GI Flashcards
Gastric Inhibitory Peptide
Stimuli: protein, fat, carbs
Site of secretion: K cells of duodenum and jejunum
Stimulates insulin release
**Inhibits gastric acid secretion
Secretin
Stimuli: acid & fat
Site of secretion: S cells of duodenum, jejunum and ileum
Stimulates pepsin secretion, pancreatic bicarb secretion, biliary bicarb secretion, growth exocrine pancreatic CK
** inhibits gastric acid secretion
Gastrin
Simulus: protein, distention, nerve
Site secretion: G cells in antrum, duodenum & jejunum
Stimulates gastric acid secretion, mucus growth
inhibited by acid
Cholecystokinin
Stimulus: protein, fat, acid
Site of secretion: I cells in duodenum, jejunum and ileum
Stimulates pancreatic enzyme secretion, pancreatic bicarb secretion, GB contraction, growth of exocrine pancreas
** Inhibits gastric emptying
Pyloric Glands
- Mainly secrete mucus
- Small amount pepsinogen
- Gastrin secretion
Pepsinogen
- Precursor to pepsin –> helps break down proteins
- Stimulated by Ach release from gastric enteric nervous plexus or acid in the stomach
Oxytonic glands
- Compose 80% stomach (fundus)
- mucus (neck) cells: release mucus
- cheif cells - release pepsinogen
- parietal cells: secrete hydrochloric acid & intrinsic factor
4 motility patterns
- Segmental: circular smooth m
- peristalsis: longitudinal smooth m
- intestinointestinal inhibition: reflex inhibition of peristalsis due to distention of segment
- Migrating motility complex: slow propulsive contact to sweep debris during fasting
motilin
Stimuli: fat, acid, nerve
Site of secretion: M cells in duodenum and jejunum
Stimulates gastric motility, intestinL MOTILITY
- ERYTHROMYCIN binds
Somatostatin
Stimuluis: acid, lipid, bile
Site of secretion: D cells in intestine and pancreas
Action: inhibits gastrin, VIP, GIP, secretin, motilin
**Stops alls ecretions
**Paracrine action
Serotoninergic receptors
- 5HT1P: intitiates peristalsis and secretory reflexes
- 5HT3: activates extrensic N sensory –> nausea & vomiting
- 5HT4: increased PREsynaptic release of Ach & calcitonin gene related peptide
- increase PSNS transmission
- Cisapride
-Doesnt work if nerve is degenerated
Risk factors of abdominal compartment syndrome
- Dec abdominal wall compliance
- increase intra-abdominal luminal content
- increased abdominal content
- capillary leak syndrome
Innervation GIT
PSNS
-Vagus: upper GI - 75% afferent, 25% efferent
-Pelvic N: distal transverse colon to rectum
SNS
- T1-L3 cord segments: short preganglion: celiac, mesenteric, hypogastric
-50% aff, 50% efferent
*Signal may bipass myenteric - muscle & mucosa
Aldosterone effect on colon
- Stimulates synthesis of Na channels
- increased Na absorption
- Increase K excretion
-Proximal 1/2 colon (distal 1/2 storing)
Nutrients from colon and their source
- Short chain fatty acids: esp acetate, propionate, & butyrate
- Source: cellulose, pectin, henocellulose
Predominant source ammonia GIT
Distal intestine/colonic bacteria have urease action on urea or dietary amines
intra-abdominal hypertension
Sustained or repeated pathologic evaluation of IAP of >12 mmhg
Abdominal compartment syndrome
Sustained increase in IAP of >20 mmHg ( with or w/o APP <60 mmHG) associated with new organ dysfunction or failure
Factors influencing intra-abdominal pressure
body position
Body condition
Pregnancy
Increased abdominal wall tone
Pain
Anxiety
External abdominal pressure application
Belly bandages
volume infusate
Physiologic Effects intra-abdominal hypertension
- Hemodynamic Effects: INcreased CVP, RAP, PCWP, MAP, SVR
- Due to increased catecholamines & volume shifts –> CO transient increase then decrease due to drop in venous return - Renal: decreased GFR - oloiguria & anuria
- Pulmonary: Decreased pulmonary compliance –> inadequate negative thoracic pressure
- CNS: increqased ICP –> increased intrathoracic P –> increased blood volume in thhe compliant system
- CS: obtunded, CN deficits, vomiting, seizures - Visceral: dec blood flow to hepatic, portal, intestinal and gastric
- Bacterial translocation Risk - Systemic: Increased ADH, Aldosterone, Renin, and increased catecholamines
How is hydrochloric acid made
- Regulated by enterochromaffin like cells –> histamine
Made in parietal cells
