Practical VETERINARY Internal Medicine.ppt

Practical VETERINARY Internal Medicine

1. Practical Internal Medicine
Don’t Throw Your Hands Up!
Keep It All Down
Managing the Vomiting Companion Animal
Wendy Blount, DVM
Nacogdoches, TX

2. Housekeeping
•Handouts other than PowerPoint slides are
already in your notebook
•You will get copies of the PowerPoint slides
after each section
•Course materials are also
downloadable at
http://wendyblount.com
•Click on “Presentation Notes”
•Click on the link for this seminar

3. Housekeeping
•Proceedings
–TOC, Abbreviations, Evaluation
–Put each PowerPoint handout behind the colored
tab for that section and in front of the first blue
subdivider
–Then you will find client handouts, diagnostic and
treatment aids, lab submission forms, etc.
•CE certificates in your notebook
–I will sign at the end of the seminar
–Please bring your completed
evaluation

4. Housekeeping
•Breakfast, coffee and registration 7:30-8am
•Morning Session 8am-12noon
•Afternoon session 1:30-5pm
•We’ll break the last 10 minutes of every hour
•Lunch break 12-12:30pm
•Dry Lab 12:30-1:30pm
–Small groups for the dry lab
–Dry lab group assignments and
schedule are in your Proceedings
•PLEASE PARTICIPATE!!
•But take private conversations out in
the hall

5. Practical Medicine Philosophy
•As referral medicine becomes more
advanced, it by default becomes more
expensive
•Growing gap between general practice and
specialty practices
•These seminars help us fill those
gaps
•Everything we talk about this
weekend can be done in a rural
mixed animal practice

6. Practical Medicine Philosophy
•Some are already doing these things
–Feeding tubes, managing DKA, liver aspirates
•Some will be ready to begin
•Some will need some hand
holding, at least at first
–TexasVets –Yahoogroups
–Moderator Rosemary Lindsey
[email protected]
•Some will be happy to be better
referring vets

7. Agenda
Saturday –8am-12noon, 12:30-5pm
•Vomiting
•Regurgitation
•Dry Lab –Liver Aspiration
Cytologies, Abaxisequipment
•Elevated Liver Ezymes
•Liver Failure
•(Sign CE Certificates)

8. Agenda
Sunday –8am-12noon, 12:30-5pm
•Diarrhea
•Pancreatitis
•Dry Lab Time if needed
•Managing Feeding Tubes
•The AcuteAbdomen
•Sign CE Certificates

9. Causes of Vomiting
•Vomiting is the most common sign
of gastric disease
•But not all vomiting dogs have
gastric disease
•Not all dogs with gastric
disease vomit

10. Causes of Vomiting –GI Disease
Distal Esophagus
Stomach
Small Intestine
Large intestine
Pancreas
Liver & Biliary Tract

11. Causes of Vomiting –ExtraGI
Abdominal Dz –Acute or Chronic
Obstruction/Irritation from outside GI Tract
Foreign Substance in GI Lumen
Neurologic Disease
Systemic Disease
Toxicity
Environmental/Behavioral

12. Causes of Vomiting
That’s about a jillion causes
How do you find the cause in a particular patient?
Acute or Chronic?
2 weeks
Mild, Moderate or Severe?
-Treat mild disease empirically
-Diagnose and Treat Severe Dz ASAP
-Proceed after discussion with
Mild-Mod chronic & Mod acute vomiting
Compartmentalize, then DAMNIT-V

13. Compartmentalization
Is the vomiting from GI disease or secondary to something else?
Is the dog relatively well and vomiting,
or very sick and also vomiting?
Are there other symptoms not attributed to the GI tract?
Systemic Diagnostics for Systemic Disease
Minimum database, imaging
diagnostic surgery
GI diagnostics
GI Lab Tests, endoscopy
diagnostic surgery

14. DAMNIT-V
D –Degenerative
A –Anomalous
M–Metabolic
N–Neoplastic, Nutritional
I–Infectious, Inflammatory,
Immune Mediated, Idiopathic
T–Toxic, Traumatic
V -Vascular

15. Distal Esophageal Disease
chronic vomiting and regurgitation
DAMNIT-V
A –hiatal hernia
N–neoplasia –leiomyoma/leiomyosarcoma
I –GERD and distal esophagitis,
Spirocerca lupi
GERD–GastroEsophageal
Reflux Disease

