15, 16)non infective enteritis, protein loosing enteropathy, perineal diseases diseases of the large intestine Flashcards

1
Q

acute haemorrhagic diarrhea syndrome

A

a. Formerly HGE
b. Toxigenic Cl. perfringens
c. Young, middle-age, small-breed; winter
d. Acute/peracute, severe
e. Vomiting → haemorrhagic diarrhea, hypovolaemia
f. PCV usually increases; neutrophilic left-shift
g. Agressive iv. fluid therapy → good prognosis
h. +- parent. ab. (if septic or non-responder to fluid)
i. Symptomatic treatment: antiemetic medic., analgesia
j. Intestinal diet

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2
Q

acute small intestinal disorders

A
unknown cause
diet related
ahds
infectious
alimentary tract parasites
ileus
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3
Q

chronic small intestinal disorders

A

food responsive
ARE
IRE/IBD

lymphangiectasia
neoplasms of SI
parasites, fungi, bacteria

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4
Q

infectious diarrhea

A

a. Viral
i. Canine parvoviral enteritis (CPV)
ii. Feline parvoviral enteritis (FPV)
iii. Canine coronaviral enteritis (CCoV; CPCoV)
iv. Other viral enteropathies of cats (FCoV/FECV, FIP; FIV; FeLV)
b. Bacterial
i. Campylobacteriosis
ii. Salmonellosis
iii. Miscellaneous bacterial enteritis
c. Fungal
i. Histoplasmosis

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5
Q

WHY USE THE TERM “CHRONIC ENTEROPATHY” RATHER THAN “INFLAMMATORY BOWEL DISEASE” IN DOGS?

A

Because of the differences between dogs and human in regards to treatment and the need for surgery to control clinical signs, it can be misleading to use the term “inflammatory bowel disease” in dogs. In effect, most dogs with this disease will not need immunosuppressant treatment. For this reason, chronic enteropathy is often used instead to describe dogs with chronic gastrointestinal signs. The advantages of using this term are:

  1. It can be used for animals in which intestinal inflammation is suspected but has not been documented (i.e. no biopsies have been taken).
  2. It does not infer which treatment will be needed to control clinical signs.
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6
Q

pathogenesis of chronic enteropathy

A

food -> intestinal microbiota -> intestinal immune systemic

loss of tolerance -> intraluminal allergens -> pathology immune response - mucosal inflammation

genetic!

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7
Q

Food Responsive Enteropathy (FRE)

A

o Food allergy – immune system involved
• Food = potential antigen → „oral tolerance”
• Causes of loss of tolerance: genetic predispose. +
• Permeability of intestinal mucosa increases
• Earlier bacterial, viral or parasitic infections
• Prolonged damage of intestinal flora
o Food tolerance – immune system NOT involved
• eg lactose intolerance in cats
→ most common allergens = PROTEINS
▪ Dogs: beef, chicken, milk, wheat
▪ Cat: beef wheat corn, fish, chicken
o Clinical signs
• PRURITUS
• recurrent chronic diarrhea
o Diagnosis, therapy
• Length of diet: pruritus = diarrhea→ evaluate
▪ DIARRHEA improve→ continue for all together 12 weeks
• Essence of diet
▪ One, NOVEL protein, (CH), high bioavailability
▪ Prescription diet: hypoallergenic/ hydrolysed or
▪ Home made
▪ Avoid „hidden” allergens
• ! Drugs; contamination in food?
• Companion pet, neighbour, grandma

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8
Q

Antibiotic Responsive Enteropathy (ARE)