Clostridium perfingens
- Gram +, anaerobic, spore forming bacilli
- 5 biotypes & 4 toxin genra
-All biotypes can harber enterotoxin (CPE) - Type A: Acute hemorrhagic diarrhea syndrome (CPE)
Diagnosis: no gold standard
- Fecal ELISA CPE
- PCR for strains
Treatment: Ampicillin, erythromycin, metronidazole*, +/- tylosin
** Can have bacterial resistance
C. Diffecile
- Gram +, anaerobic, spore forming bacilli
- 3 toxins:
A & B –> typically present together
Binary toxin - unclear significance - PCR Ag ELISA
Treatment: metronidazole +/- ampicillin
**Potentially zoonotic
** May cause acute severe diarrhea syndrome or subclinical
Enteric E coli infections
- Gram -, nonspore rods
- 7 pathotypes:
Enteropath
enterohemorrhagic
enterotoxic
necroptoxigenic
enteroinvasive
enteroaggragative
Adherent-invasive
** Unclear role of illnes - except AIEC
Pathophysiology of Pancreatitis
- trypsinogen activated early to trypsin—>trypsin activates kallirenin-kinin system –> activates inflammatory cascade–> Increased ROS –> vasodilation, decreased BP, ARF, microvascular thrombosis & DIC
- Local ischemia + phospholipase A2 + ROS –> Disrupt cell membrane–> hemorrhage, necrosis, increased cap permability & intitate arachidonic acid cascade
- Elastase–> degrades vascular elastin–> increased vascular permeability
- Chymotrypsin –> acitvates xanthine oxidase–> ROS
- Phospholipase A2 – degrades surfactent–> ALI/ARDS
Additional treatment for severe acute pancreatitis
- FFP - contains alpha2 macroglobulins, which may aid in binding of proteases and help clear them ( controversial)
- Low dose dopamine- in cats decreases vascular permeability - unsure if helps in dogs
** metoclopramide dopamine antagonist! - Nutrition: +/- cobalamin in cats
- icalcium if clinical
- Glycemic control
Viral enteritis
CPV2 + panleukopenia: SEVER (attack crypts)
Rotavirus + coronavirus - attacks tips of villi (less severe)
HGE
PCV at least 60%, normal TS
- INcreased PCV due to splenic contraction
- Normal to decreased TS due to loss in GI and redistribution
+/-c. perfingens playing tole
- May be due to abnormal immune response, endotoxin or diet changes
PLE
- Associated with different disease: lympho-plasmacytic, eosin, or granulomatous lymphangectasia, diffuse fungal or lymphosarcoma
- MOA: inflammation –> loss of GI barrier –> enterocyte & Tight junction disrupted
Granulomatous colitis
- AKA histiocytic ulcerative colitis of boxers (also seen in fenchies and border collies
- Severe large bowel diuarrhea + weight loss + inappetance
- BW: dec Albumin +/- chronic anemia
- Diagnosis: FISH stains: adherent-invasive e coli (AIEC)
Tx: fluoroquinolones for 8 weeks
Pancreatitis with TLI & CPE
Trypsin like immunoreactivity
- suggestive
- also increased in azotemia & GI disease
Pancreatic Elastase-1(CPE)
- helpful of severe
Salmonella
- Gram +, facultative anaerobic, nonspore forming bacilli
- Diagnosis: culture + PCR + clinical signs ( lethargic, fever, anorexia then vomiting, abdominal pain & diarrhea)
Treatment:
- only supportive unless systemically ill
- Abx: ampicillin + enrofloxicin if systemically ill
** zoonotic
**No abx if immunocompromized owner
Campylobacter GI illness
- Gram -, aerophilic rods
- Rare cause of diarrhea in dogs–> usually young if it does
Diagnosis: fecal real time PCR culture
Treatment: self limiting
- If decreased immune function or febrile/hemorrhagic diarrhea –> antibiotics (macrolides recommended; fluoroquinolones there is increased resistance in human med)
** possibly zoonotic–> in humans can progress to immune mediated disease (Guillain-barre syndrome)
Differentials for acquired megaesophagus
-Idiopathic
- Myasthenia gravis
- Addisons
- Toxins: lead & thalium
- Inflammatory: immune mediated polymyositis, preneoplastic myositis, lupus, dermatomyositis
- Peripleural neuropathy: larpar/GOLLP
- Severe esophagitis
- Esophageal dysmotility of terriers–> resolves as they get older
Congenital megaesophagus & breeds
- Congenital form due to sensory dysfunction where distention of vagal afferent defective
Breeds: wire haired foxhounds, minischnauzers, GSD, great danes, irish setters, Labs, Newfies, Sharpeis
Siamese
Increased BUN:Crea ratio
- Anything > 20
- DDX: GI hemorrhage, fever, burns, infections, starvation, steroid administration
