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sam dr green > disorders of the gi > Flashcards

disorders of the gi Flashcards

1
Q

transmission for canine parvo v

A
  • •Affinity for rapidly dividing cells
    • Intestines -crypt necrosis, vomiting, diarrhea
    • Bone marrow –neutropenia (immunosuppression)
  • •Transmission: fecal –oral, Highlycontagious
  • •Survival for months in environment (fomites
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2
Q

signalment for parvo

A

Age -puppies 6 weeks to 6 months

any breed can get it

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3
Q

cs of parvo

A

Vomiting
•Diarrhea
•Fever
•Anorexia
•Depression
•Dehydration
•Death (hypovolemia; sepsis)
•Heart signs
Myocarditis if infected in utero or before 8 weeks

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4
Q

dx for parvo

A
  • Sudden onset, clinical signs
  • •Age + exposure
  • •Leukopenia, neutropenia
  • •Lymphopenia, hypoalbuminemia
  • •Radiography (gas distention, ileus)
  • •Ultrasound (intussusception)
  • •Fecal antigen immunoassay (SNAP, ELISA)
  • False positive ??(5-15 days post modified live vaccine)
  • False negative (early, late in disease: 5-7 days)
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5
Q

common mistakes made with tx for parvo

A
  • Inadequate fluid therapy
  • •Overzealous fluid administration
  • •Unrecognized sepsis
  • •Unrecognized concurrent GI disease
  • Parasites
  • Intussusception
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6
Q

px for parvo

A

Most live if:
Supported long enough
Treated in a timely fashion
Survive first 4 days
•Can be fatal

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7
Q

-ve px indicators for parvo

A

Very young puppies
Septic shock
Breed differences??–crap

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8
Q

etiology for histoplasmosis

A

Histoplasma capsulatum
•Mycotic infection
•GI, respiratory, reticuloendothelial systems, bones, eyes
•Mississippi, Ohio river valleys

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9
Q

cs of histoplasmosis

A
  • Dogs
  • •Diarrhea (+/-blood, mucus)
  • •Weight loss
  • •GI histo: colon is usually target organ
  • •Diffuse, severe granulomatous, ulcerative colitis
  • •Can cause PLE(prot. losing enter)
  • •Can involve SI
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10
Q

target organ for gi histoplasmosis

A
  • colon
  • u see
    • hemato chezia,
    • straining ,
    • aurgency to defecate
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11
Q

LI dz causing PLE

A
  • lymphantegia,
  • histoplasmosis,
  • lymphoma,
  • inflamatory bowl diz
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12
Q

dx for histoplasmosis

A
  • History (chronic large bowel diarrhea, PLE)
  • •Identification of organism
  • Cytology
  • Histopathology
  • •Colonic biopsy, rectal scraping (cytology)
  • •Fundic exam (active chorioretinitis)
  • •Other systemic involvement
  • Liver, spleen, lungs, hilar lymphadenopathy
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13
Q

tx for histoplasmosis

A
  • Itraconazole
  • •Amphotericin B & Itraconazole
  • •Long term therapy (4 –6 months
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14
Q

px for histoplasmosis

A
  • Dogs may do well if treated early
  • •Multiple organ system involvement
  • Worsens prognosis
  • •CNS involvement
  • Poor prognosis
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15
Q

cs of giardia

A

Dogs > cats

  • •Asymptomatic
  • •Small bowel diarrhea
  • Can be large bowel diarrhea too!!
  • •May be self limiting
  • •Acute, chronic, or episodic
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16
Q

dx for giardia

A
  • Fecal ZnSO4 flotation-centrifugation
  • •Fecal immunoassay
    • SNAP (Idexx)
    • Microplate ELISA
    • IFA
  • Rx trial
    • Fenbendazole
    • Metronidazole
  • •Fecal smear
    • Trophozoites
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17
Q

