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Physiology > GIT > Flashcards

GIT Flashcards

1
Q

Function of the Gastrointestinal Tract (GIT)

A

Transfers organic nutrients, minerals water from EXT to INT environment
DIGESTION - chemical alteration of food into molecules that can be absorbed
ABSORPTION - movement of digested food from intestine into BLOOD or lymphatic system
EXCRETION - non-absorbable materials (fibre, bacteria intestinal cells, hydrophobic molecules) removed
HOST DEFENCE - continuous with ext of body, inactivate pathogens

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2
Q

Components of submucosa

A

blood
lymphatic vessels
connective tissue
submucosal plexus - nerve cell bodies (info relay)

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3
Q

Components of mucosa

A

epithelium - polarized. Basolateral and apical. Tight junctions
lamina propria - connective tissue
muscular muscosa - think layer of smooth muscle. Villi movement

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4
Q

Components of Muscularis Externa

A

Thick inner layer (circular muscle)
Myenteric nerve plexus (nerves to regulate muscle function)
Thin outer layer of longitudinal muscle - shorten tube

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5
Q

What is the serosa

A

Thin layer of connective tissue, connecting intestine to the abdominal wall

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6
Q

portal circulation - nutrient rich blood

A

Intestinal tract –> liver
Blood drains from the intestine, directly to liver
NUTRIENT RICH BLOOD
Liver: removal of harmful substances, process nutrients

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7
Q

What blood/circulation does the liver receive?

A 
"In Series" blood from Hepatic artery, stomach, pancreas, sm/lg intestine.
LOW OXYGEN, HIGH NUTRIENTS
Hepatic artery (oxygen-rich blood) runs through majors organs first, conglomerate to liver
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8
Q

GI Processes

A

Secretion and Motility

governed by volume and composition of lumen contents

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9
Q

Reflexes propagated by (3)

A

Mechanoreceptors
Osmoreceptors (salty)
Chemoreceptors

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10
Q

Intrinsic Neural Regulation

A

Enteric nervous system (nerve plexi)
Controls activity of SECRETOMOTOR neurons
contained within GIT walls
Dense and complex neural network (10^8)
Brain of the gut - can function independently
Two nerve networks - Myenteric plexus and submucosal plexus

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11
Q

Myenteric plexus

A

influences SMOOTH MUSCLE

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12
Q

Submucosal plexus

A

Influences SECRETION

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13
Q

Regulation of Extrinsic Neuronal Regulation

A

ANS
parasympathetic - Rest and digest (thin saliva), stim peristalsis and secretion
sympathetic - fight or flight - thick saliva, inhibits peristalsis

Influences: Hunger, sight/smell of food, emotional state

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14
Q

4 Chemical Messenger Regulators

A

Endocrine - hormone - distant target via blood
Neurocrine - neurotransmitter - post-synaptic target cell
Paracrine - diffusion through interstitial fluid
Autocrine - chemical messenger acts on cell that produced it

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15
Q

GI Hormones - all peptides, feedback control system

A

Secretin
Cholecystokinin (CCK)
Gastrin
Glucose-dependent Insulinotropic peptide (GIP)

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16
Q

CCK - cholecystokinin

A

Triggered by fatty acids and amino acids in the small intestine (I cells)
STIMULATES:
pancreas increase digestive enzyme secretion
Gall bladder contraction - bile acids break down fat

Fat and AA are absorbed, CCK is removed, stimulation is stopped –> NEGATIVE FEEDBACK

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17
Q

Peristalsis and Segmentation

A

Peristalsis –> propulsion
contraction on the oral side of food, relaxation on the other side. Moves towards anus. Smoot passage of bolus

Segmentation –> mixing with digestive enzymes
intestinal segments contract and relax, bolus does not move. Small intestine. Slows transit time for more absorption

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18
Q

Phases of GIT control (3)

A

cephalic (head) - stimulated by sight, smell, taste, chewing, emotions, parasympathetic fibres
gastric (stomach) - receptors stimulated by Distention, Acidity, Amino Acids, Peptides
intestinal - receptors stimulated by Distention, Acidity, Osmolarity, Digestive Products

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19
Q

Hypothalamus affect

A

Feeding centre in lateral region
Activation –> increased hunger

Satiety centre in ventromedial region
Activation –> feeling of fullness

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20
Q

Factors that influence food intake

A 
OREXIGENIC factors - increase intake
Neuropeptide Y (NPY) - stimulates hunger
Ghrelin - synth and released from endocrine cells in stomach. Stimulate release of NPY
ANOREXIGENIC factors - decrease intake
Leptin (adipose)
Insulin (pancreas)
Peptide YY (intestines)
Melanocortin (hypothalamus)
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21
Q

