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Physio - GI > Study Guide > Flashcards

Study Guide Flashcards

1
Q

explain the neural mechanisms controlling GI functions - local, short, long

A
  • local: myenteric -> muscle (peristalsis)
  • short: afferent to ganglion outside CNS (DRG) -> muscle (anatomical sphincter stuff)
  • long: afferent vagus -> solitary tract -> DMVN -> efferent vagal to muscle (peristalsis)
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2
Q

explain the neural mechanisms controlling GI functions - peristalsis, rhythmic segmentation, tonic contractions

A
  • peristalsis: local reflex
  • rhythmic segmentation: local and long reflex to mix shit
  • tonic contractions: local reflex to move things aborally
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3
Q

understand how intrinsic neural connections can generate intrinsic reflexes

A

local reflexes, so stretch receptor stimulates inhibitory motor neuron and excitatory motor neuron

  • inhibitory: VIP, NO relaxation aborally
  • excitatory: ACh contraction towards mouth
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4
Q

describe mechanisms involved in swallowing

A

RRGSP: raise soft palate, resp stopped, glottis closed, sphincters relaxed (UES, LES), peristalsis of bolus to epiglottis, over epiglottis and into esophagus

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5
Q

what is the swallowing reflex?

A

pressure sensors in pharynx sense food -> medulla swallowing center coordinates relaxation of UES and LES

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6
Q

what is voluntary about swallowing?

A

raising soft palate

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7
Q

what controls the LES?

A

local reflexes, VIP and NO

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8
Q

what are some of the problems with esophageal function?

A
  • achalasia: LES has too much tension, lower esophagus gets super dilated
  • GERD: LES not closed, gastric reflux into esophagus
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9
Q

what is receptive relaxation and where does it occur?

A

bolus in the esophagus (long reflex) stimulates relaxation of proximal stomach to make room for incoming food

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10
Q

what neural mechanisms control receptive relaxation?

A

long reflexes

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11
Q

explain neural control of gastric emptying

A

distention of duodenum (long reflex) inhibits gastric emptying

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12
Q

what are other non-neural controls that regulate gastric emptying?

A
  • excitatory (from gastric): gastrin, distention

- inhibitory (from intestine): acidic duodenal pH, hypertonic chyme, fat digestion

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13
Q

how is the pattern of gastric contractions immediately after eating different from that seen after fasting for several hours?

A

-interdigestive phase: MMC (migrating motility complex) controlled by motilin/deals w/ circular muscle

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14
Q

how does this influence GI functions: gastrin

A
  • increases parietal secretions

- increases chief cell secretions

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15
Q

how does this influence GI functions: glucagon

A
  • increases lipolysis
  • increases gluconeogenesis
  • inhibits glycogenesis
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16
Q

how does this influence GI functions: secretin

A

(from duodenum)

  • inhibits gastric emptying
  • inhibits gastrin
  • decreased parietal cell secretion
  • increases chief cell secretion
  • increase HCO3- secretion from pancreas
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17
Q

how does this influence GI functions: CCK

A

(from duodenum… response to fat)

  • relaxes sphincter of Oddi
  • contracts gallbladder
  • slows gastric emptying
  • stimulates pancreatic lipase
  • stimulates HCO3-
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18
Q

how does this influence GI functions: GIP

A
  • stimulates somatostatin
  • inhibits gastric emptying
  • decreases gastrin (via somatostatin)
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19
Q

how does this influence GI functions: motilin

A

-regulates MMC

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20
Q

how does this influence GI functions: VIP

A

-SM relaxation

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21
Q

how does this influence GI functions: somatostatin

A
  • slows gastric emptying
  • down-regulates gastrin
  • inhibits chief and parietal statin
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22
Q

how does this influence GI functions: GRP (from vagus)

A

-stimulates endocrine cells to release gastrin

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23
Q

describe the function of slow waves. what cells and membrane events are responsible for generating slow waves?

A

BER (basal electrical rhythm) - interstitial cells of Cajal and pacemaker type cells in proximal stomach -> spreads to longitudinal muscle -> spreads to myenteric plexus -> circular muscle -> travels along these fibers via gap junctions, which changes membrane potential

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24
Q

what contractile behaviors are seen in the small intestine and what neural mechanisms control these contractions?