16. Gastric Disease
DAMNIT-V
D -Degenerative –chronic
»gastric hypomotility
»gastric dysrhythmia
stomach motility seems normal when the stomach is empty,
but is incoordinated in response to solid food
»Dysautonomia
A –Anomalous -chronic
pyloric outflow obstruction (mucosal or muscular)

17. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy

18. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy

19. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Buster Maze Bowl

20. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Buster Maze Bowl

21. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Kyjen “Hills” Slo-Bowl

22. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Kyjen “Coral” Slo-Bowl

23. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Kyjen “Drop” Slo-Bowl

24. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Kyjen “Flower” Slo-Bowl

25. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy

26. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Buster Cubes

27. Gastric Disease
DAMNIT-V
N –Nutrition -acute
»Eating spoiled food
»Abrupt dietary change, when diet is uniform
»Gastric foreign body/material
»Eating too rapidly
Nutrition -chronic
»Dietary intolerance
Gluten in Irish Setters
»Food allergy
Green Bowl

28. Gastric Disease
DAMNIT-V
N –Neoplasia –usually chronic
Lymphoma (LSA)
»most common gastric neoplasia in the cat
»2
nd
most common gastric neoplasia in the dog
adenocarcinoma
»most common gastric neoplasia in the dog
»Most commonly in the pylorus
Leiomyoma -GIST
»Most commonly in the cardia
»Usually asymptomatic unless pyloric outflow obstruction
Schirrhous adenocarcinoma, Fibroma/FSA
SCC, plasma cell tumor, MCT
Gastric Polyp –symptomatic if pyloric obstruction

29. Gastric Disease
DAMNIT-V
I –Infectious, Inflammatory –acute or chronic
•Bacterial -Helicobactergastritis -chronic
•Fungal –phycomycosis, Histoplasma -chronic
•Parasitic
»Ascarids –puppies
»Physaloptera spp –acute
»Ollulanus spp
»Giardia spp –acute or chronic
»Neorickettsia spp (salmon poisoning) -acute
•Chronic Gastritis
superficial, atrophic, hypertrophic
•Gastric Ulcer –acute or chronic

30. Gastric Disease
DAMNIT-V
I –Idiopathic –chronic
•Chronic gastric dilatation
»Anaerobic bacteria
»aerophagia
»Hypomotility
•Acquired mucosal hypertrophy
•Acquired muscularis hypertrophy
•Duodenogastric reflux (bilious vomiting)
Immune Mediated –chronic
•Inflammatory bowel disease

31. Gastric Disease
DAMNIT-V
T–Toxic, Traumatic
•Drugs –acute or chronic
Antibiotics, NSAIDs, immunosuppressives, cardiac glycosides,
anticholinergics, emetics
•Toxins
»caustic substances –usually acute
pot pourri oil, cleaning supplies, fertilizers
petroleum distillates, organophosphates, toxic plants
»Heavy metals -chronic
lead, zinc
»Ethylene glycol -acute
•Trauma –GDV, Diaphragmatic Hernia
usually acute, but can be chronic

32. Gastric Disease
HelicobacterGastritis
•Associated with chronic gastritis, gastric and
duodenal ulcers, gastric carcinoma, gastric LSA
•Infection is often asymptomatic
•Treatment –triple therapy x 14 days
1. antibiotic 1 –metronidazole
2. Antibiotic 2 –amoxicillin or oxytetracycline
3. Antacids –bismuth or proton pump blocker
BTM–bismuth, tetracycline, metronidazole
OAM–omeprazole, amoxicillin, metronidazole

33. Small Intestine
Bile in vomit indicates duodenogastric reflux
DDx similar to gastric vomiting
DAMNIT-V
N –Neoplasia –acute or chronic
•Strangulation by a pedunculated tumor causing
volvulus (lipoma)
•Intussusception of tumor
•Obstruction by tumor or fungal mass
I –Infectious, Inflammatory
• Antibiotic responsive diarrhea –chronic
•Hemorrhagic gastroenteritis (HGE) -acute

