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Principles JC > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define the terms pharmacodynamics and pharmacokinetics

A

Codynamics: what the drug does to the body e.g to tissues, organs

Cokinetics: what the body does to the drug e.g absorption, distribution, excretion adme

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2
Q

Define a drug

A

A synthetic material of known structure used in treatment/ prevention of disease of illicitly. Something that is selectively recognised.

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3
Q

Name some drug targets in the body

A

Enzymes, carrier molecules, ion channels, receptors, rna, dna

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4
Q

Define the terms affinity, efficacy and potency

A

Affinity= likelikihood for two substances to combine

Efficacy= how effective at producing desired result

Potency= depends on the above, how much of the substance is required to produce a response. // range which an agonist is effective

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5
Q

What is the EC50 of a drug?

A

The concentration of agonist that produces 50% of max response rate.

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6
Q

Describe the effects of a non-competitive antagonist and a competitive antagonist on a concentration response curve.

A

Non- competitive; depressed max value and slope decreased, but no shift

Competitive; shift to the right no change in graph shape or height

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7
Q

Describe the effects of an agonist (body natural thing) and competitive antagonist on a concentration response curve.

A

Max response the same, but there is a parallel right shift of the curve

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8
Q

Where are ligand gated ion channels located and their function

A

Plasma membrane location

Function is to allow a rapid change in membrane potential

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9
Q

Where are g-protein coupled receptors located and what is their function. How many types are there and based on what?

A

Located on plasma membrane
Function is to cause intracellular signalling from hydrophillic molecules that cant cross the membrane

Three types Gs, Gi and Gq based on their alpha subunit

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10
Q

What is the location and function of kinase-linked receptors

A

Loated on the plasma membrane

Function is to phosphorylate the target molecule by first autophosphorylation. Occurs in the insulin glucose pathway

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11
Q

What is the function and location of the nuclear receptor?

A

Located in the nucleus and target by hydrophobic molecules

Function is to be activated and cause transcription of specific genes

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12
Q

Describe the ion channel receptor. Include the nicotinic acetylcholine receptor

A

Three types based on how many subunits of glycoprotein e.g pentamer, tetramer and trimer.
In the nicotinic acetylcholine receptor, it is a pentamer which also has a cys-loop.
The subunits combine to make a tube where there will be two binding sites for an agonist.

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13
Q

Describe the structure of a g protein and its receptor

A

Receptor:
Integral membrane protein spanning membrane 7 times. Containing Nh2 terminal extraC and a cooh terminal intraC

G-protein:
3 subunits, alpha, beta and gamma. Where beta and gamma function as a dimer, and the alpha unit’s AH domain contains the GDP/TP binding site, and its RAS domain is a GTPase. When the alpha subunit and the b/y subunit dissociate they are both signalling units.

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14
Q

Describe the adenylyl cyclase signalling pathway

A

Gs g-protein is activated from a beta-adrenoceptor to then travel intracellularly and activate adenylyl cyclase. This causes cAMP to be generated from ATP, which then promotes protein kinase A to be produced which phosphorylates ser/thr in target proteins which then drives cellular effects.

This pathway can be turned off by the activation of the Gi protein from muscarininc M2 acetylcholine receptor

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15
Q

Describe the phospholipase C effector pathway

A

Gprotein q is activated by the alpha1 adrenoceptor, this moves intracellularly to activate phospholipase C to catalyse the reaction from pip2 into ip3. Ip3 then acts on its receptor on the endoplasmic reticulum to cause an influx of calcium ions which causes cell effects.

In addition, protein kinase C is activated from the activation of PLC and the molecule DAG to phosphorylate ser/thr residues in target proteins which cause cell effects.

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16
Q

What factors determine drug disposition in the body?

A

Absorption- process that drug enters the body
Distribution- how drug is moved around body, usually general circulation
Metabolism- how the body reacts to the drug/ modifies it.
Excretion- process of the removal of the drug by the body

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17
Q

What factors affect the absorption of a drug in the body? SCLD

A
  • solubility of the drug
  • its chemical stability e.g survivable in acid or not
  • lipid water partition co-efficient e.g more soluble in lipid more able to cross membranes
  • degree of Ionisation e.g acidic or basic. The weak acids/ bases are more readily absorbed.
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18
Q

What is pka?

A

Ph value where the dissociation of drug is 50%

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19
Q

What is the henderson- hasselbalch equation? What does it determine?