tx for giardia

A
  • Fenbendazole (Panacur)
  • •Febantel (Drontal Plus)
  • •Metronidazole
    • Less effective and more side effects
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18
Q
A
  • Generally good
  • •Can be difficult to eliminate in some animals
    • Drug resistance
    • Immunodeficiency
    • Concurrent disease present
    • Reinfection common (cysts resistant in environment)
    • Other protozoal organisms mistaken for Giardiapx for giardia
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19
Q

clinical presentation of trichiminoasis

A
  • Tritrichomonas foetus
    • •Venereal disease of cattle
  • Large bowel diarrhea
    • •Chronic, waxing & waning
    • •Occasionally containing blood and mucus
    • •Mild L-P colitis
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20
Q

signalment for feline trichiminniasis

A

Young cats, purebreds
Multi -cat housing
31% of show cats

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21
Q

cat present with Anus which appear inflamed and painful and Involuntary dribbling of feces or rectal prolapse.

whats your suspicion

A
  • feline trichiminoasis
  • Cats are healthy otherwise
  • Consistency of diarrhea typically improves with abx
  • •Quickly resumes when treatment is discontinued
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22
Q

dx for feline trichiminoasis

A

Fecal PCR assay
Detects 80% -90% of cases
•Culture (In Pouch-TF)
Detects 30% -50%
•Fecal microscopy
Detects only 14%
Often mistaken for Giardia

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23
Q

which dz is often mistaken for giardia

A

feline trichiminiasis

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24
Q

tx for feline trichimianosis

A
  • Refractory to most common antibiotics
    • •Ronidazole
  • Only effective treatment known
  • Spontaneous resolution often occurs (2-3 years)
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25
Q

enterotoxic effect of clostridium perfringins

A

Permeability (inc)
•Absorption (dec)
•Cytotoxicity

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26
Q

clinical features of clostridial perfringins

A

Large bowel diarrhea
•Acute, chronic, or recurrent
•May be self limiting
•Watery to semiformed
•Variable mucus, blood, tenesmus
•Acute HGE
•Nosocomial
•High -density housing

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27
Q

dx for cl. perfringins

A
  • Fecal endospores
    • Not confirmatory
  • •Fecal toxin assay
    • ELISA (TechLab)
    • PCR genotyping
  • •Fecal culture
    • Not reliable
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28
Q

tx for clos.perfringins

A
  • Usually good
  • •Some need long term tx
    • Tylan
  • •Fiber supplementation often helpful (chronic)
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29
Q

cs of campylobacter

A

Subclinical carrier
•Large bowel diarrhea
•Watery diarrhea
•Often self limiting
•Young animals
•Crowded conditions

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30
Q

dx for campylobacter

A
  • Fecal microscopy
    • Wet mount: darting motility
    • Gram stain: “W” or gull-wing shape
  • •Fecal culture, Fecal PCR
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31
Q

dx for camphylobacter

A

Erythromycin (10 –15 mg/kg PO q 8 hrs)
•Tx 1 –3 days beyond resolution of signs

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32
Q

px for campylobacter

A

Erythromycin (10 –15 mg/kg PO q 8 hrs)
•Tx 1 –3 days beyond resolution of signs

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33
Q

etiology for salmonela poisoning

A

Neorickettsia helminthoeca
•Fluke (N. salmincola) carries organism
•Dog ingests raw fish (salmon) infected with fluke
•Rickettsia spreads to intestines, lymph nodes
•Pacific northwestern U.S.
Snail intermediate host for N. salmincola

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34
Q

clinical features of salmon poisoning

A

Dogs
•Fever
•Anorexia, vomiting, diarrhea (small bowel, +/-blood)
•Generalized lymphadenopathy
•Thrombocytopenia, lymphopenia, eosinophilia
•Hypoalbuminemia, elevated ALP

