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Year 1 Alimentary > Alimentary mechanisms > Flashcards

Alimentary mechanisms Flashcards

1
Q

What is molar?

A

One mole per litre

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2
Q

What is millimolar? And units?

A

1/1000 moles. mM.

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3
Q

What is micromolar? And units?

A

1/million moles. uM.

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4
Q

nanomolar - units and what?

A

1/billion moles. nM.

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5
Q

picomolar - units and what?

A

1/10^12. pM.

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6
Q

femtomolar - units and what?

A

1/10^15. fM.

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7
Q

Which molecules can cross membranes more easily, lipid soluble or water soluble

A

lipid soluble

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8
Q

In osmosis, how does water move?

A

Movement of water from a hypotonic solution to hypertonic solution.

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9
Q

What do tight junctions help achieve?

A

Unidirectional flow of substances, by creating cell polarity: e.g. different membrane proteins are kept on different sides of a cell.

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10
Q

What is paracellular transport?

A

Passage between cells, through tight junctions and lateral intercellular spaces.

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11
Q

What is trans cellular transport?

A

Passage through the epithelial cells.

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12
Q

What are the two transport proteins involved in membrane transport? (x2) What are channel proteins?

A

Channel proteins and carrier proteins.

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13
Q

What are channel and carrier proteins?

A

(1) Channel proteins form aqueous pores allowing specific solutes to pass across the membrane: facilitated diffusion.
(2) Carrier proteins bind to the solute and undergo a conformational change to transport it across the membrane: facilitated diffusion

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14
Q

Which has faster transport, channel or carrier proteins

A

Channel proteins allow much faster transport than carrier proteins.

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15
Q

What type of ion channels are there (x4)

A

Voltage gated, extracellular Ligand gates, Intracellular ligand gates, mechanically gated (eg change in pressure)

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16
Q

What types of carrier-mediated transport proteins are there ?

A

Uniport, symport and antiporter. Symport and antiport are coupled transport.

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17
Q

What is a uniport, symport and antiport carrier?

A

UNIPORT: One molecule transported in one direction. SYMPORT: Two molecules transported in same direction. ANTIPORT: Two molecules, transported in opposite directions - usually to balance charge.

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18
Q

What are the two types of active transport?

A

Primary and secondary active transport.

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19
Q

What is primary active transport? What is secondary active transport?

A

PRIMARY ACTIVE TRANSPORT is linked directly to cellular metabolism (uses ATP to power the transport). SECONDARY ACTIVE TRANSPORT derives energy from the concentration gradient of another substance that is actively transported.

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20
Q

What is facilitated transport/diffusion?

A

Enhances the rate a substance can flow down its concentration gradient. This tends to equilibrate the substance across the membrane and does not require energy. Uses channel and carrier-mediated diffusion proteins.

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21
Q

An example of primary active transport? (x2)

A

Na/K ATPase transport, H+/K+ ATPase transporter in stomach

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22
Q

Example of secondary active transport? (x3)

A

SGLT-1 cotransport (Na+, and glucose and galactose - when glucose in lower concentration in lumen than enterocyte), HCO3-/Cl- counter-transport, Na/H counter transport

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23
Q

Example of facilitated transport?

A

Glut-2,4,5 (Glut-5 carrier protein transports fructose on the enterocyte apical membrane; GLUT-2 is a carrier protein in the basolateral membrane so that glucose can exit from enterocyte into plasma.)

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24
Q

What percentage of ingested water is absorbed by GI tract?

A

99%

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25
Q

What is absorption of water powered by? Name for process?

A

Absorption of ions (Na+), called standing gradient osmosis

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26
Q

Where is the greatest proportion of water absorbed?

A

Small intestine, especially jejunum

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27
Q

Which molecules are incompletely absorbed?

A

Iron and Calcium

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28
Q

How much water a day absorbed by small intestine?

A

roughly 8L

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29
Q

How much water a day absorbed by Large intestine?

