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Flashcards in GI Deck (74)
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0
Q

How much water is absorbed in the GI tract every day? Where does most of the absorption occur?

A
9-10 liters!
small intestine (primarily jejunum and ileum) does 8.5 L, colon does .5 L
1
Q

Exocrine vs endocrine function (general terms)

A

Exocrine: what is dumped into the duct
Endocrine: what is dumped into the blood

2
Q

How does the pH compare between the stomach and jejunum

A

Stomach’s pH is 1 (comparable to battery acid) and jejunum is 7
Note: bicarb buffer works to change the pH

3
Q

What three arteries supply the GI and what specific organs do they go to? Where does the venous flow back through?

A

Celiac: liver, stomach, spleen, pancreas
Sup mesenteric: pancreas, small intestine, part of large intestine
Inf mesenteric: large intestine
Venous flow from all these organs back to liver, to hepatic vein, to vena cava

4
Q

When should the pyloric sphincter open and close?

A

Closed for mixing of food content in stomach, food becomes chyme, opens after mixing is complete

5
Q

When we eat STARCHES, how and where are they broken down?

A

In the mouth, salivary amylase breaks starches down to oligosaccharides. Pancreatic amylase breaks these to disaccharides (sucrose, maltose, lactose). In the small intestines, these are broken down by brush-border enzymes (sucrase, maltase, lactase) into monosaccharides (galactose, glucose, and fructose) which are absorbed by the capillaries in the villa and transported to the liver by portal vein

6
Q

When we eat protein, how and where is it broken down?

A

In the stomach, pepsin (in presence of HCl) breaks protein down to proteoses and peptones. These are broken down in the small intestine by pancreatic enzymes (trypsin) to polypeptides. Then brush-border enzymes breaks these down to amino acids which are absorbed by capillaries in the villi and transported to the liver by hepatic portal vein.

7
Q

How and where are unemulsified fats broken down in the GI system?

A

The small intestine uses emulsifying agents like bile acids, fatty acids, and cholesterol, then pancreatic lipases to make monoglycerides and fatty acids which are absorbed by LACTEALS and transported to the liver, OR they make glycerol and fatty acids which are absorbed by CAPILLARIES in the villi and transported to the liver

8
Q

What is MMC (migrating myoelectric complex)?

A

DOES NOT require stimulation from Vagus nerve, it is the sweeping movement of a bolus of food in fasting or interdigestive state, takes 1.5-2 hours, phase 3 uses the hormone motilin

9
Q

What is receptive relaxation?

A

When food comes in, mechanoreceptors send signals to move the food down by relaxing downstream muscles
Note: vagus nerve also helps with this

10
Q

What causes depolarization vs. hyperpolarization of the GI

A

Depolarization (contributes to GI movement): stretch, ACh, parasympathetic, gastrin, serotonin, substance P, tachykinin
Hyperpolarization (slow waves not causing GI relaxation): NE, sympathetics, VIP (vasoactive intestinal peptide), NO

11
Q

What is peristalsis vs. segmentation?

A

Peristalsis: contraction behind a bolus causing propulsion of food down the GI tract
Segmentation: mixing of chyme in a segment, movement in each direction
We need both!

12
Q

How do we get movement of bile into the duodenum?

A

Vagal stimulation relaxes the sphincter of Oddi, this plus the hormone CCK will stimulate gallbladder contraction, releasing bile into the duodenum

13
Q

What are micelles and what do they have to do with motility in the small intestine?

A

Bilayer (hydrophobic tail, hydrophillic head), duodenum creates it to help with absorption into the lacteal

14
Q

Where is movement slower vs faster, in the stomach or intestine?

A

SLOWER in the stomach ~3 bpm; FASTER in small/large intestine ~12-16 bpm

15
Q

What forms what haustra, where are they found, and what is its significance?

A

Haustra are the sacs formed by taneia coli that have contracted in the large intestine and it increases surface area for absorption

16
Q

Which glands produce serous, mucous, and a mixture? (Submandibular, sublingual, parotid)

A

Parotid secretes serous (with amylase)
Submandibular glands secrete mix of serous and mucous
Sublingual glands secrete mucous only

17
Q

Which hormones play a role in control of salvation?

A

ADH increases water absorption which concentrates saliva, aldosterone increases K secretion into and Na reabsorption out of saliva, PTH can cause calcium absorption
These hormones decrease salivary flow

18
Q

Which cells are responsible for secretion of saliva?

A

Acinar cells primarily secrete saliva (myoepithelial cells and striated ducts aid is salivary secretion)

19
Q

How does saliva have an antimicrobial action?

A

It can physically remove microbes and contains IgA

20
Q

What is more hypotonic, plasma or saliva?

