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GI Final Exam > Physiology > Flashcards

Physiology Flashcards

1
Q

What is secreted by each of the following salivary glands: parotid, submaxillary/submandibular, and sublingual?

A
  • Parotid: secrete fluid of water, ions, and enzymes
  • submaxillary/ submandibular: mixed glands; secrete fluid and mucin glycoproteins
  • sublingual: mixed glands; secrete fluid and mucin glycoproteins
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2
Q

How does saliva compare to plasma? What is the difference in ions?

A

saliva is hypotonic compared to plasma

  • higher levels of K and HCO3
  • lower levels of Na and Cl
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3
Q

Describe the function of each of the following: salivary acinus, striated duct, and myoepithelial cells?

A
  • acinus: produces initial saliva
  • striated duct: modifies saliva (hypotonic)
  • myoepithelial cells: contract to eject saliva as stimulated by neuronal inputs
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4
Q

Describe the formation of saliva

A

initial solution isotonic -> absorption of Na and Cl -> secretion of K and HCO3 -> net absorption of solute b/c ductal cells impermeable to water

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5
Q

What transporter is located on basolateral side of salivary duct cells?

A

Na/K ATPase (K into ductal cells; Na out)

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6
Q

What 3 transporters are located on apical side of salivary ductal cells?

A
  • Na/H anti porter (Na into cell and H out to saliva)
  • Cl/HCO3 antiporter (Cl into cell and HCO3 out to saliva)
  • K/H antiporter (H into cell and K out to saliva)
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7
Q

What is the parasympathetic innervation for the 3 types of salivary glands?

A

Facial N. (CN VII) for submandibular and sublingual

Glossopharyngeal N. (CN IX) for parotid

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8
Q

What stimulates parasympathetic activation of salivary glands? Through which receptors and what NT?

A
  • activated by smell, food, higher brain function
  • NT: ACh
  • Receptor: Muscarinic
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9
Q

What is sympathetic innervation of salivary glands? What is the result of sympathetic activation? Through what receptor and NT?

A
  • T1-T3 and superior cervical ganglion
  • increases salivary secretion (just like parasympathetic)
  • NT: NE
  • Receptor: beta adrenergic
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10
Q

Name 7 major stomach secretions

A

Acid, Pepsinogen, Intrinsic factor, Gastrin, Mucus, HCO3, and Water

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11
Q

What is the location of oxyntic glands in the stomach?

A

proximal 80% of stomach (fundus and body)

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12
Q

Name 6 types of cells located in oxyntic glands

A

parietal cells, D cells, mucous cells, ECF cells, chief cells, ECF-like cells

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13
Q

What is the location of pyloric glands in the stomach?

A

distal 20% of stomach (antrum)

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14
Q

Name 4 types of cells located in pyloric glands

A

G cells, D cells, mucous cells, ECF cells

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15
Q

What is produced by each of the following cells: parietal cells, D cells, ECF cells, Chief cells, ECF-like cells, G cells

A
  • parietal cells: acid
  • D cells: somatostatin
  • ECF cells: ANP
  • Chief cells: pepsinogen
  • ECF-like cells: histamine
  • G cells: gastrin
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16
Q

Name 2 functions of HCl in the stomach

A

lower pH to 1-2; converts pepsinogen to pepsin

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17
Q

What are 3 receptors that activate parietal cells?

A

M3 (ACh), H2 receptors (histamine), CCK-B (gastrin)

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18
Q

What is the optimal pH for pepsin? What happens if the pH becomes too high?

A
  • optimal pH = 1.8 - 3.5
  • reversibly inactivated > 5
  • irreversibly inactivated > 7-8
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19
Q

Name 4 stimuli for chief cells to release pepsinogen. Which is the most important?

