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T1 - Phase 1 - Integrated (II) > GI - Physiology - Exocrine Pancreas; Liver; Digestion & Absorption > Flashcards

GI - Physiology - Exocrine Pancreas; Liver; Digestion & Absorption Flashcards

1
Q

What are the two main goals of pancreatic exocrine secretions?

A

Neutralize acidic chyme (via HCO3-);

promote digestion (via zymogens)

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2
Q

Make the diagnosis.

A

Acute pancreatitis

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3
Q

What are the two main cell types of the exocrine pancreas?

A

Acinar;

ductal

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4
Q

Via what intracellular messenger do vagal stimulation and cholecystokinin cause increased pancreatic enzyme exocytosis?

A

Increased [Ca2+]

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5
Q

What intestinal hormone causes increased pancreatic HCO3- secretion?

What intestinal hormone causes increased pancreatic enzyme secretion?

A

Secretin;

cholecystokinin

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6
Q

An increase in intracellular [Ca2+] in the pancreatic acinar cells will cause what results?

A

Increased enzyme secretion;

increased Na+, Cl-, and H2O secretion

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7
Q

Which portion of the exocrine pancreas secretes enzymes, NaCl, and H2O?

Which portion of the exocrine pancreas secretes HCO3-?

A

Acinar cells;

ductal cells

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8
Q

Pancreatic acinar cells secrete ______________ in response to _______________ stimulation.

Pancreatic duct cells secrete ______________ in response to _______________ stimulation.

A

Enzymes, NaCl, H2O;

cholecystokinin, vagal stimulation

HCO3-;

secretin

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9
Q

What channel allows for Cl- return to the pancreatic lumen after it is exchanged for HCO3- and enters ductal cells?

A

The CFTR channel

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10
Q

What percentage of pancreatic fluid is made up of acinar secretions (enzymes, H2O, NaCl)?

What percentage of pancreatic fluid is made up of ductal secretions (HCO3-, H2​O)?

A

25%

75%

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11
Q

An increase in pancreatic fluid flow rate has what effect on HCO3- and Cl- levels in the fluid?

A

More [HCO3-];

less [Cl-]

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12
Q

Name some of the digestive enzymes secreted by pancreatic acinar cells.

A

α-amylase;

pancreatic Lipase;

various proteases (pepsin, trypsin, chymotrypsin, carboxypeptidases, elastase)

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13
Q

Describe the activation of pancreatic zymogen proteases.

A

Enteropeptidase (enterokinase) on duodenal brush border –>

activates trypsin –>

activates the others

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14
Q

How is auto-activation of trypsin within the pancreatic acinar cells avoided?

A
  1. Pancreatic enzymes exist as zymogens while in the pancreas
  2. Trypsin inhibitors can block any existing activity within the pancreas
    (e. g. trypsin inhibitory peptide and α-1 antitrypsin)
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15
Q

What is the stimulating factor that increases secretin secretion by S cells of the duodenum?

What is the stimulating factor that increases cholecytokinin secretion by I cells of the duodenum?

A

Gastric acid in the duodenum;

fatty acid and amino acids in the duodenum

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16
Q

How are secretin and cholecystokinin secretion potentiated?

A

Vagal stimulation

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17
Q

______ cells secrete secretin.

______ cells secrete cholecystokinin.

______ cells secrete glucose-dependent insulinotropic peptide.

A

S

I

K

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18
Q

What are the three stimulatory phases of pancreatic exocrine secretion?

A

Cephalic (minor role - vagus);

gastric (minor role - vagus/gastrin);

intestinal (vagus/secretin/cholecystokinin)

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19
Q

Name the two most common causes of acute pancreatitis.

For what percentage does each account?

A

Alcohol abuse (40%);

gallstones (40%) (often associated with hyperlipidemia);

genetic diseases (e.g. cystic fibrosis);

hyperparathyroidism

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20
Q

What bloodwork will you find in a paient with acute pancreatitis?

A

Elevated serum α-amylase and lipase;

decreased total cholesterol, HDL, and LDL

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21
Q

What three organs are very commonly affected in patients with cystic fibrosis?

A

Lungs,

liver,

pancreas

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22
Q

What digestive complications do patients with cystic fibrosis face?

