GIT Flashcards
before supplementary nutrition…
correct electrolyte and acid-base imbalances
stabilise
shock - reduced GIT perfusion
consider periods of at home anorexia
compromised patients - may have insulin resistance, reduced absorptive and digestive enzyme production
reasons patients may refuse to eat in hospital
stress
pain
absence of preferred food
nausea
physical incapacity
supplementary feeding - fat
calorically dense
indicated if critically ill - difficult to get nutritional volume in
contraindicated in pancreatitis
supplementary feeding - high protein
contraindicated in hepatic and renal disease and pancreatitis
energy requirements
RER = 70 x (bodyweight)^0.75
or (in animals 3-25kg)
RER = (30 x BW) + 70
resting energy requirements (RER)
calories needed for normal function in fasted patient under thermo-neutral conditions
calculating energy requirements
weigh
calculate RER
divide RER by diet content (kcal) to give daily amount
divide by total number of feeds
do not exceed 5-10ml/kg when introducing food
enteral feeding
to GIT
use gut if works
parenteral feeding
nutrients via IV
tube types
naso-oesophageal/nasogastric
oesophagostomy
gastrostomy (PEG)
enterostomy or jejunostomy
factors in choosing tube type
patient condition
injury/illness
food needed
availability of resources (including staff)
financial factors
duration of feeding required
naso-oesophageal/nasogastric
most common
through nostril
distal tract must be functional
conscious placement
3-5 days (up to 10) - short term
easy to place
no GA needed
can be used immediately and removed easily
patient can eat and drink around tube
patient may pull out
around head - bite risk
can only put liquid down - not crushed oral medication
Oesophagostomy
surgical placement into oesophagus
distal GIT must be functional
contraindicated if secondary oesophageal disorder
wider than NG so can prepare own diet
weeks/months
easy placement and any time removal
can give crushed medications
GA needed
biting risk
wound management needed for risk of infection
risk of stricture formation
Gastrostomy
into stomach through body wall
bypasses oral cavity and oesophagus
contraindicated if primary gastric disease
has to stay in for 10-14 days to allow seal to form between stomach and abdominal wall prevent leaks into abdominal cavity –> pancreatitis
can be left in for months-years
further from head so less biting
variety of diets
can give crushed medications
can’t use for 24 hours after placement
needs GA
risk of local infection
risk of pancreatitis/peritonitis
Jejunostomy (j-tube)
invasive and challenging to place
mid-long term support
bypasses upper GIT
patient can still eat by oral route if needed
jejunum has no storage capacity - trickle feeding instead of bolus
usually only referral cases
total parenteral nutrition (TPN)
IV
short term - 3-5 days
only if unable to feed enterally, increased aspiration risk or if other methods have failed
aim to meet all protein and energy needs
Partial parenteral nutrition - combined with other methods
intensive nursing needed
postural feeding
megaoesophagus
intake split into 3-4 small meals
soft wet food rolled in small balls and fed from height
sitting position
enamel
outermost layer
97% calcium and phosphorus
no circulatory system - can’t be replaced
dentin
majority of tooth
made by odontoblasts
laid down through life
nerve supply - responds to stress
pulp
living tissue
nerves, blood and connective tissue
where odontoblasts live
provides nutrition, protection and sensation - pain if damaged
gingiva
gums
both attached and free sections
cementum
anchors tooth
alveolar bone
portion of the jaw the teeth sit in
covered in periosteum
periodontal ligament
in periodontal space between tooth and alveolar bone
shock absorber
holds tooth in place
closed mouth exam
lips
oral mucosa
occulsion
open mouth exam
gingiva
cheek mucosa
palate
tongue
floor of mouth
discharge
foreign bodies
masses
swelling
inflammation
fractures
ulcers
NB: not whole tooth is visible - could be root pathology
GA dental exam
intubation
lateral recumbency
pharyngeal pack
chlorhexadine prep
mouth gag - only large dogs, not for long