A
  • Vagus N. (most important)
  • H triggers local cholinergic (ACh) reflex to stimulate chief cells
  • Gastrin and secretin enter circulation and activate chief cells
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20
Q

Describe HCl secretion from parietal cells

A
  • Na reabsorbed into cytoplasm (Na/K ATPase)
  • negative charge on canaliculus side -> Na and K passively diffuse into canaliculus
  • H2O dissociates into OH and H in parietal cell
  • H secreted into canaliculus (H/K ATPase)
  • Cl actively transported into canaliculus
  • water enters canaliculus via osmosis
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21
Q

Describe an alkaline tide

A

CO2 reacts w/ OH in cytoplasm of parietal cells to form HCO3 -> secreted into ECF -> slight increase in pH surrounding stomach

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22
Q

How does the vagus N. directly influence parietal cells to secrete HCl?

A

M3 receptor (IP3/Ca) via ACh

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23
Q

How does the vagus N. indirectly influence parietal cells to secrete HCl?

A
  • induces gastrin release via GRP directly on G cells

- activates ECL cells to release histamine

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24
Q

How does atropine affect HCl secretion?

A

blocks muscarinic (cholinergic) receptors - lower HCl secretion; does not shut down the whole system

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25
Q

How does each of the following affect HCl secretion: histamine, gastrin, ACh, somatostatin, prostaglandins?

A
  • histamine: increases
  • gastrin: increases
  • ACh: increases
  • somatostatin: decrease
  • prostaglandins: decrease
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26
Q

What cells produce histamine? What receptor does histamine use to increase acid secretion?

A

produced by ECL-like cells; uses H2 receptors

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27
Q

What 2 things potentiate the release of histamine from ECL-like cells?

A

gastrin and ACh

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28
Q

How do somatostatin and prostaglandins inhibit acid secretion?

A

directly and indirectly by inhibiting ECL-like cells

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29
Q

What 3 things does gastrin stimulate the release of?

A
  • acid via CCKB receptors
  • histamine from ECL-like cells
  • somatostatin (inhibits acid secretion)
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30
Q

How do prostaglandins inhibit acid secretion?

A

inhibit ECL-like cells (histamine) and parietal cells directly via cAMP

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31
Q

Describe passive feedback of HCl secretion

A

HCl secretion inhibits gastrin release -> reduces HCl secretion

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32
Q

What is cimetidine? What is it used to treat?

A

H2 receptor antagonist; treats GERD, duodenal and gastric ulcers

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33
Q

What is the MOA of omeprazole?

A

inhibits H/K ATPase on parietal cells to prevent them from secreting acid

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34
Q

Explain PSNS regulation of gastrin and somatostatin release? How is somatostatin released?

A
  • Vagus N. stimulates gastrin release via GRP; inhibit somatostatin
  • somatostatin released due to gastrin
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35
Q

What is the 1st phase of gastric HCl release? How much HCl is released and what stimulates it?

A

cephalic phase; 30% of HCl secretion; stimulated by smell, taste, chewing, swallowing, and conditioned reflexes (Vagus N.)

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36
Q

What is the mechanism by which the cephalic phase of HCl release works?

A
  • vagus N. stimulates parietal cells via ACh (direct)

- vagus N. stimulates gastrin secretion via GRP on G cells (indirect)

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37
Q

What is the 2nd phase of gastric HCl release? How much HCl is released and what stimulates it?

A

Gastric phase; 60% of HCl secretion; stimulated by distention of the stomach and presence of proteins

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38
Q

What is the mechanism by which the gastric phase of HCl release works?

A
  • distention activates mechanoreceptors in mucosa of oxyntic and pyloric glands (activates vagus N.)
  • distention of antrum activates local reflex of gastrin release
  • AAs and small peptides stimulate gastrin release
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39
Q

What is the 3rd phase of gastric HCl release? How much HCl is released and what stimulates it?

A

intestinal; 10% of HCl secretion; stimulated by distention of small intestine and presence of digested protein

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40
Q

What is the mechanism by which the intestinal phase of HCl release works?

A
  • distention of small intestine stimulates acid secretion via ENS
  • digested protein stimulates gastrin release (hormone mediated)
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41
Q

What is the reverse enterogastric reflex?