A

Malabsorption,

acute pancreatitis,

obstruction,

etc.

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23
Q

Does gastrin potentiate pancreatic acinar secretions (via CCK) or ductal secretions (via secretin)?

A

Acinar

(to digest the proteins the stomach has sensed and responded to by secreting gastrin)

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24
Q

Presence of fatty acids in the duodenum causes increased ___________ (hormone) secretion.

Presence of gastric acid in the duodenum causes increased ___________ (hormone) secretion.

A

Cholecystokinin;

secretin

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25
Q

What test can you use to help confirm a diagnosis of acute pancreatitis?

A

Blood work –> elevated serum α-amylase and lipase

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26
Q

What test can you use to help confirm a diagnosis of cystic fibrosis?

A

Sweat test

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27
Q

What is the likely diagnosis?

What is the primary cause?

A

Cholecystitis;

gallstones

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28
Q

What percentage of hepatic circulation comes from the portal vein?

What percentage of hepatic circulation comes from the hepatic artery?

A

75%

25%

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29
Q

What is a hepatic lobule?

A

The hepatocytes around a central vein and several associated portal triads

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30
Q

True/False.

Hepatocytes are a single layer of epithelial cells.

What type of junctions connect them?

A

True;

tight junctions

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31
Q

Describe the bile cannaliculi and apical / basolateral sides of a hepatocyte.

A

Cannaliculi and apical sides = between cells

Basolateral sides = sides facing space of Disse

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32
Q

What are the main components of bile?

A

Water (82%),

bile acids (12%),

phospholipids (4%),

cholesterol (1%)

bilirubin (<1%)

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33
Q

What cell is here described:

change fluid in bile duct lumen to make bile

A

Cholangiocytes

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34
Q

Describe the function of cholangiocytes.

A
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35
Q

Describe the changes in pH and electrolytes from hepatic bile to gallbladder bile.

A

Increase:

Sodium

Bile acid (pH decreases initially until Cl-/HCO3- exchange catches up)

Decrease:

Bicarbonate (pH decreases until Cl-/HCO3-​ exchange catches up)

Chloride

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36
Q

How are bilirubin and cholesterol excreted?

A

Through bile

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37
Q

What are the purposes of bile?

A

Fat emulsification

Antibacterial

Neutralize gastric acid

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38
Q

True/False.

Bile acids are amphipathic and form chylomicrons.

A

False.

Bile acids are amphipathic and form micelles.

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39
Q

Bile acids are the end product of __________ metabolism.

What enzyme is responsible for cholesterol synthesis?

What enzyme is responsible as the rate-limiting step of bile acid synthesis?

A

Cholesterol;

HMG-CoA reductase,

7α-hydroxylase

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40
Q

Why can statins cause cramps and neurological symptoms?

A

Changes in myelin (due to decreased cholesterol synthesis)

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41
Q

Primary bile acids are formed in the _______.

Secondary bile acids are formed in the _______.

A

Liver;

colon

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42
Q

Secondary bile acids (formed in the colon) are conjugated with:

A

Glycine or taurine

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43
Q

How are secondary bile acids reabsorbed by the colon?

A

Na+-dependent cotransport

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44
Q

Describe bile acid circulation.

A
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45
Q

What sphincter is relaxed by CCK?

A

The sphincter of Oddi

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46
Q

What substances are released secondary to CCK action at the gallbladder and common bile duct?

A

VIP and NO (relaxation of Oddi);

ACh (further gallbladder contraction)

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47
Q

______ ________ turns heme into iron and bilirubin.

A

Heme oxygenase

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48
Q

Unconjugated bilirubin is transported in the blood via ________.

A

Albumin

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49
Q

Which sex is at a greater risk of gallbladder disease?

Why?

A

Women;

oral contraceptives, estrogen

(effects on cholesterol, I think)

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50
Q

What surface has the largest surface area of the body in potential direct contact with immunogenic/toxic substance?

A

The GI tract

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51
Q

___% of Ig-secreting cells are in the GI tract.

A

80%

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52
Q

Describe the GALT.

A
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53
Q

True/False.

The enteric NS has the same number of neurons as the spinal cord (100,000,000)

A

True.

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54
Q

Describe the function of histamine and somatostatin as paracrine factors.

