Small animal GI Flashcards
diagnostic approach
- Standard approach
- History
- Physical Exam
- Labs
- Imaging
- Biopsies
vomit vs regurgitation
vomit: activley, bile, acidic, digested food and prodromal signs
regurgitation: passive, no bile, non acidic, undigested food, no prodromal signs
abdominal palpation as part of exam
- LIVER (CAN ELEVATE FRONT OF ANIMAL)
- PANCREATIC REGION
- STOMACH
- INTESTINES: Thickness, consistency, mobility
- COLON, RECTUM
STANDARD LABORATORY
EVALUATION
- CBC:
- Anemia, eosinophilia, stress leukogram, NRBC and basophilic stippling
- SERUM CHEMISTRIES:
- Electrolytes, protein losing disease, secondary causes
- URINALYSIS
- Protein loss, bilirubin, urobilinogen
ULTRASONOGRAPHY
- VISUALIZE EXTRAINTESTINAL ORGANS
(pancreas, liver, etc.) - ASSESS MURAL THICKNESS
- ASSESS LYMPH NODE SIZE
apperance of vomit
- BILE (REFLUX FROM DUODENUM
OR REFLUX GASTRITIS) - BLOOD (ULCER, TUMOR,
HEMOSTATIC DISORDER) - FOOD
- GRASS
- NON-FOOD CONSTITUENTS
steps in vommiting
PRODROMAL NAUSEA
* Licking lips, drooling, restless, yawning
* Hypersalivation-relaxes gastroesophageal sphincter
* RETROGRADE GIANT CONTRACTION
* RETCHING (CONTRACTION OF
ABDOMEN WITH CLOSED GLOTTIS)
* FLACCID STOMACH AND RELAXED
SPHINCTERS
vomiting triggered by
- Neural pathway:
- Vagosympathetic
- CRTZ: no BBB in 4th ventricle
- Vestibular
-vomiting center in medulla, - Humoral pathway (CRTZ
NEURAL CONTROL OF VOMITING
* VESTIBULAR RECEPTORS
* PERIPHERAL RECEPTORS
CONSEQUENCES OF VOMITING
Aspiration pneumonia
* Dehydration
* Electrolyte and acid-base
abnormalities
* Hyponatremia
* Hypochloremia and alkalosis with pyloric or duodenal obstruction
* Hypokalemia
* Acid base status often variable
causes of vomiting
- SECONDARY TO A VARIETY OF
DISEASES - Kidney, Liver, Pancreatic disease
- Toxin ingestion
- Infections (parvo, distemper, lepto)
- Heart disease
- Endocrine dx (Addison’s,
hyperthyroid) - CNS disease
- PRIMARY GI DISEASE
ACUTE GASTRITIS
- DIET (INTOLERANCE, BACTERIAL
OR FUNGAL TOXINS, CHEMICAL
TOXIN) - INFECTIOUS (VIRUSES,
BACTERIA) - DRUGS (NSAIDS, ANTIBIOTICS)
THERAPEUTIC GUIDELINES
SUPPORTIVE CARE: Supply fluids and electrolytes
* ANTIEMETICS
* SPECIFIC THERAPY OF PROBLEM
METOCLOPRAMIDE
anti -EMETIC drug
* DOPAMINE ANTAGONIST AT CRTZ AND AT PERIPHERAL RECEPTORS
* ANTIEMETIC AND STIMULANT FOR GI
MOTILITY
* SHORT HALF-LIFE
maropitant
- Cerenia, anti emetic
- NK 1 Receptor Antagonist
- Can be used in dogs and cats
- Good efficacy
5-HT3 Antagonists
- Ondansetron:
- One of the better antiemetics
- Cost is high
- Mirtazapine:
- Antidepressant
- Effective for vomiting and nausea, increase appetite
- Commonly recommended in cats with CRD
GASTROINTESTINAL
PROTECTANTS
Drugs
- H-2 RECEPTOR ANTAGONISTS
(CIMETIDINE, RANITIDINE,
FAMOTIDINE) - OMEPRAZOLE (PROTON PUMP
INHIBITOR) - SUCRALFATE
- MISOPROSTOL
true food allergy
- For definitive diagnosis have to show
immunologic basis of the reaction - More common to see skin than GI
manifestations - Usually diagnosed with elimination
diet/challenge
The most common allergens are proteins and glycoproteins
* Becoming an allergen or not can be
influenced by food processing
* Milk, beef, soy, wheat, oats, eggs, chicken, corn meal, pork, yeast and others have been incriminated in dogs, in cats mainly milk and fish
* Allergy can be to one or multiple components
Development of Food Allergy
- Intestinal barrier prevents most antigens from being absorbed (tight junctions, proteolysis, peristalsis, surface mucus)
- About 0.002% of protein is absorbed intact
- This absorbed protein stimulates GALT (gut associated lymphoid tissue)
- GALT produces secretory antibodies and systemic hyporesponsiveness (tolerance)
-normally antigens are processed by enterocytes or macrophages. B lymphocytes become plasma cells and produce antibodies. T suppresors cells result in a tolerance.
