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ESA 2 - Mine > M&R > Flashcards

M&R Flashcards

0
Q

Where are alpha1 adrenoreceptors found and what is their function there?

A

Liver - glycogenolysis
Pupil - increase dilation
Bladder - increase sphincter contraction = bladder relaxes
Vascular smooth muscle - vasoconstriction
Skeletal muscle - glycogenolysis and arterial dilation

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1
Q

Where are adrenoreceptors found?

A

On effectors stimulated by the sympathetic nervous system

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2
Q

Where are alpha 2 adrenoreceptors found and what is their function there?

A

GIT - decrease peristalsis and gut secretion.

- constrict sphincters

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3
Q

Where are beta 1 adrenoreceptors found and what is their function there?

A

SAN - increase HR
Ventricle - increase force of contraction
Adipose tissue - lipolysis (along with beta3)

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4
Q

Where are beta 2 adrenoreceptors found and what is their function there?

A

Lungs bronchi - vasodilation
Vascular smooth muscle - vasoconstriction
Liver - glycogenolysis
Skeletal muscle - glycogenolysis
Bladder - relaxation
Ventricle - increase force of contraction
GIT - decrease peristalsis

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5
Q

How does GalphaQ G protein work?

A

It activates phospholipase C.
This converts PIP2 —-> IP3 + DAG
IP3 acts upon IP3 receptors in the SR to open Ca2+ channels
= Ca2+ influx

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6
Q

What is the action of GalphaS G protein?

A

Activates adenylate cyclase
Increases cAMP levels
This activates:
Protein kinase A = phosphorylations (beta1 and 2)
HCN channels (beta1)
Certain K+ channel for relaxation (beta2)

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7
Q

How does GalphaI G protein usually work?

A

It acts to inhibit adenylate cyclase
Decreases cAMP levels
Less activation of protein kinase A
Less phosphorylation

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8
Q

What adrenoreceptors does adrenaline have the highest affinity for?

A

Beta2
Then alpha 1
But still acts upon all

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9
Q

What drug can be used as an alpha1 agonist?

A

Oxymetazoline (nasal decongestant)

- vasoconstriction of nasal vessels = less inflammation and mucus production

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10
Q

What drug can be used as an alpha 2 agonist?

A

Adrenaline = prolongs action of local anaesthetic

- vasoconstriction limits its diffusion/absorption and bleeding in surgery

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11
Q

What drug can be given as an alpha adrenoreceptor antagonist?

A

Terazosin

- decrease high BP by blocking vasoconstriction

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12
Q

What drug can be given as a beta1 agonist?

A

Dobutamine - used in cardio genic shock to increase HR

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13
Q

What drug can be given as a beta1 antagonist?

A

Atenolol - acts to slow heart rate, therefore reducing hearts need for O2 (angina) and decreasing BP

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14
Q

What drug can be given as a beta2 agonist?

A

Salbutamol - decrease bronchoconstriction in asthmatics

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15
Q

What can be given as a beta adrenoreceptor antagonist?

A

Propanolol

Acts the same as atenolol in slowing HR, but is less selective, so a danger to asthmatics

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16
Q

Where are muscarinic1 receptors found and what is their function?

A

Bladder - increase contraction

Exocrine glands - increase secretion

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17
Q

Where are muscarinic 2 receptors found and what is their function?

A

SAN - decrease HR
Presynaptic neurone of post synaptic ganglion at neuromuscular junction - autoregulation
Bronchi - constriction

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18
Q

What is auto regulation at muscarinic 2 receptors?

A

Where if he amount of ACh builds up, it will act upon M2 and M4 receptors on the presynapse membrane and inhibit ACh release. This prevents desensitisation.

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19
Q

Where are muscarinic 3 receptors found and what is their function?

A 
Bronchi - constriction
Bladder - constriction
Pupils - dilation
GIT - increase peristalsis and gut secretions
       - relax sphincters 
Liver - increase glycogenesis
Glands in general - increase secretion
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20
Q

What are the muscarinic and adrenoreceptors which seem to have the greatest effect?

A

Alpha 1
Beta 2
Muscarinic 3

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21
Q

What receptors are present and most active on the heart?

A

Beta 1

Muscarinic 2

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22
Q

Name a drug specific to action on an M3 receptor and its action.

A

Carbachol/pilocarpine - acts to dilate the pupil which increases the angle of the eye via contraction of the sphincter pupillae = decrease in intraocular pressure to help glaucoma etc.