A
  • interdigestive: MMC (motilin)
  • digestive: MMC stops
  • peristalsis, rhythmic segmentation, tonic contraction
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25
Q

what is gastric sieving?

A

pyloric sphincter closes as bolus approaches -> only a small amount of fluid gets through, while most fluid and solids remain in stomach for more mixing

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26
Q

what regulates movement of chyme from the small to large intestine?

A

ileocecal junction - distention of ileum causes relaxation of sphincter and vice versa, mediated by myenteric plexus

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27
Q

what happens in the colon?

A
  • water absorption
  • electrolyte absorption
  • evacuation of feces
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28
Q

what motility patterns are seen in the colon, and what functions do they serve? (6)

A
  • haustral shuttling: annular contractions of circular mm. to mix back and forth between haustra
  • haustral propulsion: haustra contract sequentially to go to anus
  • multihaustral propulsion: simultaneous contraction of many
  • mass propulsion (peristalsis): infrequent, longer distance
  • gastro-colic reflex: colonic movement soon after a meal (ACh, gastrin, CCK)
  • defecation: parasympathetic long arc (rectum relaxes and distends), internal anal sphincter relaxes, external contracts at first then relaxes
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29
Q

what is a mass movement and what does it accomplish?

A

getting things through fast after you eat

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30
Q

explain what the defecation reflex is and what might enhance it

A

enhancement of reflex from increased intra-abdominal pressure due to contraction of chest and abdominal muscles

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31
Q

describe composition of saliva

A
  • acinar cells secrete stuff into water and form presaliva that is isotonic to plasma
  • as it’s going across ductal cells, Na and Cl get pulled out and K and HCO3 go in -> makes saliva hypotonic to plasma
  • acinar cells also put in alpha-amylase and salivary lipase
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32
Q

describe cellular processes in acinar and duct cells responsible for salivary secretions

A

-ACh binds muscarinic receptors -> rise in intracellular Ca2+ that leads to solute flux
-VIP binds to receptor and leads to protein kinase activity that leads to amylase vesicle secretion
(stimulus (excitation)-secretion coupling)

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33
Q

what are the neural mechanisms controlling salivation and what sorts of stimuli excite or inhibit salivation?

A
  • CN 7, 9
  • excite: see, smell, taste
  • inhibit: dehydration
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34
Q

explain the physiological functions of gastric juice

A
  • HCl- lowers pH, CT dissolved, denatures proteins

- gastrin: stimulates gastric emptying, stimulates chief and parietal cells

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35
Q

how is HCl produced in the stomach?

A
  • CO2 and water make H2CO3 via CA
  • H+/K+ ATPase on apical side -> H+ into lumen
  • HCl/Cl exchanger on basal side, then Cl- and K+ channels on apical side -> Cl- into lumen
  • H+ and Cl- combine in lumen
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36
Q

describe the neural mechanisms that regulate the secretion of HCl in the stomach

A

vagal (ACh) - cephalic phase

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37
Q

describe the hormonal mechanisms that regulate secretion of HCl in the stomach

A

ACh acts directly on parietal cells, gastrin, histamine (activates AC to cause HCl secretion from parietal cell, from ECL cells)

38
Q

how is stomach pH regulated?

A
  • secretion produced in duodenum -> inhibitory to parietal cells
  • somatostatin (from GIP) inhibitory to parietal cells
  • secreted in response to fat in duodenum
39
Q

explain the importance of mucus and bicarbonate in creating a gastric mucosal protective barrier

A
  • prevents stomach mucosal epithelial cells from being destroyed by digestive enzymes
  • mucus is mechanical barrier, stops bacterial adhesion
40
Q

what are the intestinal secretory cells and what do they secrete?

A
  • I cells (CCK)
  • S cells (secretin)
  • K cells (GIP)
41
Q

what are the pancreatic secretory cells and what parts of pancreatic juice do they secrete?

A

-acinar: pancreatic enzymes, ductal readjustments - HCO3- is high

42
Q

how does the composition of pancreatic juice change as flow increases?

