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Gastro > Intestines physio > Flashcards

Intestines physio Flashcards

1
Q

major ions secreted in small intestine

A
  • Cl-
  • HCO3-

Na+ (less important)

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2
Q

where are the ions secreted in small intestine

A
  • crypt
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3
Q

how does Cl- secretion occur & lead to water secretion

A

apical membrane:
- Cl- secreted by intestinal cell through CFTR (cystic fibrosis transmembrane conductance regulator) into intestinal lumen
- -ve charge brings Na+ & water into intestinal lumen as well (via PARACELLULAR route)

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4
Q

how does intestinal cell maintain [Cl-] despite constant Cl- secretion

A

basolateral membrane:
- contains Na+, K+, ATPase -> pumps out 3Na+ for 2K+ -> causes Na+ deficit within cell
- contains NKCC1 (Na K Cl cotransporter) -> pumps K, Na, 2Cl into intestinal cell with help to [Na+] gradient (created by NaKATPase) -> [Cl-] is maintained

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5
Q

how does HCO3- secretion occur in intestinal cell (2)

A

same as other GIT cells
- presence of DRA (downregulated in adenoma) -> secrete HCO3- in exchange for Cl-
- presence of CFTR -> pump both Cl- and HCO3- out of intestinal cell

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6
Q

how does intestinal cell maintain [HCO3-] within cell (2)

A
  • carbonic anhydrase -> convert CO2 to H2CO3 -> dissociate, HCO3- is produced, H+ is removed from cell via NHE (Na H exchanger) on basolateral membrane

basolateral membrane:
- presence of NBC1 (Na HCO3 cotransporter) -> cotransports Na and HCO3- into intestinal cell

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7
Q

what do the intestines secrete

A

intestinal juice
- water, electrolytes, mucous
- mucus & electrolytes secreted by crypts (driven by Cl- secretion through CFTR)

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8
Q

what stimulates production of intestinal juice (4)

A
  • mechanical irritation of mucosa
  • distenstion of gut
  • ACh (vagal) , PG, guanylin
  • 2nd messengers - cAMP, cGMP, Ca
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9
Q

functions of intestinal fluid

A
  • maintain fluidity of chyme
  • alkalinise contents for enzymatic activity
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10
Q

major ions secreted in COLON

A
  • K+ (distal)
  • Cl-
  • HCO3-
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11
Q

what does the colon secrete

A
  • mucus
  • intestinal fluid (pH8-8.4), contains high K+ & HCO3- -> buffers against H+ produced by bacterial fermentation in colon
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12
Q

what stimulates colonic secretion (2)

A
  • parasympathetic nerve impulses
  • mechanical/ chemical irritation of mucosa
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13
Q

how do DISTAL colonic cells secrete K+ (ability is NOT present in intestinal cells)

A
  • Na+ enters cell via apical membrane from lumen (process can be upregulated by aldosterone)
  • increase in Na+ within cell creates electrochemical potential -> allows K+ to be secreted at apical membrane via K+ channels -> into lumen
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14
Q

2 routes for intestinal absorption

A
  • transcellular -> electrolytes, nutrients; higher transepithelial resistance (2 membranes involved) and usually active processes are needed
  • paracellular -> lower resistance & molecules flow through tight junctions (junctions are looser at duodenum and become tighter [less permeable] down the GI tract)
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15
Q

substances that are reabsorbed at small intestines (6)

A
  • water
  • nutrients (glucose, amino acids)
  • Na+ (thus H2O)
  • CO2
  • Cl-
  • K+
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16
Q

how does water reabsorption occur in small intestines & what is an effect of water reabsorption

A
  • coupled to solute movement -> absorption of water is controlled by amount of electrolyte & nutrients (mainly glucose, Na+) absorbed
    *water usually moves PARACELLULARLY

effect:
- solvent drag phenomenon -> eg K+ will be reabsorbed along with water

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17
Q

how are nutrients absorbed into small intestines

A

TRANSCELLULAR
secondary active transport
- presence of NaKATPase at apical membrane pumps Na+ out of cell -> create Na gradient from lumen
- SGLT: Na-glucose cotransporter allow absorption of glucose with Na+ into cell

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18
Q

how is Na+ reabsorbed in small intestine (2)

A

TRANSCELLULAR
- Na-glucose cotransporter
- Na-H antiport on apical membrane -> absorb Na+ in exchange for H+ secretion

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19
Q

how is HCO3-/CO2 reabsorbed into small intestine

A

TRANSCELLULAR
- Na-H antiport secretes H+ into lumen -> H+ combines with HCO3- in lumen to form CO2 -> diffuse back into cell and into blood

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20
Q

how is Cl-reabsorbed in small intestine

A
  • through PARACELLULAR junction
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21
Q

how is K+ reabsorbed in small intestine

A

PARACELLULAR
- moves via solvent drag -> dragged along with water paracellularly as it is dissolved in water

