Lipids And Cel Membranes Flashcards

1
Q

Cell to cell communication

A

Synthesis of signal
Release of signalling molecule by exocytosis diffusion to cell to cell contact
Transport signal to target cell
Detection by receptor protein
Change in cellular metabolism, function etc
Removal of signal or desensitisation

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2
Q

Two types of signalling

A

Long range and short range

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3
Q

Long range signal

A

Endocrine

Neurotransmitters

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4
Q

Endocrine

A

Where hormones is released by endocrine cells and carried in bloodstream to distal target cells

Example FSH released form pituitary acts on ovary

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5
Q

Example of neurotransmission

A

Breathing phrenic and thoracic nerves send impulses from brain to diaphragm

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6
Q

Short range signalling

A

Paracrine
Autocrine
Membrane bound proteins interact

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7
Q

Paracrine

A

Signalling molecules only affect cells in close proximity to secreting cell

Ex somatostatin release by pancreas acts locally as can neurotransmittion be local

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8
Q

Autocrine

A

Cells respond to substances that they themselves release

NT and Growth factors bind to cells that release them

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9
Q

Membrane bound proteins interact to signal

A

Signaling by plasma membrane attached proteins

Ex signalling by T cells in immune systems

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10
Q

Ex of multiple types of signalling occurring simultaneously

A

Insulin released form pancreatic beta fuels acts in autocrine paracrine and endocrine matter

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11
Q

Lipid soluble signalling molecules

A

Bind inteacellular receptors rest bing to membrane bound receptors on surface

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12
Q

Examples of cell surface receptor

A

Ligand gated ion channels
G protein coupled receptor
Kinase liked receptors

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13
Q

Example of intracellular receptors

A

Nuclear receptors

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14
Q

Signals that alter protein function are

A

Fast

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15
Q

Signals that alter protein synthesis are

A

Slow

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16
Q

Altered protein synthesis or function work by

A

Altering cytoplasmic machery and hence altering cel behaviour

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17
Q

Examples of lipid soluble molecules

A

Cortisol
Estradiol
Thyroxine
Testosterone

18
Q

What happens during lipid molecule synthesis

A

Cortisol passes through plasma membrane
Reacts with intracellular receptor protein causing conformational change
Can now pass through into nucleus
Complex activates target gene via regulatory region causing transcription to occur

19
Q

Inositol phospholipid signalling pathway

A

PIP2 is phospholipid found in enzyme bilateral

Substrate of enzyme phosplipase C (plc)

Plc liberates two signalling molecules from PIP2 - IP3 and DAG

Opens calcium channel

20
Q

What happens to calcium in response to IP3 release

A

Calcium conc inc in cell

Calcium binds to protein to regulate their function

21
Q

Substrates for PKC to activate it are

A

Tumor suppressor p53. Prevents tumor formation

CAv 1.2 - heart muscle contraction

IKKa - B cell activation

22
Q

What happens to IP3 after signal

A

Referred back to membrane as PIP2

23
Q

What are eicosanoids (prostanoid)

A

Inflammatory mediators

Local hormones - specific effect on target cel close to site of formation

Rapidly degradedo so not transported to distal sites within the body

24
Q

Main eicosanoids (prostanoids)

A

Prostaglandins
Theomboxanes
Leukotrienes

20C with double bonds

25
Q

Source of eicosanoids

A

Arachidonic acid (20:4)

26
Q

Biosynthesis of eicosanoids

Initial and rate limiting step

A

Liberation of arachidnoic acid by phospholipids A2 PLA2

PLA2 
Serotonin receptors
Glutamate receptor 1 
Some cytokine receptors
An increase in calcium
27
Q

How can arachidonic scid be metabolised

A

Cyclooxygenase and peroxidase to give prostaglandins and theomboxanes

Lipocygenases to give leukotrienes

28
Q

Prostaglandins

A

Synthesised in all tissue and cell types

Vasoconstriction dilation
Inhibitor promote platelet aggregation

EP1 - vasoconstriction
EP2 - vasodilation

Inflammatory response. Thermoregulation fever and pain

29
Q

Thromboxanes

A

Synthesised in platelets clotting

Short lived

Thromboxane A2 TXA 2 had prothrombotic properties

Stimulate platelet aggregation

Vasoconstrictor

30
Q

Leukotrienes

A

Synthesised in WBC and contain double bonds

Some contain cystine in structure - anaphylactic shock

Heavily implicated in Asthma and allergy

31
Q

Platelet activating factor

A

By product of arichdonic acid liberation not an eicosanoid

Synthesised in leukocytes and injured tissue

Platelet aggregation
Vasoconstriction
Inflammation
Immune response

32
Q

What are NSAIDs

A

Inhibit cuclooxugenases and hence the formation of prostaglandins involved in pain fever and inflammation ( blockchannel where arschidonste enters COX active site)

Inhibit blood clotting by clocking thrombocytes tmformstion in blood platelets

33
Q

How does aspirin work

A

Acetylates serine hydroxyl group preventing aracidonate bidning

IRREVERSIBLE

resybthesis of COX1 to restore activity

34
Q

Aspirin anticoagulant

A

Thirnboxnae A2 stjualtes blood platelet in clotting

COX1 inhibiton - inhibition of theomboxane formation

Long lived because platelets lack nucleus and connor make new enzyme s

35
Q

Aspirin

A

Cox1 inhibitin

36
Q

Dexamethasone

A

Glucocorticoid

Inhibitos cox2 induces PLAw inhibitor

Arthritis chemotherapy

37
Q

Iloprost

A

Activates prostacyclin receptor

Pulmonary hypertension

38
Q

Zileuton

A

5-lipoxygenase inhibitor and his inhibits leukotriene synthesis
Asthma

39
Q

Zafirukast

A

Inhibits leukotriene by blockingrecepto

Asthma

40
Q

Dipyridamole

A

Inhibits thromboxane A2 synthesis

Pulmonary hypertension

Stoke pretentious with aspirin