Gastrointestinal Flashcards

1
Q

What are the major functions of the gastrointestinal system? (4)

A
  1. digestion
  2. absorption
  3. excretion
  4. host defense
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2
Q

Components of the GIT (6) and accessory components (3)

A

mouth, pharynx, esophagus, stomach, small intestine (duodenum, jejunum, ileum), large intestine

accessory components: pancreas, liver, gallbladder

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3
Q

explain the structure of the lumen

A
  • the inside of the GIT tube.
  • many folds and processes to increase the surface area - circular folds are where the entire inner surface folds in on itself.
  • folds contains villi that project into the lumen, and crypts that project below the surface
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4
Q

explain the structure and function of the layers of the GIT (4)

slide 14-17

A

1.Mucosa:

  • epithelium: single layer of cells
  • lamina propria
  • muscularis mucosa: thin layer of smooth muscle

2.submucosa: beneath the mucosa layer, contains blood vessels, lymphatic vessels, submucosal nerve plexus, connective tissue

3.muscularis externa:

  • circular muscle: fibers in a circular pattern, contract and relax to open and close tube
  • myenteric nerve plexus: network of nerve cells that regulate muscle function
  • longitudinal muscle: lengthens and shortens to control the length of the tube

4.serosa: connective tissue layer that encases intestine and forms connections with intestine and abdominal wall

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5
Q

functions and structure of the epithelial layer of the mucosa

slide 10

A

functions:

  • selective uptake of nutrients, electrolytes and water
  • prevent passage of harmful substances
  • stem cells within crypts divide and produce daughter cells which differentiate into a variety of cells

structure:

  • polarized cells; contains apical surface (lumen facing), and basolateral surface (blood facing). Transport proteins exist at each surface due to tight junctions.
  • surface area amplified by villi (single layer of epithelial cells containing microvilli) and crypts.
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6
Q

2 pathways that chemicals or molecules can use to get across an epithelial layer

A
  1. paracellular pathway - chemicals move through cell junctions, tight junctions allow only water and small ions diffuse
  2. transcellular pathway - two step process; requires a transport protein on the apical and basolateral surface of the cell
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7
Q

How is blood supplied to the GI system?

A
  • blood supply carries away water-soluble nutrients and other molecules for usage at other sites in the body
  • blood entering the GIT is highly oxygenated, loses oxygen as it perfuses intestine
  • liver: unusual organ, receives blood from both venous and arterial circulation. it is perfused mostly by blood that has already perfused another organ.
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8
Q

Portal circulation - process, functions, components

A

process: the portal circulation carries nutrient-rich blood from the GIT to the liver via the portal vein before returning to the heart

functions: removing harmful substances (liver acts as filter with many enzymes), and processing of nutrients

components: hepatic artery - contains fully oxygenated blood that perfuses the liver. hepatic portal vein -perfuses liver with blood that has already perfused the organsof the GIT

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9
Q

What is unusual or different about the portal blood circulatory pathway?

A
  • liver is different from other organs in the body as it isn’t perfused by arterial (fully oxygenated) blood. (30% arterial blood when not eating, 10% when eating)
  • hepatic artery contains fully oxygenated blood that perfuses liver and hepatic portal vein carries blood to the liver that has already perfused stomach, pancreas, SI and LI. These two blood supplies mix, so that the liver is perfused with nutrient-rich, poorly oxygenated blood.
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10
Q

reflexes regulating GI processes are initiated (4) and propagated (3) by:

A

initiated by:
1. distention of wall by volume of luminal contents
2. osmolarity of contents
3. pH of contents
4. concentrations of specific digestion contents (monosaccarides, fatty acids, peptides and aa’s)

propagated by:
1. mechanoreceptores (pressure, stretch)
2. osmoreceptors (change in osmolarity)
3. chemoreceptors (specific chemicals)

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11
Q

Intrinsic Neural Regulation of GI processes

A

occurs through enteric nervous system

  • Myenteric plexus: found between circular and longitudinal muscle of muscularis externa, responsible for influencing and regulating smooth muscle
  • submucosal plexus: found in submuscosa, predominantly influences secretion

constant communication between these two layers

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12
Q

Role of the ANS in the regulation of GI activity

A

extrinsic pathways - long GI reflex

  • nerve fibers from PS and S pathways enter the GIT and synapse w/ neurons in both plexuses

influences motility and secretion of the GIT by:
1. hunger - 2. sight/smell of food - 3. emotional state

parasympathetic: stimulates flow of saliva, stimulates peristalsis and secretion, stimulates release of bile

sympathetic: stimulates flow of saliva (small amounts, thick), inhibits peristalsis and secretion