A

small intestine switches roles from activating acid secretion to inhibiting it

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42
Q

What hormones have a role in the reverse enterogastric reflex?

A

secretin, GIP, VIP, and somatostatin

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43
Q

What is the only essential stomach secretion? What is its function and what happens if it is not secreted?

A

intrinsic factor from parietal cells; required for absorption of B12 in the ileum; if not secreted -> pernicious anemia

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44
Q

What do mucous neck cells and gastric epithelial cells secrete?

A
  • mucous neck cells -> mucus

- gastric epithelial cells -> HCO3

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45
Q

What are 5 protective factors of the gastric mucosa?

A

HCO3, mucus, prostaglandins (inhibits acid), blood flow, gastrin (growth factors)

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46
Q

What are 7 damaging factors of the gastric mucosa?

A

acid, pepsin, NSAIDs/ASA, H. Pylori, alcohol, bile, stress

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47
Q

What are the 2 predominant causes of PUD in the US?

A

H. Pylori infection and NSAIDs

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48
Q

What is the main reason for gastric ulcers? What is the major causative agent and how is it diagnosed?

A

mainly due to defective mucosal barrier; causative agent is H. Pylori; dx based on urease activity (alkalizing agent that allows bacteria to colonize)

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49
Q

What are H secretion rates in duodenal ulcers? How does H. Pylori play a role?

A

H secretion is slightly higher; H. Pylori has an indirect influence by inhibiting somatostatin and HCO3 secretion

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50
Q

What is Zollinger-Ellison Syndrome?

A

gastrinoma (pancreatic tumor that secretes large amounts of gastrin) cause really high H secretory rates -> increased H secretion by parietal cells and increased proliferation of parietal cells

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51
Q

What is used to dx Zollinger-Ellison syndrome? What is the tx?

A

Secretin is used to dx (paradoxical increase in gastrin); tx include cimetidine, omeprazole, and surgery

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52
Q

What are 2 types of active enzymes released from the pancreas?

A

amylases and lipases

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53
Q

What is the organization of the exocrine pancreas?

A

similar to salivary glands; acinus (secretes enzymes) -> centroacinar cells -> ducts (secretes aqueous solution w/ HCO3)

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54
Q

What is the role of pancreatic ductal cells?

A

secretion of HCO3 and absorption of H

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55
Q

What is the 1st phase of pancreatic secretion and what is released (and %)? What stimulates it?

A

cephalic phase produces enzymatic secretion (10-15%); initiated by vagus N., smell, taste, and conditioning

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56
Q

What is the 2nd phase of pancreatic secretion and what is released (and %)? What stimulates it?

A

gastric phase produces enzymatic secretion (5-10%); imitated by vagus N. and stomach distention

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57
Q

What is the 3rd phase of pancreatic secretion and what is released (and %)? What stimulates it?

A

intestinal phase produces enzymatic and aqueous secretions (80%); driven by secretin

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58
Q

What is the sympathetic innervation of the pancreas and what does it do?

A

postglangionic nerves from celiac and superior mesenteric plexus -> inhibitory

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59
Q

What is the parasympathetic innervation of the pancreas and what does it do?

A

vagus N. -> stimulatory; potentiates secretin and CCK

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60
Q

What is secreted from S cells and I cells of the duodenum?

A

S cells = secretin

I cells = CCK

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61
Q

What stimuli does secretin respond to and what is its function?

A

secreted in response to pH < 5.0 in duodenum; stimulates aqueous and HCO3 secretion from ductile cells of pancreas

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62
Q

What stimuli does CCK respond to and what is its function?

A

secreted in response to fat and protein digestion byproducts in duodenum and jejunum; stimulates enzymatic secretions for pancreatic acini

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63
Q

What is secreted from Brunner’s glands in the small intestine (duodenum)?