A

1.4L

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30
Q

Where does 8L liquid come from a day, if only drink 2L?

A

Drink 2L, Saliva 1.2L, Gastric secretions 2L, Bile 0.7L, Pancreas 1.2L, intestinal secretions 2.4L

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31
Q

Movement of sodium across the epithelial layer and their locations in the GI? (x5 mechanisms) Efficiency down the GI tract?

A

(1) Na+/H+ antiport (proximal bowel).
(2) Na+/Glucose co-transport (jejunum).
(3) Na+/Amino Acid Co-transport (Jejunum).
(4) Co-transport with Cl- (ileum).
(5) Some ion channles (colon)

(This all increases intracellular NA+ and becomes MORE EFFICIENT as you travel down intestine).

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32
Q

Transport of chloride? (x2 mechanisms)

A

(1) Cl- co-transported with Na+ (ileum) as already mentioned. (2) Exchanged with HCO3- (colon) into enterocytes. Both secondary active transport.

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33
Q

Transport of K+? (x2 mechanisms)

A

(1) K+ diffuses IN via paracellular pathways in small intestine. (2) K+ diffuses OUT out via paracellular pathways in colon. Passive transport and explains why you will find K+ in faeces..

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34
Q

What happens to this high intracellular sodium?

A

Active transport of Na+ into the lateral intercellular spaces by Na+K+ATPase transport in the lateral plasma membrane, therefore [Na+] increases in intracellular space.

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35
Q

What happens to high intracellular chloride and HCO3-?

A

The movement of positive sodium out into intercellular spaces sets up an electrochemical gradient for negative ions (Cl- and HCO3-) which also move past basolateral membrane and into intercellular spaces.

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36
Q

What does movement of ions into intracellular spaces mean for standing gradient osmosis?

A

Creates a hypertonic intercellular fluid which drives transport of water from gut lumen to intercellular spaces by paracellular and transcellular pathways.

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37
Q

How does water and ions enter blood from intercellular spaces?

A

Movement of water into spaces increases pressure, which puts pressure on basement membrane, which forces water and ions into blood stream OVER the basement membrane (not basolateral membrane, but the basememnt membrane of the ECM).

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38
Q

Where is calcium absorbed?

A

Duodenum and Ileum

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39
Q

What happens to gut function when you have a Ca2+ deficient diet? Purpose?

A

Ca2+ deficient diet increases gut’s ability to absorb. This is compensatory - gut attempts to absorb more Ca2+ this way.

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40
Q

What stimulates calcium absorption? (x2)

A

Vit D and Parathyroid Hormone

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41
Q

How much ca2+ typically in diet?

A

1-6g/day

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42
Q

How much absorbed per day?

A

just under a gram

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43
Q

What is intracellular calcium concentration?

A

100nM/0.1mM

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44
Q

What is extracellular calcium concentration?

A

1-3mM. i.e. Calcium is found in high concentrations in the ECF, but low concentrations intracellularly.

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45
Q

What does high extracellular-low intracellular calcium mean for transport?

A

Doesn’t require energy for movement of calcium in cell.

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46
Q

How is calcium transported? (x2)

A

i) Intestinal calcium-binding protein (IMcal)- facilitated diffusion. ii) Ion channel

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47
Q

Why is ca2+ low in cytosol

A

acts as a signalling molecule

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48
Q

How is absorbed ca2+ prevented from acting as a signal?

A

Need to transport Ca2+ while maintaining low INTRAcellular concentrations. SO, binds to Calbindin in cytosol of enterocyte cell, preventing its action as an intracellular signal.

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49
Q

How is ca2+ transported across the basolateral membrance and into blood? (x2 mechanisms)

A

(1) Ca2+ pumped across basolateral membrane by plasma membrane Ca2+ ATPase (PMCA) against concentration gradient. PMCA has a high affinity for Ca2+ (but low capacity). High affinity maintains the very low concentrations of calcium normally observed within a cell. (2) Ca2+ also pumped across basolateral membrane by plasma membrane Na+/Ca2+ exchanger against concentration gradient. The Na+/Ca2+ exchanger has a low affinity for Ca2+ but a high capacity. Requires larger concentrations of Ca2+ to be effective. This means that it responds very quickly when there is an influx in Calcium.