A

increased flow = more bicarb

43
Q

what is the mechanism for pancreatic production of bicarbonate?

A

duct cells of pancreas have CA on either side (not inside), so the bicarb is made in the blood and the lumen

44
Q

explain the physiological functions of pancreatic juice components

A
  • secrete inactive enzymes that will be activated in the duodenum
  • HCO3 secretion
45
Q

what are the components of bile?

A
  • bile salts (glycocholate, lysolecithin, monocyceride)
  • TG
  • phospholipids
  • cholesterol esters
46
Q

what are the physiological functions of bile components in digestion?

A

bile salts for fat travel in blood (emulsify lipids)

47
Q

what is the role of Kupffer cells in the liver?

A

macrophages

48
Q

what neural and hormonal mechanisms regulate secretion of bile?

A

CCK - contracts gallbladder

vagal stimulation to gallbladder

49
Q

where is the sphincter of Oddi and what does it do?

A

common bile duct into duodenum -> relaxes to let bile and all pancreatic shit through

50
Q

how are bile components recycled?

A

reabsorbed in terminal ileum -> blood -> liver to be reused

51
Q

what role does the liver play in excretion of wastes?

A

detox and conjugation

52
Q

what is bilirubin and where does it come from?

A

globulin portion of Hb - comes from apoptotic RBCs

53
Q

if there was a decrease in pH of chyme entering duodenum, what would happen to liver, pancreatic, and stomach functions?

A
  • liver: nothing
  • pancreas: secretin increases bicarb
  • stomach: secretin inhibits gastrin and inhibits parietal cells (and increased chief cells)
54
Q

where are amylases produced in the body and how do they work?

A

salivary, pancreatic - cleave internal 1,4 alpha linkage

55
Q

what limits carbohydrate digestion by salivary amylase?

A
  • acid in stomach degrades it

- still the 1,6 alpha and terminal 1,4 alpha linkages

56
Q

where do digestion and absorption of carbohydrates take place?

A

small intestine

57
Q

describe digestion of sucrose, lactose, and branched starch molecules

A

sucrose, lactase

58
Q

what are oligosaccharidases and what role do they play on brush border membrane cells?

A

degraded by enzymes in the brush border

59
Q

how are monosaccharides transported in the small intestinal brush border cells?

A
  • glucose/galactose: with Na and an independent glucose transporter
  • fructose: facilitated diffusion
  • facilitated diffusion on basal side to get into blood
60
Q

what are pepsins, where are they produced, and what role do they play in total protein digestion?

A
  • chief cells

- break peptide bonds into free aa, dipeptides and tripeptides

61
Q

what role does gastric acid play in protein digestion?

A
  • activates pepsinogen -> pepsin
  • activates pancreatic alpha-amylase
  • ribo/deoxyribo
62
Q

what are the pancreatic proteases/peptidases?

A
  • trypsin (activated by enteropeptidases)
  • chymotrypsin
  • elastase
  • carboxypeptidases A/B
  • aminopeptidases
63
Q

how are some peptidases functionally unique?

A
  • trypsin - basic aa
  • chymotrypsin - aromatic aa, large hydrophobic aa
  • elastase - peptide bonds
  • carboxypeptidase A/B - peptide bones on carboxy end
  • aminopeptidases - peptide bones on amino ends
64
Q

what prevents the pancreatic enzymes from digesting the cellular apparatus of the pancreas?

A

they are zymogens - only become activated by trypsin, CI, or enteropeptidases

65
Q

how do peptides and amino acids get absorbed at the brush border membrane?

A
  • free aa, di and tripeptides are cotransported with Na via secondary active transport (Asp, Glu move via facilitated diffusion)
  • all move by facilitated diffusion to the blood
66
Q

where does most dietary protein get digested and absorbed?

A

small intestine?

67
Q

what are the different fat digestion enzymes, where do they originate and how do they work? (6)

A
  • lingual lipase: lingual gland, breaks down TG
  • gastric lipase: endocrine glands?, breaks down TG
  • colipase: pancreas, attach to fat droplets
  • pancreatic lipase: pancreas, breakd 1,3 position of TG
  • cholesterol ester hydrolase: pancreas, breaks water-soluble lipids
  • phospholipase A2: breaks phospholipids
68
Q

where does most dietary fat get digested?

