EXAM 3 Flashcards
Chemical digestion
Fats
LIPIDS:
Triglycerides are absoped as FATTY ACIDS & MONOGLYCERIDES
Chemical Digestion
Protiens
- AMINO ACIDS:
absorped as small peptides and amino acids - AA uptake in sodium coupled transporters
- peptides absorped faster than AA and require PepT1(ogliopeptides)
- Pepsin activated at low pH levels 1.8-3.0..irreversible inactivated at 7.2
- Bicarb layer protects mucous lining
Chemical Digestion
Carbohydrates
STARCHES absorped as MONOSACCHARIDES
A-amalyse enzyme starts in mouth..digest starches
Enzyme Release
Salivary Glands
Amylase break down starches
Lipase break down triglycerides
Carbs (Starches) are the only macronutrient that digest in the mouth
Enzyme Release
Stomach
Pepsin breaks down protiens
Lipase breaks down triglycerides
Enzyme Release
Pancreas
ACTIVE ENZYMES
a-amylase & lipase
starches and triglycerides
Enzyme Release
Intestines
Enterokinase (activate trypsin)
Diasaccharides (complex sugars)
Dipeptides (peptides)
Trypsin
A protease that ACTIVATES SECRETED XYMOGENS (Lysine & Argenine)
Breaks down peptides to ogliopeptides
Chymotrypsin cleaves to trypsin
Released in pancreas
Goblet Cells
Secrete mucus, deuodnum to ileum
Stem Cells
Repairs cell complex when old cells die
Endocrines
Hormones released in the blood
Gastrin is an example
Paracrines
Act on neighboring cells in the same tissue
Somatostatin and histamine are examples
Neurocrines
Neurotransmitters
That thanksgiving smell makes you hungry!
Hormone
Secretin
- Released from S-CELLS in DUODENUM
- INHIBITS GASTRIC ACID RELEASE
- STIMULATE PEPSIN & HCO3- SECRETION
The duodenum pH IS <4.5
Hormone
Gastrin
- Secrete gastric acid & growth of mucosa, duodenum, and colon
- Antrum and Duodenum
- Little (17AA): secrete from G Cells
- Big (34AA): secrete from duodenal
Gastrinoma
- Causes hypergastrinemia
- Increase parietal cell mass & acid secretion (low pH)
- peptic ulcer
- Decrease bile & lipase (causing diarrhea, steatorrhea, hypokalemia)
Hypokalemia
Less K+ in the blood due to loss of K+ from diarrhea, vomiting, etc.
Zollinger Ellison Syndrome
Gastrin levels increase after injecting secretin due to failure of inhibiting gastrin release
Hormone
CCK
- In the DUODENUM & JEJUNUM
- Release bile into duodenal
- Empty gallbladder
- Inhibits gastric emptying
- Fatty acids, peptieds, and AA stimulate release
Your stomach wont deliver any more food until the batch is digested, this is what it means for gastric emptying to be paused
Hormone
GLIP
Secretin family
- STIMULATES insulin release
- INHIBITS gastric acid secretion
- Oral glucose, only released when injested…meaning when there is a presence of food in the intestines that needs to be digested
Hormone
Motilin
Stimulates upper GI motility during fasting periods
Released from M-CELLS
Hormones
Somatostatin
In D cells of the corpus
1.Inhibits PARIETAL CELL acid secretion (decreasing acid release)
2.STIMULATED by ACID
3.INHIBITED by ACh D-Cells
Paracrine
Inhibits histamine and gastrin release
Hormones
Histamine
Paracrine
Released from ECL cells w/ gastrin & ACh
1. Stimulates acid secretion
2. H2 receptors block acid secretion
3. Hypergastrinemia Acid supression so gastrin remains high
CIMETIDINE & RATITIDINE
VIP
- Relaxes the smooth muscle in the gut
- Stimulate fluid secretion and electrolytes
GRP/ Bombesin
Increase gastric release
Enkephalins
Increase smooth muscle tone
* Stifness decreases GI motility
Myenteric A. Plexux
Located in the proximal esophagus to anus
Submucosal Meissner Plexus
Large Intestines Only
* Sensory, local secretion & absorption, and contraction
Nerve plexus
Ascending cholinergic
Ms contraction promels intraluminal distally towards anus
* ACh for contraction
* Peptide YY is located in colon, senses fat and protiesn, slows intestinal emptying (inhibit motility for more nutrient absorption)
IPAN
Inintiate peristalsis and dynamic contraction
Mast Cells
- Monitor sensory input from lumen
- Respond to foreign antigers chemically (histamine)
- Increase gut motility to rid foreign antigers
- TnFa can be released immediately
Peristalsis
- __
- I. contraction ahead of bolus
- continued contraction before bolus
- force bolus foward
Dysphagia
- Anestesia: aspiration of stomach contents
- Stroke: damage cranial nerves and leads to aspiration
- MS Diseases: Polio, Myestenia Gravis, Botulism
Swallowing disorders
Gastroenphageal Reflux Disease
In the lower esophageal spincter
1. Backwash of acid, pepsin, & bile into esophagus
2. Barret esophagus: tissue replaced by goblet cells, increase cancer risk
Gastric Motility
- Caudad Area: mix food with gastric juice
- nitric oxide relaxes orad area (upper stomach)
What happens during increased gastric emptying?