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13
Q
  • be able to explain how the short and long reflexes act together to activate the GIT (refer to diagram on slide 29) *
A
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14
Q

What is meant by enteric nervous system

A

refers to intrinsic nerve regulation - short GI reflex

  • controls the activity of the secretomotor neurons which play a role in secretion and motility
  • contained completely in walls of GIT
  • brain of the gut - large # of neurons
  • can function independantly of CNS
  • critical for involuntary functions; allows digestion without thought
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15
Q

Role of the GI hormones in regulation of GI activity? (4)

A

each participates in a feedback control system that regulates an aspect of the GI lumen and has an effect on more than one cell

Secretin:

  • released by S cells in the SI
  • release stimulated by acid in the SI
  • decreases acid production and stomach motility, increases HCO3-/H2O from pancreas and in bile

Cholecystokinin (CCK):

  • triggered by fatty and amino acids in the SI, secreted from I cells in SI into blood
  • stimulates pancreas to increase digestive enzyme secretion, increases bile acids for fat breakdown, decreases HCl
  • CCK release is stopped due to removal and uptake of fats and aa’s

Gastrin:

  • released by by G cells in the stomach
  • release stimulated by peptides/aa’s in stomach and parasympathetic nerves
  • increases HCl production, and GIT motility

GIP:

  • released by K cells in SI
  • release stimulated by glucose or fat in SI
  • increases release of insulin
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16
Q

What is meant by neurocrine, endocrine, paracrine and autocrine?

A

the 4 categories of chemical messenger regulation:

Neurocrine - a nerve cell sends an electrical signal that then releases neurotransmitters that act on another neuron or effector cell

Endocrine - a hormone-secreting cell releases hormones across the basolateral surface into the blood, which then travel through blood vessels to target cells in one or more distant places in the body

Paracrine - local cells release paracrine substances that travel through IF and target cells in close proximity; occurs across the apical surface of the cell into the lumen of the gland

Autocrine - local cells release autocrine substances that act on the same cell that released it

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17
Q

What type of muscle activity occurs in the GI tract? What are properties of smooth muscle?

A

Peristalsis (Propulsion)

  • circular muscle contracts above a bolus (food) - longitudinal layer relaxed
  • contracted CM moves toward the anus, contents propel in that direction; CM on the other side of the distended area relaxes - longitudinal muscle contracts = smooth passage of bolus

Properties of smooth muscle:

  • ability to contract/relax causes contents to move along tract smoothly

Segmentation (mixing):

  • contraction and relaxation of SI that allows mixing of contentx w digestive enzymes and absorption of nutrients + water. Little net movement toward LI occurs
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18
Q

basic electrical rhythm

A
  • set by slow waves - pacemaker cells throughout GIT smooth muscle cells; constant spontaneous depolar./repolar.
  • slow waves propagated through through gap junctions in muscle layers
  • excitatory hormones/neurotransmitters further depolarize the membrane to threshold = muscle contraction

frequency of contractions = basic electric rhythm
force of contraction = neural and hormonal input

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19
Q

How is ingestion of food regulated in the digestive tract

A
  • feeding centre: lateral region of hypothalamus ~ activation increases hunger. satiety centre: ventromedial region ~ activation results in fullness

orexigenic factors - increases intake

  • neuropeptide Y (neurotransmitter)
  • ghrelin: from endocrine cells in stomach during fasting + stimulates NPY release in hypothalamus

anorexigenic factors - decreases intake

  • leptin: from fat tissue
  • insulin: from pancreas
  • peptide YY: intestines
  • melanocortin: hypothalamus
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20
Q

How is water intake regulated? (4 factors)

A
  1. increased plasma osmolarity - eating salt/exersice (+ thirst)
    - osmoreceptors&thirst centre stimulated
    - vasopressin (antidiuretic) released; conserves water @ kidney
  2. decreased plasma volume (+ thirst)
    - stimulates baroreceptors in cardio. system to increase angiotensin II
  3. dry mouth and throat (+ thirst)
  4. prevention of over hydration (- thrist)
    - person stops drinking well before water is absorbed by GIT
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21
Q

Phases of Gastrointestinal Control (3)

A
  1. Cephalic (Head) - receptors in the brain stim (sight, smell, taste/chewing of food, emotional state) PS fibers activate neurons in GI nerve plexuses
  2. Gastric (Stomach) - receptors stim. by distension, acidity, aa’s and peptides. Short and long neural reflexes mediate the response (ie. gastrin and acetylcholine)
  3. Intestinal - receptors stim. by distention, acidity, osmolarity and digestive products. mediated by short and long neural reflexes and by hormones secretin, CCK and GIP.

aa’s - amino acids

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22
Q

Major salivary glands (3) and how is their structure related to function?

