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Smal animal GI > Small animal GI Learning objectives (1: conc GI dz; 2: Clin apprch to GI dz; 3: Pre, Pro, Symbiotics) > Flashcards

Small animal GI Learning objectives (1: conc GI dz; 2: Clin apprch to GI dz; 3: Pre, Pro, Symbiotics) Flashcards

1
Q

three basic gastric functions

A
  1. Gastric filling (adjustable food reservoir)
  2. Mix food with gastric secretions to start digestion
  3. gradually empty partially digested food into intestine
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2
Q

Accomodation

A

stomach adjusts size to inc volume w/o inc gastric pressure

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3
Q

accomodation is mediated by

A

vagal inhibitory fibers

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4
Q

Receptive relaxation

A
  • when a bolus of food enters stomach
    • vagal inhibitory fibers dec the lower esophageal sphincter pressure and fundic contractions
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5
Q

Disruption of gastric filling

A
  • by failure to relax
    • inflammatory dz
    • neoplastic dz
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6
Q

Receptacle for food

A

Fundus

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7
Q

Distal pump

A

Anterum

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8
Q

Disruption of gastric emptying

A

vomiting

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9
Q

In dogs, when does the stomach empty

A

12-24 hours after eating

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10
Q

Final determinant of gastric emptying

A

caloric content of the meal

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11
Q

Structural components of gastric mucosal barrier

A
  1. surface mucus
  2. bicarb secreted
  3. epithelial cell membranes
  4. gastric mucosal blood flow
  5. prostaglandins and cytoprotection
  6. basal membrane
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12
Q

Secretion of gastric juice is not

A

continuous

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13
Q

Acid is secreted by

A

parietal cells

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14
Q

the making of bicarb

A
  • each molecule of H+ secreted makes a molecule of CO2.
  • CO2 combines with water to make bicarb
  • bicarb goes into interstitial fluid
  • mucosal capillaries in interstitium absorbs bicarb
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15
Q

Damage to gastric mucosal barrier

A
  • allows H+ to leak back into the mucosa
    • saturates buffers and cell pH decreases: cell injury/death
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16
Q

Result of damage to gastric mucosal barrier

A
  • local ischemia
  • hypoxia
  • vascular stasis
  • leakage of plasma proteins and blood into lumen
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17
Q

Vomiting reflex is mediated through

A

emetic center in medulla

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18
Q

Activation of the emetic center

A
  1. from higher centers
  2. from cerebellum
  3. from viscera
  4. from extra visceral sources
  5. drugs or toxins
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19
Q

Causes for activation from higher emetic centers

A
  1. CNS tumor
  2. limbic epilepsy
  3. inc crania pressure….
  4. others
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20
Q

Causes for activation of nausea from cerebellum

A
  1. motion sickness
  2. vestibular dz
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21
Q

causes for activation of nausea from viscera

A
  1. GI distention
  2. Torsions
  3. severe pain in viscera
  4. inflammation
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22
Q

Causes for activation of nausea from extra-visceral sources

A
  1. tonsillitis
  2. heartworms
  3. tactile stimulation of pharynx
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23
Q

Causes for activation of nausea from drugs or toxins

A
  1. Apomorphine
  2. Uremic toxins
  3. Hepatotoxins
  4. Endotoxins
  5. Cardiac glycosides
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24
Q

Emetic center can be directly stimulated by

A
  1. cerebral cortex
  2. chemoreceptor trigger zone
  3. oculovestibular system (cats only)
  4. GI tract
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25
Q

Chemoreceptor trigger zone

A
  • located outside blood brain barrier so it can ‘sample’ chemicals in blood w/o it getting to brain
  • this area is usually responsible for repeat vomiting
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26
Q

CRTZ is directly stimulated by

A
  1. emetic toxins
  2. the oculo vestibular system of dogs only
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27
Q

Diarrhea def

A

inc fecal water content which results in change of frequency, fluidity, and volume of bowel movements

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28
Q

Percent of fluid in intestines that come from diet

A
  • 20%
  • remainder comes from endogenous GI secretions
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29
Q