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23
Q

What is atropine?

A

An antagonist of muscarinic ACh receptors that is often used to prevent spasms in the gut.

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24
Q

What is bethanechol?

A

An agonist of muscarinic receptors, which can be used to treat urinary retention, often due to previous surgery.

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25
Q

What role does NCX have in cell injury due to ischaemia?

A

Ischaemia = no ATP = no Na+/K+ ATPase
This means Na+ builds up intracellularly.
This causes greater Na+ gradient in the cell so NCX reverses as it is electrogenic (dependant on Na+ gradient)
Brings calcium into the cell which is toxic.

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26
Q

What pumps are used to control cellular pH?

A

Acid extruders

  • NHE (Na+ in, H+ out)
  • Na+ dependent HCO3-/Cl- exchanger (Na+ and HCO3- in, H+ and Cl- out)

Base extruders
- AE (HCO3- out, Cl- in)

27
Q

How is the action of NHE stimulated or inhibited?

A

Inhibited by the drug amiloride

Activated by growth factors as growth factors mean more metab is occurring and therefore more H+ is being produced.

28
Q

What are the methods of controlling cell volume via pumps and channels?

A

1). Conductive systems
- allow K+ down its conc gradient
= shrink
- allow Na+ or Ca2+ in
= swell

(Cl- will follow to maintain electroneutrality)

2). pH related
- AE = HCO3- in, and K+/H+ exchanger brings H+ in = H2CO3 which can then form H2O and CO2 and leave
= shrink
- this reverses
= swell

3). Cotransport systems
- efflux of free amino acids or K+/Cl- symporter out
= shrink
- Na+/K+/2Cl- symport in, Na+/Cl- symport in
= swell

29
Q

What are the ion conc’s in and outside the cell?

A

Na+ 145 out, 10 in
Cl- 122 out, 4 in
K+ 155 in, 4 out
Ca2+ 10-7 in, 1.5mM out

30
Q

What are the 3 ways of raising Ca2+ levels?

A

1) . Across the plasma membrane
2) . Rapidly releasable stores
3) . Non rapidly releasable stores

31
Q

How can Ca2+ levels be raised across the plasma membrane?

A

V-gated Ca2+ channels

Ligand gated Ca2+ channels

32
Q

How do rapidly releasable stores increase Ca2+ levels?

A

1). Ligand binds to GPCR
= GalphaQ acts on phospholipase C = IP3 reacts on IP3 receptors to open SR

2). Calcium induced calcium release
= Ca2+ acts on ryanodine receptors or in skeletal muscle, Ca2+ channels shape change is transduced onto ryanodine receptors = Ca2+ influx

33
Q

How do non rapidly releasable Ca2+ stores work?

A

The mitochondria take up Ca2+ when it is very high in microdomains close by via Ca2+ ATPase.

Can release into these microdomains by store operated Ca2+ channels opening.

34
Q

What is the evidence for involvement of mitochondria in non rapidly releasable stores?

A

1) . They buffer Ca2+ which allows mitochondria to regulate the pattern and extent of signalling.
2) . Role in apoptosis which is reliant on Ca2+
3) . Mitochondrial metabolism is activated by Ca2+, as high Ca2+ means more ATP is required for its removal, meaning more metabolism occurs.

35
Q

Name 2 Ca2+ buffers and their function.

A

Calsequestrin
Calbindin

Bind to Ca2+ and prevent its diffusion

36
Q

What are the 3 steps to restoring regular Ca2+ levels?

A

1) . Stop Ca2+ influx signals
2) . Remove Ca2+
3) . Refill Ca2+ stores

37
Q

How are Ca2+ stores refilled?

A

SERCA - pump Ca2+ into SR using ATP

This is stimulated via depleted store signals which open STIM (and ER membrane protein with a Ca2+ sensor that changes shape in low Ca2+)

This then interacts with ORAI, a plasma membrane Ca2+ channel, activating it to allow Ca2+ influx into the cell.

38
Q

How do drugs exert their effect?

A 
By binding to a target e.g.
DNA
Enzymes
Ion channels
Transporters
GPCRs
39
Q

What is the action of drug determined by?

A

The conc of drug molecules surrounding the receptor

40
Q

Why do we use molarity to calculate drug concentrations rather than simply mg/L?

A

mg/L is simply the conc of the weight of drug added to the volume.

By working out conc in molarity (dividing above by molecular weight) we can then multiply this by Avogadro’s number to obtain the number of drug molecules in the solution.

