Digestion Flashcards
GASTRIN function
Stimulate
- gastric-, oancreatic juice secretion
- motility, endyme secretion
- growth of intestinal mucosa
- fascilitate pyloric pump
CCK function
Inhibit
- gastric emptying and motility
Fuction of VIP, GIP, secretin and enteroglucan
Inhibit
- gastric juice secretion
(secretin = gastrin antagonist)
Stimulate
- pancreatic-, and intestinal juice secretion
- gall secretion
Neurohormonal regulation
Central neural regulation:
chewing, swallowing, defecation
Neurohormonal regulation
Peripheral neural regulation:
gastric, pancreatic, bile secretion, gastrointestinal motility, intestinal juice production
secretion of pepsinogen stimulated by
vagus
low blood sugar
HCl secretion (by histamines)
direct way of regulating secretion of gastric juice
vagus stim parietal cell to prod HCl
indirect way of regulating secretion of gastric juice
G-cells prod gastrin
H-cells prod histamine
–> these bind to receptor or parietal cell to prod HCl
name the aromatic amino acids and by which enzyme at which pH cleaves them
tyr
his
phe
pepsin, 1,8-3,8
Amino peptidases:
Cleave an amino-acid from the N-terminal of the peptide
Dipeptidases:
Cleave dipeptides into amino acids
Dipeptidil-aminopeptidases:
Cleave dipeptides from the N-terminal of the peptides
Na+ symport systems on luminal side of enterocytes tp these proteins
Are responsible for the transport of neutral amino acids, phe, met, pro and hydroxyproline
By facilitated transport on the luminal side of enterocytes transport these proteins
Hydrophobic neutral amino acids and alkaline amino acids
where are APUD cells found and what are they
specialized cells of the gastrointestinal tract and pancreas with endocrine function. They produce gastrointestinal hormones or peptides
what triggers depolarization in spike potential in GI
stretching of the smooth mm cell
acetylcholine from nerve endings
PS mimic
specific GI hormones
what triggers hyperpolarization in spike potential in GI
adrenaline in blood
noradrenalin from nerve endings
specific GI hormones
why is the blood leaving the stomach slightly alkaline?
HCl secretion triggers HCO3⁻ tp to interstitium
gastric secretion regulation
direct/indirect
cephalic phase
gastric phase
intestinal phase
gastric secretion; how does the secretion of the different substances occur
acetylcholine/chemical stimulis:
G-cells, H-cells, parietal cells ->gastrin, (histamin->) HCl -> pepsinogen
block of H2 receptor
cimetidin
block of acetylcholine binding to receptors
antropine
what are inhibiting factors of gastric juice secretion
- dilation of duodenum (slow down further evacuation)
- earlier mentioned hormones
- chyme being strongly acidic, hyperosmotic or rich in lipids
stimulating factors of GI dilation an the function
VIP, Gastrin, secretin, cholecystokinin
1 - slow down further evacuation
2 - increase digestion and absorption
lack of B12 leads to
anaemia
how is the activation of proenzymes activated
enteropeptidase: trypsinogen -> trypsin
trypsin: activate other enzymes
activation = cleaving enzymes
main functions of bile
emulsifying -> digestion of fats
secretion of metabolic end products and antibodies into the bile -> excretion
primary bile acids and their conjugation, where?
LIVER
cholic acid + glycine/taurine -> glycocholic acid, taurocholic acid
chenodeoxycholic acid
the function of the conjugated bile acids
(bile acids: COOH- dissociate in alkaline pH)
conjugated bile acids dissociate at physiological pH
–> increased water solubility and efficiency of bile acids in emulsifying lipids
pancreatic lipase can only digest lipids at the water/lipid interphase!!