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35
Q

dx for salmon poisoning

A
  • Presumptive
    • History -consumption of fish, exposure to streams/lakes)
  • •Definitive
    • N. salmincolaova in feces
    • N. helminthoecaorganism in cytology (FNA of lymph node)
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36
Q

tx for salmon poisoning

A
  • Supportive care
  • •Tetracycline, oxytetracycline, doxycycline
  • •Elimination of fluke (praziquantel)
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37
Q

px for salmon poisoning

A

Most respond well
•Fatal if left untreated

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38
Q

clinical features of protothecosis

A
  • Dogs (cats)
  • •Skin, colon, eyes, other body systems
  • •Large bowel diarrhea
    • ​chrnic n can be a wasting dz
  • •Weight loss, ADR
  • •Collies overrepresented
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39
Q

tx for protothecosis

A
  • Identification of organism
  • •Cytology (rectal cytology)
  • •Histopathology (colonoscopy)
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40
Q

tx for protothecosis

A

Amphotericin B, Azoles
•Equivocal efficacy

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41
Q

px for protothecosis

A

poor

42
Q

etiology for exocrine maldigestive insufficiency

A
  1. Pancreatic acinar cell atrophy due to;
    1. Hereditary predisposition
    2. Autosomal recessive
    3. German Shepherd
    4. Rough-coated Collie
  2. Chronic pancreatitis
    •Pancreatic hypoplasia
    •Pancreatic neoplasia
43
Q

sequela for exocrine pancreatic insufficiency

A
  • Maldigestion
    • •Proteases (eg, trypsin)
    • •Lipase
    • •Amylase
  • Duodenal acidity
  • Bacterial overgrowth
  • Cobalamin deficiency
  • Intestinal mucosal damage
44
Q

cs of epi

A

Dogs > Cats
•Age: 1 –5 years (average –3 years)
•Polyphagia
•Coprophagia
•Pica
•Weight loss (may be only feature)
•Diarrhea (small bowel)
•High volume, fatty
•Borborygmus
•Flatulence

45
Q

confirmatory for EPI

A

TLI (trypsin-like immunoassay) –CONFIRMATORY

46
Q

dx for epi

A

History, signalment, clinical signs
•Rule out other causes of small bowel diarrhea
•Fecal microscopy
Presumptive ONLY
Sudan (undigested fat)
Iodine (undigested starch)
•Serum enzyme assay
TLI (trypsin-like immunoassay) –CONFIRMATORY
Fasted sample (12 hour fast)
•Serum cobalamin (decreased in 75 -80%)

47
Q

tx for epi

A
  • Enzyme replacement (Pancrezyme, Viokase
  • Low fat diets (high quality)
  • •Cobalamin therapy (PRN)
  • •Abx for ARD (PRN)
  • •H2-receptor blockers (PRN)
48
Q

px for epi

A
  • Good
  • •Most dogs show clinical response in 1 week
  • •LIFELONG therapy required
49
Q

indicator for bad px in epi dog

A

Marked hypocobalaminemia (< 100 ng/L)

50
Q

common cause of epi in cats

A

triditis

51
Q

characterization of inflamatory bowl dz

A
  • Cellular infiltrative pattern
    • Lymphocytic –plasmacytic–most common
    • Eosinophilic
    • Granulomatous– fungus should be in your list
52
Q

location for IBD

A 
Small intestine (enteritis)
Large intestine (colitis)
53
Q

HOW IBD IS DEFINED

  1. TIME OF PRESENTATION OF CS
  2. LESIONS
A
  • Chronic GI signs (> 3 weeks)
  • •GI mucosal lesions
    • Mucosal L-P infiltration (other patterns)
    • Epithelial injury
    • Abnormal mucosal architecture
  • •Exclusion of other causes of chronic GI signs
54
Q

WHAT CAUSES IBD

A
  • LOT OF POTENTIAL CAUSES
    • Defect in mucosal barrier -immune mediated response
    • •Inflammatory reaction (antigens)
    • •Hypersensitivity(dietary, parasitic)
    • •Primary immune mediated
    • •Parasitic, fungal, FIP
    • •Other unrecognized antigens (parasites, bacteria, etc.)
55
Q

CS OF IBD

A
  • N.B NO CLASSICAL IBD CASE.IT CAN DO WHATEVER IT WANTS DEPENDING ON WHAT PART OF GI IS AFFECTED
  • Variable GI signs
    • Region of GI affected
    • Diffuse or selective
    • Extent of disease
  • •Unpredictable course (weeks to years)
    • Persistent clinical signs
    • Spontaneous exacerbations and remissions
    • Waxing-waning
    • Episodic
56
Q

