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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
enterotoxic effect of clostridium perfringins
Permeability (inc) •Absorption (dec) •Cytotoxicity
26
clinical features of clostridial perfringins
Large bowel diarrhea •Acute, chronic, or recurrent •May be self limiting •Watery to semiformed •Variable mucus, blood, tenesmus •Acute HGE •Nosocomial •High -density housing
27
dx for cl. perfringins
* Fecal endospores * Not confirmatory * •Fecal toxin assay * ELISA (TechLab) * PCR genotyping * •Fecal culture * Not reliable
28
tx for clos.perfringins
* Usually good * •Some need long term tx * Tylan * •Fiber supplementation often helpful (chronic)
29
cs of campylobacter
Subclinical carrier •Large bowel diarrhea •Watery diarrhea •Often self limiting •Young animals •Crowded conditions
30
dx for campylobacter
* Fecal microscopy * Wet mount: darting motility * Gram stain: “W” or gull-wing shape * •Fecal culture, Fecal PCR
31
dx for camphylobacter
Erythromycin (10 –15 mg/kg PO q 8 hrs) •Tx 1 –3 days beyond resolution of signs
32
px for campylobacter
Erythromycin (10 –15 mg/kg PO q 8 hrs) •Tx 1 –3 days beyond resolution of signs
33
etiology for salmonela poisoning
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
34
clinical features of salmon poisoning
Dogs •Fever •Anorexia, vomiting, diarrhea (small bowel, +/-blood) •Generalized lymphadenopathy •Thrombocytopenia, lymphopenia, eosinophilia •Hypoalbuminemia, elevated ALP
35
dx for salmon poisoning
* Presumptive * History -consumption of fish, exposure to streams/lakes) * •Definitive * N. salmincolaova in feces * N. helminthoecaorganism in cytology (FNA of lymph node)
36
tx for salmon poisoning
* Supportive care * •Tetracycline, oxytetracycline, doxycycline * •Elimination of fluke (praziquantel)
37
px for salmon poisoning
Most respond well •Fatal if left untreated
38
clinical features of protothecosis
* Dogs (cats) * •Skin, colon, eyes, other body systems * **_•Large bowel diarrhea_** * **_​chrnic n can be a wasting dz_** * •Weight loss, ADR * •Collies overrepresented
39
tx for protothecosis
* Identification of organism * •Cytology (rectal cytology) * •Histopathology (colonoscopy)
40
tx for protothecosis
Amphotericin B, Azoles •Equivocal efficacy
41
px for protothecosis
poor
42
etiology for exocrine maldigestive insufficiency
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
sequela for exocrine pancreatic insufficiency
* Maldigestion * •Proteases (eg, trypsin) * •Lipase * •Amylase * Duodenal acidity * Bacterial overgrowth * Cobalamin deficiency * Intestinal mucosal damage
44
cs of epi
**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
confirmatory for EPI
TLI (trypsin-like immunoassay) –CONFIRMATORY
46
dx for epi
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
tx for epi
* Enzyme replacement (Pancrezyme, Viokase * Low fat diets (high quality) * •Cobalamin therapy (PRN) * •Abx for ARD (PRN) * •H2-receptor blockers (PRN)
48
px for epi
* Good * •Most dogs show clinical response in 1 week * •LIFELONG therapy required
49
indicator for bad px in epi dog
Marked hypocobalaminemia (\< 100 ng/L)
50
common cause of epi in cats
triditis
51
characterization of inflamatory bowl dz
* Cellular infiltrative pattern * Lymphocytic –plasmacytic--most common * Eosinophilic * Granulomatous-- fungus should be in your list
52
location for IBD
``` Small intestine (enteritis) Large intestine (colitis) ```
53
HOW IBD IS DEFINED 1. TIME OF PRESENTATION OF CS 2. LESIONS
* **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
WHAT CAUSES IBD
* 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
CS OF IBD
* 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
CS OF LPE IBD
* Vomiting * Most common in cats * •Small bowel diarrhea * •Weight loss * •Lethargy * •Appetite * Increased * Normal * Decreased
57
cs of LPC ibd
* Mucoid diarrhea * •Hematochezia * •Frequent defecation * •Urgency * •Dyschezia * •Vomiting * •Weight loss (rare)
58
WHICH LI DZ CAUSES WT LOSS
1. COCCIDIOSIS AND 2. HISTO 3. THEY SHOW WT LOSS WHEN THEY HAVE COLONIC DZ
59
PE EXAM FINDINGS FOR IBD
* **NOTHING ESPECIFIC** * No abnormalities in most cases •Thickened intestinal loops-IF U ARE REALLY EXPERIENCED •(Enlarged mesenteric LN) •Cachexia •Alopecia (rare) •Effusion (rare)
60
IBD COMPLICATIONS
* 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
dx for IBD
* 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
lab findings for IBD DX
* **_NO ABNORMALITIES IN MOST CASES!_** * Nonregenerative anemia (mild) * Lymphopenia (stress) * Hypokalemia (mild) * Low albumin (PLE) * Elevated ALT & ALP * •Cholangitis * •Cholangiohepatitis
63
DISCUSS USE OF US IN DX OF IBD
* 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
ENDOSCPIC FINDINGS FOR IBD
