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GI Flashcards

1
Q

What are the layers of the GI tract?

A

Mucosa: epithelium, lamina propria, muscularis mucosae
Submucosa (submucosal plexus)
Muscularis externa: circular muscle layer and longitudinal muscle

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2
Q

What are the two plexi in the enteric nervous system (ENS) and what are their locations?

A

Submucosal (Meissner’s) plexus in the submucosa

Myenteric (Auerbach’s) plexus between the circular and longitudinal layers of the muscularis externa.

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3
Q

What is an open-type enteroendocrine cell (EEC)?

A

EEC’s that have an apical membrane that is open to the GI tract lumen. This is more common than “closed-type” EEC’s.

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4
Q

What is an enterochromaffin-like (ECL) cell?

A

They are closed-type EEC’s that secrete histamine. Histamine is the most powerful paracrine secretagogue of HCl.

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5
Q 
Gastrin:
What is the source?
What is the stimulus?
Endocrine or Paracrine?
What is the target?
What is the effect?
A

G cells (located in gastric antrum)
Stimulus: Oligopeptides
Pathway: Endocrine
Targets: ECL cells and parietal cells of gastric corpus
Effect: Parietal cells secrete protons and ECL cells secrete histamine (–> more proton secretion), slows gastric emptying.

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6
Q 
Cholecystokinin (CCK)
What is the source?
What is the stimulus?
Endocrine or Paracrine?
What is the target?
What is the effect?
A

Source: I cells in duodenum
Stimulus: Fatty acids, hydrolyzed protein
Pathway: paracrine and endocrine
Targets: Pancreatic acinar cells, vagal afferent terminals
Effect: Inhibits gastric emptying and proton secretion, stimulation of pancreatic enzyme secretion, gallbladder contraction, satiety

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7
Q 
Secretin:
What is the source?
What is the stimulus?
Endocrine or Paracrine?
What is the target?
What is the effect?
A

Source: S cells in duodenum
Stimulus: protons
Pathway: paracrine and endocrine
Targets: Vagal afferent terminals, pancreatic duct cells
Effect: Stimulation of pancreatic duct secretion (water and HCO3-), slows emptying of stomach into SI

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8
Q

What do the pelvic nerves innervate?

A

They carry parasympathetics to the descending colon and below in the GI tract.

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9
Q

How is salivary secretion controlled?

A

Control is exclusively neural (unique to GI).

Secretion is stimulated by both sympathetic and parasympathetic

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10
Q

What is secondary peristalsis? Where does it occur?

A

It is initiated by distension in the esophagus. It is a second wave of peristalsis to clean out the esophagus after passage of a bolus. It can occur multiple times to clear the esophagus.

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11
Q

What is it called when the proximal stomach relaxed along with the LES to accomodate food coming into it?

A

Receptive relaxation

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12
Q 
Pepsinogen:
Secreted by?
Secreted as?
Optimal pH?
Required?
A

Secreted by chief cells
Secreted as pepsinogen
Active at pH<3
Not required because pancreatic proteases are sufficient.

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13
Q 
Intrinsic Factor:
Secreted by?
Stimulated by?
Function?
Required?
A

Secreted by parietal cells
Stimulated by all factors that stimulate acid secretion
IF binds up vitamin B12 so that it can be absorbed in the SI
The only gastric factor required for human life.

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14
Q

Mucins:
Secreted by?
Consists of?

A

Secreted by mucous neck cells and gastric epithelial cells
Composed of 80% carbohydrate
Tetrameric with 4 arms of carbohydrate surrounding a protein core

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15
Q 
Somatostatin:
Triggered by?
Secreted by?
Target?
Effect?
A

Triggered by pH< 3 in gastric antrum
Secreted by D cells
Targets G cells (paracrine)
Effect: inhibits gastrin release and therefore gastric acid secretion

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16
Q

Histamine’s mechanism of action in parietal cells

A

Histamine –> H2 receptor –> adenylyl cyclase –> increased [cAMP] –> increased HCl secretion

