GI Flashcards
Describe the digestive system.
-GI tract = concentric muscle cylinders lined w epi
-accessory organs = teeth, tongue, salivary gland, liver, pancreas
Describe the digestive system of diff species.
- Carnivore = big stomach, short intestinal tract
- Ruminants = fermentation in forestomach
- Horse = fermentation in lg intestine
- Birds = food store (crop), glandular stomach (proventriculus), muscular stomach (gizzard)
Describe the main functions of the GI tract.
- Transport food
- Digest food into absorbable particles
- Absorption of food & transport into blood
- Regulation of water & electrolyte balance
- Immunologic barrier (GALT)
- Thermoregulation (fluid intake, panting)
Describe prehension.
*getting food into mouth
-species diff:
1. Horse = lips or incisors
2. Cattle = tongue & incisors
3. Goat & sheep = tongue & lips
4. Pigs = snout & mandible
5. Carnivorous = canine, incisors, forelimb
Describe mastication.
*1st act of digestion = teeth, jaw, tongue, cheeks
1. Carnivores
-sparse
-movement of manible is vertical
-molars & premolars in upper & lower jaws move like scissors
2. Herbivores
-long time masticating
-upper & lower jaws
-mastication movement horizontal
Describe motility & its function in the GI tract.
-after mastication, motility of diff GI tract seg is activated
-movement of GI functions:
1. Propel ingested food from one location to next
2. Retain ingested food for digestion, absorption, storage
3. Break up food physically & mix w digestive secretions
4. Circulate ingested feed = all portions in contacts w absorptive surfaces
Describe the involuntary & voluntary stages of deglutition.
- Voluntary (oral phase)
-food in oral cavity & molded into bolus
-tongue pushed back into pharynx
-food enters pharynx -> activate sensory nerve endings -> initiate involuntary part of deglutition - Involuntary (swallow reflex)
-in pharynx & esophagus -> directs food into digestive system (away from airway)
Describe the steps of deglutition.
- Soft palate elevated to close pharyngeal opening of nasopharynx preventing food from entering the internal opening of nostril
- Tongue is pressed against hard palate to close to oral opening
- Epiglottis moves back covering the entrance to the trachea preventing the movement of food into respiratory system
- Upper esophageal sphincter opens & food transported thru esophagus by peristaltic contractions = entrance to trachea reopened & respiration continues
Describe deglutition disorders.
-difficulty swallowing = neuromuscular disorder or mechanical obstruction
1. Dysphagia = 2 types
>oropharyngeal: bc malfunction of pharynx & upper esophageal sphincter
>esophageal: dysphagia bc of esophagus
2. Aspiration =
-food particles/fluid or stomach contents reach airways (can be result of dysphagia)
Describe the regulation of food intake.
*regulatory center for energy homeostasis = hypothalamus
-hunger center: nucleus paraventricularis, lateral hypothalamus, perifornical region
-satiety center: nucleus ventromedialis
1. Neuropeptides in hypothalamus
-stimulatory = neuropeptide Y (NPY), orexin
-inhibitory = melanocyte stimulating hormone (MSH) inhibit hunger & increase energy consumption
2. Non hypothalamic hormones
-stimulatory = ghrelin
-inhibitory =
>cholecystokinin (CCK)
>peptide YY (PYY)
>leptin (fat cells inhibit NPY release & activate MSH release)
>insulin (pancreas -> glu availability)
Describe agonist VS antagonist.
- Agonist
-function as reg hormone but more/less potent
-receptors bound by diff hormones
-diff agonists more/less potency when bound to receptors - Antagonist
-molecules bind to receptor & block binding of agonist
-receptor is nonfunctional
-block intracellular signaling events
-used as drugs
Describe Ghrelin.
-made in stomach by endocrine cells in muscosal epi of oxyntic glands in gastric fundus
-plasma ghrelin increases during fasting & decreases postprandially (after eating)
-function: increase appetite & food intake
Describe salivary glands.