-* Changes in this “normal” way to deal
with antigens can result in food allergy
Breakdown in Normal Antigen
Processing leading to allergy
-increased mucosal antigen uptake
-if gut is damaged there can be direct injection of antigen into the peyers patches.
-IgA deficiency
-increased permeability
- Once allergy is established permeability increases with challenge
- The increased permeability then causes further damage and excess antigen bypassing normal immune function
- May be genetic (Irish Setters and
Gluten sensitive enteropathy
mechanisms of allergic response
- Type 1 reaction easy to recognize with IgE mediated mast cell degranulation. increasing permiability change motility and stimulate mucus production,.
- Type 3 immune complex deposition and Type 4 delayed hypersensitivity are suspected to be the most common,
delay in signs makes it harder to “spot”
the problem as being allergic in origin
clinical signs of food allergy
-more common young
* Can be dermatologic (non-seasonal
pruritus, miliary dermatitis in cats)
* GI signs commonly are vomiting with or without diarrhea, changes in appetite, weight loss
* Although rare asthma, behavioral
changes and seizures may occur
How to Approach A
Chronic Enteropathy
Case
- Establish a baseline, can also use CCECAI
-These factors were more likely related to negative
outcomes with treatment. - Itchy dogs that are food responsive do less well.
- PLE and IBD dogs have less improvement vs. food
responsive dogs.
how to diagnose food allergy
-skin test: detects igE (not good)
-measurment of food specidic igE: ELISA, or RAST, a good negative predictor
- Gastroscopic food sensitivity testing
- Perform gastric endoscopy
- Drip some of the antigen on the stomach and monitor reaction (blanching, erythema. not great for mast cell mediated responses.
-elimination/ challenge diet
Elimination/ challenge diet
-at least 4 week trial, may however in
some cases need to be longer (up to 12 weeks) to exclude a food sensitivity
* No treats, pet vitamins or flavored
medications
* If good response the patient is rechallenged with typical foods to see if reaction recurs, if it does then the elimination diet is started again, provided signs clear up again a
diagnosis of food sensitivity is made
Treatment of Food Sensitivity
-Maintain novel diet
- Hydrolysates
– Proteins broken down to a form no longer allergenic
– Variety of products on market - Avoid offending antigens
- Corticosteroids
food intolerance
- Food idiosyncrasy:
– Probably most common source of GI
related food problems
– Do not require sensitization or
immunological response - Pharmacologic reactions:
– Histamine in spoiled fish
– Chocolate - Food poisoning
– Can be from spoiling - Dietary indiscretion
– Too much food
pancreatitis
- Inflammation of the pancreas
- Develops when the digestive
enzymes are activated in the
pancreas causing autodigestion
MECHANISMS TO PREVENT
AUTODIGESTION
- Enzymes are synthesized, stored
and secreted as inactive zymogens - Activation of zymogens in intestine
- Enteropeptidases (enterokinase)
cleaves activation peptides from
trypsinogen to form trypsin - Trypsin cleaves the activation
peptide off of other zymogens
Digestive enzymes segregated in
the lumen of the rER - Acinar cells contain a trypsin
inhibitor that is synthesized,
segregated, stored and secreted
with digestive enzymes
PATHOPHYSIOLOGY OF
PANCREATITIS
- Develops with autodigestion
- Abnormal mixing of lysosomes and
zymogen granules in abnormal
intracellular vacuoles - Activation of trypsinogen by
lysosomal proteases - Trypsin activates the other
digestive enzymes
-Activated enzymes increase
capillary permeability, damage the
pancreas, and activate vasoactive
amine cascade - Local extension of inflammation
- Vasoactive peptides in circulation
lead to ARDS, DIC, hypotension,
myocarditis, hepatocellular
necrosis, renal tubular damage
pancreatitis will be more severe if?