= weight conc of drugs may be same but molecules differ.

41
Q

What is a ligand?

A

A molecule that binds specifically to a receptor.

42
Q

What is drug action based on?

A

1) . Affinity - the degree to which the ligand binds to the receptor
2) . Intrinsic efficacy - the ability of the ligand to activate the receptor
3) . Efficacy - the ability of the activated receptor to form a response

43
Q

What is an agonist?

A

A ligand which binds to cause a response. Has both affinity and intrinsic efficacy.

44
Q

What is an antagonist?

A

A ligand which binds to a receptor without causing a response, therefore blocking the action of agonists. Has affinity but no intrinsic efficacy.

45
Q

What is Kd and what does it give us?

A

The dissociation constant (a measure of affinity)

The conc of ligand required to occupy 50% of receptors.

46
Q

How is Kd calculated?

A

Addition of an increasing amount of radioactive ligand to the cell, and then calculating the proportion of receptors bound.
This is then plotted.

47
Q

What is EC50?

A

The conc of ligand required to gain a 50% of max response

Therefore is a measure of potency.

48
Q

What is potency?

A

A measure of how well a drug works.

49
Q

What is potency dependant on?

A

Affinity - how well it binds
Intrinsic efficacy - how well it activates the target receptor
No. of receptors - how many need to be occupied to formulate a response

50
Q

Why may a cell have “spare receptors” and what is the effect this has?

A

In some cells, less than 100% of receptors are needed for a response because of amplification reactions, or a post receptor event which limits the response.

More spare receptors = increased sensitivity

51
Q

What type of cells tend to have spare receptors?

A

Those with catalytic ally active receptors (GPCRs, enzyme linked etc)

52
Q

How can receptor number change and what may this cause?

A

Up or down regulation

Tolerance
Tachyphalaxis (decreased reaction to a drug)

53
Q

What is the difference between concentration and doseage?

A

Conc - drug conc at site of action is known (cell/tissue)

Doseage - drug conc at site of action is unknown (body system)

54
Q

What is a partial agonist and what is this due to?

A

One where a full response is not stimulated, despite 100% of receptors being full.

Poor efficacy (good affinity, so the ability of the receptor to cause a response or of the ligand to activate the receptor is poor)

55
Q

What are the EC50 and Kd values in a partial agonist like?

A

They are equal

56
Q

How may a partial agonist become a full agonist?

A

Via upregulation of receptors -
intrinsic efficacy is still the same there are now a greater number of receptors to allow us to stimulate a full response.

57
Q

What occurs if a partial agonist has a greater affinity for a receptor than a full agonist?

A

It will antagonise the full agonist.

58
Q

What are the EC50 and Kd values of a full agonist like?

A

Kd is greater than EC50

59
Q

What is IC50?

A

The inhibitor concentration (antagonist) at 50% response

60
Q

What is Kd and Kb in terms of antagonists?

A

Kd is still the conc of radio labelled drug to take up 50% receptors.

Kb is the same but pharmacologically - the conc of antagonist

61
Q

What are the 3 types of antagonism and what occurs in each?

A

1) . Reversible competitive
- antagonist binds at same site as agonist and therefore blocks it.

2) . Irreversible competitive
- antagonist binds at same site but dissociates very slowly or not at all

3) . Non competitive inhibition
- antagonist binds at allosteric site, affecting the orthosteric site of the ligand, or efficacy of this site (primary binding site of ligand) = agonist has no/reduced effect

62
Q

Where may reversible competitive antagonism be used clinically?

A

Drugs such as naloxolene have a higher affinity at u-opioid receptors than other opioids = bind and prevent opioids stimulating = less resp depression in OD

63
Q

How may irreversible competitive antagonism be useful clinically?

A

To block alpha1 receptors in disorders which secrete adrenaline = less highBP

64
Q

How may non competitive antagonism be useful clinically?

A

Ketamine can be used for analgesia as it binds to allosteric site of an ion channel, blocking glutamate = no excitation

65
Q

How may a high affinity partial agonist be used clinically?

A

Can be given to wean from drugs such as heroin
- binds to receptors as affinity is higher but has less efficacy, so still gives partial response, but lessens risk of respiratory depression etc.

66
Q

Why does salbutamol have little effect on HR?

A

It has a higher Kd for beta2 receptors than beta1.

Given IV as salmeterol (has higher affinity for beta2 so is better) isn’t always used as it is insoluble = can’t be given IV

ESA 2 - Mine (4 decks)

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