A
  1. Parotid (water/serous secretion)
  2. Submandibular (serous/mucous secretion)
  3. Sublingual (mucous)
    - one of each gland on either side of the face

structure:

  • glands are made up of many microspopic ducts that branch out from grossly visible ducts
  • smooth muscle and epithelial cells push saliva from acinus into duct

functions:
- important for protein, electrolyte and water secretion
- important for creating alkaline and hypotonic secretion

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23
Q

What are major components of saliva and why are they important (5)

A
  1. Water (97-99.5%)
    - hypotonic, slightly alkaline (contains bicarbonate)
  2. Electrolytes
    - rich in K+ and HCO3-
    - poor in Na+ and Cl-
  3. Digestive enzymes
    - amylase (digests starch), lipase (digests fat)
  4. Glycoproteins
    - mucin [mucin + water = mucus]
  5. Other components
    - anti-microbial factors (lysozyme, lactoferrin)

Adult produces ~ 1500mL of saliva/day

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24
Q

How is saliva produced? Explain cells involved + their transport systems

A
  1. Acinar Cells ~ initially secrete an isotonic saliva (due to leaky cells)
    - proteins released by exocytosis
    - Cl-, HCO3- and K+ are released by AS
    - Na+ and H2O follow paracellularly via leaky tight junctions
  2. Myoepithelial Cells ~ contract & expel formed saliva from acinus into duct
  3. Ductal Cells ~ modify the initial saliva to a hypotonic, alkaline state
    - loss of Na + & Cl- (AT/reabsorption)
    - addition of K+ and HCO3- (AS)
    - cells tightly joined, impermeable to water

AT - active transport
AS - active secretion

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25
Q

How is salivation regulated?

A

0.5mL/min, can increase by 10-fold following stimulation

  • PS and S both stimulate salivary secretion; PS predominant pathway
  • PS stim. increases blood flow to glands → increases secretion & release of proteins from acinar cells, and stim. myoepithelial cells for contraction → increases flow

PS pathway stimulated by:
1. smell & taste
2. pressure receptors in mouth
3. nausea
Inhibited by: fatigue, sleep, fear, dehydration, some drugs

  • S effects: same as PS but with modest increase in saliva flow
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26
Q

What is the relationship between salivation and blood flow through the salivary glands? Are the salivary glands essential for life?

A

increased blood flow → increased salivation

salivary glands are not essential for life however conditions can arise from not being able to produce saliva (xerostomia) such as:
- dry mouth
- decreased oral pH leading to tooth decay or esophageal erosions
- difficulty lubricating and swallowing food
- poor nutrition (not related to poor digestion)

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27
Q

What roles/functions does saliva have in the digestion of food? Are they major or minor pathways for digestion?

A
  1. starch digestion: enzyme amylase (ptyalin) ~ inhibited at acidic pH in the stomach
    amylase cleaves internal alpha-1,4 linkages of glucose polymers amylose and amylopectin
  2. lingual lipase: breaks down fat, acid stable & active in stomach

overall amylase and lingual lipase are minor pathways for digestion

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28
Q

Xerostomia

A

“dry mouth”

caused by: birth defects, autoimmune process, some drugs, radiation treatment

consequences: dry mouth, decreased oral pH (tooth decay, esophageal erosions), difficulty in lubricating and swallowing food, poor nutition

treated by: frequent sips of water and fluoride

29
Q

functions of saliva (6)

A
  1. moistens and lubricates food
  2. initiates digestion: amylase and lingual lipase
  3. dissolves a small amount of food: allows diffusion to taste buds ~ affects appetite and food intake
  4. antibacterial actions: prevents microbial colonization
  5. aids in speech
  6. buffering action: HCO3- neutralizes acid
30
Q

How does food pass from the mouth to the stomach (4)? (explain swallowing and motility through the esophagus (3))

A

peristalsis is the main driving force of swallowing
Swallowing - reflex initiated by pressure receptors in the walls of the pharynx

  1. tongue pushes food bolus to the back of the pharynx
  2. soft palate elevates to prevent food entering the nasal passages, larynx raised, swallowing center inhibits respiration
  3. epiglottis covers glottis to prevent food or liquid entering trachea
  4. food decends into the esophagus

Esophagus - transfers food from mouth to stomach (18-25cm tube)

  • skeletal muscle = upper 1/3, lower 2/3 = smooth muscle
  • Food passes rapidly - no absorption, mucous glands for lubrication
  • specialized epithelium (“stratified squamous” 20-30 cells thick)
  • Upper esophageal sphinchter: ring of skeletal muscle below pharynx guards entrance into esophagus
  • Lower esophageal sphinchter: ring of smooth muscle at stomach
    sphinchters closed except when swallowing, vomiting and burping
  1. Relaxation of UES - food passes, sphincter closes, glottis opens, breathing resumes
  2. Peristaltic waves moves food down esophagus (1 wave 5-9s)
  3. LES opens, allows food into stomach, sphincter closes

UES - upper esophageal sphinchter
LES - lower esophageal sphinchter

31
Q

What happens when acid gets into the esophagus? How can heart burn occur?

