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GI II Exam 1 EH > Lecture 1: Review of GI Physiology > Flashcards

Lecture 1: Review of GI Physiology Flashcards

1
Q

What are 3 stimuli for the secretion of Gastrin?

A

1) Small peptides and AA’s
2) Distention of the stomach
3) Vagal stimulation (via GRP)

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2
Q

What are 2 actions of Gastrin?

A

1) Increase gastric H+ secretion
2) Stimulates growth of gastric mucosa

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3
Q

Which cells secrete CCK and their location?

A

I cells of the duodenum and jejunum

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4
Q

What are 2 stimuli for the release of CCK?

A
  • Small peptides and AA’s
  • Fatty acids
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5
Q

What are 4 actions of CCK once secreted?

A

1) Increased pancreatic enzyme secretion and HCO3- secretion
2) Contractionof thegallbladderandrelaxationofsphincter of Oddi
3) Growth of exocrine pancreas and gallbladder
4) Inhibits gastric emptying

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6
Q

Which cells secrete Secretin and their location?

A

S cells of the duodenum

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7
Q

What are 2 stimuli for the secretion of Secretin?

A

1) H+ in the duodenum
2) Fatty acids in the duodenum

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8
Q

What are 4 actions as a result of Secretin release?

A

1) Increased pancreatic HCO3- secretion
2) Increased biliary HCO3- secretion
3) Decreased gastric H+ secretion
4) Inhibits trophic effect of gastrin on gastric mucosa

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9
Q

What is the site of secretion for Glucose-dependent insulinotropic peptide (GIP)?

A

Duodenum and Jejunum

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10
Q

What are 3 stimuli for the release of Glucose-dependent insulinotropic peptide (GIP)?

A

1) Fatty acids
2) AA’s
3) Oral glucose

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11
Q

What are 2 actions of Glucose-dependent insulinotropic peptide (GIP) once released?

A

1) Increases insulin secretion from pancreatic B cells (incretin effect)
2) Decreases gastric H+ secretion

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12
Q

Which 2 hormones mediate the incretin effect?

A

1) Glucagon-like peptide 1 (GLP-1)
2) Gastric inhibitory peptide (GIP)

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13
Q

What are 3 actions of ACh in the GI tract?

A

1) Contraction of smooth muscle
2) Relaxation of sphincters
3) Increase salivary, gastric, and pancreatic secretion

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14
Q

What are 3 actions of NE in the GI tract?

A

1) Relaxation of smooth muscle in wall
2) Contraction of sphincters
3) Increase salivary secretion

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15
Q

What are 3 actions of Vasoactive Intestinal Peptide (VIP)?

A

1) Relaxation of smooth muscle
2) Increased intestinal secretion
2) Increased pancreatic secretion

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16
Q

What are the 2 actions of Enkephalins in the GI tract?

A

1) Contraction of smooth muscle
2) Decreased intestinal secretion

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17
Q

What are the 2 actions of Neuropeptide Y in the GI tract?

A

1) Relaxation of smooth muscle
2) Decreased intestinal secretion

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18
Q

What are the 2 actions of Substance P in the GI tract?

A

1) Contraction of smooth muscle
2) Increased salivary secretion

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19
Q

Which 3 NT’s cause contraction of smooth muscle in the GI?

A

1) ACh
2) Enkephalins
3) Substance P

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20
Q

Which 4 NT’s cause relaxation of smooth muscle in the GI?

A

1) NE
2) VIP
3) NO
4) Neuropeptide Y

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21
Q

Which functional layer of the GI tract consists of smooth muscle, and its contractions change the shape and surface area of the epithelium?

A

Muscularis mucosae

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22
Q

What are slow waves of GI smooth muscle?

A

Depolarization and repolarization of the membrane potential, but are NOT APs

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23
Q

What’s a phasic vs. tonic contraction of the GI tract?

A
  • Phasic = periodic contractions followed by relaxation
  • Tonic = maintain a constant level of contraction w/o regular periods of relaxation
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24
Q

The greater the # of APs on top of the slow wave the larger the _________ contraction

A

Phasic

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25
Q

Where do phasic contractions occur in the GI tract?

A
  • All tissues involved in mixing and propulsion
  • Esophagus, stomach (antrum), small intestine
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26
Q

Where do tonic contractions occur in the GI tract?

