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ACVECC > GI > Flashcards

GI Flashcards

1
Q

Gastric Inhibitory Peptide

A

Stimuli: protein, fat, carbs
Site of secretion: K cells of duodenum and jejunum

Stimulates insulin release

**Inhibits gastric acid secretion

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2
Q

Secretin

A

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

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3
Q

Gastrin

A

Simulus: protein, distention, nerve
Site secretion: G cells in antrum, duodenum & jejunum

Stimulates gastric acid secretion, mucus growth

inhibited by acid

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4
Q

Cholecystokinin

A

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

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5
Q

Pyloric Glands

A
  • Mainly secrete mucus
  • Small amount pepsinogen
  • Gastrin secretion
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6
Q

Pepsinogen

A
  • Precursor to pepsin –> helps break down proteins
  • Stimulated by Ach release from gastric enteric nervous plexus or acid in the stomach
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7
Q

Oxytonic glands

A
  • Compose 80% stomach (fundus)
  • mucus (neck) cells: release mucus
  • cheif cells - release pepsinogen
  • parietal cells: secrete hydrochloric acid & intrinsic factor
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8
Q

4 motility patterns

A
  1. Segmental: circular smooth m
  2. peristalsis: longitudinal smooth m
  3. intestinointestinal inhibition: reflex inhibition of peristalsis due to distention of segment
  4. Migrating motility complex: slow propulsive contact to sweep debris during fasting
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9
Q

motilin

A

Stimuli: fat, acid, nerve
Site of secretion: M cells in duodenum and jejunum

Stimulates gastric motility, intestinL MOTILITY

  • ERYTHROMYCIN binds
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10
Q

Somatostatin

A

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

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11
Q

Serotoninergic receptors

A
  1. 5HT1P: intitiates peristalsis and secretory reflexes
  2. 5HT3: activates extrensic N sensory –> nausea & vomiting
  3. 5HT4: increased PREsynaptic release of Ach & calcitonin gene related peptide
    - increase PSNS transmission
    - Cisapride
    -Doesnt work if nerve is degenerated
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12
Q

Risk factors of abdominal compartment syndrome

A
  1. Dec abdominal wall compliance
  2. increase intra-abdominal luminal content
  3. increased abdominal content
  4. capillary leak syndrome
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13
Q

Innervation GIT

A

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

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14
Q

Aldosterone effect on colon

A
  • Stimulates synthesis of Na channels
  • increased Na absorption
  • Increase K excretion

-Proximal 1/2 colon (distal 1/2 storing)

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15
Q

Nutrients from colon and their source

A
  • Short chain fatty acids: esp acetate, propionate, & butyrate
  • Source: cellulose, pectin, henocellulose
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16
Q

Predominant source ammonia GIT

A

Distal intestine/colonic bacteria have urease action on urea or dietary amines

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17
Q

intra-abdominal hypertension

A

Sustained or repeated pathologic evaluation of IAP of >12 mmhg

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18
Q

Abdominal compartment syndrome

A

Sustained increase in IAP of >20 mmHg ( with or w/o APP <60 mmHG) associated with new organ dysfunction or failure

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19
Q

Factors influencing intra-abdominal pressure

A

body position
Body condition
Pregnancy
Increased abdominal wall tone
Pain
Anxiety
External abdominal pressure application
Belly bandages
volume infusate

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20
Q

Physiologic Effects intra-abdominal hypertension

A
  1. 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
  2. Renal: decreased GFR - oloiguria & anuria
  3. Pulmonary: Decreased pulmonary compliance –> inadequate negative thoracic pressure
  4. CNS: increqased ICP –> increased intrathoracic P –> increased blood volume in thhe compliant system
    - CS: obtunded, CN deficits, vomiting, seizures
  5. Visceral: dec blood flow to hepatic, portal, intestinal and gastric
    - Bacterial translocation Risk
  6. Systemic: Increased ADH, Aldosterone, Renin, and increased catecholamines
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21
Q

How is hydrochloric acid made

A
  • Regulated by enterochromaffin like cells –> histamine
    Made in parietal cells
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22
Q

Clostridium perfingens

A
  • 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

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23
Q

C. Diffecile

A
  • 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

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24
Q

Enteric E coli infections

A
  • Gram -, nonspore rods
  • 7 pathotypes:
    Enteropath
    enterohemorrhagic
    enterotoxic
    necroptoxigenic
    enteroinvasive
    enteroaggragative
    Adherent-invasive