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22
Q

substances that are reabsorbed at large intestine/ colon

A

PROXIMAL COLON
mainly
- H2O
- electrolytes (Na, Cl)

some
- CO2

DISTAL COLON
mainly
- Na+
**K+ secretion

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23
Q

how are electrolytes absorbed at PROXIMAL colon

A

TRANSCELLULAR
- electroneutral NaCl absorption -> absorbs Na along with Cl

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24
Q

how is water absorbed at PROXIMAL colon

A

coupled to solute movement
- Na+ and Cl- generate osmotic gradient -> water reabsorbed PARACELLULARLY

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25
Q

how is CO2 absorbed at PROXIMAL colon (same as small intestine)

A

TRANSCELLULAR
- Na-H antiport secretes H+ into lumen -> combine with HCO3- to form CO2 -> diffuses though cell back into blood

26
Q

how is Na+ reabsorbed at DISTAL COLON

A
  • Na+ moves into distal colon via electrogenic sodium pump (controlled by aldosterone)
  • allows secretion of K+ afterwards by creating electrochemical gradient
27
Q

how is iron absorbed in small intestine (2)

A

HEME
- absorbed by heme transporter -> broken down to Fe2+ in enterocyte

Fe3+
- reduced to Fe2+ by ferric reductase -> absorbed by DMT1

28
Q

what happens to Fe2+ in enterocytes (2)

A
  • converted to Fe3+ and stored in enterocyte as Fe3+-ferritin
  • transported through ferroportin into blood
29
Q

how is iron absorption regulated (high iron stores -> less absorption; vice versa)

A

HEPCIDIN
- reduces ferroportin activity
- high iron stores -> liver increases hepcidin production -> reduce ferroportin & iron movement into blood
- Fe3+ - ferritin stores build up in enterocyte (iron is trapped in enterocyte) -> enterocyte eventually gets shed -> Fe stores disappear

30
Q

how is Vitamin B12 (cobalamine, CBL) absorbed in small intestines?

A
  • CBL is initially bound to proteins in food -> pepsin in stomach releases CBL -> CBL binds to haptocorrin (secreted by gastric glands, protects CBL from degradation)
  • gastric parietal cells secrete IF (intrinsic factor) which follows CBL-haptocorrin into small intestine
  • pancreas secrete protease into small intestine -> degradation of haptocorrin -> IF-CBL complex forms
  • IF-CBL absorbed at ILEAL enterocytes -> endocytosis and degradation to release CBL
31
Q

how are carbohydrates digested in small intestines (2)

A
  • LUMINAL salivary & pancreatic amylase
  • MUCOSAL disaccharidases (on brush borders of enterocytes)
32
Q

products of luminal digestion by amylase in small intestine

A
  • maltotriose (3x glucose)
  • maltose
  • a-limit dextrins (contain a-1,6 linkages, cannot be broken down by amylase
33
Q

what are the mucosal disaccharidases present on brush border of enterocytes (3) + their functions

A

sucrase-isomaltase (2 enzymes attached tgt)
- isomaltase splits a-limit dextrins, maltose, maltotriose
- sucrase splits sucrose, maltose, maltotriose

lactase
- splits lactose

glucoamylase
- splits maltotriose, maltose

34
Q

how are glucose and galactose molecules transported across apical membrane

A

SGLT
- sodium linked glucose transporter (secondary ACTIVE transport) -> cotransport glucose/ galatose with help of Na+ concentration gradient

GLUT5
- glucose transporter (facilitated transport/ passive diffusion) -> transport fructose down concentration gradient (maintained as fructose is rapidly metabolised into glucose & lactic acid upon entering cell)

35
Q

how do the sugars absorbed from intestinal lumen enter the blood?

A

GLUT 2
- on basolateral membrane of enterocyte -> transport glucose/ fructose/ galactose into blood via FACILITATED DIFFUSION (concentration of sugars are much higher within enterocyte)

36
Q

how are proteins digested in small intestines (3)

A
  • LUMINAL gastric pepsin (from stomach), pancreatic protease
  • MUCOSAL enterocyte peptidases (found brush border of enterocytes)
  • INTRACEULLAR peptidases
37
Q

how are proteins absorbed by small intestines

A
  • gastric & pancreatic peptidases + mucosal enterocyte peptidases -> breaks down proteins into 1) tripeptides 2) dipeptides 3) amino acids

tripeptides & dipeptides:
- absorbed via H+ cotransporter (PEPT1)

amino acids:
- absorbed via Na+ cotransporter

38
Q

what happens to tripeptides & dipeptides inside enterocytes

A
  • digested to form amino acids

*amino acids are then transported out through basolateral membrane by Na+-independent AA transporters (at least 3 distinct transporters present for diff AA groups)

39
Q

how are dipeptides/ tripeptides absorbed into the cell

A
  • NHE secretes H+ into intestinal lumen in exchange for Na+
  • H+ is coupled with di-, tri peptides and absorbed into cell via PEPT1 (peptide transporter 1)
40
Q

are di-, tripeptides OR amino acids more easily absorbed at apical membrane?

