Physiology Flashcards
1
Q
Parasympathetic innervation of the GI system uses what two postsynaptic receptors?
A
Cholinergic–> ACh
Peptidergic–> substance P + VIP
2
Q
What nerve relays the GI mechanoreceptors and chemoreceptors signals back to CNS?
A
VAGUS
3
Q
Actions of ACh on GI system?
A
Contraction of smooth muscle Relax sphincters Increase salivary secretions Increase Gastric secretions Increase pancreatic secretions
4
Q
Actions of NE on GI?
A
Relax smooth muscle
Contract sphincters
Increase salivary secretions
5
Q
Actions of VIP on GI?
A
Relax smooth muscle
Increase intestinal secretions
Increase pancreatic secretions
6
Q
GRP (bombesin) actions on GI?
A
Gastrin releasing peptide
7
Q
Enkephalins (opiates) actions on GI?
A
Contract smooth muscle
Decrease intestinal secretions
8
Q
Neuropeptide Y actions on GI?
A
Relax smooth muscle
Decrease intestinal secretions
9
Q
Substance P actions on GI?
A
Contraction of smooth muscle
increase salivary secretions
10
Q
Stimulation / actions/ site of Gastrin secretion?
A
Stimuli= small peptides + AA + GRP (distention) Action= Increase H+ (parietal cells) & gastric mucosa growth Site= G cells of Stomach
11
Q
Stimulation / actions / site of CCK secretion?
A
Site= I cells of Duodenum + jejunum Stimuli= small peptides + AA + FA Actions= increase pancreatic enzymes & HCO3 + contraction of Gallbladder + relax sphincter of iddi growth of exocrine pancreas + GB Inhibits Gastric emptying
12
Q
Stimuli / actions/ site of secretin secretion?
A
Site= S cells of duodenum
stimuli= H+ & FA in duodenum
actions= increase pancreatic & biliary HCO3
Decrease gastic H+
inhibit trophic affects of gastrin on mucosa
13
Q
Stimuli / site/ actions of GIP?
A
Site= duodenum + jejunum stimuli= FA + AA + Oral Glucose Actions = increase Insulin secretion + Decrease Gastric H secretion
14
Q
What is the difference btwn “little” (17-amino acid) Gastrin and “big” (34 AA) gastrin?
A
Little= secreted in response to meals Big= secreted during inter-digestive periods
15
Q
Two most potents AA for stimulation of GASTRIN secretion are?
A
Phenulalanine
Tryptophan
16
Q
What are the affects of High levels of Gastrin (ZES= Gastrinoma)?
A
Increase H+ secretion from Parietal cells
Hypertrophy of Gastric mucosa
DUODENAL ULCERS–> High H+
FAT malabsorption (steatorrhea)
17
Q
What is the Tx for Zollinger-Ellison syndrome?
A
H2 receptor blockers (Cimetidine)
H+ pump inhibitors (Omeprazole)
18
Q
CCK- Gastrin are related how?
A
CCK –> has Gastrin activity
Gastrin–> Can activate CCKb receptor
19
Q
Monoglycerides + FA + small peptides and AA Triglycerides
A
CCK
20
Q
Stimuli/ site/ and action of Motilin?
A
Site= upper duodenum Stimuli= Fasting Actions= initiates interdigestive myoelectric complexes 90min intervals
21
Q
Action / stimulation / site of Somatostatin?
A
Site= D cells in GI mucosa Stimuli= Decreased pH Action= inhibits Gastric H+ secretions
22
Q
What action to Histamine and ACh have in common in GI?
A
Stimulate H+ secretion by parietal cells
23
Q
What parts of the GI tract are Striated muscle instead of Smooth?
A
Pharynx
Upper 1/3 Esophagus
Anal sphincter
24
Q
Which parts of the GI tract exhibit phasic contractions?
A
Esophagus
Gastric antrum
small intestines
25
Which parts of GI are involved in Tonic contractions?
Upper Stomach
Lower Esophageal sphincter
Ileocecal and internal anal sphincter
26
Contractions in GI smooth muscle has what unique feature?
SLOW waves= oscillating depolarization and repolarization that leads to AP when membrane potential reaches Threshold
27
What parts of the GI tract have the highest and lowest slow wave rates?
```
Slowest = Stomach (3/min)
Fastest= Duodenum (12/min)
```
28
What sets the slow waves and how can it be modulated?
