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PHSI 208 > GI Tract > Flashcards

GI Tract Flashcards

1
Q

what is the relative energy content of the macromolecules?

A

Fat»protein>carbs

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2
Q

what does the digestive system require?

A
  1. mixing and movement of food through alimentary tract (motility)
  2. secretion of digestive juices for digestion
  3. absorption of digested products
  4. circulation of blood to carry away nutrients
  5. nervous and hormonal regulation of gastro-intestinal functions
  6. also functions as mucosal immune function or host defense, and excretion of waste
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3
Q

describe all of the secretions and absorptions from teh GI tract

A

1200 mL water ingested per day; 1500 mL of salivry secretions; 2000 mL from gastric secretions (1500 from pancreas and 500 mL from bile); 1500 mL from intestinal secretios;
80% or 6700 mLs are reabsorbed into blood via the SMALL INT (duodenum);
1400 mL or ~20% absorbed into blood via large int
100 mL/~1% of water still is excreted in feces

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4
Q

what leads to diarrhea?

A

malabsorption of water and electrolytes in small int, as small int absorbs 6700/~80% of fluid per day;

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5
Q

why are commensal bacteria important?

A

contribute to the digestion of of food–>e.g. fibre fermentation; provide essentail nutrients (e.g. secondary and deconj. secondary bile acids); prevent pathogenic bacteria from colonizing (e.g. c difficile, v. cholerae (in lumen), salmonella and listeria (invasive)

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6
Q

describe “poo pills”

A

capsules which contain frozen poo, or more important, frozen commensal bacteria–>will push out C difficile and prevent it from over populating

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7
Q

probiotics important to increase growth of commensal bacteria and reduce growth of pathogen bacteria

A

ya

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8
Q

what are the accessory organs of the GI tract?

A

–secrete their own eznymes and secretions; parotid salvary glands; sublingual salivary glands; submandibular sal. glands; liver; gall bladder; pancreas–pancreas, gall, and liver all secrete into duodenum

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9
Q

describe the GI motility from the oral cavity to the anus

A

upper esophageal sphincter–sk muscles
lower eso sphinc, stomach, pyloric sphinc, sphinc of Oddi, small int, illeocolic sphinc, and internal anal sphinc all under sm muscle control
external anal sphinc–sk muscle

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10
Q

what is the sphincter of oddi?

A

sphincter which separates the gall bladder from the duodenum

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11
Q

describe the mucosa of the GIT

A

mucous membrane + lamina propria + muscularis mucosa;
– Luminal surface
– Inner epithelial layer (protective function)
– Exocrine cells (secretion of digestive juices)
– Endocrine cells (Secretion of GI hormones: gastrin, CCK, secretin, GIP, motilin)
– Epithelial cells (Absorbing nutrients)

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12
Q

describe the submucosa of the GIT

A

– Layer of connective tissues – distensibility and elasticity
– Blood and lymph vessels
– Submucous plexus (network of nerves)

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13
Q

desribe the muscularis externa

A
  • -two muscle laeyrs (inner circular and outer longitudinal)

- -myenteric plexus and deep muscular plexus

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14
Q

describe the serosa of the GIT

A
  • -outer connective tissue covering the digestive tract

- -secretes watery fluid for lubrication

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15
Q

what are the ways digestion is regulated?

A
  • -autonomous sm muscle function
  • -intrinsic nerve plexus (enteric nervous system)
  • -extrinsic innervation
  • -GI hormones
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16
Q

describe how autonomous sm muscle function acts to regulate digestive functions

A

– Muscle-like but not contractile cells (“Interstitial cells of Cajal”)
– Rhythmic variations in membrane potentials (Basic Electrical Rhythm, also called “slow wave potential”)
– Pacesetter cells

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17
Q

describe how intrinsic nerve plexuses function to regulate digestion function

A

– Interconnecting network of nerve cells
– Two major networks (myenteric and submucous)
– Run the entire length of GI tract
– Influence all facets of digestive tract activity

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18
Q

describe extrensic innervation of the GIT

A

Sympathetic and parasympathetic activity

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19
Q

describe hormonal roles in regulation of digestive function

A

Released in response to local changes in luminal content into blood

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20
Q

what are ICCs and what are their functions within the gut?

