Veterinary Medicine - Gastrointestinal Diseases Flashcards
Clinical signs esophageal diseases? Also - name the clinical signs expected if complications occur (2 specific complications of esophageal diseases)
Regurgitations
Hypersalivation
Sialoadenosis
Gagging
Aspiration pneumonia: Fever, Lethargy, Anorexia, Tachypnea, Dyspnea, Cough
Nasopharyngitis +/- Nasopharyngeal stenosis: Reverse sneezing, Sneezing, Stridor, Stertor.
Oro-pharyngeal Vs. esophageal disease - Name one hallmark clinical sign for each
Oro-pharynx - Dysphagia
Esophagus - Regurgitations
What in the neurological exam can give a hint to Myasthenia Gravis?
Progressively weakening palpebral reflex
Regurgitations Vs. Vomiting: Pharynx/Esophagus/Stomach - Pain on swallowing
Possible
Frequent
No
Regurgitations Vs. Vomiting: Pharynx/Esophagus/Stomach - Ejection period after meal
Immediate
Immediate / Delayed
Delayed
Regurgitations Vs. Vomiting: Pharynx/Esophagus/Stomach - Qualities of ejected food (Digested / Undigested, Color)
Undigested, Colorless
Mostly undigested. Can be partially digested. Mostly colorless, Yellowish-greenish color also possible (more commonly associated with gastric content but not limited to)
Digested. Yellowish-greenish color (Bile)
Regurgitations Vs. Vomiting: Pharynx/Esophagus/Stomach - Ability to drink (Poor / Normal)
Poor
Normal
Normal
Regurgitations Vs. Vomiting Pharynx/Esophagus/Stomach - Swallowing attempts (Single/Multiple)
Multiple
Single
Single
Regurgitations Vs. Vomiting: Pharynx/Esophagus/Stomach - Commonly associated with secondarily causing dyspnea and coughing due to Aspiration Pneumonia
Yes
Yes
No
Reflux of food content from the stomach to the esophagus is always abnormal (True/False)
False
Normal healthy dogs can regurgitate from time to time as seen in fluoroscopic studies of the lower esophageal sphincter
Assessment & Diagnosis of Dysphagia - Physical examination / additional diagnostics
Full PE (emphasis on Initial oro-pharyngeal exam, sialoadenosis, masses, chest auscultation for signs of aspiration pneumonia)
Neurological assessment (with emphasis on cranial nerves, muscle symmetry, palpebral, swallow reflex, tongue motility)
Eating/drinking test (If not scheduled for anesthesia)
Full biochem panel (with emphasis on clues for endocrinopathies/CK levels/additionally - Cholinesterase levels, AB titers for MG)
Full oro-pharyngeal examination under sedation
Imaging: X-Ray / Fluoroscopy (Swallow study) / Endoscopy.
Pharyngeal dysphagia - Mechanical problems (DDs)
Pharyngitis: Viral (e.g. Calicivirus, Herpes), Bacterial, due to reflux
Corrosive agents
Masses (e.g. Granuloma, Abscess,
Neoplasia, Polyp, Cyst)
Sialoadenosis
Anatomical defects: Hypoplasia/Hyperplasia of soft palate
Misc. Stricture, Foreign body, Trauma
Pharyngeal dysphagia - Functional Problems (DDs)
Neurological (CNS/PNS diseases)
Junctionopathies (e.g. Myasthenia Gravis, Organic Phosphate (Chronic), Botulism)
Muscles: Myositis (Immune, Infectious, Pre-neoplastic), Muscle dystrophy, Storage diseases, Hypothyroidism
Cricopharyngeal Achalasia
Cricopharyngeal Asynchrony
Cricopharyngeal Achalasia - Treatment (2 options)
Botox injection (Short term)
Myotomy of Cricopharyngeal m.
Cricopharyngeal Asynchrony - Treatment
Conservative treatment:
-Find the food with the best texture for this specific dog
-High frequency + small quantities of food each time
-Bailey’s Chair
Esophagitis - DDs
Pill esophagitis (e.g. Doxycycline)
Reflux esophagitis (e.g. Anesthesia, 2nd to BAOS, Certain drugs)
Ingestion of caustic material
Foreign Body
Chronic Vomiting
Granuloma/Neoplasia/Inflammation involving the LES.
Reflux esophagitis (DDs)
Drugs (e.g. Anesthesia, Atropine, Anti-histamines)
Hiatal hernia
Due to upper respiratory disease (BAOS, Nasopharyngeal disease)
Coughing
Sialoadenosis - A Clinical sign / PE finding that is usually suggestive of pathology in what organ?
Esophagitis
Esophagitis - Clinical signs. Also, try to think of complications and their respective clinical signs
Mild cases - only regurgitations
Severe inflammation: Anorexia, Fever, Regurgitations, Pain on swallowing, Weight loss, Hypersalivation, Sialoadenosis
Signs of aspiration pneumonia: Fever, Cough, Dyspnea
Signs of anemia: Melena, pale mucus membranes, weakness
What is a common intra-mural sequela of esophagitis?
Stricture
Esophagitis - Treatment
Treat underlying issue
Switch to small portions + High frequency feedings
Low fat diet
Feed from above with neck extended (can use Baileys chair)
GI Protectants (Sucralfate, PPI), Pro-Motile (Metoclopramide)
Analgesia
*Gastric tube in severe cases
Sucralfate - Important thing to remember if additional drugs are also meant to be administered with it
Sucralfate can interfere with the absorption of other drugs. When giving sucralfate - separate from food and other drugs 2 hours before and after administration.
H2 Receptor blockers - Most relevant drug of the family? How long does it remain effective?
Famotidine
24-48 Hours
Proton pump inhibitors (PPI’s) - Relevant drugs, what are 2 Important points to remember with long term usage?
Omeprazole/Omepradex/Pantoprazole
1) After 4 weeks - Taper off slowly to avoid massive resurgence of acid production
2) Can cause dysbiosis
Pro-motile drugs - Names, Effects and which is considered a more effective pro motile drug?
