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163 Cards in this Set
- Front
- Back
- 3rd side (hint)
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contraction of circular smooth muscle in GI tract?
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decrease in diameter
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contraction of longitudinal smooth muscle in GI tract?
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shortening
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Extrinsic Innervation of GI tract?
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PNS and SNS
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Intrinsic Innervation of GI tract?
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Myenteric Plexus and Meissner's Plexus
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PNS is usually (1) on GI tract.
PNS innervation of GI tract is via (2) and (3) nerves. |
1 = excitatory
2 = vagus 3 = pelvic |
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PRE PNS fibers synapse in (1); POST PNS fibers leave (2) and innervate (3), (4) and (5).
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1 = myenteric and meissners plexus
2 = myenteric and meissners plexus 3 = smooth muscle 4 = secretory cells 5 = endocrine cells |
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PNS vagus nerve innervates what part of the GI tract? (4)
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1 - esophagus
2- stomach 3 - pancreas 4 - upper large intestine |
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PNS pelvic nerve innervates what part of the GI tract? (3)
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1 - lower large intestine
2 - rectum 3 - anus |
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SNS is usually (1) on GI tract.
SNS originate from (2). PRE SNS synapse on (3). POST SNS synapse on (4). |
1 = inhibitory
2 = T8-L2 in spinal cord 3 = prevertebral ganglion (Ach) 4 = myenteric and meissners plexus (NE) |
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Intrinsic Innveration of GI tract?
Consists of (1) reflexes that relay information within (2) |
enteric nervous system:
- myenteric plexus - meissner's plexus 1 = local 2 = GI tract |
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Myenteric Plexus aka. (1), is located between (2) and primarily controls (3)
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1 - Auerbach plexus
2 - outer long. and inner circular smooth mm. 3 - GI motility |
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Meissner's Plexus aka (1), is located between (2) and primarily controls (3)
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1 - submucosal plexus
2 - inner circular mm and submucosa 3 = GI secretion and blood flow |
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What are the 4 "official" GI hormones?
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gastrin
CCK secretin glucose-dependent insulinotropic peptide (GIP) |
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All of the biological activity of Gastrin resides in (1).
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1 - last 4 CT amino acids
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Gastrin is produced in (1) as little gastrin with (2) amino acids
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1 = G cells of stomach (antro-duodenal cells)
2 = 17 aa |
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ACTIONS OF GASTRIN
increases (1) stimulates growth of (2) |
1 = gastric acid secretion
2 = growth of gastric mucosa |
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Main Stimuli for Secretion of Gastrin?
- small peptides/amino acids esp. (1) - stomach (2) - vagal stimulation via (3) |
1 = Phe, Trp
2 = distension of stomach 3 = GRP (gastrin-releasing peptide) --> not blocked by atropine |
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INHIBITION OF GASTRIN
negative feedback from (1) hormone (2) |
1 = H+ in lumen of stomach
2 = somatostatin |
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Zollinger-Ellison Syndrome
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tumors of pancreas or duodenum that release gastrin
- excessive gastric acid secretion |
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CCK is homologous to (1) with the same (2) but the biological activity of CCK depends on the (3)
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1 = gastrin
2 = 5 terminal CT amino acid residues 3 = CT heptapeptide |
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CCK is produced by (1) in the (2).
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1 = I cells
2 = duodenal and jejunal mucosa |
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What stimulates secretion of CCK? (2)
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1 - small peptides and amino acids
2 - fatty acids and monoglycerides |
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ACTIONS of CCK
- stimulates contraction of (1) and relaxation of (2) - increases pancreatic (3) and (4) secretion - stimulates growth of (5) - inhibits (6) |
1 = gallbladder
2 = Sphincter of Oddi 3 = pancreatic enzyme 4 = HCO3- 5 = exocrine pancreas 6 = gastric emptying |
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Secretin is homologous to (1).
Which aa are necessary for biologic action of secretin? (2) |
1 = glucagon
2 = ALL aa are necessary |
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Secretin is produced in (1).
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S cells of duodenal-jejunal mucosa
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What are the stimuli for secretion of secretin? (2)
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1 = H+ in lumen of duodenum
2 = fatty acids in lumen of duodenum |
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ACTIONS of Secretin
- stimulates pancreatic and hepatic (1) secretion - (2) bile production - increases growth of (3) - inhibits (4) |
1 - HCO3-
2 - stimulates bile production 3 - exocrine pancreas 4 - gastric H+ secretion |
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GIP is homologous to (1) and (2).
