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Nutritional physiology > physiology test 2 > Flashcards

physiology test 2 Flashcards

1
Q

what are phospholipids made of

A

diglyceride + phosphoric acid. Found in egg yolk

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2
Q

what is the structure of sterols

A

contain four C rings. Mostly in animal tissues and egg yolk.

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3
Q

how are dietary lipids generally digestion

A

Esterases cleave ester bonds
o Lipase
o Phospholipase (pancreas)
o Cholesterol esterase (pancreas)

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4
Q

what are the 3 ways that fat is emulsified

A

force
emulsion
hydrolysis

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5
Q

how is fat emulsified by force

A

chyme passing through pyloric sphincter physically breaking down fat droplets

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6
Q

how is fat emulsified by emulsion

A

Bile acids synthesised by cholesterol in liver

Sterol ring is retained and OH groups added

Hydrophobic side chains replaced by group containing carb. Acid

Bile acids ionised to bile salts

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7
Q

how is fat emulsified by hydrolysis

A

In intestinal lumen

Lingual lipase & Gastric lipase

Hydrolyses at sn-3

Directly absorbed into portal vein

Pancreatic lipase: hydrolysesTAG –> 2 diacylglycerols –> 2 monoacylglycerol

Colipase: Hydrophobic regions associate with lipid droplet.

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8
Q

how are phospholipids digested

A

Phospholipase A2 from pancreas

Hydrolyse phospholipids

Produces lysophosphatidylcholine + FFA

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9
Q

how are sterols digested

A

Free cholesterol DOESN’T need to be digested

Cholesterol ester needs breakdown (cholesterol ester hydrolase)

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10
Q

list all the possible products of lipid digestion

A

Lyso-phosphatidylcholine

2-monoacylglycerol

Free cholesterol

Fatty acids

Phytosterols

Fat soluble vitamins

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11
Q

describe the structure of the large intestine mucosa

A

2 muscle layers (circular and longitudinal)

Incomplete longitudinal muscle layer – forms bands

Has ‘pouches’ called haustra

Simple columnar epithelium cells

No folds

Straight, tubular crypt glands in cell wall

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12
Q

list the 3 motility processes of the large intestine

A

haustral contractions

mass movements

defecation reflex

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13
Q

describe the motility of the large intestine through haustral contractions

A

Basoelectrical rhythm by pacemaker cells, lower frequency

Alternating contraction/relaxation (flattening) of haustra pouch

Mixing contents back and forth (non propulsive)

Absorption and storage

Local control – intrinsic nerve plexuses mediate contractions

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14
Q

describe the motility of the large intestine through mass movements

A

Contraction of large colon segments

Coordinated by ENS reflexes:
 Gastrocolic (stomach distension). Clears contents in prep for new meal
 Duodenocolic (duodenum stimuli e.g. chyme)

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15
Q

describe the motility of the large intestine through the defecation reflex

A

Internal anal sphincter (smooth muscle) and external anal sphincter (external0

Rectal distention initiated reflex

Relaxation of both sphincters

Controlled by local (intrinsic/extrinsic NS) and parasympathetic reflexes (vagal nerves)

Conscious control: afferent input into cerebrum

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16
Q

briefly explain constipation

A

Longer retention of contents –> excess water absorbed from faeces

Appendicitis may occurs with faecal obstruction
o Abdominal pain
o Inflammation
o Bacterial infection

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17
Q

what are some things absorbed in the large instines

A

Salt, water and electrolytes, short chain FA, vitamins

Na+ active absorbed (pump)

Cl- passive absorbed

Water osmosis

18
Q

what are chylomicrons

A

Long chain fatty acids packaged into chylomicrons in SI enterocytes

Enter circulation vis lymphatics

Lipid composition modified in circulation

Concentration of chylomicrons decreases after time after fat dense meal – due to lipoprotein lipase action (LPL)

19
Q

what are the products of lipoprotein lipase (LPL) action

A

hydrolyses TAG

Products taken up by adipocytes, myocytes, mammary gland epithelial cells (lactation)

Chylomicrons lose phospholipids, free cholesterol and apolipoproteins due to circulating HDL (now becomes chylomicrons remnants)

20
Q

explain VLDL and LDL metabolism

A

Secretin of VLDL:
o Contains Apo B100, cholesterol, cholesterol ester
o TAG

Once release into circulation, VLDL acquires other apolipoproteins from HDL

Hydrolysis in capillaries: FAs released from LPL action

In circulation for days, exchanges lipid component with other lipoproteins

LDL taken up by endocytosis

21
Q

describe HDL metabolism

A

Synthesised in liver as Apo A1

Acquires lecithin cholesterol acyl transferase in circulation – allows HDL to continue collecting cholesterol as it moves through tissues

HDL can counteract some atherosclerotic plaque through reverse cholesterol transport

HDL delivers cholesterol to liver – binds to SR-B1 on hepatocyte surface

Liver can maintain cholesterol homeostasis, and put cholesterol into bile (for elimination)