A
  • Stomach (orad)
  • Lower esophageal, ileocecal, and internal anal sphincters
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27
Q

What is the effect of ACh and NE on slow waves in the GI tract?

A
  • ACh increases the amplitude of slow waves and the # of AP’s
  • NE decreases the amplitude of slow waves
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28
Q

What are the pacemaker for GI smooth muscle?

A

Interstitial cells of Cajal (ICC) = generate and propogate slow waves

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29
Q

Where are the interstitial cells of Cajal (ICC) located?

A

Myenteric plexus

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30
Q

Which part of the brain controls the involuntary swallowing reflex?

A

Medulla

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31
Q

Describe the afferent and efferent input involved in the involuntary swallowing reflex?

A
  • Food in pharynx –> afferent sensory input via vagus/glossopharyngeal N. —>
  • Swallowing center (medulla) –> brainstem nuclei –> Efferent input to pharynx
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32
Q

Which peristaltic wave cannot occur after vagotomy?

A

Primary peristaltic wave

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33
Q

What is the secondary peristaltic wave?

Why is it significant?

A
  • Occurs if primary wave fails to empty the esophagus or if gastric contents reflux into the esophagus
  • Occurs even after vagotomy
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34
Q

What is the resting pressure in the UES, body of esophagus (upper, near diaphragm) and LES?

A
  • UES = elevated (> pharynx and body of esophagus)
  • LES = elevated
  • Body of esophagus is flaccid with pressure <0
  • Near diaphragm the pressure in esophagus is >0 (subatmospheric)
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35
Q

Describe the change in pressure within the esophagus during swallowing?

A
  • UES relaxes (opens - pressure decreases)
  • Once bolus passes, the sphincter closes and assumes its resting tone
  • Peristaltic wave: body of esophagus undergoes peristaltic contraction; wave of high pressure moving along esophagus
  • LES and orad stomach relax - receptive relaxation (pressure decreases)
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36
Q

Which nerve and chemicals are invovled in the opening of the LES?

A
  • Vagal nerve
  • Release of VIP
  • NO also may play a role
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37
Q

What is happening during receptive relaxation and is mediated by what reflex?

A
  • Decrease pressure and increase volume of the orad region
  • Vagovagal reflex
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38
Q

Which process is occuring in the caudad region of the stomach for mixing and digestion of food particles?

A
  • Most of the gastric contents are propelled back into the stomach for further mixing and reduction of particle size
  • Retropulsion
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39
Q

Large particles of undigested residue remaining in the stomach are emptied by what?

Occur at how long of an interval and only during?

A
  • Migrating myoelectric complex (MMC) = periodic, burstin peristaltic contractions
  • Occur at 90 min intervals, during FASTING
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40
Q

Which hormone plays a significant role in mediating MMC’s?

A

Motilin

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41
Q

Which 4 conditions increase the rate of gastric emptying?

A

1) Decreased distensibility of the orad
2) Increased force of peristaltic contractions of caudad stomach
3) Decreased tone of the pylorus
4) Increased diameter and inhibition of segmenting contractions of the proximal duodenum

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42
Q

Which 4 factors inhibit gastric emptying?

A

1) Relaxation of orad
2) Decreased force of peristaltic contractions
3) Increased tone of pyloric sphincter
4) Segmentation contractions in intestine

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43
Q

What is the Entero-Gastric reflex?

A

Negative feedback from duodenum will slow down the rate of gastric emptying

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44
Q

Describe the effects that acid, fats, peptides/AA’s, and hypertonicity of the duodenum play in the Entero-gastric reflex.

A
  • Acid in duodenum –> Secretin release –> inhibit stomach motility via inhibition of gastrin
  • Fats, peptides/AA’s in duodenum –> CCK and GIP release –> inhibit stomach motility
  • Hypertonicity in duodenum –> (unknown hormone) –> inhibit gastric emptying
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45
Q

How are the contractions in the small intestine different from those in the stomach, especially in regards to slow waves.

A
  • Unlike in the stomach, slow waves themselves DO NOT initiate contractions in the small intestine
  • Spike potentials (AP) are necessary for musle contractions
  • Slow wave frequency sets the maximum frequency of contractions
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46
Q

Which hormones/NT’s can stimulate contractions in the small intestine?

Which inhibit?