A
  • peristalsis stimulated
  • salivary secrection increases

heartburn can occur due to an inefficent sphincter (not closing properly), after a big meal or during pregnancy (pressure on sphincter; opens)

32
Q

What are the functions of the stomach? (7)

A
  1. storage of food
  2. mechanical breakdown of food
  3. chemical breakdown of food:
  4. secretes pepsinogen (precursor for pepsin - protein digesting enzymes)
  5. secretes HCl (dissolves food, partially digests macromolecules, sterilizes food)
  6. control the rate at which food enters the SI
  7. secretes IF (critical for absorption of vitamin B12)

reduces food to Chyme

IF - intrinsic factor

33
Q

Is the stomach essential for life? Why/why not

A

Not essential

Issues:

  • no regulation of amount of food that enters SI
  • anemia: stomach produces IF that aids vit B12 absorption
  • stomach sterilizes food and bacteria
34
Q

What are the names of the different regions of the stomach (2)? Major and minor exocrine secretions

A
  1. Fundus/body - functionally and anatomically similar, thin layer of smooth muscle that secretes mucus, pepsinogen and HCl
  2. Antrum - thicker smooth muscle layer, secretes mucus, pepsinogen and gastrin

Major secretions:

  • Mucus (protect epithelium)
  • HCl (protein hydrolysis)
  • Pepsinogen (digestion of proteins)

Minor secretions

  • IF (B12 absorption)
  • Gastrin (HCl prod and stomach motility)
  • Histamine (HCl prod)
  • Somatostatin (inhibits HCl prod)
35
Q

What cell types are present in the gastric glands and what do they do? (5)

A

1.Cheif cells
- gastric glands in all regions
- secrete pepsinogen (pepsin precursor)

2.G-cell
- gastric glands in antrum
- secrete gastrin horomone (stim. HCl prod & GI motility)

3.Enterochromaffin-like (ECL) cells
- gastric glands in all regions (more in antrum)
- secretes histamine (stim. HCl release)

4.D-cells
- gastric glands in all regions (more in antrum)
- secrete somatostatin (HCl inhibitor)

5.Parietal Cell - oxyntic cell
- gastric glands in fundus/body
- secretes HCl and IF: requires energy, lots of mitochondria

canaliculi: increase surface area of the cells and maximize secretion into the stomach lumen - active secreting cell has a better defined “canaliculus”

36
Q

Why does the stomach produce an extremely strong acid? What is the process for this production (5 components, 4 channels involved)

A

0.1M HCl - Lumen (pH 1)
- important for digestion

in parietal cells:
H+/K+ ATPase (apical)
- pumps H+ into lumen in exchange for K+ into the cell, AT, electroneutral

Carbonic anhydrase (CA) - cytosol
- catalyzes formation of carbonic acid
- carbonic acid dissociates into H+ (secretion into lumen) and bicarbonate (4 passage across other membranes)

Cl-/HCO3- exchanger (baso)
- excess HCO3- removed from cell in exchange for Cl- by SAT
- critical for maintenance of neutral cellular pH

K+ channels (apical)
- K+ recycled back into stomach lumen; diffusion through channel, loss of + charge

Cl- channels (apical)
- Cl- leaks back into stomach lumen; diffusion through channel, compensates for loss of + charge by K+

AT - active transport

37
Q

How is acid secretion regulated? How does the stomach protect itself?

A

4 chemical messengers regulate H+/K+ ATPase:

  • Gastrin (gastric horomone): (+) acid secretion
  • Acetylcholine (neurotransmitter): (+) acid production
  • Histamine (paracrine) - potentiates effects of gastrin and ACh, (+) acid secretion
  • Somatostatin (paracrine) - (-) release of acid, gastrin and histamine

Pepsinogen: secreted as inactive precursor by ENS, activated by low lumen pH, precursor prevents autodigestion

ENS - enteric nervous system
(-) - inhibits
(+) - stimulates

38
Q

What are the major factors which regulate gastric secretion and how do these factors work together after a meal is eaten?

