Digestion and Absorbtion Flashcards

1
Q

what are the two seemingly paradoxical tasks of intestinal epithelial barrier tissue?
what are the cell types here?
what are 4 features of ^ of their cytoskeleton proteins?

A
  • *intestinal epithelial barrier (IEB)** has two paradoxical tasks:
  • enable absorption of nutrients (permeable)
  • control passage of pathogens (impermeable

due to enterocytes (highly specialised cells of intestinal lining) having specialised cytokskeleton proteins:

a) brush border - increase SA for absorb
b) tight junctions - to be impermeable to toxins
c) polarity complexes (lets the cell know whats inside / outside)
d) lots of ECM to hold them in place

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2
Q

surface area of skin v mucusoa?

A

skin - 25m2
mucosae - 32m2 - 95% of absorption of nutrients occurs in the small intestine

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3
Q

why does the small intestine absorb the most?

A
  • *Anatomical features** make the small intestine so specialised for absorption. The human small intestines have the surface area of a studio apartment **(between 30 and 40 square meters).
  • intestine has folds:villi& the cells inside the villi containmicrovilli**
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4
Q

how are cells made in villus?

A

at the crypt:
- stem cells make new cells - differentiate into enterocytes and other intestinal cells like goblet cells

  • get pushed up to the top of villus and die: microbiome feed on dead cells
  • whole process is very dynamic
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5
Q

what specifically is absorbed in the ileum? (5)
and the colon (3)?

A

ileum

  • water
  • Na+
  • B12
  • intrinsic factors
  • bile acids

colon

  • water
  • **electrolytes
  • **bile acids (less)
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6
Q

what is the difference in the structure of colon and small intestine/

A

small intestine: villus & crypts

colon: no villus & crypts

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7
Q

explain what the 3 different phases of digestion?

A
  1. luminal phase: - ingested food broken down by:
    - acid in stomach
    - alkali in small intest.
    - substrate specific enzymes from gastric, small bowel mucosa & pancreas
  • *2. mucosal phase:**
  • pre-digested nutrients are taken up by brush border membrane of enterocytes and enter
  • *3. post absorptive:** nutrients absorbed via
  • lymphatics
  • portal circulation
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8
Q

why is water needed in the digestive system? (4)

A
  • Hydrolysis reactions of digestion
  • Facilitation of absorption (brings products of digestion into close proximity to microvilli)
  • Facilitation of propulsion of gut contents
  • Combination with mucin granules to make mucus
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9
Q

explain luminal, mucosal and post absorptive phases of carb digestion

A
  • *luminal phase:**
  • carboyhydates: enzymes secreted by saliva and pancreas = disaccaharides + limit dextrins

mucosal phase:
- brush border enzymes: sucrase, lactase, maltase, limit desxtrinase, glucoamylase break down molecules into glucose and galactose
- glucose and galactose enter epithelial cells via Na linked secondary transport acorss apical membrane using SGLT1
- fructose enters by fac. d.

post absorptive phase
- The sugars exit the cells across the basolateral membrane by facilitated diffusion to the portal vein - GLUT 1/2
(
The Na/K ATPase pump drives the entrance of the sugars into the blood capillary. It will be drained to the portal vein, straight into the liveR)

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10
Q

explain luminal, mucosal and post absorptive phases of llipid digestion

A

luminal phase
- mouth: lingual lipases
-
stomach:gastric lipases
- pancrease: pancreatic lipase bile salts & bile salts
= triglycerides -> free fatty acids & monoglycerides. then form micelles (contain fat soluble vitamins and cholesterol)

  • *mucosal phase:**
  • simple diffusion (bc membrane of enterocytes are also lipids - so can just diffuse through)
  • within enterocytes: molecules are reassembled by GA = chylomicrons
  • *post absorptive phase:**
  • chylomicrons secreted across basolateral membrane, but are too big to enter blood: enter lympahtic fluid
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11
Q

what is role of bile salts
what is the enterohepatic circulation?
(why bad if doesnt work)

A

bile salts: cause emulsification: breaking down of fat globules into smaller droplets

Enterohepatic circulation: recycling of bile salts

  • liver: makes bile salts
  • stored in gall bladder
  • goes into duodenum: help digest fats
  • reabsorbed in ileum
  • bulk of bile salts are absorbed in liver
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12
Q

how do commensal bacteria regulate digestion?

what happens if we have bacterial overgrowth?