A

o First named SIBO = small intestinal bacterial overgrowth
o BUT: NO real overgrowth in many cases
→ renamed: SIBO → ARE
o Primary ‒ loss of tolerance, breed predisp.: Germ. Shep.
o Secondary ‒ damage of intestinal microbiota, dysbiosis
• Consequences
o Secretion of enterotoxins
o Direct harmful effect on brush border enzymes
o Competition for nutrients (e.g. cobalamine)
• Clinical signs: CHRONIC SI DIARRHEA
o Gas production, fat malabsorption
o Weight loss (+-polyphagia/anorexia)
o Vomiting (sometimes)
• Diagnosis: NO specific test
o Most intestinal microbiota NOT culturable
o (cobalamine INCREASE, folate DECREASE)
• Aim of therapy: number of microbiota DECREASE + normal balance
o Antibiotics
▪ Metronidazole (IMMUNOMODULATING), tilozin, (OTC)
▪ Long-term, min. 4 weeks
▪ Withdrawal → relapse
• Intestinal diet

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9
Q

Immunosuppressant Responsive Enteropathy (IRE) → IBD

A
o When the term inflammatory bowel disease (IBD) is used for dogs, it typically implies that treatment trials with diet (FRE) and subsequently antibiotics (ARE) have failed, inflammation has been demonstrated and an immunosuppressant will be needed = IRE!
Histopathological types:
o LPE (lymphocytic-plasmacytic enteritis) – most common
o EGE (eosinophilic gastroenteritis)
o Neutrophilic gastroenteritis
o Granulomatous gastroenteritis
Clinical findings:
o Middle age
o Predisposed breeds: German shep., terriers, sharpei
o Chronic diarrhea
• Recurrent, even for months
o +/- weight loss, vomiting
o Inappatence
o Abd. discomfort, flatus
o Ascites, subcutan oedema
o Severe IBD → PLE!!!
Diagnosis:
o NOT specific
• Blood tests
▪ Hypoproteinaemia
▪ Leukocytosis (LPE)
▪ Eosinophilia (EGE)
▪ Cobalamine decrease; folate increase
• Abdominal ultrasonography
▪ Thickened SI loops, lymphadenopathy (EGE)
o SPECIFIC
• Endoscopic findings
• Diagnostic laparotomy
Treatment:
o Immunosuppressant drugs used for CE include
• Prednisolone (use gastroprotectors)
• Azathioprine (NOT in cats)
• Budesonide
• Cyclosporine
o Only cortices for 4 weeks
o Cortices + cyclosporine for 2 weeks
o In case of critically-ill patient:
• Fluid therapy – fluid-, electrolyte-, acid-base homeostasis
o Colloid – PLE IBD – treatment
o Feeding tube (Noe/ cat) – anorexia, malnutrition
o Parent ab – risk of bacterial translocation
a. Eg. metronidazole + enrofloxacin
b. Eg. amoxicillin-clavulanate
• VitB12 supplementation – long-term
• Probiotic – long-term, but if risk of bacteria translocation don’t!
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10
Q

Non-Responsive Enteropathy (NRE)

A

o Reconsider the diagnosis
o The microbiome has been shown to play a central role in several diseases and treatment to alter its constituents, using pre- and probiotics appears promising
o Another promising technique to alter the intestinal flora is faecal transplantation
o mesenchymal stem cells for the treatment of inflammatory conditions such as CE

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11
Q

LYMPHANGIECTASIA

A
o Predisposed breeds
• Yorkshire terrier,
• Rottweiler
o Classification
• Primary
▪ Lymphatic abnormality
• Secondary
▪ Intestinal disorders
• Inflammatory disease (IBD)
• Intestinal neoplasia
▪ Systemic disorders
• Right-sided cardiac failure
• Hepatic failure
o Clinical signs
• Prolong protein-loss Increase → ascites, hydrothorax, oedema
• Fat malabsorption and protein loss→ weight loss
• +-! Chronic Chronic diarrhea diarrhea
• Thromboembolia (rarely) → severe complication (loss of atithrombin III)
o Diagnosis
• Laboratory findings
▪ HYPOPROTEINAEMIA (TP decr, Alb decre )
▪ Hypocholesterolaemia (TotChol derease)
▪ Lymphopenia (lymphocyte decrease)
▪ Hypocalcaemia (Ca DEcrease), hypomagnesaemia (Mg INcrease)
• Endoscopic findings
▪ Mucosal edema
▪ “rice-grain” nodules
• Abdominal US
▪ Mucosal thickening
▪ Streaks in submucosa
o Specific diagnosis
• Intestinal biopsy → histology
o Treatment
• Ultra! low-fat (ULF) diet; high bioavailability
• Immunomodulation (see IBD)
• Antimicrobial therapy (see ARE)
• Diuretics  ascites
• Fluid therapy: colloids  oncotic p. increase
• Plasma:  suppl. of antitrombin III (microthrombosis premedication & treatment)
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12
Q

