)
5. Increase LES tone and prevent gastroesophageal reflux by giving Metoclopramide (or cisapride)
6. Surgically repair hiatal hernia if present.
7. Sucralfate suspension for erosions - gastric protectant and causes production of protective agents such as prostaglandin E.
How should esophageal foreign bodies be dealt with?
Diagnose by history, Radiographs, contrast radiography (to outline radiolucent foreign bodies and to demonstrate tears), or esophagscopy with endoscope.

1. •Esophageal foreign bodies should be considered an emergency situation because the incidence of complications rises with duration of the condition.
•Esophagoscopy allows removal of foreign bodies not securely anchored.
•Assessment of esophageal damage should follow removal of FB. The esophageal mucosa should be visualized throughout its entire length endoscopically. Radiographs should be taken to check for pneumomediastinum or pneumothorax.
•Only digestible foreign bodies can be left in the digestive tract unless small enough to pass.
•Systemic antibiotics will be required in cases of esophageal perforation.
•Esophagotomy is required if the object cannot be removed with esophagoscopy.

1/3 of affected animals will have complications including perforation f the esophagus, mediastinitis, pleuritis, pyothorax, mucosal laceration, esophageal stricture, diverticulum, and severe esophagitis.
What is megaesophagus?
Esophageal dilation which is associated wth hypomotility. It is more common in Dogs than cats.
There are three types: Congenital idiopathic, Adult onset idiopathic, or acquired megaesophagus.
How is megaesophagus diagnosed?
Idiopathic (congenital and adult onset) is diagnosed with thoracic radiographs following a barium swallow. Dilatation of the entire esophagus is evident. Fluoroscopy can help evaluate peristalsis and is a valuable prognostic aid.
Diagnosis of Acquired cases can be exhaustive.
Acquired megaesophagus is most commonly associated with what 2 general disorders?
neuromuscular disorder
immune mediated disorder
What is the difference between the canine and feline esophagus?
The canine esophagus is all striated muscle fibers while the feline has smooth muscle in the distal 1/3 (which gives it a herringbone like appearance).
What is the purpose of the esophagus?
to move solid and liquid material from the pharynx to the stomach.
The cervical portion of the esophagus is innervated by?
the pharyngoesophageal and recuurent laryngeal nerves.
Caudal to the heart the esophagus is innervated by what nerves?
By dorsal and ventral branches of the vagus.
The gastroesophageal junction (or Lower esophageal Sphincter) is an (anatomic or physiologic) sphincter?
What is its main function?
What controls this sphincter?
The LES is a physiologic sphincter whose main function is preventing gastroesophageal reflux.
The LES is under both vagal nerve control and gastrin (a hormone) control.
1. What are primary signs of esophageal disease?
2. What are seconday signs of esophageal disease?
1.regurgitation(during, shortly after or hours after eating), dysphagia, odynophagia, repeated swallowing movements, ptyalism

2. mucopurulent nasal discharge, dyspnea, moist cough (aspiration pneumonia)
What is the most common congenital esophageal development defect in both dogs and cats?
Persistent Right Aortic Arch (PRAA). Irish Setters and German Sheperds are more frequent victims than other breeds.
How is megaesophagus treated?
Feed dog from vertical position (on stairs is great!)
Small frequent meals
Use of enteral nutrition to support the dog, if necessary.
Treat aspiration pneumonia with broad spectrum antibiotic.

If acquired, remove or treat the underlying cause.

Spontaneous remissions are quite rare, but do happen.
What is the prognosis for megaesophagus?
In most cases it is poor, though if acquired, if a specific etiology can be established and treated (such as myasthenia gravis that only affects the skeletal muscle of the esophagus) the prognosis is a bit better.
Define Dysphagia
Difficulty in swallowing or the inability to swallow. Seen as the immediate ejection of undigested food.
Signs of Dysphagia:
1. Multiple swallowing attempts
2. Pain upon swallowing exhibited by extension and lowering of head and neck.
3. Hesitation before swallowing.
4. Excessive salivation
May be aggravated by firmer consisitency of food.
5. Associated signs include dyspnea and cough if food is aspirated.
Define Regurgitation
The act of passively ejecting esophageal contents without initation of reflex neural pathways other than the gag reflex. May be delayed (can be hours after eating)
Signs of Regurgitation
1. NO ACTIVE ABDOMINAL CONTRACTIONS. it is a passive act.
2. no extreme premonitory signs.
3. The head is held ventrally. Gravity and gagging movements propels the food out of the esophagus.
4. Food is undigested, bile free, and may be cylindrical in shape.
5. Associated signs may include dyspnea and coughing.

