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GI 2 COPY > Phys DSA > Flashcards

Phys DSA Flashcards

1
Q

What are 3 stimuli for the secretion of Gastrin?

A

1) Small peptides and AA’s2) Distention of the stomach3) Vagal stimulation (via GRP)

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2
Q

What are 2 actions of Gastrin?

A

1) Increase gastric H+ secretion2) Stimulatesgrowthofgastric mucosa

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3
Q

Which cells secrete CCK and their location?

A

I cellsof theduodenumand 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 4actions of CCK once secreted?

A

1) Increasedpancreatic enzyme secretionandHCO3-secretion2) Contractionof thegallbladderandrelaxationof sphincter of Oddi3)Growthofexocrine pancreasandgallbladder4)Inhibitsgastric 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 duodenum2) 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-secretion2) Increased biliary HCO3-secretion3) Decreased gastric H+ secretion4) 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 ofGlucose-dependent insulinotropic peptide(GIP)?

A

1) Fatty acids2) AA’s3) Oral glucose

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11
Q

What are 2 actions ofGlucose-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 3actions of ACh in the GI tract?

A

1) Contraction of smooth muscle2) Relaxation of sphincters3) 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 wall2) Contraction of sphincters3) Increase salivary secretion

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15
Q

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

A

1) Relaxation of smooth muscle2) Increased intestinal secretion2) 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 muscle2) Decreased intestinal secretion

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17
Q

What are the 2 actions of Neuropeptide Yin the GI tract?

A

1) Relaxation of smooth muscle2) 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 muscle2) Increased salivary secretion

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19
Q

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

A

1) ACh2) Enkephalins3) Substance P

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20
Q

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

A

1) NE2) VIP3) NO4) 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 areNOTAPs

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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 inmixing 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

-AChincreases the amplitude of slow waves and the # of AP’s-NEdecreases 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) =generateandpropogateslow 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 –>Efferentinput to pharynx
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32
Q

Which peristaltic wavecannotoccur 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 failsto 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 isflaccidwith 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 ofVIP-NOalso may play a role
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37
Q

What is happening duringreceptive relaxation and is mediated by what reflex?

A
  • Decrease pressure and increasevolume 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 arepropelledback 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 at90 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 orad2) Increased force of peristaltic contractions of caudad stomach3) Decreased tone of the pylorus4) 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 orad2) Decreased force of peristaltic contractions3) Increased tone of pyloric sphincter4) Segmentation contractions in intestine

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43
Q

What is the Entero-Gastric reflex?

A

Negativefeedback from duodenum willslow downtherate 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 –>Secretinrelease –> inhibit stomach motility viainhibitionofgastrin- Fats, peptides/AA’s in duodenum –>CCKandGIPrelease –> 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 themaximum frequencyof 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 Insulinstimulatecontractions- Epinephrine (adrenal glands), Secretin, and Glucagoninhibit
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47
Q

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

A

-Myenteric plexusmainly regulatesrelaxationandcontraction-Submucosal (Meissner)plexussense 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 onIPANs, initiating peristaltic reflex

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49
Q

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

A
  • Behindbolus, excitatory NT’s (ACh and Substance P) released incircular m(contracts), while this pathway is simultaneously inhibited in longitudinal m.(relaxes)=segment narrowsand lengthens- In front ofbolus, inhibitory NT’s (VIP and NO)releasedincircular m.(relaxes), while excitatory pathways activated inlongitudinalm.(contracts)= segmentwidensandshorten
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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/vitaminsandconversion 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
  • Pathwayswithinthe spinal cord thatleadtothecerebral cortex- Destruction of these pathways causeslossof voluntary controlofdefecation
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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 byvagusandsympathetic afferentsto 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 happens/contributestoachalasia of the esophagus?

A
  • Impaired peristalsis-Incomplete LES relaxationduring swallowing (stays closed)- Elevation of LES resting pressure
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58
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 acommon cause- Injury tovagus nerve
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59
Q

What is the cause of Hirschsprung disease (megacolon)?Descrbe the physiological basis.

A

-Ganglion cellsabsent from segment of colon- VIP levels low –> SM constriction/loss of coordinated movement -> colon contents accumulate

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60
Q

What is the tonicity of saliva in comparison to plasma?K+, HCO3-, Na+and Cl- concentrations?

A

-Hypotoniccompared to plasma-IncreasedK+ and HCO3–DecreasedNa+ and Cl-

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61
Q

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

A

1) Formation ofisotonic,plasma-like, solution by acinar cells2) Modification of the isotonic solution by theductal cells

62
Q

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

A
  • Combined action is absorption of Na+ and Cl-andsecretion of K+ and HCO3–Net absorptionof solute (more NaCl is absorbed than KHCO3 secreted)
63
Q

How do vasopressin and aldosterone modify the composition of saliva?

