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SI Flashcards

1
Q

What are the functions of the SIT?

A

Digestion of ingesta/food  Secretion of water and mucous

 Digestive enzyme: peptidases, nucleases, disaccharidases  Bile acids
 Pancreatic enzymes

*** Absorption of nutrients ***
Barrier to infection
Complex immunologic organprotects body against threats

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2
Q

VILLI

A

 Mucosal immune system  Lamina propria  Enterocytes

 Turnover in 3 days from base of crypts

 Microvilli membrane / brush border – nutrients absorbed  Digestive enzymes and carrier proteins, goblet cells  Crypt cells

 Secretory capacity

 Make undifferentiated epithelial cells – most of these are enterocytes which migrate from crypt up to tip of villi

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3
Q

ENTEROCYTES

A

Enterocytes main energy requirement is glutamine If absent

Decline in villi structure
Loss of epithelial integrity Decreased immune function Decreased absorptive function

In GI disease – NUTRITIONAL SUPPORT IS VITAL !!!!!!!!!

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4
Q

What kind of stools are common with SI bowl disease?

A

steorrhea

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5
Q

ACUTE ENTEROPATHY

A

Dietary Indiscretion Diet change Infection Medications

Stress (boarding, car ride, apt at your office) Secondary to pancreatitis

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6
Q

CHRONIC ENTEROPATHY

A

Food allergy or hypersensitivity Inflammatory Bowel Disease Lymphangiectasia
Infections including SIBO, parasites Neoplasia

Secondary to EPI

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7
Q

HGE VS. AHDS

A

Hemorrhagic gastroenteritis IS NOW …  Acute hemorrhagic diarrhea syndrome

Small breed dogs over-presented
Marked hemoconcentration
Marked fluids shifts
Typically requires hospitalization
Hypovolemic shock before clinical evidence of dehydration

Clinical signs including: Hematemesis and hematochezia Etiology

 Viral or
 Hypersensitivity reaction or  Clostridium perfringens **

PCV > 60% and TS not as high as expected (GI loss)

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8
Q

What’s the treatment/prognosis for AHDS?

A

Treatment  IVFs

 Antibiotics (Unasyn or Metro)  Gastroprotectants  Antiemetics
 Nutrition

Prognosis is good with aggressive supportive care  Unless severe hypoproteinemia

 OR signs of sepsis

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9
Q

What do you treat tapeworms with?

A

Praziquantel
5 mg/kg PO once

Fenbendazole 50 mg/kg PO SID 3 days

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10
Q

Toxacara

A

Ingestion of eggs or maternal transmission

Adults mature in small intestine

Young pup & kittens most affected

Can be fatal

High worm burdens Pulmonary involvement

Small intestinal obstructions possible/rare

Clinical Signs
• Vomiting of live worms • Unthrifty
• Diarrhea

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11
Q

What is common with protozoa? and who does it affect?

A

Single Celled Organisms

Found worldwide in most habitats

Infections range from asymptomatic to life threatening

Species, strain, the resistance of the host

Young and immunocompromised

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12
Q

GIARDIA DUODENALIS

How do you check it?

A

Dogs and Cats Species specific strains

 Transmission between humans & pets = RARE Re-infection can occur

DIRECT SMEAR PROTOCOL

Checking for TROPHOZOITES in diarrheic stools 1. Small, FRESH, unrefrigerated feces

  1. Mix sample into two to three drops of saline (not water) on a glass slide
  2. Add coverslip
  3. A Lugol’s iodine stain may be added to aid in identification

Subclinical infections common GOAL

 Stop diarrhea
 Elimination of infection = DIFFICULT

Apparently well animals do not need treatment more than 1x RX:

 Fenbendazole x 5 days +/- Metronidazole x 5 days  Bathing on last day

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13
Q

COCCIDIA

A

Cystoisospora a.k.a. Isospora species Species specific
Fecal oral OR predation transmission Sporozoites infect enterocytes

CLINICAL SIGNS
Weight loss, dehydration, +/- hemorrhage Adults – can be self-limiting

