Small Ani. Med 2- GI introduction

wilsbach's version from 2016-02-23 21:30


Question Answer
6 major GI fxnsDigestion, Absorption, Excretion, Water balance, Electrolyte and acid/base balance, Immune organ
what are the layers of the GI, what do they look like on U/S?5 layers alternating hyperechoic and hypoechoic layers. serosa: hyperechoic (white), muscularis propria: hypoechoic, submucosa: hyperechoic, muscularis mucosa: hypoechoic, superfical mucosa: hyperechoic
is hyperechoic white or black?white!
how do cells regen in the GI?New cells move from crypt to new villi-tip in 3 days (so takes 3 days for vili to repair)
vit B12 is aka?cobalamin
vit B9 is aka?folate
what protects cobalamin from digestion?r protein
she said if it's cats and diarrhea, a safe answer might always be...cobalamin (B12)
Folate and cobalamin (vitamin B12) review--> explain the folate (B6--she calls it, wiki says it's B9 tho) and cobalamin (B12) path from being consumed to being useable for the bodyB12(cobalamin) is ingested, in the mouth there is salivary R protein which protects the cobalamin from being digested in the stomach (there is also gastric intrinsic factor but this is not in cats). when it reaches the sm int there is a folate carrier which directly transports the folate (B9) out to become serum folate (useable). For cobalamin(B12), There is a IF receptor in the ileum which transports out the cobalamin bound to the gastric IF (IF-B12) (cats dont have the gastric IF, their IF comes from their pancreas) (so in cats if panc is dz, think about cobalamin deficiency. if ileum dz in dogs, think about cobalamin deficiency) So once the IF-B12 is taken up in ileum it is brought to the liver and then taken up into the blood stream to be useful (or circulation back into intestine). Uptake in ileum is very important.
***What implications are there for cobalamin/folate if there is intestinal damage?IF THERE IS DAMAGE IN THE distal small intestine/ileum, (such as cats with intestinal lymphoma) THEY CANNOT ABSORB THE COBALAMIN..... IF YOU HAVE PROXIMAL SMALL INTESTINE DAMAGE, this is where the folate uptake receptors are (remember folate is a product of bacteria) so folate would be low
what are the things intestinal flora are affected by? (first chance bact are whatever bact were first encountered by the animal as a neonate)
what bacterial breakdown product is used for coloncyte nutrition?butyrate
explain how the bact use non-digestible fiber
what are 2 big PROTECTIVE roles intestinal bacteria play?(1) intestinal gene expression with impact on: Nutrient uptake, Metabolism, Angiogenesis, Mucosal barrier integrity, Enteric nervous system development, Mucosal immunity: Th1/Th2 cytokine profile (2) Barrier against colonization by pathogens: Mechanical competition, Competition for binding sites Competition for nutrients, Prod. of antimicrobial substances: bacteriocins, lactic acid
Host – bacteria crosstalk: what are the 3 ways the host's gut "communicates"/interacts with the bacteria in it?(1) Surface enterocytes: antigenic exclusion (mucous & tight junct.) sense danger signals, secrete IgA, defensins, chemokines, cytokines (2) Mcells: lay on follicles, sample luminal Ag -> product to DC (dendritic cell) (3) Dendritic cell (DC) sample gut contentIngest bacteria (alive) --> present to lymphnodes
what is the classic presentation of SIBO (small intestinal bacterial overgrowth) which is now known as ARE (antibiotic responsive enteropathy) (in relation to gut-bacteria balance and function)in classic presentation The excessive bacteria USE UP all the B12 (cobalamin) and use it to make MORE folate (she keeps calling it B6 but wiki says B9 so idk man) so you will basically see INC FOLATE AND DEC COBALAMIN
what are two antimicrobials you can use to tx bacterial overgrowth (SIBO/ARE) without killing off all the regular flora which actually are trying to help in this sitaution?metronidazol+ Tylosin