A

Parietal cell produces acid: ACh, histamine, and gastrin (+) acid production, somatostatin (-)

Ach (+): stimulates release of gastrin from G-cells (+PC), stimulates ECL cells to release histamine (+PC), inhibits somatostatin release from D-cells (-PC)

Gastrin (+): stimulates histamine from ECL cells (+)

once acid secretion is high:

  • as eating, ACh stimulated by PS nerves is reduced - reduces (-) on somatostatin
  • somatostatin (-) acid secretion by: (-) histamine and gastrin
  • acid (-) gastrin release

PC - parietal cell
+ stimulant/stimulant
- inhibitor/inhibition

39
Q

What is meant by cephalic, gastric and intestinal phases of secretion?

A
  1. Cephalic: stimulation in the brain mainly via vagus nerve to stomach (sight, smell, taste) -> aceytlcholine increases acid prod.
  2. Gastric: major - occurs when food reaches the stomach, gastrin increases acid
  3. Intestinal: inhibitory phase - food that is partially broken down enters SI, due to presence of acid, fat digestion products and hypertonic sol., secretin and CCK have a (-) effect on gastrin prod.
40
Q

How is food moved into, through and out of the stomach?

A

into:

  • upon consumption SM relaxes by PS nerve stim to ENS - stomach stretches

through:

  • arriving food causes peristaltic waves - weak in stomach, strong in antrum; mixes contents, closes PyS
  • small amt of contents released into duodenum, most forced back towards body of stomach - mixes contents w enzymes & acid
  • BER: slow pacemaker cells; do not cause significant contraction, but sets frequency of contraction - strength of contraction determined by stimulatory input to antral SM cells

  • PyS is just before the SI
  • PyS: pyloric sphincter
  • BER: basic electrical rhythm
41
Q

What sometimes causes the gastric contents to move in the opposite (retrograde) direction, ie. vomiting

A
  • GIT disturbances (infection/distension/obstruction)
  • motion sickness/inner ear infection
  • Chemoreceptors in brain/GIT (detects alcohol, toxins etc.)
  • Pressure on CNS
  • Psychogenic (sights, smells etc.)

All stimuli feed into vomiting centre in medulla oblongata

42
Q

How does the structure of the pancreas relate to its dual role as an exocrine gland and an endocrine gland?

slide 122, 123

A

Main pancreatic duct: drains exocrine secretions into SI
- joins w common bile duct from liver just before duodenum
- similar to salivary glands: acinar cells @ end of the duct - produce digestive enzymes (exocytosis), duct cells produce water and bicarbonate

Sphincter of Oddi: b/w bile duct & MPD
- regulates release of liver and pancreatic contents into SI

Exocrine pancreas: secretions ultimately enter SI

Endocrine pancreas: ductless, cells surround capillaries
- i.e insulin; pancreatic islets produce horomone insulin

exocrine - secretion of substance locally through ducts to an apical epithelial surface
endocrine - ductless, release substances that travel through bloodstream (basolateral) and go to distant places
MPD - main pancreatic duct

43
Q

What are the major constituents of pancreatic juice and why are they important?

A

isotonic and alkaline
electrolytes:

  • high in HCO3- and low in Cl-, bicarbonate neutralizes acid in duodenum
  • Na+ and K+ conc. *same as plasma *(isotonic)
  • HCO3- and water (duct cells)

digestive enzymes: (acinar cells)

  • important for digestion of proteins, carbs, fats and nucleic acids
  • proteolytic enzymes - stored and secreted in inactive forms; activated in duodenum (prevents self-digestion)

isotonic: concentration of solutes inside cell = outside cell

44
Q

Why and how does the pancreas secrete an alkaline juice?

slide 126

A

in pancreatic duct cells:

  1. Chloride channel opens: allows diffusion of Cl- into duct lumen
  2. Cl- in lumen exchanged for HCO3- in cell by CFTR - carbonic anhydrase catalyzes formation of carbonic acid (dissociates into H+ and HCO3-) from CO2 and water, base leaves cell
  3. Neutral pH of cytosol maintained by Na+/H+ exchanger: SAT dependant upon electrochemical greadient generated by Na+/K+ ATPase
  4. H2O and Na+ follow paracellularly in response to Cl- electrochemical gradient across epithelium

results in water alkaline secretion, neutralizes gastric acid and washes digestive enzymes through

CFTR - cystic fibrosis transmembrance cunductance regulator
SAT - secondary active transport

45
Q

What is meant by “alkaline tide” and “acid tide”?

A

following a meal

in the stomach, acid (HCl) enters lumen
alkaline tide: large amounts of bicarbonate are pumped across basolateral surface of parietal cells in the stomach into blood

in pancreas, base moves into lumen of pancreatic ducts
acid tide: large amounts of acid are pumped across basolateral surface of duct cells in pancreas into blood

46
Q

What role does the pancreas play in digestion of food?