Young, immunocompromised can be quite sick  Anorexia, vomiting, dehydration

Diagnosis  Direct smear

 Fecal float Treatment

 Sulfadimethoxine (ALBON)
 50-60 mg/kg daily for 5-20 days (D,C)

 Others (i.e. Ponazuril)  Supportive care

Prognosis
 Good in adults and mild symptoms  Guarded in systemically ill patients

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14
Q

CRYPTOSPORIDIUM

A

Cryptosporidium parvum  ‘Coccidia-like”

Species specific BUT zoonosis possible

Transmission
 Fecal oral
 Contaminated food, water

CLINICAL SIGNS

Self limiting small bowel diarrhea

Severe life-threatening in immunocompromised  Can extend into large intestine and other organs

DIAGNOSIS
 Direct smear & Fecal float

 Difficult to find  ELISA
 PCR
 +/- Biopsy

TREATMENT
 Paromomycin

 150 mg/kg SID for 5 days (D,C)  Tylosin

 10 to 15 mg/kg TID for 14 to 21 days (C)

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15
Q

TOXOPLASMA GONDII

A

ZOONOTIC
Oocysts require 1-5 days to become infectious after passed

 Clean litter boxes daily
Disease seen in immunocompromised, immunosuppressed, fetus, elderly CATS > DOGS
Transmission

Predation – bradyzoites/muscle Fecal contamination

Significant clinical disease often from extra-intestinal effects

Unlikely to shed oocysts at the time significantly ill

DIAGNOSIS  Fecal Float

Capc.org

 Limited use
 Oocyst shedding occurs briefly after infection AND not always

associated with clinical disease 

Antibody Titers

_ IgG & IgM * useful when associated with sick pet
 Positive titers does not = oocyst shedding or clinical disease_

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16
Q

What’s the treatment for Toxo?

A

Clindamycin
 10 to 12 mg/kg orally twice daily for 4 weeks

Trimethoprim-sulphonamide
 15 mg/kg orally every 12 hours for 4 weeks.

Other meds (see CAPC) Supportive care

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17
Q

PYTHIUM INSIPIOSUM

A

Aquatic oomycete
 Fungus-like & resembles algae

 Feeds on rotting material or living plants by absorbing nutrients through fine threads

 Occasional mammal host
Tropical, subtropical, temperate climates

Mostly Gulf Coast States
 Also documented NJ,VA,NC,CA, IN,IL, KY,OK,MI,KS

Exposure to free standing waterpenetration of skin or mucosa by motile zoospores

DOGS; rare = cat, sheep, exotics, cow, human Zoonosis not been documented

Gastrointestinal distress  Vomiting

 Weight loss  Diarrhea  Hematochezia  Abdominal pain

Dermatologic disease  Non healing skin lesions

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18
Q

What are the PE findings of Pythium?

A

GI
 Palpable abdominal mass

 Dehydration
 Poor body condition

Cutaneous
 DOG: Lesions base of the tail, extremities,

ventral neck, perineum
 CAT: Cervica, inguinal, truncal  Ulcerative nodules
 Draining tracts
 +/- LN involved

Skin and GI do not occur together!

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19
Q

What is the main diagnostic for pythium?

A

CBC: eosinophilia, anemia

CHEM: hypoalbuminemia, hyperglobulinemia

UA: NSF

* Pythium ELISA – antibody detection; also used for response to therapy – titers fall with therapy

Culture – difficult

FNA of lesions – nonspecific for organism

* Biopsy of lesions
 SEVERE transmural segmental thickening (esophagus  colon +/- dissemination into other abdominal organs)  Pyogranulomatous and eosinophilic inflammation on biopsy
 GMS stain on histopath to ID organisms

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20
Q

What will you see on US for pythium? Treatment/ prognosis?