Neoplasm

A
o Types
• Alimentary lymphoma in CAT
• Lymphosarcoma
• Intestinal adenocarcinoma
• Intestinal leiomyoma / leiomyosarcoma
o Clinical signs
• Middle-aged, older animals
• Chronic diarrhea, excess weight loss, anorexia, melena, vomiting, hematemesis
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13
Q

PROTEIN LOSING ENTEROPATHY

A
o Collective term
• Lymphangiectasia (most frequent)
• IBD
• Intestinal neoplasia/lymphoma
• GI haemorrhage
o Clinical findings
• Chronic Chronic diarrhea diarrhea
• Intestinal Intestinal protein protein loss
• Ascites
• Edema, cachexia
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14
Q

INTUSSUSCEPTION

A

o Invagination (telescoping) of one part of the intestine into another
o Most often in young dogs and puppies
o Ileocolicus (mostly) or jejunojejunal (often in cats)
o Idiopathic or secondary to diseases causing dysmotility (viral, parasitic enteritis, infiltrative diseases in older cats)
o Hematochesia, vomiting, abdominal pain, palpable elongated thickened intestinal loop
o Abdominal US: multiple concentric rings
o Surgery
o Treatment of ileus:
o Medical pre-operative management:
• fluid therapy (crystalloid with K+)
• antibiotic (parenterally, wide spectrum)
o Surgical management: ASAP
• Laparotomy and enterotomy
• + Resection of devitalized intestine
• Sterile lavage of peritoneal cavity
o Post-operative care:
• fluid therapy as needed
• analgesia
• early post-op enteral feeding (ASAP - no risk of aspiration, 25% of RER, low fat, highly digestible, orally via syringe feed or feeding tube)
• prokinetic drug in paralytic ileus

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15
Q

diseases of the large intestine in cats and dogs

A
 Anatomy of the COLON
o Segments:
▪ Ascendens
▪ Transverse
▪ descendens
o Ileocolic orifice (prevent oral movement)
o Layers: → NO villi!!
▪ Mucosa
▪ Submucosa
▪ Muscularis
▪ Serosa
o Crypt:
▪ columnar epithel cells
▪ goblet cells (mucous secreting)
▪ endocrine cell, intraepithelial ly
o a. / v. mesenterica (cran / caud) – v. portae
o Parasympathicus: vagus (prox colon); n. pelvini (dist. colon)
o Sympathicus: paravertebralis gl. – n. splanchnicus
 Physiology of the large intestine
o Conservation of water, Na, Cl
▪ Absorption of fluid~ Na, SCFA
▪ Secretion: HCO3, K (colon descendens: absorption/secretion)
o Storage of waste products
▪ Segmentation (mixing)
▪ Propulsive (peristaltic, reverse and mass peristaltic)
o microbial population 10 to the power of 11/gr feces
▪ Fermentation Fermentation: dietary fibre, poorly digest. CHO→ SCFA
• ↑H2O absorption,7-10% energy, peristaltic, colonocyts proliferation
▪ primary BA→ secondary BA
o Mucous production
▪ Physiological barrier
o Immune balance
 History, clinical signs (CS)
o Large bowel diarrhoea (LBD)
o Tenesmus:
▪ Straining to defecate (remains postured for extended period or repeated attempts)
o Dyschezia:
▪ Difficult, painful defecation
o Fresh blood: haematochezia
o Generally alert, active
o Physical examination: normal
▪ Rectal digital palpation! RDP
→ CS: SBD or LBD?
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16
Q