A

Histamine – secreted by ECL cells and stimulates HCl release

Somatostatin – secreted by D cells in response to decreased GI luminal pH

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55
Q

The action of histamine at H2-receptors in the stomach is blocked by what endogenous hormone?

A

Secretin

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56
Q
A

2.

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57
Q

Gastrin is secreted by what type of cell?

CCK is secreted by what type of cell?

Secretin is secreted by what type of cell?

Glucode-dependent insulinotropic peptide is secreted by what type of cell?

A

G cells;

I cells (duodenum and jejunum);

S cells (duodenum);

K cells (duodenum and jejunum)

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58
Q

What are the stimuli for secretion of gastrin?

What are the stimuli for secretion of CCK?

What are the stimuli for secretion of secretin?

What are the stimuli for secretion of glucose-dependent insulinotropic peptide?

A

Amino acids, distention, vagal stimulation;

lipids and amino acids;

gastric acid and fatty acids;

oral glucose, fatty acids, and amino acids

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59
Q

What are three substances that directly inhibit gastric acid secretion?

A

Somatostatin;

secretin;

glucose-dependent insulinotropic peptide (aka gastric inhibitory peptide)

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60
Q

Gastrin is directly blocked by:

A

Secretin

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61
Q

Gastrin causes increased secretion of:

CCK causes increased secretion of:

Secretin causes increased secretion of:

Glucose-dependent insulinotropic peptide causes increased secretion of:

A

HCl;

pancreatic enzymes, pancreatic HCO3-;

pancreatic HCO3-; biliary HCO3-;

insulin

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62
Q

Gastrin’s non-secretory effects include:

CCK’s non-secretory effects include:

Secretin’s non-secretory effects include:

Glucose-dependent insulinotropic peptide’s non-secretory effects include:

A

Growth of gastric and intestinal mucosa, increased gastric motility;

gallbladder contraction, sphincter of Oddi relaxation, growth of pancreas and gallbladder, slowed gastric emptying;

inhibits gastrin/histamine, slowed gastric emptying;

inhibits glucagon, slowed gastric emptying

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63
Q

Describe the vessels found within a single intestinal villus.

A
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64
Q

What structural feature of the GI tract lends the highest increase in surface area to the tract (plicae circularis, villi, crypts of Lieberkuhn, microvilli)?

A

Microvilli

(600x increase)

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65
Q

True/False.

GI stem cells are mostly found between the microvilli.

A

True/False.

GI stem cells are mostly found at the bottom of the crypts of Lieberkuhn.

66
Q

Describe the histological differences between the small intestine and large intestine.

67
Q

Describe the differences in breakdown and absorption between protein, carbohydrates, and lipids.

A

Proteins: broken down into oligopeptides or amino acids –> oligopeptides then digested within enterocytes

Carbohydrates: broken down into monomers

Lipids: broken down into fatty acids –> resynthesized into triglycerides in the enterocytes

68
Q

What is the main carbohydrate we eat?

What is the main carbohydrate of dietary fiber?

A

Amylopectin (plant starch);

cellulose

69
Q

Describe how a branched carbohydrate is broken down in the GI tract.

A
  1. α-amylase cuts branched structures (such as amylopectin) into monomers
  2. Disaccharides and limit-dextrans are then cut down by further brush border hydrolases (isomaltase, sucrase, lactase, etc.)
70
Q

What transporter allows for apical glucose uptake in the GI tract?

What transporter allows for apical fructose uptake in the GI tract?

A

SGLT1

GLUT5

71
Q

What transporter allows for basolateral glucose uptake in the GI tract?

What transporter allows for basolateral fructose uptake in the GI tract?

A

GLUT2

GLUT2

72
Q

Is protein uptake in the GI tract sodium-dependent at either the apical or basolateral sides?

A

Apical only

(secondary active transport)

73
Q

What type of diarrhea can a lactase deficiency cause?

Why is there excess gas production?

A

Osmotic diarrhea;

the bacteria turn the excess sugar into H2 and CO2

74
Q

What is Hartnup disease?

To what disorder does it lead?

A

A disorder (renal and intestinal) of oligopeptide and tryptophan absorption;

pellagra (niacin defiiency leading to dermatitis + diarrhea + dementia)

75
Q

What is cystinuria?

What is the common result?

