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MPharm Stage 1 > Unit 2: Cells and Signalling > Flashcards

Unit 2: Cells and Signalling Flashcards

1
Q

Phospholipid bilayer is composed of…

A

Polar phosphate heads which are hydrophilic and point outwards
Hydrophobic fatty acid tails which line up on inside of the bilayer making it almost impossible for polar molecules like ions to cross

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2
Q

Functions of plasma cell membrane

A
  • Physical barrier between outside and inside of cell– preserves cell status as individual unit
  • Controls movement of materials into cell and secretion of materials out of cells without breaching barrier
  • Communicates with the world outside of the cell. Receptors on membrane can bind with specific chemical messengers to change activity in cell.
  • Makes physical connections with other cells
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3
Q

Function of the ribosomes

A

Site of proteinsysnthesis where mRNA is translated to protein
Free ribosomes manufactures proteins destined for the cytosol
Fixed ribosomes on RER manufactures proteins destined for secretion outside the cell.

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4
Q

Structure of endoplasmic reticulum

A
  • Network of membranes
  • Made of series of tubes and chambers aka cisternae
  • Directly connected to membrane surrounding nucleus
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5
Q

Structure of ribosomes

A

Small organelles
70S or 80S
Small and large subunit

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6
Q

Function of endoplasmic reticulum

A
  • Responsible for synthesis and storage of proteins, carbohydrates and lipids,, transport of molecules,, and detoxification of dangerous material.
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7
Q

Structure of the nucleus

A
  • Double membrane known as nuclear envelope
  • Chromatin enclosed within
  • Nuclear pores
  • Nucleolus
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8
Q

Eukaryotic cells contain…

A

A membrane bound nucleus and membrane bound organelles

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9
Q

Function of golgi apparatus

A
  • Modifies and packages cellular material for:
    –> Release outside of cell (exocytosis)
    –> Use in maintainence of cell membrane
    –> Incorporation of enzymes into lysosomes for use within the cell
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10
Q

Acetylcholinesterase inhibitors and their consequences? Examples of nerve agents

A

Novichok, Sarin, VX
Continued presence of acetylcholine in synaptic cleft desensitises receptors, acetylcholine signalling no longer functions
Causes various neurological symptoms and can be fatal due to respiratory paralysis

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11
Q

Intrinsic efficacy

A

Ability of an agonist, having bound to a receptor, to intiate a cellular response by ensuring the coupling of the agonist-receptor complex with the transduction system (G protein//ion channel)
Drug must bind and cause response to be an agonist

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12
Q

kinases

A

Enzymes which catalyse the transfer of phosphate groups from a donor molecule (ATP) to a specific target molecule (phsophorylation reaction)

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13
Q

Different classifications of neurotransmitters

A

Acetylcholine
Biogenic Amines- dopamine, epinephrine, serotonin
Amino acids- GABA, glutamate
Neuropeptides- vasopressin
Purines- ATP
Gases and lipids- nitric oxide

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14
Q

Depolarisation

A

Na+ flow into cell down chemical//electrical gradient
Until it reaches 30mV when the Na+ channels close

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15
Q

What are paracrine factors and give 2 examples?

A

Released from cells
Have local (nearby) site of action
E.g., neurotransmitters, neuropeptides, lipid mediators

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16
Q

What causes hallucinations and delusions seen in Sz? What antipsychotic medication has been used in the past and what causes its adverse effects? What do newer antipsychotics target

A

Excessive dopamine signalling
Antipsychotic medication= haloperidol= antagonist of D2 receptors, reduce dopaminergic signalling in mesolimbic pathway
Antagonism of dopamine receptors in other pathways causes adverse effects.
NEWER ANTIPSYCHOTICS (olanzapine) TARGET D2 receptors and other receptors

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17
Q

How is acetylcholine used in neuromuscular junction?

A

Neurones which supply muscles release acetylcholine
Acetylcholine receptors on muscles detect NT, muscle contracts.