- Major
-parotid, mandibular, sublingual - Small
-ventral jaw, palate, pharyngeal, lip, zygomatic
*classified according to type of secretion:
>serous, mucous, seromucus
Describe the saliva functions.
- Primary function:
-protect oral mucosa & teeth
-facilitate deglutition
-initiate enzymatic carbohydrate digestion (human & pigs -> amylase)
-pH regulation (HCO3) - Secondary function:
-immunologic function (lysozyme, lgs)
-thermoreg
-defense (alpacas)
Describe saliva components and where they’re made.
-99% water, electrolytes (Na, K, Cl, HCO3)
-in the ducts the secondary saliva (K, HCO3) made
-in acinus (glandular epi) the primary saliva (Cl, Na, H2O) made
*disturbance in saliva production = dry mouth, buccal ulceras, dysphagia, proliferation of bacterial pop
Describe the regulation & stimulation of saliva secretions.
*regulation primarily thru cholinergic signaling (AcH) & neuropeptides via para
1. Regulation:
-para -> M3 -> contract of myoepithelial cells (increase secretion, saliva more dilute)
-sym -> a1 -> secretion of sm vol of consistent saliva
2. Stimulation:
-innate (reflex) = contact w oral mucosa (mechanorecptors)
-conditioned = sight, smell, imagination of food
Describe the 4 gastric secretion mechanisms.
neurocine: secretions by enteric neurons that affect muscle cells, glands, blood cells
Describe the regulation of gastric secretion.
A digestive hormone must:
1. Be secreted by one cell & affect another
2. Be transported in blood
3. Be stimulated by food & action mimicked by a synthetic analog molecule
KNOW THE 5 ENDOCRINE GI HORMONES!
Describe the 3 glandular zones of the stomach.
- Cardia = mucus
- Fundus = HCl, enzymes
- Pylorus = mucus
Describe the different types of cells found in the stomach.
- Gastric pits = invaginations of glandular mucosa lined w mucus secreting cells at luminal surface
- Surface mucous cells = make thick mucus to protect stomach from acid
- Gastric gland = each gastric pit leads to this
- Parietal cells = located in neck of gastric glands
- Chief cells (zymogenic cells) = make proteolytic enzyme precursors like pepsinogen self replicating - not from stem cells
- Mucous neck cells = make less viscous secretion (thin mucus) to serve as progenitor cells for chief cells
- Stem cells = after division they migrate down/up into pit & differentiate into diff types of gastric pit cells
Describe parietal cells.
-secrete intrinsic factor (IF = glycoprotein) essential for vit B12 absorption in ileum
all functional cell types of gastric pit originate from stem cells in neck of gland
-injured cells make meta plastic cells that are preneoplasic (cancer cells)
-proton pump inhibitors decrease HCl
Describe chief cells.
zymogen granules
-adults:
Pepsinogen (proenzyme) -> active in stomach (acidic pH) pepsin (autoproteolysis) -> hydrolysis of proteins
-calves/lambs:
Prochymosine -> acidic pH in abomasum chymosine -> hydrolysis of milk
Describe enteroendocrine cells.
-secrete endocrine substances:
1. G cells -> gastrin
2. D cells -> somatostatin
3. I cells -> CCK
4. ECL cells -> histamine
*enteroendocrine cells secrete granules content (gastrin, histamine, somatostatin) into lamina propria then to blood capillaries
Describe mucus producing cells.
-mucins (glycoprotein) secreted by exocytosis -> protection & lube of mucosa -> surface mucosa regen 3-5 days (increase mitotic activity in isthmus of gastric pit)
Describe gastric acid secretion.
HCl secretion regulation:
1. Neural = mediated by AcH
2. Hormonal = mediated by gastrin
3. Paracrine = mediated by histamine
STIMULATORY:
>gastrin, histamine, AcH
INHIBITORY:
>somatostatin
Describe resting & stimulated stages.
