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BIOL 373 Exam Flashcards

1
Q

what are the functions of the GI system?

A

Digestion- break down macromolecules into forms that ca be transported across the epithelium

absorption- transport nutrients, water, ions, vitamins across the epithelium

motility- keep the gut contents moving

secretion- release on enzymes into the gut lumen

maintain water balance- balance between secretion and reabsorption

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2
Q

what are some problems faced by the GI tract regarding its function?

A
  1. need to digest macromolecules but not itself
  2. need to allow entry of digested nutrients but not pathogens

-GI lining is largest area of contact between external and internal environments
-protection from pathogens by various barriers:
-epithelial barrier
-mucus
-digestive enzymes
-acid
-GALT

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3
Q

anatomy of GI tract

A

stomach
small intestine- duodenum, jejunum, ileum
large intestine- colon, rectum

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4
Q

what is the mucosa surface anatomy?

A
  1. mucosa- epithelium, lamina propria, muscularis mucosa
  2. submucosa- messsiners submucosal plexus
  3. smooth muscle layers- circular muscle, longitudinal muscle, Auerbach’s myenteric plexus
  4. serosa
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5
Q

differences between small intestine and stomach anatomy

A

stomach: gastric glands, oblique muscles

small intestine: villi, crypt, peyers patch (in mucosa)

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6
Q

what features increase surface area?

A

stomach- gastric gland

small intestine- crypts

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7
Q

What are the two major patterns of contraction for gut motility?

A

peristalsis: moving food from mouth to anus, contraction and relax to move food forward

segmental contractions: mixing/churning, maximizes exposure to digestive enzymes and epithelium (little or no net movement forward)

these both occur during/after a meal

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8
Q

Tonic vs. phasic gut motility contractions

A

-most gut muscle is single unit smooth muscle, connected by gap junctions

-certain regions are tonically contracted for minutes to hours: smooth muscle sphincters keeps food from moving backwards

-other regions undergo phasic contractions for a few seconds: posterior stomach, small intestine

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9
Q

migrating motor complexes

A

this occurs between meals

sweep slowly down tract, roughly 90 minutes from stomach to large intestine

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10
Q

slow wave potentials

A

below threshold= no contraction

above threshold= opening of voltage gated Ca channels-> action potentials-> contraction

the degree of the contraction relates to the amount of Ca that enters

longer wave= more time for Ca to enter= larger contraction

amplitude and duration of contraction influenced by: hormones, paracine factors, neurotransmitters

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11
Q

Wave frequency and interstitial cells of cajal

A

slow wave frequency varies in different regions of the tract

more frequent in duodenum versus the stomach

set by pacemakers cells between smooth muscle layers

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12
Q

what is secreted in the GI tract

A

-water and ions (secreted into lumen then reabsorbed)
-enzymes
-mucus
-saliva

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13
Q

How are water and ions secreted in GI tract?

A

-mostly through membrane transporters
-water follows osmotic gradient
-water and ions in some regions can pass between cells: paracellular pathway
-similar channels and transporters to kidney but expressed on apical vs. basolateral membranes

transporters:
Na/k ATPase, NKCC cotransporter, H+/K+ ATPase
exchanger- Na+/H+, Cl-/HCO3-

Ion channels:
ENaC, K+ channels, Cl- channels (CFTR)

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14
Q

How is acid secreted?

A

acid is secreted by parietal cells

H+ is a million times higher in the lumen

  1. inside the cell CA forms bicarb from OH and CO2
  2. on the basolateral side: HCO3- out and Cl- into the cell
  3. On the apical side: H+ out and K+ in using the H+/K+ ATPase. Cl- out of the cell through Cl- channel

bicarb moving out of the cell is absorbed by blood, alkaline tide can be measured after a meal

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15
Q

How is NaCl secreted?

