GI Flashcards
1
Q
Describe the digestive system.
A
-GI tract = concentric muscle cylinders lined w epi
-accessory organs = teeth, tongue, salivary gland, liver, pancreas
2
Q
Describe the digestive system of diff species.
A
- 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)
3
Q
Describe the main functions of the GI tract.
A
- 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)
4
Q
Describe prehension.
A
*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
5
Q
Describe mastication.
A
*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
6
Q
Describe motility & its function in the GI tract.
A
-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
7
Q
Describe the involuntary & voluntary stages of deglutition.
A
- 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)
8
Q
Describe the steps of deglutition.
A
- 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
9
Q
Describe deglutition disorders.
A
-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)
10
Q
Describe the regulation of food intake.
A
*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)
11
Q
Describe agonist VS antagonist.
A
- 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
12
Q
Describe Ghrelin.
A
-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
13
Q
Describe salivary glands.
A
- Major
-parotid, mandibular, sublingual - Small
-ventral jaw, palate, pharyngeal, lip, zygomatic
*classified according to type of secretion:
>serous, mucous, seromucus
14
Q
Describe the saliva functions.
A
- 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)
15
Q
Describe saliva components and where they’re made.
A
-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
16
Q
Describe the regulation & stimulation of saliva secretions.
A
*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
17
Q
Describe the 4 gastric secretion mechanisms.
A
neurocine: secretions by enteric neurons that affect muscle cells, glands, blood cells
18
Q
Describe the regulation of gastric secretion.
A
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
19
Q
KNOW THE 5 ENDOCRINE GI HORMONES!
A
20
Q
Describe the 3 glandular zones of the stomach.
A
- Cardia = mucus
- Fundus = HCl, enzymes
- Pylorus = mucus
21
Q
Describe the different types of cells found in the stomach.
A
- 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
22
Q
Describe parietal cells.
A
-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
23
Q
Describe chief cells.
A
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
24
Q
Describe enteroendocrine cells.
A
-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
25
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)
26
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
27
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
28
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
29
Describe the 3 phases of gastric secretion.
1. Cephalic
-before food enters stomach
-sight, smell, thought, taste
2. Gastric
-induced by vagovagal reflexes from stomach to brain
-dilation of stomach
-presence of amino acids & peptides in GI lumen
3. Intestinal
-induced by presence of food in duodenum
30
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
31
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
32
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
33
Describe the sm intestine.
-lg surface area due to:
>plicae circulares, villi, microvilli
-base of villi = glands called ‘crypts of lieberkuhn’
34
Describe the cell types in the sm intestine.
1. Mature enterocytes/absorptive cells:
-absorb nutrients, secrete digestive enzymes & H2O, Cl, HCO3)
2. Goblet cells:
-secret mucus
3. Enteroendocrine cells:
-hormones like CCK, secretin, GIP
4. Paneth cells:
-antimicrobial enzymes & peptides
35
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
36
Describe peyers patch.
-immune surveillance of intestinal lumen
-generation of immune resp within mucosa
37
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
38
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
39
Describe the lg intestine.
1. Microbial metabolism
2. 1 layer cylindrical epi w crypts
3. Water absorption, vit
4. Goblet cells -> mucus
5. Secretion: sm volume, isotonic to plasma, mucin, bicarb, K rich (alkaline)
40
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
41
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
42
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)
43
Describe the liver functions.
1. Carbohydrates metabolism (gluconeogenesis, glycolysis)
2. Amino acid & protein metabolism (synthesis of plasma proteins)
3. Lipid metabolism (fatty acids oxidation, ketone bodies synthesis)
4. Storage (glycogen, lipids, vitamins, copper, iron)
5. Synthesis & secretion of bile acids, bile formation
6. Biotransformation (medicaments, xenobiotics, metabolism byproducts)
7. Synthesis of hormones & mediators
8. Synthesis of components of immune system
44
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
45
Describe the endocrine functions of the liver.