This is a hallmark sign of esophageal disease!
Define Vomiting
Coordinated, centrally mediated ejection of stomach contents.
Signs of Vomiting
1. Sense of nausea (lickling lips, salivation, repeated swallwoing movements, apprehension)
2. Retching which is the the rhythmic contraction of the abdominal muscles. This makes vomiting AN ACTIVE PROCESS WITH PRONOUNCED ABDOMINAL MUSCULAR CONTRACTIONS.
3. ejection of stomach contents is due to the contraction of the abdominal muscles.
4. The food is often digested, or at least partially digested, and has bile which is indicative of duodenal reflux.


Projectile vomiting may be seen with high intestinal obstructions.
Differentiate signs between dysphagia, regurgitation, and vomiting.
The food falls from the mouth it is dysphagia. If it is cylindrical, non-digested, and isn't accompanied with abdominal contractions, then it is regurgiation. If the animal is having abdominal muscle contractions and the food is partially or wholly digested with a bunch of bile in it, then it is considered vomit.
What are 4 metabolic alterations whibh may occur in patients with severe vomiting?
1. dehydration
2. prerenal azotemia
3. Electrolyte disturbances: loss of chloride, sodium, and potassium
4. Metabolic alkalosis with pure gastric vomiting (loss of HCl)
5. Metabolic acidosis possible with loss of bicarbonate (rich duodenal secretions).
Outline symptomatic therapy for the acutely vomiting patient.
1. Identify and remove or correct the inciting cause.
2. Withhold food/water for 1 day.
3. Correct fluid deficites and electrolyte imbalances with SQ or IV fluids.
4. After 24 hours start to give small amounts of water. When that stays down, give small amounts of bland food such as I/D, baby food, boiled chicken, rice, oatmeal, and low fat cottage cheese.
After a couple of days, start the regular diet, but phase it in slowly.
Small volumes, frequent feedings.
Consider total parenteral nutrition if vomiting persists for over 3-4 days.
Which drugs should be avoided in the acutely vomiting dog?
1. Anticholinergics (atropine, scopolamine) as they delay gastric emptying.
2. Coating agens such as kaolin/pectin and bismuth salts are rearely effective and may be vomited.
3. ORAL MEDICATIONS ARE CONTRAINDICATED...
Which drugs should be used in teh acutely vomiting dog?
Antibiotics are rarely necessary, but if there is an infectious process occuring, then they can be used, though not orally.
2. Centrally acting antiemetics (phenothiazines (best) or metoclopramide are used)
List 5 metabolic disorders in which the patient may have chronic vomiting as a symptom.
1. metabolic disease - liver, kidney dysfunction
2. Endocrinopathy - Addison's disease
3. Inflammatory Bowel Disease
4. Gastric neoplasia (lymphoma, adenocarcinoma)
5. Gastroduodenal ulceration (many causes)
When taking a history of a vomiting patient, what should be included?
1. Duration and frequency
2. Characteristics of the vomitus
3. When does it occur in relationship to eating/drinking
4. Foreign bodies, toxins, garbage?
5. Dietary changes?
6. Current drugs taken?
7. Vaccinated?
Non-gastrointestinal causes of vomiting include:
1. infectious disease such as canine distemper or leptospirosis
2. Acute pancreatitits
3. Ketoacidotic diabetes mellitus
4. Adrenocortical insufficiency
5. hepatic disease
6. renal failure
7. Drug toxicities
8. Vestibular disorders
9. pyometra
10. CNS disease
11. peritonitis
12. malignancies
Gastrointestinal causes of vomiting include:
1. Gastritis from
a. drugs or toxins
b. infectious causes
c. parasites
d. hypertrophic
e. infiltrative (such as neoplasia)
f. inflammatory such as IBD
2. viral or bacterial enteritis
3. foreign bodies or hairballs
4. gastrointestinal neoplasia
5. ulcers of either the stomach or duodenum
6. intestinal obstructions
7. Pyloric disease and/or hypertrophy
List 5 metabolic disorders in which the patient may have chronic vomiting as a symptom.
1. peritonitis
2. Chronic pancreatitis
3. chronic renal disease with uremia
4. hepatic disease with or without hyperbilirubinemia
5. hypoadrenocorticism
6. feline hyperthyroidism
7. CNS disorder causing increasd CSF pressure
8. Ketoacidotic diabetes mellitus - (will have hyperglycemia, glucosuria, and ketonuria)
List 5 common etiologies for gastrointestinal ulceration in the dog and cat.
1. Drugs such as corticosteroids, NSAIDS, or aspirin. These decrease gastric mucosal blood flow.
2. Alsterd gastric blood flow due to hypovolemia, DIC, endotoxemia
3. Locally aggressive neoplasia such as LSA or adenocarcinoma
4. Renal disease -
-high gastric ammonia serum concentrations promote vasuclitis
- hypergastrinemia may cause excessive HCl secretions