- INCREASED orad tone & DECREASED pylorus tone
- force contraction
- Empty intestines
Acinar cells
Secrete Cl- and enzymes
Isotonic
1. Na/K pump moves Na+ basolaterally inward
2. Na/K/Cl cotransporter bring cl- into cell
3. Rise in K+
4. Cl- secretes into lumen
5. Na+ driven into lumen
CCK & ACh increase acinar secretion of Na& Cl
Duct cells
Secrete bicarb and K+
High mitochondria
pH < 7.4
Secretin
Ouabaine BLOCKS HCO3-
Atrophine BLOCKS ACh and Ca2+
Pancreatitis
Decrease HCO3-
Leads to dehydration and oily stool (steatorrhea)
Alcohol & Cystic Fibrosis
Failure of the pancreas
Stomach
- Functions for food storage and protien digestion
- Cardia – Located near the gastroesophageal junction, devoid of acid-secreting cells.
Body (Corpus) – The largest portion, where acid-secreting cells are located.
Antrum – The distal region that leads to the pylorus, involved in secreting regulatory hormones. - Gastric (oxyntic) glands: Secrete digestive substances like acid and pepsinogen.
Pyloric glands: Primarily secrete regulatory hormones, including gastrin and somatostatin. - Superficial epithelial cells and mucous neck cells secrete bicarbonate and mucus, forming an alkaline barrier.
Parietal cells secrete acid and intrinsic factor, crucial for vitamin B12 absorption.
Chief cells secrete pepsinogen, which is activated by the acidic environment to break down proteins.
Endocrine cells release regulatory hormones (gastrin, somatostatin) that help manage digestion.
Cardia, Fundus, Antrum, Cells
What is Hirschsprung disease and how is it treated?
- mutations in multiple genes (e.g., endothelin-B receptor) leading to the failure of neural crest cells to migrate caudally
- Constipation Megacolon Narrowed colon segment (usually in the rectum)
- Absence of ganglion cells in the submucosal (Meissner’s) and myenteric (Auerbach’s) plexuses.
- Surgical removal of the aganglionic segment of the colon to restore normal function.
What systems are involved in neuroendocrine control of pancreatic secretion?
Parasympathetic nervous system: Main regulator during fasting (phase 3)
Cholecystokinin (CCK): Stimulates enzyme secretion during the fed state.
Adrenergic pathways: Can suppress fasting secretion through α-adrenergic tone.
What is the relationship between migrating motor complexes (MMCs) and pancreatic secretion?
Phase I: Quiescent motility, minimal pancreatic secretion.
Phase II: Increased motility, increased secretion.
Phase III: Maximal motility and peak secretion.
Phase IV: Secretion declines after phase III
Telenzepine (M1 antagonist)
reduce pancreatic enzyme secretion by more than 85% during phases II and III.
What is nonpropulsive segmentation in the colon?
Nonpropulsive segmentation is driven by slow-wave activity, resulting in circular muscle contractions that churn the colonic contents.
This movement pushes material toward the cecum (orad direction).
Haustra (the typical segmented appearance) are formed during this process, giving the colon its segmented look.
The primary function is mixing, and it helps with fluid and electrolyte absorption.
Material stays in the proximal large intestine for longer periods during this phase.
What is mass peristalsis, and when does it occur?
Mass peristalsis is a strong, propulsive contraction that moves colonic contents distally (20 cm or more).
It occurs 1-3 times a day, often triggered by eating.
During mass peristalsis, haustra disappear as the contents are propelled forward, and they reappear afterward.
Mass peristalsis is the primary form of propulsive motility in the colon.
What motor activity occurs in the distal colon?
n the distal colon, the primary motor activity is nonpropulsive segmentation through annular or segmental contractions.
This is where the final desiccation (water absorption) of colonic contents occurs.
The contents are stored in the distal colon until an occasional mass peristalsis moves them into the rectum.
How does the rectum fill, and what role does mass peristalsis play?
The rectum remains nearly empty due to nonpropulsive segmentation until mass peristalsis occurs in the distal colon.
Mass peristalsis propels contents into the rectum, triggering rectal filling.
This process facilitates the storage and eventual evacuation of fecal material.