GIP is secreted by (3) |
1 = glucagon
2 = secretin 3 = duodenum and jejunum |
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What stimulates release of GIP? (what's so special about this hormone)
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FAT, PROTEIN and CARB
- the only hormone to respond to all 3 |
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ACTION of GIP
- stimulates (1) - inhibits (2) |
1 - insulin secretion (oral glucose load is more effective)
2 - gastric H+ secretion |
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What is the stimulus for somatostatin secretion?
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- H+ in lumen of GI tract
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What inhibits somatostatin release?
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somatostatin release is inhibited by VAGAL stimulation (PNS)
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Main action of somatostatin is? (2)
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1 = inhibits release of ALL GI hormones
2 = inhibits gastric H+ secretion |
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Where is histamine secreted in the GI tract? (1)
Histamines increases (2) |
1 = mast cells of gastric mucosa
2 = gastric H+ secretion (direct, and potentiates effects of gastrin and vagal stimulation) |
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VIP is homologous to (1) and is considered a (2) hormone.
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1 = secretin
2 = neurocrine hormone (released from neurons) |
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VIP produces (1), stimulates (2) and inhibits (3).
These actions resemble (4) hormone. |
1 = relaxation of GI smooth muscle
2 = HCO3- secretion from pancreas 3 = gastric H+ secretion |
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What hormone mediates pancreatic cholera?
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VIP (vasoactive intestinal peptide)
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GRP aka (1) is released from (2) that innervate G cells.
GRP stimulates (3) |
1 = bombesin
2 = vagal nerve endings 3 = gastrin release (from G cells) |
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Enkephalins stimulate contraction of (1) particularly the (2); and inhibit (3).
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1 = contraction of GI smooth mm.
2 = pyloric, ileocecal and LES sphincters 3 = intestinal secretion of fluid and electrolytes |
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The action of opiates to treat diarrhea is mediated by ?
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enkephalins
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Striated muscle in the GI tract is located in ... (3) areas?
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1. upper 1/3 of esophagus
2. pharynx 3. external anal sphincter |
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Phasic contractions of GI smooth mm. occur in ... (3) areas?
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1. esophagus
2. stomach 3. small intestine |
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Tonic contractions occur in .... (4) areas?
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1. lower esophageal sphincter
2. orad stomach 3. ileocecal sphincter 4. internal anal sphincter |
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Pacemaker cells for GI smooth muscle?
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Interstitial Cajal cells
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What is a "slow wave" ?
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oscillating membrane potential that occurs spontaneously
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Slow waves determine the pattern of (1) but are not themselves (1).
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1 = action potentials
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Slow waves are due to opening of what kind of channels?
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Ca2+ channels for depolarization
K+ channels for hyperpolarization |
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frequency of slow waves is not influenced by (1)
frequency of slow waves sets the maximum (2) |
1 = neuronal or hormonal inputs
2 = frequency of contraction of smooth muscle |
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frequency of slow waves in stomach = (1)
frequency of slow waves in duodenum = (2) |
1 = 3 waves/min
2 = 12 waves/ min ** characteristic for each part of the GI tract |
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where is the swallowing centre located?
what nerves mediate the swallowing reflex? |
medulla
vagus N. and glossopharyngeal N. |
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intraesophageal pressure equals (1) which is lower than (2).
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1 = intrathoracic pressure
2 = atmospheric pressure |
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What is a primary peristaltic contraction in esophagus?
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area of high pressure behind food bolus, with distension in front of bolus, moves down esophagus and propels food down --> accelerated by gravity
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What is the purpose of secondary peristaltic contraction in esophagus?
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clears the esophagus of any remaining food
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Relaxation of the LES is mediated by (1) nerve and (2) neurotransmitter
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1 = vagus nerve
2 = VIP |
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Gastroesophageal reflux aka. (1) occurs when the tone of the (2) is (3)
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1 = heart burn
2 = LES 3 = decreased |
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Achalasia
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LES does not relax and food accumulates in esophagus
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Oxyntic glands are located in what region of the stomach?
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orad region
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The stomach has an additional layer of smooth muscle.. the (1) layer.
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oblique smooth muscle layer
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Receptive Relaxation is a (1) reflex that is initiated by (2). It is characterized by (3) and is potentiated by (4) hormone.
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1 = vagovagal reflex
2 = distension of stomach 3 = orad region of stomach relaxes to accomodate incoming food 4 = CCK |
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What is retropulsion?
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when distal antrum is closed, and caudad region contracts food is propelled back into stomach to be mixed
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Gastric contractions are increased by (1) and decreased by (2)
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1 = vagal stimulation
2 = sympathetic stimulation |
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Migrating Myoelectric Complex
- frequency? (1) - when? (2) - mediated by? (3) - function? (4) |
1 = every 90 minutes
2 = during fasting 3 = motilin 4 = to clear the stomach of residual food |
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Gastric Emptying is slowed by (3).