Leptin

A

ANOREXIGENIC factor - from adipose
Inhibit the release of neuropeptide Y, inhibiting food intake

no apetite regulation

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22
Q

Water intake

A

Hypothalamus - thirst centre - stimulated by:

  1. Increased plasma osmolarity - vasopressin (antidiuretic hormone) conserves water at kidney
  2. Decreased plasma volume - stimulates baroreceptors. Increases thirst due to decreased blood volume
  3. Dry mouth/throat
  4. Prevent over-hydration - stimulated by mouth, throat, GIT
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23
Q

Salivary Glands (3) and their secretion

A

Parotid - watery (serous) secretion
Submandibular - serous/mucous secretion
Sublingual - mucous secretion

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24
Q

Composition of saliva

A
  1. Water (hypotonic, slightly alkaline)
  2. Electrolytes (Rich in K+ and HCO3-, poor in Na+ and Cl-)
  3. Digestive enzymes (amylase, lipase)
  4. Glycoproteins (mucin) [mucin + water = mucous]
  5. other components (anti-microbial)
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25
Q

function of saliva

A 
moisten/lubricate food
initiate digestion
Dissolve food - diffusion allows for taste
antibacterial
speech
buffering (HCO3- neutralizes acid)
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26
Q

acinar cells

A

Part of the salivary gland

Important for protein, electrolyte and water secretion

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27
Q

ductal cells

A

Part of the salivary gland

Important for creating alkaline and hypotonic nature

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28
Q

myoepithelial cells

A

part of the salivary gland
important for pushing saliva from acinus into duct
smooth muscle and epithelial characteristics

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29
Q

formation of saliva

A

ACINAR glands secrete initial saliva (isotonic)
water, electrolytes, proteins
MYOEPITHELIAL cells contract, expelling saliva from acinus –> duct
DUCTAL cells modify initial saliva to a hypotonic, alkaline state
loss of Na+ and Cl-
secretion of K+ and HCO3

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30
Q

striated duct

A
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31
Q

regulation of salivary gland function

A

Parasympathetic

  • smell/taste
  • pressure receptors in mouth
  • nausea (protection)
  • -inhibited by fatigue, sleep, fear, dehydration, drugs

Sympathetic

  • increased, thicker*
  • increased protein secretion from acing cells
  • stimulates myoepithelial cells (increased flow)
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32
Q

Amylase in saliva

A

Starch digestion in the mouth
– inhibited in the stomach (acidic pH)

Carbohydrates are digested in the small intestine by PANCREATIC AMYLASE

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33
Q

Lingual lipase

A

Fat breakdown in the mouth

acid stable, active in the stomach

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34
Q

Digestive role of saliva is ______

A

Minor

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35
Q

“dry mouth” and causes

A

Xerostomia

congenital
autoimmune process
drug side effect
radiation

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36
Q

Consequences of a dry mouth

A

dry mouth
decreased oral pH –> tooth decay, esophageal erosion
poor nutrition due to decreased food lubriaction

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37
Q

What initiates swallowing?

A

Pressure receptors in the walls of the pharynx

liquid/food entering signals pharynx, esophagus, respiratory muscles

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38
Q

Swallowing

A
  1. Tongue pushed food to back of PHARYNX
  2. soft palate elevates to prevent food from entering nasal passages
    - -> inhibition of respiration. larynx raises. glottis closes
  3. EPIGLOTTIS covers glottis. prevents liquid or food from entering trachea
  4. food descends into esophagus
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39
Q

Esophageal phase of swallowing

A

Transfers food from mouth –> stomach
skeletal muscle on top 1/3, smooth muscle rest
no absorption, past passage via mucous gland help
exposed to rough/abrasive food
Upper and lower sphincter closed except when swallowing, vomiting, burping

  1. relaxation of upper esophageal sphincter
  2. peristaltic waves move food down esophagus
  3. lower sphincter opens, food enters stomach
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40
Q

Stomach

A

Sac-like organ between esophagus and small intestine

stores food
machanical and chemical breakdown of food

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41
Q

Pepsinogen and HCl in stomach

A

Pepsinogen - digestion enzymes for PROTEIN

HCl - dissolves food, partial digestion, sterilization

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42
Q

Pernicious Anemia

A

Stomach doesn’t secrete Intrinsic Factor like normal … Vitamin B12 is not absorbed.
RBC deficiency