A
  • Serotonin, Prostaglandins, Gastrin, CCK, Motilin, and Insulin stimulate contractions
  • Epinephrine (adrenal glands), Secretin, and Glucagon inhibit
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47
Q

Role of the myenteric plexus and submucosal (meissner) plexus of the intestinal wall?

A
  • Myenteric plexus mainly regulates relaxation and contraction
  • Submucosal (Meissner) plexus sense the lumen enviornment
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48
Q

Which cells of the intestinal mucosa sense the food bolus and what is released to initiate the peristaltic reflex?

A

Enterochromaffin cells (ECC) release 5-HT, which binds receptors on IPANs, initiating peristaltic reflex

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49
Q

What occurs behind and in front of the food bolus as it enters the small intestine and peristaltic reflex is initiated (reciprocal innervation)?

A
  • Behind bolus, excitatory NT’s (ACh and Substance P) released in circular m (contracts), while this pathway is simultaneously inhibited in longitudinal m. (relaxes) = segment narrows and lengthens
  • In front of bolus, inhibitory NT’s (VIP and NO) released in circular m. (relaxes), while excitatory pathways activated in longitudinal m. (contracts) = segment widens and shorten
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50
Q

Which type of contraction in the small intestine mixes the chyme?

A

Segmental contraction

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51
Q

What type of movement stimulates the defecation reflex?

A

Mass movements

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52
Q

Motility in the large intestine is key for?

A

Absorption of water/vitamins and conversion of digested food into feces

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53
Q

As the rectum fills with feces what occurs to the SM in the wall of rectum and internal anal sphincter?

Which reflex is this?

A
  • SM contracts and internal anal sphincter relaxes
  • Rectosphincteric reflex
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54
Q

Sensation of rectal distention and voluntary control of the external anal sphincter are mediated by pathways where?

What occurs with destruction of these pathways?

A
  • Pathways within the spinal cord that lead to the cerebral cortex
  • Destruction of these pathways causes loss of voluntary control of defecation
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55
Q

The vomiting reflex is coordinated by which brain region and the nerve impulses are transmitted via which afferents?

A
  • Coordinated by the medulla
  • Transmitted by vagus and sympathetic afferents to multiple brainstem nuclei
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56
Q

Order of events for the vomiting reflex?

A
  • Reverse peristalsis of small intestine
  • Stomach and pylorus relax
  • Forced inspiration to increase abdominal pressure
  • Movement of the larynx
  • LES relaxation
  • Glottis closes
  • Forceful expulsion of gastric contents
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57
Q

What is Gastroparesis and one of the most common causes?

Injury to what may contribute?

A
  • Slow emptying of stomach/paralysis of stomach in absence of mechanical obstruction
  • Diabetes mellitus is a common cause
  • Injury to vagus nerve
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58
Q

What is the cause of Hirschsprung disease (megacolon)?

Descrbe the physiological basis.

A
  • Ganglion cells absent from segment of colon
  • VIP levels low –> SM constriction/loss of coordinated movement -> colon contents accumulate
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59
Q

What is the tonicity of saliva in comparison to plasma?

K+, HCO3-, Na+ and Cl- concentrations?

A
  • Hypotonic compared to plasma
  • Increased K+ and HCO3-
  • Decreased Na+ and Cl-
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60
Q

What are the 2 main steps in formation of saliva and which cells mediate each part?

A

1) Formation of isotonic, plasma-like, solution by acinar cells
2) Modification of the isotonic solution by the ductal cells

61
Q

What is the combined action at the salivary ductal epithelial cell in formation of saliva and what is the net result?

A
  • Combined action is absorption of Na+ and Cl- and secretion of K+ and HCO3-
  • Net absorption of solute (more NaCl is absorbed than KHCO3 secreted)
62
Q

How do vasopressin and aldosterone modify the composition of saliva?

A
  • Decrease its [Na+]
  • Increase its [K+]
63
Q

What are the 2 unusual features in the regulation of salivary secretion?

A

1) Salivary is exclusively under the control of the ANS
2) Secretion is increased by BOTH parasympathetic and sympathetic stimulation

64
Q

Where is the oxyntic gland area vs. pylroic gland area of gastric mucosa and what does each secrete?

A
  • Oxyntic gland = located in proximal 80% of stomach (body and fundus); secretes acid
  • Pyloric gland = located in distal 20% of stomach (antrum); synthesizes and releases gastrin
65
Q

Where are parietal cells located in the stomach and what are their products?