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50
Q

How does Vit D help absorb calcium? (x3 functions) What diseases does deficiency lead to? (x2)

A

1, 25-dihydroxy D3 9the active form of Vitamin D) taken up by enterocytes: (i) Enhances the transport of Ca2+ through the cytosol; (ii) increases the levels of calbindin; (iii) Increases rate of extrusion across basolateral membrane by increasing the level of Ca2+ ATPase in the membrane. DEFICIENCY DISEASES: Deficiency causes rickets, osteoporosis.

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51
Q

What is the purpose of Iron? (x3)

A

(1) Iron can act as an electron donor and an electron acceptor. (2) Oxygen transport (red blood cells). (3) Oxidative phosphorylation (mitochondrial transport chain) - cytochromes.

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52
Q

What issue is there with iron absorption?

A

Too much is toxic, and the body has no way of actively excreting iron

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53
Q

What are the daily ingestion and absorption rates of iron?

A

Adult ingests approx 15-20mg/day but absorbs only 0.5-1.5mg/day.

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54
Q

Where is iron sourced in diet? (x2)

A

(1) INORGANIC IRON (Fe3+ ferric, Fe2+ ferrous) (2) as part of HEME (HAEM) GROUP (trapped in the meat that you eat in haemoglobin, myoglobin and cytochromes).

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55
Q

Which iron ion is absorbed

A

Fe 2+. Cannot Fe 3+

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56
Q

Where is Fe 3+ in diet? (x3 sources)

A

Fe3+ found in insoluble salts with: hydroxide, phosphate, HCO3-

57
Q

What does Vit C do to Fe 3+? Why?

A

Vit C reduces Fe3+ to Fe2+, which makes iron more absorbable. Fe3+ is harder to absorb.

58
Q

How much haem is absorbed and used as a source of iron? Compared with inorganic iron sources?

A

Heme is a smaller part of diet, but more readily absorbed. COMPARED WITH INORGANIC SOURCES: 20% of heme is absorbed; 5% of inorganic iron is reabsorbed.

59
Q

How is haem absorbed into enterocytes in the gut? (x2 transporting mechanims)

A

Dietary heme is highly bioavailable. Heme is absorbed intact into the enterocyte via (1) heme carrier protein 1 (HCP-1), and (2) receptor-mediated endocystosis. Fe2+ is then liberated by Heme oxygenase.

60
Q

What happens to Fe3+ that is taken up into enterocytes in absorption?

A

Duodenal cytochrome B (Dcytb) catalyzes the reduction of Fe3+ to Fe2+ in the process of iron absorption in the duodenum of mammals on the apical membrane of the enterocyte.

61
Q

How is inorganic Fe2+ absorbed into enterocytes in the gut?

A

Fe2+ transported via divalent metal transporter 1 (DMT-1), a H+-coupled co-transporter.

62
Q

How is Fe2+ in the enterocyte cytosol transported to the basolateral membrane and into the blood?

A

Fe2+ binds to unknown factors and carried to basolateral membrane.

  • Fe2+ moves via ferroportin ion channel into blood.
63
Q

How is iron moved around in the blood? What is the mechanism of this?

A

IRON IS TRANSPORTED IN THE BLOOD IN THE Fe3+ form.

Hephaestin is a transmembrane (found in baso-lateral enterocyte membrane) copper-dependent ferroxidase that converts Fe2+ to Fe3+.

Fe3+ binds to apotransferrin and travels in blood as a transferrin complex.

64
Q

How are iron blood levels regulated?

A

Hepcidin, the major iron regulating protein, suppresses ferroportin function which decreases iron absorption by inhibiting movement of iron out into the blood from the enterocytes.

65
Q

What is a storage method of Fe2+ in enterocytes?