A
  • Decrease its [Na+]- Increase its [K+]
64
Q

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

A

1) Salivary isexclusivelyunder the control of theANS2) Secretion isincreasedbyBOTHparasympathetic and sympathetic stimulation

65
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); secretesacid-Pyloric gland= located in distal 20% of stomach (antrum); synthesizes and releasesgastrin

66
Q

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

A
  • Body of the stomach- Secrete:Intrinsic factorandHCl
67
Q

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

A
  • Body of the stomach- Secretepepsinogen
68
Q

HCl with ______ initiates protein digestion

A

Pepsin

69
Q

Mucus cells of the antrum of stomach secrete what?

A
  • Mucus- HCO3– Pepsinogen
70
Q

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

A

Vagus nerve stimulation

71
Q

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

A
  • HCO3is 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.
72
Q

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

A

Inhibits the H+/K+ ATPase

73
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
74
Q

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

A
  • Passive feedback mechanism- As pH falls, gastrin release ininhibited- Decreases HCl secretion
75
Q

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

A

-Histaminepotentiates the actions of ACh and gastrin-AChpotentiates the actions of histamine and gastrin

76
Q

What acts on G cells to inhibit Gastrin release?

A
  • Somatostatin
77
Q

How does Vagal activation stimulate gastrin release?

A
  • Release of GRP- Inhibiting the release of somatostatin
78
Q

What 2 events stimulate the release of Somatostatin?

A
  • Gastrin itself increases somatostatin (negative feedback)- H+ in the gastric lumen also stimulates release
79
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 cellsdirectly, 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

80
Q

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

A

1) Distentionof the stomach2) Presence of breakdown products ofprotein, AA’s and small peptides

81
Q

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

A

Only thedirect pathway!

82
Q

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

A

Intrinsic Factor needed for absorption of B12 in the ileum

83
Q

Failure to secrete Intrinsic Factor leads to?Common underlying causes (hint: one is autoimmune mediated)?

A
  • Pernicious anemia- Common underlying cause isdestructionof gastric parietal cells (atrophic gastritis)- Autoimmune metaplastic atrophic gastritis –> immune system attacks IF protein or gastric parietal cells
84
Q

Mucous neck cells secrete _________Gastric epithelial cells secrete _________

A
  • Mucous neck cells secretemucus- Gastric epithelial cells secreteHCO3-
85
Q

Which agents are protective of the gastric mucosa?

A
  • HCO3-and mucus- Prostaglandins (i.e., Misoprostol)- Mucosal blood flow- GF’s
86
Q

Which agents damage the gastric mucosa?

A
  • Acid- Pepsin- NSAIDs (i.e., aspirin)-H. pylori- Alcohol- Bile- Stress
87
Q

Which enzyme allowsH. pylroito colonize the gastric mucosa and through which mechanism?How does this enzyme relate to diagnostics?

A
  • Urease- Converts urea to NH3whichalkalinizesthe enviornment- A diagnostic test is based onurease activity!
88
Q

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

A
  • Duodenal ulcer- H+ secretion is elevated
89
Q

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

A
  • H+ secretion isdecreased- Gastrin levels areincreased(due to decreased H+)
90
Q

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

A

-Gastrinsecreting tumor in thepancreas- Massively increased levels ofbothGastrinandH+- Increased parietal cells mass due to trophic effect of increased gastrin

91
Q

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

A

Low duodenal pHinactivatespancreatic lipases

92
Q

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

A
  • Secretin stimulation test- Undernormalconditions, secretin administratininhibitsgastrin release- Ingastrinomas, injection of secretin causesparadoxicalincrease in gastrin release
93
Q

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

A

-Centroacinarandductal cellsproduce the initial aqueous solutionwhich isisotonicand containsNa+, K+, Cl-, andHCO3– Initial secretion is then modified by transport processes inductal epithelial cells

94
Q

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

A

-Acinar cells- Pancreaticamylasesandlipasesare secreted asactive enzyme-Proteasesare secreted ininactiveform and converted to active form in thelumenofduodenum

95
Q

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

A

-Secretionof HCO3-intopancreatic ductal juice-Absorptionof H+

96
Q

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

A

Intestinal phase

97
Q

What do I cells of the duodenum release and what stimulates this release?What are the downstream effects on the pancreas?

A
  • ReleaseCCKin response toPhe, Met, Trp, Small peptides, andFA’s- CCK stimulatespancreatic acinar cells–> increased IP3and Ca2+- Release ofenzymes
98
Q

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

A

ACh

99
Q

What do S cells of the duodenum secreteand what is the stimuli for this secretion?What are the downstream effects on the pancreas?

A
  • Release secretinupon stimulation byH+- Secretin activates cAMP inpancreatic ductal cells- Leads to release ofaqueous solution(Na+, HCO3-)
100
Q

What potentiates the effects of Secretin on pancreatic ductal cells?

A

ACh and CCK

101
Q

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

A

Apicalsurface ofductal cellof pancreas

102
Q

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

A

Liver

103
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
104
Q

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

A

Cirrhosis

105
Q

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

A
  • Decreased hepaticurea cycle metabolismleads to accumulation ofammoniain systemic circulation-AmmoniaREADILY crosses the BBB and alters brain function
106
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
107
Q

What is the function of bile?Solves which problem?