1. angiotensinogen = prohormone
2. thrombopoietin = hormone (GF)
3. IGF (insulin like GF) = IGF1 & 2
4. hepcidin = sm peptide hormone (iron homeostasis)
46
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)
47
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
48
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
49
Describe phase II outcomes.
-conjugative/synthetic addition of a lg, polar molecule *allows drug to be water soluble for renal excretion*
50
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
51
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%
52
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
53
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
54
Describe secretion of the pancreas.
-in acinus = primary saliva
-HCO3 in duct lumen
55
Describe proteases in the pancreas.
-protein-digesting enzymes harmful to pancreatic cells & synthesized as zymogen (inactive form)
56
Describe digestive enzymes made in the pancreas.
1. Peptidases (inactive)
-trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A & B
2. Nucleases
-ribonuclease, desoxyribonuclease
3. Amylase
-a-amylase
4. Lipase
57
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
58
Describe the impairment in pancreas secretion.
1. Pancreatic insufficiency
-insufficient production of digestive enzymes by exocrine pancreas = bad digestion
-CS: steatorrhea, polyphagia, weight loss
2. Pancreatitis
-acini destroyed (multi factorial) & replaced by CT bc auto digestion
-increased risk when eating garbage
59
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
60
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)
61
Describe proteins in the stomach.
-denatured in stomach
-partially hydrolyzed by pepsin
-final digestion & absorption of proteins in sm intestine
62
Describe lipids.
-amphipathic = hydrophobic hydrocarbon & hydrophilic carboxyl
EX: prostaglandins, steroid hormones, phospholipids, PAF, sphingomyelin
63
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)
64
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
65
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)
66
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
67
Describe what’s needed for efficient absorption.
*pores of tight junctions & water permeability along sm intestine & proximal lg intestine
EFFICIENT ABSORPTION:
-increasing resorption surface
-high blood perfusion
-permeability
-mucosa uptake mechanisms
68
Describe the intestinal absorption of monovalent ions & water.
-Na transport efficient = driving force for most transport processes
-K & Cl absorbed in sm intestine thru paracellular pathway
-most water absorption in sm intestine & less in lg intestine
69
Describe intestinal absorption of Ca, Mg, phosphate.
1. Ca
-calcitriol =
>increase apical Ca channel
>increase Calbindin synthesis
>increase Ca ATPase
2. Mg
-absorbed they Mg channels & paracellular
3. Phosphate
-thru Na/Phos symporter
70
Describe the intestinal absorption of Vit B12.
HC = haptocorrin (transporter) *secreted by saliva & swallowed*
IF = intrinsic factor
71
Describe the absorption of iron & vitamins in sm intestines.
A = iron
B = vitamins
72
Describe catabolic VS anabolic pathways.
1. Catabolic
-make (ATP) as a result of degradation of energy rich molecules
2. Anabolic
-combine sm molecules to more complex that use energy (ATP->ADP) & chemical reductions (NADH)
73
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
74
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
75
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)
76
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
77
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
78
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
79
Describe glycogenesis VS glycogenolysis.
1. Glycogenesis
-store glu as glycogen
-mobilize glu in absence of dietary source
-main store in muscle & liver
2. Glycogenolysis
-glycogen into glu
-glu mobilized from glycogen granules to be sent to blood & tissues
80
Describe pentose phosphate cycle.
-in cytosol
-hexose pathway
-no ATP made or consumed
-makes NADPH & pentose ribose 5-phos
81
Describe the functions of NADPH.
1. Source of electrons (reductases)
2. Carry electrons to ETC complexes
3. Reduce enzyme cytochrome P450 (steroid hormone)
4. Respiratory burst in phagocytic cells (NADPH oxidase makes reactive O2)
5. Synthesis of NO
82
Describe lipids.
-short & medium chain FA: into portal circ (bound to albumin) & reach liver
-chylomicrons:
>TAGs converted into FFA & glycerol by enzyme lipoprotein lipase = expressed at capillaries
>FFA stored as TAG (adipocytes) or used to make energy or stay in blood (bound to plasma protein)
83
Describe FA relevance.