A

ULTRASOUND
 Segmental thickening of GI
 Thickened gastric outflow tract possible  Enlarged LNs

TREATMENT:

SURGERY
 Removal (3-4 cm margins) of limb or GI segment

MEDICATIONS
At least 2 -3 months

 Itraconazole: 10 mg/kg P) SID  Terbinafine: 5-10 mg/kg PO SID

+/- Immunotherapy (pred 1 mg/kg/day) in non-resectable cases Medications aloneless than 20% chance of survival

Prognosis:

Monitor ELISA
IF COMPLETE RESECTION and NO RECURRENCE

 ELISA usually drops by 50% or more within 3 months  Can d/c oral meds

Poor with disseminated disease, non-resection
Less than 20-25% respond to medial management alone

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21
Q

HISTOPLASMOSIS

A

Dimorphic fungus

Occurs worldwide

USA: Mississippi and Ohio River valleys

DOG & CAT- cats have more respiratory signs

TRANSMISSION
 Aerosols into lungs & thoracic LN

 Gastrointestinal tract (D > C)

3milliondogs.com

 Organisms enters bloodstream from primary site and can cause wide spread disease

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22
Q

What are the most common CS/PE findings for Histo?

A

Diarrhea (LARGE > SMALL)

Weight loss to emaciation

Chronic cough
Fever

Anemia

Hepatomegaly, splenomegaly, lymphadenopathy

Nasopharyngeal and GI ulceration

Lameness

Respiratory difficulty 

Nodules & thoracic LNs

Skin lesions Cats

Same as dog EXCEPT GI signs

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23
Q

DX, treatmetn, and prognosis for histo

A

DIAGNOSIS

Non-specific CBC, CHEM, UA

Chest Rads: nodules, enlarged LNs

U/S:
 Spleen, liver, LN enlargement

 Thickened LI and/or SI wall
Fine needle aspirates of abnormal tissue+fluid- peritoneal effusion

Biopsy of abnormal tissues

Culture

ELISA antigen test  Urine, serum, and CSF

vetfolio.com

 Cross-reactivity occurs with blastomycosis

TREATMENT & PROGNOSIS

MEDICATION *** PROLONGED THERAPY  Itraconazole

 10 mg/kg/day
 ALT: Fluconazole or Ketoconazole (mild cases)  SEVERE

 Amphotericin B

PROGNOSIS
 Acute histoplasmosis may be fatal after 2–5 weeks
 Poor condition & multisystem involvement = guarded to poor  One organ involved = better

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24
Q

CANDIDIASIS

A

Normal inhabitant of nasopharynx, GI tract, genitalia

_OPPORTUNISTIC INFECTIONS CAN BE SEEN
 Associated with disruption of MUCOSAL INTEGRITY ! _Immunosuppresive medications
 Antibiotic administration
 IV or urinary catheters

CATS
 Oral and upper respiratory disease, pyothorax, ocular lesions, intestinal disease, and cystitis

DOGS
 Peritonitis & Fungemia documented
 Perforating intestinal lesions after surgery
 Mucosal and cutaneous candidiasis has been noted in immunosuppressed dogs

25
Q

SALMONELLA

A

Gram -, facultative anaerobic  Low prevalence in normal pets

 Normal flora in up to 30% dogs & 18% cats

 Culture positive and clinical signs

 = likely association

Young, parasitized, immunocompromised, or stressed kenneled dogs Raw and/or contaminated food
ZOONOTIC

Destroyes Intestinal Villi

Ileum Cecum Colon

CLINICAL SIGNS
Acute, transient illness (diarrhea)

 Supportive care
Septic, shock, hospitalized from illness

DIAGNOSIS

  • Culture
  • Blood in septicemia • Feces

• PCR lacks validation

26
Q

How do you treat SALMONELLA?