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1 = hypertonic/hypotonic chyme
2 = fat (via CCK) 3 = H+ in duodenum |
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Role of segmentation contractions?
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mix the intestinal contents with no net forward movement
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Role of Peristaltic contractions?
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propel the chyme through small intestine
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Peristaltic reflex is coordinated by (1).
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enteric nervous system
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Gastroileal reflex is mediated by (1). Presence of food in the (2) triggers relaxation of (3) and delivery of intestinal contents to (4).
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1 = ANS
2 = stomach 3 = relaxation of ileocecal sphincter 4 = large intestine |
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In the large instestine, segmentation contractions produce (1)
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haustra
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mass movements in the large intestine occur (1)
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1-3 times/day
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Most colonic water absorption occurs in the (1).
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proximal colon
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rectosphincteric reflex
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presence of feces in rectum relaxes the internal anal sphincter
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Valsalva Maneuvre
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intra-abdominal pressure is increased by expiring against a closed glottis --> necessary for defecation
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Gastrocolic reflex
- presence of food in the (1) increases (2) and frequency of (3) |
1 = stomach
2 = motility of colon 3 = mass movements |
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Gastrocolic reflex has a rapid (1) component and a slower (2) component, mediated by (3)
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1 = PNS (stomach distension)
2 = hormonal 3 = CCK and gastrin |
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Megacolon (Hirschsprung's Disease)
- results in (1) of involved segment - dilation and accumulation (2) to constriction - (3) |
absence of colonic enteric nervous system
1 = constriction 2 = proximal 3 = severe constipation |
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Functions of Saliva (3)
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- digestion of starch and triglycerides
- lubrication - protection |
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Composition of Saliva:
- high (1) - low (2) - tonicity? (3) - enzymes? (4) |
1 = K+ and HCO3-
2 = Na+ and Cl- 3 = hypotonicity 4 = a-amylase, lingual lipase, kallikrein |
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low flow rate saliva?
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lowest osmolarity with highest K+ conc.
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high flow rate saliva?
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composition is closest to the of plasma --> does not have as much time for reabsorption of NaCl
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Function of Salivary Acinus?
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produces initial saliva with composition isotonic and almost identical to plasma
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Function of Salivary Ducts?
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- reabsorb Na+ and Cl-
- secrete K+ and HCO3- - saliva becomes hypotonic in ducts bc it is reabsorbing ions yet impermeable to water |
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Why is HCO3- low with low flow rate and increased with high flow rate? (even though it is secreted?)
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HCO3- is selectively stimulated when saliva secretion is stimulated
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Production of saliva is stimulated by both (1) but (2) is more important
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1 = PNS and SNS
2 = PNS |
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PNS stimulation of saliva is enhanced by (4)
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1 - conditioning
2 - smell 3 - food 4 - nausea |
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PNS stimulation of saliva is inhibited by (4)
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1 - dehydration
2 - sleep 3 - anticholinergic drugs 4 - fear |
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Salivary Stimulation - Mechanism
PNS acts via (1) receptor and (2) 2nd messenger SNS acts via (3) receptor and (4) 2nd messenger |
1 = muscarinic Ach receptor
2 = PLC -> IP3 and Ca2+ 3 = b-adrenergic 4 = cAMP |
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What do parietal cells secrete?
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HCl
intrinsic factor |
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What do chief cells secrete?
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pepsinogen
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What do G cells secrete?
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gastrin
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Proton pump inhibitors inhibit (1)
ex. (2) |
H+/K+ ATPase on apical membrane of parietal cells --> blocks H+ secretion
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alkaline tide
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HCO3- produced in parietal cells in absorbed into blood stream in exchange for Cl-; pH of venous blood increases
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PNS increases H+ secretion by acting directly on (1) and indirectly by stimulating (2)
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1 = muscarinic receptors (parietal cells) - Ach
2 = G cells (via GRP) |
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What receptor does gastrin act on? what 2nd messenger?
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1. CCKb on parietal cells
2. IP3/Ca2_ |
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Histamine is released by (1). and stimulates H+ secretion by (2).