A

Improper gut cysteine absorption;

renal stones

77
Q

Cystinuria or Hartnup?

A

Cystinuria

78
Q

Virtually all dietary lipids are __________ (90%).

A

Triglycerides

79
Q

Name a few luminal substances necessary for proper fat digestion and absorption by the GI tract.

A

Lipases, bile acids, and phospholipids

80
Q

Children with low sun exposure may be at-risk for what disorder of vitamin D?

81
Q

Name three lipases and a cofactor released into the proximal duodenum.

A

Glycerol ester hydrolase, cholesterol ester hydrolase, phospholipase A2;

colipase

82
Q

What is colipase?

A

An amphipathic molecule that anchors lipases to lipid droplets

83
Q

Do micelles contain triglycerides?

A

No;

free fatty acids

84
Q

How are the fat-soluble vitamins (ADEK) absorped?

A

They diffuse into micelles and then into enterocytes and then into chylomicrons

85
Q

Which is larger: chylomicrons or micelles?

Which contains triglycerides: chylomicrons or micelles?

A

Chylomicrons;

chylomicrons

86
Q

Which of the following are formed within enterocytes:

Triglycerides

Cholesterol

Micelles

Chylomicrons

A

Triglycerides;

chylomicrons

87
Q

Which macromolecules are digested within enterocytes as well as in the GI lumen?

Which macromolecules are reformed within enterocytes after being digested in the GI lumen?

A

Oligopeptides;

triglycerides

88
Q

Describe the cellular mechanism of calcium absorption in the GI tract.

89
Q

While carbohydrate/protein/lipid absorption happens in each portion of the small intestine, where does the majority occur?

A

The duodenum (then jejunum, then ileum)

(Graph A.)

90
Q

In what portion(s) of the small intestine does calcium absorption occur?

A

All three

(Graph B.)

91
Q

Where is folate absorbed in the gut?

A

Duodenum and jejunum

92
Q

Where is iron absorbed in the gut?

A

The duodenum

93
Q

Where are bile acids absorbed in the gut?

A

Mostly the ileum

94
Q

The ileum is specifically responsible for the absorption of what two substances?

A

B12;

bile acids

95
Q

About how much fluid is secreted into the gut every day?

About how much of that fluid is reabsorbed by the small intestine?

About how much of that fluid is reabsorbed by the large intestine?

A
  1. 5 L
  2. 5 L
  3. 9 L
96
Q

What is the basic mechanism of fluid reabsorption in the gut?

A

Solute reabsorption

(fluid follows solutes)

97
Q

What two types of junctions are responsible for water reabsorption in the gut?

With what two different tonicities?

A

Leaky junctions –> isosmotic absorption

Tight junctions –> absorption across gradients

98
Q

The small intestine absorbs net amounts of water and what electrolytes?

The small intestine secretes net amounts of what electrolytes?

A

Na+, K+, Cl-;

HCO3-

99
Q

The large intestine absorbs net amounts of water and what electrolytes?

The large intestine secretes net amounts of water and what electrolytes?

A

Na+, Cl-;

K+, HCO3-

100
Q

What causes congenital chloridorrhea?

What pH change is expected?

A

A deficiency of the gut Cl-/HCO3- exchanger;

metabolic alkalosis (HCO3- retention)

101
Q

What pH effect can secretory diarrhea have?

What pH effect can severe vomiting have?

A

Metabolic acidosis (HCO3- loss);

metabolic alkalosis (HCl loss)

102
Q

How can diarrhea be classified according to the reason for fluid moving to the vessel lumen?

A

Osmotic;

secretory

103
Q

True/False.

Diarrhea can be caused by either blocking gut solute absorption or increasing gut solute secretion.

107
Q

Describe the cellular mechanism of iron absorption in the duodenum.

Specifically, what is the apical transporter and other protein regulating the pathway?

A

DCT1;

hephaestin

108
Q

In what ways is absorption of glucose and amino acids in the gut similar to reabsorption in the kidneys?

A

Secondary active transport (Na+-linked) at the apical membrane;

Na+/K+ ATPases at the basolateral membrane

109
Q

Describe post-prandial sodium absorption in the duodenum, jejunum, and ileum.