diagnosis of large intstinal disease

A
o History!!! Physical examination
▪ RDP!!!! (irregular colon mucosa, feces)
o Labor: haematology, biochemistry, urine
o Feaces
o Exfoliative cytology, „rectal smear”
o XRay (native, contrast barium, pneumocolon)
o US?
o Colonoscopy
▪ fasting 18-24h, rectal enema (20-25 ml/kg)
o Biopsy (endoscop or laparotomy)
 Diagnostic tests
o History!!! Clinical examination
o Labor: CBC, biochemistry, urine
o Faeces
▪ Flotation
• Giardia, Trichuris (intermittent)
▪ Direct smear (motile trophozoites)
• Giardia, Trichomonas, Entamoeba, Balantidium
▪ Cytology (stain: Diff-Quik, Wright’s)
• Histoplasma, spirochaetes, Clostridial spores
▪ Culture (fresh!)
• Campylobacter, Salmonella, Clostridium
▪ ELISA
• Giardia Ag, Clostridium enterotoxin
17
Q

diseases of the colon

A
o Acute colitis
▪ Parasitic
I. Trichuris vulpis
II. Tritrichomoniasis▪ Bacterial
I. Salmonella
II. Campylobacter
III. Clostridium perfringens, difficile
IV. Yersinia
V. Brachyspira pilosicoli
▪ Fungal, algal
I. Histoplasma
II. Pythium insidosum
o Chronic colitis (IBD!)
▪ Lymphocytic-plasmacytic colitis (LPC) plasmacytic colitis (LPC)
▪ Eosinophilic colitis (EC)
▪ Chronic histiocytic ulcerative colitis (CHUC)
o Other diseases of the colon
▪ Irritable bowel syndrome
▪ Constipation
▪ Intussusception
▪ Neoplasia
18
Q

acute colitis

A

 LBD
 usually self-limiting
 Cause:
▪ Diet
▪ infection:
I. PARASITES
II. BACTERIA/TOXINS
III. FUNGI
 Rarely identified the cause
 Treatment: diet (24h fasting fasting)
▪ Low fat, hypoallergenic hypoallergenic, highly digestable
▪ Fibre supplementation supplementation! (fibre→SCFA)
I. Normalizing motility
II. Binding colonic irritants
III. Protecting colonic mucosa
IV. Energy source
 Metronidazol, tylosin +/- (loperamid?)
I. PARASITIC COLITIS
i. TRICHURIS VULPIS
o Intermittant diarrhea LBD (blood, mucus)
o Dg: eggs in feces, parasites by colonoscopy
o Intermittant evacuation (3 days collected feces)
o Fenbendazol (50 mg/kg 3-5 day) 3 weeks, 3 months

19
Q

ii. TRITRICHOMONIASIS - T. foetus (blagburni

A

o Motile trophozoits in fecal smear
o Distal ileum -colon
o Young cat (giardia!)
• Breeding, shelter, crowded population
• LBD, intermittant. Cow-pad like, sticky feces
• Within 2 years, self-limiting asymptomatic carrier 88%
o Diagnosis:
• feces: „Giardia trophozoits” in direct smear fresh feces, but NO cyst with Zn flotation
• PCR (cat specific primer), biopsy, culture difficult!!
o Ronidazol 30-(50) mg/kg 14 days (neurotoxic…)

20
Q

II. BACTERIAL COLITIS

A

o Part of the normal bacterial flora
o Mostly acute, small and large intestine
o Clinical signs ~ host pathogen interaction
o Zoonotic risk (Salmonella, (Salmonella, Campylobacter Campylobacter)
o Not treat infected but healthy or mild (YOPI)
o Repeated faecal culture
i. Clostridium - Cl. perfringens, Cl. dificile
ii. Salmonella typhimurium
iii. Campylobacter jejuni
iv. Yersinia enterocolitica