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18
Q

Agonist

A

Drug/Chemical that binds to receptor, mimics the action of the endogenous ligand and initiates cellular response

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19
Q

stages of interphase

A

G0
G1
S phase
G2 phase

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20
Q

Local potential

A

Change in membrane potential is limited to the area of the membrane around open ion channels
Once ion channel closes after very brief opening membrane will return to RMP

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21
Q

Dendrites

A

Recieve inputs from other neurons

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22
Q

Non-competitive antagonism

A

Binds to allosteric site- causes conformational change in receptor- prevents binding of agonist OR blocks a step downstream in sequence of events leading from receptor activation to cellular effect.

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23
Q

EPSP

A

Excitatory Postsynaptic Potential
Ligand-gated sodium channels increase local membrane potential
Made postsynaptic membrane more positive, more ‘excitable’, closer to threshold so action potential more likely to occur.

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24
Q

Types of agonism

A

Full, partial and inverse

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25
Q

Explain the significance of Ca2+ in cells

A

Responsible for initiating muscle contraction, secretion, release of neurotransmitters, and others.
Cytoplasmic Ca2+ levels are very carefully regulated so the biological effects are controlled: if Ca2+ levels RISE TOO HIGH this can lead to cell death.

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26
Q

Function of RER

A

Recieves newly manufactured protein chains from ribosomes
Modification of proteins into glycoproteins
Packaging of proteins/glycoproteins into transport vesicles to be sent to Golgi apparatus

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27
Q

Types of antagonism

A

Competitive, non competitive, physiological, chemical, pharmacokinetic

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28
Q

Repolarisation

A

Voltage-gated K+ channels open allowing K+ to flow out of the cell down its chemical/electrical gradient
Repolarises membrane, bringing membrane potential back towards equillibrium potential -80mV

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29
Q

4 major dopaminergic pathways in brain

A

Mesolimbic pathway
Mesocortical pathway
Nigrostriatal pathway
Tubero-infundibular pathway

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29
Q

How do ionotropic receptors work?

A

Part of ligand-gated ion channel protein
Activation results in conformational change in channel protein, allowing specific ions (Na+, Cl-, K+) to pass through by FD
Result in very fast transmission that occurs in miliseconds
E.g receptors for neurotransmitters like GABA, glutamate, acetylcholine

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30
Q

Structure of mitochondria

A
  • Outer membrane surrounds the entire grain-shaped molecule
  • Highly folded second inner membrane
  • Folds are called cristae
  • Contains mitochondrial matrix
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31
Q

What do old and new treatments of CF focus on?

A

Old- focus on clearing mucus from lungs and dealing with associated infections
New- target CFTR protein to fix fault caused by the mutation (only work for certain genotypes- the patients case of CF has to have been caused by a specific mutation )

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32
Q

Increasing GABA activity will…

A

cause sedative effects, and can be used in treatment of anxiety, insomnia or as anaesthetics

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33
Q

What is G1 phase and how long does it last?

A

8-12hrs at high speed OR several weeks in cells continuing normal operations
Cell increases it count of cytoskeletal filaments, ribosomes, ER, golgi, mitochondria and cytosol so there is enough for 2 cells
Manufacture of new centrioles begins

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34
Q

Which steps can be targeted by drugs to alter synaptic transmission?

A
  1. Synthesis
    > stops chemical reactions creating neurotransmitters
    > increase or decrease availability of its precursor
  2. Storage
    > block neurotramsitters from entering/leaving vesicles
    > empty neurotransmitters from vesicles
  3. Release
    > block Ca2+ channels on preS terminals
  4. Activation of receptors
    > bind to receptors in place of neurotransmitters
    > interact with preS receptors that control NT release
  5. Inactivation/Reuptake
    > inhibit enzymes that breakdown NT
    > prevent NT from returning to preS neuron in reuptake
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35
Q

When do voltage-gated sodium channels open?

A

When the membrane reaches -55mV

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36
Q

What is G2 phase and how long does it last?

