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GI Exam 1 > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

Bolus

A

rounded mass of food ready to swallow

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2
Q

Borborygmi

A

abdominal rumblings sounds (gas)

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3
Q

Chyme

A

semifluid mass of partly digested food passed from stomach to duodenum

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4
Q

Diverticulum

A

outpouching of GI wall

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5
Q

Eructation

A

belching

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6
Q

Peristalsis

A

propulsion of food through esophagus and intestines

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7
Q

Postprandial

A

after feeding

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8
Q

Sitophobia

A

fear of eating

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9
Q

Steatorrhea

A

fatty stools

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10
Q

Upper GI Structures

A

oral cavity, pharynx, esophagus, stomach, small intestine (duodenum, jejunum, ileum)

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11
Q

Lower GI Structures

A

large intestine (cecum, colon, rectum, anus)

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12
Q

Accessory Organs

A 
All secrete substances into GI tract
Salivary Glands
Exocrine Pancreas
Liver
Gallbladder
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13
Q

Sphincters purpose?

A

regulate movement into GI tract and allow some compartments to act as reservoirs

  • proximal pressure –> relaxation
  • distal pressure –> contraction
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14
Q

GI epithelial cells undergo constant renewal….

A

stem cells at base of crypts divide, differentiate, and migrate toward tips of microvilli –> apoptosis occurs 3-6 days –> cell is shed into lumen
*loss of APC –> colorectal cancer risk

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15
Q

Diverticulum

A

single pouch protruding from alimentary tract (usually false)
- individuals with diverticulosis have multiple diverticula due to lack of fiber in diet –> can progress to diverticulitis

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16
Q

Mucus

A

viscous, hydroscopic gel secreted by goblet cells
Mucin protein monomers combined into complexes by disulfide bonds
- glycosylation protects protein core from proteases
- Enterocytes are coated with transmembrane mucins

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17
Q

Digestion

A

mechanical and chemical reduction of food into nutrients

  1. Teeth –> masticate food, saliva provides lubrication
  2. Stomach –> movements and pepsin digest food creating chyme
  3. Duodenum contains brush border enzymes and additional enzymes from pancreas
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18
Q

Absorption

A

transport of nutrients across epithelium into blood
Dependent on splanchnic circulation –> all blood entering intestines leaves through portal vein to liver for detox
- AA, monosaccharides, and lipids are absorbed in duodenum and jejunum
- Bile salts/acids absorbed in ileum
- small intestines and colon absorb water and electrolytes

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19
Q

Enterohepatic circulation

A

recycling of bile salts/acids (95% of bile salts are recycled)
-return to liver via the hepatic portal vein

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20
Q

Chylomicrons absorption

A

chylomicrons are too large to pass through capillaries –> therefore they are absorbed through lacteals which empty into blood stream via thoracic duct

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21
Q

Mesenteric Ischemia

A

occlusive mechanism –> thrombi
nonocclusive mechanism –> prolonged reflexive vasoconstriction
*causes postprandial pain and sitophobia

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22
Q

Water secretion and absorption

A

Majority of fluids absorbed in small intestine
- fluids help uptake of nutrients and minimize damage to epithelium
- fluid is supplied by many GI organs
Water moves across epithelium by pressure gradients and AQP channels that follow gradients set up by ions and nutrients

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23
Q

Diarrhea

A

Osmotic diarrhea –> overgrowth of bactera –> increased production of organic acids –> pull water from blood stream into lumen by osmosis
Secretory diarrhea –> infection leads to excess secretion of chloride –> drawing water into lumen

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24
Q

Antidiarrheals

A

some work by slowing transit time –> increase absorption

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25
Q

Motility

A 
controls length of time for digestion and absorption
Esophagus --> 10 seconds
Stomach --> 4-5 hrs
Small Intestine --> 2-3 hrs
Large Intestine --> 30-40 hrs
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26
Q

Muscle in GI tract

A

most is smooth muscle

long slender cells separated into branching bundles –> gap junctions/nexuses enable contraction wave

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27
Q

GI Smooth Muscle

A

phasic contraction –> seconds
tonic contraction –> minutes/hours –> sphincters
can shorten considerably
initiate depolarization in response to stretch