A

Binds to apoferritin in cytosol to form ferritin micelle.

Ferritin is globular protein complex. Fe2+ is oxidised to Fe3+ which crystallises within protein shell.

A single ferritin molecule can store up to 4,000 iron ions.

In excess dietary iron absorption, produce more ferritin.

66
Q

How is iron lost in the diet?

A

REMEMBER, the intestinal enterocytes are being renewed daily.

SO, the irreversible binding of iron to ferritin in the epithelial cells means that when enterocytes are renewed, the iron/ferritin is lost into the lumen and excreted in the faeces.

Iron/Ferritin is also not available for transport into plasma, so all synthesised Ferritin is lost.

67
Q

What is a vitamin?

A

Organic compounds that cannot be manufactured by the body but vital to metabolism.

68
Q

Which vitamins are fat soluble? What is the type of transport for each?

A

A, D, E, K (transported to brush border in micelles. K taken up by active transport; rest by passive diffusion.)

69
Q

What does a lack of vit B12 cause?

A

retards the maturation of red blood cells - pernicious anaemia.

70
Q

Where is B12 sourced?

A

Most Vit B12 in food is bound to proteins.

71
Q

Where is Vitamin B12 freed in GI tract from protein?

A

In the stomach, low pH and the digestion of proteins by pepsin releases free vit B12. But B12 is easily denatured by HCl.

72
Q

How is B12 saved from denaturation?

A

Binds to R protein (haptocorrin) released in saliva and from parietal cells. R proteins digested in duodenum; not the stomach.

73
Q

After R protein digested, what binds B12?

A

Intrinsic Factor - a Vit B12 binding glycoprotein.

74
Q

What cells are Vit B12 intrinsic factor secreted?

A

Parietal cells.

75
Q

What is the purpose of the intrinsic factor for Vitamin B12? (x2)

A

(1) Vit B12/IF is resistant to digestion.
(2) No IF, then no absorption of vit B12. Vit B12/IF complex binds to cubilin receptor and taken up in distal ileum (mechanism unknown, but thought to involve receptor-mediated endocytosis).

76
Q

What is fate of B12? Most common location?

A
  1. Once in cell, Vit B12/IF complex broken- possibly in mitchondria
  2. B12 binds to protein transcobalamin II (TCII) and crosses basolateral membrane by unknown mechanism
  3. Travels to liver bound to TCII.
  4. TCII receptors on cells allow them to uptake complex.
  5. Proteolysis then breaks down TCII inside the cell and Vitamin B12 is stored.

OCCURS USUALLY IN THE LIVER.

77
Q

What nervous systems regulate the functions of the alimentary system?

A

INSTRINSIC (enteric) and EXTRINSIC (autonomic).

78
Q

What is the enteric nervous system made up of? How is it arranged?

A

More than 100 million INTRINSIC (meaning capable of acting independently of other nervous systems) NEURONES that extend along the length of the GI tract.
Arranged in GANGLIONATED PLEXUSES with interconnecting bundles of UNMYELINATED nerve fibres.

79
Q

What are the three types of neurones in the ENS? What neurone-class are most?

A

MOST ARE MULTIPOLAR (one axon and multiple dendrites).

· SENSORY: respond to mechanical, thermal, osmotic and chemical stimuli.

· MOTOR: axons terminate on smooth muscle cells of the circular or longitudinal layers, secretory cells of the GI tract, OR GI blood vessels.

· INTERNEURONS: neurons between neurons, reflects the capacity of the ENS to integrate the sensory input and effector output.

80
Q

What is the major function of the enteric nervous system? (x2 general and x6 specific)

A

It INTEGRATES the motor and sensory activities of the GI system.
Enables the GI tract to perform its basic REFLEX FUNCTIONS of:

· secretion,

· absorption,

· mixing,

· gut movements.

· Regulates water and electrolyte transport.

· Regulates blood flow.