A

1.Source of majority of enzymes for digestion:
- proteases: proteins → peptides + aa’s
- amylolytic enzymes: starch → sugars
- lipases: triglycerides → free fatty acids & monoglycerides
- nucleases: nucleic acids → free nucleotides

2.Packaging & Precursors
- acinar cells produce and pack pro-enzymes into zymogen granules that are stored at apical pole of cell

zymogen granules - inactve precursor enzymes

47
Q

What is autodigestion and how is it prevented? Is the pancreas essential for life?

A

autodigestion: enzymes not stored in inactive forms in the pancreas that start to digest the cell it is in

Proteases
Trypsinogen: activates by
Chymotrypsinogen
Pro-elastase
Pro-carboxy peptisdase A&B

  • pancreas is essential→ starvation would occur without, bc cannot digest and absorb food in GIT
48
Q

How is secretion of pancreatic juice regulated?

A

epithelial layer of duodenum:
1.S cells: (+) by acid to produce of secretin → released in blood to (+) pancreatic duct cells → releases HCO3-
- stomach acid is neutralized & release of secretin is stopped (NFCS)

2.I cells: (+) by digested fats and proteins to produce CCK → released into blood, (+) acinar cells in pancreatic duct which (+) zymogen granules
- fats and amino acids are absorbed, release of CCK is stopped due to their removal (NFCS)

3.Parasympathetic nerves: cause release of enzymes when hungry and smell food

  • Secretin and CCK inhibit gastrin secretion which reduces stomach motility and acid secretion

  • zymogen granules release digestive enzymes
  • NFCS: negative feedback control system
  • (+): stimulate(d)
49
Q

Functions of the liver (4)

A
  • exocrine gland; makes and secretes bile
  • metabolizing and storing nutrients (supply & demand)
  • deactivation & detoxification
  • producing circulating proteins
50
Q

How is the structure of the liver related to it’s role as an exocrine gland?

slides 148-152

A

Gall Bladder: small sac under lobule of liver
Bile ducts: branches running from the liver, join underneath to form common hepatic duct, then joins with the common bile duct
Main pancreatic duct: joins with common bile duct, release their contents into duodenum (controlled by SoO)

Blood flow: recieves mix of blood from both systemic (arterial blood, 25%) and portal circulation (venous blood, 75%)

Lobule: units of liver, hexangonal, central vein runs through center (carries mixed blood), portal triad in each corner
- portal triad: hepatic artery, hepatic portal vein, bile duct

  • hepatocytes: epithelial cells of liver, produce bile and place in canalicular networks, networks join to form bile ducts. blood flow occurs on other surface of hepatocytes

exocrine glands: secrete products into ducts which carry substance to specific locations
SoO: Sphincter of Oddi

51
Q

What is bile made of? How is it produced? What’s it’s role?

A

bile is an exocrine secretion consisting of:

  1. bile acids (breaks down fat)
  2. cholesterol
  3. salts (Na+, K+, and HCO3-) and water
  4. bile pigments
  5. phospholipids
  6. trace metals

formation of bile:
- hepatocytes: produce/secrete bile acids, phospholipids, cholesterol and bile pigments into canaliculi
- bile duct cells add HCO3, salts and water to bile
- gallbladder: stores and concentrates bile, expels into duodenem after meal

role is to digest fat:
- amphipathic bile acids and phospholipids found in bile emulsify large lipid droplets so pancreatic lipase can access them
- form mixed micelles

52
Q

Does the bile contain digestive enzymes?

A

does not contain digestive enzymes but allows them to digest the fat

53
Q

What is a micelle, what’s it’s function?

A
  • a soluble cluster of amphipathic molecules with nonpolar groups in the middle and polar groups on the outer layer
  • equilibrium exists between the micelle, free fatty acid and monoglycerides → free forms diffuse across SI epithelium
  • keep monoglycerides and fatty acids in small soluble aggregates “holding station” for small insoluble lipids
54
Q

what is the enterohepatic circulation? (3 steps)

A

enterohepatic circulation: recycling of bile acids to maintains balance of bile acids, and for secretion rate to exceed synthesis

1.Bile acids released by the liver/gallbladder into duodenum for fat digetsion

  • bile acids transported across apical surface of hepatocytes PAT
  • bile acids: canalicular networks → bile ducts → gallbladder/SI

2.Bile acids reabsorbed across ileum of SI into portal circulation

  • bile acids enter SI, digest food and move to end of SI (ileum) where bile acids move back into portal circulation
  • absorbed across enterocyte through Na+ dependant SAT
  • bile acids then move by FT across basolateral surface of enterocyte into portal blood

3.Bile acids transported back to hepatocytes

  • bile acids in portal blood carried into hepatocyte via SAT

PAT - primary active transport
SAT - secondary active transport
FT - facilitated transport

55
Q

How is the synthesis and secretion of bile regulated? (3)

A
  1. by bile salts: as absorbtion of bile salts in ileum ↑ and returns to liver, more will be sec. back into bile. synthesis ↓ w/ well working EHC
  2. by secretin: increases HCO3- by the bile duct cells and pancreas
  3. by CCK: increases contraction of the gallbladder and relaxes the SoO → bile is released into duodenum

EHC - enterohepatic circulation
SoO - sphincter of Oddi

56
Q

Is the liver essential for life? Is the gallbladder essential for life?

