acute GE - SA Flashcards
most cases of acute GE are fatal y/n
n, most self limiting
name 2 common causes of acute, non-fatal self limiting GE
- parasites
2. dietary indiscretion
name 4 general causes of severe, pos fatal GE
- enteric infection (parvo, bacterial)
- surgical dz
- HGE (acure haemorhagic d+ syndrome..)
what is the major sign of sx dz wrt GE
V+
how much fluid goes IN /day of a 20kg dog
2,700ml/d
what % of the total fluid IN is absorbed by the GIT
98%, the rest into poo
what are the remaining factors which must be considered before a tx and dx is made
what supportive tx is needed
are there underlying dz causing this - pos non-enteric ones
then all the hx, and signalment etc
there are 3 categories of GE of which are often combined in various ways
- gastritis
- enteritis
- colitis
what is haematochezia
fresh blood in poo (colitis suggested)
both gastritis and enteritis have similar causes and often combined what are they
dietary indiscretion foreign body bezoar self-limiting intoxication/drugs etc
colitis has a number of other causes - name some
whipworms, garbage ing, protozoa (giardia, crypto)
how does colitis present differently to GE
tenesmus, not vomiting
rare in cat
after symptomatic tx how long should you give a case to imprve
48hrs
what is the min database from a lab that should be gained to get a dx for suspected GE
haematology
serum biochem
urinalysis (to check systemic dz)
faaecal exam for para
what procedures are carried out to check for para in poo
virology - ELISA for ag parasitology - smears and flotation (giardia) - wet-prep for tritrichomonas (C) or PCR serology - snap test for giardia and parvo
why are radiographs a good dx tool in GE cases
assess if obstruction
u/sound
intussusceptin and forign bodies
contract - rarely req
in a per-acute emergency cases - what would your dx tools/actions be
PCV/TP - assess DH, anaemia, protein losses
blood smear for inflam, haemolysis, anaemia, PLTs
glucose - if very young, often poor gluc control
urea
urinalysis - haemolysis
what are the pros/cons of withholding food in animals w d+ and V+
- less to V+ or d+ (management easier), will make more nauseous
- good to feed - less likely to be septic
- speedier recovery if feed through d+
how do anti-emetics act?
centrally at CTZ
- metoclopraminde, chlorpromazine
anticholinergics
- atropine,
what is the generic name for cerenia
maropitant
what is maropitant - cerenia
NK-1 R antago 1xd dose (s/c inj or oral) SE = v+; CI = if sx dz or obstruction
why woudl you use gastric mucosal protectants
V+ persists or ulceration
what receptors and how do drugs act to prevent ulceration
H2-R antagonists = cimetidine (v freq dosing and SE), sucralfate (antacid and mucosal protection), antacids like MgOH
whya re NSAIDs CI?
damage GI mucosa and damage kidney if they are DH
how do anti-d+ work?
absorbants - protect mucosa, bind tox and XS water = act charcoal
motility modifiers = opioids slow transit AND anti-secretory. also = anticholinergics
what are the pros and cons of ABx use in d+ cases
- upset natural flora and cause d+ and promote R
- flora already upset and if mucosa barrier compromised = sepsis poss!
what are the indication for abx in the d+ case
haem d+
d+ and fever
known infection eg salmnella, campy, EPEC
what is the use of probiotics
limiited once d+ happening - better prev. supprot flora
if a foreign body - how shoul di tbe removed
- induce v+ (if smooth)
- ## wait for it in poo (wi 48hrs!)
what is HGE
canine haem+ enteritis so.. its CHE OR acute haem+ diar syndrome
desc the dz of HGE
toy and mini breeds
netF enterotox, not inflm, altered mucosa perm and secretion
what are the clinical signs of HGE
v+ w/wo blood, followed by d+, depression, shock and marked hamoconcentration (PCV = 60-80!!!)!
what is the reccom tx of HGE
IVFT at bolus until PCV