1. Energy = fasting period - FA bound to albumin in plasma (FFA) to tissues (coming from adipose) -> oxidation (energy production)
2. Structural components = phospholipids & glycolipids in PM
3. Hormone precursors = prostaglandins
4. Energy reserve = TAG in adipose
84
Describe B oxidation of FA.
-make a lot of ATP & Acetyl Co A
85
Describe ketone body formation in liver.
-liver (mitochondria) converts ACoA from FA oxidation into ketone bodies:
>acetoacetate
>3 hydroxybutyrate
>acetone
(All imp source of energy during fasting)
-prolonged fasting = FFA mobilized from adipose to liver -> excess ACoA for ketone body formation
*in peripheral tissue ketone bodies converted into ACoA = enters TCA
86
Describe absorbed amino acids in liver.
1. Urea
2. Liver proteins
3. Plasma proteins
4. Systemic circ (muscles, etc)
87
Describe molecules that are derived from AA.
1. Serotonin (neurotransmitter/paracrine)
2. Melatonin (hormone)
3. Dopamine/NE (neurotransmitter)
4. Histamine
88
Describe peptides.
1. Oxytocin (made in hypothalamus)
2. ADH (made in hypothalamus - water balance)
3. Bradykinin (vasoactive)
4. Angiotensin II (vasoconstriction)
89
Describe polypeptides.
1. Gastrin (stomach hormone, stim secretion of gastric glands)
2. CCK (stim pancreas & liver secretion)
3. Glucagon (made by Alfa cells of pancreas)
4. ANP (reg BP)
90
Describe AA.
1. Glucogenic AA
-make TCA intermediates & enter TCA via oxaloacetate
2. Branch chain AA (BCAA)
-source of energy in muscle (dont enter TCA)
91
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
92
Describe the 2 plexus found in the enteric NS.
-autonomic NS
-in GI wall & regulate GI functions
1. Plexus submucosus
-regulate mucus secretion & food absorption
2. Plexus myentericus
-control muscular activity (tone/contraction rhythm)
93
Describe enteric neurons.
-secrete neurotransmitter from varicosities
-lengthy axonal branches
-spread to affect wide area (lg SA)
94
Describe the 3 types of enteric neurons.
1. Dogiel type I
-sm cell body & short dendrites
-motor neurons
2. Dogiel type II
-lg cell body & 1 or 2 long dendrites
-sensory neurons
3. Dogiel type III
-multi shaped & functions
95
Describe the sensory nerve cells.
-detect change in stimuli -> regulate function
-axons go to enteric nerve cells & to CNS
*mechanosensitive cells (mechanoreceptors) = recog stretching of intestinal wall or volume changes
*chemosensitive cells (chemoreceptors) = detect presence of nutrients in GI lumen, changes in osmolarity, changes in pH
>decode stimulus -> sensitization of endocrine cells
96
Describe interneurons.
-process signals coming from other nerve cells or from CNS & propagate them to other neurons (motor neurons)
97
Describe motor neurons.
-induce change in GI tract as answer to stimulus
1. Muscle motor neurons = plexus myentericus
2. Secreto motor neurons = plexus submucosus
3. Vaso motor neurons = both plexus
98
Describe the types of neurotransmitters secreted by enteric neurons.
1. Conventional
-NE, AcH
2. Non conventional
-non noradrenergic, non cholinergic (NANC)
>NO = inhibit motility of GI tract
>VIP (vasoactive intestinal polypeptide) = vasodilation & relax smooth muscle sphincters
>substance P = excitatory - increases secretion & motility of GI tract
99
Describe PSNS & SNS in the enteric NS.
1. PSNS
-uses Ach
-stim GI functions
-origin in medulla oblongata thru vagus nerve
-distal part of GI tract
-sacral spinal cord thru pelvic nerve
-postganglionic neurotransmitter = AcH & NANC
2. SNS
-NA (postgang)
-inhibitory effect on GI tract
-symp n fiber exit thru thoracic & lumbar seg of spinal cord
-preganglionic neurons = short axons
-postganglionic neurons = long axons to target organ
-spinal cord has sym gang chain
100
Clinical case.