** Unclear role of illnes - except AIEC

25
Q

Pathophysiology of Pancreatitis

A
  • 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
26
Q

Additional treatment for severe acute pancreatitis

A
  1. FFP - contains alpha2 macroglobulins, which may aid in binding of proteases and help clear them ( controversial)
  2. Low dose dopamine- in cats decreases vascular permeability - unsure if helps in dogs
    ** metoclopramide dopamine antagonist!
  3. Nutrition: +/- cobalamin in cats
  4. icalcium if clinical
  5. Glycemic control
27
Q

Viral enteritis

A

CPV2 + panleukopenia: SEVER (attack crypts)

Rotavirus + coronavirus - attacks tips of villi (less severe)

28
Q

HGE

A

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

29
Q

PLE

A
  • Associated with different disease: lympho-plasmacytic, eosin, or granulomatous lymphangectasia, diffuse fungal or lymphosarcoma
  • MOA: inflammation –> loss of GI barrier –> enterocyte & Tight junction disrupted
30
Q

Granulomatous colitis

A
  • 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
31
Q

Pancreatitis with TLI & CPE

A

Trypsin like immunoreactivity
- suggestive
- also increased in azotemia & GI disease

Pancreatic Elastase-1(CPE)
- helpful of severe

32
Q

Salmonella

A
  • 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

33
Q

Campylobacter GI illness

A
  • 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)

34
Q

Differentials for acquired megaesophagus

A

-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

35
Q

Congenital megaesophagus & breeds

A
  • 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

36
Q

Increased BUN:Crea ratio

A
  • Anything > 20
  • DDX: GI hemorrhage, fever, burns, infections, starvation, steroid administration
37
Q

Vomiting Center

A
  • 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

38
Q

Central trigger zone receptors

A

** 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

39
Q

Vestibular nausea receptors

A
  • Motion stimulates

H1: histamine
M1: muscarinic-ACh
NMDA: glutamate

Vestibular –> CRTZ (dogs)
—> directly stimualtes vomit center in cats

40
Q

Vomit center receptors

A

Alpha2:adrenergic
5HT1A: serotonin

41
Q

Cerebral cortex vomiting receptors

A

Anticipation/stimulates anxiety:

W2 - benzo
ENKmu – opiates

–> both directly sitmulate vomit center

42
Q

Gut vomiting receptors

A
  • Stimulated by vomiting center

5HT3(serotonin)–> afferent to vomit center

Efferents:
5HT4:serotonin
D2: dopamine
M2:muscarinic
MOT:motilin

43
Q

SI obstruction on rads

A

Cats >2x height of L2
Dogs >1.6 height of L5

44
Q

Septic peritonitis findings (sensitivity and specificitiy

A

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

45
Q

Uroabdomen Findings

A

K Fluid:blood
- Dogs: 1.4:1
- Cats 1.9:1

CREA fluid:blood
- Dogs&cats: 2:1

46
Q

Regurgitation

A
  • passive ejection of food
  • Assd with esophageal or pharyngeal disease
47
Q

Osmotic diarrhea

A

Increased luminal osmoles–> draws fluid into intestinal lumen

48
Q

Secretory diarrhea

A

Net increased in intestinal fluid secretion (actual increase or due to net decreased absorption)

49
Q

Altered Permeability diarrhea

A

Normally intestines semipermable, if macroscopic or microscopic damage, see increased permeability through epithelial cells or gap junctions

** Increased risk of bacterial translocation

50
Q

Small bowel vs large bowel

A

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

51
Q

Deranged motility diarrhea

A

Increased peristaltic contractions or decreased segmental contractions

52
Q

Infectious causes of diarrhea

A
  • 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
53
Q

Diarrhea diagnostics

A

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

54
Q

Primary GI diarrhea causes

A

Food intolerance/allergy
INfectious
IBD
Lymphangectasia

55
Q

Extra GI diarrhea causes

A
  • 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
56
Q

Secondary closures of septic peritonitis

A
  1. Jackson pratt: 1 if small dog, 2 if large; decreased risk nosocomial, less intensive care, dec risk eviseration
  2. Vacuum assd peritoneal lavage: Cd 1/3-2/3 incision reapposed losely & subatmospheric P cranial extent incision
  3. 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
57
Q

Diagnostic peritoneal lavage

A

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

58
Q

IAP clases & recommendations

A

ACVECC (10 decks)

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