radiographs to see hidden pathology
occlusion
upper incisors should overlap lower
lower canines should fit into upper diastema
upper and lower premolars should interdigitate
number of teeth
missing or supernumery
retained deciduous teeth
overcrowding - common in brachycephalics
appearance of teeth
defects
shape
discolouration
fractures
oral soft tissue exam
discolouration
inflammation
oedema
Periodontal disease
common
any disease affecting soft tissue or tissues holding teeth in place
may need radiographs to see full extent
signs - gingivitis, plaque build up (can mineralise to calculus), gingival recession, bone loss, mobile teeth, tooth loss
plaque
made by bacteria –> gingivitis as immune response –> tissue destruction –> plaque mineralises to calculus and prevents healing –> attachment loss –> tooth becomes mobile and falls out
mouth directions
mesial - towards midline
distal - away from midline
buccal - towards buccal mucosa
lingual - towards tongue
labial - towards lips
palatal - towards palate
interproximal - between teeth
coronal - towards tip of crown of tooth
apical - towards root of tooth
periodontal probe
blunt ended
measures attachment loss
assess gingival inflammation
test tooth mobility
dental explorer
sharp ended
detect softened enamel
explore defects - fracture sites and tooth resorption
check for pulp exposure
don’t put in gingival sulcus
gingivitis index
0 - none
1 - mild - slight change in colour, no bleeding
2 - moderate - redness, oedema, bleeding
3 - severe - ulceration, prone to spontaneous bleeding
periodontal grading index
score for individual teeth
attachment loss estimated with probe and confirmed with x-ray - probe tends to overestimate depth
0 - healthy - pink, firmly attahced
1 - gingivitis due to calculus deposition, reversible by brushing, no attachment loss
2 - up to 25% detachment, deepened sulcus
3 - 25-50% attachment loss
4 - over 50% attachment loss, may see horizontal bone loss, severe inflammation
furcation index
furcation = area where roots divide on multi rooted tooth - measure of amount of bone loss
0 - no bone loss
1 - less than 1/3 bone loss
2 - more than 1/3 lost but not all
3 - open furcation
mobility index
measure of loss of normal support around tooth - periodontal ligament and bony support
0 - no mobility (<0.2mm)
1 - <1mm horizontal movement
2 - >1mm horizontal movement
3 - any vertical movement
dental radiography techniques
parallel - plate parallel to target with beam aimed straight at it - caudal mandibular teeth only
bisecting angle - creating shadow of teeth and capturing it - used when can’t get in parallel
extra oral - plate not inside mouth - cats and small mouths, skyline view of maxillary arcade
common dental pathology - small animal
vertical bone loss - radiograph, creates pocket
horizontal bone loss - can get probe under tooth
type 1 resorption - common in cats, remove full tooth
type 2 resorption - cats - tooth blends with jaw at root, remove top (not root so can’t remove whole thing)
trauma - chewing something hard
uncomplicated crown fracture - dentin exposed but not pulp
complicated crown fracture - pulp exposure - painful
open vs closed extraction
open - multirooted teeth, elevation of mucoperiosteal flap and bone removal (surgical extraction)
closed - usually single root teeth, incision into gingival attachment and breakdown of periodontal ligament
Colic - definition
abdominal pain - predominately GIT associated but can involve a number of systems
colic causes
smooth muscle spasm
inflammation - colitis/ulceration
distension - impaction/gas accumulation
obstruction - impaction
tension on mesentery - displacement
tissue congestion/infarction/necrosis - torsion/volvulus, strangulation –> endotoxemia
combination of above
colic - endotoxemia
if gut wall is compromised toxins will start to absorb toxins into blood stream
–> death
high HR
poor pulse quality
slow jugular refill
dark dry mucous membranes
slow capillary refill time
colic - signs
inappetence
reduced fecal output
vocalisation
agitation
pawing
lip curling
flank watching
lying down repeatedly
stretching to urinate