A

it is secreted from small intestine, colon, salivary glands

  1. Na+, K+, 2Cl- enter the cell on the basolateral side through NKCC
  2. Cl- enters the cell lumen on apical side through CFTR channel
  3. Na+ is reabsorbed on the basolateral side through Na+/K+ ATPase
  4. Negative Cl- in lumen attracts Na+ by paracellular pathway and water follows. goes from basolateral to apical side

crypt cells in small intestine and colon secrete ‘isotonic saline’ that mixes with mucus secreted by goblet cells to lubricate gut contents

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16
Q

Bicarb secretion from pancreas into duodenum

A

bicarb secreted into duodenum neutralizes acid coming from the stomach

acinar cells of pancreas secrete enzymes

epithelial cells lining ducts secrete bicarb solution

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17
Q

How is bicarb secreted?

A

secreted from epithelial cells lining ducts-> secreted into duodenum to neutralize stomach acid

  1. CA creates bicarb inside the cell (CO2 + H20 = HCO3- + H+
  2. basolateral side: Cl- enters the cell through the NKCC
  3. apical side: HCO3- leaves the cell through HCO3-/ Cl- exchanger, Cl out of the cell through CFTR channel then it reenters the cell through HCO3-/Cl- exchanger
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18
Q

How does cystic fibrosis effect the pancreas?

A

-mutation in gene that encodes in CFTR channel
-leads to a defect in the Cl- channel, and water transport
-fluid filled cysts and fibrosis (named for changes in the pancreas)
1. Cl- not transported into the ducts
2. there are various effects, water and Na+ do not transport into ducts since Cl- doesn’t
3. mucus is still produced but is greatly thickened due to lack of water
4. blockage of pancreatic ducts
5. exocrine secretions of pancreas does not get released
6. back pressure/ inflammation causing damage to pancreas

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19
Q

How are enzymes secreted?

A

-enzymes are secreted by exocrine glands or epithelial cells of stomach and small intestine
-they are synthesized by rough ER, packaged by golgi into vesicles, stored in cell under signal for release by exocytosis
-enzymes sometimes remain linked to apical membranes by protein or lipid stalks
often released as inactive precursor to prevent-auto digestion (zymogens)
-secretion regulated by neural, hormonal, paracrine signals (usually stimulated by parasympathetic)

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20
Q

How is mucus secreted?

A

-mucus consists of mucins mixture of glycoproteins
-produced by exocrine cells:
-serous cells in salivary gland
-mucous cells in stomach
-goblet cells in intestine

-signals for secretion:
-parasympathetic stimulation
-many neuropeptides
-cytokines
-infection and inflammation increase mucus secretion

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21
Q

How is saliva secreted?

A

-the salivary glands are arranged similar to exocrine pancreas (acini and ducts)
-saliva is a complex hypo-osmotic fluid
-it is a two step process:
1. fluid is secreted by acinar cells similar to ECF
2. as it passes through ducts, epithelial cells take back Na+ and secrete K+, so it eventually resembles intracellular fluid
-ducts cells have low water permeability, so water remains in saliva-> hypo-osmotic

-signals for secretion is parasympathetic, inhibited by sympathetic

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22
Q

organization of hepatic lobule. how is bile secreted?

A

hepatocytes-> bile canaliculi-> bile ductules-> common hepatic duct-> common bile duct (gall bladder)-> duodenum

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23
Q

how does blood flow work in the liver?

A

-most absorbed nutrients move into capillaries than into villi, then into hepatic portal vein
-xenobiotics must first pass through the liver before systemic circulation

75% hepatic portal vein, 25% hepatic artery-> sinusoids-> central vein-> hepatic vein

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24
Q

what are the key components of bile

A

-bile salt
-bile pigments
-cholesterol
-drugs and other xenobiotics being processed in liver and excreted in kidneys

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25
Q

Iron and RBC turnover: bilirubin

A
  1. spleen converts Hb to bilirubin
  2. liver metabolizes bilirubin and excretes it in bile
  3. bilirubin metabolites excreted in urine and feces
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26
Q

what are bilirubin metabolites responsible for

A

-normal colour of feces and urine
-yellow colour of bruising and yellow pigment of jaundice

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27
Q

what is digestion?