34. Small Intestine
DAMNIT-V
I –Infectious –viral
•Parvovirus
•Coronavirus
•Canine distemper virus
I –Idiopathic
•Reverse intestinal peristalsis
T –Traumatic -acute
•Mesenteric volvulus
•Intussusception
most commonly secondary to severe diarrhea

35. Large Intestine
Acute or chronic
DAMNIT-V
M –Metabolic -chronic
•Hypothryoidism can predispose to megacolon
I –Inflammatory
•HGE –acute or relapsing
•Colitis –acute or chronic
•IBS -irritable bowel syndrome
T–Traumatic
•Constipation –acute or chronic

36. Pancreas
Acute Pancreatitis
Chronic Pancreatitis

37. Liver & Biliary Tract
Vomiting more common when there is cholestasis
Most icteric dogs vomit
Why do dogs with non-icteric liver disease vomit?
»Decreased gastric mucus, due to abnormal protein
synthesis.
»Decreased gastric epithelial cell renewal due to
abnormal protein synthesis.
»Decreased gastric blood flow, due to altered vasoactive
factors.

38. Liver & Biliary Tract
DAMNIT-V
M –Metabolic -chronic
•Biliary sludging and/or mucocoele
•Gall stone obstruction
N –Neoplasia -chronic
•Hepatic carcinoma
•Biliary carcinoma
•LSA

39. Liver & Biliary Tract
DAMNIT-V
I –Infectious –acute or chronic
•Acute or chronic bacterial cholangiohepatitis
•Viral hepatitis –chronic
•Heterobilharzia spp–chronic
•Fungal hepatitis
I –Inflammatory, Immune mediated –acute or chronic
•Acute hepatic necrosis
•Chronic active hepatitis
T -Trauma –acute
•Biliary tract rupture

40. Abdominal Disease
Peritonitis (ascitic exudate) and resulting ileus
Abdominal pain
Impingement on the biliary and/or GI tracts by mass
DDx Peritonitis
•Septic –perforated bowel or abscess, or localized
infection
•Bile –ruptured biliary tract
•Uroabdomen –ruptured urinary tract
•chyloabdomen
•Generalized enteritis
•Pancreatitis
•Viral -FIP

41. Abdominal Disease
DDx Abdominal pain –acute abdomen
•Passing a kidney stone
•pancreatitis
•Biliary obstruction
•GI obstruction
•Rapidly growing mass in an encapsulated organ
(kidney, liver, spleen)
•Abdominal abscess
•Pyelonephritis
•Splenic torsion
•Cryptorchid testicular torsion

42. Abdominal Disease
DDx Impingement on the biliary and/or GI tracts by mass
Neoplasia
Cyst
•Pancreatic cyst
•Perirenal cyst
•Choledochal cyst
•Hepatic cyst
Abscess
Granuloma

43. Abdominal Disease
DDx Impingement on the biliary and/or GI tracts by mass
DDx Granuloma
I –Infectious -chronic
•L-form bacteria
•Ureaplasma, Mycoplasma spp
•Mycobacterium spp
•Bartonella spp
•FIP
•Many fungal infections

44. Abdominal Disease
DDx Impingement on the biliary and/or GI tracts by mass
DDx Granuloma
I –Inflammatory –necrosis or saponification of fat
•Pancreatitis
•Pansteatitis
•Pancreatic adenocarcinoma
•lymphangiectasia
I -rarely immune mediated
•Idiopathic
•Post rabies vaccine steatitis

45. Neurologic
Limbic Epilepsy
Seizure locus at the vomiting center
Responds to anticonvulsants (don’t use bromide)
Vestibular Disease
Neoplasia
Vomiting center or CRTZ
Increased CSF pressure
Many things that increase CSF

46. Systemic Disease
Why do dogs with systemic disease vomit?
Chemical stimulation of the vomiting center &
chemoreceptor trigger zone.
Drugs that suppress this center
work best
Cerenia®

47. Systemic Disease
DAMNIT-V
M-Metabolic (ileus)
»Hypercalcemia
»Acute hypocalcemia
Eclampsia
»Hypokalemia
»hypomagnesemia
»hypothyroidism
»hypoadrenocorticism
»Hyperadrenocorticism

48. Systemic Disease
DAMNIT-V
M-Metabolic (toxic)
»Uremia
»Jaundice
»Sepsis
»Acidosis (lactate, ketones, necrosis, etc.)
Metabolic (idiopathic)
»Hyperthyroidism
Metabolic (shock)