RESTING:
-H/K ATPase limited access to apical membrane
STIMULATED: (via acid secretion)
-canaliculi fuse w apical (luminal) membrane & vesicles contain H/K ATPase go to apical membrane to increase HCl secretion
Describe secretion of gastric enzymes.
-enzymatic secretion stimulated via:
1. Neural (AcH, NA)
2. Hormonal (secretin, CCK)
>release of secretin & CCK from enteroendocrine cells of sm intestine depends on presence of food particles in intestinal lumen & pH
>amino acids & fatty acids -> CCK
>low pH -> secretin
Describe the 3 phases of gastric secretion.
- Cephalic
-before food enters stomach
-sight, smell, thought, taste - Gastric
-induced by vagovagal reflexes from stomach to brain
-dilation of stomach
-presence of amino acids & peptides in GI lumen - Intestinal
-induced by presence of food in duodenum
Describe the importance of mucus secretion.
-AcH & prostaglandin E (PGE) stim mucus secretion
>low pH -> AcH & PGE secretion -> mucus
>secretion altered by gastric acid & enzymatic secretion
-NSAID block synthesis of prostaglandins that promote formation of gastric ulcers
Describe gastric ulcers.
-gastric acid: HCl (pH 1-4)
>defense system to kill microorganisms (except H. Pylori)
>colonization of mucosa & neutralizes acid pH by making enzyme urease to produce bicarb
Describe gastric ulcers in horse/pig.
PH = 4-6
-colonize bacteria -> hydrolysis of carbohydrate in short chain fatty acids & lactate -> more acidic pH -> damage mucosa -> gastric ulcer
Describe the sm intestine.
-lg surface area due to:
>plicae circulares, villi, microvilli
-base of villi = glands called ‘crypts of lieberkuhn’
Describe the cell types in the sm intestine.
- Mature enterocytes/absorptive cells:
-absorb nutrients, secrete digestive enzymes & H2O, Cl, HCO3) - Goblet cells:
-secret mucus - Enteroendocrine cells:
-hormones like CCK, secretin, GIP - Paneth cells:
-antimicrobial enzymes & peptides
Describe Brunners glands.
-tubulo alveolar glands (submucosa)
-secrete mucus thru exocytosis
-secrete glycoproteins & bicarb ions
(PH of secretions = 8-9)
FUNCTION:
-sm intestine mucosa protection by neutralizing acid containing chime delivered from stomach
Describe peyers patch.
-immune surveillance of intestinal lumen
-generation of immune resp within mucosa
Describe cells of the crypt & regen.
-division & replication of enterocytes occur in crypts
-intestinal crypt cells regen & migrate up villi
-length of villi by rate of cell loss & replacement
>turnover time of enterocytes = 4-7 days
-progenitor cells arise from stem cell & differentiate into absorptive enterocytes or secretory goblet, enteroendocrine, paneth cells
>paneth cells move down into crypt
Describe sm intestine water movement.
-mediated via osmosis
-food entering is hyperosmotic or become after digestion
-osmotically active substances draw water from lateral space (paracellular) into intestinal lumen
-solutes absorbed on other side as water follows back thru epi into vascular system
-water moves to keep isomotic (low -> high)
-water reabsorption in sm intestine:
>lg solute reabsorption
>lg SA (villi & microvilli)
>lg opening in tight junctions
>capillary network in villi
Describe the lg intestine.
- Microbial metabolism
- 1 layer cylindrical epi w crypts
- Water absorption, vit
- Goblet cells -> mucus
- Secretion: sm volume, isotonic to plasma, mucin, bicarb, K rich (alkaline)
Describe the lg intestine in the immune system.
-cecum & colon = crypts but no villi lined by goblet cells & some absorptive epi cells (absorb electrolytes & water)
-base of crypts = stem cells
Describe the GI tract & nutrients movement.
