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Physiology Flashcards

1
Q

What are the 4 major functions of the GI Track

A
  1. Motility
  2. Secretion
  3. Digestion
  4. Absorption
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2
Q

What are the 3 ways in which peptides are delivered to their targets?

A
  1. Endocrine
  2. Paracrine
  3. Neurocrine
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3
Q

Gastrin

A

17 AA whose 4C terminal AA make up active cneter

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4
Q

Cholecstokinin

A

33AA closely related to gastrin structurally and functionally

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5
Q

Differences in activities in Gastrin & CCK

A

-depends on whether tyrosine is the 6th or 7th position from the C-terminus and whether or not it’s sulfated

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6
Q

GI Endocrine Cell

A

-hormone containing granules at the basal lateral membrane and the apical membrane adjacent to the gut lumen

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7
Q

VIP SIte of Release & Actions

A

Released: mucosa and smooth muscle of GI tract
Actions: relaxes sphincters
relaxes gut circular muscle
stimulates intestinal secretion
stimulates pancreatic secretion

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8
Q

Bombesin or GRP SIte of Release & Actions

A

Released: gastric mucosa
Actions: stimulates gastrin release

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9
Q

Enkephalins SIte of Release & Actions

A

Released: mucosa and smooth muscle of GI tract
Actions: inhibits intestinal secretion

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10
Q

Somatostatin

A

Action: inhibits gastrin release & other peptide hormone release
Site of release: GI mucosa, pancreatic islets
Releasers: acid, vagus inhibits release

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11
Q

Histamine

A

Action: stimulates acid secretion
Site of release: oxyntic gland mucosa ECL-cell
Releasers: gastrin, Ach

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12
Q

Gastrinoma: Zollinger-Ellison Syndrome

A
  • overproduction of gastrin
  • duodemal ulcer, diarrhea, steatorrhea
  • high rates of acid secretion
  • inactivation of pancreatic lipase
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13
Q

Pancreatic Cholera: Werner-Morison Syndrome

A
  • over production of VIP
  • diarrhea, metabolic acidosis, dehydration, hypokalemia
  • high rates of intestinal secretion
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14
Q

Gastric Esophageal Reflux Disease (GERD)

A
  • acid reflux
  • heartburn
  • hiatal hernia, pregnancy, failure of secondary peristalsis
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15
Q

Impaired Gastric Emptying

A
  1. Failure to empty
    • fullness, loss of appetite, nausea
    • obstruction-ulcer, cancer
    • vagotomy
  2. Increased Emptying
    • inadequate regulation
    • diarrhea, duodenal ulcer
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16
Q

GI Motility

A

Interaction of 3 neural network

  • central nervous system (CNS)
  • autonomic nervous system (ANS)
  • enteric nervous system
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17
Q

Enteric Nervous System

A

-neurons located in the gut wall comprise the intrinsic neural network, which is called the enteric nervous system

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18
Q

Other factors of GI Motility

A

-include neurotransmitters, neurohumoral factors-Serotonin, food and mechanical stretch

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19
Q

Autonomic Nervous System

A
  • both sympathetic and parasympathetic nervous system innervates GI tract
  • In General: sympathetic systems slows down GI motility, parasympathetic stimulates GI motility
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20
Q

Enteric Nervous System

A
  • present in the gut
  • comprises of 2 components
    1. myenteric plexus
    2. meissner plexus
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21
Q

Myenteric Plexus

A

-present b/w circular and longitudinal muscle layer

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22
Q

Meissner Plexus

A

-located in submucosa

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23
Q

Peristalsis

A
  • gut/intestinal contraction or peristalsis has rhythmicity
  • results from pacing from pacemaker present in ENS
  • pacemaker cells are interstitial cell of Cajal
  • Peristalsis results from a complex interaction b/w interstitial cell, other enteric neurons and smooth muscle
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24
Q

GI-Pacemaker Interstitial Cell of Cajal

A
  • interstitial cell are now thought to be pacemaker cell of GI tract
  • not neural in origin
  • they are present in Enteric nervous system
  • slow waves generates from these cell which lead to peristalsis at varialbe rate
  • present throughout GI tract
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25
Q

Esophagus Motility

A
  • conduit of solids/liquids to stomach
  • upper esophageal sphincter consist of striated muscle
  • body of esophagus has both striated and smooth muscle
  • lower esophageal sphincter (LES) let food pass through esophagus into the stomach
  • LES relaxation is controlled by vagus (NO, neurotransmitter)
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26
Q

Peristalsis in Esophagus

A
  • primary: reflex esophageal peristaltic contraction wave associated with swallowing
  • secondary: residual food in the esophagus, as seen with ineffective peristalsis, may be cleared
  • tertiary: nonperistaltic contractions
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27
Q

Gastric Physiology

A
  • receptive relaxation of fundus
  • upper - handles liquids
  • lower - solid pulverized
  • gastric pacemaker - 3 cycles/min
  • antrum empties contents in duodenum when particles size 1mm
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28
Q

Small Bowel Physiology

A
  • facilitates nutrient absorption
  • organized motor pattern
  • motility pattern: fasting/fed pattern
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29
Q

Fasting Pattern/Migrating Motor Complex

A

-sweeping function/house keeping
-four phases
Phase 1: motor quiescence (40-60%)
Phase 2: increasing but irregular contraction (20-30%)
Phase 3: intense rhythmic contraction (20%)
Phase 4: a transition from phase 3 to 1 (0-5%)

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30
Q

Fed Pattern

A
  • following meal ingestion MMC converts in characteristic fed pattern
  • mixes and propel intestinal content
31
Q

