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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
Q

Canine Parvovirus pathogenesis

What cells does it affect?
When do CS start?
When is shedding detected?

A

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
Q

Myocarditis efx from Parvovirus

A

Rare; but seen in neonates
immature myocytes still rapidly dividing

27
Q

Parvovirus; CBC findings

A

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
Q

Parvovirus; Biochem findings

A

Hypoproteinemia
hyperbilirubinemia
Elevated AlkPhos/ALT
low electrolyes
hypoglycemia
Pre-renal Azo

28
Q

Parvo Sepsis/SIRS compications

A

–intestinal integrity compromised + neutropenia = risk of bacterial translocation (E.coli)
–Bacterial endotoxin → cascade of inflammatory cytokines → vasodilation, low CO, ↑vascular permeability

29
Q

Parvo efx on Coags

A

Hypercoagulabilty; hyperfibrinogenemia;
– procoagulant efx of endotoxins/cytokines on vascular endothelium → antithrombin loss from GIT + antithrombin consumption/dilution

30
Q

Causes of Acute abdominal pain

A

distension of hollow organs/capsule
ischemia
traction
inflammation 2nd to other causes

31
Q

Pure transudate

A

grossly clear
TP < 2.5 g/dl
< 1000 U/L nucleated cells
hypoalbuminemia
portal venous obstruction

32
Q

Modified Transudate

TP
cell #
examples

A

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

33
Q

Exudate

TP
# cells
examples

A

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

34
Q

Fat soluable Vitamins

A

K-E-D-A
–GI works with liver and pancreas to absorb fat soluable vitamins

35
Q

2 types of Pancreatitis

A

1: Interstital edematous pancreatitis
2: Necrotizing pancreatitis

36
Q

Risk factors for Pancreatitis

K9 vs Fel

A

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
Q

Acute Pancreatitis definition

A

–Premature activation of proteases in acinar cells
–Premature activation of trypsinogen to trypsin
–activates proenzymes = clincial manifestations

38
Q

Pathphys of Actue Pancreatitis

A

If more than 10% trypsin activated (normal inhibitory enzyme has no affect) = pancreatic inflammation/peripancreatic fat necrosis
== Sterile peritonitis

39
Q

What contributes to pancreatic inflammation?

A

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
Q

Endocrinopathies at risk of Acute Pancreatitis

A

–DM
–hypothyroidism
–hyperadrenocorticism

Yorkies, mini schnauzers

41
Q

Clin Path of Acute Pancreatitis

A

–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
Q

“Shock Gut”

A

result of villi death from hypoxemia/vasocontriction

43
Q

GIT relation with Immune System

A

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
Q

What receptors are located in CRTZ?

#5

A

Dopamine
Serotonin (5-HT3)
histamine (H1)
Muscarine (M1)
Neurokinin (NK1)
alpha-2 adrenergic

45
Q

What pathways does the vestibular system stimulate in V+C?

A

Histaminergic and cholinergic pathways

46
Q

Megaesophagus types

A

–regional or diffuse dilation of esophagus w/ minimal or nonexsistent peristalsis
Acquired vs congenital

47
Q

Congential Megaesophagus

A

uncommon; 2nd to development abnormalities in young dogs
–golden/german shepherds/shar-peis

48
Q

Acquired Megaesophagus

4 examples
Diagnostic test

A

2nd to other disorders affecting neuromuscular function

Ex; myasthenia gravis/hypothryoidism/lead toxicity/lupus

Dx; Acetylcholine receptor antibody test for MG

49
Q

AHDS
Acute-hemorraghic diarrhea syndrome

A

Possibly anaphylactic reaction from enterotoxins/clostridium
–TP generally normal - lower value with hemoconcentration from dehydration/splenic contraction

50
Q

Absorption of Non-fat molecules

A

Carbs/Protiens
–water soluable

51
Q

Pancreas role in digestion

A

–Produce enzymes for chemical digestion of carbs/protiens/fats
–Lipase, Amylase, Proteases

52
Q

Lymphatic system’s role in digestion

A

–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
Q

Liver/Gallbladder role in digestion

A

Mechanical digestion of fat via emulsification

VTS ECC 2024 (17 decks)

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