Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/61

Click to flip

61 Cards in this Set

  • Front
  • Back
GI peptides: distinction
- endocrine
- paracrine
- neurocrines
distinction is based on origin cell and route to target
- endocrine peptides travel thru the blood to target cells
- paracrine peptides diffuse through the extracellular space to neighboring cells
-neurocrines - synthesized in neurons and diffuse across synaptic gap
Gastrin
-source
-releasing factors
-functions
source: mainly antrum of stomach, also in duodenum and jejunum
release stimulated by: amino acids, peptides, gastrin releasing peptide, stomach distension; release is inhibited by H+
functions: acid release
Acid secretion in the stomach
-where from
-what stimulates it
gastrin, histamine, and Ach activate the parietal cell which secretes gastric acid
CCK
-source
-releasing factors
-functions
source: duodenum, jejunum, illeum
stimulated by: fat in food, amino acids
function: increases pancreatic enzyme secretion, bile and gastrin secretion, stomach emptying
Secretin
-source
-releasing factors
-functions
source: duodenum, jejunum, ileum
stimulated by: low pH
function: promotes HCO3 production from pancreas and bile, causes pepsin secretion (inhibits acid secretion)
GIP = glucose dependent insulinotropic peptide
-source
-releasing factors
-functions
source: duodenum and jejunum
stimulated by: glucose, AA, FA
causes: insulin secretion and inhibits gastric acid
motilin
-source
-releasing factors
-functions
source: duodenum and jejunum
stimulated by: fasting
function: causes motility
Enteric nervous system
-myenteric plexus
-submucosal plexus
- capable of regulating GI function in the absence of extrinsic innervation

-myenteric - btw circular and longitudinal muscle layers, controls muscularis externa (motility)
-submucosal - controls glandular, endocrine, and epithelial cell secretion
parasympathetic innervation
- excitatory for motility and secretion
innervation:
- IX - upper esophagus
- X - esophagus thru colon, pancreas, liver, GB
- pelvic nerve - colon, rectum, anus
sympathetic innervation
fibers from:
- celiac ganglion (esophagus thru SI)
- superior mesenteric ganglion - transverse colon
- inferior mesenteric ganglion/ hypogastric plexus - rest of colon, anus, rectum
Chewing
- 3 functions
function:
- reduction in particle size
- mixing of food with saliva ( easier to swallow, exposure to amylase and lipase)
- stimulation of taste buds
Oral or Buccal phase of swallowing
- voluntary control
- tongue moves food
muscle tone in esophagus, during rest
- upper and lower esophageal sphincter are tonically contracted - isolating the esophagus
- esophageal muscles do not maintain contraction (flaccid)
Pharyngeal phase of swallowing
- involuntary, controlled by the swallowing center in the reticular formation
- phase starts when bolus touches tonsils/ base of tongue --> afferents to swallowing center --> efferents back to sphincters/ esophageal muscles
- inhibition of respiration
- UES relaxes to let bolus enter esophagus and then contract more than normal to prevent reflux (ACh, enkephalin)
- higher pressure
esophageal phase of swallowing
- primary esophageal peristalsis/ slow peristaltic wave (initiated by the swallowing center)
- lower esophageal sphincter relaxes, then contracts (above normal level - ACh, enkephalin)
- fundus and body of stomach relax (receptive relaxation)
- relazation is mediated by vagal inhibition (NO, VIP)
- inhibition of respiration
seconday peristalsis
- function
- when it happens/ stimulated by
- not preceeded by pharyngeal activity
- stimulated by distension of esophagus (stretch receptors --> vagus nerves)
- clears the esophagus of retained food/ refluxed gastric contents
- no sensation associated
4 Anti reflux mechanisms
in what situations do people rely on different mechanisms?
- LES - high pressure
- seconday peristalsis, clearing of esophagus (important in pregnancy since other mechanisms are weaker)
- pinching action of diaphragm on esophagus (important in infants)
- reflexes (increased intragastric and intraabdominal pressure causes increase LES pressure)
Retching and Vomiting
- peristalsis in SI towards stomach
retching - not tenough force to move contents thru the UES
vomiting - additional contraction of the diaphragm and abdominal muscles & decreases in sphincter tone
Stomach functions
(4)
Storage
- receptive relaxation (relaxes during swallowing)
- accomadation (muscle relaxation due to distension
- storage allows digestion by amylase/ gastric enzymes
Mixing
- antral muscle
- facilitates digestion
Size reduction
Controlled gastric emptying
migrating myoelectric complexes
during interdigestive period, sweep undigestible stuff out of the stomach and SI
-strong intermittent contractions
-beginning is associated with motilin (stops w/ feeding/ gastrin)
- generated when the stomach is empty
-requires enteric system
antral systole
- simultaneous contraction of the terminal antrum and the pylorus
- chyme and liquids first leave the stomach
- systole causes retrograde mvmt of chyme back in to stomach (mixing) and reduction in particle size
What affects the change in gastric emptying rate?
- increased gastric volume = faster emptying rate
- depends on what is in the stomach:
~smaller empties faster
~ liquids = faster
~carbs faster than protein faster than fat
~neutral faster than acid
~isotonic faster than hypotonic faster than hypertonic
- duodenogastric reflex - distension of duodenum slows emptying
- ileogastric reflex - distension of ileum decreases emptying
- emotion can also affect emptying
interstitual cells of Cajal
- where
- what they do
- Electrical control activity/ slow wave originates here
- lies btw circular and longitudinal muscle layers within the inner dense circular muscle layer
- signal is conducted via gap junctions to rest of cells
Electrical Control Activity = Basal electrical rhythm= slow waves
- ion flux
= fluctuation of the resting membrane potential of muscle cells

