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SAM 2 > Small Intestinal Disease > Flashcards

Small Intestinal Disease Flashcards

1
Q

What comprises the small intestine?

A

Everything from the pyloric sphincter to the ileocolic junction

Duodenum- Jejunum- Ileum

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2
Q

What is the function of the small intestine?

A
  • Digestion of ingesta/food
  • Secretion of water and mucous
  • Absorption of nutrients- peptidases, nucleases, disaccharides, bile acids, pancreatic enzymes
  • Barrier to infection
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3
Q

What are villi?

A

Protrusions of the intestinal mucosa to increase surface area

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4
Q

What are the villi comprised of?

A
  • Mucosal immune system
  • Lamina propria
  • Enterocytes
  • Digestive enzymes, carrier proteins, goblet cells
  • Crypt cells
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5
Q

How long does it take for enterocytes to completely turn over?

A

3 days from the base of crypts

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6
Q

What do crypt cells do?

A
  • Some secretory capacity

- Make undifferentiated epithelial cells

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7
Q

What is the main energy requirement of enterocytes?

A

Glutamine

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8
Q

What will happen to enterocytes if they do not have enough glutamine?

A
  • Decline in villi structure
  • Loss of epithelial integrity
  • Decreased immune function
  • Decreased absorptive function
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9
Q

What are some clinical signs of small intestinal disease?

A
  • SI diarrhea
  • Melena or steatorrhea
  • Inappetence
  • Systemic illness
  • Abdominal distension or pain
  • Borborygmi
  • Flatulence (usually mild)
  • Vomiting and weight loss
  • Ravenous appetitie
  • Coat changes
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10
Q

What are acute enteropathies typically caused by?

A
  • Dietary indiscretion or change
  • Infection
  • Medications
  • Stress
  • Pancreatitis
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11
Q

What are chronic enteropathies typically caused by?

A
  • Food allergy or hypersensitivity
  • Inflammatory bowel disease
  • Lymphangiectasia
  • Infections (SIBO or parasites)
  • Neoplasia
  • EPI
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12
Q

What is HGE and AHDS?

A 
HGE= Hemorrhagic gastroenteritis
AHDS= Acute hemorrhagic diarrhea syndrome
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13
Q

What are the animals predisposed to AHDS and how does it typically present?

A

Small breed dogs

Marked hemoconcentration with fluid shifts
Typically require hospitalization

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14
Q

T/F: Dogs with AHDS will typically enter hypovolemic shock prior to having clinical evidence of dehydration.

A

True

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15
Q

What are the clinical signs of AHDS?

A

Hematemesis and hematochezia

Typically profuse and very hemorrhagic

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16
Q

What is the etiology of AHDS?

A

Usually viral, hypersensitivity, or clostridium perfringens

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17
Q

What are the expected PCV and TS levels in AHDS patients?

A

PCV >60% and TS not horribly elevated due to GI loss

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18
Q

How do you treat AHDS?

A

IV fluids, antibiotics, gastroprotectants, antiemetics, nutritional support

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19
Q

What is the prognosis of AHDS?

A

Good with aggressive supportive care

Decreases with severe hypoproteinemia or signs of sepsis

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20
Q

What helminths are found in the small intestine?

A 
Toxocara canis
Trichuris vulpis
Ancyclostoma caninum
Dipylidium caninum
Strongyloides stercoralis
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21
Q

What is the best test when you suspect worms?

A

Fecal (if negative do 3 consecutive days testing)

Can just deworm empirically

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22
Q

All the things about Diplydium caninum.

A
  • Ingestion of fleas with immature worms
  • Shed proglottids with in 2-3 weeks
  • Peri-rectal irritation and rarely small intestinal impactions
  • Teat with praziquantal or fenbendazole

Other tapeworm species: Taenia or Echinococcus

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23
Q

All the things about Toxocara canis/cati.

A
  • Ingestion of eggs or maternal transmission
  • Adults in small intestine
  • Babies most affected and can be fatal
  • Small intestinal obstruction are possible but rare

Clinical signs: vomiting or defecating live worms, unthrifty, rounded belly, diarrhea

Treatment: fenbendazole, pyrantel

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24
Q

What protozoa live in the small intestine?