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17
Q

Ach effect on parietal cells

A

Ach –> muscarinic receptors –> Membrane Ca2+ channels open and IC Ca2+ is released from IC stores –> HCl secretion

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18
Q

Gastrin mechanism of action in parietal cells

A

Binds to CCK2 receptor –> Membrane Ca2+ channels open and IC Ca2+ is released from IC stores –> HCl secretion

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19
Q

What are interstitial cells of Cajal (ICC’s)

A

Specialized cells in the intestinal wall that are involved in the transmission of info from enteric neurons to smooth muscle cells. It’s thought that they are “pacemaker” cells that can generate slow wave rhythm.

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20
Q

What type of antibodies are secreted onto mucosal surfaces in the body?

A

IgA are mucosal antibodies and they represent ~80% of daily Ig production in the body.

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21
Q 
S cells:
Where are they located?
What triggers them?
What do they release?
What is the effect?
A

Located in the small intestinal epithelium
Triggered by pH< 4.5
Release secretin
Secretin directly stimulates increased release of HCO3- by pancreatic ductular cells. Water follows HCO3-, leading to increased pancreatic juice volume and pH. ***This is CFTR-mediated so cystic fibrosis patients have pancreas-associated symptoms.

Secretin also inhibits parietal cells & G cells (gastrin)

Note that this loop is self-limiting

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22
Q

What type of cell releases CCK?

What are the 3 things that can cause CCK release?

A

I cells in the small intestine epithelium release CCK

Stimulated by:
Direct I cell contact with fatty acids or amino acids
CCK-releasing factor (released by paracrine cells)
Monitor peptide (released by pancreatic acinar cells into pancreatic juice)

CCK-releasing factor and monitor peptide are largely stimulated by neural factors, and CCK can also be stimulated by the presence of amino acids & fatty acids.

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23
Q

What endocrine/paracrine/neural factors promote pancreatic acinar cell secretion?

A

cAMP mediated:
Vasoactive intestinal peptide (VIP)
Secretin

Ca2+ mediated:
Gastrin-releasing peptide (GRP)
ACh
CCK

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24
Q

What is the Migrating Motor Complex (MMC)?
What is it used for?
What is its cycle length?

A

The MMC is peristalsis seen in the small intestine, when no bolus is present. It propagates between smooth muscle cells via gap junctions. It is used to clear the small bowel between meals and to prevent colonic bacteria from colonizing the small intestine. Its cycle length is ~90 minutes.

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25
Q

What are Brunner glands?

Where are they located?

A

Brunner glands secrete mucous and bicarbonate into the small intestinal lumen.

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26
Q

What are Lieberkuhn glands/crypts?

A

Lieberkuhn glands secrete peptidases and carbohydrate-digesting enzymes directly into the small intestine.

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27
Q

What are Paneth cells & where are they located?

A

Paneth cells are located at the base of villi in the small intestine. They secrete antimicrobial proteins (esterases, nucleases, etc.) into the small intestinal lumen

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28
Q

What does alpha amylase digest?

A

alpha amylase digests alpha-1,4 linkages between glucose molecules. beta 1,4 linkages (cellulose) cannot be digested and are secreted.

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29
Q

What carbohydrate-digesting enzymes are found at the brush border of the small intestine?

A

Lactase, sucrase, glucoamylase, and alpha-dextrinase are located at the brush border of the small intestine. Alpha dextrinase is used to hydrolyze alpha-1,6 linkages.

30
Q

What is the main carbohydrate transporter found at the BL membrane of the small intestine and what does it transport?

A

GLUT2 can transport glucose, galactose, and fructose across the BL membrane.

31
Q

What carbohydrate transporter is responsible for shuttling glucose and galactose across the apical membrane of the small intestine?

A

SGLT1

It is a sodium-dependent symporter.

32
Q

What carbohydrate transporter is responsible for shuttling fructose across the apical membrane of the small intestine?

A

GLUT5

33
Q

What causes lactose intolerance?