Metoclopramide (Pramin) - Constricts LES, Promotes stomach contractility, Anti-Emetic
Cisapride (Preplusid) - Constricts LES, Promotes contractility along the entire GI tract (except for the esophageal striated muscle)
Cisapride > Metoclopramide
Mechanical causes for regurgitations (Esophagus) - The 3 main categories are:
Intra-luminal
Intra-mural
Peri-esophageal (Extra-esophageal)
Mechanical causes for regurgitations (Esophagus) - Intraluminal - DDs
Foreign body
Esophageal foreign body - Diagnosis & Treatment
History and clinical signs
Chest X-rays
Endoscopy (Gold standard)
Removal via endoscopy is best. If not possible - pushing the foreign body to the stomach and removal via surgery is also a possibility
+/- Treatment for esophagitis
Esophageal stricture - Causes
Caustic agents
Esophagitis
Surgery
Foreign Body
Luminal or Peri-Esophageal masses
Esophageal Stricture - Diagnosis
Endoscopy
Swallow study via Fluoroscopy
Esophageal stricture - Treatment
Bougienage (Balloon dilatation) + Short course of GC (to prevent inflammation and recurrence)
Stent (in the event of recurrence)
Surgery
+ Gastric tube and treatment for esophagitis
Mechanical causes for regurgitations (Esophagus) - Intramural - DDs
Esophagitis
Stricture
S.Lupi (In relevant countries)
Neoplasia
Diverticulum
S.Lupi (Esophageal) - Diagnosis
History (Mainly lack of preventative treatment) and clinical signs
Chest X-rays:
-Soft tissue opacity in the caudal mediastinum (caudal third of esophagus)
-Aortic mineralization and aneurism
-Spondylitis (T6-T12)
Fecal analysis
Endoscopy (Gold standard) - Typical appearance of S.Lupi granuloma - Smooth bulge continuous with the esophageal wall
S.Lupi (Esophageal) - Atypical presentations
Migration through the CNS (causing paresis/plegia)
Migration through Mesenteric arteries - Ischemia to GI and necrosis. Can cause either septic peritonitis or Hemoabdomen
Cutaneous fistula
Aortic rupture - Acute collapse & hemothorax (Acute death).
Esophageal neoplasia - Common types and locations (intra-mural / Peri-esophageal masses that can lead to regurgitations)
Intra-mural: Carcinomas (Cats), Sarcomas (S.Lupi), Leiomyoma
Peri-Esophageal: Thymoma, Chemodectoma
Esophageal neoplasia - Treatment & Prognosis
Surgery / Laser
Excellent if on a thin stock
Esophageal Diverticula - Diagnosis
Contrast study
Endoscopy
Mechanical causes for regurgitations (Esophagus) - Peri-esophageal - DDs
Vascular ring anomalies (e.g. PRAA)
GI accidents (e.g. Sliding hiatal hernia, Gastro-esophageal intussusception)
Mediastinitis
Intra-thoracic neoplasia (e.g. Pulmonary neoplasm, Heart-base tumor)
Severe lymphadenopathy
Persistent right aortic arch (PRAA) - Diagnosis
Classic history - regurgitations begin upon weaning and switching to solid foods (puppyhood)
Chest X-rays +/- Contrast study
CT
Persistent right aortic arch (PRAA) - Common complications (2)
Growth retardation (with good appetite)
Aspiration pneumonia (Cough, Fever, Dyspnea)
Hiatal hernia - Signalment
Congenital - Brachycephalic breeds over-represented
Acquired: 2nd to upper respiratory tract diseases (Nasopharynx in particular), Trauma with damage to the diaphragm
Hiatal Hernia - Clinical signs
Esophagitis - Regurgitations, Melena, Hypersalivation, Sialoadenosis
Fever and anemia in severe cases
Aspiration pneumonia (Fever, Dyspnea, Cough).
Hiatal Hernia - Diagnosis
Chest X-rays: Soft tissue opacity in the caudal mediastinum (caudal third of esophagus)
False negative rates high with sliding hiatal hernia and do not rule out the disease
Endoscopy (J-Maneuver)
Fluoroscopy
Hiatal Hernia - Treatment
Treat Reflux Esophagitis (PPI, Protectants, Pro-Motiles)
Treat Respiratory Disease (Surgery for Brachycephalic)
Last Resort - Gastropexy
Megaesophagus - Most Common: Congenital/ Acquired
Acquired
Megaesophagus - 2 Most common causes for acquired megaesophagus?
1) Idiopathic
2) Myasthenia Gravis
Megaesophagus - Congenital - Most commonly affected breed
German Shepard
Megaesophagus - Congenital - Classic presentation /Clinical signs. Also, What is another major DD?
Regurgitations from weaning
Aspiration pneumonia
Growth retardation
Vascular ring anomalies (e.g. PRAA)
Megaesophagus - Acquired - DDs
Idiopathic
Neuropathies: (e.g. Inflammation, vascular, Neoplasia) mainly involving the Vagus nerve CN9 (CNS/PNS)
Junctionopathies: Organic phosphates (Chronic), Myasthenia Gravis, Botulism, Tetanus
Muscles: Myositis, Dermatomyositis, Muscle Dystrophy, Storage Diseases
Led Poisoning
Endocrinopathies: Addison’s disease, Hypothyroidism
Chronic distal impaction: Foreign body, LES achalasia
Megaesophagus - Diagnosis
Full history & PE
Full neurological exam (with emphasis on medullary CNs)
Chest X-rays (Diagnosis of megaesophagus is usually achieved via X-rays)
CBC, Panel, UA (Aspiration Pneumonia, CK, Clues for Endocrinopathies, Basal cortisol, T4)
Fluoroscopy + Swallow study (When not obvious on X-rays)
ACh Anti-body titer / Tensilon test (If other clinical signs of Myasthenia Gravis are present
Megaesophagus - Treatment & Prognosis
-Treat underlying cause if possible (And then full remission is also possible)
-High frequency/Small quantities feedings
- food with appropriate texture for the dog (based on trial & error)
-Feed from above so neck is extended upward. Can use a Baileys Chair
-Gastric tube (last resort)
-Treat episodes of aspiration pneumonia
Prognosis: Mostly poor in the long run but depends on the primary cause.