Serous secretion vs. Mucus Secretion
Serous contains salivary enzymes in a watery base
Mucus provided lubrication to help food move through the esophagus
Average daily salivatory secretion
1-1.5L of saliva daily
Major salivary glands
Parotid & Submandibular (majority of production)
Sublingual (mucins/ lubrication)
Buccal (mucous secretions)
Kalikrien Function
Secreted by all but the buccal glands. Cleaves kininogen to PRODUCE BRADYKININ that increases salivary secretion rate
Carb digestion process
A-Amylase in saliva (oligosaccharides)
40% digestion occurs in stomach
Pancreatic amylase continues digestion in small intestine
Monosaccharides occur at brush border
Brush border disaccharides
Lactase: breaks down to glucose and galactose
Maltase: breaks down maltose into glucose
Sucrase-isomaltose: breaks down sucrose into glucose and fructose
Monosaccharide Absorption
Glucose & Galactose: Absorbed by SGTL1 with Na+
Fructose: GLUT5 facilitated diffusion
Exit via GLUT2 transporter
L-Glucose
Cannot be absorbed by the body
Phlorizin
Inhibits SGTL1, reduce blood glucose
Fructose
Less insulin and leptin results in less appetite suppression
High fructose increases fat production in liver
CCK
Secreted from duodenum in response to fats
PYY
Secreted in the ileum and proximal colon, slowing gastric emptying so more nutrients are absorbed
Fat Digestion process
- Emulsification: promote enzyme breakdown
- Triglyceride breakdown: duodenum, yields momoacylglycerols and fatty acid
- Reassembly: Triacylglycerols reassembled in enterocytes
Lipase Enzymes and Breakdown
- Gastric lipase: breaks down 15% fats in stomach
- Lingual lipase
- Pancreatic lipase: Yield sn2-monoacylglycerols
- Cholesterolester hydrolase and others work in duodenum and jejunum to complete lipid hydrolysis
Gastric, lingual, pancreatic lipase cleave at sn3 positions
Fatty Acid Absorption
Mucus layer, Unstirred water layer, apical membrane enterocytes
Occurs by direct diffusion, membrane incorporation, or fatty acid translocase (FAT/CD36)
Exetimbe
Lipid medicine
Inhibits cholesterol absorption by blocking brush border protiens
Lipitor (atarvastatin)
Inhibits cholesterol synthesis by blocking HMG-CoA reductase
Chylomicrons
Formed from lipolytic products, enter lymphatic circulation, and then bloodstream
largest lipoprotiens
Taken up by liver hepatocytes for breakdown
Long chain fatty acids turn into cylomicrons for transport
Bile acid reabsorption
Bile acids: secreted into duodenum
Enterohepatic circulation: reabsorbed in distal small intestine and recycled back to liver
Conjugated bile acids: absorbed in the terminal ileum
Unconjugated bile acids: passively absrobed throughout intestine
Bile salts
Help in digestion and absorption of fats in the small intestine, critical for continued fat digestion
Intestine structure
Crypts: ion secretion
Surface epithelium: electrolyte absorption
Villi
Paneth Cells
Sense bacteria in the small intestine
trigger antimicrobal responses to prevent bacteria from penetrating mucosal surface
lysozymes, a-defensisn, c-type lectins, TNF-a
Fluid absorption in intestines
Small intestine: 75% of 8-9L daily fluids
Large intestine: 2L fluid daily, increases to 4-5L if small intestine decreases absorption
Electrolyte movement in the intestines
Potassium is absorped in small intestine and secreted in colon
Intestines secrete bicarb
Intestines absorb water, Na+, Cl-
Sodium-proton exchanger in small intestine
NHE3: apical, Na+ absorption in duodenum and jejunum
NHE1: basolateral, regulate intracellular pH
Alkaline lumen: stimulate Na+ uptake in proximal small intestine in the presence of bicarb
Na+ absorption in intestines
Na+ absorped through Na/H exchanger
Cl- absorped through HCO3-/Cl- exchanger
Na+ absorption in the distal colon va epithelian Na+ channels
Cl- absorped paracellularly and transcellularly
Chloride Bicarb Exchanger
Parallel or independent
ileum and proximal colon during interdigestive period
K+ Secretion in colon
Passive: paracellular by lumen negative voltage
Active: aldosterone and cAMP (increase the BK activity in cells)
Colon HK pump mediates absorption (can be inhibited by ouabaine)
Melena (balck stool)
Digestion of blood in upper GI bleeding
can also result from iron supplements
Maroon Stool
Incomplete digestion of blood from center small intestine or proximal colon
How does bile duct blockage affect stool color?
Prevents bile from reaching intestinal lumen
lack of stercobilin
Clay colored stool
Greasy, yellow stool
Poor fat digestion and absorption
Secretory diarrhea
cholera toxin
increase intracellular cAMP, activate chloride channels in the apical membrane causing chloride and water secretion into lumen
Osmotic diarrhea
Excess osmotically active particles in lumen
retain water leading to diarrhea
Rotavirus
Caused diarrhea by increasing Ca2+ levels leading to Cl- secretion
damage enterocytes leading to osmotic diarrhea
Motility
Chime moves too quickly= increased fluid excretion
vagotoy lead to dumping syndrome and diarrhea
Cholera toxin
10L of fluid loss per day
Oral rehydration solution: treat cholera
Causes increase in intracellular cAMP (prevent G-alpha-S from hydrolyzing GTP)
Cause excess Cl- secretion
* CFTR activity is increased leading to excess water and Na+ in lumen
Cystic Fibrosis
limit cholera toxin ability to hyperactivate CFTR
CF hererzygotes protect against cholera