A

A lack of lactase at the brush border of the small intestine causes lactose intolerance. Bacteria can then digest the excess lactose, leading to gas, diarrhea, etc.

34
Q

What is the daily requirement of protein?

A

0.6 g/kg/day

35
Q

How much protein is processed per day typically? Where does it come from?

A

~20 g from diet

~20 g from exfoliated GI epithelial cells

36
Q

What percent of amino acids are absorbed?

What do transporters group them by?

A

100% of proteins are absorbed
Transporters group amino acids by their charge (acidic, basic, neutral). Neutral AA’s are further divided by their properties.

37
Q

Describe protein digestion/absorption in the small intestine.

A

Luminal peptidases (trypsin, chymotrypsin, carboxypeptidases) digest proteins down to oligopeptides. Amino-peptidases in the brush border digest oligopeptides down to AA’s or dipeptides. AA’s are absorbed by their respective transporters, whereas Peptide Transfer Protein can transport di & tripeptides into the cyoplasm, where they will be further degraded.

38
Q

What powers peptide transporters in the small intestine?

A

Peptide transporters are symporters with H+

39
Q

How are hydrophobic amino acids absorbed in the small intestine?

A

They diffuse through the brush border membrane.

40
Q

How are single amino acid transporter deficiencies treated?

A

The body can usually compensate with di and tripeptides absorbed.

41
Q

What is Hartnup’s Disease?

A

Neutral amino acids cannot be absorbed in the small intestine and kidney. They are found in the urine (diagnostic). This can be compensated by di/tripeptide absorption.

42
Q

What do bile acids accomplish in the small intestine?

A

They emulsify fats and hydrophobic molecules, exposing them to lipases and other pancreatic enzymes.

43
Q

What is Zollinger-Ellison Syndrome?

A

ZES is characterized by a gastrin-secreting tumor in the pancreas or duodenum (gastrinoma).
Gastrin hypersecretion –> parietal cell hypersecretion & hypertrophy –> ulcers in stomach & duodenum. Steathorrea is also seen, likely because pancreatic lipases are inactivated by the low acidity of the duodenum. In this case, preduodenal lipases (usually not necessary) become important.

44
Q

Once absorbed into brush border cells, what is the fate of lipids?

A

They are bound by transport proteins (I-FABP = long chain, L-FABP = cholesterol, SCP-1 & SCP-2 = sterols) to prevent their aggregation in the cytoplasm. They are transported to the SER.

The SER catalyzes:
FA’s –> triglycerides
lysophosholipids –> phospholipids
lipid synthesis

They are then packaged into prechylomicrons –> Golgi –> lymphatics (thoracic duct).

45
Q

Where is most water absorbed in the GI system (secreted and ingested water)?

A

The small intestine

46
Q

How is Calcium absorbed in the small intestine?

How does vitamin D affect this process?

A

It is transported into the brush border cells and then binds calbindin. It dissociates at the BL membrane from calbindin and is transported across via Ca2+-ATPase or Ca2+/Na+ exchanger. Calcium absorption is more effective with acidic bile & occurs much slower than monovalent cations.

PTH –> more active vitD –> more calbindin & more Ca2+-ATPase activity –> more Ca2+ absorption

47
Q

How is vitamin B12 (cobalamin) handled in the GI tract?

Where in the GI tract is it absorbed?

A

It is complexed to R factor in the stomach.
In the pancreas, this complex is degraded and B12 binds to IF & absorbed. IF dissociates in the cytoplasm.
Transcobalamin binds to B12 to allow transport in the blood.

B12 is absorbed in the ileum.

48
Q

Do peristaltic waves propogate through the ileocolic sphincter to the large intestine?

A

No. The colon begins a new peristaltic wave.

49
Q

What is the gastrocolic reflex?

A

Distension of the stomach –> increased motility in the colon

50
Q

What is peptide YY?

A

Secreted by colonic epithelial cells into the bloodstream in response to lipids present in the colonic lumen.

It decreases gastric emptying and overall intestinal motility to allow fat digestion & absorption. Also suppresses appetite.