A 
Giardia
Tritrichomonas foetus
Coccidia
Cryptosporidium
Toxoplasma gondii
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25
Q

What are the primary clinical signs and pathophysiology of protozoa infections?

A

Clinical signs: Diarrhea +/- weight loss

Pathology: Destruction of enterocytes and villi

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26
Q

How do you diagnose Giardia?

A

Direct smear to visualize cysts or trophozoites, IFA, Antigen/ELISA

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27
Q

How do you diagnose Tritrichomonas foetus?

A

Direct fecal smear, culture, PCR preferred

CATS ONLY

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28
Q

T/F: Giardia is non-species specific so it can be passed between dogs and cats and to humans.

A

False- species specific so any cross infections would be self-limiting

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29
Q

T/F: Subclinical infection of Giardia are very common.

A

True

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30
Q

What is the goal of treatment of Giardia?

A

Stop diarrhea

Fenbendazole or metronidazole effective

Elimination of infection is very difficult

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31
Q

What are the clinical signs of coccidia infections?

A

Weight loss, dehydration, may be hemorrhagic

Typically self limiting in a healthy adult animal

Worse in young or immune compromised patients

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32
Q

How do you diagnose coccidia?

A

Direct smear or fecal floatation

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33
Q

How do you treat coccidia?

A

Sulfadimethozine, ponazuril, supportive care

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34
Q

What is the prognosis of coccidia?

A

Good in adults with mild symptoms

Guarded in systemically ill patients

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35
Q

How is cryptosporidium transmitted and what are the clinical signs?

A

Transmission: fecal oral or contaminated food/water; zoonotic potential

Clinical signs: self limiting small bowel diarrhea, can be severe/life threatening in immunocompromised patients

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36
Q

How do you diagnose cryptosporidium?

A

Direct smear or fecal float, ELISA, PCR, biopsy

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37
Q

How do you treat cryptosporidium?

A

Paromomycin or tylosin

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38
Q

What is a major concern with toxoplasma?

A

Zoonosis

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39
Q

What are the parasitology facts about toxoplasma?

A
  • Oocysts require 1-5 days to become infectious
  • Disease only seen in immunecompromised patients
  • Disease mostly seen in cats
  • Transmission: predation or fecal contamination
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40
Q

What are the clinical signs of toxoplasma?

A
  • Pneumonitis
  • Vomiting or diarrhea
  • Encephalitis
  • Lymph node, liver issues
  • Chorioretinitis
  • Fever, weight loss, lethargy
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41
Q

T/F: Animals are unlikely to be shedding oocysts while they are significantly ill.

A

True- they have to have intestinal disease in order to shed oocysts and will typically show severe clinical sings only when extra-intestinal

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42
Q

How is toxoplasma diagnosed?

A

Fecal flotation and antibody titers (more useful)

Antibody titers do not predict oocyst shedding or clinical disease

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43
Q

How do you treat toxoplasma?

A

Clindimycin or trimethoprim-sulfonamide

Supportive care

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44
Q

What fungal infections do you see in the small intestine?

A

Pythiosis, histoplasmosis, candidiasis

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45
Q

What is pythium insidiosum?

A

An aquatic oomycete that will infect mammal hosts, typically in gulf coast states

Lives in standing water and infects via skin or mucosal penetration by motile zoospores

Most common in dogs and zoonosis has not been documented

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46
Q

What are the clinical signs of GI pythiosis?

A

Vomiting, weight loss, diarrhea, hematochezia, abdominal pain

Palpable abdominal mass, dehydration, poor body condition

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47
Q

What are the clinical signs of cutaneous pythiosis?

A

Non-healing skin lesion, Very ulcerated and granular looking with draining tracts

May have LN involvement

Dogs: base of tail, extremities, ventral neck, and perineum
Cats: cervical, inguinal, and truncal

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48
Q

T/F: Skin and GI pythiosis often occur together.

A

FALSE- very rarely occur together

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49
Q

What will your diagnostics show in pythiosis?

A

CBC: eosinophilia, anemia
Chem: hypoalbuminemia, hyperglobulinemia
Pythium ELISA (culture difficult)
Biopsy- severe transmural segmental thickening with pyogranulomatous and eosinophilic inflammation ; GMS stain to observe organisms
Rads: poor serosal detail with weight loss, mass lesion in abdomen or esophagus
Ultrasound: segmental thickening of GI, thickened gastric outflow tract, enlarged LN

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50
Q

How do you treat pythiosis?