A
  • Body of the stomach
  • Secrete: Intrinsic factor and HCl
66
Q

Where are chief cells located in the stomach and what do they secrete?

A
  • Body of the stomach
  • Secrete pepsinogen
67
Q

HCl with ______ initiates protein digestion

A

Pepsin

68
Q

Mucus cells of the antrum of stomach secrete what?

A
  • Mucus
  • HCO3-
  • Pepsinogen
69
Q

What is the most important stimuli for pepsinogen secretion in the stomach?

A

Vagus nerve stimulation

70
Q

What is responsible for the “alkaline tide” observed in gastric venous blood following a meal?

A
  • HCO3 is absorbed from the cell into the blood via a Cl−-HCO3 exchanger.
  • Absorbed HCO3 is responsible for the “alkaline tide” (high pH) that can be observed in gastric venous blood after a meal.
71
Q

What is the action of Omeprazole in the treatment of ulcers?

A

Inhibits the H+/K+ ATPase

72
Q

What is the action of Cimetidine used in the treatment of peptic ulcers, GERD, etc..?

How does this relate to potentiation interactions as well?

A
  • Antagonist of Histamine (H2) receptors –> reduces H+ secretion
  • Also blocks potentiated effects of ACh and Gastrin
73
Q

What type of feedback mechanism regulates HCl secretion in the stomach?

A
  • Passive feedback mechanism
  • As pH falls, gastrin release in inhibited
  • Decreases HCl secretion
74
Q

How do Histamine and ACh have potentiation effects in the secretion of HCl?

A
  • Histamine potentiates the actions of ACh and gastrin
  • ACh potentiates the actions of histamine and gastrin
75
Q

What acts on G cells to inhibit Gastrin release?

A
  • Somatostatin
76
Q

How does Vagal activation stimulate gastrin release?

A
  • Release of GRP
  • Inhibiting the release of somatostatin
77
Q

What 2 events stimulate the release of Somatostatin?

A
  • Gastrin itself increases somatostatin (negative feedback)
  • H+ in the gastric lumen also stimulates release
78
Q

Describe the direct and indirect pathway by which the vagus nerve stimulates HCl secretion by parietal cells (NT’s involved in each path)?

A

1) Vagus nerves innervate parietal cells directly, where they release ACh as the neurotransmitter.
2) Vagus nerves also innervate G cells, where they release GRP as the NT (indirect path) –> Gastrin released into circulation, which travels back to parietal cells causing increased H+ secretion

79
Q

What are the 2 stimuli for HCl secretion in the gastric phase?

A

1) Distention of the stomach
2) Presence of breakdown products of protein, AA’s and small peptides

80
Q

Which pathway of HCl secretion mediated by the Vagus nerve will be blocked by Atopine?

A

Only the direct pathway!

81
Q

What is the only secretion by the stomach that is required (essential)?

A

Intrinsic Factor needed for absorption of B12 in the ileum

82
Q

Failure to secrete Intrinsic Factor leads to?

Common underlying causes (hint: one is autoimmune mediated)?

A
  • Pernicious anemia
  • Common underlying cause is destruction of gastric parietal cells (atrophic gastritis)
  • Autoimmune metaplastic atrophic gastritis –> immune system attacks IF protein or gastric parietal cells
83
Q

Mucous neck cells secrete _________

Gastric epithelial cells secrete _________

A
  • Mucous neck cells secrete mucus
  • Gastric epithelial cells secrete HCO3-
84
Q

Which agents are protective of the gastric mucosa?

A
  • HCO3- and mucus
  • Prostaglandins (i.e., Misoprostol)
  • Mucosal blood flow
  • GF’s
85
Q

Which agents damage the gastric mucosa?

A
  • Acid
  • Pepsin
  • NSAIDs (i.e., aspirin)
  • H. pylori
  • Alcohol
  • Bile
  • Stress
86
Q

Which enzyme allows H. pylroi to colonize the gastric mucosa and through which mechanism?

How does this enzyme relate to diagnostics?

A
  • Urease
  • Converts urea to NH3 which alkalinizes the enviornment
  • A diagnostic test is based on urease activity!
87
Q

Which type of ulcer is most common and secretion of what is elevated?

