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Physiology > Digestion & Absorption 1 > Flashcards

Digestion & Absorption 1 Flashcards

1
Q

Define digestion.

A

Breakdown of complex large molecules into smaller simpler molecules

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2
Q

Define absorption.

A

Transport of small molecules through cell membs into blood or lymphatic capillaries

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3
Q

What are the 2 mechanisms that enzymes operate by?

A

-Lock and key model -> both enzyme & substrate have a specific configuration & unique shape that fit together

-Induced fit model -> substrate induces enzyme to adopt the form of substrate - enzymes are flexible & favour geometric adoption for binding & catalysis of substrate

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4
Q

Role of enzymes?

A

Cleavage - split large/complex molecules into smaller/simpler molecules

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5
Q

What do proteins, fats & carbohydrates break down to (by the action of enzymes)?

A

-Prots = AAs
-Fats = FAs & glycerol
-Carbs = monosaccs (glu, gal, fru)

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6
Q

Components of the digestive tract?

A

-Mouth
-Oesophagus
-Stomach
-Small intestine
-Large intestine

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7
Q

Name the components of the GI tract.

A

-Mouth
-Oesophagus
-Stomach
-Small intestine
-Large intestine
-Anus

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8
Q

Name the accessory organs - associated with alimentary tract.

A

-Salivary glands
-Liver
-Gallbladder
-Pancreas

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9
Q

Name the x2 processes occurring in mouth - involved in digestion.

A

-Mechanical digestion
-Chemical digestion

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10
Q

What is mechanical digestion?

A

-In mouth
-Chewing/mastication

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11
Q

x3 functions of mastication?

A

-Reduce size of ingested particles –> inc. SA
-Mix food w/ saliva -> lubricates & exposes to digestive enzymes
-Prevents damage to lining of pharynx & oesophagus

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12
Q

What is chemical digestion?

A

-In mouth
-Mixing ingested particles w/ saliva -> which contains enzymes

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13
Q

What x2 enzymes are involved in chemical digestion - found in saliva!?!

A

-α-amylase
-Linguinal lipase

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14
Q

Role of α-amylase?

A

-Breaks down carbs –> going from polysaccs to di & tri - saccharides
-Cleaves internal α-1,4-glycosidic bonds in starch
–> produces:
maltose
maltotriose
α-limit dextrins

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15
Q

Role of linguinal lipase?

A

-Breaks down fats
-Hydrolyses dietary lipids - by hydrolysing ester bonds

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16
Q

Outline basic role of lipase.

A

-Hydrolyses triglycerides
-Uses x2 H2Os - to break x3 ester bonds
-Forms x1 glycerol & x3 FAs

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17
Q

Outline basic role of amylase.

A

-Hydrolyses starch
-Uses water molecule - to hydrolyse α-1,4 linkages in polysaccharides into limit dextrins & maltose by addition of a water molecule

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18
Q

x3 regions of oesophagus?

A

-Cervical
-Thoracic
-Abdominal
(getting progressively lower - nearer to stomach than mouth)

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19
Q

Mechanism oesophagus uses to pass food from mouth to stomach?

A

Peristalsis

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20
Q

What is peristalsis?

A

Involuntary contraction & relaxation of longitudinal & circular muscles

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21
Q

Name x2 important features in oesophagus that prevent reflux of food/control movement of food into & out of oesophagus?

A

-Upper oesophageal sphincter
-Lower oesophageal sphincter

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22
Q

How much gastric juice does stomach produce per day?

A

2 L

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23
Q

pH of stomach?

A

pH 1-3.5 = acidic

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24
Q

Purpose of acidic environment of stomach?

A

-Break down food - proteins
–> by activating pepsinogen to the enzyme pepsin
-Activates enzyme
-Denature proteins
-Kills bacteria entering stomach

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25
Q

What are the 5 constituents of gastric juice?

A

-Intrinsic factor
-H+
-Pepsin
-Mucus
-Water

26
Q

Purpose of mucus in gastric juice?

A

-Lubricant
-> protects mucosa/wall of stomach from damage
-Mucus + HCO3- (bicarbonate ions) = neutralises acid - maintains surface of mucosa at higher pH (closer to neutral)

27
Q

Purpose of water in gastric juice?

A

-Medium for action of acid & enzymes
-Solubilises many food consituents

28
Q

Purpose of intrinsic factor in gastric juice?

A

-Glycoprot.
-Produced by parietal cells
-Vitamin B12 binds to IF -> forms IF-Cbl complex –> so IF important for absorbing B12 by ileum
–> vitamin B12 = vital micronutrient

29
Q

Describe the mechanism of stomach acid secretion.

