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VTS ECC 2024 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Mechanical vs Chemical Digestion

A

Mechanical; GIT movements to physically breakdown food
Chemical; reaction needed to break bonds of macromolecules to be small enough for absoprtion across intestinal membrane

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2
Q

CNS regulation of GI functions

PANS vs SANS

A

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

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3
Q

Submucosal plexus

A

controls secretions/blood flow

lenght of GIT

Meissners plexus

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4
Q

Myenterix Plexus

A

Smooth muscle controls movements of GIT

length of GIT

Auerbach Plexus

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5
Q

Chloecystokinin (CCK)

Stimulate by
What does it inhibit?
Where is it located?

A

–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

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6
Q

Gastrin

What is it secreted by?
What does it stimulate?

A

Hormone secreted by G-cells (endocrine cells) in pyloric region
stimulates gastric emptying

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7
Q

Cardiac Sphincter

A

thickening @ gastric end of esophagus that prevents acids from stomach back flowing/refluxing

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8
Q

Visceral peritoneum

A

Covers organ surfaces

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9
Q

Parietal peritoneum

A

lines body wall

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10
Q

Mesentary

A

connecting peritoneum that suspends intestines from abd. wall
innervated with blood vessels and nerves

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11
Q

Omentum

A

double layered connecting peritoneum that links stomach to abdominal wall/other organs
contains fat

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12
Q

Gastric circulation

A

Main blood supply → celiac artery (1st branch of abdominal aorta)
Veins leaving stomach join portal vein → travels to liver

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13
Q

Rugae

A

transient gastric folds/mucosa
allows stomach to expand
↑ surface area for absoprtion

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14
Q

Gastric mucosa structure

A

simple columnar epithelium → contains surface mucous cells to produce mucus = protects lining from acidity

Gastric ulcers form from inadequate mucus production

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15
Q

Glandular cells in Stomach

#4

A
  1. Mucus neck cells → secretes thin mucus near duct opening → divides/creates new cells
  2. Parietal cells → gastric glands → secrete H+/Cl- in lumen
  3. Chief cells → secretes pepsinogen (inactive form of pepsin) → converts to pepsin via stomach acid (HCl) → initiates chemical digestion
  4. G-cells → located in pyloric region → secrete gastrin → stimulates gastric emptying
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16
Q

“pacemaker” of the stomach

A

–specialized smooth muscle cells in stomach/intestine
–regulates contraction of gastric/intestinal smooth muscle
–no constant resting membrane potentials
–regulated by ANS

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17
Q

Autonomic nervous system efx on GIT

A

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

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18
Q

Emesis

Which receptors are involved?

A

–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

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19
Q

2 phases of Chemical digestion

A
  1. luminal → lg macromolecules breakdown into short polymer chains (Hydrolysis)
  2. Membranous chemical digestion
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20
Q

Hydrolysis

A

chemical reaction where bond is broken down by insertion of H2O molecule

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21
Q

Amylase

A

Pancreatic Enzyme that breaks down starch carbohydrates into maltose

found in saliva/small intestine

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22
Q

Small Intestine tract pathway

A
  1. Duodenum → recieves chyme differentiated between ascending/descending. Ends @ duodenojejunal flexure
  2. jejunum → longest part of SI → bulk of chemical digestion/absorption takes place
  3. Ileum → end of SI; “peyers patches” aggregates lymphoid tissue. controlls bacteria populations; ends @ ileocecal junction
23
Q

Small Intestine microanatomy

#2

A

–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

24
Q

Small intestine secretions

A
  1. CCK → cholecystokinin triggers your gallbladder and pancreas to contract
  2. Secretin → lowers HCl production in stomach and increases panc/biliary HCO3 secretion
25
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
26
Myocarditis efx from Parvovirus
Rare; but seen in neonates immature myocytes still rapidly dividing
27
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
28
Parvovirus; Biochem findings
Hypoproteinemia hyperbilirubinemia Elevated AlkPhos/ALT low electrolyes hypoglycemia Pre-renal Azo
28
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
29
Parvo efx on Coags
Hypercoagulabilty; hyperfibrinogenemia; -- procoagulant efx of endotoxins/cytokines on vascular endothelium → antithrombin loss from GIT + antithrombin consumption/dilution
30
Causes of Acute abdominal pain
distension of hollow organs/capsule ischemia traction inflammation 2nd to other causes
31
Pure transudate
grossly clear TP < 2.5 g/dl < 1000 U/L nucleated cells hypoalbuminemia portal venous obstruction
32
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 ## Footnote Other examples: Torsions, diaphragmatic hernia, lymphoma
33
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 ## Footnote Other examples: Chylohorax/Pyothorax
34
Fat soluable Vitamins
K-E-D-A --GI works with liver and pancreas to absorb fat soluable vitamins
35
2 types of Pancreatitis
1: Interstital edematous pancreatitis 2: Necrotizing pancreatitis
36
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
37
Acute Pancreatitis definition
--Premature activation of proteases in acinar cells --Premature activation of trypsinogen to trypsin --activates proenzymes = clincial manifestations
38
Pathphys of Actue Pancreatitis
If more than 10% trypsin activated (normal inhibitory enzyme has no affect) = pancreatic inflammation/peripancreatic fat necrosis == Sterile peritonitis
39
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
40
Endocrinopathies at risk of Acute Pancreatitis
--DM --hypothyroidism --hyperadrenocorticism ## Footnote Yorkies, mini schnauzers
41
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
42
"Shock Gut"
result of villi death from hypoxemia/vasocontriction
43
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
44
What receptors are located in CRTZ? | #5
Dopamine Serotonin (5-HT3) histamine (H1) Muscarine (M1) Neurokinin (NK1) alpha-2 adrenergic
45
What pathways does the vestibular system stimulate in V+C?
Histaminergic and cholinergic pathways
46
Megaesophagus types
--regional or diffuse dilation of esophagus w/ minimal or nonexsistent peristalsis Acquired vs congenital
47
Congential Megaesophagus
uncommon; 2nd to development abnormalities in young dogs --golden/german shepherds/shar-peis
48
Acquired Megaesophagus | 4 examples Diagnostic test
2nd to other disorders affecting neuromuscular function | Ex; myasthenia gravis/hypothryoidism/lead toxicity/lupus ## Footnote Dx; Acetylcholine receptor antibody test for MG
49
AHDS Acute-hemorraghic diarrhea syndrome
Possibly anaphylactic reaction from enterotoxins/clostridium --TP generally normal - lower value with hemoconcentration from dehydration/splenic contraction
50
Absorption of Non-fat molecules
Carbs/Protiens --water soluable
51
Pancreas role in digestion
--Produce enzymes for chemical digestion of carbs/protiens/fats --Lipase, Amylase, Proteases
52
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
53
Liver/Gallbladder role in digestion
Mechanical digestion of fat via emulsification

VTS ECC 2024 (17 decks)

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