A
  • Duodenal ulcer
  • H+ secretion is elevated
88
Q

What is H+ secretion and Gastrin levels like with a Gastric Ulcer?

A
  • H+ secretion is decreased
  • Gastrin levels are increased (due to decreased H+)
89
Q

What is Zollinger-Ellison syndrome caused by and what are the characteristic findings?

A
  • Gastrin secreting tumor in the pancreas
  • Massively increased levels of both Gastrin and H+
  • Increased parietal cells mass due to trophic effect of increased gastrin
90
Q

Why is steatorrhea a common finding in Zolinger-Ellison syndrome?

A

Low duodenal pH inactivates pancreatic lipases

91
Q

Which test is used in the diagnosis of gastrin-secreting tumors?

What are the findings?

A
  • Secretin stimulation test
  • Under normal conditions, secretin administratin inhibits gastrin release
  • In gastrinomas, injection of secretin causes paradoxical increase in gastrin release
92
Q

Which cells of the pancreas produce the aqueous secretion and what is the role of each cell type?

A
  • Centroacinar and ductal cells produce the initial aqueous solution which is isotonic and contains Na+, K+, Cl-, and HCO3-
  • Initial secretion is then modified by transport processes in ductal epithelial cells
93
Q

Which cells of the pancreas secrete enzymes and which are secreted as active and inactive forms?

A
  • Acinar cells
  • Pancreatic amylases and lipases are secreted as active enzyme
  • Proteases are secreted in inactive form and converted to active form in the lumen of duodenum
94
Q

What is the net result of modification of the intial pancreatic secretion by ductal cells (secretion and absorption)?

A
  • Secretion of HCO3- into pancreatic ductal juice
  • Absorption of H+
95
Q

During which pancreatic secretion phase are the enzymatic and aqueous secretions stimulated?

A

Intestinal phase

96
Q

What do I cells of the duodenum release and what stimulates this release?

What are the downstream effects on the pancreas?

A
  • Release CCK in response to Phe, Met, Trp, Small peptides, and FA’s
  • CCK stimulates pancreatic acinar cells –> increased IP3 and Ca2+
  • Release of enzymes
97
Q

What potentiates the effects of CCK on the pancreatic acinar cells?

A

ACh

98
Q

What do S cells of the duodenum secrete and what is the stimuli for this secretion?

What are the downstream effects on the pancreas?

A
  • Release secretin upon stimulation by H+
  • Secretin activates cAMP in pancreatic ductal cells
  • Leads to release of aqueous solution (Na+, HCO3-)
99
Q

What potentiates the effects of Secretin on pancreatic ductal cells?

A

ACh and CCK

100
Q

Where is the CFTR that is mutated in cystic fibrosis located?

A

Apical surface of ductal cell of pancreas

101
Q

Failure of which organ can result in hypoalbuminemia and resulting edema?

A

Liver

102
Q

How may CFTR mutations lead to recurrent acute and chronic pancreatitis?

A
  • Ability to flush active enzymes out of duct may be lost
  • Active enzymes in duct may lead to a breakdown of pancreas
103
Q

What is one of the most common causes of portal HTN?

A

Cirrhosis

104
Q

How does liver dysfunction (i.e., cirrhosis or portosystemic shunting) lead to hepatic encephalopathy?

A
  • Decreased hepatic urea cycle metabolism leads to accumulation of ammonia in systemic circulation
  • Ammonia READILY crosses the BBB and alters brain function
105
Q

What is the composition of bile and what are the 2 main components?

A
  • Bile salts (50%)
  • Phospholipids (40%) - i.e., lecithin
  • Bile pigments - i.e., bilirubin
  • Cholesterol
  • Ions and H2O
106
Q

What is the function of bile?

Solves which problem?

A
  • Vehicle for elimination of substances from the body
  • Solves the insolubility problem of lipids
107
Q

What are the 5 components/locations of bile secretion and absorption of bile salts?

A

1) Synthesis and secretion of bile salts by liver
2) Bile salts are stored and concentrated in gallbladder
3) CCK-induced gallbladder contraction and sphincter of Oddi relaxation
4) Absorption of bile salts into portal circulation
5) Delivery of bile salts to the liver

108
Q

Which hormone stimulates the uptake of ions and H2O into the bile duct?

A

Secretin

109
Q

Which hormones/NT stimulate contraction of the gallbladder for the release of bile?