101
Describe slow waves.
-GI tract contraction via rhythm determined by freq of slow waves in smooth muscle membrane potential (resting)
-NOT ACTION POTENTIAL
-caused by interstitial cells of Cajal (ICC)
>electrical pacemakers
>form network between smooth muscle cells
>cyclic changes in membrane potential due to ion channel currents
—gen slow waves
—stim spike potential
—stim muscle contraction
102
Describe spike potentials.
-action potentials
-occur automatically when resting membrane potential is more pos than -40mV
-higher slow wave potential rises = greater freq of spike potential
103
Describe the reflex in gut wall.
*for GI control*
1. reflexes in gut wall = control GI secretion, peristalsis, mixing contractions, local inhibitory effects
104
Describe reflex from gut to prevertebral sympathic ganglia & back to GI tract.
2. reflex from gut to prevertebral sympathetic ganglia & back to GI tract = transmit signals long distances to other areas of GI tract
a) gastrocolic reflex = stomach -> evacuate colon
b) enterogastric reflex = colon -> sm intestine (inhibit stomach motility & stomach secretion)
c) colonoileal reflex = colon -> inhibit emptying of ileal contents into colon
105
Describe the reflex from gut to spinal cord/brainstem & back to GI tract.
3. reflex from gut to spinal cord/brainstem & back to GI tract
-reflex from stomach & duodenum to brainstem & back to stomach = control gastric motor & secretory activity
-pain reflex = inhibiton of entire GI tract
-defecation reflex = from colon & rectum to spinal cord & back to make colonic, rectal, abdominal contractions
106
Describe the peristaltic reflex.
-stretching of intestinal wall during passage of bolus triggers reflex that constricts lumen behind bolus & dilates the lumen ahead of it
-coordination of longitudinal & circular musculature
-propulsive movement of chyme
*peristalsis = syncytial sm muscle cells
1. stretch of intestinal wall stimulates afferent neurons (mechanosensitive/receptor neurons) -> interneurons:
a) proximal to site of distention -> excitatory motor neurons stim -> Ach & substance P -> sm muscle contraction
b) distal to site of distention -> inhibitory motor neurons stim -> NO, ATP, VIP -> sm muscle relax
*direction of chyme propulsion (oral to aboral)
*coordinated directional movement circular & longitudinal do the opp
107
Describe the vagovagal reflex.
-afferent & efferent fibers of vagus n respond to gut stimuli via dorsal vagal complex in brain
-stim of mechanical receptors located in gastric mucosa stim vagus afferent fibers
-control contraction of GI muscle layers in resp to distension of tract by chyme
*reflex active during receptive relaxation of stomach in resp to mastication of food/deglutition
*food in stomach = reflex goes from stomach to brain & back to stomach = 'active relaxation' of sm m in stomach wall
108
Describe the functional regions of the stomach.
1. distal region = grinding function (gastric pump)
-breaks solid pieces of food into small intestinal digestion
2. proximal region = storage
-retain food as its waits for entry into sm intestine
109
Describe why inflow into the gastric pump happens.
1. tonic contraction of fundus (gastric store)
2. strong peristaltic wave in corpus
3. passage into grinder & pylorus
4. empty fluid & pre digested particles into duodenum
*interstitital cells of Cajal -> slow waves in smooth muscle -> spike potential & contraction of smooth muscle
110
Describe the functions of intestinal motility.
1. mix food w digestive juices (GI secretion)
2. enhance contact between intestinal wall & food
3. peristalsis = propulsive movement of chyme to distal (aboral) direction
111
Describe the 2 phases of motility in the sm intestine.
1. digestive period = food in gut
2. interdigestive period = little food in gut
112
Describe the digestive period.
1. peristaltic waves (propulsive pattern)
-fast aboral migrating contractions (fast to slow: duodenum->jejunum->ileum)
2. segmentation contractions (nonpropulsive pattern)
-localized contractions of circular muscle
-small seg of intestine contract tightly dividing gut into 2 seg (constricted & dilated lumen)
*doesnt contribute to net aboral propulsion but imp when nutrient conc is high
113
Describe the interdigestive period.