-water & nutrients enter ECF then vascular system
-forces drive movement of solutes & water between extra/intravascular fluids via osmotic & hydrostatic forces
-absorbed nutrients enter capillaries by diffusion from interstitium (drives water to capillary)
-venous blood from GI tract (except terminal colon & rectum) collected into hepatic portal vein & pass thru liver to vena cava back to heart
-lymph drain from gut bypass liver entering blood thru thoracic duct
Describe the anatomy of liver.
-liver lobule: portal venule, arteriole of hepatic artery, bile duct -> sinusoids, hepatocytes, bile canaliculi
-endothelial wall: fenestrated -> passage of big molecule (glu, amino acids, etc)
Describe the liver functions.
- Carbohydrates metabolism (gluconeogenesis, glycolysis)
- Amino acid & protein metabolism (synthesis of plasma proteins)
- Lipid metabolism (fatty acids oxidation, ketone bodies synthesis)
- Storage (glycogen, lipids, vitamins, copper, iron)
- Synthesis & secretion of bile acids, bile formation
- Biotransformation (medicaments, xenobiotics, metabolism byproducts)
- Synthesis of hormones & mediators
- Synthesis of components of immune system
Describe the synthesis of plasma proteins.
-liver makes the body circulating plasma proteins
-albumins
-lipoproteins:
>VLDLs = transport of triglycerides from liver to other organs
>LDLs = transport of cholesterol esters from liver to other organs
>HDLs = remove cholesterol from peripheral tissue & transport to liver
-glycoproteins = haptoglobin, transferrin
-prothrombin & fibrinogen
-nonimmune alpha & beta globulins
Describe the endocrine functions of the liver.
- angiotensinogen = prohormone
- thrombopoietin = hormone (GF)
- IGF (insulin like GF) = IGF1 & 2
- hepcidin = sm peptide hormone (iron homeostasis)
Describe biotransformation.
-reactions that do conversion of toxic molecules in nontoxic, water soluble, & easier to excrete substances
-most drugs liposoluble (stay long in body)
-imp for termination of action & elimination from body
-liver is site of biotransformation (cytochrome P450) microsomal enzymes
-drug metabolism = increase polarity (more water soluble)
Describe the phase I & II.
Phase I: ‘oxidation’
-hydroxylation (add OH)
-carboxylation (add COOH)
-in sm ER & mitochondria
-reaction w cytochrome P450
Phase II: ‘conjugation’
-conjugation w glucuronic acid, glycine or taurine
-makes product of phase I more water soluble so it can be easily eliminated
Describe phase I outcomes.
-induce chemical change (oxidation) drug is more conducive to phase II
1. inactivation
2. activation from a ‘pro-drug’ to active form of drug
3. modification of activity = formation of active metabolites can have equal, greater, or lesser activity to that of the parent compound
4. formation of toxic metabolites
Describe phase II outcomes.
-conjugative/synthetic addition of a lg, polar molecule allows drug to be water soluble for renal excretion
Describe bile acid production.
-bile made in hepatocytes & is modified in epi cells of gallbladder
-gallbladder = bile storage & bile conc. thru electrolyte & water reabsorption
-bile acids synthesized from cholesterol & conjugated w amino acids (glycine, taurine) to make bile salts
>amphipathic & secreted into duodenum where they emulsify fat droplets in sm intestine
Describe the liver relationship with bile acids.
-bile excreted into common bile duct
-sphincter of smooth muscle cells ‘sphincter of oddi’ guards entrance of bile into duodenum
-bile stored in gallbladder (no digestion in duodenum)
-20% bile loss thru feces
-enterohepatic circ & hepatic syn of bile acids = 5%
Describe the emptying the gallbladder after a meal.
-high AA & FA in duodenum -> high CCK -> contraction of smooth muscle & relax of oddi sphincter
-reflex -> increase AcH -> contract of smooth muscle
Describe the structure of the pancreas.
2 glandular tissue:
>endocrine (secrete hormones)
>exocrine (secrete digestive enzymes)
—acinar gland (acini connected by ducts)
—looks like salivary gland
*vagus & CCK stim pancreatic enzymes
Describe secretion of the pancreas.