CS OF LPE IBD

A
  • Vomiting
    • Most common in cats
  • •Small bowel diarrhea
  • •Weight loss
  • •Lethargy
  • •Appetite
    • Increased
    • Normal
    • Decreased
57
Q

cs of LPC ibd

A
  • Mucoid diarrhea
  • •Hematochezia
  • •Frequent defecation
  • •Urgency
  • •Dyschezia
  • •Vomiting
  • •Weight loss (rare)
58
Q

WHICH LI DZ CAUSES WT LOSS

A
  1. COCCIDIOSIS AND
  2. HISTO
  3. THEY SHOW WT LOSS WHEN THEY HAVE COLONIC DZ
59
Q

PE EXAM FINDINGS FOR IBD

A
  • NOTHING ESPECIFIC
  • No abnormalities in most cases
    •Thickened intestinal loops-IF U ARE REALLY EXPERIENCED
    •(Enlarged mesenteric LN)
    •Cachexia
    •Alopecia (rare)
    •Effusion (rare)
60
Q

IBD COMPLICATIONS

A
  • Vitamin malabsorption
    • •Cobalamin depletion
    • •Vitamin K deficiency (cats)
    • VIT B12 IS ABSORBED IN ILEUM SO IF U HAV si DZ WONT B ABLE TO ABSORB IT
  • Bacterial Overgrowth
    • disbiosis happens in every SI dz
  • Effusions & edema
    • •Protein loss (PLE)
  • Triaditis (cats)
    • •Cholangitis / Cholangiohepatitis
    • •Pancreatitis
  • GI Lymphoma
61
Q

dx for IBD

A
  • Preliminary
    • PE, MDB, fecal
    • •Infectious diseases (bacteria, protozoa, etc.)
    • •TLI/Cobalamin/Folate-Do b4 doing bx
    • •Imaging (radiographs, ultrasound)= useless
  • Endoscopic biopsy
  • Response to treatment
    • •Corticosteroids, other immunosuppressive
    • •Fenbendazole trial
    • •Novel protein diet trial
    • •Antibiotic trial (metronidazole, etc.)
    • corticosteroids ,other immnosupressives
62
Q

lab findings for IBD DX

A
  • NO ABNORMALITIES IN MOST CASES!
  • Nonregenerative anemia (mild)
  • Lymphopenia (stress)
  • Hypokalemia (mild)
  • Low albumin (PLE)
  • Elevated ALT & ALP
    • •Cholangitis
    • •Cholangiohepatitis
63
Q

DISCUSS USE OF US IN DX OF IBD

A
  • good to US before scoping to localise the area before scoping
  • Thickness
  • Stratification of layers
  • Masses
    • U WONT SEE MASSES WITH IBD
  • Mesenteric LNs
  • Associated viscera
    • •Pancreas, liver, biliary tract, etc.
  • NOT reliable to DDx lymphoma vs. IBD
64
Q

ENDOSCPIC FINDINGS FOR IBD

A
  • Erythema
  • Friability
  • Granularity
  • Thickening, folding
  • Indistensibility
  • Hemorrhages, erosions
65
Q

BX FINDINGS FOR IBD

A

Immune cells in the mucosa ARE normal

66
Q

IBD VS SMALL CELL LYMPHOMA

A
  • Well-differentiated low-grade lymphocytic lymphoma vs. IBD
    • •Immunohistochemistry
    • •Flow cytometry
    • •Lymphocyte clonal assay (CSU)
67
Q

DISCUSS THEURAPEUTICS TRIALS IN IBD

A
  • Diet modification
  • Fenbendazole
  • Antibiotics
  • •Microflora & immune modulation
  • Probiotics
    • DNT MAKE MUCH DIFFERENCE
  • •Microflora & immune modulation
  • Sulfasalazine (5-ASA)
    • •Colitis (dogs)
  • Cobalamin
  • Environmental enrichment (indoor cats)
68
Q