A

Saliva

Note: Rate of flow also determines tonicity.. as rate increases, osm increases bc not as much reabsorption can happen

20
Q

What increases and decreases salivary flow?

A

Increases: parasympathetic, Ach, cephalic phase of CNS, nausea, esophageal distention, tasty foods
Decreases: sympathetic, NE, hormones (ADH, aldosterone), sleep, dehydration, drugs, aging

21
Q

What is lactose broken down into?

A

Galactose and glucose

22
Q

What is sucrose broken down into?

A

Fructose and glucose

23
Q

What is maltose broken down into?

A

2 glucoses

24
Q

How is fructose transported across brush-border membrane?

A

GLUT5

25
Q

How is glucose transported across brush-border membrane?

A

SGLT1

26
Q

How does galactose cross the brush-border membrane?

A

SGLT1

27
Q

How do all three monosaccharides cross basolateral membrane to the capillary?

A

GLUT2

28
Q

What do mucous neck cells do?

A

Protection (from acidity) by secreting mucous

Replace cells in lumen after desquamation

29
Q

What do parietal cells do?

A

Secrete HCl, intrinsic factor, and R protein

Digest food, kill bacteria, convert pepsinogen to pepsin (HCl), vitamin B12 absorption (IF and R protein)

30
Q

What do chief cells secrete?

A

Pepsinogens and gastric lipase for fat and protein absorption

32
Q

What stimulates chief cells to secrete pepsinogen?

A

Vagus, gastrin, histamine, secretin, and CCK

33
Q

What do endocrine cells (in the gastric cells) secrete and what do they do?

A

somatostatin (by D cells specifically, inhibits gastrin and HCl release)
gastrin (by G cells specifically, stimulates parietal cells)
histamine (by ECL cells specifically, stimulates HCl secretion)

34
Q

What does HCl do?

A

Digests food
Kills bacteria
Converts pepsinogen to pepsin

35
Q

What does Intrinsic Factor do?

A

Binds to B12 primarily in duodenum for absorption

*the only INDISPENSABLE gastric secretion

36
Q

What does Gastrin do?

A

Stimulates gastric motility and HCl secretion
Decreases gastric emptying (to increase mixing time)
G cells release gastrin

37
Q

What is the difference between mucous, mucosa, and mucin?

A

Mucous is the bicarbonate rich fluid secreted, serves as a buffer. Mucosa are the epithelial cells that line the stomach. Mucin is a glycoprotein that causes the viscosity in the mucous (it traps the bicarb).

38
Q

What effect does somatostatin and histamine have on Hcl?

A

Somatostatin inhibits Hcl secretion and histamine stimulates Hcl secretion

39
Q

What is ghrelin?

A

A hormone that increases when fasting, acts on the hypothalamus to stimulate hunger, it opposes the satiety leptin and peptide YY

41
Q

What stimulates HCl secretion? What inhibits it?

A

Stim: parasympathetics, ACh, gastrin, histamine
Inhibits: Secretin (acts on G cells), somatostatin (acts on parietal and G ells), GIP (acts on parietal cells), peptide YY (indirect), and prostaglandins (acts on ECL and G cells)

42
Q

How can H pylori form ulcers?

A

H pylori can release urease which breaks off ammonia and can create a buffer. It cleaves mucin and breaks through the barrier by making it less acidic, this allows for more bacteria to colonize and injure the surface mucous cells.

43
Q

What happens in the first phase of gastric secretion (cephalic phase)?

A

Chemoreceptors and mechanoreceptors on the tongue, buccal canal and nasal mucosa elicit vagal effects of gastrin, acid, and enzymes

44
Q

What happens in the second phase of gastric secretion (gastric phase)?

A

Food is in the stomach, vagal effects (gastrin stimulation, acid, enzymes, pH changes), highly acidic chyme enters the duodenum, feedback to HCl secretion to gastric emptying

45
Q

What happens in the third phase of gastric secretion (intestinal phase)?

A

Mucosal secretions and secretions from pancreas, liver, and gallbladder travel down the hepatic duct and through sphincter of Oddi to enter duodenum

46
Q

What are crypt cells of the small intestine?

A

have CFTR, which secrete Cl into the lumen of the gut, Na and water follow. Simulated by secretin

47
Q

What are paneth cells of the small intestine?

A

host defense, secrete zinc and lysozymes that attack bacteria

48
Q

What do globlet cells of the small intestine secrete?

A

Mucus

49
Q

What do endocrine cells of the small intestine secrete?

A

Gastrin, CCK, secretin, GIP, motilin, serotonin

50
Q

What are the Brunner’s glands of the small intestine?

A

located in the first part of duodenum before sphincter of Oddi, secrete thick mucus and proteases, stimulated by secretin and vagus, inhibited by sympathetic nervous system

51
Q

What increases and decreases intestinal secretions?