A

mucous -> protects duodenum from acid

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64
Q

What is secreted from crypts of lieberkuhn in small and large intestine?

A

goblet cells secrete mucus

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65
Q

What effect does excessive alcohol intake cause on the liver?

A

most common cause of cirrhosis; leads to accumulation of fat within hepatocytes -> steatohepatitis which is fatty liver w/ inflammation -> scarring of the liver

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66
Q

Explain how hepatitis leads to increased portal blood pressure

A

inflammation causes a thick collagen basement membrane to develop -> free flow of materials is impacted -> less capillaries to spread out the blood (less in parallel) but the same amount is flowing through a smaller space

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67
Q

How does portal HTN affect hydrostatic and oncotic pressures?

A

increased hydrostatic pressure (pushes fluid out of capillary) and decreased oncotic pressure (pulls fluid back into capillary)

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68
Q

Name 6 consequences of portal HTN

A
  • ascites
  • esophageal varices
  • hepatic encephalopathy
  • malnutrition
  • caput medusae
  • hemorrhoids
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69
Q

Bile is composed of what 6 things?

A

bile salts, bile pigments (bilirubin), cholesterol, phospholipids, ions, and water

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70
Q

Where are primary and secondary bile acids synthesized as well as bile salts conjugated?

A
  • primary bile acids = hepatocytes
  • secondary bile acids = small intestine
  • bile salts = liver
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71
Q

In what form do bile sals transport lipids?

A

as micelles (amphipathic) which increase the surface area of lipids and expose them to lipases

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72
Q

How does secretin affect bile concentration?

A

stimulates release of HCO3, water, and Na from ductile cells -> increases the volume and pH of bile and decreases bile salt concentration

73
Q

What is the state of the gallbladder during the interdigestion period?

A
  • gallbladder fills w/ bile
  • gallbladder is relaxed
  • sphincter of Oddi is closed
74
Q

What mediates the contraction of the gallbladder and opening of the sphincter of Oddi upon ingesting food?

A

CCK

75
Q

How does CCK mediate the contraction of the gallbladder?

A
  • directly by acting on the gallbladder

- indirectly but communicating w/ Vagus N. afferents -> efferents cause gallbladder to contract through ACh

76
Q

Name 4 things that decrease gallbladder contractility

A

SNS, secretin, pancreatic polypeptide, and somatostatin

77
Q

What is the purpose of enterohepatic circulation? What organs are involved?

A

recycles bile acids/salts

- involves the liver, gallbladder, bile duct, duodenum, ileum, and portal circulation

78
Q

Name 2 channels that uptake bile acids into hepatocytes

A

NTCP and OATP (also plays a role in bilirubin transport)

79
Q

Name 2 channels that uptake bile acids into canaliculi

A

BSEP and MRP2 (mutations associated w/ liver diseases and hyperbilirubinemia)

80
Q

How much of bile acids are recycled per day as opposed to being excreted in feces? How is this affected by removing the ileum?

A

90-95% recycled; 5-10% excreted

- if the ileum is removed, cannot recycle bile acids and production must go up

81
Q

How is bilirubin made and by what system? How is it transported in blood?

A
  • bilirubin is released during RBC breakdown by the reticular endothelial system (RES)
  • circulates bound to albumin
82
Q

What is the key enzymes in the conjugation of bilirubin in the liver?

A

UDP-glucuronyl transferase (UGT)

83
Q

What is bilirubin converted to in the intestines?

A

urobilinogen

84
Q

What 3 routes can urobilonogen take once in the small intestine?

A
  • reabsorbed to the kidney (excreted as urobilin)
  • reabsorbed back to the liver (enterophatic circulation)
  • excreted in the feces (as stercobilin)
85
Q

What 3 liver enzymes are measured in serum using LFTs?

A
  • alanine aminotransferases (ALT)
  • aspartate aminotransferase (AST)
  • alkaline phosphatase (AlkPhos)
86
Q

What do elevated aminotransferases or AlkPhos generally mean?

