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Medicine Year 1 - Semester 2 - Part 1 > Lipids in Cell Membranes (2) > Flashcards

Lipids in Cell Membranes (2) Flashcards

1
Q

State the function of phospholipids

A

Participate in cell-cell communication mechanisms by giving rise to intracellular second messengers.

Serve as precursors for compounds that are released from cells and act on other cell types, called eicosanoids.

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2
Q

Describe the steps in cell-cell communication

A

Synthesis of signal

Release of signalling molecule by the signalling cell (via diffusion, exocytosis, cell-cell contact)

Transport of signal to the target cell

Detection of the signal by a specific receptor protein.

A change in cellular metabolism, function or development triggered by the receptor-signal complex.

Removal of the signal OR desensitisation.

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3
Q

Describe signal transduction

A

Detection of the signal by a specific receptor protein.

A change in cellular metabolism, function or development triggered by the receptor-signal complex.

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4
Q

Describe transport of signals

A

Signals can be short or long range.

In animals, signalling by extracellular molecules can be classified into different types.

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5
Q

State the 2 types of long-range signalling

A

Endocrine signalling
Neurotransmission

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6
Q

Describe endocrine signalling

A

Hormone released by endocrine cell and carried in bloodstream to distal target cells.

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7
Q

Give an example of endocrine signalling

A

FSH released from the pituitary acts upon the ovary.

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8
Q

What type of signalling is endocrine signalling ?

A

Long range

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9
Q

Describe neurotransmission

A

This is where a signal is passed along a network of neurons, through a series of neurotransmitter release receptor activation events.

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10
Q

Give an example of neurotransmission

A

Breathing

The phrenic and thoracic nerves send impulses from the brain to the diaphragm.

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11
Q

State some short-range signalling types

A

Paracrine
Autocrine

Membrane bound proteins can interact to signal

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12
Q

Describe paracrine signalling

A

Signalling molecules only affect target cells in close proximity to secreting cells.

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13
Q

Give an example of paracrine signalling

A

Somatostatin release by pancreas cells acts locally.

Neurotransmission can also be considered to be a type of paracrine signalling.

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14
Q

Describe autocrine signalling

A

Cells respond to substances that they themselves release.

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15
Q

Give an example of autocrine signalling

A

Some neurotransmitters and growth factors bind to the cells that release them.

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16
Q

Describe how membrane bound proteins can interact to signal

A

This is where you have a signalling molecule expressed on the cell surface and it binds to a receptor on an adjacent target cell.

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17
Q

Give an example in which membrane bound proteins interact to signal

A

Signalling by T cells in the immune system

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18
Q

Give an example of where multiple types of signalling can be occurring simultaneously

A

Insulin released from pancreatic B cells acts in an autocrine, a paracrine and an endocrine manner.

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19
Q

How do signalling molecules act ?

A

Act on membrane bound receptors that control the production of intracellular chemicals (second messengers)

DO NOT ENTER CELLS

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20
Q

State the function of ‘second messengers’

A

Mediate cell activity

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21
Q

State the exception to how most signal molecules act

A

Lipid soluble signalling molecules

  • they bind intracellular receptors
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22
Q

Describe how signalling molecules bind to cell-surface receptors (extracellular receptors)

A

Extracellular receptors which are on the cell surface, bind to a hydrophilic signalling molecule.

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23
Q

Describe how signalling molecules bind to intracellular receptors

A

Intracellular receptors (often reside in the nucleus)

Signalling molecules are hydrophobic and so can pass through the membrane, to get to the nucleus where they bind to the receptor.

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24
Q

Function of intracellular receptors

A

Usually involved in the switching on/off of genes and making new proteins.

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25
Q

State the 4 types of receptors

A

Ligand gated ion channels
(Ionotropic)

G protein coupled receptors
(Metabotropic)

Kinase-linked receptors

Nuclear receptors

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26
Q

State some examples of Ligand gated ion channels
(Ionotropic) receptors

A

Nicotinic
ACh receptor

(ms)

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27
Q

State some examples of G protein coupled receptors
(Metabotropic)

A

Muscarinic
ACh receptor

(s)

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28
Q

State some examples of Kinase-linked receptors

A

Cytokine receptor

(hours)

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29
Q

State some examples of Nuclear receptors

A

Oestrogen receptor

(hours)

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30
Q

Describe what happens when an extracellular signalling molecule binds to a cell-surface receptor

A
  1. Switching on of genes (altered protein synthesis)
  2. Proteins already in the cell with an altered function

Both processes give rise to alteration in cytoplasmic machinery in the cell and a change in cel behaviour.

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31
Q

State some lipid soluble molecules

A

Steroid hormones (lipids)

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32
Q

Describe the action of lipid soluble molecules

A

Pass through the cell membrane

Combine to a receptor within the nucleus

Switch on transcription of genes

Results in protein synthesis and an altered functional response.

33
Q

Describe the action of cortisol

A

Cortisol binds to a receptor in the cytoplasm

When it recognises its receptor, it is translocated to the nucleus and it switches on gene transcription.

34
Q

State the phospholipid that resides in the cell membrane and is present in significant amounts

A

Phosphatidylinositol 4,5 bisphosphate

(PIP2)

35
Q

Where is Phosphatidylinositol 4,5 bisphosphate (PIP2) found ?

A

Found in the lipid bilayer

36
Q

What is Phosphatidylinositol 4,5 bisphosphate (PIP2) ?