A

Liver is essential for life; needed for the breakdown of fats, metabolizing & storing nutrients and detoxification

Gallbladder is not essential; functions to store and secrete bile acids, however the liver can secrete bile acids directly into the duodenum. There will be less regulation however.

57
Q

What are the major functions of the small intestine? How is it’s structure related to these functions?

slide 179-180

A

Functions: digestion & absorption (protein, fat, carbohydrates, electrolytes, water, minerals, vitamins)

Structure features:

  • duodenum (closest to stomach, smallest): mixes digestive enzymes w food, absorbs nutrients, iron and calcium, releases secretin and CCK
  • Jejunum: digestion & absorption
  • Illeum (closest to LI, longest): digestion & absorption of bile acids and vit. B₁₂
  • Pyloric sphincter → b/w the stomach and duodenum
  • surface area: increased by folds of kerckring (circular folds), villi that cover the folds, and microvilli

SI - 2.4 cm wide tube, 3m long
most of the chyme entering the SI is digested and absorbed in the duodenum and jejunum

58
Q

Major cell types in the villous and crypts (4) What are the functions of these cells? Where are they derived from?

slide 182

A

stem cells in the crypts rapidly divide and differentiate into different types of epithelial cells:

  1. Absorptive cell (enterocyte): absorbs, has microvilli at the apical surface that make the brush border membrane
  2. Goblet cells: secretes mucus
  3. Enteroendocrine cells: (I/S cells), release horomones secretin/CCK
  4. Paneth cell: secrete antibacterial proteins
59
Q

What are the “brush-border enzymes” and why are they important?

A

enzyme anchored to the brush border with catalytic acitivity in the lumen

  • important for breaking down carbohydrates and peptides into sugars and amino acids prior to transport across enterocyte
60
Q

How are the major foods (carbs, protein, fats) digested?

A

carbohydrate:

  • starch (amylose/amylopectin) → maltose, maltotriose and alpha-limit dextrins (salivary and pancreatic amylases)

products of amylase broken down into monosaccharides by BBE:

  • maltose/maltotriose → glucose (maltase, sucrase or alpha destrinase)
  • alpha-limit dextrins → glucose (alpha dextrinase)
  • sucrose → glucose+fructose (sucrase)
  • lactose → glucose+galactose (lactase)

proteins:

  • pepsin in the stomach & pancreatic proteases in SI (trypsin, chymotrypsin)
  • broken down to aa’s by: carboxypeptidase (pancreatic protease) and aminopeptidase (brush-border enzyme)

fats:

  1. lipid droplets emulsified by mechanical disruption and bile acids/phospholipids
  2. pancreatic lipase act releases FFA and monoglycerides
  3. products of lipase are incorporated into micelles: slowly release FA and monoglycerides across SI epithelium

BBE - brush border enzymes
FFA - free fatty acids

61
Q

How are the major foods (carbs, protein, fats) absorbed? Include names of transporters

189, 194

A

carbohydrates:

  • only monosaccarides are absorbed by GIT
  • glucose & galactose: cross apical surface of enterocyte via SGLT (SAT pathway), cross basolateral surface via GLUT
  • Fructose: crosses apical membrane via GLUT5, crosses basolateral surface via GLUT2

proteins:

  • free aa’s absorbed by SAT coupled to Na+, or SAT coupled to H+
  • aa’s cross enterocyte’s basolateral surface via FD
  • multiple different SAT transporters at apical+basolateral surface for different aa’s

fat:

  • free fatty acids and monoglycerides released from micelles are absorbed across epithelium by diffusion
  • ER in the cell processes products back to triglycerides (maintains the conc. gradient)
  • in ER: triglycerides aggregate into protien-coated lipid droplets → packaged in Golgi to be secreted into blood as chylomicrons
  • absorbed by lymphatic system, which eventually enters systemic circulation → fat components taken up by tissues via lipase found on epithelial cells of blood vessels

SGLT - sodium-dependant glucose transporter
GLUT - facilitated glucose transporter
aa’s - amino acids
SAT - secondary active transport
FD - facilitated diffusion

62
Q

Why is the body’s handling of fat so different from that of carbohydrates and protein?