5. Acute and chronic liver disease
Briefly outline rational therapy for a patient with gastrointestinal ulceration.
1. Remove and correct primary cause if possible.
2. Don't give anything by mouth as gastirc distention will increase the HCl secretion and stomach motility .
3. Fluids to correct electrolyte loss and volume deficiency.
4. Oral antacids are not recommended.
5. H2 blockers such as Cimetidine or ranitidine (preferable as it is 5-12X mor e potent and lasts longer). these both protect the parietal cells from histamine.
6. Omeprazole which blocks the proton pump so H+ isn't excreted.
7. Sucralfate which forms a barrier layer against the HCl in the stomach. It also inactivates pepsin and absorbs bile acids. This should be gien 1 - 2 hours after Ranitidine or cimetidine as it decreases their activity.
8. Misoprostil can be used in NSAID induced gastritis as it has cytoprotective properties. It is a Synthetic PGE analog.
9. Antiemetics may or may not be needed. Metoclopramide is better for reflux diseases as it only increases stomach motility.
10. Antibiotics are probably useful only if the stomach wall is fully perforated.
11. Avoid Steroids as they can cause their own ulcers
12. When starting to feed by mouth again, small, frequent meals that are low fat, fiber, and protein.
What is the cause of GDV?
unknown
What is the pathophysiology of GDV?
1. S
How is GDV diagnosed?
1. Radiography (right lateral view) The pylorus will be cranial and dorsal to the fundus and there can be a piece of tissue that separates the pylorus from the fundus. Kind of looks like two bubbles.
How is the GDV managed?
1. Decompress stomach
2. Get baseline data base, radiographs, and blood- gas determination.
3. Restore blood volume and correct electrolyte deficiencies. Use jugular vein!
4.After fluid therapy can give glucorticoids, but may or may not help.
5. NaHCO3 if severe metabolic acidosis.
6. Antibiotics if septic
7. lidocaine if ventricular arrythmias are present.
8. give deferoximine (inhibitor of reactive oxygen metabolites) to reduce reperfusion injury.
9. AFTER patient is stabilized, go to surgery.
Prognosis for GDV?
Depends on how quickly therapy is started. The faster the better.
Compare and contrast simple and strangulated intestinal obstructions.
In both the lumen is occluded, but in simple obstruction the blood supply is retained and there is distension proximal to the obstruction due to fluid and gas buildup. In a strangulation obstruction, there is edema of the bowel wall which leads to tissue hypoxia and infarction which leads to loss of the wall integrity and the passage of intestinal bacterial toxins into the peritoneum from an intestinal perforation.
Does the location of the obstruction lend to different signalment?
Yes, a more proximal obstruction will have heightened clinical signs including severe, persistent vomiting and metabolic alkalosis (due to the loss of HCl) which leads to dehydration, electrolyte imbalance, and shock. These guys will also have diarrhea. In more distal obstruction, the signs can be more chronic, there is often less vomiting so don't have the dehydration, etc. Straining and diarrhea may also be noted.
What is the typical radiographic appearance of a linear foreign body in a cat?
Plication of the small bowel.
What are the four genereal mechainsms for diarrhea in the dog and cat?
1. Osmotic diarrhea
2. Secretory diahrrea
3. Abnormal mucosal permeability
4. Alterations in motility
What is the definition of diarrhea?
the passages of feces that contain an excess amount of water which results in an abnormal increase in stool liquidity and weight.
Non-gastrointestinal causes of vomiting include:
1. infectious disease such as canine distemper or leptospirosis
2. Acute pancreatitits
3. Ketoacidotic diabetes mellitus
4. Adrenocortical insufficiency
5. hepatic disease
6. renal failure
7. Drug toxicities
8. Vestibular disorders
9. pyometra
10. CNS disease
11. peritonitis
12. malignancies
Gastrointestinal causes of vomiting include:
1. Gastritis from
a. drugs or toxins
b. infectious causes
c. parasites
d. hypertrophic
e. infiltrative (such as neoplasia)
f. inflammatory such as IBD
2. viral or bacterial enteritis
3. foreign bodies or hairballs
4. gastrointestinal neoplasia
5. ulcers of either the stomach or duodenum
6. intestinal obstructions
7. Pyloric disease and/or hypertrophy
List 5 metabolic disorders in which the patient may have chronic vomiting as a symptom.
1. peritonitis
2. Chronic pancreatitis
3. chronic renal disease with uremia
4. hepatic disease with or without hyperbilirubinemia
5. hypoadrenocorticism
6. feline hyperthyroidism
7. CNS disorder causing increasd CSF pressure