-time where stomach & sm intestine are empty between meals (80-120min)
-motility pattern = 'migrating motoric complex' MMC
>helps push undigested material out of intestine
>control bacterial pop
114
Describe the 3 phases of MMC.
Phase I = motoric rest, no contractions
Phase II = intermittent & irregular contractions
Phase III = strong peristaltic contractions from stomach & migrate to colon
115
Describe the motility patterns of the lg intestines.
*mixing activity in colon of all species
*horse & pig = colonic segmentation 'haustra sacculations'
1. peristaltic waves
2. antiperistatical waves = oral migrating contractions that impede the movement of ingest -> intense mixing activity
116
Describe pathologic contractions.
-giant contractions = high amp & long lasting contraction
1. oral migration -> vomit
2. aboral migration -> diarrhea
117
Describe vomiting.
-defense mechanism & CS activated to elim GI content
-reflex of striated m
-coordinated in brainstem
118
Describe vomiting stimuli.
1. before food intake (color, smell, emotion, look)
2. after food intake (particle in intestinal lumen) -> visceral efferents -> vomiting center
3. after absorption (particle in blood) -> stim chemoreceptor trigger zone (CTZ) in 'area postrema'
119
Describe the seq of events of vomiting.
1. antiperistaltic wave origin in duodenum
2. propulsion of ingest toward stomach
3. contraction of abdominal m to increase intra-ab pressure
4. expansion of chest cavity (glottis stays closed to lower intrathoracic pressure)
5. relax lower esophageal sphincter
6. open upper esophageal spincter
120
Describe diarrhea.
-increase in freq of defecation/fecal vol
-increased water content
-water in gut from:
>ingested water
>water secreted by glands of GI tract
>water secreted/lost directly thru mucosal epi
-through absorption in intestine - amount of secreted water exceeds amount ingested
-diarrhea = mismatch between secretion & absorption
121
Describe malabsorptive diarrhea.
-absorption inadequate to recover all secreted water
-viral, bacterial, protozoan infections
-destruct villi & reduce length (rate of cell loss higher than rate of replacement)
-shortened villi = loss absorptive intestinal SA
-mature enterocytes affected that have enzymes of BB & transport proteins
122
Describe secretory diarrhea.
-rate of intestinal secretion increases & overwhelms absorptive capacity
-pathogenic bacteria make enterotoxins & bind to enterocytes & stim adenylyl cyclase activity & production of cAMP -> opening of Cl channels
123
Describe defecation reflex.
*internal sphincter (sm m) & external sphincter (striated m)
-internal sphincter = parasym (sacral spinal seg) & sym (lumbar) innervated
>sym stim = constriction of sphincter
>parasym stim = relax sphincter
-internal sphincter = tonically contracted (continence)
-voluntary constriction of external anal spincter (block reflective activation of defecation) *trained animals*
124
Describe the retrosphincteric reflex.
-feces accumulate in rectum -> peristaltic movement of feces into rectum & relaxation of internal anal sphincter -> urge to defecate (contract colon & rectum & increase intra ab pressure)
125
Describe the ruminant stomach.
-fermentative digestion in forestomach (stratifed squamous) or after stomach & sm intestine (cecum & colon in horse)
-microbes resp for fermentative digestion = bacteria, fungi, protozoa
-enzymes for digestion are microbial origin (not made by host like monogastric animals)
-fermentation requires secretion, motility, temp
-fermentative digestion + regurg + remastication = finely divided material (greater SA for microbial digestion)
126
Describe the ruminal environment.
1. substrate availability = food intake regulated by vol, structure, energy, palatability
2. temp = 1 degree C above body temp
3. fluids = drinking water & saliva
4. pH = 5.5-7
127
Describe the ruminal ecosystem.
-protozoa ingest lg # of bacteria
-role in starch in protein digestion
-symbiosis
128
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
129
Describe carbohydrates VS lignin.