More fluid exchanged each day in GI than

A

there is in extracellular volume

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30
Q

Diarrhea can be from

A
  • inc secretion
  • dec absorption
31
Q

Most water is absorbed in

A
  • upper small intestines
    • 50%
32
Q

Colon and water absorption

A
  • absorbs about 90% of water presented to to
    • more efficient
33
Q

cereal based diets

A
  • have more fiber
    • fiber absorbs water
    • volume of fecal water output is doubled with cereal diets
34
Q

Diseases of proximal small intestine associated with

A
  • much greater fluid loss than in distal tract
35
Q

Efficiency of absorption related to

A
  • tightness of intercellular junctions
    • tighter in distal SI and colon
    • inflammation disrupts junction = diarrhea
36
Q

Acute diarrhea often self limiting because

A
  • rapid cell turnover rate of villus means injured cells are replaced quickly
    • if cause is eliminated and crypts aren’t severely damaged, function restored in 2-3 days
37
Q

Villus main components

A
  1. crypt => secretory cells, undifferentiated cells that migrate to tip
  2. maturation zone
  3. Tip => absorptive cells, slough off after 3-5 days
38
Q

four pathophysiologic mechanisms of diarrhea

A
  1. Osmotic
  2. Secretory
  3. Exudative
  4. Disordered motility
39
Q

Osmotic diarrhea

A
  • Exocrine pancreatic insufficiency best example
  • Often seen in dysbiosis: small intestinal bacteria overgrowth
  • an excess of poorly absorbably osmotically active solutes
  • occurs when nutrients are maldigested or malabsorbed
  • seen in
    • pancreatic/enteric dz
    • laxatives
    • others
40
Q

Secretory diarrhea

A
  • Excessive fluid secretion stimulated, often in SI
  • E. Coli common cause using heat labile toxin (LT)
  • Can be from fat malabsorption (hydroxyl fatty acids)
    • steatorrhea
41
Q

Exudative diarrhea

A
  • Inc mucosal permeability causes leakage of
    • fluid
    • electrolytes
    • proteins
  • ulcers leaking blood and mucus
42
Q

Exudative diarrhea examples

A
  • inflammatory bowel dz
  • parasite infections
  • bacterial infections
43
Q

Diseases associated with exudative diarrhea cause

A
  • Protein Losing Enteropathy
44
Q

Other causes of Exudative diarrhea

A
  • Lymphangiectasia
  • dec oncotic pressure (hypoalbuminemia)
  • inc hydrostatic pressure
    • righ sided congestive heart failure
    • portal hypertension
45
Q

Disordered motility

A
  • inflammation suppresses the phasic contractions (migrating motor complexes) and stimulates giant migrating motor complexes
  • makes fluid move faster than can be absorbed
46
Q

Most diarrhea is classified as

A

mixed

47
Q

14 signs of GI dz

A
  1. vomiting
  2. regurgitation
  3. diarrhea
  4. abdominal pain - seen more in acute dz
  5. tenesmus-straining while defecating - associated w/ lwr GI, Urinary or repro dz
  6. dyschezia-painful defecation - associated with anal or perianal lesions
  7. hematochezia
  8. constipation
  9. flatus - seen more in brachycephalics (swallow air)
  10. ptyalism-salivation
  11. shock
  12. weight loss
  13. anemia - can be from GI hemorrhage or defect RBC production
  14. change in appetite
48
Q

Vomiting can be associated with

A
  • GI dz
  • Abdominal dz
  • Systemic / endocrine/ metabolic dz
  • Neurological dz
49
Q

Vomiting of food more than 10-12 hours after a meal

A

delayed gastric emptying

50
Q

Causes of regurge

A
  1. Esophageal inflammatory dz
  2. Extraluminal Esophageal compression
  3. Intraluminal esophageal obstruction
  4. Neuromuscular dysfunction
51
Q

Regurge def

A

passive, few pre-episode signs, ptyalism, semiformed material

52
Q

Vomiting

A

active, abdominal contractions, retching/heaving, ptyalism, swallowing, can be very variable

53
Q

Small intestine diarrea signs

A
  • bulky or fatty stools
  • Melena
  • Few diarrhea bowel movements a day
54
Q

Acute SI diarrhea

A
  • < 48 jour duration
  • seldome has mucus
  • brown/red color
  • sense of urgency and inc frequency
  • symptomatic therapy effective
55
Q