A

Increased by contact with chyme and distention, local enteric reflexes, parasympathetic response
Decreased by sympathetic nervous system

52
Q

What does gastrin stimulate?

A

Acid and mixing (lowers motility)

53
Q

What does secretin stimulate?

A

Pancreatic buffer secretion (bicarb), decreases gastrin which decreases acidity

54
Q

What does CCK (cholecystokinin) stimulate?

A

Increases pancreatic enzyme secretion, contracts gallbladder, relaxes sphincter of Oddi (decreases gastric emptying, increases motility)

55
Q

What does GIP (Gastric Inhibitory Peptide) inhibit?

A

Inhibits acid secretion

Increases pancreatic insulin secretion (to decrease gastric emptying)

56
Q

What does Motilin stimulate?

A

Phase 3 contractions of MMC

57
Q

What does Peptide YY decrease?

A

HCl

58
Q

How do pancreatic acinar (outside) and inner centroacinar cells differ?

A

Outside acinar cells produce enyzmes

Inner centroacinar cells secrete electrolye solutions rich in bicarb

59
Q

What are pancreatic cells’ endocrine and exocrine secretions?

A

Endocrine: secrete insulin, glucagon, and somatostatin which can affect gastric secretion and motility
Exocrine: enzyme and electrolyte secretions

60
Q

What stimulates pancreatic enzymes to be secreted?

A

CCK and insulin (for electrolyte secretions, secretin and vagovagal reflexes stimulate secretion)

61
Q

What are (the pancreatic enzymes) trypsinogen, chymotrypsinogen, and pro-carboxypeptidase activated by and what do they form?

A

trypsinogen - activated by enterokinase, forms trypsin
chymotrypsinogen - activated by trypsin to form chymotrypsin
pro-carboxypeptidase - activated by trypsin to carboxypeptidase (Trypsin inhibitor)

62
Q

What do pancreatic lipase and pancreatic amylase aid in?

A

Lipase/pre-colipase - lipid digestion

Amylase– starch digestion

63
Q

What helps stop the pancreatic secretions?

A

SS, glucagon, pancreatic polypeptide, and peptide YY

64
Q

What does the colon secrete?

A

Mucus (from goblet cells)
H, HCO3 for acid/base balance
K because colon is sensitive to aldosterone

65
Q

Why do we need brush-boarder enzymes?

A

For starch breakdown, salivary alpha-amylase starts the breakdown in the mouth, pancreatic amylase continues the breakdown in the small intestines, and we end up with disaccharides and small glucose polymers. We need brush-boarder enzymes to break these down so we can absorb the starches.

66
Q

How are proteins digested and absorbed?

A

In the stomach, HCl digests proteins and stimulates secretion of pepsinogens, these cleave to pepsin by the acidity. Pepsins aid in protein digestion.
In the pancreas, proteases are secreted as zymogens into the duodenum. Trypsin inhibitor keeps from pancreatic enzymes chewing up too much. The pancreas also secretes nucleases which into purine and pyrimidine.

67
Q

How are lipids digested and absorbed?

A

In the mouth, lingual lipase cleaves TAGs to FAs and DGs (diglycerides). In the stomach, gastric lipase cleaves TAGs to FAs and DGs. In the small intestine, CCK helps release bile and pancreatic enzymes are released (pancreatic lipase cleaves TAGs to FAs and monoglycerides with help of co-lipase molecule). Cholesterol esterase and phospholipase A2 help break down lipids too.
Micelles transport lipids to enterocytes, finally broken down in the SER.

68
Q

How does Phospholipase A2 work?

A

Activated by trypsin and cleaves phospholipids such as lecithin into lysolecithin

69
Q

When co-lipase is activated by trypsin, how does it help to form micelles?

A

It binds to bile salts so that lipase molecules can form a complex, this is important in the formation of micelles

70
Q

Where are bile salts secreted, where are they absorbed?

A

Secreted in the liver
Absorbed in the terminal ileum
(90% are reabsorbed)

71
Q

What does bile do in the duodenum and jejunum?

A

In the duodenum, bile emulsifies and digests fats

In the jejunum, helps with micelle formation

72
Q

Where does fecal production begin?

A

Late transverse colon

73
Q

What are feces composed of? What are the main electrolytes in the feces

A

75% water, 25% solids
solids: cellulose, bacteria, electrolytes like calcium and phosphates, fat, mucus, digestive enzymes
main electrolytes: K and bicarb

74
Q

How is gas formed?

A

Bacterial metabolism of carbohydrates; stomach (O2, N2), duodenum (CO2), ileum and colon (CO2, H2, CH3, H2S, NH3); polyamines (putrescine, spermine); flatulence
Poor carb digestion/absorption leads to flatulence