A

TREATMENT
 None for primary infection & when transient

 No evidence it is effective and no need if pet’s signs resolve
 Need to treat for bacterial translocation in very ill animals

 TYPICALLY WHEN WE SEE THEM & TEST THEM
 IV antibiotics like fluroquinolones, amoxicillin, TMS, chloramphenicol

PROGNOSIS
 Good unless septic (fair-guarded)

27
Q

ESCHERICHIA COLI

A

Mammalian flora naturally contains E. coli  Gram-negative, anaerobic, rod-shaped bacterium

Most non-pathogenic RARE to cause disease

 Dogs & Cats  Acute disease

 Puppy – unclean, crowded breeding environments  Immunocompromised – with Parvovirus
 Food & water contamination including raw food

CLINICAL SIGNS

  • Diarrhea
  • Vomiting
  • Dehydration
  • Lethargy
  • DIAGNOSIS
  • Culture
  • Blood in septicemia

• Feces

E. COLI

TREATMENT IN HOSPITAL
 IV supportive care
 Antibiotics like fluroquinolones, unasyn, others

PROGNOSIS
 Good unless septic (fair-guarded)

28
Q

SALMON POISONING DISEASE

A

DOG

SALMON

FLUKE
 Nanophyetus salmincola

BACTERIA
 Neorickettsia helminthoeca & elokominica

Pacific Northwest
ACUTE DISEASE (as little as 7 days after fish meal)

Parasitology.cvm.ncsu.edu

High fever

 Hematemesis

 Diarrhea  Nonhemorrhagic enteritis  +/- Hematochezia

 Vomiting
 Lethargy
 Anorexia
 Nasal and ocular discharge  Enlarged lymph nodes

DIAGNOSIS
 Fluke eggs in feces

 History of of ingested fish
 Inclusion bodies in macrophages in lymph node  PCR
 Serology
 Chem, UA: non-specific
 CBC: Thrombocytopenia (94%)

29
Q

Where can you find neorickesttsa for Salmon poisoning disease?

A

within lymphocytes

30
Q

What’s the treatment and prognosis for SPD?

A

TREATMENT
 Hospitalized support

 Antibiotics  Oxytetracycline

 (7 mg/kg IV TID) 7 day  Doxycycline

 (10 mg/kg BID) 7 day  Praziquantel for fluke

PROGNOSIS

 Fair to good with

aggressive supportive care

 Death in up to 90% of untreated animals with SPD

 Elokomin fluke fever (EFF)

 Milder form

 10% death in untreated animals

31
Q

A client brings you a sick cat with neuro and ocular signs. On labwork, you determine the cat to be positive for Toxo. The owner is concerned about parasite shedding and contracting toxo. What do you advise?

A

Treat the patient. Scoop the litter box daily. Risk of oocyst( the contagious bit) shedding is unlikely

32
Q

What is the prognosis of canine parvo?

A

If survive the first 3-4 days then likely to make a full recovery.

33
Q

What can you use diagnosis feline panleukopenia?

A

canine parvo snap test

34
Q

INTESTINAL NEOPLASIA

FELINE

A

Lymphoma

Adenocarcinoma

Mast cell

35
Q

Canine intestinal neoplasia

A

Lymphoma

Adenocarcinoma

Smooth muscle tumors – leiomyoma, leiomyosarcoma, GIST (gastrointestinal stromal tumor)

36
Q

SMALL CELL LYMPHOMA

A

INFILTRATIVE  Diffuse disease

 +/- Thickening of SI on AUS  Biopsy diagnosis

Treatment:  Chlorambucil

 Prednisone

Prognosis:
 Survival up to 3 years reported

37
Q

INTUSSUSCEPTION

Most common cause of Extraluminal obstruction

where does it commonly happen

A

1 site = Ileocolic Junction

38
Q

What is the most common intestinal hernia CS?

A

INTESTINAL HERNIA

Small intestinal loops slip outside abdominal cavity into SQ tissues  Can lead to strangulation and necrosis of intestines

 Intermittent GI signs

39
Q

Exocrine Pancreatic Insufficiency

A

Insufficient secretion & production of pancreatic enzymes

MALDIGESTION

Acinar Atrophy – genetic or immune mediated

 Chronic Pancreatitis
 Aplasia or Hypoplasia – congenital
 Usually multiple enzymes

 One report of Canine Lipase Deficiency alone causing signs

Breed: German Shepard, Rough Coat Collie, Eurasians

40
Q

What the main CS for EPI?