A

ACh and CCK

110
Q

Which 2 transporters are located on the basolateral membrane of hepatocytes and mediate the re-uptake of bile salts from portal blood?

Which is Na+-dependent and which is Na+-independent?

A

1) Na+-dependent transport protein, Na+ taurocholate contransporting polypeptide (NTCP)
2) Na+-independent transport proten, organic anion transport proteins (OATP)

111
Q

Which transporter for bile acids is located on the basolateral side of the hepatocyte and which 2 are on the apical side for secretion?

A
  • NCTP is on basolateral side for uptake into liver
  • Bile salt excretory pump (BSEP) and Multidrug Resistance Protein 2 (MRP2) are located on the apical side from bile acid secretion
112
Q

Which transporter on the enterocytes of the small intestine is responsible for re-uptake of bile acids and which is responsible for secretion into portal circulation?

A
  • Apical sodium dependent bile acid transporter (ASBT) is reponsibe for re-uptake into enterocyte
  • Organic solute transporter alpha-beta (OSTalpha-OSTbeta) is responsible for export into portal circulation
113
Q

Which type of transport for bile acids occurs in the ileum and how efficient is this process in the reuptake?

A
  • Active and passive transport
  • Highly efficient, >90% of bile acids delivered to portal blood
114
Q

What are the 2 main causes of neonatal jaundice?

Which type of bilirubin is increased?

A

1) Bilirubin production elevated due to increased breakdown of fetal RBC’s (shortened lifespan of fetal erythrocytes)
2) Low activity of UDP glucuronyl transferase
- Increased levels of unconjugated (indirect)

115
Q

Which type of bilirubin is increased in Hemolytic Anemia?

A

Unconjugated bilirubin

116
Q

Gilbert syndrome is due to mutations in gene that codes for?

What type of bilirubin is increased?

A
  • Gene that codes for UDP glucuronyl transferase
  • Increased levels of unconjugated bilirubin
117
Q

What is Crigler-Najjar syndrome Type 1 due to?

When does it start?

Associated with what kind of damage?

A
  • NO function of UDP glucuronyl transferase; starts earlier in life
  • Kernicterus: form of brain damage caused by accumulation of unconjugated bilirubin in the brain and nerve tissues
118
Q

What is Crigler-Najjar syndrome Type 2 and when is its normal onset?

How severe?

Which type of bilirubin accumulates?

A
  • Starts later in life
  • Less than 20% function of UDP glucuronyl transferase
  • Increased levels of unconjugated bilirubin
  • Less likely to develop kernicterus
119
Q

What is the defect in Dubin-Johnson syndrome?

Common findings?

Which type of bilirubin is increased?

A
  • Mutations in multidrug resistance protein 2 (MRP2): hepatocytes unable to secrete conjugated bilirubin into bile
  • Increased conjugated bilirubin in the serum w/o elevation of liver enzymes

- LIVER HAS BLACK PIGMENTATION

120
Q

In Rotor syndrome there is a buildup of what?

Due to gene mutation in?

A
  • Buildup of both conjugated and unconjugated bilirubin in blodd, but majority = conjugated
  • Gene mutations lead to abnormally short, nonfunctional OATP1B1 and OATP1B3 proteins or total absence
  • Unable to transport bilirubin from the blood into the liver for secretion into bile
121
Q

Biliary tree obstruction would lead to increased levels of what type of bilirubin?

A

Conjugated bilirubin

122
Q

Gallstones impacted where may cause jaundice, biliary-type pain and risk of cholangitis and pancreatitis?

A

Distal bile duct

123
Q

Where are villi of the small intestine the longest and the shortest?

A
  • Longest in the duodenum
  • Shortest in the terminal ileum
124
Q

Which cells of the intestinal epithelium are part of the mucosal defenses against infection and secrete agents that destroy bacteria or produce inflammatory responses?

A

Paneth cells

125
Q

Which transporters on the luminal/apical side of the small intestine are necessary for transport of glucose, galactose, and fructose?

A
  • SGLT 1 –> glucose and galactose
  • GLUT 5 –> fructose
126
Q

What type of transport does SGLT1 on the apical side of the enterocytes utilize?

A

Secondary active transport

127
Q

Which transporters on the basolateral side of enterocytes transport glucose, galactose, and fructose into the blood?