Stomach - What are the 4 main defense mechanisms against acidity
Tight epithelium
Mucosal barrier with HCO3-
Vast blood supply to the mucosa
PGE2 (Promotes the former three)
Stomach - Helicobacter can be part of the normal flora in cats and dogs (T/F)
True
Stomach - 2 Causes for stomach-originating dysbiosis
Atrophy of the stomach glands due to chronic disease
Prolonged use of anti-acids (e.g. PPIs)
Gastric disease - Clinical signs
Vomiting
Retching
Hematemesis
Melena, Burping
Nausea, Hypersalivation
Tympany
Abdominal pain
Weight loss (Chronic)
Vomiting - What questions are important to ask the owners?
First! Differentiate between vomiting and regurgitations! Different set of DDs:
-Content digested/undigested
-How long does it occur in relation to meal time
-Color/colorless
-Abdominal contraction y/n (the biggest differentiating sign)
-Blood?
-Volume?
-Frequency?
-When did it start?
-Vaccinated?
-What does he eat?
-Has access to the outside?
-Other clinical signs?
Vomiting - Intra-GI - DDs
Food: Garbage intoxication, dietary indiscretion, Intolerance
Inflammation: Infectious (e.g. Parvovirus, Distemper, Giardiasis)/Non-Infectious (e.g. Chronic inflammatory enteropathies)
Gastric ulcers
GI Accidents (e.g. Foreign body, Intussusception)
Neoplasia
Bilious vomiting
Vomiting - Extra-GI - DDs
-Hepatopathies
-Nephropathies (e.g. AKI, CKD)
-Pancreatitis
-Biliary tract disease
-Endocrinopathies (Addison’s disease, DKA, Hyperthyroidism)
-Abdominal disease (e.g. Peritonitis)
-Vestibular Disease
-Drugs\Toxins (e.g. Organic phosphates, Apomorphine)
-Shock, Sepsis, SIRS, Endotoxemia
-Electrolytes/Acid-Base Disorders
Vomiting - Treatment
Treat underlying cause
Correction of fluids, electrolytes
Anti-Emetics (e.g. Maropitant, Ondansetron, Metoclopromide)
GI-Protectants in case of ulcers (e.g. PPI)
Analgesia (if indicated)
Change of diet (e.g. low fat, tuna, rice, hypoallergenic). Can either be for a few days or for an extended period of time depending on the etiology
Anti-emetics - Name the main drugs (3)
Metoclopramide
Maropitant
Ondansetron
Metoclopramide - 2 Contraindications
GI accidents (e.g. Foreign body, Intussusception)
GI Bleeding (Can interfere with clot formation
Cerenia - In addition to being an effective anti-emetic, what is the drugs added effect and through what mechanism?
Analgesia (Substance P blocker through NK-1 Receptor)
GI Protectants - Name the main drugs
Anti-acids: H2 Blockers (e.g. Famotidine)
PPI (e.g. Omepradex)
Adsorbents: Sucralfate
PGE2: Misoprostol (Cytotec)
Describe the diet aspect in treating a simple acute case of gastritis and vomiting (Types of food and general composition)
Switch to easily digestable diet for 5-7 days - High in carbs, moderate protein, low fat & low fibers. Can switch to commercial diet or home made (e.g. rice, chicken, tuna). Switch back to previous food gradually over the course of 3-4 days
Usually acute gastritis is diagnosed tentatively from history and clinical signs. What would make you want to go further with additional diagnostics?
Hematemesis
Systemic clinical signs
Which specific glucocorticoid is most notorious for causing gastric ulcers
Dexamethasone
Gastric ulcers - General categories of causes (4)
Acid over-production
Decreased perfusion
Direct damage to the mucosa
Decreased prostaglandin production
Gastric ulcers - causes
Acid over-production: Kidney failure (Gastrin, uremia), Liver failure (Gastrin), Neoplasia such as MCT (Histamine), Gastrinoma
Damage to the mucosa: Foreign body, Gastritis, Pancreatitis, neoplasia (e.g. Leiomyoma)
Decreased perfusion: Addison’s disease Sepsis, SIRS, DIC, Shock
Decreased PGE production: NSAIDs > Steroids
Misc. Stress-related mucosal disease, Ulcers of working dogs.