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28
Q

Contraction/Relaxation of Smooth Muscle Pathway

A

ACH binds to muscarinic –> influx of Ca –> activation of calmodulin dependent MLC kinase –> phosphorylation of myosin –> increased myosin-ATPase –> binding of myosin to actin –> contraction –> dephosphorylation of myosin by MLC phosphatase –> relaxation

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29
Q

Peristaltic contractions

A

propel intestinal contents forward

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30
Q

Segmenting contractions

A

contractions of circular muscles –> mixing contents, no propulsion

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31
Q

Migrating Motor Complex

A

relaxation of sphincters and contraction of smooth muscle in stomach and intestines occurs during fasting by MOTILIN

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32
Q

Submucosal Nerve Plexus

A

within small and large intestines –> within submucosa

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33
Q

Myenteric Nerve Plexus

A

between circular and longitudinal muscle layers –> from esophagus to anus

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34
Q

Afferent neurons of enteric nervous system

A
  • excited by fast distention of gut wall or chemical signals

- many sensory neurons stimulated by 5-HT from enterochromaffin cells

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35
Q

Efferent neurons of enteric nervous system

A
  • found primarily in myenteric plexus (unipolar)

- excited by EPSPs, respond with sustained trains of APs

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36
Q

Parasympathetic activity

A

mostly cholinergic of vagus

- stimulates activity of enteric plexuses –> increased motility and secretory activity

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37
Q

Sympathetic acitivity

A

mostly adrenergic

- inhibits activity of enteric plexuses –> decreased motility and secretory activity

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38
Q

Neurotransmitters of Enteric

A
  1. ACh –> primary excitatory transmitter –> increases intracellular Ca –> relaxation
  2. Gastrin Releasing Peptide –> released from vagus to stimulate G cell secretion of gastrin
  3. Substance P –> excitatory transmitter generally released with ACh
  4. Vasoactive Intestinal Peptide –> promotes motility, relaxes smooth muscle, stimulates fluid secretion
  5. Nitric Oxide –> inhibitory NT co-released with VIP from inhibitory neurons –> relaxation
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39
Q

GI Hormones

A
  1. Gastrin –> released by G cells of stomach in response to detection of AA –> pepsinogen and H+ release
  2. CCK –> released by I cells in D/J in response to detection of fat and AA –> secretion of pancreatic enzymes and bile salts
  3. Secretin –> released by S cells in D/J in response to acid detection –> release bicarb and inhibit gastric motility
  4. Gastric Inhibitory Peptide –> released by K cells in D/J in response to detection of carbs and fat –> inhibits gastric acid secretion and stimulate insulin
  5. Motilin –> secreted by endocrine cells –> released cyclically during fasting to initiate MMC
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40
Q

Microbiota

A

greatly outnumber us in cell number

reside in outer mucus layer of large intestine –> constitue 60% of fecal mass

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41
Q

Achalasia

A

failure of LES to relax

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42
Q

Aspiration

A

inhalation of oropharyngeal or gastric contents into respiratory tract

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43
Q

GERD

A

heartburn due to inappropriate closure of LES –> acid in esophagus

44
Q

Deglutition

A

swallowing

45
Q

Dysgeusia

A

distorted ability to taste

46
Q

Halitosis

A

bad breath

47
Q

Manometry

A

test to measure pressure in GI tract

48
Q

Mastication

A

chewing

49
Q

Xerostermia

A

dry mouth

50
Q

Saliva contents

A 
Generally an exocrine secretion
Water --> majority
Digestive enzymes
Mucins --> lubricate
Defense Molecules
Growth factors
Bicarbonate
Sex Steroids
51
Q

Salivary glands

A

Parotid –> entirely serous (25% volume)
Submandibular –> mixed (70% volume)
Sublingual –> mucous (5% volume)

52
Q

Flow rate affecting saliva [ ]

A

fast flow rate = hypertonic and basic

slow flow rate = hypotonic

53
Q

Parasympathetic Nervous system affecting saliva

A

acts through VIP and ACh on muscarinic receptors –> increased watery saliva

54
Q

Sympathetic Nervous system affecting saliva

A

acts through NE on beta-1 and alpha-1 to increase viscous saliva

55
Q

Oral Cavity Digestion

A

Mastication
Salivary amylase –> hydrolyzes alpha-1,4 glycosidic linkages
Lingual lipase –> breaks down TG