Origin= Interstitial cells of CAJAL of Myenteric plx
Modulators= Hormone and neural inputs
PSNS + gastrin= increase AP freq + force contractn
SNS + GIP + secretin= decrease freq + force
29
What is considered to be the Pacemaker of GI motility?
Cells of CAJAL
30
Where is the swallowing center located?
Medulla
31
What mediates the relaxation of the lower esophageal sphincter?
Vagal peptidergic fibers== Release VIP
| **Upper stomach (orad) also relaxes to receive food
32
What factors slow or inhibit gastric emptying?
Low pH
| FAT (CCK)
33
What are the Neurotransmitters involved in contraction and relaxation during peristaltic contractions?
```
Constrictors= ACh + Substance P
Relaxers= VIP + NO
```
34
Describe vomiting reflex?
Reverse peristalsis starting @ Small intestines
Relaxation of stomach and pylorus
Forced Expiration to increase abdominal pressure
Relaxation of Lower ESO sphincter
35
What is retching?
Act of vomiting without OPENing of Upper esophageal sphincter = contents fall back into stomach
36
What is the Gastrocolic reflex?
Distention of stomach increases Colon motility via afferent PSNS and efferent CKK and gastrin
37
What stimulates salivary glands?
Both SNS & PSNS
38
What is saliva made of?
```
Water
Electrolytes (high [HCO3] + [K+])
alpha Amylase
Lingual lipase
kallikrein
mucus
```
39
Describe the tonicity of Saliva?
HYPOTONIC
Higher K+ and HCO3
Lower Na+ & Cl-
40
Formation and secretion of Saliva?
Acinar cells produce initial saliva
| Ductal cells modify the saliva
41
What do acinar cells produce in salivary glands?
Isotonic fluid--> normal (plasma) Na, K , HCO, Cl-
42
What factors decrease Saliva secretion?
Sleep
Dehydration
Atropine
Anticholinergics
43
What factors stimulate secretion of HCL in stomach?
Gastrin
ACh via GRP
Histamine
44
What factors decrease HCL secretion?
```
LOW pH in stomach
Chyme in duodenum
Somatostatin
Atropine
Cimetidine
Omeprazole
```
45
What are the characteristics of Pancreatic secretions?
```
Pepsinogen
Intrinsic Factor
High [HCO3]
Isotonic
Lipase + amylase + protease
```
46
What factors stimulate Pancreatic secretions?
PSNS--> Pepsinogen + Lipase + protease + aml
Secretins--> HCO3
CCK-
47
What is overall function of ductal cells during salivary modification?
Absorb NaCl
Secrete K+ & HCO3
Cells are water impermeable creating HYPOtonic saliva
48
What is the function of Kallikrein?
cleaves High molecular wght Kininogen into bradykinin (potent vasodilator)
49
What are the four components of Gastric Secretions?
HCl
pepsinogen
Intrinsic factor
Mucus
50
What are the products of Oxyntic/Parietal cells and Chief/peptic cells located in the BODY of stomach?
```
Parietal= HCl + IF (Absorption of HCO3)
Chief= Pepsinogen
```
51
Pyloric glands in the ANTRUM of stomach contains what 2 cells types/function?
G cells= Gastrin secretion
| Mucus cells= mucus + HCO3 + pepsinogen
52
What is the MOA of omeprazole?
Block H+ K+ ATPase on the Apical side of Parietal cells
53
What is responsible for the pH of Gastric venous blood?
HIGH pH due to Absorption of HCO3--> Eventually released back into GI from Exocrine pancreas
54
MOA of HCl release from gastric cells via ACh + Histamine + Gastrin?
Vagus->ACh->M3->IP3/Ca->HCl release (xAtropine)
ECL cells->H2->cAMP->PKA->HCL (xCometidine)
Gcells-> Gastrin-> CCKb->IP3/Ca->HCL
55
How do Atropin and Cimetidine affect HCl release from Parietal cells?
Atropine blocks Vagal stimulation (anticholinergic)
| Cimetidine Blocks H2 receptors/ blocks histamine action of Parietal cells
56
What is potentiation?
Ability of two stimuli to produce a combined response greater than the sum of individual responses --> ACh + Gastrin both increase Histamine release from ECL cells
57
How does Vagus nerve innervate parietal cells and G cells?
ACh->Parietal cells-> Direct stimulation of HCl
| GRP-> G cells -> Gastrin-> HCl release
58
What can stimulate HCl release?