8. Ketoacidotic diabetes mellitus - (will have hyperglycemia, glucosuria, and ketonuria)
List 5 common etiologies for gastrointestinal ulceration in the dog and cat.
1. Drugs such as corticosteroids, NSAIDS, or aspirin. These decrease gastric mucosal blood flow.
2. Altered gastric blood flow due to hypovolemia, DIC, endotoxemia
3. Locally aggressive neoplasia such as LSA or adenocarcinoma
4. Renal disease -
-high gastric ammonia serum concentrations promote vasculitis
- hypergastrinemia may cause excessive HCl secretions
5. Acute and chronic liver disease
Briefly outline rational therapy for a patient with gastrointestinal ulceration.
1. Remove and correct primary cause if possible.
2. Don't give anything by mouth as gastirc distention will increase the HCl secretion and stomach motility .
3. Fluids to correct electrolyte loss and volume deficiency.
4. Oral antacids are not recommended.
5. H2 blockers such as Cimetidine or ranitidine (preferable as it is 5-12X mor e potent and lasts longer). these both protect the parietal cells from histamine.
6. Omeprazole which blocks the proton pump so H+ isn't excreted.
7. Sucralfate which forms a barrier layer against the HCl in the stomach. It also inactivates pepsin and absorbs bile acids. This should be gien 1 - 2 hours after Ranitidine or cimetidine as it decreases their activity.
8. Misoprostil can be used in NSAID induced gastritis as it has cytoprotective properties. It is a Synthetic PGE analog.
9. Antiemetics may or may not be needed. Metoclopramide is better for reflux diseases as it only increases stomach motility.
10. Antibiotics are probably useful only if the stomach wall is fully perforated.
11. Avoid Steroids as they can cause their own ulcers
12. When starting to feed by mouth again, small, frequent meals that are low fat, fiber, and protein.
What is the cause of GDV?
unknown
What is the pathophysiology of GDV?
1. S
How is GDV diagnosed?
1. Radiography (right lateral view) The pylorus will be cranial and dorsal to the fundus and there can be a piece of tissue that separates the pylorus from the fundus. Kind of looks like two bubbles.
How is the GDV managed?
1. Decompress stomach
2. Get baseline data base, radiographs, and blood- gas determination.
3. Restore blood volume and correct electrolyte deficiencies. Use jugular vein!
4.After fluid therapy can give glucorticoids, but may or may not help.
5. NaHCO3 if severe metabolic acidosis.
6. Antibiotics if septic
7. lidocaine if ventricular arrythmias are present.
8. give deferoximine (inhibitor of reactive oxygen metabolites) to reduce reperfusion injury.
9. AFTER patient is stabilized, go to surgery.
Prognosis for GDV?
Depends on how quickly therapy is started. The faster the better.
Compare and contrast simple and strangulated intestinal obstructions.
In both the lumen is occluded, but in simple obstruction the blood supply is retained and there is distension proximal to the obstruction due to fluid and gas buildup. In a strangulation obstruction, there is edema of the bowel wall which leads to tissue hypoxia and infarction which leads to loss of the wall integrity and the passage of intestinal bacterial toxins into the peritoneum from an intestinal perforation.
Does the location of the obstruction lend to different signalment?
Yes, a more proximal obstruction will have heightened clinical signs including severe, persistent vomiting and metabolic alkalosis (due to the loss of HCl) which leads to dehydration, electrolyte imbalance, and shock. These guys will also have diarrhea. In more distal obstruction, the signs can be more chronic, there is often less vomiting so don't have the dehydration, etc. Straining and diarrhea may also be noted.
What is the typical radiographic appearance of a linear foreign body in a cat?
Plication of the small bowel.
What are the four genereal mechainsms for diarrhea in the dog and cat?
1. Osmotic diarrhea
2. Secretory diahrrea
3. Abnormal mucosal permeability
4. Alterations in motility
What is the definition of diarrhea?
the passages of feces that contain an excess amount of water which results in an abnormal increase in stool liquidity and weight.
Non-gastrointestinal causes of vomiting include:
1. infectious disease such as canine distemper or leptospirosis
2. Acute pancreatitits
3. Ketoacidotic diabetes mellitus
4. Adrenocortical insufficiency
5. hepatic disease
6. renal failure
7. Drug toxicities
8. Vestibular disorders
9. pyometra
10. CNS disease
11. peritonitis
12. malignancies
Gastrointestinal causes of vomiting include:
1. Gastritis from
a. drugs or toxins
b. infectious causes
c. parasites
d. hypertrophic
e. infiltrative (such as neoplasia)