49. Systemic Disease
DAMNIT-V
N –Neoplasia (paraneoplastic effects)
•High gastrin levels
Gastrinoma
MCT
•Hypercalcemia
•Systemic inflammation
I –Infectious (unknown mechanism)
»Feline heartworm disease
»Systemic fungal infection

50. Systemic Disease
DAMNIT-V
T -Toxicity
»Hypercalcemia
Cholecalciferol rodenticide
Eczema cream (calcipotriol –Dovonex®) toxicity
»NSAIDs
»corticosteroids
»Acidosis –ethylene glycol

51. Systemic Disease
Why do dogs with renal failure vomit?
Direct toxicity to the gastric mucosa my renal toxins
Decreased renal metabolism of gastrin by the
kidneys, leading to elevated gastrin levels, and
increased HCl secretion in the stomach.
Drugs that protect the GI tract and stop
gastric acid secretion work best
sucralfate
Proton pump blockers >> H2 blockers

52. Systemic Disease
Why do dogs with NSAID toxicity vomit?
Direct toxicity to the gastric mucosa
Inhibition of gastroprotective prostaglandins
»Piroxicam, ibuprofen and naproxen undergo more
complete enterophepatic circulation, and thus have
prolonged half life in the dog and cat.
»COX2 selective are not as GI toxic as COX non-
selective, but both can cause problems.
Prostaglandin analogs work best
misoprostol ( Cytotec® )

53. Systemic Disease
Why do dogs with corticosteroid toxicity vomit?
Decreased mucosal cell growth and mucus production
Increased gastric acid secretion
High doses required for acute toxicity
Chronic toxicity when other risk factors present:
NSAIDs, hypotension, bile acid reflux, spinal cord
disease, liver disease, renal disease, Addison’s
disease, mast cell tumor degranulation, gastrinoma.
H2 blockers & sucralfate work best

54. Environmental/Behavioral
Motion sickness
Heat Stroke
Pain
Fear
Excitement

55. Dozens of Causes of Vomiting
Did that help us diagnose and treat our
vomiting patients?
Not a Lot!

56. Dozens of Causes of Vomiting
Did That Help?
Not a Lot!

57. Working Up the Vomiting Patient
Empirical Treatment first if indicated
Pattern Recognition
Step Wise Work-Up

58. Step 1 –Empirical Treatment
1. Cerenia PO SID x 1-4 days
2. Metronidazole 10-15 mg/kg PO BID x 7 days
250 mg tab –¼ tab per 10 lbs
500 mg tab –¼ tab per 20 lbs
Max dose 500mg
3. Deworm
pyrantel or Profender for cats
fenbendazole for dogs

59. Physaloptera spp.
Always deworm vomiting animals
Presentation:
acute or chronic onset of profuse vomiting
weight loss is usual
Sometimes anorexic, sometimes not
Diagnosis:
Almost never see the eggs on fecal
Deworming empirically prevents the
need for diagnosis by endoscopy

60. Physaloptera spp.

61. Physaloptera spp.

62. Physaloptera spp.

63. Clues in the Signalment
Deep chested breeds -GDV
Poodles–hypoadrenocorticism
Brachycephalic breeds -GERD,
hiatal hernia, pyloric mucosal
hypertrophy
GSD –antibiotic responsive
diarrhea

64. Clues in the History
If weight loss associated with
increased appetite -diabetes,
hyperthyroidism & IBD
Most common clinic sign of
gastric neoplasia –anorexia,
then weight loss, then vomiting

65. Step-Wise Plan for
Diagnosing Vomiting
1.Minimum Database
2.Imaging, GI Lab, ACTH Stim
–radiographs +contrast, US
3.Flexible Endoscopy
4.Surgery with biopsies
5.Fluoroscopy
6.Empirical Tx for limbic epilepsy
& motility disorders

66. Step-Wise Plan for
Diagnosing Vomiting
1.Minimum Database
•CBC
•Profile
•Electrolytes/blood gases
•Urinalysis
•Fecal
•T4/free T4 for older cats
•HW Test for dogs
•Coagulation panel if hematemesis