rolling/trashing
sweating excessively
straining
signs of pain - colic
mild - restelessness, pawing, flank watching - gas build up, inflammation, smooth muscle spasms
moderate - lying flat, groaning - impaction or simple obstruction
severe - very fractious, violenet rolling - acute colic, severe strangulation
end stage - dull, unresponsive - eg. endotoxemia
colic - treatment priorities
analgesia and triage
assess severity
construct treatment plan
colic differentials
false colic - non-GI source - liver disease, urinary disease, peritonitis, intra-abdominal abscess, intra-abdominal neoplasia, reproductive disorders
non abdominal - oesophageal obstruction, rhabomyalysis, laminitis, pleuropneumonia
colic - risk factors
recent changes - feeding, management, stabling, exercise
dental history
parasites
viruses
colic - CV assessment
increased HR - more driven by CV status than pain
pulse quality
jugular refill
mucous membranes - tacky then 5% dehydrated, dry and red then need fluid therapy (horses are big so takes lots of fluid to rehydrate)
capillary refill time
boborygmi
sound of fluid and gas in intestines
motility - colic
hyper motility - increased smooth muscle activity - spasm colic
local hypomotility - localised stasis of GIT
general absence of sound - GIT ileus - common in most colics
analgesia - colic
xylazine (alpha-2) - first choice - short acting. But has CV effects so take into account
NSAIDs - don’t use right away, GI effects
opioid - butorphanol (torbugesic)
further diagnostics - colic
nasogastric intubation - fluid/ingesta from stomach - >2l is abnormal - relfux usually needs referral
trans-rectal exam - impaction, distension, displacement, masses - risk of rectal tears
abdominocentesis - asses changes in peritoneal fluid - serosanguinous colour or increased protein (leakage of blood components), increased lactate (anaerobic tissue metabolism), ingesta (GIT rupture), high WBC (peritonitis)
abdominal ultrasound - kidneys, small intestines, spleen, intestinal wall thickness, distension of small intestine, peritoneal fluid (structures not palpable by trans-rectal palpation)
colic - treatment
NSAIDs
Alpha-2s
Opioids
Spasmolytics (anticholinergics) - buscopan - rapid onset smooth muscle relaxant
fluid therapy - stomach tube - contraindicated if NG reflux or if suspected small intestinal lesion
purgatives - liquid paraffin coats impaction, epsom salts breaks impaction down
causes of weight loss
reduced intake - not wanting to eat, not being able to, not being allowed, not being fed enough
poor absorption - inadequate presentation of food, GI disease, neoplasia, parasites
decreased utilisation - disorder of nutrient metabolism (liver), cushings (not really weight loss, just look ropey)
excessive loss - protein losing enteropathy
increased requirement - exercise, bacterial infection, chronic viral infection, neoplasia
Hypoalbuminemia
low albumin - protein lowing enteropathy or nephropathy
reduced production - liver disease (Severe), malnutrition
chronic inflammation - negative acute phase proteins
Anemia
common finding in weight loss
decreased RBC production and lifespan
abdominocentesis
assess changes in peritoneal fluid
low sensitivity
good specificity for inflammation/bacteria, and neoplasia
peritoneal inflammation/bacteria - increased protein and lactate and serosanguinous colour change
neoplasia - tumours mat exfoliate cells, low grade peritoneal inflammation
gastroscopy
assess gastric ulceration - associated with weight loss through desire to eat rather than absorption
oral glucose absorption test (OGAT)
assesses absorptive capacity of small intestine
12 hour fast, baseline oxalate-fluoride
give glucose
take bloods every hour for 5-6 hours
normal - double after 2 hours then absorbed by end
partial malabsorption - 15-65% increase at 2 hours, slower to peak
total malabsorption - serum glucose not above 15% of baseline
fecal blood test
frank blood in feces - bleeding in rectum/colon
biopsies
trans-endoscopic duodenal biopsy - pinch biopsy - mucosal tissue
rectal biopsy - mucosa and submucosa
surgical - full thickness
can show inflammation