-in acinus = primary saliva
-HCO3 in duct lumen
Describe proteases in the pancreas.
-protein-digesting enzymes harmful to pancreatic cells & synthesized as zymogen (inactive form)
Describe digestive enzymes made in the pancreas.
- Peptidases (inactive)
-trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A & B - Nucleases
-ribonuclease, desoxyribonuclease - Amylase
-a-amylase - Lipase
Describe the hormones of the pancreas.
-pancreatic cells have receptors for AcH, CCK, secretin
*adjusted by food
-AcH & CCK stim secretion of enzyme & Cl rich fluid
-secretin stim bicarb rich secretion
*high starch = high amylase
*high fat & protein = high lipase & peptidase
Regulation:
Cephalic, gastric, intestinal phase
Describe the impairment in pancreas secretion.
- Pancreatic insufficiency
-insufficient production of digestive enzymes by exocrine pancreas = bad digestion
-CS: steatorrhea, polyphagia, weight loss - Pancreatitis
-acini destroyed (multi factorial) & replaced by CT bc auto digestion
-increased risk when eating garbage
Describe carbohydrate functions.
*most abundant
FUNCTIONS:
1. Energy
2. Store energy
3. Cell membrane component (communication)
4. Structural component (cell wall of bacteria)
-all carbohydrates made from monosaccharides
>disaccharides = linked by glycosidic bonds
>oligosaccharies = 3-10 mono
>polysaccharides = 10+ mono
Describe carbohydrates in digestion.
*humans & pigs digestion of carbohydrates in mouth = amylase
-dietary carbohydrates = starch, glycogen, sucrose, lactose
-digestion of carbohydrates via pancreatic enzymes & finished by enzymes in intestinal mucosa
-absorption of carbohydrates in duodenum & upper jejunum via:
>Na dependent transport mechanism (SGLT1) at apical membrane
>facilitated transport mechanisms at apical (GLUT5) & basolateral membrane (GLUT2)
Describe proteins in the stomach.
-denatured in stomach
-partially hydrolyzed by pepsin
-final digestion & absorption of proteins in sm intestine
Describe lipids.
-amphipathic = hydrophobic hydrocarbon & hydrophilic carboxyl
EX: prostaglandins, steroid hormones, phospholipids, PAF, sphingomyelin
Describe emulsification of lipids.
*in duodenum
GOAL:
1. Reduce size of lipid droplets
2. Increase SA of hydrophobic lipid droplets
-both imp for lipase function which binds at interface droplet/aqueous solution
-bile acids emulsify fat droplets
>bile acids (liver) have sterol ring w side chain of amino acid (taurine/glycine)
Describe the digestion of lipids.
*dietary lipids: cholesterol esters, phospholipids, triglycerides
-lipid digestion start in stomach (gastric lipase)
-bile acids emulsify lg fat drops
-emulsified fat drops too lg to enter space between microvilli
-pancreas lipases hydrolyze triglycerides into monoglycerides & FFA
Describe mixed micelles.
-monoglycerides, FFA, cholesterol, liposoluble vit = mixed micelles
-mixed micelles approach BB of enterocytes & absorbed
-short chain FA dont form mixed micelles (can be directly absorbed)
Describe what happens once the mixed micelles are absorbed.
-LCFA go into ER for re-esterification (resynthesis) of more complex lipids:
MAG + FFA -> TAG
-chylomicrons released by exocytosis into lymphatic vessels -> thoracic duct -> L subclavian vein -> blood
Describe intestinal absorption of Ca, Mg, phosphate.
- Ca
-calcitriol =
>increase apical Ca channel
>increase Calbindin synthesis
>increase Ca ATPase - Mg
-absorbed they Mg channels & paracellular - Phosphate
-thru Na/Phos symporter
Describe the intestinal absorption of Vit B12.