A

Because of fats chemical properties, they are not water soluble and tend to aggregate in aqueous solutions.
This means there are mechanisms the body uses to keep the fats from aggregating.
Additionally they have the ability to diffuse across cell membranes, so the diffusion is controlled by micelles and they travel through the lymphatic circulation because it is leakier

63
Q

How does the body absorb iron? What are ferritin and transferrin?

A

iron is actively transported into the enterocyte and incorporated into the protein ferritin: a protein iron complex that acts as a storage form of iron
* excreted from body when enterocytes sough of villi tips

when iron is not stored it is released on the blood side of the enterocyte attatched to protein trasferrin:
* no mechanism for iron excretion - accumulates in tissues (can cause toxicity; skin pigmentation and heart failure)

Extra info: absorption of heme iron (found in meat) is better (10-15%), vegetarians have low iron diets, blood loss means iron loss and risk of anemia

64
Q

How does the body regulate the level of iron?

A

when iron stores are ample: expression of ferritin protein is upregulated = reduced iron absorption

when iron stores are depleted: production of intestinal ferritin decreases = increased absorption

65
Q

How much fluid is presented to the small intestine every day? How is fluid secreted and absorbed?

slide 209-210

A

8-9L - volume of fluid absorbed by SI > volume absorbed by LI

  • absorption at the villi, secretion from the crypts
  • epithelium generates an osmotic gradient; water follows through tight junctions (paracellular transport)
  • important electrolytes: Na+, Cl-, HCO3-
  • inward gradient = absorption, outward gradient = secretion

absorption:

  • depends on Na+ gradients generated during secondary active nutrient uptake (glucose or aa’s)
    1. Glucose brought into cell by SAT (Na/K ATPase)
    2. glucose + Na brought in by SGLT
    3. Cl- follows positively charged Na+, along with water, paracellularly
  • differs slightly in LI since there is no nutrients being absorbed

secretion:

  • depends on Cl- gradients generated by NKCC1 transporter
    1. NKCC1 allows accumulation of Cl- in enterocyte based on inwardly-directed Na+ gradient
    2. CFTR on BBM opens allowing Cl- to diffuse down its gradient (opening is stimulated by cAMP)
    3. Na+ attracted to (-) Cl gradient and water follows
  • identical in SI

NKCC1 - secondary active Na+/K+/2Cl- transporter
BBM - brush border membrane

66
Q

motility in SI during digestion and after absorption

A

digestion: segmentation continously breaks intestinal contents into smaller divisions, frequency set by BER, force of contraction determined by neurohormonal input

after absorption: segmentation stops, replaced by migrating myoelectric complex (MMC)

  • begins in lower portion of stomach, travels 2ft to SI then dies out, overlapping wave starts further down SI (~2h)
  • pushes undigested material from SI to LI and prevents bacteria from remaining in SI
  • initiated by horomone motilin released by SI, ceases when next meal is consumed
67
Q

What are the different regions of the large intestine and what are their major functions?

A
  1. Ileocecal valve: sphincter bw the cecum and ileum, open when ileum contracts (post-meal), closed when LI distended, retains LI contents including bacteria
  2. Cecum/appendix (no function)
  3. Ascending/traverse/descending/sigmoidal colon: reabsorption of water, reservoir for storage of wastes and indigestible materials prior to defecation, absorption of products of bacterial metabolism
    4.Rectum: resevoir for feces
  4. Anus: two sphincters control defecation (internal anal sphincter - SM, involuntary & external anal sphincter - SkM, voluntary)

SM - smooth muscle
SkM - skeletal muscle

68
Q

How does the fluid absorption differ in the large and small intestine?

A
  • no nutrients are absorbed in the LI
  • SI - Na+ dependant nutrient transporter on apical surface
  • LI - no Na+ dependant nutrient transporter; has a Na+ channel which allows Na+ to move into the cell down it’s conc gradient
  • Cl- follows the + charge of Na+ and then water is also carried along with it paracellularly
  • water absorption occurs predominantly in the crypts in LI as there are no villi
69
Q

How does undigested food etc. move through the large intestine and how is it eliminated from the body?

A
  • segmentation: much slower in basic electrical rhythm in LI (one every 30m), allows retention in the colon for 18-24h
  • propulsion: 3-4x a day intense contraction (mass movement) spreads rapidly over LI pushing contents toward anus → occurs after eating and prior to defacation

REFLEX:

  • rectum contracts, internal anal sphincter relaxes, outer anal sphincter contracts (initially)
  • increased perastaltic activity in the sigmoid colon, increasing pressure = reflex relaxation of the external anal sphincter
  • feces voided
  • toilet training means brain can over ride the reflex of outer sphincter to delay defecation