22
Q

what are some interventions for high cholesterol levels

A

Statins – make less cholesterol in liver

Cholestyramine – medication binds bile acids and prevents reabsorption

Ezetimibe – medication interferes with dietary cholesterol uptake from NPC1l1 transporter

Plant sterols – replaces cholesterols in mixed micelles and interferes with intestinal absorption

23
Q

why does the liver need cholesterol

A

Liver needs most cholesterol for bile production

Regulates intracellular cholesterol homeostasis in hepatocytes

24
Q

what happens if cholesterol levels in the liver is too low

A

LDL receptors on cell membrane can bring in cholesterol from circulation

Can make cholesterol from acetyl CoA

25
Q

what happens if cholesterol levels in the liver is too high

A

Liver acts to decrease cholesterol

26
Q

explain water movement

A

Transcellular mechanism – across cells via aquaporins

Paracellular path – between cells via solute driven diffusion

Water movement dependant on osmotic gradients

Maintained by active solute transport.

Standing gradient:
o Sodium moves through enterocyte into lateral space (space between cells)
o Creates high osmotic pressure in lateral space
o Water then enters driven by high osmotic pressure
o Osmotic pressure decreases, hydrostatic pressure increases
o Water is flushed into capillaries

27
Q

where is calcium stored

A

99% skeleton

28
Q

list some dietary sources of calcium

A
  • Nuts
  • Dairy
  • Broccoli
  • spinach
  • Baked beans and legumes
  • Dried figs
29
Q

list some functions of calcium

A

o Muscle contraction
o Nerve conductivity
o Enzyme activation
o Blood clotting
o neurotransmitter secretion

30
Q

how is calcium absorbed

A

Alimentary absorption (gut) or renal absorption (more effective)

Obligatory loss of calcium through skin, sweat, faeces

Insoluble calcium salts are solubilised in low pH – stomach

SI has 2 transport mechanisms:
o Transcellular. Carrier mediated active transport. 60% absorption. saturable
o Paracellular absorption: passive diffusion. Non saturable. Jejunum and ileum

31
Q

what are the transporters involved in calcium absorption

A

Calcium transporter 1 (CaT1). Moves Ca across brush border

Calbindin. Systolic binding protein. Moves Ca through enterocyte

Calcium ATP-ase pump

32
Q

what are some factors affecting calcium absorption

A

1 – 24 dihydroxy vitamin D
o Upregulates CaT1 and calbindin
o Improved calcium absorption

Rate of transit through intestine

Life stages:
o Infants, children, adolescences pregnant and lactation increases absorption
o Decreased with age and lower oestrogen levels

Diet
o Protein and sugars, and vitamin D increase
o Free fatty acids and fibre decrease

33
Q

list some functions of iron

A

Haemoglobin synthesis and oxygen transport

DNA synthesis

Electron transport

34
Q

how is iron absorbed

A

Transporters across luminal membrane from 2 active transporters:

Haem via HAEM CARRIER PROTEIN 1(hydrolysed prior from proteases)

Hydrolysed in cell to ferrous iron

Non haem via DIVALENT METAL TRANSPORTER 1

Ferric iron concerted to ferrous iron at brush border from duodenal cytochrome b

2 fates after absorption: used immediately or absorbed

35
Q

what is the fate of iron if it’s needed for immediate use

A

ferroportin transports Fe2+ across basolateral membrane

Fe2+ oxidised to Fe3+

Binds to transferrin for transport in blood

36
Q

what is the fate of iron if it’s needed for storage

A

Stored in epithelial cells as ferritin (short term)

Excreted in faeces with epithelial turnover (3 days)

37
Q

list some factors affecting iron absorption

A

Ascorbic acid (promotes) – converts ferric iron to ferrous iron and chelated iron in gut lumen

Organic acids – citric acid enhances absorption

Inhibited by polyphenols (vegetables, some grains, tannin in tea

phytates

38
Q

list some dietary sources of iodine

A

marine food

eggs

variety of meats

grains and legumes

Iodine: organic form, amino acid bound

Iodide: free form. Mostly in thyroid gland, some circulating

39
Q

list some functions of iodine

A

Key constituant of thyroid hormones

Involved with thyroxine

Essential for normal growth and development

40
Q

what is the process of iodine absorption

A

Iodine releases and reduce to iodide before absorption

Rapidly absorbed din stomach and duodenum

Absorbed active transport at enterocyte apical surface by sodium-iodide transporter

Exit across basolateral surface into bloodstream by chloride channel (CLC-2)

Exit across basolateral surface into bloodstream by chloride channel (CLC-2)

Thyroid follicular cells actively take up free iodide immediately from blood

41
Q

what are the 3 states of energy balance

A
  1. Constant body weight
  2. Unused energy stored.
  3. Body must use stored energy to supply needs
42
Q

what are the 3 key nuclei involved in hypothalamic control of energy balance

A

o Arcuate nucleus
o Lateral hypothalamic area
o Paraventricular nucleus

Nutritional physiology (3 decks)

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