56
Q

Physiology of Taste

A

Taste ligands bind to GPCR –> secondary messengers –> release NTs –> taste signals to nucleus tractus solitarius –> gastric acid secretion

57
Q

Causes of Xerostomia

A

Sjogren, Meds, Head/Neck radiation, Dehydration, Sialothiasis, Nerve damge, Postmenopause

58
Q

Consequences of Xerostomia

A
  • Increased risk of opportunistic infections
  • Halithosis –> production of hydrogen sulfide
  • Decrease in oral pH –> tooth decay
  • Decrease in taste
  • Problems with speech
  • Dysphagia
59
Q

Central Input for Swallowing

A

mucosal mechanoreceptors transmit messages through glossopharyngeal and vagus –> medullary swallowing center

  • somatic nerves –> contract top 1/3
  • autonomic nerves –> regulates smooth muscle in bottom 2/3
60
Q

Swallowing a bolus

A
  1. tongue contacts hard palate pushing bolus against and closing soft palate
  2. Breathing inhibited as bolus passes airway (epiglottis is closed to prevent aspiration)
  3. Food moves down into esophagus by perastalsis
61
Q

Mechanoreceptors sense distention or pH

A

contractions (ACh) above and relaxation (NO/VIP) below

62
Q

Secondary Peristalsis

A

restricted to smooth muscle –> elicited by distension of esophagus or acid in esophagus`

63
Q

Retrograde movements

A

eructation, vomitting, regurgitation

- don’t require additional movements except relaxation of sphincters

64
Q

Diffuse esophageal spasms

A

uncoordinated contractions –> regurg

65
Q

Control of LES

A

depends on enteric plexus neurons

  • closed between swallows –> cholinergic
  • relaxed during swallows –> NO/VIP
66
Q

Functions of stomach???

A
  1. highly acidic environment (defense against germs)
  2. reservoir for food storage
  3. fragments bolus into chyme –> maximal absorption
  4. protein digestion –> acid hydrolysis and pepsin
  5. empty contents into small intestine controllably
67
Q

Bezoar

A

ball of foreign material trapped in stomach

68
Q

Emesis

A

vomiting

69
Q

dyspepsia

A

indigestion (pain in upper abdomen)

70
Q

Gastroparesis

A

delayed emptying

71
Q

Migrating Motor Complex

A

clears undigested material from GI tract

72
Q

Regurgitation

A

flow of material that has not reached stomach back up esophagus

73
Q

Rugae

A

stomach folds which expand as stomach fills

74
Q

Scintigraphy

A

dual-radiolabeled solid and nutrient meal to measure gastric emptying

75
Q

Trituration

A

grinding of food into small molecules

76
Q

Gastrin

A
  • polypeptide with variable length that binds CCK2 receptors

- secreted by G cells in antrum –> activates parietal cells in fundus/body to secrete acid

77
Q

Triggers for Gastrin

A
  1. Seeing food or stomach distension –> vagal stimulation of gastrin
  2. aromatic AA in lumen
78
Q

Substances that activate parietal cells to secrete acid??

A

Gastrin, histamine, and ACh

- all activate the H/K ATPase which pumps H into gastric lumen which is followed by Cl- to make HCl

79
Q

ACh stimulating acid release

A
  1. Binds muscarinic receptors on parietal cells
  2. Activates ECL cells to release histamine
  3. Acitvates enteric neurons to release GRP –> release gastrin
80
Q

Gastrin stimulating acid release

A
  1. Bind to parietal cells

2. Activates ECL cells to release histamine

81
Q

Histamine stimulating acid release

A
  1. released from ECL cells –> activates parietal cells via cAMP pathway
82
Q

Parietal cell stimulation secretes acid how?

A

Upon stimulation, tubulovesicular membranes fuse with luminal membrane –> increases # of H/K ATPase channels in apical membrane

  • protons are generated via carbonic anhydrase
  • Na/K ATPase maintains K gradient
  • HCO3 exported basolaterally –> alkaline tide
83
Q

Inhibitor of gastrin release?

