W2 Physiology: lipid digestion and absorption of calcium, iron and vitamins Flashcards

1
Q

what is emulsification and how does it occur

A
  • When solid fats and oils are converted into an emulsion of small oil droplets suspended in water
    1. mouth (chewing)
    2. Gastric churning with enzyme and squeezing through pylorus
    3. segmentation and peristalsis in SI mixing chyme with pancreatic and biliary secretions
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2
Q

how are emulsification droplets stabilised?

A

by the addition of amphiphilic coat

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3
Q

Contents of amphiphilic coat

A

Products of lipid digestion eg monoglyceride
cholesterol
biliary phospholipid
bile salts (when droplets are reduced to unilamellar mixed micelles)

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4
Q

Process of digestion of fats

A
  1. mouth- lingual lipase
  2. Gastric phase- gastric lipase
  3. Duodenum- pancreatic (TAG) Lipase
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5
Q

what triggers production of gastric lipase?

A

gastric lipase is secreted in response to gastrin release from chief cells

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6
Q

optimum pH of gastric lipase

What is gastric lipase resistant to?

A

ph4

pepsin

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7
Q

why is gastric lipase inactive in the duodenum

A

digestion by pancreatic protease and unfavourable pH

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8
Q

where are short and medium chain FA absorbed?

A

stomach

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9
Q

which cells secrete pancreatic lipase

What is this triggered by

A

acinar cells of pancreas

in response to CCK which also stimulate bile flow

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10
Q

what substances and conditions does full activity of pancreatic lipase require

A

colipase co-factor, alkaline pH, Ca2+, bile salts, fatty acids

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11
Q

where is bile salt released from and what into?

A

bile salt is released from the gall bladder into the duodenum

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12
Q

what is the release of bile salt triggered by

A

CCK

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13
Q

function of bile salts

A
  • act as DETERGENTS to help emulsify large lipid droplets to small lipid droplets
  • increases SA for pancreatic lipase to act
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14
Q

describe the structure of bile salts

A

AMPHIPATHIC

hydrophilic and hydrophobic parts

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15
Q

result of failure to produce bile salts

A
  • lipid malabsorption, steatorrhea (fatty faeces)

- secondary vitamin deficiency (A,D,E,K)

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16
Q

why may someone have steatorrhea

A

failure to produce bile salts- lipid malabsorption

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17
Q

problem that bile salts present and how this is solved

A

block access of lipase enzyme to TAG

colipase from the pancreas binds to bile salts and lipase allowing access to tri- and di-acylglycerols

18
Q

is colipase directly secreted as itself from the pancreas?

A

no

colipase is secreted as inactive procolipase then activated by trypsin

19
Q

what are the final products of lipid digestion stored in

A

mixed micelles

20
Q

methods by which mixed micelles can enter enterocyte

A

passive diffusion
membrane fatty acid translocases
fatty acid binding protein
fatty acid transport protein

21
Q
  • size of short chain and medium chain FA

- how short chain and medium chain FA pass through enterocyte

A
short chain (<6), medium chain (8-12)
diffuse through enterocyte, exit through basolateral membrane and enter villus capillaries
22
Q

size of long chain FA

what happens to the long chain FA

A

> 12

long chain FA and monoglycerides are resynthesised into triglycerides in ER and incorporated into chylomicrons

23
Q

how are chylomicrons formed?

what then happens to chylomicron

A
  • triglycerides are formed in ER by monoglyceride and long FA
  • cholesterol added and phospholipid synthesis
  • APO-B 48 added to from chylomicron
  • chylomicron exits enterocyte by exocytosis and enters the central lacteal then carried in lymph vessels to systemic circulation via thoracic duct
24
Q

transport of cholesterol absorption

A

endocytosis in clatherin coated pits by NPC1L1

25
Q

action of ezetimibe and what is it used for

A
  • binds to NPC1L1 preventing internalisation and cholesterol absorption
  • used in conjunction with statins in hypercholesterolemia
26
Q

transport in Ca2+ absorption

which is the main one?

A

passive and active (mainly active)

27
Q

what is action calcium absorption regulated by?

A

1,25-dihydroxyvitamin D3 and parathyroid hormone

28
Q

what does long term iron balance in the body depend on

A

Absorption of iron across the duodenum

29
Q

Form of Dietary iron and daily requirement

A

Fe3+

12-15mg (5-10% absorbed)

30
Q

what can iron deficiency cause

A

microcytic anaemia

31
Q

effect of excess of dietary iron

A

toxic to pancreas, heart, liver

32
Q

can Fe3+ be transported across enterocyte

A

no

most iron in diet is Fe3+, but only Fe2+ can be absorbed across duodenal enterocytes

33
Q
  • how is Fe3+ reduced to Fe2+

- what promotes this

A
  • Fe3+ accepts an electron

- HCl in stomach, Vitamin C, ferric reductase (duodenal cytochrome B), Gastroferrin

34
Q

what is Gastroferrin secreted by and its action on

A

secreted by gastric parietal cells

reversibly binds to Fe2+, preventing formation of insoluble anion salts

35
Q

what is ferratin

A

storage form of iron

36
Q

daily requirement of Vitamin B12

A

5-15ug

37
Q

another name for vitamin B12

A

Cobalamin

38
Q

describe vitamin b12 absorption

A

stomach acids removed vitamin B12 from protein
Haptocorin (from salivary enzymes) binds to VB12
Stomach parietal cells release intrinsic factor
Pancreatic protease digest Haptocorin, releasing VB12
with then binds to intrinsic factor in SI
Vitamin B12-Intrinsic factor complex absorbed in terminal ileum by endocytosis

39
Q

what are the fat soluble vitamins?

A

A, D, E, K

40
Q

what are the water soluble vitamins

A

B, C, H

not B12