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Physiology > Digestive System (Day 2) > Flashcards

Digestive System (Day 2) Flashcards

1
Q

Ability of bile salts to emulsify fats

A

conversion of hydrophobic CHOLESTEROL –> amphipathic BILE ACIDS
–> in liver

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2
Q

Digestion and Absorption of Fats

A

Digestion begins in duodenum: bile stabilizes fat emulsion and lipase (from pancreas) breaks it down into fatty acids and glycerol

Phospholipase A (from pancreas) digests phospholipids into fatty acids and lysolecithin.

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3
Q

Fat Emulsification/Digestion

A

Digestion produces fats (free FA) incorporated into micelles, producing mixed micelles

These diffuse to absorptive surface and FA pass into cells

Steps:

  1. Emulsification of fat droplets by bile salts
  2. Hydrolysis of triglycerides in emulsified fat droplets into FA and monoglycerides
  3. Dissolving of FA and monoglycerides into micelles to procude “mixed micelles”
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4
Q

Absorption/Transportation of fats

A

Fatty acids, monoglycerides, and lysolecithin move into bile micelles and are transported to brush border.

The fat molecules then leave the micelles and diffuse into the epithelial cells of the villi.

Inside the epithelial cells, they are regenerated into triglycerides, cholesterol, and phospholipids and combined with proteins to form chylomicrons.

Chylomicrons are secreted by exocytosis into the central lacteal of the villus

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5
Q

Fluid/Electrolyte Secretion and Absorption

A

Oral fluid intake = 2000 ml/day; digestive secretions = 7000 ml/day; all but 100 ml is reabsorbed, mainly in SI, but also in LI

Mostly water & ions [Na+, K+, Cl-, HCO3-, H+]

Secreted ions are reabsorbed, water follows osmotic gradients created by solute transfer

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6
Q

Control of digestive function occurs at each level of the GI Tract

A
  1. Cephalic Phase: stimulation of gastric activiity
  2. Gastric Phase: stimulatino of gastric activity
  3. Intestinal Phase: inhibition of gastric activity, stimulation of digestion in intestine
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7
Q

Cephalic Phase: Mechanism

A

short duration, prepares stomach for arrival of food

Mechanism: neural - reflex signals from medulla oblongata via vagal preganglionic fibers to synapses in submucosal plexus

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8
Q

Cephalic Phase: Actions

A
  1. direct neural stimulation of acid, mucus, enzyme secretion
  2. indirect via stimulation of gastrin release from G cells, gastrin stimulates motility and acid secretion
  3. indirect via stimulaiton of histamine release from ECL cells
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9
Q

What are conditioned reflexes?

A 
taste
smell
chewing
swallowing
hypoglycermia
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10
Q

Gastric Phase: Mechanisms

A

duration: 3-4 hours, enhances secretion, mix, acidify, and increase SA of chyme, begin hydrolysis of PRO

Mechansims:

  1. neural reflexes triggered by strech, rising pH
  2. hormonal (gastrin) release triggered by vagal signals, peptides, AAs
  3. local release of histamine (stimulates acid secretion) triggered by stretch
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11
Q

Gastric Phase: Actions

A

increased production and secretion of acid and pepsinogen, increased motility and mixing waves

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12
Q

Gastric Emptying

A

Chyme metered out into duodenum as stomach empties

Emptying is regulated by intestinal signals to prevent

Liquids empty fastest, solids slowest, nutrient-specific control (senseing of physiochemical properties)
–> ex. H, fat, pi

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13
Q

Intestinal Phase: Mechanisms

A

duration: hours, acts to control gastric emptying rate,
to limit gastric acid secretion, and to optimize conditions for enzymatic
digestion in intestinal lumen

Mechanisms:
1) NEURAL—short reflex (enterogastric reflex) triggered by distension
of duodenum
2) HORMONAL—stimulation of secretin, CCK, GIP, by presence of H+, CHO, AAs, lipids

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14
Q

Intestinal Phase: Actions

A

Feedback inhibition of gastric acid/pepsinogen secretion, gastric motility, promotion of intestinal/pancreatic/biliary secretion, intestinal motility

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15
Q

Gastrointestinal Hormones: Gastrin

A

Secreted by the stomach

stimulates partietal cells to secrete HCl, stimulates chief cells to secrete pepsinogen, maintains structure of gastric mucosa