A
  • aminotransferases: hepatocyte injury

- AlkPhos: gallstones (damage to bile duct)

87
Q

What are 3 abnormal values that may be seen w/ impaired hepatic function?

A
  • bilirubin
  • albumin
  • prothrombin time (PT)
88
Q

Difference between direct and indirect bilirubin?

A 
indirect = uncogjugated
direct = conjugated
89
Q

What could impaired liver function do to albumin levels?

A

decrease albumin levels -> decrease oncotic pressure

90
Q

What could impaired liver function do to PT?

A

increases PT as the ability of the liver to form new clotting factors decreases

91
Q

What is Jaundice a sign of?

A

hyperbilirubinemia

92
Q

Name 5 causes of hyperbilirubinemia and whether the excess bilirubin is conjugated or uncojugated

A
  • excess production of bilirubin (hemolytic anemia)(unconjugated)
  • decrease uptake of bilirubin into hepatocytes (uncojugated)
  • defective UGT enzyme (uncojugated)
  • disturbed secretion of bilirubin into canaliculi (conjugated)
  • bile duct obstruction (conjugated)
93
Q

What is hemolytic anemia and what type of bilirubin will be increased?

A

excessive breakdown of RBCs -> uncojugated

94
Q

What are the 2 main causes of neonatal jaundice? What type of bilirubin in increased?

A
  • increased bilirubin production due to breakdown of fetal erythrocytes
  • low activity of UGT enzyme
  • uncojugated
95
Q

What is the purpose of phototherapy to help with neonatal jaundice?

A

light changes trans-bilirubin to cis-bilirubin (more water soluble and can be excreted)

96
Q

What is Gilbert’s syndrome? What usually causes flare ups? What type of bilirubin is increased?

A
  • mutation in the gene that encodes UGT (defect in conjugation of bilirubin)
  • uncojugated increases
  • flare ups caused by physiological stress (seen by adolescence)
97
Q

What is Crigler-Najjar Syndrome? Which type is more severe? What type of bilirubin is increased?

A
  • loss of function mutations in UGT
  • unconjugated increases
  • Type 1 is much more severe than Type 2
98
Q

Explain Type 1 Crigler-Najjar Syndrome compared to Type 2?

What is the treatment?

A
  • starts earlier in life; jaundice appears at birth; results in kernicterus - form of brain damage caused by accumulation of uncojugated bilirubin
  • tx is a liver transplant
99
Q

Explain Type 2 Crigler-Najjar Syndrome compared to Type 1?

What is the treatment?

A
  • starts later in life and survival goes into adulthood; less likely to develop kernicterus
  • tx is phenobarbitol (no response in Type 1)
100
Q

What is Dubin-Johnson Syndrome? What may worsen it? What type of bilirubin is increased?
What is unique about the liver?

A
  • defect in ability of hepatocytes to secrete conjugated bilirubin into bile (mutations in MRP2)
  • mild jaundice throughout life; may be worsened by alcohol, BC, infection, or pregnancy
  • conjugated
  • liver has black pigmentation
101
Q

What is Rotor Syndrome?What type of bilirubin is increased? What is unique about the liver?

A
  • gene mutations in OATP (bilirubin cannot leave enterocytes - recycling compromised)
  • conjugated and unconjugated can be increased
  • lack of liver pigmentation
102
Q

Name 4 causes of gallstones?

A
  • too much water absorption from bile
  • too much absorption of bile acids
  • too much cholesterol in bile
  • inflammation of epithelium
103
Q

What stimulates bile acid independent bile formation?

A

secretin

104
Q

Why are microvilli the longest in the duodenum?

A

absorption occurs most in the duodenum and then lessens as it moves through the small intestine

105
Q

What are enterocytes and what is there function?