1. Carbohydrates = cellulose, hemicellulose, pectin
>hydrolyzed by cellulase
>monosaccharides released from polysaccharide
--monosaccharides not available for absorption by animal (further metabolized by microbes)
2. Lignin
-indigestible
130
Describe pyruvate.
-in aerobic & anaerobic bacteria
131
Describe proteins in ruminant digestion.
-proteins are vulnerable to fermentation bc they’re made of carbon = reduced to make energy for anaerobic microbes
-microbes make endopeptidases -> form short chain peptides as end products -> absorbed into microbial cell bodies -> peptides used to make microbial protein OR degraded to make energy (VFA pathway)
132
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*
133
Describe how AA enter the VFA pathway.
-AA must be deaminated first
-AA -> NH3 + carbon skeleton
-carbon structure of AA can be used for VFA synthesis
*exception is branch chain AA
134
Describe microbial proteins.
-a lot of dietary protein is fermented in rumen
-ruminant depends on microbial protein to meet needs
-microbes washed out of rumen = microbial protein reaches the abomasum & SI
-protein can be made in rumen from protein & non protein sources like: NH3, nitrates, urea
135
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
136
Describe urea recycling in mono gastric VS ruminants.
-monogastric = urea excreted by kidneys
-ruminants = urea excreted into rumen
>urea can be resynthesized into protein that contribute to AA -> under conditions of low dietary protein, ruminants conserve nitrogen
137
Describe fats & lipids.
-fats rare in plants
-microorganisms make enzymes for lipid digestion like lipases & phospholipases
-fats supplemented to increase ration energy density
-cattle diet has polyunsaturated fatty acids
138
Describe the different types of fast & lipids.
1. TAG = found in cereal grain, oilseed, animal fat, byproduct feed, milk
2. Glycoproteins = found in forages
3. Phospholipids = form cell membrane of animal cells & surface of milk fat globules
*imp in fat digestion in SI of cows
4. FFA = minor in dairy feed & major in fat supplements
139
Describe microbial lipases.
-fat hydrolization
-results in: glycerol, sugar, FFA
-glycerol & sugar -> VFA
*fatty acids synthesized in rumen & pass to abomasum & SI = absorption
140
Describe the concentration ratios in ruminants.
-typical acetic/propionic/butyric acid conc ratio = 70:20:10 (high forage diets) to 60:30:10 (high grain diet)
-
141
Describe what vitamins microbes synthesize.
-vit C, K, B
>VitB1 (thiamin) = deficiency after change in feed from roughage to concentrate
>VitB12 (cobalamin) - deficiency in cobalt poor soils or diets w too much grain
*calves/lambs cant synthesize vit so need supplement in diet (small fermentative activity)
142
Describe the common substances found in the rumen.
VFA, minerals (Na, Cl, Mg, Ca), buffers (H2PO4, HCO3), glu (small amount)
143
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
144
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
145
Describe the absorption of Na, K, Cl, Mg, Ca in rumen.
1. Na
-electrogenic transport = Na channel
-electroneutral transport = Na/H exchanger
-basolateral Na/K ATPase
2. Cl
-Cl/HCO3 exchanger
-basolateral channel
3. K
-apical & basolateral channel
-high luminal K+ conc
4. 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)
5. Ca
-basolateral Na/Ca exchanger & CaATPase
146
Describe the functions of the omasum.
1. Conc of ingest (absorption of water)
2. SCFA (VFA) absorption
3. Na & Cl absorption
4. HCO3 reabsorption
147
Describe rumen motility.
-walls of forestomach motile (ENS) -> motility patterns:
1. Mixing (primary contractions)
>function to reduce particle size of forage
2. Eructation (secondary contractions)
>function to force gas toward cr part of rumen
148
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
149
Describe frequency of contractions.
-1-3 recticulo rumen contractions per min
-more freq during eating & gone during sleep
-rate & strength of contraction depend on structure of diet
-fibrous feed = stim most freq & strongest contraction
150
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
151
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)
152
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
153
Describe gases in rumen motility.