HC = haptocorrin (transporter) secreted by saliva & swallowed
IF = intrinsic factor
Describe the absorption of iron & vitamins in sm intestines.
A = iron
B = vitamins
Describe catabolic VS anabolic pathways.
- Catabolic
-make (ATP) as a result of degradation of energy rich molecules - Anabolic
-combine sm molecules to more complex that use energy (ATP->ADP) & chemical reductions (NADH)
Describe the first stage of energy metabolism.
absorptive phase
-during active digestion & absorption of nutrients from gut
-insulin released
-glu taken up by liver & converted to glycogen & FA
-FA sent out of liver in VLDL to adipose tissue or muscle
-AA used for protein synthesis or deaminated for gluconeogenesis
Describe the second stage of energy metabolism.
post absorptive phase
-between meals
-nutrients being mobilized from storage pools to tissues
-glucagon released
-glycogenolysis & gluconeogenesis stim
-AA mobilized from muscle
Describe the third stage of energy metabolism.
prolonged energy deficiency
-food deprivation
-glu & AA conserved
-FA mobilized in form of non esterified FA (NEFAs)
-form ketone bodies in liver (mitochondria)
Describe glycolysis.
-portal blood -> glu to liver
-glu transport into cells via GLUT (tissue specific & insulin induced)
-ATP producing pathway
>with O2 = 2 pyruvate + 2 NADH + 2 ATP
—pyruvate to mitochondria to make AcoA that enters TCA
—NADH oxidized during ETC (regen of NAD+)
—ETC: 3 ATP made for each NADH oxidized
>without O2 = 2 lactate + 2 ATP
—RBCs & muscle take advantage of anaerobic glycolysis
Describe TCA.
-final pathway where carbohydrates, AA, & FA converge
-energy made by TCA
-TCA occurs close to ETC (both in mitochondria)
-aerobic (O2 used as electron acceptor in ETC)
-makes NADH & FADH2
Describe gluconeogenesis.
-production of glu from non sugar molecules like AA, lactate, glycerol
-fasting = hepatic glycogen stores depleted & glu made from precursors other than carbohydrates
-NOT REVERSE GLYCOLYSIS
-requires enzymes localized in mitochondria & cytosol
-imp tissue for gluconeogensis = liver & kidney
*glycerol -> glycerol phos
*lactate -> pyruvate
*AA -> TCA -> oxaloacetate
Describe pentose phosphate cycle.
-in cytosol
-hexose pathway
-no ATP made or consumed
-makes NADPH & pentose ribose 5-phos
Describe the enteric NS structure.
-GI smooth muscle function as syncytium
-cells arranged in bundles of 1000 parallel fibers & sep by loose CT
-within bundles = electrically connected via gap junctions
Clinical case.
Describe the fate of carbohydrates, proteins, lipids in ruminant.
-chemical structure of VFAs (acetic acid, propionic acid, butyric acid) made by fermentative digestion
-cell wall of plants have carbohydrates = imp substrate for fermentative digestion
*all dietary proteins & carbohydrates subjected to fermentative digestion in forestomach -> products: glu, other monosaccharides, short chain polysacc released in fluid phase -> glu & sugar not available to host (absorbed into cell body of microbes) -> in microbial cell, glu enters glycolytic pathway -> make 2 pyruvate from 1 glu & 2 NADH & 2 ATP used by microbes -> fermentative digestion (anaerobic) = products are VFA/SCFA
Describe protein metabolism by rumen microbes.
-proteases on microbe surface make peptides
-intracellularly = peptides hydrolyzed into AA
-amino acids contribute to:
>synthesis of microbial protein
>metabolized to VFA & NH3 (ammonia)
AA also synthesized intracellularly from VFA & NH3
Describe urea recycling.
-urea = nitrogen waste product of protein catabolism
>syn in liver of ruminant from 2 sources:
1. Urea from deamination of endogenous AA
2. Nitrogen absorbed as NH3 from rumen
Describe the concentration ratios in ruminants.