Gastric ulcers - Clinical signs
Vomiting
Hematemesis, Melena
Abdominal pain
Pale mucus membranes (severe cases)
Gastric ulcers - NSAIDs - Typical anatomical location of gastric ulcers
Antrum
Gastric Ulcers - Treatment
Treat underlying cause
Fluids, Electrolytes, Colloids (in cases of severe hypoproteinemia)
GI-Protectants (e.g. PPIs, Famotidine, Sucralfate, Misoprostol in case of NSAIDs-derived ulcers)
Anti-emetics (e.g. Maropitant, Ondansetron, Metoclopramide)
Analgesia (e.g. Buprenorphine, Butorphanol, Tramadol)
Antibiotics (If indicated)
*Surgery in specific cases (Neoplasia, Perforation)
Chronic gastritis - DDs
Chronic inflammatory enteropathies
Chronic foreign body (Rare but possible)
Hypertrophic gastritis
Atrophic gastritis
Helicobacter (Controversial)
Helicobacter - Considered always a cause of disease (T/F)
False
Found in 40-100% of both clinical and non clinical dogs and cats
Helicobacter - Same Isolates as Humans (T/F)
False
Helicobacter - Treatment (+ Duration of treatment)
2 Weeks: Amoxicillin, Metronidazole, Omeprazole
Gastric block/Delay in emptying - Mechanical DDs
GI Accidents (e.g. Foreign body, GD, GDV, Intussusception)
Pyloric Stenosis - Congenital (Brachycephalic) / Acquired (Hypertrophic Gastritis)
Neoplasia, Abscess, Granuloma, Polyp
Extra-gastric block (e.g. Organomegaly, Bad past gastropexy)
Gastric block/Delay in emptying - Ileus - DDs
Inflammation: Gastritis, Ulcers Pancreatitis, Peritonitis
Electrolyte imbalance: Hypokalemia, Hypercalcemia
Increased sympathetic innervation (e.g. Pain, Stress, Trauma, Shock)
Dysautonomia
Drugs (e.g. Opiates, Anti-cholinergic)
Gastric Ileus - Treatment
Treat underlying cause
Correct Fluids, Electrolyte
Treat Inflammation, Ulcers
Pro-motiles (e.g. Metoclopramide, Cisapride)
Anti-Emetics
GI-Protectants (in case of ulcers)
Analgesia (If indicated)
Weight lose with normal /increased appetite - DDs
Malabsorption/Maldigestion
Intestinal Parasites
Hyperthyroidism
Diabetes Mellitus
Melena - DDs
Coagulopathies: Thrombocytopenia, Thrombocytopathy, Decrease in clotting factors (in rare cases)
Swallowed blood:
1) Upper GI bleeding (e.g. Mouth, Esophagus)
2) Lower respiratory tract
Gastric & small intestinal ulcer (e.g. GI inflammation/Infection, Neoplasia, GI accidents, Addison’s disease, Pancreatitis, Liver failure, Portal hypertension, Severe uremia, NSAIDs)
Melena - Main CBC & Panel findings
CBC:
Anemia (Microcytic-hypochromic. mostly regenerative)
Thrombocytosis (Iron deficiency)
Panel:
Hypoproteinemia
Hypocholesterolemia
Increased urea (due to digestion of plasma proteins)
PLE - Clinical signs / Common PE findings / Associated pathology
Lethargy
Anorexia / Normal / Increased appetite
Weight loss
Vomiting, Diarrhea
Melena, Hematemesis
Ascites/Peripheral edema/Pleural effusion (Tachypnea, Dyspnea), Pericardial effusion
Thrombus formation (Loss of anti-coagulation factors)
Dysbiosis - Causes
Achlorhydria (e.g. Atrophic gastritis, Chronic use of PPIs
Mucosal disease (e.g. Chronic inflammatory enteropathies, Neoplasia, Infectious diseases of the GI)
Accumulation of ingest (e.g. Ileus, Chronic impaction, EPI)
Chief complaint of diarrhea - Questions to ask the owners
-Since when? (Acute/Chronic)
-Differentiate between small and big intestine diarrhea (Volume, Frequency, Consistency, Tenesmus, Urgency, Melena/Hematochezia, Mucus)
-Vaccination status?
-Deworming?
-What does he eat?
-Additional clinical signs?
-Access to the outside?
-Eats outside?
-Came in contact with a sick animal?
-Underwent surgery?
-On medications?
-Appetite?
-Weight loss?
Acute diarrhea - Intra-GI - DDs
Dietary indiscretion, Garbage intoxication
Infectious:
-Worms (e.g. Ascarids, Strongyloides)
-Viruses (e.g. Parvovirus, Distemper, Rota, Panleukopenia, FIV, FeLV, FECV)
-Protozoa (Coccidiosis, Giardiasis, Cryptosporidium, Trichomonas)
-Bacterial (e.g. E.coli, Campylobacter, Sallmonelosis)
GI Accidents (e.g. Foreign body, Intussusception, Volvulus) - Unless complete impaction - usually doesn’t present with diarrhea then.
Acute diarrhea - Extra-GI - DDs
Pancreas: Pancreatitis
Hepatopathies (e.g. Liver failure Biliary tract diseases (e.g. Cholangitis)
AKI (With severe uremia)
Endocrinopathies: DKA
Abdominal: Peritonitis, Prostatitis. Sepsis, SIRS, Endotoxemia
Drugs
Toxins (Organic Phosphates)
Vascular: R-CHF, Portal Hypertension
Ileus - Hypokalemia, Hypercalcemia.
Diarrhea - 3 Clinical findings that indicate further diagnostics
1) Melena / Hematochezia
2) Systemic clinical signs
3) Chronic diarrhea (>3 Weeks)
Acute diarrhea +/- vomiting (With or without blood) & Polycythemia - 2 Main differentials (One is a general differential and one is a specific pathology of the GI)
1) Dehydration
2) Acute hemorrhagic diarrhea syndrome (AHDS. Formerly known as HGE)
Dehydration vs. AHDS - What is a classic lab parameter that can help differentiate between the two?