A

2-5 hrs
Remaining proteinsynthesis completed
New centrioles completed

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37
Q

Structure of cytoskeleton

A
  • Made of variety of proteins e.g. actin and tubulin
  • Also may have extracellular structures built around the core e.g. flagella and cilia
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38
Q

Axon

A

Carries info in form of electrical signals//action potential
Axon meets cell body at axon hillock

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39
Q

Ligand

A

Anything that binds to a larger molecule

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40
Q

Mesolimbic pathway

A

neurones project from ventral tegmental area to ventral striatum

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41
Q

Equillibrium potential for sodium

A

+60mV

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42
Q

Antagonist

A

Drug/Chemical that blocks action of endogenous ligand, therefore blocks normal cellular response, inhibiting action of agonist

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43
Q

Tolerance

A

Where responsiveness diminishes more slowly than with tachyphylaxis. Larger doses required for same response

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44
Q

What are autocrine factors and give 2 examples?

A

Released from cells
Act on the same cells
E.g., hormones, lipid mediators and neurotransmitters

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45
Q

When do hormones become inactive?

A

When it diffuses out of the bloodstream and binds to receptors on target cells
Absorbed/broken down by cells of liver/kidney
Broken down by enzymes in plasma/interstitial fluid

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45
Q

Pharmacokinetic antagonism

A

Where one drug affects absorption/distribution/metabolism/excretion of another

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46
Q

Treatment for Parkinsons Disease and how it works

A

Parkinsons diseases causes the loss of dopaminergic neurones
L-DOPA is the reatment
It is a substrate for production of dopamine
More dopamine available for remaining neurones reducing symptoms

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47
Q

Explain how adenylate cyclase/cAMP receptors work and name examples of where they are used

A

First messenger (hormone/neurotransmitter) in ECF combines with the receptor.
Adenylate cyclase enzyme is activated via G protein
Second messenger cAMP is generated inside the cell, activating cAMP-dependent protein kinase, initiating cellular response.

EXAMPLES:
1. Vasopressin (ADH hormone)
2. Epinephrine (Adrenaline) and Glucagon)
3. Histamine

48
Q

Explain how Phospholipase C/inositol phosphate system receptors work and name examples of where they are used

A

AKA calcium mobilising receptors
First messenger (hormone or neurotransmitter) in ECF combines with receptor and phospholipase C enzyme is activated via G protein
Second messengers (DAG and IP3) are generated inside the cell. These activate cellular response mechanisms (including the release of intracellular Ca2+ from endoplasmic reticulum )

EXAMPLES:
1. Acetylcholine
2. Epinephrine (adrenaline

49
Q

What are the 2 things receptors can act as?

A

Transducers- responding to external stimuli
Transporters- bring molecules into cell interior by process of receptor-mediated endocytosis

50
Q

Voltage-gated ion channels

A

Sensitive to membrane potential of cell
E.G. voltage gated sodium channels will be closed at RMP but if it rises, this will cause the pprotein which make up the channel to shift, opening the channel.

51
Q

What is S phase and how long does it last?

A

6-8 hrs
DNA replicated– helicases disrupt H bonds between base pairs THEN DNA polymerase attaches to strands adding comp DNA nucleotides in a similar process to transcription BUT this time copies are made of both strands.

52
Q

What is primary active transport?

A

Where the transport protein contains an ATPase
ATPase hydrolyses ATP to generate the energy required for transport, e.g. ion pumps

53
Q

Function of SER

A
  • Synthesis of phospholipids and cholestrol
  • Synthesis of steroid hormones, including sex hormones
  • Synthesis and storage of triglycerides and glycogen
  • Detoxification of drugs and alcohol
54
Q

Disorders which affect myelination

A

Multiple Sclerosis - damage to myelination in CNS
Guillain-Barre syndrome - damage to myelination in PNS
Both autoimmune disorders

55
Q

Anaphase

A

Centromeres binding the chromatids together are cleaved and individual daughter chromosomes are dragged in opposite directions to opposite ends of the cell.

56
Q

What are endocrine factors and give 2 examples?

A

Released from cells
Enter circulation to ‘act at a distance’
E.g., hormones and cytokines

57
Q

What is secondary active transport?

A

E.g. co-transport
Transporter will make use of existing difference in electrochemical potential between cell and fluid
Pumping ions out of the cell via primary active transport creates electrochemical potential so ATP is still indirectly consumed.