81
Q

How is the enteric nervous system linked to other nervous systems? (x3 points)

A
  1. It operates without the influence of the CNS or autonomic nervous system – i.e. if the SNS and PNS are cut from the gut, many motor and secretory activities continue as controlled by the ENS.
  2. However, the CNS via the sympathetic and parasympathetic nerves (ANS) communicate with the intrinsic neurones of the ENS and bring about modulation of GI tract functions.
  3. Axons of the intrinsic neurones of ENS also project to sympathetic ganglia, the pancreas, gall bladder, trachea, spinal cord and brain stem.
82
Q

What are the two types of ganglia in the ENS?

A

Myenteric (Auberbach’s) plexuses.
Submucosal (Meissener’s) plexuses.

83
Q

Where are the three ENS plexuses found in the GI wall?

A

MYENTERIC: between the circular and longitudinal smooth muscle layers.

SUBMUCOSAL: in the submucosa.

MINOR PLEXUSES: including deep muscular plexus (found inside circular muscle), and the ganglia supplying biliary system and pancreas.

84
Q

What is the function of the Myenteric plexus?

A

Controls activity of the muscularis externa. Controls gut motor function.

85
Q

What is the function of the Submucosal plexus?

A

Senses environment within the lumen and regulates blood flow, epithelial and endocrine cell function.

86
Q

What viscera is the ENS associated with?

A

From the oesophagus to the anus.

87
Q

What is the purpose of the autonomic nervous system on the GI tract? (forget about the ENS for now)

A

Regulates smooth muscle, cardiac muscle and glands.

88
Q

What is the structure of the sympathetic nervous system?

A

Cell bodies of preganglionic neurons in the thoracic and lumbar spinal cord.

Cell bodies of postganglionic neurones in the pre- and para- vertebral ganglia.

89
Q

What do the thoracic splanchnic nerves of the SNS innervate?

A

Carry innervation to fore and midgut.

90
Q

What do the lumbar splanchnic nerves of the SNS innervate?

A

Carry innervation to the remainder of the gut.

91
Q

What is the neurotransmitter of the GI tract SNS?

A

Norepinephrine.

92
Q

What is the structure of the parasympathetic nervous system?

A

Cell bodies of the preganglionic neurons in the brainstem and sacral spinal cord (cranio-sacral).

Cell bodies of the postganglionic neurons are close to the target organs. Preganglionic neurons synapse in ganglia close to the gut wall or directly with enteric plexi.

93
Q

What nerves of the PNS innervate the gut?

A

· VAGUS NERVE innervates most of the GI tract – down to the transverse colon.

· The remainder of the colon, the rectum and the anus receive PNS fibres from the pelvic nerves.

94
Q

What is the neurotransmitter of the GI tract PNS?

A

Acetyl choline.

95
Q

What are the general functions of the PNS and SNS in the GI tract?

A

PARASYMAPTHETIC: Excitation usually stimulates the activities of the GI tract – promotes gut motility, secretion and digestion.

SYMPATHETIC: Action inhibits gut motility and secretion, and causes vasoconstriction and contraction of sphincters.

96
Q

***How does the autonomic and enteric nervous system interact to carry out its FUNCTIONS?

A

· Sympathetic nerves innervate the blood vessels directly (vasoconstriction of coeliac, superior and inferior mesenteric arteries) AND most terminate on neurones in the ENS plexuses.

· Parasympathetic nerves do not innervate the GI tract directly, though it does interact with the ENS.

  • ENS regulates smooth muscle, secretory cells, endocrine cells and blood vessels of the GI tract.
97
Q

What is the ANS and ENS negative feedback cycle?

A

Chemo and mechanoreceptors in the wall of the GI tract negatively feedback onto the myenteric and submucosal plexuses of the ENS via LOCAL AFFERENTS; and negatively feedback on the central nervous system via SPLANCHNIC AND VAGAL AFFERENTS.

The CNS goes on to regulate the ANS, which also affects the ENS.