Via what mechanism?

A
  • GLUT 2
  • Facilitated diffusion
128
Q

In lactose intolerance, undigested lactose remains in the lumen of intestine and causes what?

A

Holds onto H2O and causes osmotic diarrhea

129
Q

How is the inactive enzyme trypsinogen converted into trypsin?

A

By brush border enzyme, Enterokinase

130
Q

Which enzyme converts all of the inactive proteases to their active forms?

A

Trypsin

131
Q

What are the 3 endopeptidases?

A

1) Trypsin
2) Chymotrypsin
3) Elastase

132
Q

How are pancreatic proteases inactivated?

A

Digestion of themselves and each other!

133
Q

Which protein products are the only absorbable form?

How are larger products broken down into more absorbable forms?

A
  • Only AA’s, dipeptides and tripeptides are absorbable
  • Oligopeptides must be further hydrolyzed by brush-border proteases, yielding AA’s, diepeptides and tripeptides
134
Q

How does the type of AA affect the co-transport across the apical side of the enterocyte?

A

4 separate cotransporters: one each for neutral, acidic, basic, and imino AA’s

135
Q

What is the mechanism for the absorption of protein from inside the enterocyte to the basolateral (blood) side?

A

Facilitated diffusion

136
Q

Which ions are necessary for the co-transport of AA’s and di-/tripeptides across the apical (luminal) side of the enterocyte?

A
  • Na+ for AA’s
  • H+ for dipeptides and tripeptides
137
Q

How are lipids able to be emulsified in the stomach in the absence of bile acids?

A

Dietary proteins

138
Q

Which hormone is released to allow sufficient time for lipids to get digested properly and acts by slowing the rate of gastric emptying?

A

CCK

139
Q

How is the problem of active pancreatic lipase being inactivated by bile salts in the small intestine solved?

A

Colipase binds to pancreatic lipase and displaces bile salts

140
Q

How is Colipase activated?

A

Activated by trypsin

141
Q

Which enzyme breaks down phospholipids and into what products?

A
  • Phsopholipase A2
  • Lysolecithin and FA’s
142
Q

What are the 5 steps involved in the movement of lipids from the lumen of the small intestine across the epithelial cells?

A

1) Solubilization by micelles
2) Diffusion of micellar content
3) Reesterification
4) Chylomicron formation
5) Exocytosis of chylomicron into lymph

143
Q

What are the components of a Chylomicron?

A
  • Phospholipids and ApoB on surface
  • TAG’s and cholesterol core
144
Q

Explain the effect of ileal resection on the recirculation of bile acids and its effect on fat absorption?

A
  • Interrupts enterohepatic circulation of bile salts
  • Synthesis of new bile salts cannot keep pace w/ the fecal loss
  • Total bile salt pool is reduced
145
Q

Describe the mechanism of B12 absorption along the GI tract starting from the stomach until absorption into the blood stream?

A
  • B12 is complexed w/ R protein (from saliva) in stomach
  • Pancreatic proteases in duodenum cause B12 to dissociate from R protein
  • Intrinsic Factor (IF) from gastric secretions binds free B12, which then travels to distal ileum
  • Binds IF receptor and allows B12 to move into mucosa and then blood where it complexes with transcobalamin II
146
Q

Deficiency of vitamin B12 can lead to what type of anemia, why?

A
  • Pernicious anemia
  • B12 is important in DNA synthesis in RBC’s
147
Q

How does Gastrectomy and Gastric Bypass affect absorption of Vitamin B12?

A
  • Gastrectomy causes loss of parietal cells (source of IF)
  • Gastric bypass: exclusion of the stomach, duodenum, and prox. jejunum alters absorption of Vit B12
148
Q

Which part of the small intestine is responsible for the majority of Ca2+, Fe2+, and folate absorption?

A

Duodenum

149
Q

What is the MOA for cholera toxin leading to secretory diarrhea?

A
  • Toxin subunit move inside intestinal crypt cells and catalyze ADP ribosylation of αs subunit of the Gs protein coupled to AC
  • Inhibits GTPase activity, causing GTP to be permanently bound to αs subunit, AC permanently activated, cAMP levels remain high, and Cl- channels are kept open
  • Resulting Cl- secretion is accompanied by secretion of Na+ and H2O –> secretory diarrhea

GI II Exam 1 EH (12 decks)

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