Depolarization: Ca++ and Na+ influx
plateau = Ca++/Na+ influx balanced with K+ efflux (via Ca++ gated K+ channels)
repolarization – K+ efflux via Ca++ gated channels

Varying size, doesn’t always lead to contraction
Electrical response activity (ERA)
- at the plateau of the ECA, when depolarization is sufficient to activate voltage gated Ca++ channels
→ cause muscle contractions

multiple ERAs – more Ca++ enters muscle cells causing a stronger contraction
ECA and ERA control with neuroendocrine agents
- neuroendocrine agents can NOT initiate ECA, but can induce ERAs (cause more of the ECAs to have ERAs) by changing ion channel activity

- excitiatory: Ach and gastrin – indue ERAs, stronger contraction
- inhibitory: norepinephrine, VIP, NO, epinephrine – reduce ERAs, weaker, shorter contractions
Inhibitors of the movement of chyme
-drug
-reflex
- morphine reduces chyme mvmt by causing an increase in muscle tone
- adynamic ileus – inhibition of muscle activity due to obstruction
- intestino/conoic/peritoneo-intestinal reflexes – distension of intestine or colon or peritoneal area → inhibits muscle activity
Ileocecal sphincter
- function
- reflexes
Function:
- delay transit into colon (allowing time for reabsorption)
- prevent bacterial overgrowth
reflexes
- distension in the lower ileum → relaxation (chyme can enter colon)
- upper cecum distension → ⇑ contraction to prevent backflow
LI Structural modifications (3) and what they cause
- tenia coli (3 bundles of longitudinal muscles, nonuniform shortening)
- reduced electrical coupling (less coordinated contraction)
- 2 sets of pacemaker cells - allow localized contractions
rectophincteric reflex
distension of rectum causes the enteric and parasympathetic nerves to relax the internal anal sphincter, mental perception of urge to defecate
Gastroileal reflex
- entry of food into the empty stomach results in the relaxation o
of the ileo -cecal sphincter leading to the emptying of ileum
Colonocolonic reflex
distention of one part of the colon leading to relaxation ofother parts (final result: decreased resistance and increased aboral movement)
Gastrocolicreflex/Duodenocolic
reflex
entry of food into the empty stomach or chyme into the duodenum results in increases of aboral propulsive movement in the
colon.
Functions of Saliva
- lubricate (for swallowing)
- dissolve (for taste)
- protect – alkaline pH, lysozyme, lactoferrin, Ig
- facilitate speech
- carb and fat digestion (amylase and lipase)
Source of Saliva
- parotid = serous secretions, amylase
- sublingual – mucous secretions
- submaxillary – mixed
- buccal glands – mucins
2 stage secretion model of Saliva
- what the 2 parts are
-product
1° acinus produces an isotonic secretion
2° ductile epithelial cells modify the secretion by reabsorbing Na+ and Ca++ and secreting HCO3- and K+,
--> produces a hypotonic solution high in K+ and HCO3-
Sympathetic and Parasympathetic control of salivation
- amt of output
- composition of secretions
salivary nucleus of the medulla stimulates parasypmathetics, which cause:
o sustained increased salivation
o protein poor
sympathetics:
o transient decreased salivation
o protein rich