21
Q

CLOSTRIDIUM PERFRINGENS

A

iii. …CLOSTRIDIUM PERFRINGENS:
o „Antibiotic-responsive colitis” (?) „Clostridium colitis”
o Predisposing factors (diet, ab, infect) → enterotoxigen sporulation, CPE synthesis ↑↑
o Symptom: mild – fatal acute HGE - intermittant LBD!
o Diagnosis: Difficult
o spore in feces (smear) / cultur Cl.p. / toxin feces
o CPE toxin feces ELISA + PCR cpe gene
o ≈ spore number, CPE toxin, diarrhea
o Treatment:
o TYLOSIN!! 10-20 (40) mg/kg 2x
o amoxicillin, metronidazole, ampicillin
o rost supplementation supplementation!!

22
Q

CHRONIC COLITIS (IBD)

A

I. Lymphocytic-plasmacytic colitis (LPC) plasmacytic colitis (LPC)
II. Eosinophilic colitis (EC)
III. Chronic histiocytic ulcerative colitis (CHUC)
o Colon infiltration by inflammatory cells
o LPC, EC, (CHUC! = IBD)
o Idiopathic (dg. exclusion)
o Symptoms:
• chronic (>3 weeks) diarrhea LBD, anorexia?
• middle aged (6 years) dog, cat
• RDP: thicker mucous membrane
o Doesn’t improve: antiparasitic/ diet change/ ab
o DD: Systemic diseases, chronic parasitism, dietary sensitivity, infectious diseases, neoplasia
o Diagnosis histological evidence of mucosal inflammation
• Severity: extent of epithelial-glandular alterations.
• colitis/ enterocolitis (cat: enterocolitis)
o Pathophysiology: multifactorial
• defective mucosal barrier function (Ag —immun syst)
• abnormal immune response to
▪ Luminal pathogen
▪ Normal abnormal constituent
▪ TLR (Toll-like receptor) mutation
▪ Recognize microbe assoc molecular pattern, tolerance
▪ Activation→ proinflamm cytokin production↑
• dysbiosis (disturb intestinal microbiome)
• Genetic susceptibility
• Diet Ag: effect on the microbiom and the mucosa

23
Q

LYMPHOCYTIC-PLASMACYTIC COLITIS (LPC)

A

o Most common form of chronic colitis
o Middle-aged /older
o Signs: cyclical, tenesmus, mucoid faeces, haematochezia
o Colonoscopy: ↑ mucosal friability, granularity, loss of submucosal vascularity, erosions

24
Q

II. EOSINOPHILIC COLITIS (EC)

A

o Allergic manifestation to dietary /parasitic antigens?
o Middle-aged animals
o Signs: like LPC + roughened irregular mucosa by rectal palpation
o Colonoscopy: more friable and ulcerated than LPC

25
Q

III. CHRONIC HISTIOCYTIC ULCERATIVE COLITIS (CHUC)

A

o Boxer predisposed predisposed (bulldog, mastiff, malamute)
o Mostly male young
o Cause: AIEC (Adherent-Invasive E. Coli)!
• + aberrant immunosystem, mutant TLR
▪ Persist in macrophage, replicates, not able to eliminate the aberrant immunosystem
• Genetical defect
o Symptoms: severe LBD + lethargy, anorexia
o Hystopathology: Dg: PAS+ macrophag in mucosa
• PAS+ macrophage (AIEC bact residuum)
• Granulomatous inflammation
o Colonoscopy:mmfriable, thicker, granularity, erosion, ulcer
o Enrofloxacin!! (5)-10 mg/kg (4-6 w). Prognosis: better