Ex. of an H2 receptor blocker (3) |
1 = enterochromaffin cells (ECL)
2 = activating H2 receptors 3 = cimetidine |
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Potentiation
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response to simultaneous admin. of 2 stimulants is greater than the sum of either alone
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low pH (< 3.0) (1) gastrin secretion and thus (2)
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1 = inhibits
2 = inhibits H+ secretion |
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Direct pathway of somatostatin inhibition of gastric H+ secretion
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binds Gi coupled receptor, decreases cAMP (antagonizes histamines effects)
--> same mechanism seen with prostaglandins |
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indirect pathway of somatostatin inhibition of gastric H+ secretion
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inhibits release of histamine and gastrin
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Peptic Ulcer Disease
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loss of the protective mucous barrier and/or excessive secretion of H+ and pepsin
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damaging factors leading to peptic ulcer disease (7)
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alcohol
NSAIDs smoking stress H.pylori infection H+ pepsin |
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protective factors against peptic ulcer disease (5)
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mucous
HCO3- prostaglandins mucosal blood flow GFs |
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Gastric ulcers have decreased (1) and increased (2); they are caused by (3)
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1 = H+ secretion
2 = increased gastrin (bc decreased negative feedback) |
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How does H.Pylori survive in acidic stomach environment?
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contains urease --> alkalinizes local environment
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diagnostic test for H.pylori?
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drinking a solution of 13C urea, which is converted to 13CO2 urease and measured in expired air
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duodenal ulcers are characterized by (1) and (2); it can be caused by (3)
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1 = increased H+ secretion
2 = increased gastrin secretion in response to a meal 3 = h.pylori |
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three drugs that block gastric H+ secretion
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atropine - inhibits Ach muscarinic R. on parietal cells
cimetidine - blocks H2 histamine R. omeprazole - inhibits H+K+ ATPase |
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Composition of Pancreatic Juice:
- high (1) - same (2) as plasma - higher (3) than plasma - lower (4) than plasma - tonicity? (5) - enzymes? (6) |
1 = volume
2 = Na+, K+ 3 = HCO3- 4 = Cl- 5 = isotonicity 6 = pancreatic amylase, lipase and proteases |
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at low flow rates, pancreatic secretion is composed mainly of (1) and (2)
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1 = Na+
2 = Cl- |
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at high flow rates, pancreatic secretion is composed mainly of (1) and (2)
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1 = Na+
2 = HCO3- |
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Secretin acts on pancreatic (1) cells to increase (2) via (3) 2nd messenger
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1 = ductal cells
2 = HCO3- secretion 3 = cAMP |
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CCk acts on the pancreatic (1) cells to increase (2) and potentiates the effect of (3) via (4) 2nd messenger.
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1 = acinar cells
2 = pancreatic enzyme secretion 3 = secretin 4 = IP3/Ca2+ system |
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What does bile contain? (4)
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bile salts
phospholipids cholesterol bile pigments (bilirubin) |
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What do choleretic agents do?
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increase bile formation
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What are the primary bile acids?
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cholic acid
chenodeoxycholic acid |
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What are the secondary bile acids?
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deoxycholic acid
lithocolic acid |
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What amino acids do bile acids get conjugated with?
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glycine and taurine
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Contraction of the gallbladder is caused by (1) and (2)?
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1 = CCK
2 = Ach |
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Where is the Na+-bile acid cotransporter located? What is its role?
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terminal ileum
impt. for recirculation of bile acids |
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which form of carbohydrates can be absorbed?
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monosaccharides
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alpha amylase
- function? - location? |
- degrades a-1,4 glycosidic bonds in starch yielding maltose, maltotriose and a-limit dextrins
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main monosaccharides used for energy? (3)
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glucose
fructose galactose |
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Absorption of Glucose/Galactose in small intestine?
- transporters? |
SGLT Na+-dependent cotransport on luminal membrane
GLUT2 on basolateral membrane via facilitated diffusion |
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method of fructose absorption?
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facilitated diffusion, down conc. gradient
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optimum pH for pepsin activity?
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pH 1 - 3
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in what form are proteins absorbed?
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amino acids
di and tri peptides |
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method of amino acid absorption?
- luminal mb? (1) - basolateral mb? (2) |
1 - Na+dep. aa co-transport
2 - facilitated diffusion via specific aa. carrier (neutral, acidic, basic and imino acids) |
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how are di and tri peptides absorbed?
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H+ dependent co-transport across luminal membrane; hydrolyzed by proteases in the cytoplasm
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Colon has a (1) epithelium.
Small intestine and gallbladder have a (2) epithelium. |
1 = tight
2 = leaky |
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Absorption of Na+ in intestinal cells? (4)
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1. passive diffusion
2. Na+glucose/ Na+ aa cotransport 3. NaCl transport 4. Na+/H+ exchange |
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Absorption of Cl- in intestinal cells? (3)
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1. passive diffusion - paracellular (follows Na+)
2. Na+/Cl- cotransport 3. Cl- / HCO3- exchange |
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dietary K+ is (1) in the small intestine via (2) and secreted in the (3)
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1 = absorbed
2 = paracellular route 3 = colon (stimulated by aldosterone) |
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H20 absorption is (1) in the small intestine/gallbladder; whereas, in the colon, H20 permeability is (2).