IBD DIET

A
  • Digestible GI diets
  • Novel protein diets
    • •Duck, venison, rabbit, kangaroo, etc.
  • •Avoid beef, wheat, and corn gluten
  • Hydrolyzed protein diets
    • •Oligopeptides that are less antigenic
  • Cobalamin injections PRN
69
Q

VIT B12 AND FOLATE TX FOR IBD

A
  • COBALAMIN (VIT B12)
  • Intestinal absorption (assuming normal diet)
  • •Absorbed in Ileum
  • •Pancreatic intrinsic factor needed for absorption
    • produced b stomach n pancrease in dog bt only by pancrease in cats
    • dificincy of intrinsic factors could lead to vit b12 def.
      if tli is low then it may be a cause of vit. b12 def
  • Folate
  • •Intestinal absorption (assuming normal diet)
  • •Absorbed in proximal SI
  • •Produced by bacterial microflora.
    • BAC. consime vit b12 n prodce folate
70
Q

causes of decreased cobalamin

A
  1. •(Dietary deficiency)
  2. •EPI (74% of cases)
    • u are nt producing enough extrinsic factors leading to malabsoption
  3. •Malabsorption (ileum)
    1. •Antibiotic responsive diarrhea (previously –SIBO)

n.b its gonna be on the exam (what he said in class)

71
Q

what causes decreased folate

A

Dietary deficiency
•Malabsorption (proximal small intestine)

72
Q

complications of cobalaminabsoption

A

EPI,

ARD (SIBO),

IBD,

other intestinal dz

73
Q

abx responsive diarrhoea

A

Previously known as SIBO
Presumptive diagnosis
Serum cobalamin & folate
Metronidazole
Tylosin (Tylan)

74
Q

cause of PLE

A
  • Mucosal cell injury
    • •Increased permeability to plasma proteins
  • Mucosal erosions & ulcerations
    • •Loss of protein-rich exudate (and blood)
  • Lymphatic obstruction
    • •Extravasation or leakage of protein-rich lymph
75
Q

sign. for PLE

A
  • Dogs > cats
  • Genetic susceptibility
    • •Lundehound (Lymphangiectasia)
    • •Soft-coated Wheaten Terrier (PLE/PLN)
    • •Yorkshire Terrier (Lymphangiectasia
76
Q

causes of PLE

A
  • Lymphangiectasia
  • IBD
  • Lymphoma
  • Histoplasmosis
  • Any other infiltrative disease
  • Young dogs
    • •Hookworms
    • •Chronic intussusception
77
Q

etiology of lymphactasia

A
  • Lymphatic obstruction
  • •Pericarditis
    • lymphatics goes to the venous side increase in venous pressure right sided heart failure
  • •Infiltrative mesenteric LN disease
  • •Infiltrative intestinal mucosal disease
  • •MOST are idiopathic (or cryptogenic)
78
Q

lymphactasia results in

A
  • Dilation and rupture of intestinal lacteals
  • Leakage of lymphatic contents
79
Q

cs of lymphactasia

A
  • Chronic diarrhea (SI)
    • •May be intermittent
    • •May be ABSENT
    • tq-may nt hav no gi sings at all
      even if they get them they are nt always consistent
  • Weight loss
    • common presenting sign
  • Effusion & edema
    • •Ascites
    • •Pleural effusion
    • •Pitting edema
80
Q

lab findings of lymphactasia

A
  • Total Protein decreased
  • Albumin decreased
  • Globulin decreased
  • Cholesterol decreased
  • Total Calcium decreased
  • Ionized Ca++ decreased
  • Magnesium decreased
  • Lymphocytes decreased
  • AT –III decreased
81
Q