Total solids (TS)
Dehydration - high (proportional to increase in HCT)
AHDS - Low
Intestinal diseases & Eosinophilia - DDs
GI parasites
Neoplasia / Para neoplastic
Addison’s disease
Eosinophilic IBD
Food responsive diarrhea
Intestinal Diseases & Thrombocytosis - DDs
Iron deficiency
Inflammation
Intestinal Diseases & Lymphocytopenia - DDs
Stress-leukogram
Lymphangiectasis
Intestinal diseases - Classic panel findings
Hypoproteinemia (PLE, GI bleeding)
Hypocholesterolemia (PLE, GI bleeding)
High urea (GI bleeding)
Hypokalemia / Hyponatremia / Hypochloridemia (Vomiting, Diarrhea)
Hyperkalemia (Addison’s disease)
Elevated liver enzymes (e.g. Reactive hepatopathy)
Amylase (Enteritis)
Causes for decrease in B12
EPI
Dysbiosis
Ilial diseases
Short bowel syndrome
Congenital B12 receptor deficiency
Nutritional deficiency
Name 3 ancillary blood parameters that can help assess digestion & absorption
TLI
B9 (Folate)
B12 (Cobalamin)
Folate (B9) - Name one cause for increased levels and one cause decreased levels
Decreased: Proximal small intestinal disease
Increased: Dysbiosis
Acute Diarrhea - Treatment
Short course dietary change
Supportive treatment if necessary:
-Fluids, Electrolytes, Glucose
-Appetite stimulant
-Anti-emetics
-GI-Protectants (If GI ulceration is suspected)
-Pre & Probiotics
Acute hemorrhagic diarrhea syndrome - AHDS (Formerly known as HGE) - Signalment
Young to middle aged (median age - 5 years old) small breed dogs (But can be in any breed and age)
Acute hemorrhagic diarrhea syndrome - AHDS (Formerly known as HGE) - Main clinical signs
Acute Hematemesis & Hematochezia / Melena
Acute hemorrhagic diarrhea syndrome - AHDS (Formerly known as HGE) - Classic lab finding
Hemoconcentration (Classically HCT > 58%) with normal to low TS
Acute hemorrhagic diarrhea syndrome - AHDS (Formerly known as HGE) - Proposed etiologies
Clostridium perfringens endotoxins
Food allergy
Dysbiosis
Acute hemorrhagic diarrhea syndrome - AHDS (Formerly known as HGE) - Main DDs (Name 4)
Addison’s disease
Pancreatitis
Parvovirus
Coagulopathies
Acute hemorrhagic diarrhea syndrome - AHDS (Formerly known as HGE) - Treatment & Monitoring & Prognosis
Fluids, Correct electrolytes, glucose (If indicated), Colloids (in severe hypoproteinemia)
Enteral feeding
GI support (Anti-emetics, GI protectants, Appetite stimulant)
Analgesia
*Antibiotics (Ampicillin/Metronidazole) - (controversial and not indicated in all cases)
PCV/TS Every 6-24h
Good-excellent if treated in time. Big improvement expected in 24h and full recovery within a few days
Viral enteritis - Causative agents (dogs and cats)
Dogs - Parvovirus, Distemper, Rota, Noro, Corona
Cats - FeLV, FIV, FECV, Panleukopenia
Viral enteritis - Signalment
Young animals
Unvaccinated
Immunosuppressed
Kennels/Crowded-housing
Viral enteritis - Parvovirus in dogs - Typical bloodwork findings
CBC:
-Inappropriately low neutrophils (Within normal range) / Neutropenia
-Mild anemia
Panel:
-Hypoproteinemia
-Hypoglycemia
-Hyponatremia
-Hypokalemia
-Hypochloridemia
-Azotemia
Parvovirus - Treatment & Monitoring (Bloodwork)
-Intensive fluid therapy (Preferably through a central catheter)
-Correct electrolytes (Mainly potassium), Hypoglycemia
-Colloids if severely hypoproteinemic
-GI support: Anti-emetics (Multiple if necessary), Pro-motiles, GI protectants. -Apatite stimulant (Only after vomiting and severe nausea has subsided
-Analgesia
-Antibiotics for 2nd infections (Combination of Beta-lactam + Aminoglycoside considered treatment of choice)
-De-worming
-Keep warm & clean
PCV/TS, Creatinine, Glucose, Albumin, Electrolytes
*Once in 3-4 days - rechecking CBC for rebound neutrophilia is recommended (Associated with the recovery stage of the disease)
Parvovirus - Diagnosis
Mainly based on Sig., History and clinical signs
Biggest clue is from the CBC - Inappropriately low neutrophils / Neutropenia (not specific)
Definitive diagnosis - Serology from fecal sample / PCR from blood samples
Bacterial enteritis - Signalment (4 Main Ones)
Young animals
Immunosuppressed / Congenital immunodeficiency
Kennel/Low hygiene crowded living conditions
Secondary to other GI diseases (e.g. Chronic inflammatory enteropathies, Viral infections)
Bacterial Enteritis - Main pathogens (4)
Campylobacter
E.Coli
Salmonella
Clostridium
Bacterial enteritis - Diagnosis
Mainly signalment and history
Fecal smear: Large homogenous (or disproportional) population of a single type of bacteria (Suggestive of dysbiosis) along with Large amount of neutrophils
Bacterial enteritis - General treatment + Specific antibiotic treatment for specific bacteria
Supportive Tx:
-Fluid, Electrolytes
-Short course of dietary change - Easily digestible (Commercial or home made)
Anti-emetics
GI protectants
Appetite stimulant
Analgesia
Antibiotics: Salmonella - Fluoroquinolones. E.Coli - Aminoglycosides, TMS, Fluoroquinolones. Clostridium - Penicillin, Metronidazole. Campylobacter - Macrolides
Fungal enteritis - What is the most common type of pathogen? Usually secondary to…? (2)
Yeast
Immunosuppression, GI inflammation
Parasitic enteritis/colitis - Main pathogen
Worms:
-Round worms (e.g. Ascarids such as Toxocara and toxocaris, Strongyloides)
-Cestodes (e.g. Dyplidium Caninum)
-Hookworms (e.g. Ancylostoma)
-Whipworms (e.g. Trichuris (Colon))
Protozoa:
-Giardia
-Cryptosporidium
-Coccidiosis (Colon)
-Trichomonas (Colon).
Parasitic enteritis/colitis - Protozoa - name the main diagnostic methods for each of the following: Coccidia, Giardia, Cryptosporidium
Coccidia - Direct fecal smear, Fecal flotation
Giardia - Direct fecal smear, Antigen-specific kit (Feces)
Cryptosporidium - Antigen-specific kit (Feces)
Parasitic enteritis/colitis - Protozoa - When looking on fecal smears - what parasite can be easily mistaken for Giardia?