A

combination of mechanical and enzymatic processes
-occurs int he mouth, stomach, small intestine
-chewing, churning, expose more surface area to enzymes

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28
Q
A
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29
Q

what is absorption?

A

crossing the gut epithelium
-mostly in small intestine
-use many of the same transporters as in the kidney

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30
Q

are digestion and absorption regulated?

A

not directly regulated
-influenced by motility and secretion, which are regulated

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31
Q

how does absorption in the small intestine occur?

A

lumen-> apical membrane-> epithelial cell-> basolateral membrane-> interstitial-> capillary or lymph

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32
Q

carbohydrates

A

-constitute about half caloric intake, mostly starch and glucose
-can only be absorbed through membrane transporter
-we only have transporters for monosaccharides
-artificial sweetners can interact with sweet receptors but can not be digested as a way to cross into enterocytes

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33
Q

how are carbohydrates digested?

A

glucose polymers-> (amylase)-> disaccharide-> monosaccharide

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34
Q

how are carbohydrates absorbed?

A
  1. glucose/ galactose enter with Na+ on SGLT apical side and exit through GLUT2 on the basolateral side
  2. fructose enter through GLUT5 on apical side and exit through GLUT2 on basolateral side
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35
Q

how is protein absorbed?

A

proteins break down into peptides
-di and tri peptides transport with H+
-amino acids transport with Na+

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36
Q

how is protein digested?

A

In two different ways, through endopeptidase and exopeptidase

  1. endopeptidase
    -endopeptidase digests internal peptide bond
    -making smaller peptides
    -examples are trypin, pepsin, chymptrypisn
  2. exopeptidase
    -digests terminal peptide bonds to release amino acids
    -examples are aminopeptidase, carboxypeptidase

products of protein digestion are amino acids, di and tri peptides

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37
Q

Fats

A

-triglycerides, most of our fat calories are in this form. cholesterol, phospholipids, long chain fatty acids, fat soluble vitamins

-digestion complicated by solubility issues
-leave stomach as large droplets mixed with aqueous chyme
-low surface available to interact with enzymes
-broken down into smaller particles through action of bile slats

38
Q

Bile salts (bile acids)

A

come from cholesterol-> primary bile acid modified by gut bacteria-> secondary bile acid-> conjugated bile acid or conjugated in liver-> conjugated bile acid

39
Q

how is fat digested part 1?

A

-bile salts coat lipids to make emulsion of large droplets

-the hydrophobic side associates with lipids
-the polar hydrophilic side associates with water

-pancreatic lipases can act on triglycerides in droplets, aided by collapse from pancreas and break them down to amino acids and monoglyceride

40
Q

how is fat digested part 2?

A

formation of micelles
-all fats digested in smaller components except cholesterol
-micelles can then move close to surface of enterocytes and lipids can diffuse across apical membrane into cells

41
Q

how is fat absorbed?

A
  1. bile salts coat fat droplets
  2. pancreatic lipase and colipase break down fats into monoglycerides and fatty acidsstored in micelles
    3a. monoglycerides ad fatty acids diffuse from micelles across apical membrane into cell
    3b. cholesterol is transported into the cell
  3. abosrbed fats combine with cholesterol and proteins in intestinal cells to form chylomicrons
  4. chylomicrons removed by lymphatic system
42
Q

how are nucleic acids digested and absorbed?

A

nucleoprotein-> digested into nucleic acids-> then into nucleotides and nucleosides-> absorbed by Na+ coupled transport-> broken down

43
Q

how are vitamins digested and absorbed?

A

fat soluble (A,D,E,K)
-absorbed in small intestine with fats

water soluble (C, most Bs)
-absorbed in small intestine through membrane transporters

exception B12
-cobalamin, participates in metabolic pathway in every cell, important in RBC synthesis
-absorption requires protein secreted by gastric parietal cells

44
Q

how are water and ions absorbed?

A

absorbed by small and large intestine
1. Na+ enters cell through many pathways
2. the Na+/K+ ATPase pumps Na+ into ECF
3. water and K+ move through paracellular pathway

ions move across apical side, main driver on basolateral side is Na+/K+ATPase then water follows by osmosis

45
Q

how are iron and calcium absorbed?