26
Q

OTHER DISEASES OF THE COLON

A
OTHER DISEASES OF THE COLON
I. Irritable bowel syndrome
II. Constipation
III. Neoplasia
IV. Intussusception
27
Q

I. IRRITABLE BOWEL SYNDROME (IBS)

A

o Uncommon, non-inflammatory large bowel disease
o Fiber responsive responsive LBD?? overlap
o Abnormal colonic myoelectrical function
o Chronic, intermittent LBD
• Tenesmus, faecal mucus/haematochezia
o Large-breed dogs; stress-induced
o Exclusion diagnosis
• Dietary, parasitic, infectious, IBD
o Normal colonoscopic biopsy
o Treatment: to correct abnormal motility
• Dietary fibre, anxioliticum
• Loperamide

28
Q

II. CONSTIPATION

A

o Constipation:
• infrequent and difficult evacuation of feces
• decreased intestinal motility
o Obstipation:
• intractable constipation (+ accumulation of feces)
o Occurrence: Middle-aged, older cats, dogs
o Aetiology:
• Dietary: excess fibre, bones, hair accumulation
▪ Inactivity, obesity, drugs, endocrine diseases
▪ Colonic obstruction (prostate, pelvic fracture, stricture, tumour, perineal hernia, narrow pelvis)
• Megacolon, lumbosacral spinal cord disease
o Clinical signs: tenesmus, palpatory findings, typical feces (corn forceps!)
o Diagnosis: history, clinical signs, radiography
o Treatment:
• Water enema, removal of faeces
• Laxatives
• (lactulose)
• Fibre supplementation
• Prokinetic (cisapride)
• Colectomy
▪ Idiopathic megacolon, refractory severe constipation

29
Q

colonic neoplasia

A
▪ Dogs
1. Adenocarcinoma
2. Lymphosarcoma
3. Leiomyosarcoma
▪ Cats
1. Adenocarcinoma
2. Lymphosarcoma
3. Mast cell tumours
30
Q

IN GENERAL: TREATMENT OF LARGE BOWEL DISEASE

A

A. DIETARY
a. Novel protein (hypoallergenic)
 FA → SBD
b. Highly digestible
 Smaller faecal mass (mucosal disease, constipation, recto-anal disease)
c. High fibre
 Influence luminal SCFA, colonic motility
 1-2 tablespoon/25 kg psyllium, pumpkin, mixed fibres
d. FOS (fructooligosacharide)
B. NSAIDS
a. Not suggested in cats!!!
b. 5-Aminosalicylic acid (5-ASA) active moiety
c. Anti-leucotriene, free radical scavenging
d. Side effect: KCS
 mesalazine, balsalazide, olsalazine, (sulfasalazine)
C. ANTI-INFLAMMATORY/IMMUNOSUPPRESSIVE DOSE
a. prednisolone or methylprednisolone
b. budesonide
c. chlorambucil
d. cyclosporin
e. azathioprine??
D. ANTIBIOTICS
a. Effective against, anaerob, ↓ enterotoxin production
 metronidazol 10-15 mg/kg 2x
 tylosin 10-20 (40) mg/kg 1-2x
 amoxicillin, ampicillin, (klindamicin)
 enrofloxacin: (CHUC) 5 mg/kg 1x

31
Q

perineal disease

A
o Diseases of anorectum
• fecal incontinency
• anal sac
o impaction, sacculitis, proctitis, abscessation
• perianal fistula
• perineal hernia
• neoplasm
o anal sac adenocarcinoma
• perineal swelling
o paraprostatic cyst
• circumanal gland adenoma
• prolapsus ani
o Anorectum:
o Anal sacs (+ para-anal glands)
• Invaginations of inner area of cutaneous zone
• Combined secretion from glands + desquamated epithelial cells →malodorous oily fluid
• Become impacted →infection, abscessation
• Proctitis, sacculitis
▪ Circumanal glands (perianal)
• Androgen-sensitive glands → grow throughout a male dog’s life → androgen exposure → form adenoma