Chronic SI diarrhea

A
  • 7-10 days or longer
  • large volume
  • no mucus or fresh blood
  • steatorrhea
  • little urgency
  • tenesmus
  • frequency 2-3x / day
  • weight loss

*must get a specific dx and therapy

56
Q

Large intestine diarrhea signs

A
  • sudden urgency
  • tenesmus and dyschezia
  • excessive mucus
  • fresh blood
  • small-volume
  • high freq ( >5x/day)
57
Q

Chronic Large intestinal diarrhea

A
  • 7-10 days
  • small volume
  • lots of mucus (maybe some blood)
  • urgency, tenesmus, sometimes dyschezia

*can either do symptomatic therapy or get specific dx

58
Q

Acute Large Intestinal diarrhea

A
  • Uncommon
  • < 48 hours
  • lots of mucus and probably blood
  • urgency
  • sudden inc in frequency

*give symptomatic therapy, may turn into chronic

59
Q

5 mechanisms of weight loss

A
  1. decreased nutrient intake
  2. maldigestion/malabsorption
  3. malassimilation (failure to use nutrients)
    • liver/kidney failure
  4. excessive utilization
  5. inc loss of nutrients

*intestinal parasites common cause (what mechanism?)

60
Q

Proper approach to dx

A
  1. take a hx
  2. physical finding from thorough exam
  3. create ddx
  4. diagnostic studies
61
Q

3 groups of confirmatory dx procedues

A
  1. clinical lab studies
  2. radiographic and other imaging
  3. specific diagnostic procedures
62
Q

Clinical laboratory studies

A
  1. Essential studies (serum proteins and liver enzymes most imp)
    • CBC
    • chem panel
    • fecal
    • UA
  2. Confirmatory studies
    • amylase and lipase test
    • PLI (Pancreatic lipase is better than A&L)
    • TLI (for exocrine panc. insuff.)
    • Serum folate/cobalamin test
    • Fecal alpha-1 proteinase inhibitor (for PLE)
63
Q

Radiographic and other imaging

A
  1. survey rads (abdomen/thorax)
  2. contrast radiography (upper GI barium and barium enema)
  3. ultrasound for tissue sampling, not dx
64
Q

Microbiota (microflora) def

A
  • all living microorganisms that inhabit GI tract
    • archaea
    • bacteria
    • protozoa
    • viruses
65
Q

Microbiome def

A
  • mutual interaction of the organisms in GI with host cells
66
Q

Microbial characterization: bacterial culture

A
  1. useful when looking for something specific
  2. allows assessment of viability, sensitivity to testing, genotype analysis, identifying metabolic properties
  3. limited for defining unknown or anerobic organisms
  4. Few choices for culture techniques (no developed culture for vast majority of microorganisms
67
Q

microbial characterization: Analyzing RNA or DNA

A
  1. done via intestinal contents, tissue bx, feces
  2. PCR using 16S rRNA (what); amlicons ‘fingerprint’ (who)
  3. Quantitative rtPCR and FISH: how much is there, where in epithelium
68
Q

Microbial characterization: FISH, fluorescent in-situ hybridization

A
  • allows us to visualize location of bacteria in epithelium
69
Q

Cats unique bacterial characteristics

A
  • Higher number bact in Duodenum
  • greater number anaerobic bacteria
70
Q

Control mechanisms of bacteria in GI

A
  1. gastric acid
  2. bile
  3. intestinal motility
  4. intestinal mucus
  5. immune response
  6. bacteria
71
Q

Prebiotics

A
  • nondigestible dietary carbs
    • stimulate the growth and metabolism of protective enteric bacteria
  • encourages lactobacillus and bifidobacterium
  • inc fecal short-chain fatty acid conc
  • examples
    • lactosucrose
    • FOS (fructooligosaccharides)
    • psyllium
    • bran
72
Q

Probiotics

A
  • living microorganisms that impart a health benefit
  • must survive small intestine and colon to have effect
  • possibly improve epithelial barrier function
  • modulate immune system
  • alter microbiota to prevent pathogenic bacteria
  • not good in immune copmromised patients
  • must make sure manufacturer is reputable
73
Q

Synbiotics def

A

combo of both prebiotics and probiotics

Smal animal GI (5 decks)

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