67. Clues in the MDB
Polycythemia-HGE, neoplasia
•Albumin normal with HGE, high with
dehydration, globulins high with neoplasia
Low albumin and globulin –protein
losing enteropathy, GI blood loss
•HCT normal with PLE, low with GI blood
loss
Low albumin, normal globulin –
liver disease, protein losing
nephropathy, vasculitis

68. Clues in the MDB
Azotemia
•High BUN with normal creat and phos -GI
blood or high protein diet
•High BUN, high creat, high phos -Check
urine specific gravity to confirm renal
disease
Liver Disease Pattern
•High liver enzymes
•High bili with normal PCV
•Low albumin, glucose
•Abnormal cholesterol, triglycerides

69. Clues in the MDB
Cat –icterus w/normal PCV and liver
enzymes
•Pancreatitis
•FIP
•Lymphoma
Diagnostic Trifecta for FIP
•Lymphopenia <1500/ul
•Titer 1:160 or greater
•Globulins >5.1 g/dl
•Positive predictive value 89%
•Negative predictive value 99%
•Histopath and fluid analysis supportive
•Fluid analysis chart–pancreatitis section

70. Clues in the MDB
Pancreatitis pattern
•icterus
•hypocalcemia
•Acidosis
•Hyperglycemia
•Elevated fPL or cPL, TLI
•Elevated lipase
•lipemia
•Amylase not helpful if azotemic
•Abdominal pain
•Whacked out insulin response if diabetic
•Ketonuria if diabetic

71. Clues in the MDB
Ethylene glycol toxicity pattern
•Period of ataxia at onset
•Increased anion gap
•Calcium oxalate crystals in the urine
Neoplasia pattern
•Really sick with pretty boring bloodwork
•Intermittent low grade fever
•Hypercalcemia
•Increased globulins
•Increased white count

72. Clues in the MDB
Addison’s Disease pattern
•Signs wax and wane
•Hematemesis, hematochezia
•Azotemia with moderately concentrated
urine (1.020’s)
•Hypoalbuminemia
•Hypercalcemia
•High potassium and/or low sodium
•Remember whipworms can cause
hyperkalemia and hyponatremia, as can
repeated abdominocentesis

73. TAMU GI Lab Tests
•TLI/PLI –do you have significant
pancreatic disease?
•B12/folate –do you have
significant intestinal disease?
•Bile acids –do you have
significant liver disease?
•Tritrichomonas PCR –chronic
diarrhea in cats

74. Gastrin
•Made by gastric mucosa, pancreas
•Eliminated by the kidneys
•Increased with MCT, CRF, chronic proton
pump administration, gastrinoma
•Stimulates the gastric mucosa to make HCl
Causes problems:
•GERD
•Distal esophagitis and regurgitation
•Ulcers in esophagus, stomach, duodenum
•Chronic gastritis, duodenitis

75. When to do a barium study?
•NOTjust prior to an abdominal US
•NOTjust prior to a scope
•NOTif perforation is suspected
•If evidence of mural GI disease –to
check for obstruction
•If you suspect a foreign body
•If you suspect a motility disorder
•Abdominal contents are
malpositioned
•If you suspect a diaphragmatic hernia

76. Barium study for vomiting
Avoid drugs that inhibit GI motility
•Opiates
•beta agonists (bronchodilators)
•Anticholintergics (atropine, aminopentamide)
1.Shoot scout films
2.Give barium
–4-6 ml/lb small dogs and cats
–2-4 ml/lb large dogs
3.Within 5 minutes for gastrogram
4.30 minutes, and every hour until
barium is gone from stomach

77. Barium study for vomiting
Thumb Rules
•Barium should be in duodenum within 20 minutes
•Stomach should be empty within 3-4 hours
•Barium coated food can remain in the stomach for
12-15 hours

78. When to recommend endoscopy?
•No evidence of systemic disease
outside the GI tract
•Not suspecting lymphoma, which is
more often in the muscularis
•Low albumin –poor surgical risk
•Abnormal B12/folate indicate
significant intestinal disease
•Owner wants low morbidity
procedure

79. Preparation for endoscopy
•Withhold water the morning of scope
Upper GI:
•Withhold food and barium for 24 hours
•Withhold food for 48 hours for lower GI
Lower GI:
•Withhold food and barium for 48 hours
•Biscodyl 5 mg PO 24 hours before
•Enemas 24, 12 and 1-2 hours before
•Or use GoLytely

80. When do you suspect a
Motility Disorder?
•Minimum database and imaging NSAF
•Prolonged GI transit on contrast study without
obstruction
•Regurgitation without an identifiable cause
•Other signs of peripheral neuropathy
–Laryngeal paralysis
–Spinal or cranial nerve deficits (LMN)
–constipation
•Other signs of dysautonomia
•Presence of hypothyroidism, Cushing’s Disease,
Addison’s Disease, Myasthenia Gravis, spinal
cord disease, uremia, hypercalcemia,
hypocalcemia, etc.