A

epithelial cells of the small intestine that play a role in absorption of nutrients and secretion of HCO3 as protection

106
Q

Goblet cells vs Paneth cells

A

Goblet cells: mucus-secreting cells

Paneth cells: secrete defensins as part of mucosal defenses against infection

107
Q

Name 4 routes of passage into enterocytes

A

pinocytosis, passive diffusion, facilitated diffusion, and active transport

108
Q

Describe the layers solutes must cross moving from enterocyte to lumen of blood (7)

A
  • unstirred layer of fluid (mucus layer w/ immunological products)
  • glycocalyx
  • apical membrane
  • cytoplasm of cell
  • basolateral membrane
  • basement membrane
  • wall of blood capillary/wall of lymphatic vessels
109
Q

Which nutrient is mainly absorbed into the lymphatics?

A

fats

110
Q

What cannot be absorbed if the ileum is resected?

A

bile salts and vitamin B12

111
Q

What are the 3 primary sugars of the human diet? What starts digesting them in the mouth?

A
  • sucrose, lactose, and starch

- salivary amylase breaks down starch into maltose starting in the mouth

112
Q

What starts breaking sugars down in the duodenum?

A

pancreatic amylase

113
Q

What are the brush border enzymes that break down sugars? What forms are they broken into?

A
  • maltase = maltose -> glucose + glucose
  • trehalase = trehalose -> glucose + glucose
  • lactase = lactose -> glucose + galactose
  • sucrase = sucrose -> glucose + fructose
114
Q

What transporter bring glucose and galactose into intestinal epithelial cells? What process?

A

SGLT1; active transport

115
Q

What transporter bring fructose into intestinal epithelial cells? What process?

A

GLUT5; facilitated diffusion

116
Q

What transporter moves glucose, fructose, and galactose into the blood?

A

GLUT2

117
Q

How does lactase deficiency cause osmotic diarrhea?

A

lactose remains in intestine and unabsorbed -> holds H2O in the lumen -> diarrhea

118
Q

What is used to test the ability of the intestines to break down a sugar vs absorb it?

A

D-xylose -> 25 grams ingested during fast and urine collected for the next 5 hours -> if you collect less than 4 grans after 5 hours, it means the intestines are not absorbing

119
Q

Endopeptidases vs Exopeptidases

A

Endopeptidases - hydrolyse interior bonds between peptides

Exopeptidases - hydrolyze one AA at a time

120
Q

Which endopeptidase is secreted from the stomach rather than the pancreas? Is it essential?

A

pepsin; responsible for 10-20% protein breakdown in stomach -> not essential (can still break down protein in small intestine if pepsin not available)

121
Q

What is the brush border enzyme for protein breakdown and what is its function?

A

enterokinase -> activates trypsinogen to trypsin -> trypsin activates all other endopepidases an exopeptidase from pancreas

122
Q

What stimulates activation of the pancreas to secrete enzymes?

A
  • vagus N. through ACh
  • secretin -> works on ductal cells
  • CCK -> works on acinar cells
123
Q

What activates pepsin from pepsinogen?

A

low pH in stomach

124
Q

What enzymes does trypsin activate?

A
  • trypsin
  • chymotrypsin
  • elastase
  • carboxypeptidase A and B
125
Q

By what mechanism are proteins absorbed into small intestine and into blood?

A
  • Na-AA co-transporters on apical side (brings AAs into cell)
  • facilitated diffusion into the blood (Na/K ATPase creates Na gradient)
126
Q

What is chronic pancreatitis caused by?

A

deficiency in pancreatic enzymes -> ductal and acinar cells lose ability to produce HCO3 -> improper pH -> won’t secrete enzymes

127
Q

In what 2 ways could you have a congenital absence of trypsin?

A
  • if pancreas is not producing trypsinogen

- could have problem w/ enterokinase and can’t convert trypsinogen to trypsin

128
Q

What is cystinuria caused by?

A

defect or absence in Na/AA cotransporters in small intestine -> di-basic AAs all excreted

129
Q

What is Hartnup disease?

A

AR defect in neutral AA co-transporter; cannot absorb neutral AAs (such as tryptophan) and sx include pellagra (4Ds)

130
Q

How is cystic fibrosis connected to pancreatic defects?