A

Surgical removal or effected tracts

Iraconazole, terbinafine +/- immunotherapy for at least 2-3 months

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51
Q

What is the prognosis of pythiosis?

A

Poor with disseminated disease and no resection
less that 20-25% respond to medical management

Overall pretty grave

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52
Q

What is histoplasmosis?

A

Dimorphic fungus that occurs worldwide
Occurs in dogs and cats
Transmission: aerosols into lungs and thoracic LNs, GI tract, may enter bloodstream from primary site and cause wide spread disease

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53
Q

What are the clinical signs of histoplasmosis?

A 
Diarrhea (usually large)
Weight loss to emaviation
Chronic cough
Fever
Anemia, hepatomegaly, splenomegaly, lymphadenopathy
Nasopharyngeal and GI ulceration
Lameness
Respiratory difficulty
Skin lesions

Cats do not get GI signs

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54
Q

How do you diagnose histoplasmosis?

A

Chest rads: nodules, enlarged LNs
US: spleen liver and LN enlargement with thickened LI/SI wall
FNA or biopsy of abnormal tissues
ELISA antigeen tests

CBC, CHEM, and UA all have non-specific findings

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55
Q

How do you treat histoplasmosis?

A

Prolonged therapy with anti-fungals

Intraconazole, fluconazole or ketoconazole

Amphotericin B in severe cases

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56
Q

What is the prognosis of histoplasmosis?

A

Acute: may be fatal after 2-5 weeks
Poor condition/multisystem involvement: guarded to poor
One organ involved: still not great but better

57
Q

What are all the things with candidiasis?

A

Normal flora but opportunistic infections associated with the disruption of mucosal integrity can be seen

Cats- oral and URI, pyothorax, ocular, intestinal, cystitis

Dogs- Peritonitis and fungemia, perforating lesions after sx, mucosal and cutaneous candidiasis has been noted in immunosupressed animals

58
Q

What bacterial diseases are associated with the small intestine?

A 
Campylobacter
Salmonella
Clostridium
E. coli
Yersinia
Mycobacterium
59
Q

What are the top 3 bacteria associated with intestinal disease?

A

Campylobacter
Salmonella
E. coli

All associated with acute diarrhea

60
Q

What animals are prone to bacterial infections?

A

Young, kenneled, immunocompromised

Can happen in apparently healthy pets

61
Q

Are fecal cultures useful when diagnosing bacterial infections of the GIT?

A

Not really since most pathogenic bacteria can be found in small numbers in a healthy GIT

Must be interpreted with clinical signs and other lab data

Performed only in chronic diarrhea or severely debilitated animals

62
Q

What is salmonella?

A

Gram - facultative anaerobic bacteria that is part of the normal flora of the intestinal tract

Seen in young, parasitized, immunocompromised, or stressed animals

Ingestion of raw/contaminated food

Zoonoticc

63
Q

T/F: Salmonella destroys intestinal villi.

A

True- just like protozoa

64
Q

What are the clinical signs of Salmonella?

A

Acute transient diarrhea - can be supportively treated

Septic, shock, hospitalized from illness

65
Q

How do you diagnose salmonella?

A

Culture: blood or feces depending on disease type
PCR: lacks validation

66
Q

How do you treat salmonella?

A

None if primary and transient

IV abx and supportive care with severe illness

67
Q

What is the pronosis for salmonella?

A

Good unless septic

68
Q

What is E. coli?

A

Normal flora gram - anaerobic rod shaped bacterium that is mostly non-pathogenic

Rarely causes disease unless immunocompromised or particularly virulent strain

69
Q

What are the clinical signs of E. coli infections?

A

Diarrhea, vomiting, dehydration, lethargy

70
Q

How do you diagnose E. coli?

A

Culture of blood or feces

71
Q

How do you treat E. coli and what is the prognosis?

A

IV supportive care and antibiotics

Good prognosis unless septic

72
Q

What is the causative agent of salmon poisoning disease?

A

Neorikettsia helminthoeca or elokominica transmitted by Nanophyetus salmincola

73
Q

What are the clinical signs of salmon poisoning disease?