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43
Q

Fundus and body (stomach)

A

Upper 2/3 of stomach
thin layer of smooth muscle
Secretion of mucus, pepsinogen, Hal

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44
Q

Antrum (stomach)

A

bottom 1/3 of stomach
Thick smooth muscle layer
Secretion of mucus, pepsinogen, gastrin

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45
Q

Major and Minor secretions of stomach

A

Chemical messengers secreted into ducts, then to epithelial surface
does not enter blood

Endocrine:
Mucus - prevents self digestion
HCl - hydrolysis of protein, sterilization
Pepsinogen - digestion of proteins

minor:
Intrinsic Factor (B12)
Gastrin (Endocrine - stimulates HCl production, stomach motility)
Histamine (Paracrine - HCl production)
Somatostatin (Paracrine - HCl production)

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46
Q

Parietal Cell

A

found in gastric glands in fundus/body region
oxyntic cell
secretes HCl and Intrinsic Factor
CANALICULI increase surface area of cells, maximize secretion into stomach lumen
[canaliculus - actively secreting cell]
lost of mitochondria (energy needed for acid secretion)

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47
Q

Gastric glands

A

Chief cell - all regions
secrete pepsinogen
- precursor of pepsin
- accelerates protein digestion

Enteroendocrine cell - antrum (G-cell)
secretes gastrin
- HCl production
- GI motility

Enterochromaffin-like cells - all regions
secrete histamine
- HCl release

D-cells - all regions
secretes somatostatin
- HCl secretion

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48
Q

SOMATOSTATIN

A

secreted by D-cells

NEGATIVE regulator of HCL secretion

49
Q

Acidification of Stomach Lumen

A
  1. H+/K+ ATPase - H+ into lumen in exchange for K+ into cell. ACTIVE transport, electroneutral
    • -> regulated by Gastrin (gastric molecule), Acetylcholine (NT), Histamine (paracrine), and somatostatin (paracrine)
  2. Carbonic Anhydrase (CA) - formation of H2CO3 from H2O and CO2
  3. Cl-/HCO3- exchanger - OH- is effluxes from cell in exchange for Cl-. neutral cellular pH
  4. K+ channels - K+ enters stomach lumen via diffusion thru a channel
  5. Cl- channels - Cl- enters stomach lumen via diffusion thru a channel
50
Q

Cl-/HCO3- exchanger

A

Stomach:
EXCESS BASE
Cl-/HCO3- exchanger - OH- is effluxes from cell in exchange for Cl-
neutral cellular pH

Pancreatic:
ducts secrete watery all secretion to neutralize gastric acid

51
Q

Pepsinogen Secretion and Activation

A

Secreted by chief cells (inactive precursor)
- stimulated by enteric nervous system
- parallels release of HCl
Cleaved and activated by pepsin (via acidic pH in stomach)

ADVANTAGE OF INACTIVE PRECURSOR:
irreversibly inactivated when it enters small intestine - prevents auto digestion

52
Q

Phases of Gastric Secretion

A
  1. Cephalic phase (parasympathetic)
    - ACh release by parietal cells
    - anticipatory, excitatory
    - via Vagus nerve
  2. Gastric phase
    - major phase
    - excitatory
    - via gastrin
  3. Intestinal phase
    - inhibitory due to presence of acid, fat, digestion products
    - hypertonic solutions in duodenum (stomach slows down, ingestion)
53
Q

Regulation of gastric secretion

A

3 Stimulators:

  • Acetylcholine, gastrin, histamine
    • directly increase acid secretion by parietal cell

1 Inhibitor:

  • Somatostatin
    • decreased acid secretion by parietal cell

Once acid secretion is at a high rate:

  • PS input (cephalic phase) is reduced
    • Negative feedback occurs
54
Q

Gastric Motility

A

Consumption of meal –> smooth muscle relaxation –> stomach volume increases to 1.5 L without added pressure
Relaxation - PS nerves to ENS
Arrival of food causes peristaltic waves - weak contraction in body of stomach, strong in antrum
Pyloric sphincter closes - small amount of stomach content released to duodenum
mix contents with enzymes and acid
PACEMAKER CELLS in smooth muscle layer

55
Q

Vomiting

A

Vomiting centre - medulla
Caused by:
- psychogenic (smell, sight)
- GIT disturbances (infection, distension)
- Motion sickness, inner ear infection
- Chemoreceptors (Brain or GIT, influenced by alcohol, toxins)
- Pressure on CNS