A

#1 = Weight loss
 Can occur as only sign in the cat

 Loose stools steatorrhea
 Excess presence of fat in the feces  Pale, oily appearance, foul smelling

 Ravenous appetite  Poor hair coat  Borborygmi  Flatulence

 Can be subclinical

41
Q

How do you diagnose EPI?

A

CBC, CHEM, UA
 Rule out other causes

TLI level

 Species specific

 Measures trypsin, trypsin bound to proteinase inhibitors, & trypsinogen

B12
 OFTEN LOW IN EPI and needs supplementation

42
Q

TREATMENT
EXOGENOUS PANCREATIC ENZYME

A

Dried Pancreatic Extract powder (pork, beef)  DOG: 1 tsp/10 kg Pancrelipase

 CAT: 1 tsp/meal Pancrelipase
 MANY FORMULAS AVAILABLE
 MIX IN FOOD 20 mins before feeding

 SE: Gingival bleeding & irritation

FRESH PANCREAS
 30 - 90 g = 1 tsp of the dried extract  Can freezemaintains activity

B12 SUPPLEMENTATION

Pancreatic Tablets & Capsules  Typically less effective

43
Q

HYDROLYZED DIETS

A

Split proteins to such a small size that immune system cannot recognize them as foreign

 IDEAL = 1 KD = too bitter  MOST are 7-10 KD

 Some can still mount antigenic response  Cannot cross link IgE for TYPE 1
 TYPE 4 still possible

44
Q

IDIOPATHIC ANTIBIOTIC RESPONSIVE DIARRHEA

A

Small Intestinal Bacterial OvergrowthARD

No reliable test

MECHANISMS  Host-bacterial interactions

 Bacterial overgrowth – difficult to quantify

SECONDARY
 Defects in mucosa
 Aberrant mucosal immune response  Qualitative change in enteric flora (dysbiosis)

ARD TREATMENT

DIAGNOSIS
• Biopsy can be normal or concurrent disease

• Treatment trial 4 - 6 weeks Abs

 Metronidazole  Tylosin  Oxytetracycline

10-15 mg/kg PO BID 20 mg/kg PO BID 10-20 mg/kg TID

Can need to be repeated or long-term treatment in some Diet

 Variable response but positive outcomes seen in some with high quality +/- low fat

45
Q

What are bx diagnosis diseases?

A

Inflammatory Bowel Disease 

Several types

Lymphangectasia

Lymphoma

46
Q

INFLAMMATORY BOWEL DISEASE

A

WHAT IS IT ?

  • Disease of dogs and cats with chronic GI signs for which no other causes is documented
  • Affected animals who fail to respond to parasiticides, antibiotics, and diet
  • On histopath, mucosal changes include inflammatory infiltrate - Extent varies from focal to diffuse disease
  • Inflammatory infiltrates include lymphocytes, plasma cells, eosinophils, neutrophils, macrophages or some combo thereof, in numbers more than consistent with the normal immune defense
  • Can involve stomach AND/OR small intestine AND/OR the large intestine
47
Q

Why do they get IBD?

A

Multifactorial cause likely
1. Disruption of the physiologic interaction of innate and adaptive immune response

  1. Defective mucosal barrier  influx of food antigens and microbes into Lamina Propria where they trigger proinflammatory cytokines from T cells
  2. Can include inappropriate reaction to commensal bacteria, food antigen, idiopathic/ primary abnormality of the innate immune system

Pattern Recognition Receptors = PRR
 HEALTH: maintain hyporesponsiveness to luminal contents, diet, and protects the mucosa  EXAMPLES

 Toll-Like Receptors – TLR
 NOD2- Nucleotide oligomerization domain

48
Q

Most common IBD

A

MOST COMMON  Lymphoplasmacytic infitrate

49
Q

What are the type of IBD?