A

-Gastrin secreted by G cells
-Gastrin binds to CCK2 receptors on parietal cell
-ACh secreted by parasymp NS
-Gastrin & ACh activate Phospholipase C (PLC) which is found in parietal cell
-PLC catalyses formation of inositol triphosphate (IP3)
-IP3 causes release of intracellular Ca2+ & activates calmodulin kinase
-Calmodulin kinases phosphorylates a variety of proteins leading to H+ secretion

-Gastrin released by G cells
-ECL cells have CCK-2 receptors for gastrin
-Gastrin stimulates ECL cells to release histamine
-Histamine binds to parietal cells & activates adenylate cyclase (AC) to form cAMP
-cAMP activates protein kinase A
-Protein kinase A phosphorylates a variety of proteins leading to H+ secretion

—> x2 mechanisms of H+ secretion - both lead to phosphorylation of proteins that leads to H+ secretion!!!

(H+ is produced by he break down of water:
HOH -> OH- + H+)
–> H+ is actively pumped into gastric lumen across the mucosal memb via the gastric K+/H+ ATPase pump
-K+ in exchange is pumped into parietal cell from lumen
-Cl- enters parietal cell across basolateral memb in exchange for HCO3- into blood
(HCO3- come from: OH- from water breakdown & CO2: OH- + CO2 -> HCO3-)
-Cl- pumped into gastric lumen

*So H+ & Cl- both in gastric lumen together:
H+ + Cl- -> HCl

(((H2O + CO2 -> H2CO3
then…
H2CO3 -> H+ + HCO3-)))
or
(((H2O -> OH- + H+
then…
OH- + CO2 -> HCO3-)))
Either way -> end up with H+ & HCO3-

30
Q

Describe process of protein digestion in stomach.

A

-Prot stimulates G cells to release gastrin into blood (ACh stimulates gastrin release)
-Gastrin binds to CCK2 receptors of ECL cells & stimulates ECL cells to release histamine
-Histamine stimulates parietal cells (acid producing cells)
-Gastrin ALSO stimulates parietal cells to release HCl & stimulates chief cells to release pepsinogen (an endopeptidase)
-Acid/HCl -> activates pepsinogen - converting it to pepsin
-Pepsin cleaves prots

31
Q

Structure of gastric glands?

A

-Gastric mucosa is made up of pits & glands
-> lined by mucus or surface ep cells
-At base of the pits are gland openings
-> project into mucosa towards serosa

*Pits = openings on ep
*Glands = invaginations/projectiosn in mucosa towards serosa

Cells making up gastric glands
-Normal ep cells = simple columnar
-Regenerative cells - prolif into any other of thse cell types
-Mucous neck cells = secrete mucus (neutralises HCl)
-Parietal cells = secrete HCl
-Chief cells = secrete pepsinogen (inactive)
-Enterochromaffin cells (a type of enteroendocrine cell) = secrete histamine (stimulated to do so by gastrin)
-G cells = secrete gastrin
-D cells = secrete somatostatin

32
Q

Protein digestion mechanism operates by -ve feedback
-> so how is it inhibited & why?

A

-Low antral pH (lower region of stomach)
-Causes D cells to release somatostatin
-Somatostatin inhibits G cells from releasing gastrin…
–> this prevents over secretion of acid (HCl)

33
Q

Summarise the different secretory cells in stomach.

A
34
Q

Describe the digestion of dietary fats in the stomach?

A

-Neurohormonal stimuli (e.g., gastrin & cholinergic mechanisms) stimulates…
-Chief cells in fundus - secrete gastric lipase
-Gastric lipase hydrolyses ester bonds in triglycerides (x3 H2O break x3 ester bonds) = x3 FAs + x1 glycerol (from triglycerides)

35
Q

Describe the digestion of carbohydrates in stomach?

A

(Salivary amylase has been denatured due to acidic pH in stomach = no enzymes available to break down starch)
-Mechanical breakdown of carbs = ongoing
-Strong peristaltic contractions of stomach - mix carbs into uniform mix of chyme

-Gastric HCl hydrolyses SMALL amount of sucrose -> fructose + glucose

36
Q

Describe mechanical digestion in the stomach?

A

-Food mixes w/ gastric juices
-Peristaltic contractions of stomach wall churns contents
**Mixing wave = type of peristalsis = mixes & softens food w/ gastric juices -»»> CREATING CHYME!!!
-Propulsion = forward motion of contents
-Retropulsion = backward motion of contents

–> Food broken down into smaller pieces

37
Q

Describe the process of gastric emptying?

A

-Stomach holds food ~4-6 hrs
-Peristaltic contractions increase in strength
-Some liquid chyme passes pyloric sphincter -> into duodenum
-Only particles 1mm3 or smaller emptied

38
Q

What is the small amount of absorbed products in stomach?

A

Non-polar substances -> e.g., alcohol & aspirin

39
Q

What biochemical molecule empties out stomach fastest?

A

Carbs

40
Q

What part of stomach is duodenum continuous with?

A

Pylorus

41
Q

What does the SI lead to in colon?

A

Ostium ileale

42
Q

What ducts enter duodenum?

A

-Common bile duct
-Pancreatic duct

43
Q

What occurs in SI -> absorption & digestion??

A

Final breakdown/digestion of carbs, prots, fats (which was started in stomach - or even mouth for carbs!)

44
Q

Structure of SI epithelium?

A

Crypts of Leiberkuhn = invaginations of ep around the villi

45
Q

What cells make up the crypts of Leiberkuhn of the SI?