58
Q

Nigrostriatal pathway

A

projects from substantia nigta to dorsal striatum
involved in motor control and parkinsons disease

59
Q

Prophase

A

Nucleolus disappears, DNA coils tighter, individual chromosomes become visible
Sister chromatids attached by centromere where kinetochore protein complexes are assembled.
Centrioles generate spindle fibres and use motor proteins to move themselves along spindle fibres to opposite ends of cell nucleus

60
Q

Prometaphase

A

Nuclear envelope breaks down, kinetochore of each chromatid attached to spindle fibres running between centrioles

61
Q

Spindle fibres

A

chromosomal microtubules

62
Q

How do kinase-linked receptors work?

A

Receptor has extracellular area to bind the ligand and intracellular enzymatic area (kinase).
Slower than metabotropic receptor responses
Involved in regulation of growth, differentiation and responses to metabolic signals.

63
Q

Four families of receptors

A

Ionotropic receptors
Metabotropic recepetors
Kinase-linked receptors
Nuclear(intracellular) receptors

64
Q

Affinity

A

Measure of how strongly the drug binds to the receptor, characterised by KD
KD = concentration of drug required to occupy 50% of receptors
Higher affinity= lower KD

65
Q

What type of mutation is sickle cell anaemia caused by and is it a recessive or dominant disorder?

A
  • Recessive inherited disorder
  • Caused by a single substitution mutation in the HBB haemoglobin gene
66
Q

What is the RMP of neurones?

A

-70mV

67
Q

Physiological antagonism

A

Two agonists, each acting at their own receptors, induce opposing effects in cells and tissues.
Important in physiological regulation of body functions e,g, rate of heart where acetylcholine decreases HR, whereas noradrenaline increases HR.

68
Q

Main inhibitory neurotransmitter in brain and its receptors

A

GABA
GABAA = ionotropic receptors
GABAB = metobotropic receptors

69
Q

Tachyphylaxis

A

Rapid protection
Responsiveness to a drug diminishes rapdily after initial administration or during continued administration

70
Q

Nonsence mutation

A

Deletion and insertion

71
Q

Function of peroxisomes

A
  • Responsible for the digestion of large fatty acids
  • Site of Beta oxidation
  • Reactive hydrogen peroxide generated during fatty acid breakdown
  • Damaging material is kept safe inside peroxisome and further degraded to water and oxygen before release.
72
Q

Competitive antagonism

A

Bind to the same site as agonist so compete for binding site
Increase in amount of agonist overcomes
Has affinity not efficacy

73
Q

Tubero-infundibular pathway

A

involved in hormone secretion

74
Q

How do hormones interact with receptors?

A

Either hormones like peptide hormones will interact receptors on the plasma membrane OR some hormones like steroid hormones bind to intracellular receptors and activate or deactivate specific genes. This can alter rate of DNA transcription and pattern of proteinsynthesis

75
Q

How do nuclear (intracellular) receptors work?

A

Bind lipid-soluble ligands e.g. steroid hormone molecules
Complex then binds to DNA and regulates gene transcription
Usually require hours or days for full response
Long lasting responses- remain long after agonist binding
E.g. steroid hormones such as mineralcoticoid aldosterone

76
Q

IPSP

A

Inhibitory Postsynaptic Potential
Ligand-gated chloride channels open, ions enter cell
Made postsynaptic membrane more negative, more ‘inhibitory’, further from threshold so action potential less likely to occur.

77
Q

How do metabotropic receptors work?

A

AKA G protein-couples receptors

Agonist molecule combines with receptor proteins in membrane resulting in conformational change in receptor- causes activation of membrane-associated enzyme
Leads to formation of intracellular second messengers
Used in slower neurotransmission processes than ionotropic e.g. hormone action

78
Q

Why does a potential difference exist across the cell membrane?

A

Ions are distributed unevenly outside and inside cells.
High conc of sodium and chloride ions OUTSIDE the cell (extracellular)
High conc of potassium and various anions INSIDE the cell (intracellular)
This creates an electrochemical gradient across the membrane

79
Q

3 groups of hormones

A

Amino acid derivatives
Peptide hormones
Steroid hormones

80
Q

What is G0 phase?