Glottis closes off trachea
diaphragm and ab muscles contract
reverse peristalsis
Stomach contents move up through esophagus, out the mouth

56
Q

Benefit and Negatives of Vomiting

A

Benefits:

  • removal of harmful substances (bacteria, toxins)
    • prevents re-consumption in the future

Negative:

  • dehydration
  • electrolyte imbalance
  • metabolic alkalosis (loss of H+)
  • acid erosion on enamel
57
Q

Ulcers

A

damaged/eroded area of the GIT mucosa, in acidic regions
Imbalance between aggressive factors (acid, pepsin) and protective factors (HCO3-, mucus)
Helicobacter pylori –> bacterial infection
Non bacterial factors - NSAIDS - decrease prostaglandin (stomach lining protection)

Treatment:
Abx
H+/K+ ATPase inhibitor

58
Q

Pancreas

A

EXOcine and ENDOcrine gland

Exocrine –> digestion (apical surface)

  • secretions that go into guts
  • source of enzymes
  • produced in excess
  • HCO3- secretion

Duct cells - secrete H2O and HCO3- to neutralize acid

Endocrine –> regulation hormones (Ductless glands)

59
Q

What are Pancreatic Juices

A

Isotonic, alkaline, 1-2L/day
contains electrolytes
–> high HCO3-, low Cl-
–> Na+, K+ same as in plasma
–> HCO3- and H2O secreted by duct cells
–> HCO3- neutralizes gastric acid in duodenum

Digestive enzymes - secreted by acinar cells
Proteolytic enz stored and secreted in inactive forms (prevent auto digestion)

60
Q

CFTR - Cystic Fibrosis Transmembrane Conductance Regulator

A

Cystic Fibrosis - thick mucous in pancreas

61
Q

Ductular cell secretion

A
  1. Chloride channel opens (CFTR)
  2. Cl- in lumen is exchanged for HCO3-
  3. H2O and Na+ paracellularly response to electrochemical gradient
  4. Neutral pH of cytosol is maintained by exchange of H+ (exported from cell) for Na+ (imported)

ducts secrete watery all secretion to neutralize gastric acid

62
Q

Alkaline tide

A

After big meal:
Parietal cells in stomach produce a lot of acid
–> large amount of HCO3- is pumped across the basolateral surface into blood stream

HCO3- (stomach) and H+ (pancreas) meet in portal vein
Two processes balance each other to maintain acid base balance

63
Q

Acid tide

A

After big meal:
Duct cells in pancreas produce and secrete HCO3-
–> large amount of H+ is pumped across the basolateral surface into blood stream

HCO3- (stomach) and H+ (pancreas) meet in portal vein
Two processes balance each other to maintain acid base balance

64
Q

Digestive function of Pancreas

A

source for majority of enzymes for meal digestion
Acinar cells synthesize and pack pro-enzymes into zymogen granules, stored in the apical pole of cell
neurohormonal input results in the exocytosis into lumen of duct

65
Q

Proteases

A

Digestion of PROTEINS into PEPTIDES and AMINO ACIDS

66
Q

Amylolytic enzymes

A

Digestion of STARCH into SUGARS

67
Q

Lipases

A

Digestion of TRIGLYCERIDES into FREE FATTY ACIDS and MONOGLYCERIDES

pancreatic lipase is water soluble, only works on the surface of lipid droplets

68
Q

Nucleases

A

Digestion of NUCLEIC ACIDS into free nucleotides

69
Q

Where are enzymes activated? How?

A

secreted in INACTICE form
activated in the DUODENUM

Cleavage of trypsinogen –> trypsin (protease that activates other proteases)

70
Q

Pancreas prevention of auto digestion

A

Storage –> inactive form (until it reaches small intestine)
Trypsin inhibitors antagonize prematurely activated trypsin
Trypsin can degrade itself if activated before small intestine is reached

71
Q

Endopeptidases

A

Hydrolyze interior peptide bonds from protein and polypeptides

72
Q

Exopeptidases

A

Hydrolyze bonds at C-terminal end

73
Q

Regulation of Pancreatic HCO3- Secretion

A

Acid enter duodenum from stomach
Reduced pH triggers secretin from cells in small intestine into blood
Circulating secretin stimulates:
- Pancreas (Duct cells) to increase HCO3-secretion
- Liver (Duct cells) to increase HCO3- secretion