A

proximal small intestine

69
Q

where are lipids absorbed mainly?

A

proximal small intestine

70
Q

what roles do bile salts and lecithin play in fat digestion?

A
  • bile salts emulsify fat for transport

- lecithin is a type of bile salt?

71
Q

what happens to lipids inside the intestinal epithelial cell

A

free, but then packaged into micelles with apoproteins

72
Q

what are chylomicrons and what special role do they play?

A

make micelles with the free fatty acids in the intestinal mucosal cells and transport the lipids from the cell to the lymph

73
Q

how do chylomicrons get into the circulatory system?

A

thoracic duct

74
Q

what role would tight junctions play in intestinal water and electrolyte fluxes?

A

water goes through, Na and I… sodium does this in early small intestine more so, K exclusively moves across tight jxn, and water can move across tight jxn

75
Q

explain how electrolyte transport is similar and different in the small and large intestine

A
  • SI: cotransport, active transport, passively

- LI: electrogenic transport only (down its electrochemical gradient)

76
Q

what mechanisms are important for the absorption of calcium in the GI tract?

A

Ca binding protein in brush border that binds Ca and gets moved into the cell via CA ATPase (2 in for 1ATP)
-active vit D is a steroid hormone that activates translation of mRNA -> Ca binding protein -> makes Ca absorption easier

77
Q

what mechanisms are important for the absorption of Fe in the GI tract?

A
  • DMT in the DUODENUM absorbs free iron

- heme is facilitated diffusion

78
Q

what is unique about the absorption of vit B12 and why is this so important in humans?

A

B12 needs IF to bind to recognize site on mucosal cell, B12 needed for neuro shit…. in ILEUM

79
Q

how do disease states disrupt water and electrolyte balance?

A

cholera - upregulates cAMP, Gs, inhibits Na/Cl symport so it keeps the Na in the lumen -> diarrhea

80
Q

how is the absorption of water-soluble vitamins different from fat-soluble vitamins?

A
  • water soluble in distal SI: facilitated diffusion, cotransport, active transport
  • fat soluble in proximal SI: facilitated diffusion, cotransport, active transport
81
Q

How do pancreatic hormones control nutrient traffic during the fed and fasted states?

A

glucagon:
- increased gluconeogenesis, lipolysis, glycogenolysis, protein breakdown
- decreased glycogen synthase

insulin:
- increased glycogen synthase, lipogenesis
- decreased gluconeogenesis

82
Q

which gut hormones are important in regulating food intake?

A

ghrelin stimulates LH? to increase feeding

83
Q

what are the important brain regions involved in control of ingestive behavior and what controls do they exert?

A

LH - hunger, lesion = anorexia

VM - satiety, lesion = over-eating

84
Q

how do different gut signals get to brain areas that control appetite?

A

BBB

85
Q

what role do pancreatic hormones play in the control of food intake?

A
  • insulin - decrease feeding, excessive increases feeding
  • glucagon - increase feeding? not on the list
  • ghrelin - increase feeding
86
Q

what are the endocrine and metabolic changes associated with T1DM?

A

Ab’s against beta cells of pancreas -> decreased insulin, so glucose can’t get into cells (hyperglycemia)

87
Q

what are the endocrine and metabolic changes associated with T2DM?

A

insulin resistance or down-regulation of insulin receptors

88
Q

how is the control of food intake altered in uncontrolled diabetes?

A

excess insulin - causes hunger

89
Q

how are signals of adiposity important in body weight control and how do they work?

A

leptin decreases neuropeptide Y, and CRH increases SNS, leading to increased insulin

90
Q

how can we use our knowledge of basic physiological findings to devise better treatments for obesity?

A
  • amphetamines: directly inhibit feeding center in brain
  • sibutramine: decreases food intake
  • leptin agonist, ghrelin antagonist
  • orlistat: lipase inhibitor (reduce intestinal digestion of fat)

Physio - GI (5 decks)

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