Describe absorption of VFA in the rumen.
-2 mechanisms depending on ionization state of VFA:
1. Ionized VFA (Ac-): cant diffuse, need carrier (HCO3-/Ac-antiport)
2. Nonionized (HAc): lipophilic, diffuse thru apical membrane
Describe rumen acidosis.
-fermentable carbohydrates (starch rich diet) = increase in VFA -> pH in rumen more acidic
-ionization grade of VFA depends on pH of rumen (normal pH 5.5-7)
-VFA = pK 4.8 (50% ionized & 50% nonionized)
-acidic pH in rumen stim prolif of lactate making bacteria -> exacerbation of acidosis
Describe the absorption of Na, K, Cl, Mg, Ca in rumen.
- Na
-electrogenic transport = Na channel
-electroneutral transport = Na/H exchanger
-basolateral Na/K ATPase - Cl
-Cl/HCO3 exchanger
-basolateral channel - K
-apical & basolateral channel
-high luminal K+ conc - Mg
-electrogenic transport = Mg channel (depends on potential difference between apical & basolateral side)
*high K conc (young pasture/K+ fertilized pasture) -> grass tetany (hypo magnesium) - Ca
-basolateral Na/Ca exchanger & CaATPase
Describe primary contractions.
A. Bolus enters rumen & stays in area near cardia (has air bubbles)
B. Biphasic contraction of reticulum
1) first contraction is weak
2) second contraction is forceful (bigger particles pushed in dorsal sac)
C. Cd moving contraction of dorsal sac moves ingesta into dorsal sac
D. Cr moving contraction of dorsal sac mixes ingesta -> bacterial fermentation -> makes gas in dorsal sac
E. Small particles in ventral sac
F. Contraction of ventral sac sep big & small material -> small goes over cr pillar to cr sac
G. Contraction of cr sac sep material into big & sm
H. Reticulum contract -> reticulo-omasal orifice relax & sm particles (dense) forced thru opening into omasum
Describe digestibility and feed.
-digestibility & physical characteristic of feed influence rate of particle passage from rumen & rate of feed intake
-poorly digested fiber = longer to break down compared to good quality
Describe secondary contractions.
-occur at end of primary contraction cycle
1. Cr moving contraction starting in cd-dorsal blind sac
2. Forward moving contraction of dorsal sac -> moves gas forward the cardia -> gas enter esophagus & eructated (burp)
Describe the regurgitation reflex.
-function to bring lg particles from rumen back to mouth to be chewed (reduce particle size)
1. Begin w contraction at mid-dorsal rumen -> pushes gas cap cd & big particles toward cardia
2. Lower esophageal sphincter relaxes & bolus enters the esophagus & propelled to mouth by anti peristalsis
*1 regurgitation every few min
Describe glucose homeostasis in ruminants.
-carbohydrate digestion in ruminants occur in forestomach thru fermentative digestion -> no digestible carbohydrate enters intestine
-glu from gluconeogensis
-imp precursor of glu in ruminants = VFA propionate
-propionate enters Krebs cycle at level of succinate
>4 C intermediate that leads to formation of oxaloacetate = entry metabolite for gluconeogenesis
-almost all propionate absorbed from rumen extracted from portal blood by liver & never enters sys circ
-ruminants conserve glu
-FA syn in adipose tissue using acetate as precursor molecule & never glu
-insulin levels reg by conc of VFA
-ruminants in constant state of potential glu deficiency
-high producing dairy cows = glu they make goes to lactose (milk sugar) & remaining tissues function on diff fuels
Describe micro biome.
-microorganisms colonizing host = distinct physio-chemical properties
-bacteria, archae, fungi, algae, small protists
*dominant phyla depend on species, early life exposure, diet
-vary on location & host species
EX:
>termite hindgut micro biome
-degrade cellulose backbone of wood & nitrogen fixation
>cats
-obligated carnivore
-doesnt make enzymes needed for cellulose degradation