2’ bile acids and their function
cholic acid -> deoxycholic acid
chenodeoxycholic acid -> lithocholic acid
increaced lipid solubility- > increased absorption of the bile acids into enterohepatic circulation
the main regulators of bile secretion
increased bile secretion
- n. vagus
- cholecyctokinin (CCK prod)
stimulate bile production and inhibit bile salt synthesis
- bile salts into enterohepatic circulation
- secretin
- -> diluted bile
what enzyme cleave an alpha-1,4-glucosidic bond in the oral cavity (glucose)
ptyalin (salivary amylase)
what transporters are needed for fructose, glucose and galactose to be transported into the blood stream?
fructose - GLUT-5
glucose/galactose - first co-tp with Na⁺ then GLUT-2 once inside cell
end product of fermentation of cellulos
mostly VFA - but in RU also urease is produced by hydrolizing carbmine
End products of carb digestion used in ruminant pH regulation
ABSORPTION
VFA incr. absorption if the pH in rumen decrease
LACTIC ACID (from easily digested carbs), usually little content in rumen but if sudden increace acidosis occur - damage to mucosa
AMMONIA from fermentation of protein and urea, decreased absorption if pH decrease
what are triglycerides(lipids) digested into
2 fatty acids and 1 2-monoglyceride
+bile salts -> micelle
chylomicron
micelle diffuse into cell -> sER
2-monoglyceride + fatty acids -> triglyceride
— > cholesterol and phospholipid -> cholemicron
cholemicron + apolipoproteins -> tp and metabolism is now possible (too big to enter caps) -> exocytocis on basolat side -> lymph caps -> thoracic duct -> blood -> entothelial cell -> fat tissue for storage/use in muscle tissue
brush border digestion of proteins:
peptidases (endo or exo) into tri/di peptides/free aa’s
8-10 Na⁺/Aa. co-transporters at luminal border
and fascilitated diffusion
peptide digestion by which hormone where
(all produced in pancreas!!)
stomach - pepsin (aromatic) small intestines - trypsin (arg, lys) - carboxypeptidases (free C-terminals) - chemotrypsin (tyr, phe)
increased Na⁺ absporption by hormones
large/small intestines - glucocorticoids
colon - aldosterone
sodium incr -> K⁺ increase as well
what incr/decr food intake in birds
incr: egg prod, low temperature
decr: high temp and high protein content in food
what birds have gall bladder
hen duck goose
pidgeon guinea fowl doesnt
when is the resp quotent incr./decr
incr: acidosis(resp compensation), hyperventilation
decr: after exercise - O2 dept
The 4 motility functions of the reticulum
- Create liquid flow to cranial sac
- Less dense/fermented material in reticulum to dorsal sac
- Reg flow to omasum
- Make Regurgitation possible by filling cardia and caudal sac
(Dilate to let cardia above liquid level for eructation,
Motility contractions start from reticulum)
Glands and products of bird stomach
Glandular part:
Mucous gland - mucin
Complex gland - HCl, pepsinogen and mucin
Motility of the avian stomach
Primary contraction
Gizzard -> duodenum -> gizzard -> glandular stomach (-> duodenum)
Secondary contraction
Gizzard contract -> content into glandular stomach
Avian cecum, functions
- Mixing contractions and propolsive contractions (stronger, peristalsis and antioeristalsis)
- Microbial fermentation, VFA absorption ONLY
- Water absorption from urea solution
Avian vs rabbit re-injestion of feces function
COPROPHAGIA
Rabbit: proteins, microbial vitamins
Birds: end-prods of microbial digestion and vitamin supply
Factors of the endocrine system that increase the metabolic rate
Adrenalin
Noradrenalin
Growth hormone
Thyroid hormone (incr secretion)
Describe the combination of direct and indirect method of calorimetry
CO2 and O2 consumption + heat production of animal is measured
–> gives exact and reliable data
Excrete(O2) and temperature(prod) is also measured
Respiration quotent, normal value
CO2/O2 (vol/time)
0,7-1,0
Circa value bc.: Gas prod/consumpt are influenced by many factors
Qualitative
How can we measure the amount of oxidized carbs/fats/proteins
N excrete in urine and expired CO2 and inspired O2
Acclimasation aka
Shift of the thermoneutral zone
How does calorigenic effect from thyroid hormones affect the body heat
It prolongs the effect of the heat production by incr. BMR
Name the 3 factors of dry heat loss
Conduction
Convection - air/water touching body
Radiation
Receptor of heater cells allowing the leakage of calcium
Modified Ryanodine receptor
Calcium from SR -> countinous activation of the calcium pump -> heat
Epinephrine and thyroxine incr pump activity
- futile cycle process