81. Treating Motility Disorders
•Prokinetics work best
•Metoclopramide works only on the stomach
•Cisapride may also work on the esophagus and
colon, at least somewhat
•Erythromycin and ranitidine have prokinetic
characteristics
–Erythromycin lower dose 0.25-0.5 mg/kg PO TID
•Reduced dietary fiber and fat speed gastric
emptying
•Worsened by aminopentamide (Centrine®),
opiates, beta agonists

82. DDx Hematemesis
•Blood swallowed
•Blood coming from the erosive
disease in the stomach
•Blood coming from erosive
disease in the duodenum and
refluxed into the stomach
•Trauma
•Coagulopathy

83. DDx Hematemesis
Blood swallowed and then vomited
and/or produces melena
–Trauma or coagulopathy can result in bleeding from any
of these areas
1.Respiratory tract
»Neoplasia
»Pulmonary thromboembolism
2.Caudal nasopharynx (rostral nasal cavity bleeding
usually results in epistaxis)
»Neoplasia
»Fungal infection
3.Oral cavity
»Dental disease
»Neoplasia

84. DDx Hematemesis
Bleeding from the duodenum, refluxed
into the stomach.
–Ulcerative/erosive duodenal disease –
see differentials for gastric
ulcerative/erosive disease.
–Parasites –Coccidia, hookworms.
–See also Melena in the Diarrhea
Section.

85. DDx Hematemesis
Causes of erosive gastritis
»Liver failure.
»Kidney failure.
»Hypoadrenocorticism.
»Gastric neoplasia –see chronic vomiting.
»Pancreatic neoplasia –gastrinoma.
»Toxicity –NSAIDs, glucocorticoids, lead
»Toxicity –caustic substances
»cleaning supplies
»pot pourri oil
»Trauma to the gut.
»Shock –anaphylaxis, hypovolemia, septic, HGE.
»Anesthesia (hypovolemia).
»Spinal trauma.

86. DDx Hematemisis
Coagulopathy
1.Factor deficiency
»Liver failure
»Anti-vitamin K rodenticide toxicity
»congenital
2.Platelet problem
»Thrombocytopenia
»Platelet function defect
3.Blood vessel problem –vasculitis,
hypertension, hyperviscosity
4.Combination -DIC

87. DDx Hematemisis
Recurring Hematemisis and
Hematochezia are special
indications for ACTH Stim
Even if electrolytes are normal

88. Tx Hematemisis
•Treat underlying cause
•Continue proton pump or H2 blockers for 14
days after hematemesis resolves

89. H2 Blockers
•Cimetidine (Tagamet®) 2.5-5 mg/lb PO IM IV
TID-QID.
–Inhibits hepatic microsomal enzymes.
–May increase half life of drugs that are metabolized in
the liver –theophylline, warfarin, phenobarbital.
–Can cause mental depression.
•Ranitidine (Zantac®) 1 mg/lb PO SQ IM IV BID-
TID
–5x as potent as cimetidine.
–Also a prokinetic, by inhibiting acetylcholinesterase.
–Inhibits hepatic microsomal enzymes as cimetidine, but
to a lesser extent.

90. H2 Blockers
•Famotidine (Pepcid®) 0.25-0.5 mg/lb PO IV SID-
BID.
–Inhibits hepatic microsomal enzymes as cimetidine, but
to a lesser extent.
–20x as potent as cimetidine.
•Nizatidine (Axid®) 1.25-2.5 mg/lb PO SID.
–5x as potent as cimetidine.
–Also a prokinetic.