A

Na+-linked secondary active transport;

Na+/H+ exchangers

110
Q

Describe sodium absorption during the inter-digestive phase in the ileum and colon.

A

Na+/H+ and Cl-/HCO3- exchangers;

Na+ leak channels

111
Q

Where does passive Cl- absorption predominate in the GI tract?

Where do Cl-/HCO3- exchangers predominate in the GI tract?

A

Jejunum, distal colon;

ileum, proximal colon

112
Q

Describe the mechanism of NaCl secretion in the crypts of Lieberkuhn.

A

CFTR transporters;

paracellular Na+ leakage

113
Q

Describe the changes in K+ absorption and secretion from the small intestine to the large intestine to the distal colon.

114
Q

Describe some of the mechanisms of NaCl absorption and K+ secretion by the colon.

A

Na+-linked cotransporters;

Na+/H+ exchangers;

Cl-/HCO3- exchangers;

K+ leak channels

115
Q

Malfunction/deficiency of the DRA / AE1 channels in this diagram of a colonic cell would result in what effects?

What is the name of this condition?

A

Alkalosis and osmotic diarrhea

(due to HCO3- retention and Cl- secretion);

congenital chloridorrhea

116
Q

In relative terms, describe the pHs of the following GI tract segments:

Salivary glands

Stomach

Biliary tree

Pancreas

Jejunum

Ileum

Colon

A

Alkaline

Highly acidic

Alkaline

Highly alkaline

Alkaline

Alkaline

Acidic

117
Q

What is the main controlling factor for intestinal ion transport?

A

Chemical mediators: absorbtagogues and secretagogues

118
Q

Name some of the secretagogues increasing ion secretion in the intestines.

A

Acetylcholine,

nitric oxide,

VIP,

histamine,

prostaglandins,

bile acids,

gastrin,

long-chain FAs

119
Q

Name some of the absorbtagogues increasing ion secretion in the intestines.

A

Opioids,

norepinephrine,

somatostatin

120
Q

What effect do cAMP, cGMP, and Ca2+ have on intestinal anion secretion?

And NaCl absorption?

A

Increase;

inhibition

121
Q

What intracellular mediator(s) increase(s) intestinal anion secretion and inhibit(s) NaCl absorption?

A

cAMP, cGMP, Ca2+

122
Q

What sections of the stomach have parietal cells?

A

Body + fundus

123
Q

What section of the stomach is the primary location of G cells?

A

The antrum

124
Q

Which of the three factors that increase gastric acid secretion (histamine, gastrin, acetylcholine) increase intracellular Ca<strong>2+</strong> in the parietal cells they bind?

Which of the three factors that increase gastric acid secretion (histamine, gastrin, acetylcholine) increase intracellular cAMP ​in the parietal cells they bind?

A

Gastrin (CCKR), acetylcholine (M3);

histamine (H2)

125
Q

Name that respective intracellular messenger that each of the following utilizes to stimulate increased HCl secretion by parietal cells:

Gastrin

Histamine

Acetylcholine

A

Ca2+

cAMP

Ca2+

126
Q

Which is more likely to cause ulcer formation, acute or chronic NSAID use?

A

Acute

(chronic does increase risk though)

127
Q

How does a urease breath test work?

A

A patient ingests labeled urea;

labeled CO2 being breathed out is then measured to see if urease is present in the stomach;

if so, this indicates H. pylori infection

128
Q

H. pylori uses urease to turn ________ into ________.

A

Urea;

NH3 + CO2

129
Q

What is the mechanism of H. pylori-induced ulcer formation?

A

Urease creates ammonia –> neutralizing HCl so the H. pylori can approach the epithelium;

the H. pylori inhibit somatostatin at the epithelium –> causing increased HCl production

130
Q

Why can ulcer pain decrease after eating?

A

Food acts as a buffer

131
Q

True/False.

The mucus and unstirred water layers of the stomach contain high concentrations of HCO3-.

132
Q

How is H. pylori infection treated?

A

Triple therapy:

a PPI (omeprazole)

+ 2 antibiotics

133
Q

What mnemonic can be used to remember the causes of pancreatitis?

A

I GET SMASHED

Idiopathic

Gallstones EtOH Trauma

Steroids Malignancy/Mumps Autoimmune Scorpion sting Hypertriglyceridemia/Hypercalcemia ERCP Drugs

134
Q

Use the mnemonic I GET SMASHED to list some major risk factors for pancreatitis.