A

Cell is not preparing to divide.
Rapidly dividing cells like stem cells never enter G0
Matured skeletal muscle cells and others remain in G0

81
Q

Mesocortical pathway

A

projects from VTA to prefrontal cortex

82
Q

Metaphase

A

Through microtubules, each centriole pulls on chromosomes
Chromosomes line up between two centrioles in an area referred to as metaphase plate//equatorial plane.

83
Q

Autocoids/Local hormones

A

chemical messengers that have paracrine action (produced at one site active at another)

84
Q

Main excitatory neurotransmitter in brain

A

Glutamate

85
Q

Supersensitivity and when it occurs

A

Receptors become supersensitive to stimulation by agonists.
Occurs when:
> receptor population is blocked from access of agonist molecules (could be due to high exposure of antagonists previously)
> when the receptor is deprived of agonist (motor nerve to skeletal muscle is damaged so nicotinic receptors are deprived of acetylcholine so muscle shows sensitivity to acetylcholine due to… 1) increased coupling of receptors, 2) increased number of receptors 3) translocation of receptors out of neuromuscular endplate to sarcolemma)

86
Q

Examples of metabotropic receptors

A
  1. Adenylate cyclase/cAMP system:
  2. Phospholipase C/inositol phosphate system
87
Q

Function of cytoskeleton

A
  • Cells structural support
  • Influences shape, strength and flexibility of cell, movement and motility of organelles
88
Q

Function of lysosomes

A
  • Vesicles that engulf and digest their targets
  • Clear damaged organelles, invading bacteria and viruses, or other organic waste
89
Q

What does the cell cycle control system do?

A

Biochemical checkpoints which
- Allow feedback signals about upstream processes to control the progress of downstream events
- Sensitive to external regulation to alter the thresholds required for cells to pass between phases of the cycle (G1 to S, and G2 to M)

90
Q

Endogenous ligand

A

Those that occur normally in the body and bind to receptors e.g. neurotransmitters

91
Q

Equillibrium potential

A

If an ion could freely cross the membrane, EP is the point at which there would be no net movement of the ion across the membrane (equalised)

92
Q

Where is acetylcholine synthesised and broken down

A

Synthesised= presynaptic terminal by enzyme choline acetyltransferase (ChAT)
Broken down= in synpase by acetylcholinesterase

93
Q

Dependence

A

Person developed physical/physiological requirement for drug to avoid precipitation of withdrawal symptoms if drug administration isnt repeated

94
Q

Inverse agonism

A

Reduce activity by deactivating an activated receptor
Has negative efficacy

95
Q

What amino acid is serotonin synthesised from and what is it broken down by?

A

Monoamine sythesised from trytophan
Broken down by monoamine oxidase

96
Q

Telophase

A

New nuclear envelope forms around each set of daughter chromosomes
In each growing nucleus, chromosomes relax back into chromatin and a nucleolus becomes visible

97
Q

Partition coefficient equation and what each part means

A

P=Co / Cw
P= measure of lipophilic character of substance
Co= conc of solute in organic solvent
Cw= conc of solute in water

98
Q

Saltatory conduction

A

Myelin sheath acts as insulator
Allows signal to travel faster
Voltage gated sodium channels clustered at nodes of ranvier and the action potential jumps to each node

99
Q

What can cause tachyphylaxis, tolerance or desensitisation?

A

Changes/loss in receptors
Increased metabolism
Physiological adaptation
Depletion of mediators
Cellular extrusion of drugs

100
Q

Chemical antagonism

A

Two drugs interact in solution causing loss of biological activity when administered together

101
Q

How is dopamine made and broken down?