A

loss of Cl channels -> not able to secrete HCO3 -> cannot neutralize acid -> activate trypsin before reaching small intestine -> auto digestion of pancreas

131
Q

What enzyme converts cholesterol to primary bile acids?

A

7a-hydroxylase

132
Q

What enzyme converts primary bile acids into secondary bile acids?

A

7a-dehydroxylase by bacteria in small intestine

133
Q

What are bile acids conjugated w/ to produce bile salts in the liver?

A

taurine and glycine

134
Q

How is pancreatic lipase secreted? What is needed for it be be activated? What is its function once it is activated?

A
  • secreted as active enzyme
  • requires colipase to be activated (colipase is activated by trypsin)
  • displaces bile salts from fats
135
Q

How is cholesterol ester hydrolase secreted? What is its function?

A
  • secreted as active enzyme

- catalyzes production of free cholesterol

136
Q

How is phospholipase A2 secreted? What activates it and what is its function?

A
  • secreted as proenzyme
  • activated by trypsin
  • phospholipid breakdown
137
Q

What are the 5 steps of fat absorption?

A
  • solubilization by micelles
  • diffusion of micelles across apical membrane
  • re-esterification (add back on FFA to reform fat)
  • chylomicron formation (for circulatory transport)
  • exocytosis of chylomicrons into lymphatics
138
Q

Why would small intestinal bacterial overgrowth (SIBO) cause a deficiency in bile salts?

A

bacteria deconjugate bile salts which impares micelle formation

139
Q

What deficiencies occur if you lose intestinal microvilli?

A

folate, vitamin B12, and fat soluble vitamins (ADEK)

140
Q

Fat soluble vs water soluble vitamin absorption

A
  • Fat soluble: same mechanism as lipids

- Water soluble: Na-dependent cotransporters except B12 (intrinsic factor)

141
Q

What does a deficiency in vitamin B12 cause? Common cause of vitamin B12 deficiency?

A
  • pernicious anemia -> failure of RBC maturation

- stomach does not produce enough IF

142
Q

What does calcium absorption depend on ?

A

presence of vitamin D as well as calcitriol and PTH

143
Q

How could you develop vitamin D deficiency?

A

lack of vitamin D in diet and by sunlight

144
Q

Explain how iron is absorbed? What facilitates iron entry into enterocytes?

A
  • liver secretes apotransferrin into bile -> duodenum
  • apotransferrin binds to free Fe and w/ hemoglobin to produce transferrin
  • transferrin binds to receptors on membranes of intestinal epithelial cells
  • Fe enters enterocytes w/ help of ferric reductase which requires vitamin C
145
Q

In which part of the intestines is calcium absorbed?

A

duodenum, jejunum, and colon

146
Q

Which part of the intestine is important for sodium absorption?

A

jejunum

147
Q

Which part of the brain is key in regulation of food intake?

A

hypothalamus

148
Q

What are the 2 anorexigenic signals in the arcuate nucleus and what is their function?

A

POMC/CART; decreases food intake and increases EE

149
Q

What are the 2 orexigenic signals in the arcuate nucleus and what is their function?

A

neuropeptide Y (NPY) and AgRP); increases food intake and decreases EE

150
Q

What is the function of the NTS?

A

nucleus tractus solitarius regulates sympathetic activity and energy expenditure

151
Q

Where does a-MSH come from? What does it target and what is its function?

A

released from POMC/CART neurons -> binds to MCR-4 (neurons) or MCR-3 (NPY/AgRP) and inhibits their activity -> decreases food intake

152
Q

What 3 things activate the POMC/CART pathway and inhibit the AgRP/NPY pathway?

A

Insulin, leptin, and CCK

153
Q

What activates the AgRP/NPY pathway?

A

ghrelin

154
Q

What is released by NPY/AgRP neurons? What does it target and what is its function?

