Gastrointestinal Flashcards
Mechanical vs Chemical Digestion
Mechanical; GIT movements to physically breakdown food
Chemical; reaction needed to break bonds of macromolecules to be small enough for absoprtion across intestinal membrane
CNS regulation of GI functions
PANS vs SANS
Enteric nervous system →
–Submucosal plexus and Myenteric plexus
* receptors/sensory neurons/motor neurons
– Controls motor/sensory function “pacemaker cells”
– influenced by ANS → PAN branch enhances digestion. SAN inhibits digestion
–Afferent neurons from variety of receptors monitor changes in GIT
Submucosal plexus
controls secretions/blood flow
lenght of GIT
Meissners plexus
Myenterix Plexus
Smooth muscle controls movements of GIT
length of GIT
Auerbach Plexus
Chloecystokinin (CCK)
Stimulate by
What does it inhibit?
Where is it located?
–stimulated by presence of chyme/higher AA/fatty acids
inhibits gastric emptying to allow controlled rate of emptying
–located in duodenal mucosa
– allows for more time for acidic chyme to neutralize
Gastrin
What is it secreted by?
What does it stimulate?
Hormone secreted by G-cells (endocrine cells) in pyloric region
stimulates gastric emptying
Cardiac Sphincter
thickening @ gastric end of esophagus that prevents acids from stomach back flowing/refluxing
Visceral peritoneum
Covers organ surfaces
Parietal peritoneum
lines body wall
Mesentary
connecting peritoneum that suspends intestines from abd. wall
innervated with blood vessels and nerves
Omentum
double layered connecting peritoneum that links stomach to abdominal wall/other organs
contains fat
Gastric circulation
Main blood supply → celiac artery (1st branch of abdominal aorta)
Veins leaving stomach join portal vein → travels to liver
Rugae
transient gastric folds/mucosa
allows stomach to expand
↑ surface area for absoprtion
Gastric mucosa structure
simple columnar epithelium → contains surface mucous cells to produce mucus = protects lining from acidity
Gastric ulcers form from inadequate mucus production
Glandular cells in Stomach
#4
- Mucus neck cells → secretes thin mucus near duct opening → divides/creates new cells
- Parietal cells → gastric glands → secrete H+/Cl- in lumen
- Chief cells → secretes pepsinogen (inactive form of pepsin) → converts to pepsin via stomach acid (HCl) → initiates chemical digestion
- G-cells → located in pyloric region → secrete gastrin → stimulates gastric emptying
“pacemaker” of the stomach
–specialized smooth muscle cells in stomach/intestine
–regulates contraction of gastric/intestinal smooth muscle
–no constant resting membrane potentials
–regulated by ANS
Autonomic nervous system efx on GIT
Ca++ channels open when threshold reached = allows Ca++ into muscle cells = contraction
* Acetylcholine from PANS elevates baseline resting membrane potential = slow waves
* Norepinephrine from SANS opposite efx = lowers resting membrane potential = less likely to cross threshold = reduces smooth muscle contractions
Emesis
Which receptors are involved?
–Controlled by V+ center in medulla
abdominal muscle contraction/inspiration ↑ pressure in abdomen = forces stomach to expelled contents
–cardiac sphincter relaxes
–V+ center contains serotonin and Alpha-2 adrenergic receptors
2 phases of Chemical digestion
- luminal → lg macromolecules breakdown into short polymer chains (Hydrolysis)
- Membranous chemical digestion
Hydrolysis
chemical reaction where bond is broken down by insertion of H2O molecule
Amylase
Pancreatic Enzyme that breaks down starch carbohydrates into maltose
found in saliva/small intestine
Small Intestine tract pathway
- Duodenum → recieves chyme differentiated between ascending/descending. Ends @ duodenojejunal flexure
- jejunum → longest part of SI → bulk of chemical digestion/absorption takes place
- Ileum → end of SI; “peyers patches” aggregates lymphoid tissue. controlls bacteria populations; ends @ ileocecal junction
Small Intestine microanatomy
#2
–Villi/microvilli form brush barrier to ↑ surface area for membranous digestion
–Lacteals → lymphatic capillaries found in villi; carry absorbed lipids/fat soluable substances to thoracic duct → empties into vena cava
Small intestine secretions
- CCK → cholecystokinin triggers your gallbladder and pancreas to contract
- Secretin → lowers HCl production in stomach and increases panc/biliary HCO3 secretion
Canine Parvovirus pathogenesis
What cells does it affect?
When do CS start?
When is shedding detected?