Us findings of lymphactasia

A
  • Hyperechoic mucosal striations
    • •Diffuse in 70%
    • •Multifocal in 30%
  • Diffuse mucosal thickening
    • •Usually without loss of layering
  • Associated peritoneal effusion
82
Q

tx for lymphactasia

A
  • Ultra -low fat diet
    • •Commercial –Royal Canin LF
    • •Homemade –Turkey / potato
  • Corticosteroids
    • tx inflamatory component and lipogranulomas
  • Other IBD Rx
83
Q

px for lymphactasia

A
  • Variable
  • Some need long term pred
  • Some can be managed with diet alone
  • Peracute deaths due to PTE reported
84
Q

etiology for stress colitis

A
  • idiopathic(stress)
  • no inflamation present
85
Q

clinical features of stress colitis

A
  • Dogs
  • •Acute onset large bowel diarrhea
86
Q

dx for stress colitis

A

Diagnosis of exclusion

87
Q

tx for stress colitis

A
  • Fiber (Hills W/D, metamucil, etc.)

•5-ASA, abx

88
Q

neoplasia of the SI

A

Lymphoma
Adenocarcinoma
Leiomyoma (hypoglycemia)
Leiomyosarcoma (hypoglycemia)

89
Q

which dz can be difficult to distinguish from lymphoma

A

ibd

90
Q

sign. for Chronic Histiocytic Ulcerative Colitis

A

Young Boxer dogs (M)

aka boxer’s colitis

91
Q

cs of Chronic Histiocytic Ulcerative Colitis

A
  • Large bowel diarrhea
    • •Severe with bleeding
    • •Progressive wt. loss
92
Q

dx for Chronic Histiocytic Ulcerative Colitis

A
  • bx
  • Histiocytic inflam and ulcers
  • •PAS+ macrophages
  • •Adherent-invasive E. coli
  • •FISH
93
Q

tx for chronic histiocytic ulcerative colitis

A

Rx: Enrofloxacin (3 wks)

94
Q

neoplasias of the LI

A
  • Adenocarcinoma
  • Rectal polyps
    • •In older dogs
    • •Hematochezia
    • •Dyschezia (straining)
    • •Lobulated bleeding mass
95
Q

list the perineal/perianal dz

A
  • Perineal hernia
  • Perianal fistulas
  • Anal saculitis
  • Anal sac (apocrine gland) adenocarcinoma
96
Q

etiology for megacolon

A
  • primarily a cat dz
  • Idiopathic (70%)
    • Likely myopathic
  • •Obstructive (25%)
    • Pelvic canal stenosis (malunion)
    • Rectal stricture
    • Anorectal neoplasia
    • Neurogenic (5 %) -lumbosacral dz
97
Q

clinical featres of idiopathic colitis

A
  • Feline disease (dogs rarely affected)
  • •Colonic hypomotility
  • •Idiopathic smooth muscle dysfunction
  • •Colonic dilatation
  • •Recurrent constipation
  • •Impaction
  • •Irreversible dilatation
98
Q

dx for idiopathic megacolon

A
  • Abdominal palpation
    • Massively dilated colon
  • •Radiographs
  • •Elimination of other causes
99
Q

tx for idiopathic megacolon

A
  • Medical first
    • Deobstipation
    • Fiber (Metamucil, pumpkin)
    • Stool softeners (lactulose)
    • Prokinetics (Cisapride)
  • •Surgery
    • Subtotal colectomy
100
Q

drug tx for idiopathic megacolon

A
  • Cisapride (Propulsid)
    • •5-HT4-serotonergic agonist
    • •Increases Ach release
    • Myenteric plexus
    • •Stimulates colonic smooth muscle
    • •No CNS or antiemetic effects
      • Does not cross BBB
101
Q

discuss procedure for deostipation in idiopathic megacolon

A
  • Rehydration first!!!!!
  • •General anesthesia
  • •Endotracheal intubation
  • •Lubrication & saline
  • •Manual extraction (be careful)
    • Finger
    • Abdominal palpation
    • Sponge forceps
102
Q

px for idiopathic megacolon

A
  • Many respond initially to medical tx (early)
  • •Subtotal colectomy needed in others
  • Some initial wt. loss, regained within 3-7 weeks
  • Watery to mucoid stools during first 3-7 weeks
  • Mucoid / semi-solid / formed stools by 3-6 months
  • Owner satisfaction -excellent in majority of cases

sam dr green (10 decks)

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