A

Pka- ph= log (AH/A-) for acids
Pka-ph= log (BH+/B) for bases

Negatives on bottom, positives top

Calculates the degree of ionisation of a drug e.g how acidic/basic it is

20
Q

Define oral and systemic availability. Think definition of oral

A

Oral availability- fraction of drug reaching systemic circulation after ORAL INGESTION

Systemic availability- fraction of drug reaching systemic circulation after ABSORPTION

21
Q

What are some common routes of drug administration? (7) give a positive/neg about each

A

Oral- simple / can be inactivated by acids
Inhalation- good 4 volatile agents/ manual dexterity
Buccal/sublingual- rapid absorption/ infrequent route
Transdermal/subcutaneous- slow absorbed/ may irritate skin
Intravenous- rapid onset/ sterile prep needed
Rectal- nocturnal admin/ infrequent route
Intramuscular

22
Q

What are the main body fluid compartments? (6) IVF TIP

What must a drug be in order to move freely between the compartments?
How can you determine which molecule prefer which compartments?

A 
Plasma water
Interstitial water- most here as receptors here
Vascular compartmens
Intracellular water
Fat (adipose)
Transcellular water

Unionised drugs move freely or/ ionised but not bound to proteins

Vd (volume of distribution)= amount of drug administered/ plasma concentration

  • vd<10l = vascular compartments
  • vd>10L= extracellular water
  • Vd> 30L= drug everywhere
23
Q

What are the equations for:

1) the rate of elimination?
2) calculating loading dose
3) volume of distribution

A

1- rate of E= plasma conc. (Cp) x Clearance (Cl)
2- loading dose= Cp x volume of distribution (Vd)
3- Vd= dose/ clearance

24
Q

What is the minimum effect conc. (MEC), max tolerated conc (MTC) and the therapeutic ratio (TR)

A

The lowest drug dose to produce an effect= MEC
Max drug dose without becoming toxic= MTC

Range of the two above terms is the therapeutic ratio

25
Q

What is a first order elimination reaction?

What is a half life of a drug? How many half lives does it take for a drug to be removed from body?

A

Where the drug is eliminated by the plasma concentration. E.g elimination is proportional to the drug concentration

Time for the drug to fall to half its inital concetration. No change in half life of a drug based on concentration of the drug. BUT if double concentration of drug then increase action of drug by 0.5 half lives.

5 half lives

26
Q

True or false. In first order kinetics elimination is the product of plasma concentration of the drug and its clearance.

A

True

Elimination = CL x Cp (plasma conc)

27
Q

What is a steady state concentration of a drug?

What is the equation of rate of elimination at steady state?

A

Where the rate of administration = rate of drug elimination

Elimination= Cl (clearance) x Cpss (plasma conc at steady state)

28
Q

What is the function of a loading dose?

What are the equations to calculate the loading dose?

A

To get a drug into the therapeutic window quicker than the natural 5 1/2 lives

If oral admin
LD= (Vd x target plasma conc) / oral availability (fraction of drug entering systemic circulation)

If Iv admin
LD= vd x target plasma conc

29
Q

Describe a zero order elimination reaction

Why does this occur

A

Where the rate of elimination of the drug is the same regardless of the plasma concentration of the drug. Hence linear relationship not exponential.

Usually in a enzyme controlled reaction where the enzyme becomes saturated

30
Q

Define depolarisation and hyperpolarisation of a cell.

A

Depolarisation: when the cell becomes more positive

Hyperpolarisation: when the cell becomes more negative

31
Q

Describe the action potential pathway of a cell e.g hyper/depolarisation, threshold etc

A

When the threshold of a cell has been reached, the voltage gated ion channels open allowing the influx of na+. This causes depolarisation of the cell to the point where a signal is sent. There is then rapid hyperpolarisation by the excretion of k+ ions. The body over compensates so goes below the resting potential 70mV, this is then the refactory period of depolarising to the resting potential.

32
Q

What can affect the rate of transmission of a neurone?
What are the names of the cells that insulate a neurone?
What are the gaps between the insulation called?