Trichomonas
Parasitic enteritis / colitis - Name the drug of choice for each of the following: Worms, Giardia, Cryptosporidium, Coccidia, Trichomonas
-Good empiric treatment for worms - Fenbendazole
-Tape/Round worms: Drontal
-Round worms: Ivermectin
-Giardia: Fenbendazole/Metronidazole (or a combination of the two)
-Coccidia: Toltrazuril, Ponazuril, Sulfadimethoxine
-Cryptosporidium: Macrolides
-Trichomonas: Ronidazole
Chronic inflammatory enteropathies - Food-responsive enteropathy - Signalment & possible clinical signs
Young (but can be at any age)
Weight loss
Hyporexia / Normal / Increased appetite
Chronic diarrhea, Chronic vomiting
Borborygmus
Pruritus
In severe cases: Complications of hypoalbuminemia due to PLE (Peripheral edema, Ascites, Tachypnea/dyspnea due to pleural effusion)
Chronic inflammatory enteropathies - Food-responsive enteropathy - Diagnosis
History and clinical signs
*Empirical deworming
Food trial - Change to a diet composed of a novel protein/hydrolyzed protein for 3-4 weeks (Preferably also low fat but not obligatory)
If cessation of clinical signs is achieved (usually within 2 weeks) - after a month switch back gradually to the previous diet
If clinical signs return - diagnosis is achieved
*Recommended diagnostics if possible/Indicated clinically: CBC, Panel, UA, Abdominal US, Fecal tests. Additional tests: Basal cortisol, TLI, B12 & Folate, Coagulation panel.
Gluten-sensitivity - Poster breed
Irish setter
Chronic inflammatory enteropathies - Antibiotic-responsive diarrhea - Signalment & Clinical signs (and important history clue)
Young German shepherds and its mixes.
Large breeds.
Chronic diarrhea
Weight loss with decreased / normal / increased appetite
Retarded growth
+/- Borborygmi
Flatulance
+/-Vomiting
Previous antibiotic treatment worked for a short while and then clinical signs returned
Chronic inflammatory enteropathies - Antibiotic-responsive diarrhea - Diagnosis and important testing
Signalment, history and clinical signs
*Empirical deworming
1) Rule out food responsive diarrhea. If cessation of clinical signs is not achieved (usually within 2 weeks)
2) Response to antibiotic treatment: Tylosin / Metronidazole / Oxytetracycline for 4-6 weeks and taper-off slowly
If clinical signs return - Tentative diagnosis is achieved
*Recommended diagnostics if possible/Indicated clinically: CBC, Panel, UA, Abdominal US, Fecal tests. Additional tests: Basal cortisol, TLI, B12 & Folate, Coagulation panel.
Chronic inflammatory enteropathies - Antibiotic-responsive diarrhea - Treatment
Tylosin (/Metronidazole/Oxytetracycline) - 4-6 Weeks and slowly taper off
If clinical signs return during/after tapering off - return to previous dosage and try tapering off again / permanent treatment
Food - Highly digestible, low fat +/- hypoallergenic (might also be a component of FRE)
Pro/Prebiotics
B12 Supplements
Chronic inflammatory enteropathies - True IBD - Signalment
German Shepard, Basenji, Shar-Pei
Can be any breed and any age
Chronic inflammatory enteropathies - True IBD - Diagnosis
Signalment, history and clinical signs
*Empirical deworming
1) Rule out food responsive diarrhea. If cessation of clinical signs is not achieved (usually within 2 weeks):
2) Response to antibiotic treatment: Tylosin / Metronidazole / Oxytetracycline for 4-6 weeks and taper-off slowly
If no cessation of clinical signs is achieved (usually within 5-7 days):
3) Endoscopy - No remarkable findings
Histology - Necessary to demonstrate inflammation - Lympho-plasmocytic / Eosinophilic infiltrates (can be inconclusive)
**Main method of diagnosis - Response to GC and slowly taper off
*Recommended diagnostics if possible/Indicated clinically: CBC, Panel, UA, Abdominal US, Fecal tests. Additional tests: Basal cortisol, TLI, B12 & Folate, Coagulation panel
Chronic inflammatory enteropathies - True IBD - Proposed pathology (3 Main elements)
1) Genetic predisposition
2) Breaking of tolerance against antigens (Inflammation, Stress, dietary change)
3) Infective agent/dysbiosis
Chronic inflammatory enteropathies - True IBD - Treatment
GC - Prednisone/Prednisolone/Budesonide
*2nd Immunosuppression if steroids insufficient (e.g. Cyclosporine, Chlorambucil, Cellcept, Azathioprine)
Anti-coagulants (e.g. Clopidorgrel, Low dose aspirin)
Dietary change (Hypoallergenic/Low fat) - might help
B12 Supplementation
Pro/prebiotics
In cases of severe PLE - Colloids
*Can also try fecal transplantation
Chronic inflammatory enteropathies - True IBD - Monitoring & Negative prognostic indicators
Monitoring is clinically-based, according to the Canine Chronic Enteropathy Activity Index (CCEAI):
-Behavior & activity
-Vomiting, Diarrhea
-Apatite
-Weight loss/gain
(Each is scored from 0-3 from normal to worse)
Additional CCEAI monitoring:
-Pruritus
-Albumin
-Ascites
-ALP, ALT
-Total Protein
Negative prognostic indicators:
-Dogs worse than cats
-Hypoalbuminemia
-Hypercoagulability
-Concurrent Pancreatitis
-Clinically/Endoscopically/Histologically worse disease
Euthanasia - 10-20%
Chronic inflammatory enteropathies - True IBD - Clinical improvement is associated with histological improvement (T/F)
False
Lymphocytic-plasmocytic IBD Vs. Small cell-lymphoma (SCL) - Signalment, How to differentiate, Treatment
SCL - Older dogs and cats
IBD - Generally young-adult animals
Immunohistochemistry:
Monoclonal (SCL)
Polyclonal (IBD)
Treatment: Cornerstone is the same - Prednisone/Prednisolone + Chlorambucil.