can be definitive for intestinal lymphoma or infiltrative intestinal disease
upper GI conditions - cattle
mouth, teeth, throat
choke - eg. feeding potatoes - can lead to free gas bloat - pass stomach tube down and see if it hits anything
frothy gas bloat - gas trapped in pockets in rumen - eg. eating clover
bloat from vagal nerve pressure - eg. hardware disease, lymph node enlargement, pneumonia, tumour - leads to free gas bloat, can release in some bits because no obstruction but can’t do it actively
hardware disease - cattle
metal wedged in reticulum - varying penetration into pericardium
collect with a magnet
acidosis - cattle
subclinical - pH < 5.5
acute clinical - pH < 5 - very sick
subacute ruminal acidosis (SARA) - effect on production but not enough that you’d notice except from over time - usually nutritional issues
assess - ruminocentesis - rumen pH and microbial activity
ketosis - cattle
post partum
energy deficit
fatty liver - cows have poor hepatic function for mobilising body fat
pear drop small
indistinct signs - production down, bit depressed
diagnosis - elevated ketones in milk, urine or blood
cattle energy requirements
assumed 700kg -
dry -
- maintenance - 80MJ
- pregnancy - 20MJ
- milk production - 0MJ
peak lactation -
- maintenance - 80MJ
- pregnancy - 0 MJ
- milk production - 300MJ
maintenance = 10% bodyweight + 10
GIT displacements/torsion - cattle
left displaced abomasum - ketosis (loss of GI tone –> enlarged abomasum filled with gas –> slides under rumen) - usually after calving, ping on left side of abdomen
right displaced abomasum +/- volvulus - right sided ping
abomasal ulceration - black feces, can rupture and kill by peritonitis
caecal dilation - palpate per rectum
caecal torsion - can release toxins when untwisted
small intestinal torsion
viral causes GI disease - ruminants
rotavirus - young, 2-12 weeks- peracute diarrhoea, high mortality
coronavirus - young, 1-3 weeks - shedding up to 2 weeks
BVD - 6 months - 2 years - diarrhoea not main sign
bacterial causes GI disease - ruminants
e. coli - neonates - environmental bacteria
salmonella - calves and older - acute mucoid watery diarrhoea, spread in feces
clostridia - different strains, closridium perfringens
johnes - mycobacterium paratuberculosis - slow burn, notifiable
parasitic causes of GI disease - ruminants
protozoa
- cryptosporidium parvum - young - oocysts in feces, hygiene important
- coccidiosis - eimeria - older calves (around weaning), persists in environment - rectal prolapse
worms
- strongyles - usually when turned out at pasture
- liver fluke - older animals grazed in wet areas, autumn winter time
nutritional causes of GI disease - ruminants
milk scours
peri-weaning scours
SARA
grain overload
dietary changes - up to 6 weeks to stabilise to new diet
gorging
wrong mix of milk powder
feeding of whole milk
usually young animals
environmental and husbandry causes of GI disease - ruminants
failure of passive transfer
poor equipment hygiene
poor housing hygiene
mixing of age groups - leaves younger more vulnerable
stress
healthy calf parameters
temp - 38-38.9
rr - 15-30bpm
CRT - <2 secs
mm - pink and moist
quick standing for feeding
semi firm feces
ear and head position upright
no cough
diagnosis - GI disease in calves
scour check kit - rotavirus, coronavirus, crypto, e. coli
fecal worm egg counts
fecal culture - salmonella, johnes, clostridial toxin, rotavirus, coronavirus
serology - johnes, BVD
bulk milk surveillance - fluke, BVD, IBR, johnes, salmonella
postmortem/abattoir feedback - fluke, other parasites, gross anatomy changes
incisor examination - horse
overbite
underbite
slant/smile mouth
cribbing
calculus
mobility
diastema
look for draining tracts
canine and wolf teeth examination - horse
calculus
fractured canines
displaced wolf teeth
blind wold teeth - unerupted
mandibular wolf teeth
cheek teeth examination - horse
interdental spaces
buccal mucosa
dental overgrowth
dental fractures
displaced teeth
supernumerary teeth
diastema
dental exam sedation - horse
alpha-2 agonist - romifidine, xylazine or detomidine
opiate - butorphanol or morphine