A

release NPY which binds to Y1Rs on second order neurons to stimulate food intake

155
Q

What is the function of AgRP?

A

MCR-4 antagonist that blocks the action of a-MSH

156
Q

What is the role of the vagus N. in satiety and feeding?

A

vagal afferents talk to NTS -> vagal efferents talk to stomach to control energy homeostasis

157
Q

What secretes ghrelin? What is its function?

A
  • secreted by oxyntic cells of stomach

- stimulates neurons that release NPY, increases appetite, gastric motility, gastric acid secretion, and adipogenesis

158
Q

How does insulin affect NPY/AgRP and POMC/CART systems? What is its overall function?

A
  • activates POMC/CART
  • inhibits NPY/AgRP
  • overall decreases appetite and increases metabolism
159
Q

What secretes peptide YY (PYY) and what is its function?

A
  • released by L cells of the ileum and colon after a meal

- binds to Y2R on NPY/AgRP neurons to inhibit food intake

160
Q

What secretes leptin? What is its function?

A
  • secreted by adipocytes
  • inhibits NPY pathway and stimulates POMC pathway
  • overall, decreases appetite and increases metabolism
161
Q

What is adulthood obesity usually associated with?

A

leptin resistance

162
Q

What secretes CCK and what is its function in feeding behaviors?

A
  • secreted by I cells of duodenum

- elicits satiety

163
Q

What secretes GLP-1 and what is its action?

A

co-secreted w/ PTT from L cells of intestine

- reduces food intake, suppresses glucagon secretion, and delays gastric emptying

164
Q

What affect do pancreatic polypeptide, Amylin, and glucagon all have?

A

reduce food intake

165
Q

Describe an adjustable gastric band (lap band)

A

an adjustable band around the upper portion of the stomach -> activates ENS due to premature distention of stomach

166
Q

Describe a sleeve gastrectomy

A

left lateral portion of stomach is removed which leaves a banana shaped and sized stomach

167
Q

Describe a duodenal switch

A

sleeve gastrectomy is performed and large portion of small intestine is bypassed -> decreased absorption of nutrients

168
Q

Describe a Roux-en-Y. What does it do the levels of GLP-1 and PYY

A

involves creating a small stomach pouch and bypassing 3-5 ft of small intestine
- increases hormone levels (decrease desire to eat)

169
Q

What type of hormonal changes are seen in anorexia nervosa?

A

ghrelin resistance (fasting, so chronically elevated); increased levels of PYY

170
Q

Name 4 apical membrane transporters in the jejunum

A

Na-glucose, Na-galactose, Na-AA, Na-H

171
Q

What happens to HCO3 in the cells of the jejunum?

A

transported into blood via HCO3 transporter on basolateral membrane

172
Q

Which part of the intestine has a net absorption of NaCl? How does this occur?

A
  • ileum

- Na-H exchanger and Cl-HCO3 transporter move H and HCO3 into the lumen and Na and Cl into the cell

173
Q

Which electrolyte is absorbed in the colon and which is secreted? What affect does aldosterone have on the Na channels?

A
  • Na absorbed; K secreted

- aldosterone induces synthesis of Na channels -> more Na absorbed and more K secreted

174
Q

What affect does diarrhea have on K?

A

increased K loss in the colon -> hypokalemia

175
Q

What activates Cl channels on the apical membrane of intestines? How do they do this?

A

ACh and VIP -> generates cAMP to open the Cl channels and secrete Cl

176
Q

What 2 electrolytes are mainly lost during diarrhea? What does this cause?

A

mainly HCO3 (metabolic acidosis) and K (hypokalemia)

177
Q

What type of diarrhea does lactase deficiency cause?

A

Osmotic diarrhea -> lactose remains in intestines and retains water

178
Q

What can cause secretory diarrhea?

A

overgrowth of pathogenic bacteria such as E. Coli and cholera -> causes excessive secretion of fluid by crypt cells

GI Final Exam (6 decks)

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