A
  • Vehicle for elimination of substances from the body- Solves the insolubility problemof lipids
108
Q

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

A

1) Synthesis and secretion of bile salts byliver2) Bile salts are stored andconcentratedingallbladder3)CCK-inducedgallbladder contraction and sphincter of Oddi relaxation4) Absorption of bile salts intoportal circulation5) Delivery of bile salts to the liver

109
Q

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

A

Secretin

110
Q

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

A

ACh and CCK

111
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+-independenttransport proten, organic anion transport proteins(OATP)

112
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 basolateralside foruptakeinto liver-Bile salt excretory pump (BSEP)andMultidrug Resistance Protein 2 (MRP2)are located on theapicalside from bile acid secretion
113
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

-Apicalsodium dependent bile acid transporter (ASBT)is reponsibe for re-uptake into enterocyte-Organic solute transporter alpha-beta(OSTalpha-OSTbeta) is responsible for exportinto portal circulation

114
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
115
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 ofunconjugated (indirect)

116
Q

Which type of bilirubin is increased in Hemolytic Anemia?

A

Unconjugated bilirubin

117
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 ofunconjugated bilirubin
118
Q

What is Crigler-Najjar syndrome Type 1 due to?When does it start?Associated with what kind of damage?

A

-NOfunction of UDP glucuronyl transferase; startsearlier in life-Kernicterus: form of brain damage caused by accumulation of unconjugated bilirubinin the brain and nerve tissues

119
Q

What is Crigler-Najjar syndrome Type 2 and when is its normal onset?How severe?Which type of bilirubin accumulates?

A
  • Startslater in life- Less than 20% function of UDP glucuronyl transferase- Increased levels ofunconjugated bilirubin-Less likelyto develop kernicterus
120
Q

What is the defect in Dubin-Johnson syndrome?Common findings?Which type of bilirubin is increased?

A
  • Mutations inmultidrug resistance protein 2 (MRP2):hepatocytes unable to secrete conjugated bilirubin into bile- Increasedconjugated bilirubinin the serum w/o elevation of liver enzymes- LIVER HAS BLACK PIGMENTATION
121
Q

In Rotor syndrome there is a buildup of what?Due to gene mutation in?

A
  • Buildup ofbothconjugated and unconjugated bilirubin in blodd, but majority = conjugated- Gene mutations lead toabnormally short, nonfunctional OATP1B1andOATP1B3 proteinsor total absence- Unable to transport bilirubin from the blood into the liver for secretion into bile
122
Q

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

A

Conjugated bilirubin

123
Q

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

A

Distal bile duct

124
Q

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

A

-Longestin theduodenum-Shortestin theterminal ileum

125
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

126
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
127
Q

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

A

Secondaryactive transport

128
Q

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

A
  • GLUT 5- Facilitated diffusion
129
Q

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

A

Holds onto H2O and causesosmotic diarrhea

130
Q

How is the inactive enzyme trypsinogen converted into trypsin?

A

Bybrush borderenzyme,Enterokinase

131
Q

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

A

Trypsin

132
Q

What are the 3 endopeptidases?

A

1) Trypsin2) Chymotrypsin3) Elastase

133
Q

How are pancreatic proteases inactivated?

A

Digestion of themselves and each other!

134
Q

Which protein products are the only absorbable form?How are larger products broken down into more absorbableforms?

A
  • Only AA’s, dipeptides and tripeptides are absorbable- Oligopeptides must be further hydrolyzed bybrush-borderproteases, yielding AA’s, diepeptides and tripeptides
135
Q

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

A

4 separate cotransporters: one each forneutral, acidic, basic,andimino AA’s

136
Q

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

A

Facilitated diffusion

137
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

138
Q

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

A

Dietary proteins

139
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

140
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

141
Q

How is Colipase activated?

A

Activated bytrypsin

142
Q

Which enzyme breaks down phospholipidsand into what products?

A
  • Phsopholipase A2- Lysolecithin and FA’s
143
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 micelles2) Diffusion of micellar content3) Reesterification4) Chylomicron formation5) Exocytosis of chylomicron intolymph

144
Q

What are the components of a Chylomicron?

A
  • Phospholipids and ApoB on surface- TAG’s andcholesterolcore
145
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
146
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 todistal ileum- BindsIF receptorand allows B12 to move into mucosa and then blood where it complexes withtranscobalamin II
147
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
148
Q

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

A

-Gastrectomycauses loss ofparietal cells(source ofIF)-Gastric bypass:exclusion of the stomach, duodenum, and prox. jejunum alters absorption of Vit B12

149
Q

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

A

Duodenum

150
Q

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

A
  • Toxin subunit move inside intestinal crypt cells and catalyzeADP ribosylationofαssubunit of the Gsprotein coupled to AC- Inhibits GTPase activity, causing GTP to be permanently bound toαssubunit, 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 2 COPY (14 decks)

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