Vagus
Gastin
Caffeine
ETOH
59
What are the 3 phases of HCl release?
Cephalic-> Taste/smell/ Vagal ACh or Gastrin
Gastric-> Distention Vagus ACh/Gastrin + AA and small peptides
Intestinal Phase-> AA and peptides Gastrin
60
What are the direct and indirect ways Somatostatins block HCl secretions?
Direct-> inhibit Adenylyl cyclase on Parietal cells
| Indrect-> inhibits Histamine and Gastrin release
61
What is the affect of Prostaglandins in HCl secretions?
Inhibits Histamine's stimulatory action of parietal cells (inhibits Adenylyl cyclase)
62
What are the two major barriers of Peptic ulcers?
1. Mucus (contains alkaline buffers HCO3)
2. HCO3 contained in mucus and beneath mucus
3. Mucosal blood flow
4. Growth factors
63
What leads to peptic ulcers?
Loss of mucous barriers
Excessive H+ or pepsin release
Combine the TWO
64
What are the damaging factors affecting GI mucosa?
```
H+ and pepsin
H. pylori
NSAIDS
Stress
Smoking
ETOH
```
65
What is the pathogenesis of H pylori causing Gastric ulcers?
```
G- bacterium colonizes Mucus and epithelial cells.
Releases Cytotoxins (cagA toxin)
cag A breaks down mucus
```
66
What permits H pylori to colonize the LOW pH stomach environment?
Urease-> generates NH3 to alkalinize the environment
67
What is a Diagnostic test for H pylori infections?
C-urea -> CO2 + NH3
| CO2 is then measured
68
How does a H pylori cause a duodenal ulcer?
bacteria inhibits Somatostatin release
69
What are the affects of a Zollinger Ellison syndrome (gastrinoma)?
High Gastrin = High H+ & increased Parietal cells mass
high H+ overwhelms duodenal HCO3= Ulcers
High H+ inactivates Pancreatic Lipase= Steatorrhea
70
When/where is Pepsinogen secreted?
Chief cells
| Vagal stimulation->High H+ -> Pepsinogen= Pepsin
71
What happens in the absence of Intrinsic factor secretion by Parietal cells?
Pernicious anemia
| **Beware of Gastrectomies= Vit B12 supplements required
72
Sites of release & actions of Gastrin?
```
Release= Antrum + duodenum
Action= Antrum + Duodenum + Jejunum
```
73
Sites of release and action of CCK?
BOTH= Duodenum + Jejunum + ileum
74
Sites of Secretin secretion and action?
```
Secretion= Duodenum
Action= Duodenum + Jejunum + Ileum
```
75
Site of GIP & Motilin secretion and action?
BOTH= Duodenum + Jejunum
76
Stimulatory and inhibitory factors for Gastrin release?
```
Stimuli= Proteins + Distention + Vagus
Inhibitory= LOW pH
```
77
Stimuli for actions of Secretins?
```
Stimuli= LOW pH
Actions= Inhibit Acid secretion + stimulate pancreatic HCO3 and enzymes + growth
```
78
ALL secretins have what action in common?
Secretin + GIP + VIP + Glucagon= Inhibit Acid release
79
What are the GI hormones + Neurocrines + paracrines?
```
Hormones= Gastrin + CCK + Secretin + GIP + motilin
Neurocrines= VIP + Bombesin (GRP) + Enkephalin
Paracrine= Somatostatins + Histamine
```
80
Site of release and actions of VIP?
```
Site of release= mucosa and Smooth muscle
Actions= Relax sphincters
relax circular muscle
Stimulate Intestinal secretions
Stimulate pancreatic secretions
```
81
SIte of release and actions of Bombesin (GRP)?
```
Site= Gastric mucosa
Action= Stimulate Gastrin release (via VAGUS)
```
82
Site of release and actions of Enkephalins?
```
Site= mucosa + smooth muscle
Action= Simulate smooth muscle contractions + inhibits intestinal secretion
```
**used in Diarrhea
83
What are the stimuli & inhibitors of Somatostatin release?
```
Stimuli= ACID
Inhibitory= Vagus nerve
```
84
Four high yield facts about Zollinger-Ellison syndrome (gastrinoma)?
Over production of Gastrin
Duodenal ulcer, Diarrhea, Steatorrhea
High rates of Acid secretion
Inactivation of pancreatic LIPASE
85
Three high yield points about Werner-Morison syndrome or Pancreatic Cholera?