A

Part of a category of monoamines called catecholamines, synthesised from amino acid called tyrosine
1. Tyrosine to L-DOPA by tyrosine hydroxylase
2. L-DOPA to dopamine by DOPA decarboxylase
3. Dopamine loaded into synaptic vesicles by VMAT
4. After being released into synpase, dopamine is transported back to preSN by dopamine transporter
5. Dopamine broken down by monoamine oxidase

101
Q

Hyperpolarisation and include info about refractory period

A

After action potential, membrane potential goes slightly lower than usual- some K+ channels remain open
There is a refractory period (neuron typically cannot fire another action potential) split into two phases: absolute refractory period (immediately after, where voltage gated sodium channels still deactivated) and relative refractory period (voltage gated sodium channels now ready but membrane is still hyperpolarised)

102
Q

Henderson-Hasselbach equation and rearranged

A

pKa= pH -log [conjugate base]/[conjugate acid]

Rearranged:
[conjugate base]/[conjugate acid]= 10(pH-pKa)

103
Q

What are some examples of acetylcholinesterase inhibitors that are clinically beneficial and their benefits?

A

Neostigmine, pyridostigmine
Used in treatment of Myasthenia Gravis
Less potent and reversible

104
Q

Which forms of drugs readily diffuse across the membrane?

A

Lipid-soluble, non-ionised form of the drugs
Most used in clinical practice are weak acids/bases that exist in ionised and unionised forms depending on pH.

105
Q

How SSRI’s and SNRIs work and example of SSRI

A

Fluoxetine
Selective Serotonin Reuptake Inhibitor
Blocks reuptake of serotonin from synpase- increase serotonin signalling

Serotonin Norepinephrine Reuptake Inhibitor
Also blocks reuptake of norepinephrine

106
Q

What inbuilt mechanisms prevent cell division if there is significant damage to a cell?

A
  • Ends of chromosomes have repeating sections of code called telomeres acting as a protective cap for the chromosomes. Telomeres become damaged and shorten during cell division- when they become too short tumour suppressor genes produce growth inhibitors.
  • Senescence (old age) or apoptosis (programmed cell death)
  • Tumour suppressor genes prevent cell replication– when damage to DNA is detected, initiating mechanisms for DNA repair, and inducing apoptosis if damage is irreparable.
107
Q

What can barbiturates be used as?

A

As an agonist of GABAA receptors, benzodiazepines, and also Z-drugs.

Cause channel to open more frequently
ALCOHOL causes channel to stay open for longer
Both allow more chloride ions to flow in

108
Q

Equillibrium potential for potassium

A

-80mV

109
Q

What kind of disease is cystic fibrosis and which genes are mutated? What do these mutations cause? How does CF affect transporters?

A
  • Recessive inherited disorder
  • Mutations in CFTR gene causes various health issues like build up of thick mucus in lungs
  • CFTR transports chloride ions
  • Symptoms of CF result from improper transport of chloride
110
Q

Ligand-gated ion channels

A

Have binding site on them- specific substances (ligands) attach to the ion channel and cause it to open.
Could be endogenous ligands (internal, less selective) e.g. neurotransmitters, or drugs

111
Q

How is RMP restored?

A

By sodium potassium ATPase which pumps 3Na+ ions OUT of the cell for every 2K+ ions INTO cell to restore cells RMP

112
Q

Missence mutation

A

Substitution

113
Q

How can threshold be reached?

A

Lots of ligand-gated ion channels activated together, local potential rises more due to increased amount of sodium ions entering cell
If the local potential is strong enough, it will reach threshold for generating an action potential

114
Q

How and why does the membrane potential change?

A

Changes by external signals received by the cell
Happens because the cell becomes more permeable to particular ions so they are able to move across the membrane

115
Q

Variability

A

Differences in magnitude of response among individuals in same population given same dose of a drug

116
Q

What is the cell cycle control system? What is telomeres?

A
  • Have biochemical checkpoints which regulate when the cells pass through each phase of the cycle
  • Ends of chromsomes have repeating sections of code called telomeres- these act as a protective cap for chromsomes, as the cells divide more these get more damaged. If they get too damaged then tumour supressor genes will begin to produce growth inhibitors.
117
Q

Steroid hormones

A
  1. Diffusion through membrane lipids
  2. Binding of hormone to cytoplasmic or nuclear receptor
  3. Binding of hormone-receptor complex to DNA
  4. Gene activation
  5. Transcription and mRNA production
  6. Translation and protein synthesis
  7. Alteration of cellular structure/activity
  8. Target cell response

MPharm Stage 1 (14 decks)

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