what is an epulis and who tends to get them?benign growth in mouth-- brachycephalic breeds, esp boxers, tend to get these
what does the acute onset of a Esophagel foreign body present like (and who is the poster child for esoFBs?)regurgitation, dysphagia, odynophagia, gagging, excessive salivation... terriers are poster child for eso FB esp young males
what is odynophagia?painful swallowing
what are he 3 components of vomiting?nausea + retching + expulsion
what does nausea look like in a dog?Licking of lips (bicarb rich), Yawning, depression, shivering, hiding
why do dogs lick/swallow when they are nauseous? bicarb rich fluid to neutralize gastric acid
where is there reduced and where is there inc motility of the GI in vomiting?Reduction of motility in the gastric, lower esophageal sphincter, and esopahgus. Then there is Increased retrograde motility of proximal intestine
what is retching? Retching= contraction of abd. muscles & diaphragm => negative intrathoracic pressure & positive abdominal pressure
what is the physiology doing during the expulsion phase of vomiting?Nasopharynx closure & glottis closure & positive intrathoracic pressure during expulsion
where does INITIATION of vomiting occur?Emetic center which is a nuclei in brain stem. (medulla oblongata)
what are the receptors in the emetic center of the brain? 5HT3 serotonergic, NK1 neurokinergic, α2 adrenergic (pic of cat next to this one)
activation of the emetic center of the brain can be indirect or direct. what are the diff indirect vs direct ways?(1) INDIRECT: bloodborne via chemoreceptor trigger zone (CRTZ, at base of 4th ventricle, no BBB) (2) Direct= vagal, sympathetic, vestibular, cerebrocortical pathways
what are some chemicals which stimulate the chemoreceptive trigger zone to indirectly stimulate the emetic center of the brain?drugs, toxins/uremic toxins, electrolytes, osmolar disorders, vestibular, acid base disturbances
CRTZ has additional receptors-- what are these receptors and who has them?D2 dopaminergic + H1 histaminergic + M1 cholinergic [ CATS DO NOT HAVE D2 dopaminergic + H1 histaminergic here]
indirect stim of emetic center=___ and direct=___indirect= chemoreceptive trigger zone, Direct=vagal, sympathetic, vestibular, cerebrocortical pathways
direct stimulation of emetic center is through vagal, sympathetic, vestibular, and cerebrocortical pathways. Where are the various receptors in the abdominal viscera which take these paths?Duodenum (highest receptor conc of GI tract), Kidneys, uterus, urinary bladder--> sympathetic nerves. Pharynx/Tonsillae---> glossopharyngeal nerve
which part of the GI has the highest direct-emetic-center-pathway receptor conc of GI tract?Duodeinum
along with receptors in organs, the direct pathway to the emetic center (vagal, sympathetic, vestibular, cerebrocortical pathways) can be affected by cytotoxicity....what are the chemicals/ their receptors?substance P & serotonin, going to the 5HT & NK1 receptors
***which direct-to-emesis-center-receptors are less developed in cats, what are the clinical implications of this?D2 & H1 receptors less developed in Cats!! This means that Cats are NOT sensitive to apomorphine & histamine for induction of vomiting.
which drugs are effective to make cats vomit? which arent?α2 adrenergic receptors well developed => sensitive to medetomidine (and Xylazin) to induce vomiting ((have barely any D2 and H1 receptors--> meaning apomorphine and histamine aren't gonna be effective in maing them vomit)
how can you administer apomorphine? what does it do? Who can you use this in?Apomorphine for induction of vomiting --> Iv or conjunctival!! (REMEMBER ONLY IN DOGS, CATS DONT HAVE WELL DEVELOPED D1 RECEPTORS IN THE CHEMORECEPTIVE TRIGGER ZONE!)