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16
Q

GI Hormones: Secretin

A

secreted by SI

Effects:
volume & HCO3 secretion from pancreas: raises pH of incoming chyme –> allows pancreatic enzymes to be active
—> promotes favorable environment for enzymatic digestion

17
Q

GI Hormones: CCK

A

secreted by CI

Effect:

1) pancreatic enzyme secretion
2) bile secretion via stimulation of gallbladder contraction—responsible for enzymatic digestive activity, fat emulsion stability, and absorption of digestion products of fat

18
Q

Regulation of pancreatic juice and bile secretion

A

When chyme enters duodenum, two hormones are produced

  1. Secretion: by drop in pH
  2. CCK: by response to the presence of partially digested PRO and FAT in chyme
  • pancreatic enzyme production of trypsin, lipase, and amylase is stimulated by ACh from vagus nerve and CCK
  • Pancreatic bicarbonate production is stimulated by secretin
  • Liver produces bile continuously, but arrival of food into duodenum stimulates increased bile production
19
Q

Regulation of pancreatic juice and bile secretion happens when…

A
  1. bile acids are returned to the liver after intestinal absorption via enterohepatic circulation
    - -> so we don’t continuously have to make bile salts
  2. Secretin/CCK stimulate increased bicarbonate secretion into bile
  3. CCK (in response to presence of fat in chyme) stimulates gallbladder contraction
20
Q

Enterohepatic Circulation

A

recycling of bile salts regulates hepatic synthesis of bile acids from cholesterol, and therefore, controls plasma cholesterol levels

  • 5% of bile salts lost in feces, rest are reabsorbed
  • can “exploit” this process to reduce plasma cholesterol levels
21
Q

Pancreatic and Biliary Secretion

A

control by both vagal stimulation and intestinal hormones

22
Q

Pancreatic Exocrine Secretion

A

acid in duodenum –> secretin –> stim secretion of HCO3 by pancreas

Fat, AAs in duodenum –> CCK –> stim secretion of enzymes by pancreas

23
Q

Biliary Secretion

A

Fat in duodenum –> CCK –> stim of bile secretion by gallbladder and relaxation of Sphincter of Odi

24
Q

Pancreatic Exocrine Secretion: enzymes from acinar cells

A 
trypsinogen
chymotrypsinogen
lipase
amylase
HCO3 from ductal cells

Proteases secreted as inactive, zymogen from: activated only in lumen of gut

25
Q

zymogen

A

(or proenzyme)
an inactive enzyme precurser
requires a biochemical change for it to become active
–> activated only when needed to be

26
Q

Pancreatic Enzymes

A

enteropeptidase is found on brush border

Most are inactive (zygomens) until they reach the SI

  • Enteropeptidase activates typsinogen –> trypsin (to digest PRO)
  • Trypsin activates other enzymes
27
Q

Vitamins: Fat-Soluble

A

A, D, E, K

absorbed by fat

28
Q

Vitamins: water soluble

A

C, and most B vits

carrier mediated transport

29
Q

Vitamin B12

A

require gastric-secreted IF, uptake by enterocytes in terminal ileum

IF produced/secreted by into the stomach and parietal cells - the SAME cells which secrete gastic acid
–> thus anything which affects acid secretion is going to similarly affect IF secretion –> absorption of Vit B12

30
Q

What happens w/decreased Vit B12?

A

anemia

31
Q

Where does most physiological significant digestion/absorption occur?

A

SI w/exception of fat, most nutrients enter the blood and go to the liver via hepatic portal system

32
Q

Fat Absorption/Transport

A

via chylomicroms (CM) in lymph, CM enter ciruulation at thoracic duct (bypass liver) –> dlievers fat to muscle, adipose –> reduced size “remnant” particle then taken up by the liver

33
Q

Why does fat tranport via CM occur via lymph instead of directly via blood?

A

CM (100-500 nm) are too large to pass through relatively tight vascular endothelium

34
Q

Colonic Motility

A
  • segemnting contractions (esp in ascending colon)
  • mass movement tirggered by gastro-colic reflex
  • entry into and distension of rectum triggers defecation reflex
35
Q

Defensins

A

secreted by paneth cells

–> mucosal barrier

36
Q

Immune-inflammatory response

A

normally self-limiting, but dysregulation can cause disease (ex. IBD)

Physiology (29 decks)

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