- Will be most severe if protease
inhibitors are consumed (local and
in circulation) - More severe with hypoperfusion
ETIOLOGY OF
PANCREATITIS
- Nutrition (obesity, fat content)
- Hyperlipoproteinemia
- Drugs (azathioprine, diuretics,
antibiotics) - Duodenal reflux with vomiting or
trauma - Alcohol ingestion
- Ischemia
- Duct obstruction
- Hypercalcemia
- Infection (toxo, FIP)
- Cushing’s disease
- Zinc
RISK FACTORS IN ACUTE
PANCREATITIS
- Mean age 8 +/- 3 years
- Breed (Schnauzers, Yorkies,
poodles) Siamese cats - Obesity
- Prior GI disease, DM, Cushing’s
- NO RISK with oral GCs, anesthesia,
trauma
FELINE RISK FACTORS IN
PANCREATITIS
- Triaditis or triad disease
- A combination of pancreatitis, IBD
and cholangiohepatitis
COMPLICATIONS OF
PANCREATITIS
- Cardiac arrhythmias
- DIC
- Dyspnea (ARDS, effusion, pulm.
edema, PTE) - ARF
- DM
- Sepsis
- Bile duct obstruction, abscess,
pseudocyst
diagnosis of pancreatisis in dogs
- History, physical exam
- Amylase, lipase
- Ultrasound
- PLI, cPL, Precision PSL
diagnosis of pancreatitis I in cats
- History, physical exam
- Clinical signs:
- Lethargy and anorexia
- Vomiting (35-46%)
- Abdominal pain (19-25%)
- Amylase, lipase not useful
- CBC about half have a leukocytosis
liver enzy elevated
-hyperglycemia
-hyperkalemia
-low Ca - Pancreatic specific lipases
- Ultrasound
treatment of pancreatitis
- Fluid therapy, should be aggressive
- Antiemetics (not just vomiting,
also nausea) - Early feeding (enteral preferred)
- Analgesia
EXOCRINE PANCREATIC
INSUFFICIENCY
Progressive loss of exocrine
pancreatic acinar cells
* Inadequate digestive enzyme prod.
* Failure to absorb nutrients
properly
* Large functional reserve
* Signs when 85-90% of pancreas
lost
EPI history
- Weight loss
- Polyphagia
- Coprophagia
- Pica
- Diarrhea, responds to fasting,
steatorrhea - Borborygmus
- Flatulence
etiology of EPI
- Pancreatic acinar atrophy (PAA)
- Chronic pancreatitis
- Idiopathic
- Neoplasia
- Feline ?????
PATHOPHYSIOLOGY OF EP
- Nutrient malabsorption
- failure of intraluminal digestion
- abnormalities in sm. int. mucosa
function - absence of trophic influence
- SIBO: * May be lack of antibacterial
pancreatic secretions - May account for sm. int. mucosal
changes, villus atrophy, changes in enxymes of BB
EPI AND DIARRHEA
Osmotic:
* volume of feces increased in
proportion to % oral intake escaping
absorption
* CHO osmotically active
- Secretory:
- hydroxyfatty acid production by
bacteria - release enterotoxins, deconjugate
bile salts