91. Proton Pump Blockers
–More effective than H2 blockers for mast cell
degranulation.
–Stronger suppressors of gastric acid secretion
than H2 blockers.
–Diminishes proteolytic effect of pepsin.
–Maximum effect at the 5
th
dose (may need to
use with H2 blockers for the first 3-4 days).
–Prolonged use (greater than 4 weeks) can
cause reversible gastric mucosal hypertrophy.
–Rebound hypersecretion of HCl can occur if
stopped abruptly (high gastrin levels due to
lack of feedback).

92. Proton Pump Blockers
–Omeprazole (Prilosec®)
»5 mg (1/2 capsule) PO SID, for dogs <11 lbs.
»10 mg PO SID, for dogs 11-45 lbs.
»20 mg PO SID, for dogs greater than 45 lbs.
–Lansoprazole (Prevacid®)
»15 mg PO SID for small dogs
»30 mg PO SID for large dogs.
–Esomeprazole (Nexium®)
»0.7 mg/kg PO SID for dogs.
»Granules in capsule inactivated if sprinkled on
food.
–Pantoprazole (Protonix®) –10-40 mg PO SID; 1
mg/kg IV SID.
–Rabeprazole (Aciphex®) –5-20 mg PO SID.

93. Antiemetics
Central Antiemetics
•Phenothiazines-Act at both the CRTZ and the
vomiting center.
–Use only in well hydrated patients, without low blood
pressure, as they are hypotensives.
–Prochlorperazine (Compazine®) 0.25 mg/lb SQ IM TID
–Chlorpromazine (Thorazine®) 0.15-0.25 mg/lb SQ TID.
•Antihistamines -Act at the CRTZ
–Diphenhydramine (Benadryl®) 05-2 mg/lb PO IM or
SLOWLY IV.
–Dimenhydrinate (Dramamine®) 2-4 mg/lb PO TID.
–Meclizine (Antivert®) 12.5 mg PO SID for small dogs
and cats; 25 mg PO SID for medium to large dogs.

94. Antiemetics
Central Antiemetics
•Central Anticholinergics
–Scopolamine (Hyoscine®) 0.02 mg/lb SQ IM QID.
–Acts at vestibular center and CRTZ.
–Side effects ileus, dry mouth, sedation.
•Yohimbine (Yobine®)
–Acts at the CRTZ and the vomiting center.
–0.15-0.25 mg/lb SQ IM BID.

95. Antiemetics
Peripheral Antiemetics
•Cisapride (Propulsid®)
–Antiemetic and prokinetic.
–Acts peripherally on the GI tissue –does not cross the
blood brain barrier, so no associated extrapyramidal
side effects.
–0.05-0.25 mg/lb PO TID.
•Anticholinergics
–Aminopentamide (Centrine®) 0.1-0.4 mg IM SQ BID-
TID.
–Side effect –ileus (undesirable when there is ileus or
motility disorder).

96. Antiemetics
Peripheral and Central Antiemetics***
•Metoclopramide (Reglan®) -Antidopaminergic
and antihistaminic, acts at the CRTZ
–Antiemetic as well as prokinetic
–0.2-0.4 mg/kg PO, SQ, IV TID-QID.
–CRI –0.5-1 mg/lb/day IV.
–Reduce dose by 50% in pets with renal failure
–Side effects hyperactivity and constipation
(extrapyramidal signs) -more common in the cat
–For severe metoclopramide side effects, give Benadryl.
–Because serotonin receptors dominate in the feline
CRTZ rather than dopamine, metoclopramide may not
work as well as an antiemetic in cats, when compared
to dogs.

97. Antiemetics
Peripheral and Central Antiemetics***
Block vagal afferent neurons, and act at the CRTZ
NK antagonists –inhibit substance P
–Maropitant (Cerenia®) 1 mg/kg SC SID, 2 mg/kg PO
SID for acute vomiting, no more than 5 days in a row
(skip 1-2 days)
–8 mg/kg PO 2 hours prior to travel for motion sickness,
for no more than 2 days in a row (skip 3 days)
5HT antagonists
–Ondansetron (Zofran®) 0.05-0.15 mg/lb PO or slowly
IV SID-TID.
–Dolasetron (Anzemet®) 0.4-0.6 mg IV SID-BID.
–Side effects sedation and head shaking.