Overproduction of VIP
Diarrhea, Metabolic acidosis, Dehydration, HypoK
High rates of Intestinal secretions
**Watery diarrhea= ALL night does not stop
86
Name 5 features of GERD (causes and symptoms)?
```
Acid reflux
Heartburn
HIatal hernia
Pregnancy
Failure of 2nd peristalsis
```
87
What mediates the pressure change in the Fundus of the stomach right before food enters via relaxation of LES?
Accommodating/ Relaxing reflex= Vago-vagal
88
What is the contraction method for gastric emptying?
Segmental constriction= Used to propel some food into Duodenum while some back into stomach
**MIXING food
89
How long does the average gastric emptying process last?
2-3 hrs
90
How do High fat, High CCK, and High acid affect Gastric emptying?
```
Fat= Slow gastric emptying (CCK)
CCK= relax smooth muscle= decrease
Acid= increases Peristalsis= Increase
Tonicity= Isotonic rapidly empties
```
91
What causes fullness, loss of appetite, nausea, obstruction ulcer, Cancer, and vagotomy?
Decreased/ failure of Gastric Emptying
92
What causes inadequate regulation, diarrhea, and duodenal ulcers?
Increased Gastric Emptying
93
What affects to Vagal and SNS stimulation have on Slow waves?
They either Increase (vagal) or decrease (SNS) the AMPLITUDE of the slow wave= affects the strength and # of AP contraction respectively
94
What determines Gastric AP contractions?
AMPLITUDE of Slow wave
95
Small intestine Fed motor pattern is described as?
Segmentation contractions used to Increase SA coming in contact with Food to increase Absorption
96
During the FED state what is the pattern of Small bowl motility?
Migrating Motor complex-> caused by MOTILIN secretion= contraction/90min
97
How is contraction and slow wave different in small intestines from that of stomach?
Small intestines= Slow waves have Constant Amplitude
| **Contractions are triggered by AP @ peak of slow wave NOT By the change in amplitude as seen in stomach
98
How are slow waves, APs, and contractions affected by vagal and SNS stimulation in the small intestines?
NO Change in Slow wave FREQUENCY
| Vagus= increase # of AP + Contractions
99
How do contraction # increase from FED state to Fasting state in small intestines?
Increase in the # of SPIKES (APs)--> approaching the MAX (same as Slow wave frequency)
100
What is the Rectosphinteric reflex?
Passive filling of the Rectum causes Active peristalsis which causes the Relaxation of the Internal Anal sphincter= Want to poop feeling
101
What is the cause of Achalasia and megacolon?
Absence of Ganglia (***NO VIP***) causing Failure to RELAX smooth muscle
102
What are the most important function of the Acid in the stomach?
Inhibit bacterial growth
| 2nd: activate pepsin
103
What kind of cells are located in the Antrum of the stomach?
G cells --> secrete Gastrin
| ** NO parietal cells because LOW pH inhibits Gastrin release
104
What is the function of Parietal cells during fasting?
Release SMALL amounts of HCL--> inhibit Gastrin release
105
What is the Alkaline tide?
Stomach venous blood has HIGHER pH than arterial blood due to Reabsorption of HCO3 and secretion of H+
106
WHat is the function of Carbonic anhydrase in the parietal cells?
CA turns the OH- left over from break down of H2O and combines it with CO2 to Form HCO3, THIS allows for Continuous H+ production while also increasing the [Cl-] inside the cells (HCO3/Cl- exchanger on Basolateral membrane)
107
Where are the K+ H+ ATPase located inside the Parietal cells?
Lumenal side of Tubulovesicles--> NEVER face cytoplasmic side
108
What change occurs form resting -> secreting parietal cells that allows for K+ H+ ATPase secretion into lumen of stomach?
Tubulovesicles are triggered to fuse with Intracellular Canaliculus--> Proton pump is then fused with membrane facing outward
109
What are the four features of Parietal cells that allow it to Secrete High [H+]?
1. Carbonic anhydrase
2. Proton pump (K+H+ ATPase)
3. Tubulovesicles containing proton pump
4. Electrical gradients (mucosal side VERY negative due to HIGH Cl-)
5. Gastric mucosal barrier
110
How are Cl- and H+ ions transported across lumenal membrane relative to concentration and electrical charge?
```
Cl-= against both
H+= With Electrical Against Concentration
```
111
What products breakdown the the Gastric mucosal barrier?