Infection of rapidly dividing cells (lymphoid tissue/intestine/bone marrow)
–Fecal-oral transmission
–CS occur 4-10 days post infection
–Initially replicated in oropharyngeal lymphoid tissue →enters ciruclation for systemic viremia
–fecal viral shedding deteched day 4 post infection
Myocarditis efx from Parvovirus
Rare; but seen in neonates
immature myocytes still rapidly dividing
Parvovirus; CBC findings
Lymphopenia → lymphocytolysis (destruction of lymphocytes)
Neutropenia follows → peripheral consumption/destruction of WBC precursors in bone marrow
Anemia → poor regeneration, iatrogenic or GI hemorrhage, inflammation-related reduction of RBC lifespan, erythropoiesis supression
–Degenerative left shift with leukopenia = poor outcome
Parvovirus; Biochem findings
Hypoproteinemia
hyperbilirubinemia
Elevated AlkPhos/ALT
low electrolyes
hypoglycemia
Pre-renal Azo
Parvo Sepsis/SIRS compications
–intestinal integrity compromised + neutropenia = risk of bacterial translocation (E.coli)
–Bacterial endotoxin → cascade of inflammatory cytokines → vasodilation, low CO, ↑vascular permeability
Parvo efx on Coags
Hypercoagulabilty; hyperfibrinogenemia;
– procoagulant efx of endotoxins/cytokines on vascular endothelium → antithrombin loss from GIT + antithrombin consumption/dilution
Causes of Acute abdominal pain
distension of hollow organs/capsule
ischemia
traction
inflammation 2nd to other causes
Pure transudate
grossly clear
TP < 2.5 g/dl
< 1000 U/L nucleated cells
hypoalbuminemia
portal venous obstruction
Modified Transudate
TP
cell #
examples
serous/serosangineous
TP 2.5-5g/dl
1000 - 5000 U/L nucleated cells
passive liver congestion/Liver dz
impaired lymphatic drainage
RS-CHF
Dirofilarisis
Neoplasia
Other examples: Torsions, diaphragmatic hernia, lymphoma
Exudate
TP
# cells
examples
cloudy
TP >3.5 g/dl
cell# > 5000-7000 neutrophils
most common with acute abd pain
can be septic OR nonseptic
Other examples: Chylohorax/Pyothorax
Fat soluable Vitamins
K-E-D-A
–GI works with liver and pancreas to absorb fat soluable vitamins
2 types of Pancreatitis
1: Interstital edematous pancreatitis
2: Necrotizing pancreatitis
Risk factors for Pancreatitis
K9 vs Fel
most causes = idiopathic
K9 = hypertriglyeridemia, endocrine dz, prior sx, hyperCa++, Duct obstruction, biliary reflux, trauma, drug reactions, dietary factors
Fel = less clear; GI/gallbladder disorders
– cats only have one pancreatic duct that joins bile duct
Acute Pancreatitis definition
–Premature activation of proteases in acinar cells
–Premature activation of trypsinogen to trypsin
–activates proenzymes = clincial manifestations
Pathphys of Actue Pancreatitis
If more than 10% trypsin activated (normal inhibitory enzyme has no affect) = pancreatic inflammation/peripancreatic fat necrosis
== Sterile peritonitis
What contributes to pancreatic inflammation?
Trypsin and chymotrypsin → inactivate neutrophil migration = production of Reactive Oxygen Species (ROS)/Nitric oxide
–Contribute to cell necrosis → increased capillary permeability = altered circulation = worse inflammation
–ultimately produce cytokines → vasodilation, hypotension, coags, fibrnolytic pathways → micro clots
Endocrinopathies at risk of Acute Pancreatitis
–DM
–hypothyroidism
–hyperadrenocorticism
Yorkies, mini schnauzers
Clin Path of Acute Pancreatitis
–Neutrophilic leukocytosis with Left shift
–Neutropenia possible
–Leukopenia = worse prognsis in cats
–thrombocytopenia, PT/PTT elevation
–Azotemia 2nd to dehydration/GI loses
–HypoAlb 2nd to GI loss/ sequestration
–Elevated Lipase levels
-fPLI/cPLI assays most sensitive for dx
“Shock Gut”
result of villi death from hypoxemia/vasocontriction
GIT relation with Immune System
GIT = major entry point for allergens/bacteria/virus pathogens
–Immune system cells and Mast cells located in GIT
–Constant state of inflammation due to innumerable antigens
–IBD = when inflammation becomes excessive enough to cause disease
–Intrinsic bacteria in GIT assist with normal digestive/absorption processes
–Also prevent pathogenic bacteria from colonizing in GIT
What receptors are located in CRTZ?
#5
Dopamine
Serotonin (5-HT3)
histamine (H1)
Muscarine (M1)
Neurokinin (NK1)
alpha-2 adrenergic
What pathways does the vestibular system stimulate in V+C?
Histaminergic and cholinergic pathways
Megaesophagus types
–regional or diffuse dilation of esophagus w/ minimal or nonexsistent peristalsis
Acquired vs congenital
Congential Megaesophagus
uncommon; 2nd to development abnormalities in young dogs
–golden/german shepherds/shar-peis
Acquired Megaesophagus
4 examples
Diagnostic test
2nd to other disorders affecting neuromuscular function
Ex; myasthenia gravis/hypothryoidism/lead toxicity/lupus
Dx; Acetylcholine receptor antibody test for MG
AHDS
Acute-hemorraghic diarrhea syndrome
Possibly anaphylactic reaction from enterotoxins/clostridium
–TP generally normal - lower value with hemoconcentration from dehydration/splenic contraction
Absorption of Non-fat molecules
Carbs/Protiens
–water soluable
Pancreas role in digestion
–Produce enzymes for chemical digestion of carbs/protiens/fats
–Lipase, Amylase, Proteases
Lymphatic system’s role in digestion
–Route of transport for Fats absorbed by GIT
–Fat goes into Lymphatic system → absorbed into lumen → chylomicrons (chyle) → interstitium → lymph capillaries → lymph vessles → empties in to Thoracid duct
Liver/Gallbladder role in digestion
Mechanical digestion of fat via emulsification