51
Q

What are the primary functions of the colon?

A

Sodium and water reabsorption.

52
Q

Why is the rectum normally empty?

A

Humans can consciously move fecal matter back into the sigmoid colon. This accounts for why diverticulitis is much more common in the sigmoid colon.

53
Q

What nerve innervates the internal and external anal sphincters?

A

The pudendal nerve. The internal anal sphincter is reflexively opened while the external anal sphincter is under voluntary control

54
Q

What is a hepatic triad?

A

A branch of the hepatic artery, the portal vein, and the bile duct.

55
Q

Liver:
What are zone 1 cells?
Zone 3 cells?

A

Zone 1 cells are closest to the hepatic triad. They are important in detoxification of toxic substances and are most sensitive to these substances.
Zone 3 cells are important in the production of bile.
Zone 2 cells are in the middle. These, and zone 3 cells can function as Zone 1 cells during liver pathology.

56
Q

How does the liver detoxify exogenous (drugs) and endogenous toxins? (3 phases)

A

Phase 1: Cytochrome P-450 –> oxidation and hydroxylation
Phase 2: Conjugation with water soluble molecules
Phase 3: Excretion with bile –> feces
(or in urine if small enough)

57
Q

What is a hepatic sinusoid?

What cells phagocytize bacteria in this space?

A

A hepatic sinusoid is the space that connects hepatica arterial blood & portal blood to the central vein. Kupffer cells are macrophages that are found there.

58
Q

What are the largest two components of bile?

A

Bile acids = 65%

Phosphotidylcholine = 20%

59
Q

What effect does ileal resection have on bile salt synthesis & secretion?

A

Increased synthesis but decreased secretion, since reabsorption is greatly inhibited.

60
Q

Saturation of what substances in the bile can lead to gallstones?
What other physiological factors can lead to gallstones?

A

Cholesterol –> white stones
Bile pigments –> pigmented stones

Gallbladder hypomotility or long duration between meals can predispose one to gallstones

61
Q

How is bilirubin formed and excreted?

A

Phagocytosis of RBC’s –> liberated heme iron –> biliverdin –> bilirubin –> travels on albumin in bloodstream –> taken up by BL membrane of hepatocytes (OATP) –> conjugation –> secretion into bile canaliculi (multidrug-related protein 2/MRP2).

Conjugated bilirubin cannot be reabsorbed by intestine.

62
Q

How is bile concentrated in the gallbladder?

A

Net flow is Na+ reabsorption (Cl- follows). This causes hydrostatic pressure in the interstitial space and bulk flow into the capillaries. Bile acids are too large to move past the epithelial cells of the gallbladder.

63
Q

What is a stone in the gallbladder called?
In the bile ducts?
Inflammation of the gallbladder?
Inflammation of the common bile duct?

A

Cholelithiasis
Choledocholithiasis
Cholecystitis
Cholangitis

64
Q

Why is bilirubin accumulation dangerous?

A

It can cross the BBB and is toxic to the brain.

65
Q

What enzyme conjugates bilirubin to make it more water soluble and allows its excretion?

A

UDP glucoronyl transferase (hepatocytes)

This enzyme begins being synthesized after birth. This is why babies often are jaundiced

66
Q

What are the sources of NH3 in a human and why is it dangerous?

A

Protein degradation and colonic bacteria produce NH3.

It can freely cross membranes, including the BBB and is toxic to the brain.

67
Q

How is NH3 handled by the body?

A

The liver can convert NH3 to urea, to allow excretion in the urine.

68
Q

What are the main causes of liver cirrhosis?

A

Drugs (alcohol), poisons, and hepatitis.

69
Q

What are Caput Medusae?

A

Engorged abdominal veins caused by portal hypertension.

70
Q

What is considered hyperbilirubinemia?

A

> 2 mg/dL

81
Q

What symporter does carbohydrate transport rely on in the intestine?
Amino acid symport?

A 
Carbs = Na+ dependent
AA's = H+ dependent

FHB (8 decks)

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