```
Aspirin= turns to acid and overwhelms the buffers
ETOH= toxic to the cells
```
112
What are the measured affects of Loss of Gastric mucosal barrier?
1. Loss of H+--> leaks back into damaged cells
2. HyperK+ due to damaged cells releasing it into lumen
3. Increased Na+
113
What are the ion vs flow rate affects in the Stomach?
1 Increased Flow= Increased H+ & Increased K+
| Decreased Na+ & level Cl-
114
What are the blood findings in a person with Chronic vomiting?
Metabolic Alkalosis
| HYPOKalemia
115
What are the lab findings in a person with Chronic Diarrhea?
Metabolic Acidosis
116
What is the makeup of secretion in a NON-oxyntic fluid secretion? non stimulated stomach
Isotonic Fluid= NaCl + HCO3 + K+
117
What is the makeup of Oxyntic fluid secretion in a stimulated stomach?
HCl + K+
118
What are the receptors located on Parietal cells that trigger HCl release?
ACh + Gastrin--> PL-C/ IP3
| Histamine--> cAMP
119
What are the ways that Gastrin increases HCl release from Parietal cells?
Direct-> Bind IP3/ Ca receptor
| Indirect= Binds ECL cells and stimulates Histamine production and release
120
What is the relationship btwn Gastrin and histamine in response to HCl release?
Potentiation-> Both together increase HCl release higher than the sum of individual stimulation
** Histamine Potentiates ACh as well
121
Normal diurnal basal gastric secretion shows that highest when?
Midnight= GERD worst around that time
122
30% of Gastrin secretion is during the Cephalic phase (Vagus). The Amount of acid secreted is affected by what?
Self-selected preference for the foods LIKED= More Acid secretion
123
What are the triggers for the Cephalic phase of Gastrin secretion?
```
Smell|
Taste
Chewing
Swallowing
Hypoglycemia
**ALL potentiated by VAGUS
```
124
How does Vagus potentiates Cephalic gastrin release?
Direct ACh to Parietal cells
| GRP directed to G cell to release Gastrin= Increases HCl release from parietal cells
125
What are the effects of Dilatation/ distention of stomach?
HCl release via 3 mechanisms:
1: short intramural reflex= ACh= stimulate parietal
2: Vago-vagal= direct ACh
3: Vago-vagal= GRP/ Gastrin
126
What are the mechanisms for Gastrin release?
```
Vagus= ACh -> GRP-> Gastrin release
Vagus= ACh> inhibits Somatostatin
Distention= ACh-> Gastrin release
```
127
How does Protein meal affect Somatostatin release?
Proteins neutralize pH= Inhibiting the stimulatory actions of LOW pH on SS release
128
What is the majority of the pancreas made up of?
```
90%= Exocrine (HCO3 + enzymes)
2%= Endocrine (Islets of Langerhaan)
```
129
DIscuss the enzyme and aqueous secretions of the Exocrine pancreas?
Acinar cells= secrete Enzymes
Centroacinar = secrete aqueous (HCO3)
Ductal cells= Modify Aqueous secretion
130
Exocrine pancreas enzymes are synthesized where and secreted due to what?
synthesized-> RER
| Stimuli= PSNS + CCK
131
What are the Carbohydrate digesting enzymes and where are they synthesized?
Salivary gland= Amylase
Pancreas= Amylase
Intestinal mucosa= Sucrase + Maltase + Lactase + Trehalase + alpha Dextrinase
132
What are the protein digestive enzymes and where are they synthesized?
Stomach= Pepsin
Pancreas= Trypsin + Chymotrypsin + Carboxypeptidase + Elastase
Intestinal mucose= Amino-oligopeptidase, Dipeptidase + Enterokinase
133
What are the Lipid digestive enzymes and where are they synthesized?
Saliva= Lingual lipase
Pancreas= Lipase, Phospholipase A2, Cholesterol ester hydrolase
134
What is the net result of pancreatic secretion?
HCO3 into Pancreatic ductal juice
| Net absorption of H+ in venous blood
135
What happens to the content of pancreatic juice when the rate of secretion in Increased?
K + Na = Constant
HCO3 = Increases -> levels off
Cl-= Decreases -> levels off
136
How does Increased Salivary flow alter the content of Saliva?
```
K+ = Constant
Na+ = Increases Dramatically
Cl- = Increases steadily
HCO3 = Increases and then Levels off
```
137
What is the explanation for the affect of Rate of flow on Pancreatic juice content?
