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)
2
Q
What are 2 actions of Gastrin?
A
1) Increase gastric H+ secretion
2) Stimulates growth of gastric mucosa
3
Q
Which cells secrete CCK and their location?
A
I cells of the duodenum and jejunum
4
Q
What are 2 stimuli for the release of CCK?
A
- Small peptides and AA’s
- Fatty acids
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
6
Q
Which cells secrete Secretin and their location?
A
S cells of the duodenum
7
Q
What are 2 stimuli for the secretion of Secretin?
A
1) H+ in the duodenum
2) Fatty acids in the duodenum
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
9
Q
What is the site of secretion for Glucose-dependent insulinotropic peptide (GIP)?
A
Duodenum and Jejunum
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
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
12
Q
Which 2 hormones mediate the incretin effect?
A
1) Glucagon-like peptide 1 (GLP-1)
2) Gastric inhibitory peptide (GIP)
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
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
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
16
Q
What are the 2 actions of Enkephalins in the GI tract?
A
1) Contraction of smooth muscle
2) Decreased intestinal secretion
17
Q
What are the 2 actions of Neuropeptide Y in the GI tract?
A
1) Relaxation of smooth muscle
2) Decreased intestinal secretion
18
Q
What are the 2 actions of Substance P in the GI tract?
A
1) Contraction of smooth muscle
2) Increased salivary secretion
19
Q
Which 3 NT’s cause contraction of smooth muscle in the GI?
A
1) ACh
2) Enkephalins
3) Substance P
20
Q
Which 4 NT’s cause relaxation of smooth muscle in the GI?
A
1) NE
2) VIP
3) NO
4) Neuropeptide Y
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
22
Q
What are slow waves of GI smooth muscle?
A
Depolarization and repolarization of the membrane potential, but are NOT APs
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
24
Q
The greater the # of APs on top of the slow wave the larger the _________ contraction
A
Phasic
25
Where do phasic contractions occur in the GI tract?
- All tissues involved in **mixing and propulsion**
- Esophagus, stomach (antrum), small intestine
26
Where do tonic contractions occur in the GI tract?
- Stomach (orad)
- Lower esophageal, ileocecal, and internal anal sphincters
27
What is the effect of ACh and NE on slow waves in the GI tract?
- **ACh** increases the amplitude of slow waves and the # of AP's
- **NE** decreases the amplitude of slow waves
28
What are the pacemaker for GI smooth muscle?
Interstitial cells of Cajal (ICC) = **generate** and **propogate** slow waves
29
Where are the interstitial cells of Cajal (ICC) located?
Myenteric plexus
30
Which part of the brain controls the involuntary swallowing reflex?
Medulla
31
Describe the afferent and efferent input involved in the involuntary swallowing reflex?
- Food in pharynx --\> **afferent** sensory input via **vagus/glossopharyngeal N.** ---\>
- Swallowing center **(medulla)** --\> brainstem nuclei --\> **Efferent** input to pharynx
32
Which peristaltic wave **cannot** occur after vagotomy?
Primary peristaltic wave
33
What is the secondary peristaltic wave?
Why is it significant?
- Occurs if primary wave fails to empty the esophagus or if gastric contents reflux into the esophagus
- Occurs even after vagotomy
34
What is the resting pressure in the UES, body of esophagus (upper, near diaphragm) and LES?
- **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)
35
Describe the change in pressure within the esophagus during swallowing?
- **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**)
36
Which nerve and chemicals are invovled in the opening of the LES?
- Vagal nerve
- Release of **VIP**
- **NO** also may play a role
37
What is happening during receptive relaxation and is mediated by what reflex?
- **Decrease pressure** and **increase volume** of the **orad region**
- Vagovagal reflex
38
Which process is occuring in the caudad region of the stomach for mixing and digestion of food particles?
- Most of the gastric contents are **propelled** **back** into the stomach for further mixing and reduction of particle size
- **Retropulsion**
39
Large particles of undigested residue remaining in the stomach are emptied by what?
Occur at how long of an interval and only during?