A

Minimal Change Granulomatous or Neutrophilic Lymphoplasmacytic Eosinophilic
Lymphangectasia

50
Q

MINIMAL CHANGE ENTEROPATHY

Characteristics and treatment

A

CHARACTERISTICS
• Low clinical disease score

  • Albumin > 2.0 (rr: 3.0-4.2 g/dL)
  • Normal B12
  • Normal to minimal inflammation on histopathology

TREATMENT  Deworm

 Fenbendazole

 5 days at 50 mg/kg PO SID  Diet Trial
 Antibiotic trial

Petmed.com

 If good response, trial to probiotics
 Chronic therapy with tylosin 5 mg/kg PO SID may be necessary in some pets

51
Q

What do you want to do first?

A

Deworming, Diet Trial, and Antibiotic Trial

52
Q

GRANULOMATOUS OR NEUTROPHILIC ENTEROPATHY

Characteristics

A

CHACTERISTIC  Infrequent diagnosis

 Macrophages/Histiocytic and/or Neutrophilic Infiltrate  PROMPTS you to look for INFECTIOUS DISEASE

NEXT STEPS
 Image chest and abdomen to look for other evidence of infectious disease  Bacterial, fungal, parasitic testing
 FISH (fluorescence in situ hybridization to look for invasive bacteria)  Culture of mucosal biopsy, LN, other organs
 Special stains on histopathology (GMS, PAS)

53
Q

What’s the treatment/ prognosis for GNE?

A

TREATMENT
 Treat underlying infectious disease

Umich.edu

 Antibiotic trial (E coli, Stept, Campylobacter, Yersina, Mycobacteria)  Immunosuppressive medications IF infectious disease excluded

 Slow taper after see clinical response PROGNOSIS

 Can be guarded to poor if underlying etiologic agent not identified

54
Q

LYMPHOPLASMACYTIC ENTEROPATHY

characterisitics

A

CHARACTERITIC
 Lymphocyte and Plasma Cell infiltrate

 Variable clinical disease presentation  Mild

 PLE
• 67% with normal albumin • 33% with low albumin

 Systemically ill
Diet has shown 60 – 88 % response rates

TREATMENT
• Hydrolyzed or novel antigen diet

  • Responders tend to be younger dogs w/ normal albumin
  • Antibiotics trial
  • Immunosuppressants when no response to above When clinical signs resolve, consider slow taper
  • Anti-clot medications with hypoalbuminemia • Clopidogrel
  • Low Dose Aspirin

WITH CLINICALLY ADVANCED DISEASE

MAY START ALL THERAPY SIMULTANEOUSLY

55
Q

EOSINOPHILIC ENTEROPATHY

A

CHARACTERISTIC
• Eosinophilic predominant infiltrate
• Reaction to parasites or diet or fungal organisms possible

PROGNOSIS
 Good in dogs  Guarded to poor in cats

56
Q

LYMPHANGESTASIA

A

Exudation of protein-rich lymph into intestine

Severe malabsorption of fat and other nutrients leading to PLE & clinical signs

Weight loss Ascites Vomiting

Wikivet.net

ENDOSCOPY

White granules/blebs on mucosal surface

Abnormal distension of lymphatic vessels within mucosa

Surgery = potential dehiscence in advanced disease

57
Q

treatment of lymphagestesia

A

DIET
• Hydrolyzed and LOW FAT

ANTIBIOTICS
 Metronidazole or tylosin to reduce risk of bacterial translocation

IMMUNOSUPPRESANTS
• Prednisolone 1-2 mg/kg PO BIDtaper to LED

  • May need parenteral administration
  • Cyclosporine or other immune modulating medications in advanced disease

ANTI-CLOT MEDICATIONS
 Low dose aspirin or clopidogrel

DIURETICS
 For ascites

PROGNOSIS
 Fair to guarded pending response to treatment and severity of clinical sign at presentation

58
Q

What kind of feeding tube is her favorite?

A

esopahgostomy tube- requires GA

59
Q
A

SAM (13 decks)

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