Basal flow (slow) = Isotonic NaCl + H2O solution
| Stimulated Flow= activates centroacinar and ductal cells to Increase HCO3 and decrease Cl
HCO3 Na + H2O
138
What activates the release of Aqueous and enzymatic pancreatic secretions?
Aqueous= H+ in the Duodenum
Enzymatic= Digestive products in duodenum
(proteins,AA, FA)
139
Describe the 3 phases of Pancreatic juice secretion?
1. Cephalic= smell, taste, conditioning-> Vagus
* Enzymes ONLY
2. Gastric= Distention--> Vagus
* *Enzymes ONLY
3. Intestinal= CCK + ACh + Secretins
* *80% Both enzymatic + aqueous
140
What is the stimulus for the secretion of Enzymes from the Acinar cells in the Pancreas?
CCK-A + ACh receptors
I cells in Duodenum= secrete CCK in presence of AA, peptides, FA-
ACh from Vago-vagal reflex directly acts on Acinar cells
141
Most important Amino acids in relation to CCK secretion are?
Tryptophan
Methionine
Phenylalanine
142
What are the stimuli for the secretion of Aqueous solution from the Ductal cells?
CCK + ACh + Secretins
143
What part of the GI is involved in Enterohepatic circulation of bile salts?
Ileum
144
What is the composition of bile?
```
50% Bile salts
40% phospholipids
4% cholesterol
2% bilirubin
H2O + NaCl
```
145
What are the primary & secondary bile acids?
Primary= hepatocyte synthesized--> cholic acid + chenodeoxycholic acid
Secondary= dehydroxylated primaries by intestinal bacteria--> deoxycholic + lithocholic acids
146
What two amino acids are conjugated by the liver to form bile acids?
Taurine
| Glycine
147
What is the role of bile salts and what property allows them to do that?
Emulsify lipids= Amphipathic properties
* *Form Micelles
* Phospholipids are also amphipathic
148
Yellow colored byproduct of Hemoglobin metabolism?
Bilirubin
149
Describe the process from hemoglobin breakdown to urobilinogen in Urine and feces (Sterobilin)?
Hemoglobin degraded by RE cells (spleen)
Deconjugated Bilirubin circulates bound to Albumin
Liver extracts + conjugates with Glucuronide
"Direct" conjugated bilirubin enters BILE
Intestinal bacteria convert it into Urobilinogen
Gives Feces and Urine its color
150
What is the mechanism for Carbohydrate absorption?
Mechanism: Na/Glucose cotransport
Na/galactose cotransport
Facilitated diffusion
151
What is the mechanism of protein absorption?
Mechanism: Na/amino acid cotransport
H+ dipeptide cotransport
H+ tripeptide contransport
152
What is the mechanism of Lipid absorption?
Bile salts form micelles in the small intestines
Diffusion of FA + monoglycerides and cholesterol into intestinal cells
Reesterification in the cell to Triglycerides and phospholipids
Chylomicrons form in the cell (apoprotein 100) and transferred to LYMPH
153
What is the mechanism of Fat & water soluble vitamin absorption?
1. Micelles form with bile salts and products of lipids
DIffusion into intestinal cells
2. Na+ dependent cotransport
154
Where and what is the mechanism for absorption of?
1. B12
2. Bile salts
3. Ca++
4. Fe++
1. Ileum--> Intrinsic Factor
2. Ileum--> Na/ bile cotransport
3. small intestine--> vitamin D dependent binding
4. small intestine-> binds apoferritin in cell then BINDS transferrin in Blood
155
What are the only carbs absorbed in the GI system?
Monosaccharides--> Glucose, galactose, fructose
156
Describe the digestion of starch from mouth to absorption?
Mouth-> salivary amylase-> dectivated in stomach
Pancreatic amylase cleaves 1,4 glycosidic bonds
yielding dextrins, maltose, or maltotriose
These disaccharides are broken into Glucose which is absorbed
157
What is the mechanism of Glucose, fructose, and galactose absorption?
Glucose + galactose= Na+ cotransport (SGLT 1)
| Fructose= GLUT 5 facilitated diffusion
158
What is lactose intolerance?
Lactase deficiency= Brush boarder enzyme
| **Causes Osmotic diarrhea because Lactose is not broken down and absorbed
159
What are the two classes of proteases?