Achalasia

A

-greek meaning “doesn’t relax”
-esophageal motor disorder, failure of LES relaxation on swallow
Treatment: sphincter dilatation with fish whale bone

32
Q

Incidence & Etiology of Achalasia

A
  • 1 in 100,000
  • autoimmune, degenerative, infectious???
  • selective loss of post-ganglionic inhibitory neurons (no NO)
  • Pathology: Lymphocyte infiltrate in myenteric plexus & loss of ganglion cells
33
Q

Symptoms of Achalasia

A
  • Dysphagia for solid (91%) and liquid (85%)
  • chest pain locating in area of xiphoid process in 40%
  • heart burn is reported in 40%
  • weight loss in 60%
  • regurgitation of food/Globus
  • association with adrenal insufficiency and alacrimin in children (Allgrove Syndrome)
34
Q

Diagnosis of Achalasia

A
  • history and physical
  • endoscopy
  • barium radiography
  • manometry
35
Q

Endoscopy

A
  • performed to evaluate condition that mimics Achalasia (pseudoachalasia)
  • dilated esophagus with food and pills
  • lower esophageal sphincter appear tight
  • examine gastro-esophgeal junction and fundus of stomach for any malignancy
36
Q

Barium Swallow

A
  • can be used as primary screening test (95% diagnostic accuracy)
  • dilated esophagus with bird beak appearance of distal part
  • severe dilation can lead to sigmoid esophagus
  • poor peristalsis on fluoroscopy
37
Q

Manometry

A
  • involves measurement of pressure using special catheter

- esophageal, antroduodenal and ano-rectal manometry are most common

38
Q

2 Manometry Criteria to Diagnose Achalasia

A
  • incomplete LES relaxation (LES fail to relax in response to swallow)
  • aperistalsis in the body of esophagus (distal 2/3)
  • supportive feature hypertensive LES, Low amplitude esophgeal contraction
39
Q

Treatment of Achalasia

A
  1. Medical: calcium blocker, nitrates
  2. Endoscopic: Botulinum injection, balloon dilation
  3. Surgery: heller’s myotomy
40
Q

Complications of Achalasia

A
  • malnutrition
  • aspiration
  • malignancy: untreated achalasia is associated with an increased risk of squamous cell esophageal cancer
41
Q

Diseases Associated with Achalasia-Like motility disorders

A
  • malignancy, especially gastric carcinoma
  • Chagas Disease: secondary to Trypanosoma cruzi infection
  • Amyloidosis
  • Sarcoidosis
  • Neurofibromatosis
42
Q

Motility Disorders Characterized by?

A
  • heartburn, regurgitation, dysphagia

- chest pain

43
Q

Abnormal Pattern Classified in what disorders?

A
  • diffuse esophageal spasm
  • nutcracker esophagus
  • hypertensive lower esophageal sphincter
44
Q

Diffuse Esophageal Spasm (Discoordinated Motility)

A
  • repetitive contractions (>/= 3 peaks)

- prolonged duration contractions

45
Q

Nutcracker Esophagus

A

hypercontracting esophagus

-increased distal peristaltic amplitude and duration

46
Q

Motility

A

-movement of gut, propels food by smooth muscle

47
Q

Secretion

A

-salivary glands, lining secrets mucus, acid from parital cells

48
Q

Digestion

A

-neutrients, proximal small intestine

49
Q

Serosal Surface

A

outside lining

50
Q

Mucosa

A

inner lining

51
Q

Endocrine

A

-release from one part, travels through blood stream, acts on another part of body

52
Q

Paracrine

A

-acts on cells near their location that have a specific receptor

53
Q

Neurocrine

A

-synthesized in cell body, migrate down axon and released by action potential

54
Q

Effect of sulfination on gastrin?

A

no effect

55
Q

Effect of sulfination on CCK?

A

-must have sulfate group, if not only has effects like gastrin does

56
Q

2 Effects of CCK?`

A
  1. stimulates gallbladder contraction

2. stimulates pancreatic enzyme secretion

57
Q

Receptor Gastrin acts on?

A

CCK-2 (B)

58
Q

Receptor CCK acts on?

A

CCK-1 (A)

59
Q

Why are all amino acids needed for activity of secretin family?

A

-because it exists in active form in a helical configuration so you need all amino acids to make the tertiary structure

60
Q

Where is gastrin released from?

A
  1. antrum
  2. duodenum
    - also in jejunum
61
Q

Where is CCK released from?

A
  1. duodenum
  2. jejunum
  3. ileum
62
Q

Where is Secretin released from?

A
  1. duodenum

- also in jejunum and ileum

63
Q

Where is GIP released from?

A
  1. duodenum

2. jejunum

64
Q

Where is Motilin released from?

A
  1. duodenum

2. jejunum

65
Q

What causes gastrin release?

A

protein, distention, nerve

-inhibited by acid

66
Q

What causes CCK release?

A

protein, fat

67
Q

What causes Secretin release?

A

acid

68
Q

What causes GIP release?

A

protein, fat, carbohydrates

69
Q

What causes motilin release?

A

nerve

70
Q

Actions of gastrin?

A

acid secretion

mucosal growth

71
Q

Actions of CCK?

A

stimulates pancreatic HCO3- secretion
pancreatic enzyme secretion
gallbladder contraction
pancreatic growth

INHIBITS: gastric emptying

72
Q

Actions of Secretin?

A

inc. pancreatic HCO3- secretion
bile HCO33- secretion
pancreatic growth

INHIBITS: acid secretion

73
Q

Actions of GIP?

A

insulin release (stimulates)

INHIBITS: acid secretion

74
Q

Actions of Motilin?

A

stimulates gastric motility

stimulates intestinal motility

GI (19 decks)

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