A

interstitial cells of cajal;

  • -generate SLOW wave activity
  • -coordinate active propagation of SLOW waves
  • -transduce motor neural inputs from enteric NS to muscle
  • -mechanosense the stretch of GI muscles
  • -when destroyed due to diabetes, this leads to impaired gastric motility–gastroparesis
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21
Q

where are ICCs found?

A

inthe MyP and DMP; but the ones in MyP are dominant and thus create/influence gastric motility patterns the most–as in, pacemaking activity is dependent upon the ICCs in the MyP; DMP ICCs have a slower frequency

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22
Q

How do ICCs work to set a pacemaking activity?

A

ICCs are connected by gap junctions–make them a single-unit tissue; they require functional c-kit receptors which guide the MyP ICCs to migrate to the MyP region; ; the c-kit is a receptor-type tyrosine kinase which binds to ligand stem cell factor
without c-kit, no slow waves will be generated and the nerve ganglia and MyP ICCs develop abnormally

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23
Q

how can basal membrane potential be altered?

A
  1. stretch 2. ACh 3. Parasymps 4. NE 5. Symps 6. NO
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24
Q

what are the motility patterns from the bottom 1/3 of the stomach to the ileum (end of the small int?)

A
  1. Peristalsis
  2. Segmentation–food reacts with digestive enzymes; moved back and forth
  3. Mass movement–contractions of large int which move undigestible food material towards the anus
  4. Migrating motor complex–MMC starts in the bottom third of the stomach; propagates down to the end of the small int—housekeeping function—leads to the growling of the stomach when hungry; motilin is the hormone responsible for this—>twists the bottom third of the stomach, pushes everything out to the ileum (end of a small intestine); MMC also clears out bacteria which may be over-proliferating in gut
25
Q

describe the long and short neural reflexes and hormonal regulation of GIT

A

external influences, such as emotional state or properties of food (lipid content, eg) send signals to the CNS via long nerves; the CNS in turn sends signals to the autonomic nervous system via long nerves; the ANS influences the enteric NS via the vagus nerve (long nerve); the ENS in turn acts on endocrine cells (via short nerve) GI sm muscles (va short nerve) or exocrine cells (via long nerve); endocrine cells release GI hormones via short neural reflexes; released into blood and act on exocrine cells/sm muscle via short neural reflexes;
the gi sm muscles cause a change in secretory activity motility via short neural reflexes, and the exocrine glands cause a change via long

26
Q

what is the purpose of the secretion mouth/pharynx?

A

1500mL saliva/day
Facilitate swallowing
Keeps mouth moist Solvent (taste buds) Aids speech Antibacterial action Keeps mouth/teeth clean

27
Q

what are teh contents of saliva?

A 
99.5% water/0.5%
electrolytes and proteins
   Lingual lipase (breaks down fats)
   Amylase (breaks down carbs)
   mucins
   IgA (antibodies, for disinfection and protecting the mouth/pharynx)
   Lysozyme disinfecting agent
   Lactoferrin disinfecting agent
   Bicarbonate neutralizes stomach acid
28
Q

what organs secrete saliva?

A

parotid gland, on jaw by ear; submandibular gland, underjaw; sublingual gland, …??

29
Q

describe regulation of saliva glands

A

Salivary center in medulla of brainstem
Parasympathetic nerves Sympathetic nerves Conditioned reflex, taste, smell,
pressure on glands, and nausea ↑
Sleep, fatigue, dehydration, fear ↓

30
Q

salivary gland is the only gland which is innervated by symp and parasymp, and the result is the same—to increase salivation rate

A

ya

31
Q

xerostomia–damage to salivary glands; esp when parasymp damage–>leads to atrophy, almost no saliva produced; symp results in less saliva but rich in mucus

A

ya

32
Q

describe xerostomia

A

• Impaired salivary secretions
• Sjögren’s syndrome-autoimmune attack of salivary
glands
• Drug side effects (e.g., antidepressants,
antihypertensives, psychotropics)
• Head/neck radiation to tumours

33
Q

clinical manifestations of xerostomia?