```
Endopeptidases= hydrolyze INterior peptide bond
Exopeptidases= hydrolyze one AA @ a time from C terminal side
```
160
What are examples of endopeptidases and exopeptidases?
```
Endo= Pepsin + Trypsin + chymotrypsin + elastase
Exopep= Carboxypeptidases A & B
```
161
Describe the role of pepsin in protein digestion?
Begins the process @ Low stomach pH
Inactivated in high pH of duodenum
NOT essential to digestion
162
After proteins enter duodenum, what are the next steps in digestion?
Trypsin activated by Enterokinase
Trypsin activates all other brush boarder enzymes
Break down proteins and absorb
Pancreatic proteases digest themselves and each other
163
In what form are proteins absorbed?
AA + Dipeptides + tripeptides
164
What is the mechanism of absorption for L- amino acids and dipeptides/ tripeptides?
```
L-AA= Na+ cotransport
Di/tripeptides= H+ cotransport
```
165
The absence of what enzymes affects all other pancreatic enzymes and Drastically affects protein absorption?
TRYPSIN
166
Genetic disorder in which cotransporters for Dibasic amino acids cystine, lysine, arginine, ornithine is absent in both small intestines and kidneys?
Cystinuria
167
What is the function of the stomach in lipid absorption?
Initiates enzymatic digestion by mixing, increasing SA, and hydrolyzing using Lingual and gastric Lipases
* *slowly empties Lipids into Duodenum so it can ALL properly come in contact with BILE
* *CCK slows gastric emptying for this reason
168
What is the role of the small intestines in lipid digestion?
Pancreatic lipase= hydrolyzes TGs into MAG+2FAs
| **Inactivated by Bile salts thus NEEDS Colipase to maintain activity
169
Explain the absorption of lipids digestion products cholesterol, monoglycerides, lysolecthin, and FFA?
All are bound to Micelles--> diffuse TO brush-boarder-> Lipids are released and diffuse into cell-> Most lipids absorbed by midJejunum.
**Micelles DO NOT enter cell
170
What happens to the lipid digestive products once they enter intestinal cells?
They are RE-esterified with FFA and packed into CHYLOMICRONS
171
What is a chylomicron composed of?
TGs
Cholesterol
Core of Phospholipids
Apoprotein B 48
172
What is the fate of chylomicrons?
They are Exocytosed into Lymphatics as Lacteals
173
What are the affects of ileal resection?
Pernicious anemia
| Steatorrhea--> No enterohepatic circulation of Bile salts so Bile storage is depleted
174
Decreased intestinal absorption due to decreased in intestinal cells and reduced microvillar surface area?
Tropical sprue
175
What are the water-soluble vitamins and mechanism of absorption?
Vitamins B1, B2, B6, biotin, folic acid, nicotinic acid, and pantothenic acid--> Na dependent cotransport in small intestines
**Except for Cobalamin (B12)
176
Describe the absorption of Vitamin B12 (cobalamin)?
1. released from food by Pepsin
2. Free B12 binds R protein from Saliva
3. Pancreatic proteases degrade R protein
4. B12 then binds Intrinsic factor
5. B12+ IF resistant to pancreatic proteases
6. Ileum absorption via special transporter
177
Describe the absorption of Fe++ (iron)?
1. Absorbed as either Free iron or heme iron
2. Digested by lysosomal enzymes inside intestinal cells
3. Binds Apoferritin and transports across basolateral membrane into blood.
4. Binds Transferrin during circulation
178
Paracellular movement of H2O and electrolytes is possible at what part of the GI?
Small intestines= Leaky tight junctions= paracellular movement possible
COLON= "Tight" tight junctions= no PC movement
179
Neonate with failure to pass meconium in the immediate postnatal period followed by obstructive constipation. Dx?
Hirschsprung Disease= Congenital Aganglionic Megacolon
180
What is the pathogenesis of Hirschsprung disease?
Failure of Neural crest cells to migrate and produce the Meissner submucosal plexus and Auerbach myenteric plexus
**Tyrosine kinase RET mutation in familial form
181
What is the difference btwn mucosal infaction and mural infarction?
```
Mucosal= NO deeper than muscularis mucosa
Mural= Mucosa and submucosa
Transmural= all three layers
```
182
What are the causes of mucosa, mural, and transmural infarctions?
Mucosal + mural= acute/chronic hypo perfusion
| Transmural= Acute vascular obstruction
183
What are some common causes of acute arterial obstruction?