98
Q

What is the role of the afferents of extrinsic nerves of the GI tract (ANS)? (x3)

A

Afferents are sensory to PAIN, NAUSEA AND FULLNESS. (Efferents are the SNS and PNS which coordinate GI activities.)

99
Q

What happens when there is enteric neural dysfunction/degeneration? (x3)

A

· Inflammation

· Irritable bowel syndrome

· Degeneration associated with age – hence why you see constipation more in old age etc.

100
Q

Where are hormones produced in the GI tract?

A

Produced by endocrine cell sin the mucosa and submucosa of the stomach, intestine and pancreas.

101
Q

***What gut hormones are produced and where along the GI tract?

A

STOMACH: Gastrin, somatostatin.

DUODENUM: cholecystokinin (CCK), secretin and somatostatin.

PANCREAS: insulin, glucagon, somatostatin.

ILEUM AND JEJUNUM: PYY, GIP (glucose-dependent insulinotropic peptide OR gastric inhibitory peptide), somatostatin.

BOWEL: PYY, somatostatin.

102
Q

How is gut hormone release controlled?

A

Enteroendocrine cells which release hormones, have receptors in their apical surface (on microvilli) which sense nutrients e.g. fatty acids, amino acids, glucose…

103
Q

What is the function of the GI endocrine system? (x4)

A

· Regulation of the mechanical processes of digestion (e.g. smooth muscle of GI tract and sphincters, gall bladder).

· Regulation of the chemical and enzymatic processes of digestion (e.g. secretory cells located in the wall of the GI tract, pancreas and liver).

· Control of post-absorptive processing involved in assimilation of digested food and CNS feedback regulating intake e.g. GIP stimulates insulin from pancreas and PYY acts on CNS to suppress appetite.

· Effects on the growth and development of the GI tract e.g. GLP-2 promotes small intestinal growth.

104
Q

What examples are there of paracrine actions in the GI tract? (x2)

A

(1) Histamine released from stomach wall cell is a key physiological stimulus to HCl secretion by gastric parietal cells; (2) Somatostatin from the stomach can inhibit acid secretion by paracrine mechanisms.

105
Q

How is gastrin release controlled? (x3 and x1)

A

STIMULATED by amino acids and peptides in the lumen of the stomach, gastric distension (enlargement) and vagus nerve directly.

INHIBITED when pH in the stomach falls below pH 3.

106
Q

What is the function of gastrin?

A

Stimulates gastric acid secretion.

107
Q

What cells synthesis somatostatin?

A

Endocrine D cells.

108
Q

What is the function of somatostatin? (x5)

A

UNIVERSAL INHIBITOR: release in response to mixed meal and inhibits (i) gastric secretion, (ii) motility, (iii) intestinal and pancreatic secretions, (iv) intestinal nutrient and electrolyte transport, (v) growth and proliferation. Can be paracrine AND endocrine.

109
Q

What is the clinical application of somatostatin?

A

Analogues are used to treat neuroendocrine tumours e.g. octreotide.

110
Q

What is the (i) site of production, (ii) stimulus, (iii) functions (x2) of SECRETIN?

A

(i) Secreted by S cells of the upper duodenum and jejunum; (ii) major stimulus is the presence of acid in the duodenum (pH falls below 4.5); (iii) stimulates pancreatic bicarbonate secretion; high concentrations: inhibition of gastric acid and gastric emptying in the stomach.

111
Q

How are the effects of secretin potentiated?

A

By CCK.

112
Q

What is the (i) site of production, (ii) stimulus, (iii) functions (x4) of CHOLECTYSTOKININ (CCK)?

A

(i) Secreted by cells most densely located in the small intestine; (ii) release stimulated by fat and peptides in the upper small intestine, independent of the vagus nerve; (iii) stimulates pancreatic enzyme release, delays gastric emptying, stimulate gallbladder contraction and decreases food intake and meal size.

113
Q

What is the (i) site of production, (ii) stimulus, (iii) functions, (iv) receptor antagonists of GIP?