* Erythema * Friability * Granularity * Thickening, folding * Indistensibility * Hemorrhages, erosions
65
BX FINDINGS FOR IBD
Immune cells in the mucosa ARE normal
66
IBD VS SMALL CELL LYMPHOMA
* Well-differentiated low-grade lymphocytic lymphoma vs. IBD * •Immunohistochemistry * •Flow cytometry * •Lymphocyte clonal assay (CSU)
67
DISCUSS THEURAPEUTICS TRIALS IN IBD
* 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
IBD DIET
* 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
VIT B12 AND FOLATE TX FOR IBD
* **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
causes of decreased cobalamin
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
what causes decreased folate
Dietary deficiency •Malabsorption (proximal small intestine)
72
complications of cobalaminabsoption
EPI, ARD (SIBO), IBD, other intestinal dz
73
abx responsive diarrhoea
Previously known as SIBO Presumptive diagnosis Serum cobalamin & folate Metronidazole Tylosin (Tylan)
74
cause of PLE
* **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
sign. for PLE
* Dogs \> cats * Genetic susceptibility * •Lundehound (Lymphangiectasia) * •Soft-coated Wheaten Terrier (PLE/PLN) * •Yorkshire Terrier (Lymphangiectasia
76
causes of PLE
* Lymphangiectasia * IBD * Lymphoma * Histoplasmosis * Any other infiltrative disease * Young dogs * •Hookworms * •Chronic intussusception
77
etiology of lymphactasia
* 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
lymphactasia results in
* Dilation and rupture of intestinal lacteals * Leakage of lymphatic contents
79
cs of lymphactasia
* 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
lab findings of lymphactasia
* Total Protein decreased * Albumin decreased * Globulin decreased * Cholesterol decreased * Total Calcium decreased * Ionized Ca++ decreased * Magnesium decreased * Lymphocytes decreased * AT –III decreased
81
Us findings of lymphactasia
* Hyperechoic mucosal striations * •Diffuse in 70% * •Multifocal in 30% * Diffuse mucosal thickening * •Usually without loss of layering * Associated peritoneal effusion
82
tx for lymphactasia
* Ultra -low fat diet * •Commercial –Royal Canin LF * •Homemade –Turkey / potato * Corticosteroids * tx inflamatory component and lipogranulomas * Other IBD Rx
83
px for lymphactasia
* Variable * Some need long term pred * Some can be managed with diet alone * Peracute deaths due to PTE reported
84
etiology for stress colitis
* idiopathic(stress) * no inflamation present
85
clinical features of stress colitis
* Dogs * •Acute onset large bowel diarrhea
86
dx for stress colitis
Diagnosis of exclusion
87
tx for stress colitis
* Fiber (Hills W/D, metamucil, etc.) •5-ASA, abx
88
neoplasia of the SI
Lymphoma Adenocarcinoma Leiomyoma (hypoglycemia) Leiomyosarcoma (hypoglycemia)
89
which dz can be difficult to distinguish from lymphoma
ibd
90
sign. for Chronic Histiocytic Ulcerative Colitis
Young Boxer dogs (M) aka boxer's colitis
91
cs of Chronic Histiocytic Ulcerative Colitis
* Large bowel diarrhea * •Severe with bleeding * •Progressive wt. loss
92
dx for Chronic Histiocytic Ulcerative Colitis
* **_bx_** * Histiocytic inflam and ulcers * •PAS+ macrophages * •Adherent-invasive E. coli * •FISH
93
tx for chronic histiocytic ulcerative colitis
Rx: Enrofloxacin (3 wks)
94
neoplasias of the LI
* Adenocarcinoma * Rectal polyps * •In older dogs * •Hematochezia * •Dyschezia (straining) * •Lobulated bleeding mass
95
list the perineal/perianal dz
* Perineal hernia * Perianal fistulas * Anal saculitis * Anal sac (apocrine gland) adenocarcinoma
96
etiology for megacolon
* primarily a cat dz * **_Idiopathic (70%)_** * Likely myopathic * •**_Obstructive (25%)_** * Pelvic canal stenosis (malunion) * Rectal stricture * Anorectal neoplasia * Neurogenic (5 %) -lumbosacral dz
97
clinical featres of idiopathic colitis
* Feline disease (dogs rarely affected) * •Colonic hypomotility * •Idiopathic smooth muscle dysfunction * •Colonic dilatation * •Recurrent constipation * •Impaction * •Irreversible dilatation
98
dx for idiopathic megacolon
* Abdominal palpation * Massively dilated colon * •Radiographs * •Elimination of other causes
99
tx for idiopathic megacolon
* **Medical first** * Deobstipation * Fiber (Metamucil, pumpkin) * Stool softeners (lactulose) * Prokinetics (Cisapride) * **•Surgery** * Subtotal colectomy
100
drug tx for idiopathic megacolon
* **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
discuss procedure for deostipation in idiopathic megacolon
* Rehydration first!!!!! * •General anesthesia * •Endotracheal intubation * •Lubrication & saline * •Manual extraction (be careful) * Finger * Abdominal palpation * Sponge forceps
102
px for idiopathic megacolon
* 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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