A

-Regenerative cells = prolif to become any of these cell types
-Paneth cells = release bacteriotoxic peptides & some growth factors
-Enterocytes = absorbative cells -> form brush border of microvilli
-Enteroendocrine cells = release signalling molecules (e.g., CCK & motilin hormones)
-Goblet = secrete mucus into lumenal (ext) side

46
Q

Role of enterocytes?

A

-Make up brush border - microvilli
-Contain brush border enzymes tethered to microvilli - to complete enzymatic digestion of nutrients
-Release absorbed materials: ions, water, sugar, peptides, lipids -> to serosal (int) side

47
Q

Role of goblet cells?

A

-Secrete mucus - to lumenal (ext) side
–> acts as protective barrier

48
Q

Role of enteroendocrine cells?

A

-Release signalling molecules - e.g., CCK & motilin hormones
–> coordinate & regulate activities of digestive system

49
Q

Role of paneth cells?

A

-Release bacteriotoxic peptides & some growth factors
-Vital part of innate imm syst -> antimicrobial peptides called defensins - contributing to host defense against microbes in SI

50
Q

Mechanism within duodenum that inhibits gastric emptying?

A

-Intestinal recs in duodenum activated when chyme enters duodenum
-Triggers:
*CCK = inc. distensibility of orad stomach
*Acid = inhibits motility & emptying
*Other hormones - secretin, gastric inhibiting peptide (GIP) - inhibits emptying

–> causes liver & gall bladder to release bile & pancreas to release digestive enzymes (trypsin, lipase, amylase)

51
Q

Describe how carbohydrates are digested in SI?

A

-Pancreatic amylase - after secretin & CCK secretions
–> hydrolyses starch to maltose, maltotriose & α –Limit dextrins

-Brush border enzymes
-> hydrolyse oligosaccs & disaccs

52
Q

Name the brush border enzymes.

A

-Lactase – lactose -> glucose and galactose
-Sucrase – sucrose -> glucose and fructose
-Isomaltase – α1,6 bonds of limit dextrins
-Maltase – Maltose -> glucose and glucose

53
Q

Describe fat digestion in SI?

A

-Bile - acts as an emulsifier = increases the surface area
-Lipase action = lipids -> fatty acids and glycerides
-Bile salts envelop the fatty acids and monoglycerides-> micelles
-At the brush border of the small intestine the fatty acids and monoglycerides diffuse out of the micelles into the absorptive cells

54
Q

Describe protein digestion in SI?

A

-Proteases (e.g. trypsin, chymotrypsin) - exopeptidase
-Brush border enzymes (peptidases) hydrolyse to dipeptides and amino acids for absorption

55
Q

What is absorbed in SI?

A

*Simple sugars
-Glucose
-Fructose
-Galactose

*AAs

*Na+

56
Q

How does absorption occur in SI?

A

-Simple sugars & AAs - absorbed by enterocytes
-Absorbed nutrients moved into circulation by blood capillaries & lacteals OR lymph channels

Glucose uptake
1-SGLT1 carrier used
-Transport 2Na+ & glu - from lumen of SI into ep cell -> moving Na+ provides energy to move glu against its conc grad = CO-TRANSPORT - SECONDARY ACTIVE TRANSPORT
2- GLUT2 carrier used
-Glu then moves by fac diff into interstitial space

Fructose uptake
1- GLUT5 carrier used - fac diff from lumen of SI into ep cell
2- GLUT2 carrier used
-Fructose then moves by fac diff into interstitial space

Na+/K+ pump maintains conc grad of Na+ for co-transport with glu!
-3Na+ (COUNTER TRANSPORT - SECONDARY ACTIVE TRANSPORT) - from ep cell into interstitial space - keeps Na+ conc low in ep cell - so can be pump glu via FD
-2K+ from interstitial space into ep cell

X2 TYPES OF SECONDARY ACTIVE TRANSPORT:
-CO-TRANSPORT
-COUNTER TRANSPORT

57
Q

What structural features of SI enable efficient absorption in SI?

A

-Folds called “plicae circulares”
-Villi
-Microvilli

58
Q

Purpose of LI in dig/ab?

A

-Storage & elimination of remaining waste
-Peristalsis is slower -> pushes waste material towards anal end of tract (to rectum then anus)
-Absorption of water & electrolytes (K+, Na+, Cl-)
**NO DIGESTIVE ENZYMES!!!

59
Q

What is a sort of form of digestion occurring in LI?

A

Bacterial flora
-> aid in digestion of of non-digestible carbs (including dietary fibre & undigested carbs)

-This is via anaerobic fermentation by colonic bact

-Methane & H2 = produced

-Bact make vitamin K - is then absorbed

60
Q

What are the x2 types of (dietary) fibre?

A

-Soluble - slows transit time - e.g., pectins from fruit/veg, hemicelluloses from cereals

-Insoluble - draws water into stool = soften & increase faecal weight = improved bowel movement consistency & speed up transit time e.g. cellulose from plant material

Physiology (10 decks)

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