A

dynamic equilibrium between diet-gut microbiome-bile acid pool size:

normally - we have conjugated bile acids, created by liver. Conjugated bile acids (primary bile acids): more efficient in emulsifying fats because at intestinal pH they become more ionized than the unconjugated bile acids.

Commensal bacteria: participate in the synthesis of bile acids. Microbial enzymes de-conjugate bile acids & make them less effecient: (secondary bile acids).

so we have a pool of primary and secondary bile acids: if have bacterial overgrowth in gut: form too much secondary bile acids = struggle to digest fats

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13
Q

explain luminal, mucosal and post absorptive phases of protein digestion

A

luminal phase
- stomach: pepsin released by pepsinogen (zymogen / proenzyme). pepsinogen is activated by HCl, which is releaed from parietal cells in the gastric pits.
- small intestine: further digestion from pancreatic enzymes

mucosal phase:
- brush border enzyme: enterokinase converts trypsinogen -> trypsin
then:
trypsin activates:
a) chymotrysinogen -> chymotrypsin
b) procarboxypetidae -> carboxypeptidase

  • a.a. enter the epithelial cells via Na-linked secondary active transport across the apical membrane (same system for sugar)
  • *post-absorptive phase;**
  • a.a. transporte across basolateral membrane by fac. d
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14
Q

** why do vitamins need to be absorbed from the food?

what are two type of vitamins?
how are each absorbed?^
into which system are they absorbed? **

A

vitamins cant be manufactured by body

1. fat soluble vitamins: A, D, E & K

  • absorbed with lipids: readily dissolve in **lipid droplets, micelles and chylomicrons
  • absorbed into lymph fluid**

2. water soluble vitamins: B & C

  • follow flux of water (B&C)
  • absorbed into portal vein
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15
Q

B12 can be only observed where? & what must it first be complexed with?

what is B12 aka?

describe the absorptive pathway of B12 :)

A
  • B12: absorbed only in terminal ileum, after being complexed with stomach-derived intrinsic factor
  • B12: aka cobalamin

absorptive pathway:

  • bound to dietary protein
  • first dissociated by HCl and pepsin, in stomach
  • reattaches itself via haptocorrin (from saliva thats now in stomach)
  • dissociated from haptocorrin and binds with stomach-derived intrinsic factor
  • absorbed only in terminal ileum in enterocytes (although 60-80% still goes into faeces)
  • *-** reassociates with transcobalamin and then goes to portal circulation
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16
Q

if you have an issue with terminal ileum - what can you predict is going to have malabsorbtion?

A

B12

17
Q

*important*

A
18
Q

causes of general malabsorption come from diseases of which body parts ? (2) e.g.? (3)

A

most commonly: small intestine diseases - e.g. coeliac disease, crohns disease, post-infectious malabsortion
also: pancreatic diseaess

19
Q

most common cause of malabsorption in developed world is = ?
most common cause of malabsorption in developing world is = ?

A

developed world = coeliac disease

developing world = post-infectious malabsoprtion and tropical spure

20
Q

what causes coeliac disease? - what isoform do they have? which 3 antibodies this this create?

what does it cause in the cells ? (3)

A
  • *coeliac disease:**
  • *- autoimmune disease**
  • (95% of CD) have isoform of DQ2 or DQ9 of human leukocyte antigen (HLA) HLA-DQ protein
  • due to HLA-DQ, get high levels of antibodies: antigliadin, tissue transgluataminase, antiendomyisial

causes

  • complete villi atrophy
  • marked crypt hyperplasia (bc trying to replace the villi, which are being replaced)
  • major inflammation
21
Q

what is specifc malabsorbtion? give two examples of things that are a specific malabsorbed lol

A
  • failure of process governing absorption of one class or type of nutrient
  • e.g B12 or dissacharide sugars
22
Q

dissacharidase deficiences are mostly what?

A

mostly genetic - e.g. most of world is lactose intolerent

23
Q

what do mutations in:

  • LCT gene
  • SLC5A1 gene

cause?

which phase of digestion they effect?

A

mutation in gene LCT - affects _mucosal phase o_f dissachardide absorption. lactose intolerance

gene SLC5A1 - encodes for Sodium dependent GLucose tranpsorter one: SGLT1. so mutation causes glucose-galactose malabsorption. again: mucosal phase

24
Q

why do unabsorbed dissacharides cause diarrhoea? (2)

A

add to the osmotic load of the colon
AND
sugars get fermented - causes gaseous distension (e.g. H2) :(