98. Prokinetics
–Reduce gastroesophageal reflux.
–Help control vomiting by accelerating
gastric emptying.
–Improve coordination of antrum, pylorus
and duodenum.
–Increases propagation distance of
peristaltic waves.
–Contraindicated in cases with obstruction
(can precipitate perforation).
–Can usually wean prokinetics to the
lowest effective dose.

99. Cytoprotective Agents
•Bind to the ulcer/erosion to create a
physical protective barrier.
•Inactivate pepsin.
•Adsorb bile acids, which can be
inflammatory.
•Sucralfate (Carafate®) 0.5 g/15 lb PO
BID-QID.
•Barium sulfate 2-6 ml/lb PO (same as for
upper GI series).
•Side effect constipation.

100. Mucosal Protective Agents
•Increase mucosal mucus and bicarbonate
production.
•Decrease mucosal acid production.
•Promote mucosal blood flow.
•Indicated for NSAID gastritis.
•Misoprostyl (Cytotec®) 1-2.5 ug/lb PO
TID.
•Side effects include:
–Abdominal cramping.
–Vomiting, diarrhea.
–Abortion.

101. Dysautonomia
First cases in Scottish horses in the 19 century
First reported in the cat in 1982, first dog in 1983
Degeneration of autonomic ganglia and failure of
autonomic function
History:
•Vomiting, regurgitation, diarrhea
•Anorexia weight loss, lethargy
•Dyspnea, coughing
•Photophobia
•Dysphagia, dysphonia
•dysuria
•Onset over 1-2 weeks

102. Dysautonomia
Exam:
•Decreased anal tone
•Absent PLR, moderate mydriasis
•Third eyelid prolapse
•Dry mucous membranes and eyes
•Crusty nose, nasal discharge
•Dyspnea, pulmonary crackles, fever
•Cachexia, weakness
•Global LMN weakness and CP deficits on neuro exam
•Large urinary bladder that is easy to express
•Heart rate and blood pressure relatively low

103. Dysautonomia
Diagnosis:
•Thoracic rads may show megaesophagus and/or
aspiration pneumonia
•Other neurologic deficits are absent
•Ileus, bladder distension on abdominal imaging
•Schirmer Tear Test less than 10mm OU
•CBC, panel, CSF tap may be normal if no systemic
complications

104. Dysautonomia
Diagnosis:
Pilocarpine test
•Place 1-2 drops 0.05% pilocarpine in one eye
•Check PLR every 15 minutes for one hour
•Normal dogs show minimal response
•If dysautonomia, miosis due to denervation hypersensitivity
•Can be false negatives
•Chronic OP toxicity can produce similar results
•Adding atropine will reverse the miosis in OP toxicity
but not dysautonomia
No tachycardia in response
to atropine injection

105. Dysautonomia
Treatment:
Bethanechol 1.25-5 mg PO BID or 0.05 mg/kg SC BID
•SC seems to work better
•Can help with urination and secretion
•Can gradually increase to effect
•Side effect –can increase vomiting and aspiration pneumonia
Pilocarpine eye drops
•Can assist tear production and photophobia
Artificial tears OU PRN, Genteel, Soothe XP
Elevated feedings, prokinetics, permanent Gtube

106. Dysautonomia
Prognosis:
Grave
Mortality 70-90%
Those who survive have significant disability and progressively
debilitate

107. Dysautonomia
Pathology:
50% have megaesophagus
20% have aspiration pneumonia
Can diagnose with histopath on necropsy
Widespread degeneration of the autonomic nerves and ganglia
More than 50% are rural, outdoor dogs
Exposure to Clostridium toxins and/or
paraneoplastic disease
may play a role in pathogenesis

108. Handouts
•.pdf of this PowerPoint –behind the red tab
•TAMU GI Lab Submission Form
•Client Drug Handouts
–Amoxicillin
–Oral antacids
–Bethanechol
–Bisacodyl
–Bismuth subsalicylate
–Cimetidine
–Cisapride
–Erythromycin
–Famotidine
–Fenbendazole
–Maropitant
–Metoclopramide
–Metronidazole
–Omeprazole
–Praziquantel
–Pyrantel pamoate
–Ranitidine
–Sucralfate

109. Handouts
•Client Handouts
–Diaphragmatic hernia
–Endoscopy
–Hemorrhagic gastroenteritis