Physiology Flashcards
What are the 4 major functions of the GI Track
- Motility
- Secretion
- Digestion
- Absorption
What are the 3 ways in which peptides are delivered to their targets?
- Endocrine
- Paracrine
- Neurocrine
Gastrin
17 AA whose 4C terminal AA make up active cneter
Cholecstokinin
33AA closely related to gastrin structurally and functionally
Differences in activities in Gastrin & CCK
-depends on whether tyrosine is the 6th or 7th position from the C-terminus and whether or not it’s sulfated
GI Endocrine Cell
-hormone containing granules at the basal lateral membrane and the apical membrane adjacent to the gut lumen
VIP SIte of Release & Actions
Released: mucosa and smooth muscle of GI tract
Actions: relaxes sphincters
relaxes gut circular muscle
stimulates intestinal secretion
stimulates pancreatic secretion
Bombesin or GRP SIte of Release & Actions
Released: gastric mucosa
Actions: stimulates gastrin release
Enkephalins SIte of Release & Actions
Released: mucosa and smooth muscle of GI tract
Actions: inhibits intestinal secretion
Somatostatin
Action: inhibits gastrin release & other peptide hormone release
Site of release: GI mucosa, pancreatic islets
Releasers: acid, vagus inhibits release
Histamine
Action: stimulates acid secretion
Site of release: oxyntic gland mucosa ECL-cell
Releasers: gastrin, Ach
Gastrinoma: Zollinger-Ellison Syndrome
- overproduction of gastrin
- duodemal ulcer, diarrhea, steatorrhea
- high rates of acid secretion
- inactivation of pancreatic lipase
Pancreatic Cholera: Werner-Morison Syndrome
- over production of VIP
- diarrhea, metabolic acidosis, dehydration, hypokalemia
- high rates of intestinal secretion
Gastric Esophageal Reflux Disease (GERD)
- acid reflux
- heartburn
- hiatal hernia, pregnancy, failure of secondary peristalsis
Impaired Gastric Emptying
- Failure to empty
- fullness, loss of appetite, nausea
- obstruction-ulcer, cancer
- vagotomy
- Increased Emptying
- inadequate regulation
- diarrhea, duodenal ulcer
GI Motility
Interaction of 3 neural network
- central nervous system (CNS)
- autonomic nervous system (ANS)
- enteric nervous system
Enteric Nervous System
-neurons located in the gut wall comprise the intrinsic neural network, which is called the enteric nervous system
Other factors of GI Motility
-include neurotransmitters, neurohumoral factors-Serotonin, food and mechanical stretch
Autonomic Nervous System
- both sympathetic and parasympathetic nervous system innervates GI tract
- In General: sympathetic systems slows down GI motility, parasympathetic stimulates GI motility
Enteric Nervous System
- present in the gut
- comprises of 2 components
1. myenteric plexus
2. meissner plexus
Myenteric Plexus
-present b/w circular and longitudinal muscle layer
Meissner Plexus
-located in submucosa
Peristalsis
- 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
GI-Pacemaker Interstitial Cell of Cajal
- 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
Esophagus Motility
- 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)
Peristalsis in Esophagus
- 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
Gastric Physiology
- receptive relaxation of fundus
- upper - handles liquids
- lower - solid pulverized
- gastric pacemaker - 3 cycles/min
- antrum empties contents in duodenum when particles size 1mm
Small Bowel Physiology
- facilitates nutrient absorption
- organized motor pattern
- motility pattern: fasting/fed pattern
Fasting Pattern/Migrating Motor Complex
-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%)
Fed Pattern
- following meal ingestion MMC converts in characteristic fed pattern
- mixes and propel intestinal content
Achalasia
-greek meaning “doesn’t relax”
-esophageal motor disorder, failure of LES relaxation on swallow
Treatment: sphincter dilatation with fish whale bone
Incidence & Etiology of Achalasia
- 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
Symptoms of Achalasia
- 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)
Diagnosis of Achalasia
- history and physical
- endoscopy
- barium radiography
- manometry
Endoscopy
- 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
Barium Swallow
- 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
Manometry
- involves measurement of pressure using special catheter
- esophageal, antroduodenal and ano-rectal manometry are most common
2 Manometry Criteria to Diagnose Achalasia
- 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
Treatment of Achalasia
- Medical: calcium blocker, nitrates
- Endoscopic: Botulinum injection, balloon dilation
- Surgery: heller’s myotomy
Complications of Achalasia
- malnutrition
- aspiration
- malignancy: untreated achalasia is associated with an increased risk of squamous cell esophageal cancer
Diseases Associated with Achalasia-Like motility disorders
- malignancy, especially gastric carcinoma
- Chagas Disease: secondary to Trypanosoma cruzi infection
- Amyloidosis
- Sarcoidosis
- Neurofibromatosis
Motility Disorders Characterized by?
- heartburn, regurgitation, dysphagia
- chest pain
Abnormal Pattern Classified in what disorders?
- diffuse esophageal spasm
- nutcracker esophagus
- hypertensive lower esophageal sphincter
Diffuse Esophageal Spasm (Discoordinated Motility)
- repetitive contractions (>/= 3 peaks)
- prolonged duration contractions
Nutcracker Esophagus
hypercontracting esophagus
-increased distal peristaltic amplitude and duration
Motility
-movement of gut, propels food by smooth muscle
Secretion
-salivary glands, lining secrets mucus, acid from parital cells
Digestion
-neutrients, proximal small intestine
Serosal Surface
outside lining
Mucosa
inner lining
Endocrine
-release from one part, travels through blood stream, acts on another part of body
Paracrine
-acts on cells near their location that have a specific receptor
Neurocrine
-synthesized in cell body, migrate down axon and released by action potential
Effect of sulfination on gastrin?
no effect
Effect of sulfination on CCK?
-must have sulfate group, if not only has effects like gastrin does
2 Effects of CCK?`
- stimulates gallbladder contraction
2. stimulates pancreatic enzyme secretion
Receptor Gastrin acts on?
CCK-2 (B)
Receptor CCK acts on?
CCK-1 (A)
Why are all amino acids needed for activity of secretin family?
-because it exists in active form in a helical configuration so you need all amino acids to make the tertiary structure
Where is gastrin released from?
- antrum
- duodenum
- also in jejunum
Where is CCK released from?
- duodenum
- jejunum
- ileum
Where is Secretin released from?
- duodenum
- also in jejunum and ileum
Where is GIP released from?
- duodenum
2. jejunum
Where is Motilin released from?
- duodenum
2. jejunum
What causes gastrin release?
protein, distention, nerve
-inhibited by acid
What causes CCK release?
protein, fat
What causes Secretin release?
acid
What causes GIP release?
protein, fat, carbohydrates
What causes motilin release?
nerve
Actions of gastrin?
acid secretion
mucosal growth
Actions of CCK?
stimulates pancreatic HCO3- secretion
pancreatic enzyme secretion
gallbladder contraction
pancreatic growth
INHIBITS: gastric emptying
Actions of Secretin?
inc. pancreatic HCO3- secretion
bile HCO33- secretion
pancreatic growth
INHIBITS: acid secretion
Actions of GIP?
insulin release (stimulates)
INHIBITS: acid secretion
Actions of Motilin?
stimulates gastric motility
stimulates intestinal motility