A

(i) Secreted by mucosal K cells (predominant in the duodenum and jejunum; (ii) GIP released following ingestion of a mixed meal; (iii) stimulates insulin secretion; (iv) GIP receptor antagonists reduce postprandial (post-meal) insulin release.

114
Q

What is the (i) site of production, (ii) stimulus, (iii) functions (x5) of PEPTIDE YY (PYY)?

A

(i) Cells found throughout the mucosa of the terminal ileum, colon and rectum. Released from L cells (ii) post-prandially (particularly protein); (ii) PYY reduces intestinal motility, gallbladder contraction and pancreatic exocrine secretion. It also inhibits intestinal fluid and electrolyte secretion and PYY3-36 inhibits food intake.

115
Q

What are the three stimuli of thirst? Which is most potent?

A

(1) Body fluid osmolality is increased (more potent i.e. requires smaller change), (2) blood volume is reduced, (3) blood pressure is reduced.

116
Q

What is the effect of ADH?

A

Acts on the kidneys to regulate the volume and osmolality of urine.

When plasma ADH is low, a large volume of urine is excreted (water diuresis); when plasma ADH is high, a small volume of urine is excreted (anti diuresis).

117
Q

Where are osmoreceptors found?

A

Found in the hypothalamus, OVLT (Organum vasculosum) and SFO (Subfornical organ).

118
Q

How do osmoreceptors work?

A

Sense changes in body fluid osmolality. Cells shrink or swell in response (expand when plasma more dilute and vice versa). They send signals to the ADH producing cells in the hypothalamus to alter ADH release.

119
Q

What are the two responses by the body when there is increased plasma osmolality?

A

Invokes drinking and ADH release (which increases water conservation in the kidney. Vice versa when plasma osmolality is decreased.

120
Q

Why is sensation of thirst decreased by drinking, even before sufficient water has been absorbed by the GI tract to correct osmolality? How short-lived is this?

A

Receptors in the mouth, pharynx, oesophagus relieve this feeling of thirst SHORT TERM. Thirst is only completely satisfied once plasma osmolality is decreased or blood volume or arterial pressure is corrected.

121
Q

How is the renin-angiotensin-aldosterone system linked to thirst?

A

RAAS reabsorbs salt, and therefore also increases reabsorption of water. Therefore, when Angiotensin II is synthesised, it doesn’t just affect salt absorption and vasoconstriction etc., it also increases THIRST sensation by activating SFO neurons.

122
Q

What is the role of the hypothalamus in body weight?

A

Integrates signals from different chemicals and different areas of the body e.g. periphery (vagus nerve input from stomach distension, adipose tissue, GI tract…). RESULT = regulates food intake and type of food they intake. Overall, hypothalamus therefore controls our body weight homeostasis.

123
Q

Why is the hypothalamic mechanism of appetite regulation so complex?

A
  1. Body may require specific nutrients rather than general food; so, hypothalamus makes you hungry for specific nutrients to make up for their short supply.
  2. Hunger isn’t the same in all circumstances. Hypothalamus makes you feel all kinds of hunger e.g. can differ is you are skinny/fat or haven’t eaten for 2hrs/24hrs.
  3. Loss of appetite can feel different: Differences in not wanting to eat because of nausea/feeling full/don’t like the food.

SO, there’s a lot of redundancy in the system.

124
Q

What is the structure of the hypothalamus?

A

Paraventricular nucleus – neurones which extend to posterior pituitary or release things like TRH.

Arcuate nucleus – really important in regulation of food.

125
Q

How does the arcuate nucleus receive signals?

A

It is a circumventricular body, meaning that it is not completely isolated by the blood brain barrier. IMPORTANT: allows receptors access to peripheral hormones which tell us about nutritional state and allows us to respond to hormones.

126
Q

What are the two populations of neurones in the arcuate nucleus?

A

NPY/Agrp neuron: stimulates food intake; POMC neuron: inhibits food intake.

127
Q

How are the two neuron populations arranged in the hypothalamus? Why?