74
Q

CCK

A

Triggered by fatty acids and amino acids in the small intestine

Circulating CCK stimulates:

  • pancreas increase digestive enzymes
  • gall bladder contraction (bile acids break down fat)

Negative feedback control system
–> fats and amino acids are absorbed and CCK stimulation is stopped

75
Q

phases of Pancreatic Secretion

A
  1. Cephalic Phase (via PS nerves)
  2. Gastric Phase (via PS nerves)
  3. Intestinal Phase
76
Q

Components of Liver and Biliary System

A

Bile Duct (from liver)
Sphincter of Oddi (controls content release into small intestine)
Gallbladder
COMMON HEPATIC DUCT
COMMON BILE DUCT
Pancreas
HEPATIC PORTAL VEIN - 75% blood volume, rich in nutrients, poor in oxygen
CENTRAL VEIN - blood back to inferior vena ceva

77
Q

Lobule

A

Hexagonal structure with:

  • central vein running through the centre
  • portal trains at each corner (composed of hepatic artery, portal vein, bile duct)
78
Q

What forms bile ducts

A

Hepatocytes
Bile Duct epithelial cells
BILE CANALICULI

79
Q

Portal triad

A

Composed of:

  1. hepatic artery
  2. portal vein
  3. bile duct

bathed in blood, filters

80
Q

hepatic sinusoid

A
81
Q

functions of liver

A

Exocrine gland (formation and secretion of bile)
Metabolism and storage of nutrients (liver matches supply to demand)
Deactivation and detoxification (drugs, hormones, waste products, toxins)
Production of circulating proteins (blood coagulation factors, lipoproteins)

82
Q

Constituents of Bile (secreted by liver)

A
  1. Bile Acids
    • synthesized within hepatocyte from cholesterol
    • amphipathic
  2. Cholesterol
    • slightly amphipathic
  3. Salts and Water
    • Na+, K+, HCO3-
  4. Phospholipids
    • phosphatidylcholine (amphipathic)
  5. Bile Pigments
    • bilirubin
  6. Trace Metals
83
Q

Emulsification

A

Mechanical disruption to make lipid droplets small

Emulsifying agent prevents droplets from re-forming

84
Q

what is a micelle? how is it formed?

A

Soluble cluster of amphipathic molecules - holding station for small insoluble molecules

    • non polar groups in the middle
    • polar groups on the outer layer

Formed by emulsification via bile acids
product of lipase digestion

85
Q

Formation of bile

A

Hepatocytes: produce and secrete bile, phospholipids, cholesterol, bile pigments,

Bile Duct: adds HCO3-, salts, H2O to bile

Gallbladder: stores and concentrates bile between meals, releases into duodenum after a meal

86
Q

Enterohepatic circulation of bile acids

A
87
Q

Steps for bile acid recycling

A
  1. Bile acids are released by the liver/gallbladder into duodenum for fat digestion
  2. Bile acids are reabsorbed across the small intestine (ileum) into portal circulation
  3. Bile acids are transported back into hepatocytes
88
Q

Regulation of Heoatobiliary secretion

A

Bile Salts - as ileum absorbed bile salts, more is produced. reduced when enteropathic circulation is working

Secretin - produced and released by S-cells. Increased HCO3- secretion by bile duct cells

Cholectstokinin -

89
Q

Gallstones

A

Cholesterol stones
high concentration of cholesterol results in precipitation

Consequences:
Location - obstruction, infection impacting gall bladder, liver, pancreas
pain, nausea, jaundice, malabsorption

90
Q

Pigment stones

A

Result of excessive hemolysis

pigments form precipitates with Ca2+

91
Q

Gallstone treatment

A

Cholecystectomy (remove gall bladder) - reduce fat in diet
Remove stones
Drugs to dissolve stones

92
Q

Location and sections of Small Intestine

A

Between stomach and large intestine

  • duodenum
  • jejunum
  • ileum
93
Q

Major function of Small intestine

A

digestion and absorption of protein, fat, carbohydrate, electrolytes, water, minerals, vitamins

94
Q

Function of Duodenum

A

mixing of pancreatic digestive enzymes and bile with food
absorption of nutrients, iron, calcium
release endocrine hormones secretin and CCK