A

High fever, hematemesis, diarrhea +/- hematochezia, vomiting, lethargy, anorexia, nasal and ocular discharge, enlarged lymph nodes

74
Q

How do you diagnose salmon poisoning disease?

A
  • Fluke eggs in feces
  • History of ingested fish
  • Inclusion bodies on macrophages in lymph nodes
  • PCR or serology
  • Thrombocytopenia

Chem and UA non specific

75
Q

How do you treat salmon poisoning disease and what is the prognosis?

A

Hospitalized support and antibiotics (oxytetracycline, doxycycline) and praziquantel for the fluke

Prognosis is fair to good with aggressive supportive care but death in 90% of untreated cases

76
Q

What viruses effect the small intestine?

A

Parvo, distemper, feline panleukopenia, coronavirus, FIV, FELV

77
Q

All things canine parvo.

A
  • Type 2 pathogenic
  • Fecal oral transmission highly contagious
  • Infects enterocytes and bonemarrow
  • Typically seen in puppies
  • Severe hemorrhagic diarrhea
  • Dx: ELISA test useful but can cross react with vaccine
  • Tx: Aggressive supportive care
  • Prog: full recovery if they survive the first few days
78
Q

All things feline parvo.

A
  • Clinical signs similar to canine parvo but less severe enteritis usually
  • 50-90% fatal without aggressive support
  • Causes cerebellar hypoplasia in peri-natal infection
  • Can use canine snap test to diagnose
79
Q

All things coronavirus.

A

Canine- limited enteric pathology

Feline- self-limiting to moderate diarrhea and rarely causes CS; may mutate and manifest as FIP

80
Q

What are the most common intestinal neoplasms in cats?

A

Lymphoma, adenocarcinoma, mast cell

81
Q

What are the most common intestinal neoplasms in dogs?

A

Lymphoma, adenocarcinoma, smooth muscle tumors

82
Q

All things small cell lymphoma.

A

Infiltrative /diffuse type disease diagnosed via biopsy

Tx: chlorambucil and prednisone

Prognosis: survival up to 3 years with treatment

83
Q

What are the criteria that you can classify intestinal obstruction by?

A

Extraluminal vs Luminal

Mechanical vs. Functional

84
Q

What are some conditions that can cause intestinal obstruction?

A
  • Mass lesions
  • Foreign bodies
  • Ganulomatous disease
  • Inflammatory disease
  • Hypertrophy
  • Inussusceptions
  • Hypomotility or ileus
  • Volvulus or torsion
  • Hernia
85
Q

What is an intussusception?

A

Telescoping of one bowel loop into the adjacent segment

Often associated with parvovirus, masses, or diffuse ileus

86
Q

T/F: Intussuscpetion is the most common cause of extraluminal obstruction.

A

True- most commonly at the ileocolic junction

87
Q

What animals are predisposed to intussusceptions?

A
  • Young animals with severe gastroenteritis
  • Causes of gasteroenteritis
  • Neoplasia
  • Postparturient bitches
88
Q

What are the clinical signs and physical exam findings of animals with intussusceptions?

A

CS: vomiting, diarrhea, anorexia

PE: Abdominal pain, tube like structure, associated illness

89
Q

How do you diagnose and treat intussusceptions?

A

Dx: palpation of tube like mass, radiographs, ultrasound (double walled structure)

Tx: spontaneous reduction possible, surgery, treat underlying disease

90
Q

All things intestinal volvulus.

A

Rare often fatal twisting of the intestines

Acute onset of CS, patients typically present in shock

Surgery is obligatory as bowel is mot often diffusely necrotic

91
Q

What is an intestinal hernia?

A

Intestinal loops slip outside abdominal cavity into the SQ tissues

Can lead to strangulation and necrosis of intestines with intermittent GI signs

92
Q

What is the difference between direct and indirect intestinal hernias?

A

Direct- rent in the body wall from trauma or surgery

Indirect- existing ring of tissue such as umbilical ring, inguinal ring, or scrotum

Aka congenital and acquired

93
Q

How do you diagnose and treat intestinal hernias?

A

Dx: Palpate, radiographs, ultrasound
Tx: Sugery

94
Q

What is EPI?

