in order to dx IBD you need to see what two things?
Chronic persistent or chronic recurrent GI signs AND histologic inflammation of lamina propria
how do you dx IBD?
exclusion of other ddx, endoscopy & histopath (so need to do CBC/Chem/UA, then fecal exam AND diagnostic tx, GI panel (PLI, TLI, Cobalamin, folate, ACTH Stim), test TT4, FeLV, FIV, do Abdominal ultrasound, try a dietary trial (some improvement after 2 wk) abx trial (tylosin, OTC, metronodazole--> do endoscopy
what causes IBD?
Probably loss of tolerance to microbiome (Genes + immune dysregulation + decreased complexity of microbiome)
ok.....TLI vs PLI, what are these tests telling us
(1) TLI= Trypsin-Like Immunoreactivity. This tests for EPI. Trypsinogen/trypsin (trypsin only activated from trypsinogen in serum if pancreas inflammation) so is synthesized exclusively by the acinar cells pancreas, and measurement of this zymogen by assay of TLI provides an excellent indirect index of pancreatic function. So if TLI low, EPI. (1) PLI: pancreatic lipase immunoreactivity. if high levels of PLI in blood, there is inflammation in the panc
IBD: so you do CBC/Chem,Urinalysis,Fecal analysis (flotation/protozoa/rectal scraping…), PLI, TLI, Cobalamin, folate, ACTH Stim, TT4, FeLV, FIV, Abdominal ultrasound....and you get nothing. THEN you do a dietary trial and it is successful. What do you have?
Food responsive diarrhea= FRD
IBD: so you do CBC/Chem,Urinalysis,Fecal analysis (flotation/protozoa/rectal scraping…), PLI, TLI, Cobalamin, folate, ACTH Stim, TT4, FeLV, FIV, Abdominal ultrasound....and you get nothing. THEN you do a dietary trial ...and you get nothing. Then you do a Abx trial and you get success...what do you have?
Antibiotic responsive diarrhea= ARD
IBD: so you do CBC/Chem,Urinalysis,Fecal analysis (flotation/protozoa/rectal scraping…), PLI, TLI, Cobalamin, folate, ACTH Stim, TT4, FeLV, FIV, Abdominal ultrasound....and you get nothing. THEN you do a dietary trial ...and you get nothing. Then you do a Abx trial and...you get nothing. Your next step is endoscopy, with possible dx being? (Which is most common)
granulomatous (histiocyte is a kind of macrophage)
IBD: so you do CBC/Chem,Urinalysis,Fecal analysis (flotation/protozoa/rectal scraping…), PLI, TLI, Cobalamin, folate, ACTH Stim, TT4, FeLV, FIV, Abdominal ultrasound....So you do this basic min. database and you get nothing, but your animal is hypoalbuminemic, unstable, or has worsening clinical signs. what should you do next?
USUALLY you would do diet trial, then abx trial, THEN endoscopy. but because they are unstable, go right to endoscopy.
what is the tx for IBD? how can it vary between cat and dog?
Prednisolone for both! DOG: Cyclosporine. CAT: pred + chlorambucil
how can you do a canine follow-up on your tx of their IBD?
CRP (C-reactive protein- a type of nutritional assay), CIBDAI (canine IBD activity index) & biopsies (cat is just clinical and bx)
PLE means you will have low albumin. what other dzs cause low albumin that you will have to exclude?
Renal loss (UPC=urine protein creatinine ratio) (in renal, low albumin but globulins still normal), Third space loss (pleural effusion, ascites), Skin burns, Liver failure (no production)-- ALT/ALP, bile acids pp & fasted, us, biopsy
*how can you tell renal protein loss from GI protein loss?
in RENAL, ONLY ALBUMIN WILL BE LOW. IN GI, ALBUMIN AND GLOBULINS ARE LOW
in lymphangiectasia, the main protein you lose is..
what are the four primary causes of protein losing enteropathy?
WEIGHT LOSS!!!, +/- Diarrhea, +/- vomiting, +/- inappetence, EDEMA, pleural effusion, abdominal effusion ( in smaller print she also had: deficiency of fat soluble vitamins (ADEK), thromboembolism from AT deficiency, hypocalcemia -> tetany/seizures, hypomagnesemia, possible bleeding from Vitamin K deficiency)
what are the 4 major lab findings you will see with PLE?
(1) Panhypoproteinemia (aka both albumin and globulin. PAN is with intestinal dz, if only low albumin prolly liver or kidney dz). (2) Hypocholesterolemia (not absorbing fats correctly either) (3) Hypocalcemia (4) Lymphopenia (if lymph vessels damaged, prolly dumping some lymphocytes into the intestines etc)
how do you dx PLE?
biopsies (surgery > endoscopy) (some clinicians administer corn oil 3-4h pre-biopsy to dilate lactaceals)
what dietary therapies can you implement to tx PLE?
flatulance can be normal, or it can be a result of dz from what 3 places?
stomach, small int, colon
what is flatulance?
Excessive formation of gas in stomach or intestines
PE sign of flatus might be
abdominal distension can lead to borboygmi--> flatus or also
Gastric dilatation / volvulus: explain how the stomach flips
usually turns clockwise (when viewed from ventrally)
if you open up a GDV, which side do you want to grab, and which way do you want to pull?
so grab from L side and turn it back to right side when it is all rotated
Re-occurrence of bloating from GDV: … after surgery, what can we do ? First, exclude other disorders. How do you do this?
Try some drugs like Metoclopramide (inc gastric emptying), Cisapride (inc GI movement), Ranitidine (dec stomach acid) -- so if the stomach was just angry, maybe it distended for that reason
if there is reoccurring bloating, and you eliminate out other motility diseases and irritation, what might be your next step in trying to figure it out?
perhaps try to eliminate amount of gas being produced which might lead to the bloating-- Erythromycin (Also has prokinetic effects) and Simethicone (anti-gas agent)
if you have tried your first step of trying to elim other causes (metaclopramide, cisapride, ranitidine) which might lead to dysmotility, that doesnt work, so then you try to eliminate possible gas formation problems (erythromycin inc motility), and that doesnt work....then what can you try as your 3rd and last effort?
teach owner to pass a tube , 2nd surgery
Re-occurrence of bloating --> Metoclopramide where does it work? who do you not give it to?
METOCLOPRAMIDE. works on smooth muscle upper gi tract & dopamine receptors CNS. do not give to seizure-patients .... can give PO, SC, IV
Cisapride--> how does this work, when should you dec dose?
Stimulation of the serotonin receptors increases acetylcholine release--> prokinetic agent. decrease dose if pain/cramping
Ranitidine--> how does this work?
H2 receptor antagonist.... questionable effect on gi kinetics
bloating right after surgery... what are some possibilities for this to happen?
(1) is the Gastropexy in the right place? If it isnt, might be causing outflow obstruction. (2) Is there an underlying disorder? Consider: (a) primary motility disorder (b) cancer
how can you check for a primary motility disorder?
Barium contrast studies-- 10-12h max for gastric emptying!
Pages linking here (main versions and versions by same user)