```
Atherosclerosis
Aortic aneurysm
Hypercoagulable states
Oral contraceptives
Embolization of cardiac vegetation
```
184
Intestinal hypoperfusion can be associated with what causes?
cardiac failure
Shock
dehydration
vasoconstrictive drugs
185
What are the variables that determine the severity of ischemic bowel disease?
Severity of vascular compromise
Time frame
Vessel affected
186
What areas of the GI system are particularly susceptible to ischemia?
Watershed zones= Splenic flexure
| Sigmoid colon
187
What causes GI surface epithelial atrophy and necrosis with consequent sloughing BUT normal or hyperproliferative crypts?
Ischemic intestinal disease= Crypts have majority of blood supply because they house the regenerative cells
188
Older patient with history of cardiac and vascular disease with sudden onset severe abdominal pain and tenderness, N/V, bloody diarrhea?
Ischemic Bowel disease
189
What viral infection can cause ischemic GI disease as a consequence of tropism and infection of endothelial cells?
CMV
190
Most common acquired GI emergency of neonates, particularly prematures and low birth weights often beginning with Oral feeding?
Necrotizing enterocolitis
191
Malformation of submucosa and mucosal blood vessels in cecum of Right colon presenting @ 6th decade with Lower intestinal bleeding, hemorrhage?
Angiodysplasia
192
Thin walled dilated submucosal vessels that protrude beneath anal or rectal mucosa above the anorectal (pectinate) line?
Internal hemorrhoids
193
Passing of Isotonic stool that persists during Fasting?
Secretory diarrhea
**Osmotic ceases with fasting
194
Excess stool caused by inadequate nutrient absorption with Steatorrhea and relieved by Fasting?
Malabsorptive diarrhea
195
What are the four phases of nutrient absorption?
1. intraluminal digestion=breaking down to absorbable size
2. Terminal digestion= hydrolysis by enzymes @ the brush boarder of intestinal mucosa
3. Transepithelial transport
4. Lymphatic transport of Lipids
196
What are the signs and symptoms of malabsorption?
Diarrhea
flatus
abdominal pain
weight loss
197
What is the cause of Cystic fibrosis malabsorption?
Mutated CFTR (Cl- channel) interferes with HCO3, Na, H2O secretion= causes thickened secretion
* *Meconium Ileus newborn
* *Pancreatic insufficiency in adults
198
Autoimmune mediated enteropathy triggered by the ingestion of gluten-containing foods?
Celiac disease
199
Biopsy of Duodenum mucosa shows Increased numbers of intraepithelial CD8+ T cells with intraepithelial lymphocytosis, crypt hyperplasia and VIllous atrophy?
```
Celiac disease (Gluten sensitive enteropathy)
**Often affects Duodenum heavily due to high gluten exposure
```
200
Pt 30-60 yo with Iron deficiency anemia, diarrhea, bloating, and fatigue. GI biopsy shows lymphocytosis and villous atrophy?
Celiac disease
201
Children btwn 6-24 mo presenting with irritability, abdominal pain, distention, anorexia, diarrhea, failure to thrive, weight loss, and muscle wasting with Characteristic Pruritic skin blisters?
Pediatric Celiac disease = Dermatitis Herpetiformis
202
What is the differential for a celiac disease pt On Strict Gluten FREE diet with sudden onset of abdominal pain, diarrhea, and weight loss?
High RISK for:
Enteropathy associated Tcell Lymphoma
Intestinal Adenocarcinoma
Refractory sprue (no longer responding to Diet)
203
syndrome of stunted growth and impaired intestinal function that is common in developing countries?
Environmental Sprue (tropical)
204
Pt with recent enteric viral or bacterial inception presents with explosive diarrhea with watery, frothy stools and abdominal distention?
Acquired Lactose deficiency
205
Mutation in the microsomal triglyceride transfer protein rendering the enterocytes unable to to export lipoproteins and FFA?
Abetalipoproteinemia = Spur cells in peripheral blood
206
Chronic and relapsing abdominal pain, bloating, changes in bowel habits including diarrhea and constipation?
IBS (irritable bowel syndrome)
207
Middle-aged women with chronic watery diarrhea, grossly normal intestines BUT presence of dense subepithelial collagen layer, increased numbers of intraepithelial lymphocytes, and mixed inflammatory infiltrates within lamina proria?
Collagenous colitis
**lymphocytic colitis= same without Thickened collagen layer