A
  • di-, tripeptides as PEPT1 more efficient
41
Q

how are whole proteins absorbed

A
  • endocytosis of proteins by enterocyte/ M cells
  • some are degraded while others exit basolateral membrane as whole proteins
42
Q

what is emulsification

A
  • breaking down of fat globule into fat/ emulsion droplets
43
Q

characteristic of bile that helps with emulsification

A
  • amphipathic -> can surround fat droplets while hydrophilic sites face out and hydrophobic sites face inwardds
44
Q

what causes intragastric digestion of fats (2)

A
  • gastric lipases (20-30%) -> intragastric lipolysis
  • lingual lipases (from saliva)
45
Q

what causes luminal digestion of fats

A
  • emulsification
  • lipolysis by gastric lipase (pH4.5-6, majority inactive in stomach); PANCREATIC lipase (pH>7)

*pancreatic lipase is enhanced by colipase

46
Q

types of pancreatic lipase

A
  • glycerol ester hydrolase (MAIN)
  • cholesterol esterase
  • phospholipase A2
47
Q

how is glycerol ester hydrolase activated

A
  • binds to colipase to form complex -> has better access to lipids in emulsion & micelle + exposes active site of lipase to substrate + target fat water interface

*bile acids wrap around fat droplet and prevents glycerol ester hydrolase from breaking fat down -> colipase opens up the bile acid covering

48
Q

what are fat droplets broken down into by lipase?

A

micelle
- extremely hydrophobic materials (eg cholesterol) are stored within interior of micelle
- requires minimum amount of bile salts to be formed

49
Q

how are micelles absorbed

A
  • diffusion through unstirred water layer (possible as bile salts are hydrophilic) -> RATE LIMITING STEP
  • micelle reaches enterocyte and lipid content is rapidly removed once contacted with microvilli
50
Q

what proportion of lipids are absorbed

A
  • almost all (>95% for triglycerides) -> fat in stools is from colonic bacteria & desquamated intestinal cells
51
Q

where are bile salts reabsorbed

A

terminal ileum (receptor mediated process)

52
Q

where are SCFA (short chain fatty acids) found, eg acetate, propionate, butyrate

A
  • not dietary
  • synthesized by bacteria -> PRIMARY nutrient for colonic epithelial cells
53
Q

what does absorption of SCFA by colon stimulate?

A
  • Na & water absorption at colon (SCFA is water soluble)
54
Q

absorption of medium chain fatty acids (C6-12)

A
  • more water soluble thus micelle formation is unnecessary
  • esters are absorbed directly (hydrolysis not needed)
  • MFCA are more efficiently absorbed
  • NO NEED re esterification and chylomicron formation for absorption
  • exits via portal blood (unlike long chain fatty acid, too long to enter blood)
55
Q

absorption of long chain fatty acids (LCFA)

A
  • post-absorptive handling (re-esterification)
  • drains into lymphatic duct, thoracic duct then systemic circulation
56
Q

why is post-absorptive handling required for long chain fatty acids

A

LCFA cannot dissolve in blood -> needs to be re esterified and drained via lymphatics

57
Q

process of post-absorptive handling

A

occurs in epithelial cell of small intestine
- fatty acid components (cholesterol, mono glyceride, fatty acids) are re-esterified into cholesterol esters/ phospholipids/ triglyceride -> grouped together to form CHYLOMICRON
- chylomicron is exocytosed into extravascular space -> drains into lymph node -> thoracic duct -> systemic circulation

58
Q

what are the nutrients absorbed at different parts of the small intestine

A

Proximal small intestine
- fat, sugar, peptides & amino acids, iron, folate, Ca, water and electrolytes

Middle small intestine
- sugar, peptides & amino acids, Ca, water and electrolytes

Distal small intestine
- bile salts, Vit B2, water & electrolytes

Colon
- water & electrolytes

59
Q

tissue permeability of small intestine & large intestines to water

A

Jejunum:
- leaky (HIGHH fluid reabsorption)

Ileum:
- moderately leaky (HIGHH fluid reabsorption)

Cecum
- moderately tight (LOW fluid reabsorption)

Colon
- tight (HIGH fluid reabsorption, although no where as high as jejunum/ ileum)

60
Q

potential difference of small intestines & large intestine

A

jejunum < ileum < cecum < colon
- tighter epithelial cells -> greater potential difference when ions are reabsorbed

61
Q

absorptive mechanisms of water in small intestines & large intestines

A

Jejunum:
- Na-nutrient
- Na-H+

Ileum:
- Na-Cl
- Na-nutrient
- Na-bile acid

Cecum:
- Na+
- SCFA

Colon:
- Na-Cl
- SCFA

62
Q

reasons for diarrhea (4)

A

HYPERMOTILITY of intestine (inflammation)
- less absorption time

HYPEROSMOLARITY
- unabsorbed nutrients (eg vit B12 malabsorption, excess lactose in lactose intolerance)
- osmotic, malabsorption

LOSS OF ABSORPTIVE CAPACITY
- loss of villi, loss of length (eg resection)
- malabsorption

ENHANCED SECRETION OF WATER & ELECTROLYTES
- secretory diarrhoea
- bacterial toxins – cholera, E. coli, Clostridium difficile
- tumours – VIP, carcinoid

Gastro (20 decks)

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