- Migrating myoelectric complex **(MMC)** = periodic, burstin peristaltic contractions
- Occur at **90 min intervals,** during **FASTING**
40
Which hormone plays a significant role in mediating MMC's?
Motilin
41
Which 4 conditions increase the rate of gastric emptying?
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
42
Which 4 factors inhibit gastric emptying?
1) Relaxation of orad
2) Decreased force of peristaltic contractions
3) Increased tone of pyloric sphincter
4) Segmentation contractions in intestine
43
What is the Entero-Gastric reflex?
**Negative** feedback from duodenum will **slow down** the **rate of gastric emptying**
44
Describe the effects that acid, fats, peptides/AA's, and hypertonicity of the duodenum play in the Entero-gastric reflex.
- **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
45
How are the contractions in the small intestine different from those in the stomach, especially in regards to slow waves.
- 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
46
Which hormones/NT's can stimulate contractions in the small intestine?
Which inhibit?
- Serotonin, Prostaglandins, Gastrin, CCK, Motilin, and Insulin **stimulate** contractions
- Epinephrine (adrenal glands), Secretin, and Glucagon **inhibit**
47
Role of the myenteric plexus and submucosal (meissner) plexus of the intestinal wall?
- **Myenteric plexus** mainly regulates **relaxation** and **contraction**
- **Submucosal (Meissner)** **plexus** sense the lumen enviornment
48
Which cells of the intestinal mucosa sense the food bolus and what is released to initiate the peristaltic reflex?
**Enterochromaffin cells** (ECC) release **5-HT**, which binds receptors on **IPANs**, initiating peristaltic reflex
49
What occurs behind and in front of the food bolus as it enters the small intestine and peristaltic reflex is initiated (reciprocal innervation)?
- 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**
50
Which type of contraction in the small intestine mixes the chyme?
Segmental contraction
51
What type of movement stimulates the defecation reflex?
Mass movements
52
Motility in the large intestine is key for?
Absorption of water/vitamins **and** conversion of digested food into feces
53
As the rectum fills with feces what occurs to the SM in the wall of rectum and internal anal sphincter?
Which reflex is this?
- SM contracts and internal anal sphincter relaxes
- Rectosphincteric reflex
54
Sensation of rectal distention and voluntary control of the external anal sphincter are mediated by pathways where?
What occurs with destruction of these pathways?
- Pathways **within** the spinal cord that **lead** **to** the **cerebral cortex**
- Destruction of these pathways causes **loss** of **voluntary control** of **defecation**
55
The vomiting reflex is coordinated by which brain region and the nerve impulses are transmitted via which afferents?
- Coordinated by the **medulla**
- Transmitted by **vagus** and **sympathetic afferents** to multiple brainstem nuclei
56
Order of events for the vomiting reflex?
- 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
57
What is Gastroparesis and one of the most common causes?
Injury to what may contribute?
- **Slow emptying of stomach/paralysis** of stomach in absence of mechanical obstruction
- Diabetes mellitus is a **common cause**
- Injury to **vagus nerve**
58
What is the cause of Hirschsprung disease (megacolon)?
Descrbe the physiological basis.
- **Ganglion cells** absent from segment of colon
- **VIP levels low** --\> **SM constriction**/**loss** of **coordinated movement** -\> colon contents accumulate
59
What is the tonicity of saliva in comparison to plasma?
K+, HCO3-, Na+ and Cl- concentrations?
- **Hypotonic** compared to plasma
- **Increased** K+ and HCO3-
- **Decreased** Na+ and Cl-
60
What are the 2 main steps in formation of saliva and which cells mediate each part?
1) Formation of **isotonic,** plasma-like, solution by **acinar cells**
2) **Modification** of the isotonic solution by the **ductal cells**
61
What is the combined action at the salivary ductal epithelial cell in formation of saliva and what is the net result?
- 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
How do vasopressin and aldosterone modify the composition of saliva?
- **Decrease** its **[Na+]**
- **Increase** its **[K+]**
63
What are the 2 unusual features in the regulation of salivary secretion?