Vomiting Center
- Stimulated by vagal and sympathetic impulses of GI inflammatory or overdistention
- Triggered by vestibular, CTZ & cerebellum
CTZ: area posterna of 4th ventrical lacks BBB –> drugs may stimulate
Central trigger zone receptors
** Activated by apomorphine, uremic toxins, hepatotoxins, endotoxin, & cardiac glycosides
D2: dopaminergic
H1: Histamine
Alpha2: Adrenergic
5HT3: Serotonin
M1: Muscarinic-ACh
NK1: neurokinin
ENK mu,beta: opiates
*8Vestibular system directly activates
Vestibular nausea receptors
- Motion stimulates
H1: histamine
M1: muscarinic-ACh
NMDA: glutamate
Vestibular –> CRTZ (dogs)
—> directly stimualtes vomit center in cats
Vomit center receptors
Alpha2:adrenergic
5HT1A: serotonin
Cerebral cortex vomiting receptors
Anticipation/stimulates anxiety:
W2 - benzo
ENKmu – opiates
–> both directly sitmulate vomit center
Gut vomiting receptors
- Stimulated by vomiting center
5HT3(serotonin)–> afferent to vomit center
Efferents:
5HT4:serotonin
D2: dopamine
M2:muscarinic
MOT:motilin
SI obstruction on rads
Cats >2x height of L2
Dogs >1.6 height of L5
Septic peritonitis findings (sensitivity and specificitiy
Dogs:
BG >20mg/dL 100% sens/spec
Lactate >2 mmol/L 100% sens/spec
Cats:
BG>20 86%sens, 100% spec
Lactate >2 not preported
Uroabdomen Findings
K Fluid:blood
- Dogs: 1.4:1
- Cats 1.9:1
CREA fluid:blood
- Dogs&cats: 2:1
Regurgitation
- passive ejection of food
- Assd with esophageal or pharyngeal disease
Osmotic diarrhea
Increased luminal osmoles–> draws fluid into intestinal lumen
Secretory diarrhea
Net increased in intestinal fluid secretion (actual increase or due to net decreased absorption)
Altered Permeability diarrhea
Normally intestines semipermable, if macroscopic or microscopic damage, see increased permeability through epithelial cells or gap junctions
** Increased risk of bacterial translocation
Small bowel vs large bowel
Small:
- mucus uncommon
- blood uncommon
- normal to increased stool volume
- +/– melena
- increased to normal frequency
- uncommon to have urgency or tenesmus
Large:
- mucus common
- blood common
- normal to decreased stool volume
- no melena
- increased frequency
- common urgency, common tenesmus
Deranged motility diarrhea
Increased peristaltic contractions or decreased segmental contractions
Infectious causes of diarrhea
- Parasites: acyclostoma sp, toxocara, toxoascaris, trichuris
- Bacteria: salmonella, campylobacter, C diff, C perfingens, enteropathogenic ecoli
- Viral: parvo, panleuk
- Fungal: histo, pythium, cryptococc
- Protozoa: tritrich, giardia, cryptosporidium, isospera
- Rickettsial: Neorickettsia species
- Algal: prototheca
- SIBO- controversial
Diarrhea diagnostics
CBC/chem/ua
Screen GT4, addisons, occults liver disease
Fecal, zinc sulfate (giardia), direct
Fecal culture, enterotox screen
Parvo ELISA
Exfoliative rectal cytology –> fungi, algea, neoplastic
TLI for EPI
Folate & cobalamin if suspected SIBO
AUS
Biopsy
Primary GI diarrhea causes
Food intolerance/allergy
INfectious
IBD
Lymphangectasia
Extra GI diarrhea causes
- Hepatobilliary: dec albumin–> dec biliary salts
- Pancreatic Disease: EPI, pancreatitis–> obstructive CBD, SI, inflamm LI
-CHF R sided: intestinal & hepatic congestion - Endocrine disorders: HyperT4, addisons, sometimes hypoT4
- noncirrhotic portal hypertension
- Post CPA
- Septic diarrhea - bacterial endotoxin impairs colonic water & Na absorption –> inc small and large motility
Secondary closures of septic peritonitis
- Jackson pratt: 1 if small dog, 2 if large; decreased risk nosocomial, less intensive care, dec risk eviseration
- Vacuum assd peritoneal lavage: Cd 1/3-2/3 incision reapposed losely & subatmospheric P cranial extent incision
- Open drainage: rectus abdomen loosely closed with 1-6 cm gaps –> reassemble sterile bandages with an outer layer impermeable to water
- Change 2x/ day in 1st 24 hours, then daily
Diagnostic peritoneal lavage
Dialysis or larege bore catheter–> instill 22ml/kg warm, sterile saline then retreive sample and submit for culture
DPL counts 500-10500 with nondegen neuts normal post op to 3 days
DPL count: predominately degenerative neut with count >/=5K indicates peritonitis
IAP clases & recommendations