A

two of the very few substance which intestinal absorption is regulated
decrease levels-> detector-> signal-> intestinal uptake

iron:
-iron and H+ cotransport through DMT1
-heme also transported across apical membrane
-heme is broken down into Fe and polypherin
-Fe is transported across basolateral membrane by ferroportin

calcium:
-paracellular absorption not regulated
-calcium crosses through calcium channel
-transport of calcium across basolateral membrane is regulated by Vitamin D3

46
Q

describe long reflexes

A

integrated in CNS
-sensory information from GI tract to CNS
-feedforward reflexes that originate outside GI tract
-include cephalic reflexes in response to sight, small, thought of food, effects of motion
-efferent limb always autonomic:
-parasympathetic-> excitatory
-sympathetic-> generally inhibitory

47
Q

describe short relfexes

A

integrated within gut, in enteric nervous system (gut brain)
-neurons in submucosal plexus receive signals from lumen, regulate secretion
neurons in myenteric plexus regulate motility

48
Q

describe reflexes involving gut peptides?

A

-can act locally (paracine) or travel via blood (endocrine)
-effects on motility
-effects on both exocrine and endocrine secretion
-some gut peptides can also act on brain

49
Q

what are the similarities between the enteric and central nervous system?

A

-has intrinsic neurons that lie entirely within the gut
-release more than 30 different neurotransmitters and neuromodulators: not epinephrine, norepinephrine, and acetylcholine but otherwise similar to molecules used in CNS
-has glial support cells
-diffusion barrier- capillaries surrounding ganglia are not very permeable
-acts on integrating centre-> gut function can be regulated without CNS

50
Q

what was Pavlov’s contribution to the history of gut hormones?

A

-acid chyme passing into duodenum-> pancreatic juice secreted
-vagus afferents from duodenum to brain-> vagal efferents from brain to pancreas-> pancreatic juice secreted into duodenum

-pancreatic secretion was thought to be controlled only by vagus nerve

51
Q

what was Bayliss and Starlings contribution to the history of gut hormones?

A

-took out nerves surrounding pancreas and duodenum
->put acid in duodenum
->pancreas still secreted
-hypothesis: acid caused release of signal from duodenum into blood
-tested hypothesis: collected lining of duodenum
-added acid to it
-injected it intravenously (straight into circulatory system)
-resulted in pancreatic secretion

intestine stimulated pancreatic secretion called secretin
blood-borne regulators-hormones

52
Q

what are the families of gut hormones?

A
  1. gastrin family- includes gastrin, CCK
    -major targets are stomach, intestine and accessory organs
  2. secretin family
    -secretin, VIP, gastric inhibitory peptide (GIP), GLP-1
    -both endocrine and exocrine glands
  3. motility
    -acts on gut smooth muscle
    -regulates migrating motor complexes
53
Q

how does the mouth initiate digestion?

A

-saliva-> secretion under autonomic control:
-soften and lubricates food
-digestion: salivary amylase, some lipase
-antimicrobial: lysozyme, immunoglobins
-chewing
-transfer to stomach, swallowing

54
Q

describe the swallowing reflex

A
  1. tongue pushes bolous against soft palate and back of mouth, triggers swallowing reflex
  2. breathing inhibited as bolus passes closed airway
  3. food moves downward into esophagus, propelled by peristaltic waves and aided by gravity

-swallowing reflex integrated in medulla
-sensory afferents in cranial nerve IX and somatic motor and autonomic neurons mediate reflex

55
Q

what is the transition into the stomach?

A

-lower esophageal sphincter guards entry into stomach
-if lower esophageal sphincter is not closed, acid from stomach will go into lower esophagus
-this creates gastroesophageal reflux disease (GERD, heartburn)

56
Q

explain the cephalic phase (neural control)

A

integrated with long vagal reflexes

  1. anticipation/ presence of food in mouth-> activation of neurons in medulla-> efferent signal to salivary gland, autonomic signals via vagus to enteric nervous system (gut brain)-> increase motility and secretion in stomach, intestine, accessory organs
57
Q

gastric phase (neural control)

A

once food enters stomach, series of short reflexes

distention (stretching) or peptides and amino acids once food enters stomach initiate short reflexes-> sensory input to enteric nervous system-> increased motility and secretion in stomach, small intestine, accessory organs

58
Q

what are the 3 functions of the stomach?