A
  • the length of the axon
  • Ri (axial resistance)
  • Rm (resistance of the internal cavity) as it increases speed of transmission increases
  • insulation glial cells (if in the PNS then schwann cells)
  • gaps known as nodes of ranvier
33
Q

What are the subdivisions of the PNS

A

1) AutonomicNS
A. Sympathetic
B. Parasympathetic

2) somatic efferent (exit from CNS)- motor fibres to skeletal 
     Somatic afferent (towards CNS)- sensory fibres from skin/skeletal      muscles
34
Q

What kind of receptors do the sympathetic and parasympathetic mainly utilise?

A

Sympathetic= adrenoceptors alpha (1,2) and beta (1,2,3)

Parasympathetic= muscarinic cholinoreceptors

35
Q

Describe the motor neurones in the sympathetic and parasympathetic e.g post/pre

A

The presynaptic neurone is acetylcholine acting on nicotinic cholinoreceptors.

The postsynaptic neurone in the:
1. Sympathetic is adrenergic releasing noradrenaline that acts on adrenoceptors

2. Parasympathetic is cholinergic releasing acetylcholine to act on muscarinic cholinoceptors
36
Q

In the sympathetic chain the neurones can either synapse at the prevertebral or the paravertebral ganglia. Whats the differece?

A

Prevertebral ganglia are outwith the sympathetic chain so the post ganglionic neurone will be at the target organs

Paravertebral ganglia are located on the sympathetic chain so the post ganglionic neurone joins peripheral nerves via grey rami

37
Q

What is an adrenoceptor

A

A g-protein coupled receptor with 5 subtypes of alpha 1&2 and beta 1,2,3.

38
Q

Give some examples of what organs the sympathetic nervous system stimulates and what receptor they act on

A

The heart by acting on Beta 1 adrenoceptors (one heart)

The lungs by acting on the beta 2 adrenoceptors (two lungs)

The intestines by acting on alpha 1&2 and beta2

The vessels by alpha1 or in skeletal muscle by beta 2

The bladder relaxation of the detrusor muscle (to allow storage of urine) by beta 2/3 and by constricting urethral sphincter alpha1.

The penis by alpha 1

39
Q

Describe the stages in the cholinergic transmission of the preganglionic neurone in the synapse

A
  1. Choline is uptaken into the neurone by a transporter and then bound with acetyl co-enzyme A by acetyl transferase to create acetyl choline.
  2. This is stored in a vesicle
  3. When a voltage gated channel opens it gives the neurone an action potential which then opens the calcium channels to allow influx of ca2+.
  4. This allows the vesicles to exocytose their contents into the synaptic cleft to act on their nicotinic receptors
  5. Once a signal has been sent then the NT is then degraded by ACHe and it is reuptaken into the neurone and stored
40
Q

Describe the process of sympathetic post ganglion transmission

A
  1. Noradrenaline is synthesised
  2. This is stored in a vesicle
  3. When a voltage gated channel opens it gives the neurone an action potential which then opens the calcium channels to allow influx of ca2+.
  4. This allows the vesicles to exocytose their contents into the synaptic cleft to act on their adrenoreceptors
  5. Once a signal has been sent then the NT is then reuptaken by U1/U2 into the neurone and then degraded by MAO or COMT
41
Q
  1. What transporter does cocaine block?
A
  1. U1 in the sympathetic pathway meaning noradrenaline isnt reuptaken into the neurone
42
Q

What protein does amphetamine inhibit? What is this effect?

A

MAO in the sympathetic pathway so there isnt degradation of noradrenaline and it gets re-exocytosed into the synaptic cleft

43
Q

What does the drug prazosin do? To which receptor? Agonist/antagonist?

A

Blocks the alpha 1 receptor hence antagonist. Alpha 1 responsible for constriction in vasculature, ejaculations, constriction of sphincters, reducing gi mobility

44
Q

What does the drug atenolol do? To which receptor? Agonist/antagonist?

A

Blocks beta 1 adrenoceptors so an antagonist. Beta 1 increases heart rate and force of heart contractions,

45
Q

What does the drug salbutamol do? To which receptor? Agonist/antagonist?

A

It stimulates the beta 2 adrenoceptor hence is an agonist. This causes bronchodilation, decresed mucus production, relaxes skeletal muscles, constricts sphincters, relaxes detrusor muscle of bladder

46
Q

What does the drug atropine do? To which receptor? Agonist/antagonist?

A

Blocks m1, m2 and m3 receptors. It is a competitive agonist. Therefore it blocks all parasympathetic activity.

Principles JC (10 decks)

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