both: if denervated – decresased secretion
Oxyntic component of Gastric secretion
- what it consists of
- what each factor does
- what stimulates it
consists of:
H+, Cl-, intrinsic factor (parietal cells )
Stimulated by:
feeding
Increases greatly with increased secretory rate

functions:
o Acidic pH activates pepsinogen and lipase
o HCL depantures proteins, stabilizes minerals, inactivates microbes
o Intrinsice factor – required for B12 absorption
Control of Acid secretion
-phases of digestion associated with secretion
-what enzymes are involved in control/ their receptors and effects
Most acid is secreted when food is in the stomach, a lot is also secreted when food is smelled/ tasted/ chewed/ swallowed
Stimulate HCl release:
o Gastrin --> CCK/ gastrin receptor and stimulates Ca++ release
o Ach binds M3 receptor and also stimulates Ca++ release
o Histamine bines H2 receptor an stimulates cAMP

inhibitors of gastrin and cAMP, decreasing HCl:
Somatostatin, secretin, GIP, prostaglandins transforming and epidermal growth factors
Non oxyntic component of gastric secretions
-whats included
-what stimulates it/ secretion mechanisms
includes:
mucous, Na+, HCO3- (mucous cells)
pepsinogen (chief cells)


HCO3- is secreted into the lumen from the epithleial cells by:
o Cl-/ HCO3- exchanger which is stimulated by glucagon
oHCO3- transporter stimulated by prostaglandin E

Mucous secretion:
Parasympathetic→ (+)neck mucus cell
Mechanical/chemical irritation → (+) surface mucus cells
Disruption of the mucosal barrier
- mucosal barrier is made by the non oxyntic component of gastric juice
- aspirin – acidification, inhibits prostaglandin (decreased HCO3- and mucus secretion)
- NSAIDs - inhibits prostaglandin (decreased HCO3- and mucus secretion)
- Ethanol – inhibits intracellular enzymes
- Bile acids – solubiliza plasma membrane
- H pylori – inflammation, immune response
Production of pancreatic secretions
- cells involved
- what they produce
- acinar cells – synthesize the enzymes and stored in zymogen granules until they need to be secreted)
- centroacinar and ductal cells – produce the initial, isotonic, aqueous component of pancreatic secretion; this aqueous secretion is then modified by the ductal epithelial cells:
o Cl-/HCO3- exchanger secretes HCO3- into the pancreatic juice (which causes a net absorption of H+ into the blood)
2 functions of pancreatic secretions
- HCO3- to neutralize chyme from stomach in the duodenum
- Emzymes to digest: pancreatic amylase, lipase, proteases (have to be converted to active form)
Control of secretion (autonomic and hormonal)
- aqueous portion
- enzymatic portion
Aqueous portion:
o H+ in the lumen of the intestine →(+) secretin secretion →(+) ductal cells
o AcH and CCK also stimulate ductal cells

Enzymatic portion
o peptides, AA, FA → (+) secretion of CCK → (+) acinar cells
o Ach stimulates acinar cells
bile salts
- functions
o amphipathic
o emulsify lipids by surrounding the lipids, creating small lipid droplets in the intestinal lumen increasing the surface area for the digestive enzymes
o form micelles w/ the products of lipid digestion – at the core of the micelle – lipid products, at the edges – bile salts – allows lipid products to move in the aqueous solution of the lumen
Gallbladder control
- chyme reaches the SI: AA, peptides, FA→(+) CCK is secreted to stimulate the contraction of the gallbladder and relaxation of sphincter of Oddi → bile flows into the duodenum
Recirculation of the bile salts – Enterohepatic circulation
- bile salts are absorbed (from the ileum) into portal circulation by Na+-bile salt cotransporters
- hepatocytes extract bile salts from the portal blood, so only a small amt of bile salts have to be remade
Starch Breakdown (digestion)
1st stach digested with alpha amylase in the saliva (inactivated when it reaches the stomach), stach digested with pancreatic amylase in duodenum → produces disaccharides
- THEN, disaccharides digested by brush border enzymes (alpha dextrinase, maltas, sucrase) → glucose