A
  1. storage
    -neurally mediated receptive relaxation of upper stomach
  2. digestion
    -mechanical and chemical processing into chyme
    -secretion begins before food arrives
  3. protection
    -against microbes-> acid
    self protection-> mucus-bicarbonate barrier
59
Q

parietal cells, secrete, stimulus, function of secretion

A

-secrete H (acid)
-stimulus gastrin, histamine, acetylcholine
-activates pepsin from pepsinogen
-denatures proteins
-anti-microbial

60
Q

ECL cells secrete, stimulus, function of secretion

A

-secrete histamine
-stimulus acetylcholine and gastrin
-stimulate acid secretion from parietal cells
-binds to H2 receptors on parietal cells

61
Q

chief cells secrete, stimulus, function of secretion

A

-secrete pepsinogen-> pepsin
-secrete gastric acid
-stimulus acetylcholine, acid secretion
-pepsin digests proteins and gastric lipase digests fat

62
Q

D cells secrete, stimulus, function of secretion

A

-secrete somatostatin
-stimulus acid in the stomach
-stops secretion of acid and pepsin (parietal cells, ECL cells, G cells)

63
Q

G cells secrete, stimulus, function of secretion

A

-secrete gastrin
-stimulus acetylcholine, peptides, amino acids
-triggered by long and short reflexes

64
Q

what is the integration of cephalic and gastric phases?

A
  1. food or cephalic reflexes initiate gastric secretion
  2. gastrin stimulates acid secretion by direct action on parietal cells or indirectly through histamine
  3. acid stimulates short reflex secretion of pepsinogen
  4. somatostatin release by H+ onto D cells is feedback signal that modulates acid and pepsin release
65
Q

what is the purpose of mucus in the stomach?

A

bicarbonate barrier- protects itself from acid

-breakdown of mucus bicarb barrier- peptic ulcer
-acid and pepsin damage mucosal surface, creating holes that extend into submucosa and muscular layers

66
Q

what are the preventions and treatments of peptic ulcers?

A

-main treatment was antacids:
-substrates that neutralized acid

-H2 receptor antagonist-> block histamine action

-proton pump inhibitor- block H+/K+ ATPase since parietal cells secrete acid in this way

67
Q

how are parietal cells stimulated? (acid secretion)

A

-gastrin
-histamine
-acetylcholine

cause H+/K+ ATPase expression on parietal cells

68
Q

what is the intestinal phase?

A

-stomach produces chyme by actions of acid, pepsin, peristalsis
-intestinal phase begins with controlled entry of chyme into small intestine
-sensors in duodenum feed back to stomach to control delivery of chyme, feed forward to intestine to promote digestion, motility and nutrient utilization

69
Q

integration of gastric and intestinal phases

A
  1. food into stomach
  2. acid secretion, pepsin and lipase secretion, gastric motility
  3. chyme into small intestine-> enteric nervous system says less
  4. carbs, fats and proteins, acid
  5. GIP and GLP-1, CCK, secretin
  6. insulin secretion, pancreatic enzyme secretion, pancreatic bicarbonate secretion
70
Q

enterohepatic circulation of bile salts

A

bile salts are released into the duodenum, absorbed in terminal ileum, enter portal circulation, travel back to liver
-recycled several times during a meal

71
Q

how are pancreatic zymogens activated?

A
  1. pancreatic secretions including zymogens enter lumen of small intestine
  2. enteropeptidase in brush border activates trypsin from trypsinogen
  3. trypsin activates zymogens
72
Q

what is diarrhea?

A

imbalance between intestinal absorption and secretion

  1. osmotic diarrhea= unabsorbed osmotically active solutes
  2. secretory diarrhea= bacterial toxins increase Cl- secretion eg. cholera
73
Q

what is the role of the large intestine?