A

tooth decay (lack of protective agents, e.g. lysozyme); esophageal erosions; difficulty in lubricating/swallowing food; opportunistic infections (impaired host defense–if you lose the disinfecting agents in your saliva, you lose your first line of defense against pathogens)

34
Q

describe the process of esophageal relaxation to let food through

A

the pharyngo-esophageal sphincter opens under sk muscle control–the pressure drops to 0 mmHg and the sphincter opens; the portions of the esophageal body relax to allow food to pass; final, the gastro-esoph sphinc relaxes (almost simulataneously with the UES) due to NO (inihibtor);

35
Q

what is the purposeof the UES?

A

prevents air from entering the esoph when breathing

36
Q

what is the purpose of the LES?

A

prevents reflux of gastric content;

37
Q

what is achalasia?

A

difficulty swallowing; food gets stuck, reduced inhibitory nerve input;

38
Q

how does NO relax the LES?

A

NO diffuses across cell membranes, activates a kinase which produces cGMP—>opens K channel—>membrane hyperpol—>muscle relaxes

39
Q

what is GERD, what can it lead to, and what are the treatments?

A 
Gastroesophageal reflux disease; 
• Esophagitis (erosions of mucosa and ulcers)
• Lumen stricture
• Columnar cells replace squamous epithelium
• Adenocarcinoma
GERD Treatments:
• Treated with proton pump inhibitors
• Also H2 histamine receptor antagonists
40
Q

describe the motility of the esophag

A

peristalsis–sequential activation of muscles in pharynx and esoph. –sequential contraction and relaxation
–top part of esoph contracts due to ACh; below, the esoph relaxes to allow bolus to pass (due to NO/VIP); then, the lower part contracts again via ACh etc–
–circular muscles contract/relax, and longitudinal muscles contract
1. Primary peristaltic wave
Initiated by swallowing center (medulla)
2. Secondary peristaltic wave
Initiated by distension–happens when food is still
present in eso—irritates mucosa, initiates second
peristaltic wave

41
Q

secretions of the esophagus?

A

Protective Entirely mucus
Lubrication
Protect from acid and enzymes if gastric reflux should occur; no digestion or absorption occurs

42
Q

what is the purpose of the pyloric sphincter?

A

separates antrum (lower part of stomach) from duodenum

43
Q

what is the purpose of gastric rugae?

A

ehances SA of the stomach; for enhanced secretion of acids or enzymes

44
Q

what are the parts of the stomach and their purposes?

A

fundus–digestible food ruminates for awhile here to mix with digestive juices and enzymes; water sits too but for not as long
body–lots of rugae, for further digestion
antrum–food is pulverized here and turns into gastric chyme–has a different motility pattern than that of the fundus;
after pulverization the chyme passes through the pyloric sphinc into the duodenum

45
Q

functions of the stomach?

A
  1. Store ingested food
  2. Secrete HCl and enzymes to begin protein digestion 3.Secrete Ghrelin (control of feeding, stim. hunger, released from oxyntic gland), gastrin (acid secretion) from pylorus and antrum
  3. Mix and pulverize ingested food to produce chyme
46
Q

what are the gastric motilities?

A
  1. Filling–stomach can go from 50 mL to 1 L in vol; high plasticity and receptive relaxation via NO;
  2. .Storage– weak mixing of food from fundus
  3. Mixing–strong antral peristaltic contractions
  4. Emptying–dependent upon the strength of antral contractions
47
Q

what is the pressure-vol rlnship of the stomach?

A

as stomach receives food, it relaxes; increases in volume, but pressure doesn’t change—also a function of receptive relaxation
after the pressure-volume relationship has been surpassed you can no longer ingest any more food

48
Q

what factors affect gastric emptying and how?

A

1.Amount of chyme in the stomach
Distension stimulates motility and emptying–
mechanoreceptors stim’d by distension
2.Degree of fluidity of chyme
Increased fluidity allows more rapid emptying
3.Presence of fat, acid, hypertonicity or distension in the
duodenum
Inhibit gastric motility and emptying
“Enterogastric reflex”–when any food content is in
small int—> sets of reflex—> neurons in small int send
signal to pyloric anteric nervous system—>reduces
gastric emptying
-Neural and hormonal factors (secretin,
cholecystokinin, and gastric inhibitory peptide – GIP)
4.Outside influences – e.g. Emotion, pain, hunger
(stimulates or inhibits)–motilin—> hormone released
when no more food in stomach; sets up motility pattern
MMC (in last lecture); increases motility of the stomach

49
Q

what are the gastri secretion of the stomach, and where are they secreted from?