A

Idiopathic

Gallstones EtOH Trauma

Steroids Malignancy/Mumps Autoimmune Scorpion sting Hypertriglyceridemia/Hypercalcemia ERCP Drugs

135
Q

What cofactor does the pancreas secrete to aid lipase in digesting lipids?

What does the pancreas secrete to inhibit trypsin activity?

Why?

A

Colipase;

trypsin inhibiting protein (TIP),

to prevent pancreatic autodigestion

136
Q

Name two proteins that the duodenum secretes.

One is solely to decrease gastric acid secretion, and one is to aid in protein digestion.

A

Urogastrone;

pepsinogen

137
Q

What is urogastrone?

A

A duodenal peptide that inhibits the action of gastrin

138
Q

Where are bile acids reabsorbed in the GI tract?

139
Q

Why might a patient present with diarrhea following resection of the terminal ileum?

A

Secretory diarrhea

(bile acids remain in lumen and Cl- secretion is increased)

140
Q

Which is more soluble, bile salts or bile acids?

A

Bile salts (better able to emulsify fat)

141
Q

How are bile acids reabsorbed in the ileum?

Where do they go?

A

Via Na+-linked cotransport;

the portal vein

142
Q

What is chenodeoxycholic acid?

A

A primary bile acid

(can be used to dissolve gallstones)

143
Q

What is the rate-limiting enzyme for bile acid production?

A

7α-hydroxylase

144
Q

What three products does α-amylase produce?

A

Maltose,

maltotriose,

α-limit dextrans

145
Q

What bonds can α-amylase cleave?

A

Non-terminal α-1,4 bonds

(forming maltose, maltriose, and α-limit dextrans)

146
Q

Name the substrate each of the following enzymes acts upon:

Isomaltase

Lactase

Sucrase

A

Maltose, maltotriose, α-limit dextrans;

lactose;

sucrose

147
Q

After α-amylase cleaves amylopectin α-1,4 bonds to produce maltoses, maltrioses, and α-limit dextrans, what enzyme further degrades these products?

What bonds can it cleave?

A

Isomaltose;

α-1,4 (maltose, maltriose) and α-1,6 (α-limit dextrans)

148
Q

How are gut amino acid transporters classified according to their nomenclature?

A

Upper case letter (e.g. B): Na-dependent

0 Superscript (e.g. B0): neutral amino acids

Lower case letter (e.g. b): Na-independent

+ Superscript (e.g. b+): charged amino acids

149
Q

What type of gut amino acid transporter is missing in Hartnup disease?

A

Na-dependent for neutral amino acids

(B0)

150
Q

Are patients protein-deficient in either Hartnup’s disease or cystinuria?

151
Q

In which locations does most Na-linked cotransport occur in the gut?

A

Duodenum > Jejunum >> Ileum

152
Q

In which locations does most Na+/H+ exchange occur in the gut?

A

Jejunum, ileum, proximal colon

153
Q

In which locations does most passive Cl- absorption occur in the gut?

A

Jejunum, distal colon

154
Q

In which locations does most K+ secretion occur in the gut?

A

Distal colon

155
Q

In which locations does most Cl-/HCO3- exchange occur in the gut?

A

Ileum, proximal colon

156
Q

What transporter in the duodenum allows for Fe3+ uptake?

What transporter in the small intestine allows for glucose​ uptake?

A

DCT1

SGLT1

157
Q

What transporter in the colon allows for short-chain fatty acid uptake?

What transporter in the colon allows for Cl-​ (uptake) and HCO3- exchange?

A

SMCT1

DRA/AE1

158
Q

A deficiency of what transporter in the colon leads to congenital chloridorrhea?

A

DRA/AE1

(a Cl-/HCO3- exchanger)

159
Q

True/False.

Apical transport of amino acids into the enterocytes is bidirectional.

A

False.

Basolateral transport of amino acids into the enterocytes is bidirectional.

160
Q

What cotransporter allows for glucose uptake in the gut?

What cotransporter allows for glucose uptake in the kidneys?

A

SGLT1

SGLT2

T1 - Phase 1 - Integrated (II) (23 decks)

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