A

Exocrine pancreatic insufficiency

Insufficient secretion and production of pancreatic enzymes leading to maldigestion

95
Q

What are some etiologies of EPI?

A
  • Acinar atrophy
  • Chronic pancreatitis
  • Aplasia or hypoplasia

Congenital in GSD, rough coated collies, eurasians

96
Q

What are the clinical signs of EPI?

A

1 is weight loss

Loose stools and steatorrhea
Ravenous appetitie
Poor hair coat
Borborygmi
Flatulence
Can be subclinical
97
Q

How do you diagnose EPI?

A

CBC, CHEM, UA: rules out other causes
TLI levels: species specific
B12: often low in EPI and requires supplementation

98
Q

How do you treat EPI?

A

Dried pancreatic extract powder or fresh pancrease in the diet (pancrealipase powder)

B12 supplementation

99
Q

Why does EPI treatment fail?

A

Concurrent intestinal disease
Too much acid in the stomach (start on antacid)

Prognosis usually excellent but requires lifelong therapy

100
Q

When should you biopsy a patient with a suspected primary enteropathy?

A

To prioritize and optimize therapy or when empiric therapy fails or patient status dictates definitive answer

101
Q

What are examples of empiric therapy?

A

Deworming
Diet change
Antibiotic trial
Probiotics

102
Q

What conditions are extremely responsive to diet change?

A

Food allergies or hypersensitivity

103
Q

How do you diagnose and what are treatment options for food allergy or hypersensitivity?

A

Dx: resolution of CS with diet change

Tx: Hydrolyzed diets, novel antigen diets

104
Q

How long will it take to see a clinical response to a food responsive disease?

A

Around 2 weeks

May take a couple different diets before medication trial

105
Q

What are hydrolyzed diets?

A

Proteins are split up into a very small sized so that the immune system cannot recognize them as foreign

Most are around 7-10 KD

106
Q

What is idiopathic antibiotic responsive diarrhea?

A

Due to small intestnial bacterial overgrowth

No reliable test or specific etiology

107
Q

What are some mechanisms that cause IARD?

A

Host-bacterial interactions or bacterial overgrowth secondary to defects in mucosa, aberrant mucosal immune response, qualitative changes in enteric flora (dysbiosis)

108
Q

What are the clinical signs of ARD?

A
  • Small bowel diarrhea
  • +/- colitis and weight loss
  • Stunted growth
  • Borborygmi and flatulence
  • Appetite change
  • Vomiting
109
Q

How do you treat ARD?

A

Metronizadole, tylosin, oxytetracycline

Diet trials can be done but has a variable response- high quality protein with low fat seems to have the best outcome

110
Q

What are the most common diseases diagnosed on biopsy?

A

Inflammatory bowel disease
Lymphangectasia
Lymphoma

111
Q

What parts of the GIT can be accessed with gastroduodenoscopy?

A

Esophagus, stomach, proximal duodenum

112
Q

What parts of the GIT can be accessed with colonoscopy?

A

Anus, rectum, colon, +/- ileum

113
Q

What are some reasons to perform endoscopic biopsies?

A
  • Concurrent concerns for colitis
  • Concerns for lower SI disease
  • Concerns for neoplasia
114
Q

Why would a surgical biopsy be better than an endoscopic biopsy?

A
  • When disease is deeper than the mucosal layer
  • When other organs are affected
  • When you have a diffuse lesion requiring surgical removal
115
Q

What are the pros and cons of endoscopy?

A

Pro: minimaly invasive, same day GI and recover well, can biopsy many regions

Con: deeper layers missed, cannot access jejunum, cannot sample/assess other organs

116
Q

What tests can be done to evaluate a biopsy?

A

H&E staining
IHC for cellular contents and differentiation of inflammation
Special stains for organisms

FISH analysis- for AIEC on colonic biopsy

117
Q

What is AIEC?

A

Adherent invasive E. coli

118
Q

What is inflammatory bowel disease?

A
  • Chronic GI disease of dogs and cats
  • Fails to respond to deworming, antibiotics and diet
  • Histopath reveals mucosal changes and inflammatory infiltrate
  • Can involve any or all of the GIT
119
Q

What causes IBD?