A

It is the substrate of the enzyme phospholipase C (PLC)

37
Q

Function of phospholipase C

A

Liberates 2 signalling molecules from PIP2

  • IP3
  • DAG

(these molecules are second messengers)

38
Q

Function of Calcium

A

Activates cellular pathways
Ca2+ conc increases in the cell in response to IP3 release.

Calcium binds to proteins to regulate their function

39
Q

State some substrates for PKC’s

A

Tumour suppressor p53 (transcription factor)
Cav 1.2 (calcium channel)
IKK alpha (cytokine)

40
Q

Function of Tumour suppressor p53 (transcription factor)

A

Prevents tumour formation

41
Q

Function of Cav 1.2 (calcium channel)

A

Heart muscle contraction

42
Q

Function of IKK alpha (cytokine)

A

B cell activation
- Immune function

43
Q

What are eicosanoids ?

A

Inflammatory mediators

(local hormones)

44
Q

Where are eicosanoids derived from ?

A

Phospholipid derived

45
Q

Why are eicosanoids considered as ‘local hormones’ ?

A

They have specific effects on target cells close to their site of formation. (autocrine/paracrine)

They are rapidly degraded, so are not transported to distal sites within the body.

46
Q

State some features of eicosanoids

A

Unstable
Don’t last very long

47
Q

Name the 3 main types of eicosanoids

A

Prostaglandins
Thromboxanes
Leukotrienes

48
Q

Eicosanoid meaning

A

‘Eicosa’ - 20 carbon atoms
‘Enoic’ - Double bonds

49
Q

What is the main source of eicosanoids ?

A

Arachidonic acid

50
Q

State some features of arachidonic acid

A

A 20 Carbon, unsaturated fatty acid, containing 4 double bonds.

(20:4)

51
Q

What is the initial and rate limiting step in eicosanoid synthesis ?

A

Liberation of arachidonic acid by phospholipase A2 (PLA2)

52
Q

How is PLA2 activated ?

A

By a variety of receptor mediated signals

53
Q

State some ways in which PLA2 is activated

A

Serotonin receptors
Glutamate receptor 1
Some cytokine receptors
Increase in intracellular calcium levels

54
Q

Describe eicosanoid biosynthesis

A

Through the action of PLA2, phospholipids can be converted into arachidonic acid.

[By-product of platelet-activating factor]

The arachidonic acid can then be processed by 2 different classes of enzymes.

55
Q

State how arachidonic acid can be metabolised

A

BY 2 classes of enzymes :

  • Cyclo-oxygenase
  • Lipooxygenases
56
Q

State the function of cyclo-oxygenases

A

Cyclo-oxygenases (and peroxidase) metabolise arachidonic acid to give prostaglandins and thromboxanes.

57
Q

State the function of Lipoxygenases

A

Lipoxygenases metabolise arachidonic acid to give leukotrienes.

58
Q

Where are prostaglandins synthesised ?

A

Synthesised in all tissues and cell types

59
Q

Function of prostaglandins

A

Inducing vasoconstriction/ vasodilation

Gives rise to redness, swelling and heat

Inhibits/promotes platelet aggregation.

60
Q

What does the effects of prostaglandins depend on ?

A

Depends upon receptor

61
Q

Function of EP1 receptor

A

Vasoconstriction

62
Q

Function of EP2 receptor

A

Vasodilation

63
Q

Key functions of prostaglandins

A

Inflammatory response
Thermoregulation (Fever)
Pain

64
Q

Where are thromboxanes synthesised ?

A

Synthesised in platelets (clotting)

65
Q

Describe some features of thromboxanes

A

Short lived (autocrine/paracrine)

66
Q

Function of thromboxanes

A

Stimulates platelet aggregation

Vasoconstrictor

67
Q

State the function of leukotrienes

A

Immune response

Heavily implicated in asthma and allergy

68
Q

Describe the structure of leukotrienes

A

Contains a conjugated triene system of double bonds

Some contain amino acid cysteine in their structure

69
Q

What is the function of cysteine in leukotrienes ?

A

Anaphylactic shock

70
Q

Where are PAF synthesised ?

A

By-product of arachidonic acid liberation

Synthesised in leukotrienes.

Also synthesised by injured tissue.

71
Q

Function of PAF

A

Stimulates platelet aggregation

Vasoconstriction

Inflammation

Immune response (also anaphylaxis)

72
Q

What are NSAID’s ?

A

Non-steroidal anti-inflammatory drugs

73
Q

State the function of NSAIDs

A

Inhibit :

  • Formation of prostaglandins involved in fever, pain and inflammation
  • Blood clotting by blocking thromboxane formation in blood platelets
74
Q

Name some NSAID’s

A

Aspirin
Derivatives of ibuprofen

75
Q

Describe the action of ibuprofen

A

Block the hydrophobic channel by which arachidonate enters the cyclooxyrgenase active site.

76
Q

Describe the action of aspirin

A

Aspirin acetylates a serine hydroxyl group near the active site, preventing arachidonate binding.

77
Q

What types of inhibitors are aspirin and ibuprofen ?

A

Aspirin : Irreversible inhibitor

Ibuprofen : Reversible inhibitor

78
Q

Why is the action of aspirin long lived in platelets ?

A

Platelets lack a nucleus and so do not make new enzyme.

Cox1 inhibited, stays inhibited

79
Q

Function of aspirin

A

Anti-clotting effect

Inhibition of thromboxane formation (via Cox1 inhibition) in blood platelets

Medicine Year 1 - Semester 2 - Part 1 (51 decks)

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