f. inflammatory such as IBD
2. viral or bacterial enteritis
3. foreign bodies or hairballs
4. gastrointestinal neoplasia
5. ulcers of either the stomach or duodenum
6. intestinal obstructions
7. Pyloric disease and/or hypertrophy
List 5 metabolic disorders in which the patient may have chronic vomiting as a symptom.
1. peritonitis
2. Chronic pancreatitis
3. chronic renal disease with uremia
4. hepatic disease with or without hyperbilirubinemia
5. hypoadrenocorticism
6. feline hyperthyroidism
7. CNS disorder causing increasd CSF pressure
8. Ketoacidotic diabetes mellitus - (will have hyperglycemia, glucosuria, and ketonuria)
List 5 common etiologies for gastrointestinal ulceration in the dog and cat.
1. Drugs such as corticosteroids, NSAIDS, or aspirin. These decrease gastric mucosal blood flow.
2. Alsterd gastric blood flow due to hypovolemia, DIC, endotoxemia
3. Locally aggressive neoplasia such as LSA or adenocarcinoma
4. Renal disease -
-high gastric ammonia serum concentrations promote vasuclitis
- hypergastrinemia may cause excessive HCl secretions
5. Acute and chronic liver disease
Briefly outline rational therapy for a patient with gastrointestinal ulceration.
1. Remove and correct primary cause if possible.
2. Don't give anything by mouth as gastric distention will increase the HCl secretion and stomach motility .
3. Fluids to correct electrolyte loss and volume deficiency.
4. Oral antacids are not recommended.
5. H2 blockers such as Cimetidine or ranitidine (preferable as it is 5-12X mor e potent and lasts longer). these both protect the parietal cells from histamine.
6. Omeprazole which blocks the proton pump so H+ isn't excreted.
7. Sucralfate which forms a barrier layer against the HCl in the stomach. It also inactivates pepsin and absorbs bile acids. This should be gien 1 - 2 hours after Ranitidine or cimetidine as it decreases their activity.
8. Misoprostil can be used in NSAID induced gastritis as it has cytoprotective properties. It is a Synthetic PGE analog.
9. Antiemetics may or may not be needed. Metoclopramide is better for reflux diseases as it only increases stomach motility.
10. Antibiotics are probably useful only if the stomach wall is fully perforated.
11. Avoid Steroids as they can cause their own ulcers
12. When starting to feed by mouth again, small, frequent meals that are low fat, fiber, and protein.
What is the cause of GDV?
Unknown
How is GDV diagnosed?
1. Radiography (right lateral view) The pylorus will be cranial and dorsal to the fundus and there can be a piece of tissue that separates the pylorus from the fundus. Kind of looks like two bubbles.
How is GDV managed?
1. Decompress stomach
2. Get baseline data base, radiographs, and blood- gas determination.
3. Restore blood volume and correct electrolyte deficiencies. Use jugular vein!
4.After fluid therapy can give glucorticoids, but may or may not help.
5. NaHCO3 if severe metabolic acidosis.
6. Antibiotics if septic
7. lidocaine if ventricular arrythmias are present.
8. give deferoximine (inhibitor of reactive oxygen metabolites) to reduce reperfusion injury.
9. AFTER patient is stabilized, go to surgery.
Prognosis for GDV?
Depends on how quickly therapy is started. The faster the better.
Compare and contrast simple vs strangulated intestinal obstructions.
In both the lumen is occluded, but in simple obstruction the blood supply is retained and there is distension proximal to the obstruction due to fluid and gas buildup. In a strangulation obstruction, there is edema of the bowel wall which leads to tissue hypoxia and infarction which leads to loss of the wall integrity and the passage of intestinal bacterial toxins into the peritoneum from an intestinal perforation.
Does the location of the obstruction lend to different signalment?
Yes, a more proximal obstruction will have heightened clinical signs including severe, persistent vomiting and metabolic alkalosis (due to the loss of HCl) which leads to dehydration, electrolyte imbalance, and shock. These guys will also have diarrhea. In more distal obstruction, the signs can be more chronic, there is often less vomiting so don't have the dehydration, etc. Straining and diarrhea may also be noted.
What is the typical radiographic appearance of a linear foreign body in a cat?
Plication of the small bowel
What are the four general mechanisms for diarrhea in the dog and cat?
1. Osmotic diarrhea
2. Secretory diahrrea
3. Abnormal mucosal permeability
4. Alterations in motility
What is the definition of diarrhea?
the passage of feces that contain an excess amount of water which results in an abnormal increase in stool liquidity and weight.
1. Describe osmotic diarrhea.