Receptor antagonists AGAINST vomiting--> Dolasetron, Ondansetron Metoclopramide high dose work on which receptor to stop vomiting?5HT3 serotonergic
Receptor antagonists AGAINST vomiting--> Maropitant (Cerenia®)work on which receptor to stop vomiting? NK1 neurokinergic
so like you can agonize the receptors of the CRTZ, you can antagonize to stop vomiting.. what are the 6 receptors we play with here5HT3 serotonergic, NK1 neurokinergic, α2 adrenergic, D2 dopaminergic, M1 cholinergic, H1 histaminergic
Receptor antagonists AGAINST vomiting--> diphenhydramine works on which receptor to stop vomiting?H1 histaminergic
Receptor antagonists AGAINST vomiting-->Metclopramide (D2), Chlorpromazin, Prochlorperizine work on which receptors (4) to stop vomiting?α2 adrenergic, D2 dopaminergic, M1 cholinergic, H1 histaminergic
When do you treat pts with antiemetics? (exs)ONLY!!!!! if there is a KNOWN CAUSE of the vomiting!! ex) Chemotherapy patients, Secondary to organ failure (Kidney disease, Pancreatitis, Liver disease…)
if an owner says their dog is vomiting, it can be.. vomiting, cough, dysphagia/ regurgitation---> Your medical history will differentiate!!
Cough vs regurg vs vomit: which have Abdominal effort?C and V...... REGURG HAS NO ABD EFFORT
Cough vs regurg vs vomit: which have nausea?ONLY VOMITING HAS NAUSEA
Cough vs regurg vs vomit: what color would you expect the expectoration to me?cough and regurg would be white, VOMITING WOULD BE YELLOW BECAUSE OF THE STOMACH ACID (yellow= acid. Green= bile)
dysphagia vs regurg vs vomit: Abdominal effort?ONLY vomiting
dysphagia vs regurg vs vomit: nausea?ONLY vomiting
dysphagia vs regurg vs vomit: ejected food (is it digested?)only vomiting has digested food
dysphagia vs regurg vs vomit: swallowing attempts?++/+++ for dysphagia, all others are normal
dysphagia vs regurg vs vomit: what is drinking like?ABNORMAL only in dysphagia
dysphagia vs regurg vs vomit: when does the stuff come out?dysphagia there is an immediate expulsion, the other two are delayed
possible reasons for hematemesis?Ulceration, coagulopathy, blood from other sources
whn doing oral exam DONT FORGET to..look under the tongue!
how do you safely open the mouth and keep it open?come in from behind canines (side of mouth) and then press on hard palate to keep it open
so you're palpating the neck and you feel TWO bumps! which one is the submandibular LN and what is the other one?first one in front is LN, one behind is glandular submandibularis
Vomiting: Differential diagnoses: first off, what are the three places the vomiting can be triggered from?Central (CNS), Outside gastrointestinal tract, Inside gastrointesinal tract
what are CENTRAL DDx for vomiting? (general reasons)Toxins, Inflammation, Neoplasia, Pain/Pressure, Stress, Anatomic
what are the toxins you might consider that could cause vomiting?(leads to CENTRALLY caused vomiting) ****NSAIDs, Doxycyclin/Tetracyclin, Erythromycin, Penicillamine / Zinc, Cardiac glycosides, (Lead, Ethylene glycol, strychnine, medetomidine, chemotherapy agents, xylazine, apomorphine )
what are the places outside the GI tract where if there is a problem, it can cause vomiting?liver , kidney, adrenals, uterus, prostate, pancreas, peritoneum, spleen, lymphnodes, endocrine
what are the (general) things that are IN the GI tract and can cause vomiting?infection (parasites, bacteria, viral, fungal), inflammation (colon, duodenum), toxins (garbage), diet, obstruction, neoplasia, motility
vomiting workup flow chart
what are your two choices if you wanna do a Contrast study, and what should you keep in mind with these choices?Barium, Iodine Do not use barium if suspect perforation or prior to endoscopy

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