1) Salivary is **exclusively** under the control of the **ANS**
2) Secretion is **increased** by **BOTH** parasympathetic and sympathetic stimulation
64
Where is the oxyntic gland area vs. pylroic gland area of gastric mucosa and what does each secrete?
- **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
Where are parietal cells located in the stomach and what are their products?
- Body of the stomach
- Secrete: **Intrinsic factor** and **HCl**
66
Where are chief cells located in the stomach and what do they secrete?
- Body of the stomach
- Secrete **pepsinogen**
67
HCl with ______ initiates protein digestion
Pepsin
68
Mucus cells of the antrum of stomach secrete what?
- Mucus
- HCO3-
- Pepsinogen
69
What is the most important stimuli for pepsinogen secretion in the stomach?
Vagus nerve stimulation
70
What is responsible for the "alkaline tide" observed in gastric venous blood following a meal?
- 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
What is the action of Omeprazole in the treatment of ulcers?
Inhibits the H+/K+ ATPase
72
What is the action of Cimetidine used in the treatment of peptic ulcers, GERD, etc..?
How does this relate to potentiation interactions as well?
- Antagonist of Histamine (H2) receptors --\> reduces H+ secretion
- Also blocks potentiated effects of ACh and Gastrin
73
What type of feedback mechanism regulates HCl secretion in the stomach?
- **Passive** feedback mechanism
- As pH falls, **gastrin** release in **inhibited**
- Decreases HCl secretion
74
How do Histamine and ACh have potentiation effects in the secretion of HCl?
- **Histamine** potentiates the actions of ACh and gastrin
- **ACh** potentiates the actions of histamine and gastrin
75
What acts on G cells to inhibit Gastrin release?
- Somatostatin
76
How does Vagal activation stimulate gastrin release?
- Release of GRP
- Inhibiting the release of somatostatin
77
What 2 events stimulate the release of Somatostatin?
- Gastrin itself increases somatostatin (negative feedback)
- H+ in the gastric lumen also stimulates release
78
Describe the direct and indirect pathway by which the vagus nerve stimulates HCl secretion by parietal cells (NT's involved in each path)?
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
What are the 2 stimuli for HCl secretion in the gastric phase?
1) **Distention** of the stomach
2) Presence of breakdown products of **protein**, AA's and small peptides
80
Which pathway of HCl secretion mediated by the Vagus nerve will be blocked by Atopine?
Only the **direct pathway**!
81
What is the only secretion by the stomach that is required (essential)?
Intrinsic Factor needed for absorption of B12 in the ileum
82
Failure to secrete Intrinsic Factor leads to?
Common underlying causes (hint: one is autoimmune mediated)?
- 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
Mucous neck cells secrete \_\_\_\_\_\_\_\_\_
Gastric epithelial cells secrete \_\_\_\_\_\_\_\_\_
- Mucous neck cells secrete **mucus**
- Gastric epithelial cells secrete **HCO3-**
84
Which agents are protective of the gastric mucosa?
- HCO3- and mucus
- Prostaglandins (i.e., Misoprostol)
- Mucosal blood flow
- GF's
85
Which agents damage the gastric mucosa?
- Acid
- Pepsin
- NSAIDs (i.e., aspirin)
- *H. pylori*
- Alcohol
- Bile
- Stress
86
Which enzyme allows *H. pylroi* to colonize the gastric mucosa and through which mechanism?
How does this enzyme relate to diagnostics?
- Urease
- Converts urea to NH3 which **alkalinizes** the enviornment
- A **diagnostic test** is based on **urease activity!**
87
Which type of ulcer is most common and secretion of what is elevated?
- Duodenal ulcer
- H+ secretion is elevated
88
What is H+ secretion and Gastrin levels like with a Gastric Ulcer?
- H+ secretion is **decreased**
- Gastrin levels are **increased** (due to decreased H+)
89
What is Zollinger-Ellison syndrome caused by and what are the characteristic findings?
- **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
Why is steatorrhea a common finding in Zolinger-Ellison syndrome?
Low duodenal pH **inactivates** pancreatic lipases
91
Which test is used in the diagnosis of gastrin-secreting tumors?