2. Give one clinical example.
1. Increased solutes in bowel lumen secondary to impaired absorption.

2. a. Dietary overload - too many carbs
b. poor absorption of ions
c. Malassimilation (malabsorption and/or maldigestion of nutrients) Exocrine pancreatic insufficiency (EPI)
1. Describe secretory diarrhea.

2. Give one clinical example.
1. increased flow of fluid and electrolytes into the intestinal lumen resulting in large amounts of Na, K, HCO3, and water lost.

2. a. Bacterial enterotoxins
b. Hydroxylated fatty acids
c. Unconjugated bile acids
1. Describe abnormal mucosal permeability diarrhea.

2. Give one clinical example.
exudation of fluid, electrolytes, and protein into the intestinal lumen from mucosal damage.

2. a. protein losing enteropathy (hallmark is panhypoproteinemia)
b. Cellular infiltration (inflammatory, neoplastic, or infectious)
c. invasive bacteria.
d. mucosal ulceration with blood loss
e. lymphatic obstruction (intestinal lymphangiectasia)
1. Describe diarrhea due to alterations in motility.

2. give one clinical example.
1. This rarely causes diarrhea.
Transit time can be either too slow or too fast.

2. Transit time too fast -
a. Feline hyperthyroidism ?
b. IBS?

Transit time too slow
a. favors bacterial growth
Ileus - mechanical or functional
What are characteristics of small bowel diarrhea?
1. often associated with maldigestion or malabsorption
2. Voluminous diarrhea, loss of body weight, failure to gain weight, malnutrition.
3. water, stinky, feces often with color changes.
4. Steatorrhea is common, visible mucus or red blood is uncommon.
5. Flatulence and borborygmus are common with malassimilation.
6. may have melena.
What are characteristics of large bowel diarrhea?
1. hematochezia
2. small quantities of semisolid feces frequently.
3. urgency and tenesmus common
4. vomiting is uncommon but may happen.
5. normal appetite and minimal weight loss.
6. systemic signs aren't often noticed.
What is the value in performing a routine data base in an animal with chronic diarrhea?
A CBC can give you clues as to how the animal is doing and what may be the underlying cause of the diarrhea such as an eosinophilia can suggest endoparasitism, hypoadrenocorticism, or eosinophilic enteretis.
Serum Chemistries and an urinalysis can rule out metabolic or extraintestinal disorders. Also, it can localize the diarrhea to the large or small bowel as large bowel diarrhea will have normal findings.
PANHYPOPROTEINEMIA STRONGLY SUGGESTS A PROTEIN-LOSING ENTEROPATHY (hypoalbuminemia suggests liver disease or glomerular injury).
Fecal exams can also look for parasites or infectious agents as the cause of the diarrhea.
What is a TLI assay?
Trypsin-like immunoreactivity assay.
This is the diagnostic test of choice for EPI (exocrine pancreatic insufficiency).