A
  1. oxyntic mucosa–mucus, enzymes, HCl, and Ghrelin

2. pyloric gland area–gastrin

50
Q

what do the parietal cells of the oxyntic tissue of gastric cells release?

A

HCl–for digestion, activation of pepsinogen, and killing bacteria
Instrinsic factor–needed for Vit B12 abs–>no Vit B12 leads to pernicious anemia

51
Q

describe parietal cell acid secretion

A

acid secretion stim’d by ACh, histamine, and gastrin; this converts a resting parietal cell into an acid secreting one–the receptors for ACh, histamine, and gastrin occur on the BASOLATERAL membrane (facing blood side) of the parietal cell–all 3 are synergistic and lead to maximal acid secretion;
intracellular canaliculi expand because they fuse to tubulovesicles (involved in H+/K+ ATPase)
-parietal cells contain a lot of mito to power the ATPAse pump

52
Q

describe the alkaline tide

A

during MAX ACID SECRETION, the blood supply to the stomach becomes alkaline because:
the H+/K+ ATPase is pumping protons out through the apical membrane to make the lumen more acidic (primary active transport); the drop in H leads to CA becoming very active and converting CO2 + H2O to H2CO3; H2CO3 loses a proton and becomes HCO3; HCO3 is then transported to theblood of the capillaries surrounding the stomach through the basolateral membrane via a chloride exchanger (secondary active transport) to maintain the charge

53
Q

what are the chief cell secretions?

A

pepsinogen–starts protein digestion as it is a protease

gastric lipase–starts fat digestion of TAGs and MAGs to FAs

54
Q

descibe the phases of gastric acid secretion

A
  1. Cephalic influences
    –30% of total acid secretion
    –occurs without food reaching the stomach (thinking about food, conditioned reflexes–pavlov; taste, smell, fear, depression
    –neural influences through vagus nerve–nerve impulses sent to stomach to stimulate acid secretion
  2. Gastric phase (50% total acid secretion)
    –local reflex responses–e.g. when stomach recieves food
    –response to gastrin from G cells in the presence of protein in the antrum
    –gastrin stims parietal and chief cell secretions and gastric motiltiy (acts of sm muscles, slight depol–increase contractility)
  3. Intestinal phase (5-10% of total acid secretion)
    –acid secretion slows down when gastric chyme enters intestine–duodenum– Dominantly inhibitory via neural and hormonal mechanism, via the enterogastric reflex; lipids and low pH cause inhibition of gastric secretion.
    –CCK and secretin are stim’d by lipids and low pH, respectively—contribute to inhibiting gastric secretion (only during intestinal phase)
    short neural reflex—inhibs gastric acid reflex
55
Q

describe digestion in the stomach

A
  • -proteins digested via pepsin
  • -fat digested from gastric lipase
  • -carb digestion begins in mouth and continues into the stomach – only briefly, stops because of acid–amylase is likely denatured
56
Q

absorption in the stomach?

A

–very limited; epithelial cells impermeable to most stuff; a few short-chain FAs can get through and some drugs and alcohol (weak acids like aspirin)

57
Q

How can the stomach contain strong acid and proteases without destroying itself?

A

gastric mucosal barrier–mucus shields the parietal, chief, and epithelial cells from HCl–>HCl cannot permeate,

  1. Luminal membrane not permeable to H+
  2. Tight junction prevents leakage of HCl between cells
  3. Layer of mucus coating offers additional protection (mucus layer also has bicarbonate)
  4. Damaged cells rapidly replaced every 3 days
58
Q

how to peptic ulcers form?

A

Helicobacter pylori
Chemical exposure (NSAID’s)
Stressful situations
(increase gastric secretions)

59
Q

—gastric bypass surgery removes 2/3 of the upper part of the stomach—removes intrinsic factor
gastric lipase and pepsinogen released by chief cells

A

ya

PHSI 208 (32 decks)

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