A

Somatostatin –> secreted from D cells in antrum when pH<3

  • a rise in pH decreases Somatostatin secretion
  • it prevents G cells from releasing gastrin by inhibiting formation of cAMP and prevents ECL cells secretion of histamine
84
Q

Interdigestive phase

A

low acid secretion, D cells secrete somatostatin to maintain low levels of gastrin

85
Q

Cephalic phase

A

dorsal vagal complex integrates input from higher centers to activate vagus. GRP activates gastrin and ACh activates ECL and parietal cells

86
Q

Gastric phase

A

distension of stomach activates vagal afferents –> AA activate gastrin secretion and food raises pH –> decreasing somatostatin

87
Q

Intestinal phase

A

introduction of gastric contents into small intestine –> activates duodenal G cell secretion of gastrin –> activation of secretin and other enterogastrones

88
Q

Intrinsic factor

A
  • required for B12 absorption in ileum
  • glycoprotein secreted by parietal cells
  • PPI inhibit parietal cells but not intrinsic factor part
  • Lack of B12 caused by autoimmune destruction of parietal cells –> pernicious anemia
89
Q

Pepsinogen secretion

A
  • inactive proenzyme protease
  • secreted by chief cells is gastric glands in response to ACh and gastrin…..inhibited by secretin
  • activated in acidic envrionment –> pepsin (proteolytic enzyme)
90
Q

Mucous gel layer in stomach

A
  • surface epithelial cells secrete mucus and bicarb in response to PGE2
  • NSAIDs block PGE2 –> gastric irritation
91
Q

Trefoil factors

A

signal repair and regeneration of injury epithelium

92
Q

Zollinger-Ellison Syndrome

A

caused by gastrin-secreting tumor

- results in excess H secretion

93
Q

Peptic Ulcer Disease

A

-hyperacidity –> deterioration of gastro-mucosal barrier

94
Q

Achlorhydria

A

reduced acid secretion

- caused by aging, gastric resection, autoimmune attack

95
Q

Gastric motility

A

when food enters stomach –> very little change in pressure –> receptive relaxation
- dorsal vagal complex integrates input to alter gastric secretion and relaxation

96
Q

Gastrocolic reflex

A

induces need to defecate

97
Q

Gastroileal reflex

A

causes ileocecal valce to relax and transfer contents into large bowel

98
Q

Gastric digestion

A

low pH denatures proteins –> parietal cells
pepsin releases peptides –> chief cells
gastric lipase produced FFA
mechanical movements emulsify

99
Q

Gastric trituration

A

emptying of liquids –> tonic (body and fundus)

emptying of solids involves antral pump –> phasic (antrum)

100
Q

Peristalsis occurs at Basic Electrical Rhythm

A
  • establishes max frequency of wave that is propagated over stomach
  • amplitude can be altered (para (+), sympathetic (-))
  • contractions speed up and strengthen as they approach pyloric sphincter
101
Q

Gastric emptying

A

when food enter duodenum –> many signals feed back to slow gastric emptying time

  • pure glucose –> faster emptying
  • protein –> intermediate emptying
  • solid meal/fat –> slow emptying
102
Q

Gastric contractions inhibited by…..

A
  • acid in duodenum

- fat in duodenum (CCK)

103
Q

Pyloric stenosis

A

congenital condition where pylorus fails to relax

104
Q

Gastroparesis

A

reduced gastric emptying often to diabetic neuropathy –> treat with prokinetic drugs

105
Q

Dumping syndrome

A

rapid gastric emptying from gastric bypass, vagotomy, high sugar meals

106
Q

Peptic ulcer disease

A

scarring and ulcers near pylorus can delay emptying

107
Q

Vomiting (emesis)

A

expulsion of contents of one’s stomach contents through reverse peristalsis of intestine

  • lots of stuff can cause it, all influence emetic center in CNS
  • increased salivation to neutralize acidity
  • preceded by retching
  • glottis closes to prevent aspiration, contraction of ab muscles and diaphragm

GI Exam 1 (7 decks)

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