- disaccharides in food – are digested by brush border enzymes trehalase, lactasem sucrase → glucose, galactose, fructose

only glucose, galactose and fructose can be absorbed by epithelial cell
Absorption of monosacharrides across the apical (into ep cell) and basolateral (into blood) membranes
- glucose and galactose: absorbed into epithelial cell by Na+ glucose cotransporter SGLT1
- Fructose is absorbed into the epithelial cell by GLUT5 transporter by facilitated diffusion (can’t be absorbed agst gradient)
- Glucose, galactose, and fructose – all absorbed into blood via GLUT2 facilitated diffusion
Protein breakdown (digestion)
- 1st proteins digested w/ pepsin in stomach (pepsinogen produced by chief cells and activated by ⇓pH - ⇑pH of duodenum in activates)
- 2nd proteins digested with pancreatic proteases (trypsin – which is activated by enterokinase in the brush border and then activates other enzymes: chymotrypsin, elastase, carboxypeptidase A and B) →AAs, di and tripeptides, larger peptides
- 3rd brush border proteases in SI break down larger peptides -->di/tri peptides
absorbable form: di and tripeptides, AAs
Protein absoprtion:
- products of breakdown
- how their absorbed at apical and basolateral membranes
AAs
apical/ ep cell membrane from lumen:
- Na/AA cotranporters (separate transporters for neutral, acidic, etc)
AAs - basolateral/ blood membrane:
- transported into blood by facilitated diffusion
Di/tripeptides,
apical:
- H+/ditripeptide cotransporter
basolateral:
Within the cell, di/tripeptides are either broken down to AAs or just absorbed as is.
Lipids
- 3 ingested forms
- how each gets broken down/ enzymes used
- where
1. Triglycerides:
stomach -lingual and gastric lipases (triglycerides→ glycerol and FAs)
SI - pancreatic lipase (triglycerides→monoglyceride, FAs)

2. Cholesterol ester:
SI- cholesterol ester hydrolase ( →free cholesterol, FAs)

3. Phospholipid
SI- phopholipase A2 (→lysolecithin and FAs)
Lipid absorption
-how they get absorbed into epithelial cell
-what happens to get them into the bloodstream
- solubolized in lumen as micelles
- @ epithelial cell, lipids are released from the micelle and diffuse down concentration gradient into the epithelial cell in duodenum, jejunum
- inside epithelial cell – lipid digestion products are reesterified to reform original lipids
- lipids are packaged with apoproteins and carried in chylomicrons which are put in vesicles and exocytosed into lymphatic capillaries → bloodstream
pancreatic insufficiency
can’t breakdown triglycerides → in feces
zollinger Ellison syndrome
- too much acid from parietal cells- → acidic environment of the duodenum (not neutralized) → lipases can’t work (not prime pH) → triglycerides in feces
bile salts deficiencies/ ways they get inactivated
- deficiency of bile salts – can’t form micelles to absorb lipid products → lipid products are in feces (phospholipids, monoglycerides, FAs, cholesterol)
- bacterial overgrowth/ ⇓ pH – deactivates bile salts to bile acids (which is absorbed easily, too soon – prior to micelle formation) → lipid products in feces
Fat soluble vitamins
- what they are
- how absorbed
- vitamins A, D, E, K
- absorbed w/ lipids (packaged into micelles and then chylomicrons →blood)
Water soluble vitamins
-what they are
-where they are reabsorbed
Jejunum:
B1, B2, B3, folate;
B6 (duodenum & jejunum), B7 (proximal intestine)
Ileum:
C, B12 (distal ileum)
Ca++ absorption
dependent on D 1,25 dihydroxycholecalciferol
dietary vitamin D3 – converted in the liver, again in the kidney to finally 1,25 diydroxycholecalciferol which promotes Ca++ absorption from SI
o [deficiency in Vitamin D or conversion to active form → rickets, osteomalacia]
Iron absorption
- absorbed as free iron (Fe++) or heme iron (bound to Hb, once inside epithelial cells, Hb-iron is digested to release free iron)
- free iron in epithelial cell binds apoferritin which is transported into blood
- in blood, iron is bound to transferrin for transport
Where are the following most absorbed:
-carbohydrates
- proteins
Carbohydrates: most in the duodenum, completed by mid jejunum
protein: mainly jejunum and ileum