A
  1. Disruption of physiologic interaction of innate and adaptive immune response
  2. Defective mucosal barrier
  3. Inappropriate reaction to normal GIT components
120
Q

What are pattern recognition receptors?

A

Health: maintain hyporesponsiveness to luminal contents, diet, and protects the mucosa

121
Q

What is the most common infiltrate in IBD?

A

Lymphoplasmacytic infiltrate

122
Q

What is the pathogenicity of IBD?

A
  • Loss of normal villous structure
  • Goblet cell changes
  • Crypt abscesses and cysts in advanced disease and lymphangectasia
  • Moderate to severe infiltrates are often associated wit protein losing disease
123
Q

What are the types of IBD?

A
  1. Minimal change
  2. Granulomatous or neutrophilic
  3. Lymphoplasmacytic
  4. Eosinophilic
  5. Lymphangectasia
124
Q

What are the characteristics of minimal change enteropathy?

A
  • Low clinical disease score
  • Albumin >2.0
  • Normal B12
  • Normal to minimal inflammation on histopathology
125
Q

What is the treatment for minimal change enteropathy?

A
  • Deworm
  • Diet trial
  • Antibiotic trial with probiotics (chronic therapy may be necessary)
126
Q

What are the characteristics of granulomatous or neutrophilic enteropathy?

A
  • Infrequent diagnosis
  • Macrophages/histiocyticc and/or neutrophilic infiltrate
  • Prompts to look for infectious disease (must rule out)
127
Q

How do you treat granulomatous or neutrophilic enteropathy?

A
  • Treat underlying infectious disease
  • Antibiotic trial
  • Immunosupressive medications if infectious disease is excluded

Guarded to poor prognosis if underlying etiologic agent isn’t identified

128
Q

What are the characteristics of lymphoplasmacytic enteropathy?

A
  • Lymphocyte and plasma cell infiltrate
  • Variable clinical presentation
  • May be PLE
  • Typically systemically ill
  • Typically diet responsive (60-88%)
129
Q

What is the treatment for lymphoplasmacytic enteropathy?

A
  • Hydrolyzed or novel antigen diet
  • Antibiotics trial
  • Immunosuppressants when no response to above
  • Anti-clotting medications with hypoalbuminemia

Better response when younger dogs with normal albumin

130
Q

What are the characteristics, prognosis, and treatment of eosinophilic enteropathy?

A
  • Eosinophil infiltrates
  • Typically reaction to parasites or food allergy
  • Good prognosis in dogs
  • Guarded to poor prognosis in cats
  • Tx: deworm, diet, immunosuppressant therapy
131
Q

What are characteristics of lymphangectasia and crypt cell cysts?

A

Local or generalized lymphatic disease
Common cause of PLE

Basenhi, SCWT, Torkie, and Lundehunds over represented

132
Q

What does lymphangectasia look like on endoscopy?

A
  • White granules/blebs on mucosal surface

- Abnormal distension of lymphatic vessels within mucosa

133
Q

What is the treatment for lymphangectasia and crypt cell cysts?

A 
Diet: hydrolyzed and low fat
Antibiotics: metronidazole or tylosin
Immunosuppresants: prednisolone or cyclosporine may need parenteral administration
Anti-clot medications
Diuretics- in cases of ascites
134
Q

What is the prognosis of lymphangectasia and crypt cell cysts?

A

Fair to guarded pending response to treatment and severity of clinical signs

135
Q

What are potential causes of protein losing enteropathy?

A
  • Inflammatory disease
  • Lymphangectasia
  • Infiltrative neoplasia
  • Infectious disease
  • Endoparasites
  • Intussusception
  • Portal hypertension
136
Q

What is the treatment for protein losing enteropathy?

A
  • Treat the underlying disease
  • Diuretics as needed
  • Abdominocenteisis (do not remove all the way)
137
Q

What is the prognosis of PLE?

A

-Guarded to good

Depends on severity of pets condition and response to therapy

138
Q

What are some negative indicators for prognosis?

A

Low albumin, low B12, Neoplasia

139
Q

What are the best way to provide enteral nutrition in a GI disease patient?

A

Nasogastric or nasoesophageal tubes
Esophagostomy tubes
PEG tubes- used more for chronic cases

SAM 2 (21 decks)

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