95
Q

Function of jejunum

A

digestion and absorption

96
Q

function of Ileum

A

digestion and absorption

bile acids and vitamin B12

97
Q

Folds in small intestine

A

Folds of Kerckring/Circular folds
increase surface area

villus - protrudes
crypt - invagination

98
Q

4 cells derived from stem cells

A 
- Absorptive cell (enterocyte)
     absorption
     brush border enzyme
- Goblet cell
     lubricate food 
     protect from stomach acid
- Enteroendocrine cell (I or S cells)
- Paneth cell 
     antimicrobial
99
Q

Brush Border Enzyme

A 
small projections (microvilli) of epithelial cells
covers villi of small intestine
absorptive sufrace

BBE: enzyme anchored to brush border, catalytic activity in lumen
breaks down carbohydrates and peptides into sugars and amino acids before transporting across the enterocyte

100
Q

Carbohydrate digestion

A

Starch (amylose and amylopectin) broken down into maltose, maltotriose, and alpha-limit dextrin
cleavage of alpha1,4 and alpha1,6 bonds
sucrose —> glucose + fructose
lactose —> glucose + galactose

101
Q

Protein digestion and absorption

A

Proteins broken down may pepsin (sm int) and pancreatic proteases (trypsin and chymotrypsin)
Free amino acids are abs by 2° active transport

102
Q

Fat Digestion and absorption

A

lipid droplets are emulsified via mechanical disruption and bile acids
release free fatty acids and monoglycerides
products are incorporated into micelles (breakdown of triglycerides)
Breakdown of micelles results in the diffusion of fatty acids and monoglycerides across intestine epithelium

Extracellular fat droplets - “chylomicrons”

103
Q

Chylomicron

A

contains triglycerides, phospholipids, fat soluble vitamins. cholesterol

Lipoprotein lipase on endothelial cell of blood vessels release triglycerides from chylomicrons as monoglycerides and free fatty acids (energy)

104
Q

absorption of iron

A

Fe2+ actively transported into enterocyte and incorporated into ferritin –> storage
Transferrin - plasma protein - transport through blood

105
Q

Iron-Deficiency Anemia

A

reduced number and size of RBC
tired, light headed, headaches
Not enough iron (diet), iron loss, poor absorption, intestine disease

106
Q

Water and Electrolyte Abs and Secretion

A

Absorption - villi
Secretion - crypts

Osmotic gradient
ABS - Na+ gradient
SEC - Cl- gradient

107
Q

Water transport and electrolyte transport

A
108
Q

MMC (motility sm intestine)

A

MIGRATING MYOELECTRIC COMPLEX
pushes any undigested material from the small intestine to large intestine
prevents bacteria from remaining in the small intestine

Regulated by motilin
feeding inhibits motilin

109
Q

Lactose intolerance

A

Lactose - milk sugars
lactate (BBE) digests lactose into glucose and galactose
loss of lactase expression after weaning
decreased water abs in gut, bacteria in lg intestine digest lactose (gas, diarrhea)

110
Q

Monosacchraides in lactose

A

lactose —————-> glucose + galactose

via lactase

111
Q

Vibrio cholera

A

vomiting and excessive diarrhea
increases cAMP production in crypto of small intestine
activates Cl- channel, water follows (diarrhea)

112
Q

Anus sphincters

A

Ileocecal valve
between cecum and ileum
closed when lg int is distended

cecum/appendix

Ascending/transverse/decending/sigmoidal colon
reabs water
reservoir for storage of waste

rectum - hold feces

anus - control defecation

113
Q

Colon crypt cell types

A

ONLY CRYPTS, no villi
ABSORPTIVE CELLS/ENTEROCYTES
GOBLET CELLS
PANETH and ENDOCRINE

bacteria - metabolize fibre, produce vitamins (Vit K), gas production

114
Q

Water absorption in large intestine depends on:

A

Na+ gradients (ABS)

Cl- gradients (SEC, NKCC1)

115
Q

Components of GIT

A

Mouth (chopper)
Pharynx
Esophagus
Stomach (blender, acid sterilizer, reservoir)
Small Intestine - duodenum (run vessel), jejunum, ileum (catalytic & absorptive)
Large intestine (residue combusted, desiccator, pelleter)
Accessory organs - pancreas (enz supplier, neutralizer), liver, gallbladder

116
Q

Paracellular transport

A

Across epithelium - BETWEEN CELLS
Limited by tight junction seal
Water and small ions diffuse through

117
Q

Transcellular pathway

A

THROUGH CELL
two steps:
transport protein on apical and basolateral cell surface

118
Q

Defecation

A

feces - water, undigested food, bacteria old cells

REFLEX - contraction, peristalsis,

Physiology (3 decks)

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