Eosinophilic IBD - Signalment, name a clinical sign often associated with Eosinophilic IBD
Young adult dogs
Boxer, Doberman, German shepherd over-represented
Bleeding due to ulcers/erosions
Eosinophilic IBD - Main DDs (4)
Addison’s disease
Parasites
Paraneoplastic syndrome
Food allergy
Eosinophilic IBD - Name the unique variant in middle aged cats, Location, Classic appearance and treatment
Feline sclerosing eosinophilic Fibroplasia
Stomach
Small Duodenum
Granuloma-like/Mass - Can cause impaction/perforation
Antibiotics + GC
Lymphangiectasis - Predisposed breeds
Yorkshire terrier, Maltese, Rottweiler
Lymphangiectasis - Causes
Congenital
Secondary:
-Inflammatory diseases of the small intestine (e.g. IBD), Fibrosis, Neoplasia.
-Blockage of thoracic duct.
-R-CHF
Lymphangiectasis - Classic bloodwork findings
CBC:
Lymphopenia
Panel:
Hypocholesterolemia
Hypoproteinemia
Hypocalcemia
Hypomagnesemia
Lymphangiectasis - DDs for hypocholesterolemia
Addison’s disease
Liver failure
Lymphangiectasis
EPI
PLE
Hyperthyroidism
Multiple myeloma
Snake envenomation
Lymphangiectasis - 3 main differentials which also present with hypoalbuminemia and hypocholesterolemia? In standard blood tests (CBC/Panel) - what helps differentiate between them?
Atypical Addison’s disease: Lymphocytosis
Lymphangiectasis: Lymphocytopenia
Liver failure: Hypocholesterolemia, Hypoalbuminemia
PLE and Lymphangiectasis: Hypocholesterolemia and Hypoproteinemia (Loss of both albumin and globulins)
Lymphangiectasis - Diagnosis
Signalment, History and Clinical signs
CBC (Lymphocytopenia) & Panel findings (Hypocholesterolemia, Hypoproteinemia, Hypocalcemia, Hypophosphatemia)
On rare occasions - prolonged clotting times
Abdominal US - Hyperechoic mucosal striations (dilated intestinal lacteals)
Endoscopy - dilated lacteals can be seen microscopically as white plaques scattered across the intestinal mucosa
Histology
Lymphangiectasis - How can you help your US findings be more prominent and conclusive?
Give high fat meal a few hours before the US - makes the lacteals more prominent
Lymphangiectasis - Treatment
Treat underlying cause if exists
Dietary change (most important element of treatment): Extremely low-fat diet
Vitamin D supplement
Anti-coagulants (If indicated).
Short Bowel Syndrome - How much of the small intestine can you remove?
85%
Short Bowel Syndrome - Treatment
Initially - Parenteral feeding and then start with an easy to digest food
Fat-soluble - vitamin supplementation
In case of Ileum/Ileo-cecal valve removal: B12 Supplementation, Antibiotics for secondary dysbiosis, Ursodiol, Bile acid absorbents
Pre-Colonoscopy Enema - Preparation
36 Hour fast
24 Hours before procedure - Polyethylene glycol
Right before - Wash colon with hot water
Phosphate Enema - Recommended in Animals? Why?
No
Can cause hyperphosphatemia
Colitis - What is important feeding considerations? (2 elements)
High digestibility
Digestible fiber
Chronic Colitis - Immunomodulatory drugs
Metronidazole (/Tylosin)
Sulfasalazine
Immunosuppressive drugs
Histiocytic ulcerative colitis (HUC) - Signalment & Clinical signs & lab findings
Young boxers (0.6-4 Years)
Signs of colitis (chronic):
-Runny diarrhea
-Small quantity
-high frequency
-Urgency
-Mucus secretions
-Tenesmus
-Hematochezia
-Hypoproteinemia, Anemia
Histiocytic ulcerative colitis (HUC) - Histological findings
Macrophages which stain positive in PAS
Lymphocytic-plasmocytic & Eosinophilic Infiltrates
Ulcers
Histiocytic ulcerative colitis (HUC) - Diagnosis
Signalment (Young Boxers)
History - Signs of chronic colitis
Biopsy and histology - PAS-positive granulomatous infiltrates
Histiocytic ulcerative colitis (HUC) - Causative Agent
Adhesive-invasive E.Coli
Histiocytic ulcerative colitis (HUC) - Treatment and Prognosis
Fluoroquinolones for a prolonged period (9 weeks)
Good if treatment is effective - can see improvement in a week
Poor if E.Coli is resistant to Fluoroquinolones
Chronic Colitis - Prototheca - Signalment & Clinical Signs
Young dogs
Signs of colitis (chronic):
-Runny diarrhea
-Small quantity
-high frequency
-Urgency
-Mucus secretions
-Tenesmus
-Hematochezia
CNS Signs
Uveitis
Skin nodules (Cutaneous form)
Chronic Colitis - Prototheca - Diagnosis (4 methods)
Rectal Scrape
Biopsy
Fecal PCR
CSF PCR
Chronic Colitis - Prototheca - Treatment & Prognosis
In cases of GI disease only: Itraconazole + Nystatin
In cases of disseminated disease: Itraconazole + Amphotericin B
Poor
Chronic Colitis - Tritrichomonas Foetus - Signalment
Young cats
Multi-cat household/Kennels.
Chronic Colitis - Tritrichomonas Foetus - Name the parasite that is morphologically very similar to Trichomonas Foetus
Giardia
Chronic Colitis - Trichomonas Foetus - Diagnosis (2 main methods)
Fecal Smear
Fecal PCR
Chronic Colitis - Tritrichomonas Foetus - Treatment & Prognosis
Ronidazole for 2 weeks
Spontaneous remission can be seen 9 months after diarrhea began
Relapses also possible
Good
Chronic Colitis - Tritrichomonas Foetus - Ronidazole side effects
CNS Signs
Irritable Bowel Syndrome - Signalment & Clinical signs
Working dogs and hyperactive breeds
Abdominal pain
Diarrhea and/or Constipation
Irritable Bowel Syndrome - Treatment
Increased activity
Highly digestible food, low in fiber
Irritable Bowel Syndrome - Name of the disease in dogs
Chronic idiopathic large bowel diarrhea
Constipation/Obstipation - Mechanical obstruction - DDs
Intraluminal: Dry solid feces (2nd to dehydration, Lack of activity, Stress, Bones in feces, Orthopedic/Neurological problems), Foreign body (Rare).