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1 = isoosmotic
2 = decreased |
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what is the primary ion secreted into the intestinal lumen?
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Cl-
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Cholera Toxin
- mechanism? - causes? |
1 - permanently activates Gs by ADP ribosylation, increases cAMP and Cl- are open; Na+ and H20 follow Cl- out
2 - secretory diarrhea |
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water-soluble vitamins are absorbed via (1)
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Na+ dependent co-transport
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fat soluble vitamins ex. (1) are absorbed via (2)
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1 = vitamins A, D, E ,K
2 = incorporation into fat micelles |
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How is vitamin B12 absorbed?
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intrinsic factor must be present to complex vit. B12 and bind receptor on ileal cells
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Absorption of Ca2+ depends on...
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1,25 dihydoxycholecalciferol and calbindin D-28K
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In what form is iron absorbed?
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heme iron
free Fe2+ |
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Peptides that INCREASE FOOD intake (9)
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G O B G G M N A E
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ghrelin
orexin a and b beta-endorphin galanin GHRH MCH neuropeptide Y agouti-related peptide endocannabinoids |
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peptides that DECREASE FOOD intake (14)
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L P P P C M G G I V C I I T
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leptin CK
PYY PP POMC CRH MSH glucagon GLP-1 insulin vasopressin CART IL1 IL6 TNFa |
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Motilin
- where is it produced? (1) - when is it produced? (2) - function? |
1 = enterochromaffin cells
2 = released periodically during fasting 3 = initiates migrating motor complex |
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Obestatin
- function? (1) |
counteracts effect of motilin
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pancreatic polypeptide
- where is it made? - what stimulates its release? - function? |
1 = F cells in pancreatic islets
2 = protein digests (Phe, Trp) AND vagal cholinergic activity 3 = inhibits pancreatic secretion, induces satiety |
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PYY
- where is it made? (1) - what stimulates its release? (2) - functions? (3) |
1 = L cells of ileum/colon
2 = fatty meal and cholinergic stimulation 3 = inhibits secretin-CCK effects and inhibits food intake |
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NPY
- where? (1) - main functions? (2) |
1 = neurons of CNS esp. hypothalamus
2 = controls food intake and appetite AND blocks transmission of pain signals in brain |
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Constrictors of GI Smooth MM?
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Ach
Substance P |
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Relaxants of GI Smooth MM?
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VIP
PACAP ATP GABA NO |
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Mechanism of Peristalsis?
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stretching of gut --> release of 5HT from EC-cell --> stimulates cGRP neurons to release Ach/SP behind stretch AND release relaxants ahead of stretch
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LES tone is increased by? (5)
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Ach
gastrin H.pylori motilin ghrelin |
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LES tone is decreased by? (5)
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secretin
CCK GIP VIP/NO P4 (pregnancy) |
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swallowing center (1) the respiratory centre
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inhibits
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Afferent limb of swallowing reflex
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trigeminal, glossopharyngeal, vagal
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Efferent limb of swallowing reflex
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trigeminal, facial, hypoglossal, vagal
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Innervation of Colon
- proximal SNS ? (1) - distal SNS? (2) - rectum/internal anal sphincter? (3) - external anal sphincter? (4) |
1 = superior mesenteric ganglion
2 = infereior mesenteric ganglion 3 = hypogastric plexus 4 = pudendal N. |
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Tenia coli are formed from (1).
Which plexus is concentrated in tenia? (2) |
1 = longitudinal smooth mm.
2 = myenteric plexus |
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haustral contractions
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local circular mm. contractions
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adynamic paralytic ileus
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- inhibition of smooth mm. of gut and disappearance of motor activity
- following trauma or surgery - may be due to activation of opiod receptors or excessive NE discharge |
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blind loop syndrome
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- normal passage of intestinal contents is disturbed due to blind loop
--> massive overgrowth of bacteria with malabsorption and steatorhea |
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Saliva Composition at Low rates of secretion?
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low Na+ and Cl - (lots reabsorbed)
high K+ and HCO3- (lots secreted) |
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xerostomia
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deficient salivation
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EGF and saliva
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saliva is rich in EGF which helps stimulate GI mucosal cell proliferation, repair and healing
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"gastric barrier"
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surface mucosa cells in the pyloric region secrete a thick, HCO3- rich mucous AND epithelial cells are connected by TJ that contribute to resistance of mucosal damaga
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