The exocrine pancreatic tissue secrets a constant level of trypsinogen directly into the blood stream. If the test shows a lower than normal amounts of trypsinogen then EPI can be shot to the top of the differentials list. This is a low cost, highly diagnostic test for EPI.
What signs would an animal be displaying to elicit running the TLI assay?
Weight loss with normal to increased appetite.
Coprophagia/pica may be observed
Increased passage of large volumes of semi-solid feces
Flatulence, borborygmus, steatorrhea
Dry hair coat and general loss of body condition.
What is the significance of Campylobacter jejuni infection in cats and dogs?
It has zoonotic potential and is spread by the fecal-oral route. It is found in animals in healthy and unhealthy animals. Erythromycin may (may not) eliminate the carrier state.
It can cause small bowel diarrhea.
Where are bacteria more apt to be found?
in the large bowel as the HCl in the stomach kills them. Mainly anaerobes (1000:1). Changing the microflora balance can cause diarrhea.
What type of diarrhea does E. coli cause?
secretory diarrhea due to the secretion of water and electrolytes due to enterotxin stimulation.
Should antibiotics be used with a Salmonella infection? Why/Why not?
Only if there is bacteremia present as they don't help with the intestinal issues and they may lengthen the time that the animal is a carrier. This is a Zoonotic disease.
What type of colitis does Clostridium difficile cause?
pseudomembranous colitis.

Clostridium perfringens has been shown to cause nosocomial diarrhea in dogs.

Either of these can be identifed during a fecal.
What are 4 common causes of acute hemorrhagic diarrhea in a young adult dog?
1. Canine parvovirus
2. Salmonella
3. Hemorrhagic Gastroenteritis
4. severe hookworm infestation
5. small intestinal obstruction
6. Histoplasma capsulatam
7. coccidia
What is the therapy for parvoviral enteritis?
1. Fluid/electrolyte replacement
2. Parental bacteriocidal antibiotics
3. Dextrose to prevent hypoglycemia
4. if anemia and hypoproteinemia are present, may need tranfusions.
5. Nothing by mouth until vomiting has stopped.
6. Antiemetics
7. Good nursing care.
8. Begin water and food with small amounts of water, then small amounts of low-fat, low-protein, low fiber food.
What are the clinical signs of lymphocytic-plasmacytic enteritis in dogs and cats?
1. most common sign is chronic, unresponsive small intestine diarrhea.
2. vomiting
3. weight loss
What is the difference between coronavirus and parvovirus?
Coronavirus is less severe than parvovirus. It affects the upper 2/3 of the villi instead of the crypts. It does not spread systematically.
What is significant about Canine hemorrhagic gastroenteritis?
1. severe hemoconcentration with out dehydration because of rapid fluid loss from GI tract before intestitial tissues can correct.
2. Treat with aggressive fluid therapy and ab due to mucosal disruption.
What is the most common cause of chronic gastroenteritis in dogs and cats?
IBD