A

Completely separate, because they perform two opposing functions, so signals do not want to be integrated.

128
Q

What does POMC turn into in the arcuate nucleus?

A

POMC breaks into ACTH in the pituitary. In the arcuate nucleus, it is turned into a neuropeptide called alpha-MSH which suppresses appetite.

129
Q

How does the arcuate nucleus respond to circulating factors and deliver a response?

A
  • Incomplete B-B barrier is indicated by dotted line.
  • Circulating factors cross this barrier and bind to receptors on the neurons and decide whether to suppress or stimulate food intake downstream.
  • Cell bodies and receptors of these neurones are found in the arcuate nucleus, but the axons extend all over the brain. A lot signal into the paraventricular nucleus which then mediates the feeling of appetite.
130
Q

How does the melanocortin system work? (x2)

A
  1. The melanocortin system responds to POMC in the arcuate nucleus: POMC is released, and broken down into alpha-MSH, and interacts with the melanocortin 4 receptor (MC4R) in the paraventricular nucleus to decreases food intake.
  2. Agrp is also released and interacts with the same receptor. However, it is an endogenous antagonist of that receptor, and so decreases stimulation of decreased food intake.
131
Q

What are the implications of mutation in the melanocortin system?

A

Melanocortin receptors are found all over the body.

If there’s mutation resulting in POMC deficiency, means that all molecules POMC makes is lost – so, there is…

  1. lack ACTH = no corticosteroid regulation.
  2. Melanocortin receptor also affects hair colour – so you get red hair.
  3. Also become obese because they have no alpha-MSH, so cannot restrain food intake.
132
Q

What other brain regions are associated with food intake? (x3)

A

Higher centres: AMYGDALA (emotion and memory), other parts of the hypothalamus e.g. lateral hypothalamus, and vagus to brain stem to hypothalamus.

133
Q

What are the two peripheral inputs into the brain that control appetite?

A

LONG TERM SIGNAL: leptin; SHORT TERM SIGNAL: Ghrelin, PYY.

134
Q

How does the leptin mechanism of body weight homeostasis work?

A
  • · Leptin is produced proportion to amount of fat in the body – called adipostat mechanism.
  • · Made by adipocytes in white adipose tissue.
  • · Leptin is a circulating hormone – hypothalamus senses the concentration of hormone, then alters neuropeptides to increase or decrease food intake and thermogenesis (expenditure).
  • · Low when low body fat and opposite when high body fat.
  • · Hormone decreases food intake and increases thermogenesis.
135
Q

What are three potential pathways of lectin system abnormality, that can lead to obesity?

A
  1. Absent leptin so hypothalamus isn’t stimulated to decrease food intake and increase rates of metabolism.
  2. Regulatory defect, so when you get more adipose tissue, leptin does not increase levels in the blood or respond sufficiently.
  3. Leptin resistance in the hypothalamus.
136
Q

What is the common lectin abnormality that leads to obesity?

A

For most who are obese, they have LEPTIN RESISTANCE. So, leptin is ineffective for weight control.

137
Q

Treatment for those who have absent leptin or leptin regulatory defect?

A

Small number of patients have this problem – so treatment is leptin injections.

138
Q

What is the effect of PYY on appetite? Longevity?

A
  • Secretion of PYY increases post-prandially.
  • PYY 3-36 modulates neurons in the arcuate nucleus – inhibits NPY release and stimulates POMC neurons = decreased appetite.
  • BUT PYY 3-36 has short-term effects – photo.
139
Q

What is the effect of Ghrelin on appetite? Structure?

A
  • Ghrelin is a peptide and has a fatty acid attached, which is important in binding to its receptor and travelling in the circulation.
  • Ghrelin works in the opposite direction to PYY – goes up when you haven’t eaten, and drops post-prandially.
  • Ghrelin modulates neurons in the arcuate nucleus – stimulates NPY/Agrp neurons and inhibits POMC neurons = increased appetite.

Year 1 Alimentary (8 decks)

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