A

removes most of remaining water-> formation of feces
-motility:
-ileocecal valve relaxes each time a peristaltic wave reaches it, also relaxes when food leaves the stomach
-segmental contractions except when mass movements occur (wave of contractions that send a bolus forward trigger distention of rectum-> defecation reflex)

74
Q

what is the intracellular trafficking of cholera toxin?

A
  1. enters cell via pentameric B subunits
  2. travels backwards direction through golgi
  3. sequence on A2 subunit recognized as signal to be taken to ER
  4. mimics being a misfolded protein and gets dumped on cytosol
  5. A1 subunit modifies the Galpha subunit and makes it stay on, bound to GTP
  6. persistent activation of adenyl cyclase
  7. persistent elevation of cAMP
  8. sustained activation of CFTR channel
75
Q

why is the frequency of cystic fibrosis so high?

A

CF heterozygotes have some advantage over non-CF homozygotes
-heterozygotes have 50% functional CFTRs
-enough for normal function but resist death to cholera due to reduced Cl- secretion
-survive to pass the gene on to offspring
-however cholera epidemics did not hit Northern Europe until 19th century
-CFTR channels involved in other diseases that were around earlier

76
Q

how is metabolism regulated?

A

endocrine- primary role
-products of endocrine pancreas

neural- regulation of food intake
-endocrine pancreas also innervated

77
Q

what are the three possible fates of ingested biomolecules?

A

fuel- metabolized to provide energy

build- synthesis reactions for growth and maintenance of tissues

store- as glycogen or fat

78
Q

what are the two states of metabolism?

A

fed/ absorptive state= anabolic, products of digestion being absorbed and used for synthesis or stored

fasted/ post-absorptive state= catabolic, body taps into stores

79
Q

what are the nutrient pools available for immediate use?

A

-amino acids
-free fatty acids
-glucose

80
Q

how do enzymes control direction of metabolism?

A
  1. in fed state metabolism is under influence of insulin= glucose to glycogen reaction increases, enzymes for glycogen breakdown inhibited= net glycogen synthesis
  2. fasted state metabolism under the influence of glucagon= enzymes that break down glycogen are more active and enzymes that synthesize glycogen are inhibited= net glucose synthesis
81
Q

what is the goal of fasted state metabolism?

A

-maintain plasma glucose levels
-achieved through pathways that yield glucose or provide ATP
-brain is acutely dependent on glucose

82
Q

what are the nutrient storage depots for the fasted state?

A

carbs:
-glycogen in liver- can be broken down and exported as free glucose
-glycogen in muscle- can be broken down but not exported as free glucose, it can be exported as pyruvate or lactate

fats: triglycerides in adipose-> export glycerol-> liver-> gluconeogenesis

liver- handling glycerol it can produce ketone bodies

83
Q

what is ketogenesis?

A

-formation of ketone bodies
-if lipolysis proceeds faster than acetyl CoA can be used in TCA cycle, ketone bodies are formed
-can enter blood stream and serve as energy substrates for brain during times of starvation
-typically generated by low carb, high protein/ fat diets

ketogenesis can become dangerous
-they are strong acids that can disrupt acid-base balance

84
Q

Homeostatic vs non-homeostatic eating

A

homeostatic: eating when hungry, energy fuels are depleted and not eating when not hungry, when energy fuels are sufficient
-metabolically driven hunger

non-homeostatic: eating in absence of hunger, eating despite large fat reserves, involves cognitive, reward, emotional factors

85
Q

models for regulation of homeostatic eating

A

two centres in hypothalamus:
hunger or feeding centre, satiety centre

glucostatic theory: intake regulated by glucose levels, monitored by centres in the hypothalamus
-plasma glucose low-> satiety centre suppressed-> feeding centre dominant

lipotsatic theory: signal from fat stores to brain modulates eating behaviour
1994 discovery of protein hormone synthesized in white adipose tissue= leptin

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biol 373 (4 decks)

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