Hallmark sign is large and or small bowel diarrhea.
What is the treatment of lymphocytic-plasmacytic enteritis?
1. metronidazole (safer) or oral prednisone
2. bland, low-fat hypoallergenic diet. small amounts, increased frequency
3. increased dietary fiber reduces colon inflammation
What is PLE?
An excessive loss of both albumin and globulin into the GI lumen causing a panhypoproteinemia.
PLE occurs secondary to?
1. Intestinal lymphangiectasia (caused by rupture of lacteals and loss of lymph)
2. Severe mucosal disease (protein loss due to exudation, bleeding, or increased mucosal permeability)
3. IBD, Intestinal histoplasmosis, and intestinal lymphosarcoma all cause PLE.
Clinical signs of PLE are?
1. chronic watery diarrhea (mucosal inflammation)
2. Weight loss due to protein caloric malnutrition
3. Pitting edema, ascites, or hydrothorax from reduced oncotic pressure from ruptured lacteals
Clinicopathologic findings of PLE?
1. panhypoproteinemia
2. lymphopenia
3. hypocholesterolemia
4. steatorrhea
5. hypocalcemia
What are the 2 most common neoplasm which occur in the GI tracts of dogs and cats?
1. lymphosarcoma
a. responds variably to chemotherapy
2. Adenocarcinoma
a. poor prognosis
b. most common primary intestinal tumor in the dog.
c. usually located in the feline jejunum
d. usually located in the canine colon.
1. SIBO is?
2. caused by?
3. indirect evidence is?
1. Small intestine bacterial overgrowth.
2. obstruction
stasis
decreased gastric/pancreatic secretions
3. increased serum folate and decreased vitamin B12 levels
Whate are the clinical indications for using antibiotics in patients with acute or chronic gastroenteritis?
1. Not called for unless you have direct evidence that it has a bacterial cause (Campy or Salmonella).
2. May use if there is severe mucosal damage and you are worried about secondary sepsis such as with parvo or HGE
3. May use if there is bloody diarrhea, fever, leukocytosis or -penia, leukocytes in the fecals, or signs of shock.
4. be careful as they may upset the normal GI flora and cause more problems.
Treatment of IBD colitis?
1. treatment is for control as it is rarely curative.
2. Diet of hypoallergenic or homemade diets that are high fiber as they need the bulk to reduce straining.
Drug therapy:
Most antibiotics are useful, but sulfasalazine and metronidazole can be quite useful. Sulfasalazine works because of the antiprostaglandin action and the antileukotriene effect of the salicylates. It has to be used for a minimum of 30 days to be able to see if it helps. Because of the salicylates, use cautiously in cats.
Metronidazole has antiimflammatory properties and it suppresses the cell-mediated immunity. It also lowers the dose of corticosteroids if they are used. Corticosteroids are used to suppress the immune agents.
How is IBD colitis definitively diagnosed?
Biopsy specimens obtained using protoscopy or colonscopies. These specimens are both diagnostic and prognostic.
What is the etiology and how is Irritable bowel syndrome diagnosed?
1. etiology is unknown
2. diagnosed via exclusion
3. intestinal biopsies and other diagnostic tests are normal.
What are 4 host defense mechanisms that prevent pancreatic autodigestion?
1. synthesis of INACTIVE zymogens
2. once synthesized, they are stored withing the rough endoplasmic reticulum.
3. Acinar cells produce pancreatic secretory trypsin inhibitor which inactivate any enzymes that are free in the pancreas. Alpha macroglobulins
inhibit any enzymes that get into circulation.
4. Secretin and cholecystokinin (CCK) are released from the proximal small bowel and stimulate secretion of bicarbonate- and enzyme-rich components of pancreatic juice. This is regulated by cephalic stimulation and hormonal control.
What is the most common cause for EPI in the dog?
1. Juvenile pancreatic atrophy. Affects young 6-24 month old German sheperds. Acinar tissue is lost without any inflammatory changes while islet tissue and endocrine pancreatic function remain normal.

Other causes are chronic recurrent pancreatitis, pancreatic neoplasia, or funcional pancreatic insufficiency when there is severe protein-caloric deficiency (resolves upon adequate intake of protein).
What are the typical clinical signs seen with EPI?
1. Weight loss with normal to increased appetite
2. coprophagia/pica possible
3. increased passage of large volumes of semi-solid feces
4. flatulence, borborygmus, steatorrhea
5. Dry hair coat and general loss of body condition.
What are 4 common causes of acute pancreatitis in the dog?
1. nutritional imbalances
2. Ischemia
3. Trauma
4. Drugs (diuretics)
5. Duodenal reflux into pancreatic ducts
6. hepatobiliary disease in cats
7. chornic renal disease as uremia causes vasculitis and hypergastrinemia.
What is the routine data base that should be performed in a dog or cat with suspected acute pancreatitis.
1. CBC, chem, U/A, serum lipase, and abdominal radiographs.
2. elevated TLi assays
3. diagnosis is exclusionary
What is a rational therapy for a dog/cat with acute pancreatitis?
1. Nothing by mouth for a few days.
2. IV fluids
3. Antibiotics not needed
4. Corticosteroids, probably not necessary
5. Anticholinergics are NOT used as they don't work well in fasting animals.
6. Analgesics are necessary.
7. Antiemetics as needed.
8. Surgery if there is an abscess or efffusive peritonitis.
9. Plasma transfusions to replace alpha macroglobulins
10. reintroduce water first, then low fat, low protein, high carb diet. small amounts frequently.
What are the 2 cornerstones of therapy?
Nothing by mouth for several days to decrease pancreatic secretory activity.

Aggressive IV fluid therapy to correct fluid and electrolyte insufficiencies.
The pancreas lies next to what organs?
duodenum, stomach, kidneys, and transverse colon.

In the cat, the common bile duct enters the pancreas and runs next to the pancreatic duct to the major duodenal papilla. With acute pancreatitis, extra hepatic biliary obstruction can occur.