What are the findings?
- Secretin stimulation test
- Under **normal** conditions, secretin administratin **inhibits** gastrin release
- In **gastrinomas**, injection of secretin causes **paradoxical** increase in gastrin release
92
Which cells of the pancreas produce the aqueous secretion and what is the role of each cell type?
- **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
Which cells of the pancreas secrete enzymes and which are secreted as active and inactive forms?
- **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
What is the net result of modification of the intial pancreatic secretion by ductal cells (secretion and absorption)?
- **Secretion** of HCO3- into **pancreatic ductal juice**
- **Absorption** of H+
95
During which pancreatic secretion phase are the enzymatic and aqueous secretions stimulated?
Intestinal phase
96
What do I cells of the duodenum release and what stimulates this release?
What are the downstream effects on the pancreas?
- 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
What potentiates the effects of CCK on the pancreatic acinar cells?
ACh
98
What do S cells of the duodenum secrete and what is the stimuli for this secretion?
What are the downstream effects on the pancreas?
- Release **secretin** upon stimulation by **H+**
- Secretin activates cAMP in **pancreatic ductal cells**
- Leads to release of **aqueous solution** (Na+, HCO3-)
99
What potentiates the effects of Secretin on pancreatic ductal cells?
ACh and CCK
100
Where is the CFTR that is mutated in cystic fibrosis located?
**Apical** surface of **ductal cell** of pancreas
101
Failure of which organ can result in hypoalbuminemia and resulting edema?
Liver
102
How may CFTR mutations lead to recurrent acute and chronic pancreatitis?
- Ability to flush active enzymes out of duct may be lost
- Active enzymes in duct may lead to a breakdown of pancreas
103
What is one of the most common causes of portal HTN?
Cirrhosis
104
How does liver dysfunction (i.e., cirrhosis or portosystemic shunting) lead to hepatic encephalopathy?
- **Decreased** hepatic **urea cycle metabolism** leads to accumulation of **ammonia** in systemic circulation
- **Ammonia** READILY crosses the BBB and alters brain function
105
What is the composition of bile and what are the 2 main components?
- Bile salts (50%)
- Phospholipids (40%) - i.e., lecithin
- Bile pigments - i.e., bilirubin
- Cholesterol
- Ions and H2O
106
What is the function of bile?
Solves which problem?
- Vehicle for elimination of substances from the body
- Solves the **insolubility problem** of lipids
107
What are the 5 components/locations of bile secretion and absorption of bile salts?
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
Which hormone stimulates the uptake of ions and H2O into the bile duct?
Secretin
109
Which hormones/NT stimulate contraction of the gallbladder for the release of bile?
ACh and CCK
110
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?
1) Na+-**dependent** transport protein, Na+ taurocholate contransporting polypeptide **(NTCP)**
2) Na+-**independent** transport proten, organic anion transport proteins **(OATP)**
111
Which transporter for bile acids is located on the basolateral side of the hepatocyte and which 2 are on the apical side for secretion?
- **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
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?
- **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
Which type of transport for bile acids occurs in the ileum and how efficient is this process in the reuptake?
- Active and passive transport
- Highly efficient, \>90% of bile acids delivered to portal blood
114
What are the 2 main causes of neonatal jaundice?
Which type of bilirubin is increased?
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
Which type of bilirubin is increased in Hemolytic Anemia?
Unconjugated bilirubin
116
Gilbert syndrome is due to mutations in gene that codes for?
What type of bilirubin is increased?
- Gene that codes for UDP glucuronyl transferase
- Increased levels of **unconjugated bilirubin**
117
What is Crigler-Najjar syndrome Type 1 due to?
When does it start?
Associated with what kind of damage?
- **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
What is Crigler-Najjar syndrome Type 2 and when is its normal onset?
How severe?
Which type of bilirubin accumulates?
- Starts **later in life**
- Less than 20% function of UDP glucuronyl transferase
- Increased levels of **unconjugated bilirubin**
- **Less likely** to develop kernicterus
119
What is the defect in Dubin-Johnson syndrome?
Common findings?