Intramural: Neoplasia, Polyps, Granuloma, Perineal hernia, Perianal fistula, Perianal sacs enlargement, Stricture
Extra-Intestinal: Abdominal mass, Pelvic Fractures, Prostatic enlargement, Enlargement of abdominal lymph nodes (e.g. sub-lumbar)
Constipation/Obstipation - Functional problems (Ileus) - DDs
Idiopathic megacolon (Cats).
Metabolic: Hypokalemia, Hypercalcemia, Hypothyroidism
Drugs: Opiates. Sympathetic stimulation (e.g. Pain, Stress)
Dehydration
Dysautonomia
Peritonitis
PNS Injury (Sacral Region)
UMN injury (e.g. Degenerative myelopathy, Lumbosacral stenosis, Trauma).
Constipation/Obstipation - Diagnosis
Physical exam (Rectal exam as well)
Neurological Exam
CBC, Panel
T4+TSH
X-rays
Colonoscopy
Constipation/Obstipation - Treatment
Treat underlying issue if possible
Correct hydration and electrolytes (Fluid therapy assists in liquifying the feces - very important)
Enema
Laxatives (e.g. Lactulose, Polyethylene Glycol)
Lubricant (e.g. Vaseline)
food with soluble fibers (can also add Psyllium)
Pro-motiles (only after removal of obstruction!)
Constipation/Obstipation - What are the pro-motiles that are available to us. What is the “last resort” one and why?
Cisapride
Erythromycin
Remeron (Also Apatite Increase)
Ranitidine (H2 Blocker but also weak pro motile)
Bethanecol - Powerful Parasympathomimetic. Can cause Organic-phosphate-like Intoxication signs
Constipation/Obstipation - Idiopathic Megacolon - Signalment, Treatment
Middle aged cats (Males»_space; 70%)
Colectomy
Septic peritonitis + Eosinophils on cytology of abdominal fluid. Suggestive of?
S. Lupi
PLE - Common pathology in both cats and dogs (T/F)
False
Rare in cats
Fungal enteritis - Usually a marker of what pathology
Dysbiosis
Fungal enteritis - Diagnosis and when to treat?
Rectal smear
When a large homogenous population is seen
3 Major DDs for chronic diarrhea in German shepherds
EPI
ARD
True IBD
Protein-losing enteropathy - Name the 3 major DDs
Chronic inflammatory enteropathies
Lymphangiectasis
GI Neoplasia
Chronic diarrhea - Intra-GI - DDs
Chronic inflammatory enteropathies (Food-responsive diarrhea, Antibiotic responsive diarrhea, True inflammatory bowel disease (True IBD))
GI Worms,
Lymphangiectasis
Giardiasis
Neoplasia
GI accidents (Rarely chronic but possible)
Chronic diarrhea - Extra-GI - DDs
Pancreas: Chronic pancreatitis, EPI. Biliary tract disease (e.g. Lymphoplasmacytic cholangiohepatitis, Mucocele). Hepatopathies (e.g. chronic hepatitis). Nephropathies (e.g. CKD). Endocrinopathies (e.g. Hyperthyroidism, Addison’s disease)
Parvovirus - Common complications
Sepsis
Peripheral edema (Hypoalbuminemia)
Intussusception
Phlebitis (Prolonged hospitalization, Contamination)
Hairballs - 2 Major categories of causes
Excessive grooming
Decreased/Abnormal GI motility
Hairballs - Causes (Divided to 2 Categories and Detailed)
Excessive Grooming: Stress | Abdominal Pain | Musculoskeletal Pain | Neuropathies | Claw Pain | Skin Parasites and Allergies | Dry Skin | Dermatophytes
Decreased/Abnormal GI Motility: Esophagitis | Stricture| FB | Neoplasia | Megaesophagus | Mediastinal Diseases | Hernia | Gastric Ulcers | Gastritis | Enteritis (Infectious and Non Infectious | Ileus | Parasites | Intussusception | Abdominal Disease | Pancreatitis |Allergies | Cholangiohepatitis | Cholecystitis
What can give you a clue to the presence (or past presence) of a sublingual foreign body in cats
Sublingual granuloma
Hairballs - Treatment
Treat underlying cause
Hydration
Petrolatum / Hairball remedies
Remove excess hair (Comb / Roller)
Protein-losing enteropathy (PLE) - 3 Common causes in puppies / Young dogs
Parvovirus
Chronic Intussusception
Worm Infestation
Protein-losing enteropathy (PLE) - Treatment
Treat any Extra-GI underlying cause (e.g. Addison’s disease, Cardiac disease, Liver disease, Intussusception, Parvovirus)
Change diet (Novel/Hydrolyzed protein. Low fat preferred)
Antibiotic treatment (Tylosin/Metronidazole generally preferred)
Glucocorticoid treatment (Prednisone/Budesonide)
Additional immunosuppressive treatment if no response
Anti-thrombotics (e.g. Clopidogrel / Low-dose aspirin)
Probiotics
Cobalamin Supplement
Constipation / Obstipation / Megacolon - Treatment
Treat underlying cause if possible
IV fluids
Enema if indicated
- Warm Water
+/- Mineral Oil
Can also trickle PEG with NG tube
Diet - Psyllium, High fiber diet
Laxatives: Lactulose / Polyethylene Glycol (PEG)
Pro-motiles (e.g. Cisapride)
When an animal has low-normal cobalamin levels - What test should you perform to determine if the animal could benefit from cobalamin supplements?
Methylmalonic Acid levels