-gases made during rumination = CO2 mostly & methane
-traces of nitrogen, oxygen, hydrogen (intermediates)
-eructation freq 1/min
-eructation center =
>in medulla
>receive afferent fibers from mechanoreceptors in dorsal sac of rumen (where gas accumulates)
154
Describe ruminants clinical correlations.
1. Tympanism
-bloating
-eructation fails
>blockage of esophagus
>impaired vagal n function
>rabies
>ingestion of legumes
2. Legume bloat
-cattle feed on alfalfa/clover pasture (waxy saponins)
-gas trapped & normal free gas cant go on top of dorsal sac of rumen
>presence of gas not detectable by mechanoreceptors of dorsal sac
155
Describe the control of reticulorumen motility.
-ENS & Vagus n
-stretch receptors, chemoreceptor -> monitor distention, consistency of ingesta, pH, VFA conc, ions
-control center for reticulorumen motility in brainstem (dorsal vagal nucleus) -> efferent go to rumen w Vagus n
156
Describe the esophageal/reticular groove.
-invagination of wall of reticulum from cardia to reticulo-omasal orifice
-diverts milk away from rumen & directly to abomasum
-reticular groove closure = reflex (brainstem impulse thru Vagus n) *in calves*
-afferent stimuli from central (anticipation of suckling -> Cephalic phase) & from pharynx (suckling)
-when stimulated, muscles of groove contract = close to form tube from cardia to omasal canal
157
Describe ruminant ketosis.
-hypoglycemia
-freq in high production dairy cows (6wk after calving/late gestation)
-acetate & butyrate enter Krebs:
*acetate, butyrate -> acetyl CoA -> citrate
(Occurs when theres enough oxaloacetate)
>if not enough or amount of acetyl co a is excessive (excess oxidation of fat) = accumulate as acetoacetyl co a & degraded to ketone bodies (acetone, acetoacetate, beta-hydroxybutyrate)
158
Describe hindgut fermentation.
-horse & rabbit rely on fermentation in colon for energy
-substrate for hindgut fermentation = structural & nonstructural carbohydrates & proteins
-fermentation products = VFA & absorption mechanisms like in ruminants
-ingesta pass thru stomach & SI -> lg intestine -> exposure to gastric acids & digestive enzymes = increase digestion rate in hindgut
-some proteins escape SI digestion & absorption = arrive in hindgut
-urea recycling into colon & cecum like in rumens
*horses cant recover & utilize microbial proteins (pass thru feces)
*cecotrophy in rabbits help recover microbial proteins
159
Describe the conditions for maintaining fermentation similar to the rumen.
1. Substrate supply
2. Control pH (buffers)
3. Osmolality
4. Anaerobiosis
5. Retention of fermenting material
6. Removal of waste product & residue
160
Describe the motility pattern in the cecum & ventral colon.
CECUM:
-mixing nature w low amp contractions that move ingesta from haustras
VENTRAL COLON:
-haustral segmentations
-propulsive peristalsis
-retropulsive peristalsis
-sm particles flow distal leaving ventral colon & big particles retained
161
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
162
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
163
Describe gut microbiota characterization.
-PCR = DNA extraction = predict bacteria functions
164
Describe micro biome products.
1. Amino acids
2. Neuroactive compounds/neurotransmitters
3. Microbial metabolites
4. Nutrients
165
Describe what alters micro biome.
-diet
-disease
-environmental exposure
-climate change
-stress
-land use change
-captivity VS free ranging
166
Describe metabolites.
-gut microbial associated metabolites translocate from intestinal lumen to organs thru circulatory system & induce tissue specific immune resp
-shapes immune resp:
>thru colonization of GI tract
>thru metabolites
*EX: intestinal colonization by segmented filamentous bacteria promote diff of CD4 Th17 cells
167
Describe the gut brain axis.
-microorganisms can induce host production of metabolites & neurotransmitters
-mediate gut brain signaling & made some neuroactive compounds themself
-microbial derived molecules signal to brain via neuronal pathways of vagus n or modulate immune system
EX: lactobacillus