Which type of bilirubin is increased?
- 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
In Rotor syndrome there is a buildup of what?
Due to gene mutation in?
- 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
Biliary tree obstruction would lead to increased levels of what type of bilirubin?
Conjugated bilirubin
122
Gallstones impacted where may cause jaundice, biliary-type pain and risk of cholangitis and pancreatitis?
Distal bile duct
123
Where are villi of the small intestine the longest and the shortest?
- **Longest** in the **duodenum**
- **Shortest** in the **terminal ileum**
124
Which cells of the intestinal epithelium are part of the mucosal defenses against infection and secrete agents that destroy bacteria or produce inflammatory responses?
Paneth cells
125
Which transporters on the luminal/apical side of the small intestine are necessary for transport of glucose, galactose, and fructose?
- SGLT 1 --\> glucose and galactose
- GLUT 5 --\> fructose
126
What type of transport does SGLT1 on the apical side of the enterocytes utilize?
**Secondary** active transport
127
Which transporters on the basolateral side of enterocytes transport glucose, galactose, and fructose into the blood?
Via what mechanism?
- **GLUT 2**
- **Facilitated diffusion**
128
In lactose intolerance, undigested lactose remains in the lumen of intestine and causes what?
Holds onto H2O and causes **osmotic diarrhea**
129
How is the inactive enzyme trypsinogen converted into trypsin?
By **brush border** enzyme, **Enterokinase**
130
Which enzyme converts all of the inactive proteases to their active forms?
Trypsin
131
What are the 3 endopeptidases?
1) Trypsin
2) Chymotrypsin
3) Elastase
132
How are pancreatic proteases inactivated?
Digestion of themselves and each other!
133
Which protein products are the only absorbable form?
How are larger products broken down into more absorbable forms?
- Only AA's, dipeptides and tripeptides are absorbable
- Oligopeptides must be further hydrolyzed by **brush-border** proteases, yielding AA's, diepeptides and tripeptides
134
How does the type of AA affect the co-transport across the apical side of the enterocyte?
**4 separate cotransporters**: one each for **neutral, acidic, basic,** and **imino AA's**
135
What is the mechanism for the absorption of protein from inside the enterocyte to the basolateral (blood) side?
Facilitated diffusion
136
Which ions are necessary for the co-transport of AA's and di-/tripeptides across the apical (luminal) side of the enterocyte?
- **Na+** for AA's
- **H+** for dipeptides and tripeptides
137
How are lipids able to be emulsified in the stomach in the absence of bile acids?
Dietary proteins
138
Which hormone is released to allow sufficient time for lipids to get digested properly and acts by slowing the rate of gastric emptying?
CCK
139
How is the problem of active pancreatic lipase being inactivated by bile salts in the small intestine solved?
**Colipase** binds to pancreatic lipase and displaces bile salts
140
How is Colipase activated?
Activated by **trypsin**
141
Which enzyme breaks down phospho**lipids** and into what products?
- Phsopholipase A2
- Lysolecithin and FA's
142
What are the 5 steps involved in the movement of lipids from the lumen of the small intestine across the epithelial cells?
1) Solubilization by **micelles**
2) **Diffusion** of micellar content
3) **Reesterification**
4) **Chylomicron** formation
5) Exocytosis of chylomicron into **lymph**
143
What are the components of a Chylomicron?
- **Phospholipids** and **ApoB** on surface
- **TAG's** and **cholesterol** core
144
Explain the effect of ileal resection on the recirculation of bile acids and its effect on fat absorption?
- 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
Describe the mechanism of B12 absorption along the GI tract starting from the stomach until absorption into the blood stream?
- 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
Deficiency of vitamin B12 can lead to what type of anemia, why?
- Pernicious anemia
- B12 is important in DNA synthesis in RBC's
147
How does Gastrectomy and Gastric Bypass affect absorption of Vitamin B12?
- **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
Which part of the small intestine is responsible for the majority of Ca2+, Fe2+, and folate absorption?
Duodenum
149
What is the MOA for cholera toxin leading to secretory diarrhea?
- **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**
