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Pharmacology > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

What psychological responses are produced through drug-receptor interactions?

A

When a drug binds to its receptor & changes shape of receptor it can…

  • change the CONTRACTILITY of a tissue e.g. muscle
  • change the EXCITABILITY of neurones & neural stimulation e.g. morphine & diazepam work by increasing threshold of depolarisation for A.P
  • changes in GENE TRANSCRIPTION e.g. insulin causes expression of gene needed for a protein which transports glucose across the cell membrane

Extent of change depends on drugs AFFINITY & EFFICACY

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2
Q

Define partial agonist

A

Binds to & activates specific receptor. But only has partial intrinsic efficacy = means you get some of the effect but not all the effect

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3
Q

Define antagonist

A

Chemical which interferes or inhibits the effect of another drug. Binds to receptor & inhibits it. Binds using covalent bonds

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4
Q

Define competitive antagonist

A

Chemical which binds to receptor at the same active site as the agonist & competes for same binding site. Has NO intrinsic efficacy e.g. narcan

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5
Q

Define a non-competitive antagonist

A

Binds to a allosteric (non-agonist) site on the receptor to prevent activation of the receptor

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6
Q

Define adrenergic agonist

A

Drug that stimulates the response from the adrenergic receptors e.g. adrenaline & salbutamol

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7
Q

Define adrenergic antagonist

A

Drug the inhibits the response from the adrenergic receptors e.g. propranolol (beta-blockers)

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8
Q

Define a chemical antagonist

A

Binds to the active drug & inactivates it

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9
Q

What is a physiological antagonist

A

2 agents with opposing effects, they cancel one another out e.g. prostacyclin on platelet aggregation

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10
Q

Which antagonist binds irreversibly to the receptor?

A

Non-competitive antagonist- bind covalently e.g. aspirin

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11
Q

Albuterol and salbutamol are both beta 2 agonists. Why is salbutamol safer?

A

Because albuterol also has beta 1 properties = causing tachycardia & tachyarrhymias

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12
Q

Why can’t propranolol be given to asmatics?

A

Propranolol is a beta 2 antagonist. Therefore would block salbutamol

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13
Q

What is an inverse agonist?

A

An agent that binds to the same receptor as an agonist but causes a psychological response opposite to that of agonist

E.g. BZs -once bound the receptor cannot shift to active conformation

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14
Q

What is an allosteric interaction?

A

A secondary binding site on receptors usually enzymes. It can change the affinity of the primary binding site by changing its conformation. Can activate or inhibit

E.g. alcohol increases effect of BZs (allosteric interaction)

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15
Q

Define affinity

A

How well a drug can bind it it’s receptor. Depends on shape

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16
Q

Define efficacy

A

Maximum response achievable from a drug - (how effect the drug is).

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17
Q

Define specificity

A

Degree to which the drug is specific to its aim e.g. reduces side effects

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18
Q

Define potency

A

The amount of drug required to create an effect - how strong the drug is

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19
Q

How many drugs in the BNF work on 7 transmembrane / g-protein coupled

A

70%

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20
Q

How does a G-protein transduce the signal across the cell membrane?

A
  1. Ligand e.g. NA, morphine attaches to receptor
  2. Receptor changes shape to accommodate molecule = receptor activates.
  3. G protein made of 3 sub units. Activated receptor touches G protein = changes shape of G protein
  4. Alpha subunit drops of & either….
    -bumps into cell enzyme = activated enzyme (secondary messenger cascade)
    OR
    -bumps into ion channel & opens ion channel e.g. morphine activates potassium channel
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21
Q

Give 3 examples that work on second-messenger coupled receptors in the ANS

A

Atropine, adrenaline + ACh

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22
Q

What receptors does atropine bind to?

A

Muscarinic ACh receptors but doesn’t activate = mAChR antagonist

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23
Q

The first synapse is always what?…. in both sympathetic & parasympathetic muscle tissue?

A

Nicotinic

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24
Q

What is the ganglion?

A

Collection of cell bodies outside CNS

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25
Q

What does inotropic mean?

A

Relates to the contractility of a muscle.

E.g. adrenaline is a + inotrope (increases contractivity of heart)

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26
Q

What dose chronotrope mean?

A

Changes speed of HR

E.g. adrenaline is a + chronotrope (speeds up HR)

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27
Q

What would the signs + symptoms be if a pt has a transected spinal cord at C6?

A

PNS doesn’t go down spinal cord so wouldn’t be affected. SNS would be…. this means the PNS would be unapposed causing…

  • bradycardia
  • Bronchoconstriction
    • SOB
  • blood vessels are controlled by SNS… therefore below the transection, the blood vessels would dilate, causing area above to look pale as the blood vessels are constricted above.
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28
Q

What are the effects of atropine on the heart & GI tract?

A

Heart - removes vagal inhibition

GI tract - removed parasympathetic stimulation = motility & secretions reduced

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29
Q

Adrenergic transmission is activated by what?

A

Catecholamines (sympathomimetics - mimic the SNS)

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30
Q

Why do you give adrenaline in cardiac arrests?

A

Not because it’s a cardiac stimulant but to causes constriction of peripheral blood vessels = goes into CNS

Alpha 1 receptors

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31
Q

How does the drug Britaline (ADHD medication) work?

A

Works on alpha 2 receptors (theses are involved in concentration & inabition of behaviour) by simulating beta 2 = stimulate concentration

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32
Q

What happens if NA/A acted on beta 1 receptors?

A

Beta 1 mainly on heart muscle cells = increase rate & force of contraction. Same effect on skeletal muscle

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33
Q

What happens if NA/A acted on beta 2 receptors?

A

Beta 2 receptors mainly on smooth muscle (including respiratory) = relaxation & glycogenolysis (production of glucose)

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34
Q

Adrenaline is a non-specific agonist on all receptor sub-types. What is its effect on alpha 1, beta 1 & beta 2 receptors?

A

Alpha 1 - vascoconstriction - increased total peripheral resistance

Beta 1 - increased rate & force of heart contraction

Beta 2 - bronchodilator & increased blood sugar

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35
Q

What can you use to treat a beta blocker overdose?

A

Glucagon

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36
Q

Activation of H1 receptors in response to an infection… what are benefits?

A

Histamine dilates the capillaries around the injury/sting/bite so that WBCs can get to it (counteract infection)

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37
Q

Why is H1 receptor activation in allergic reactions bad?

A

You get an over the top reaction

  • blood vessels dilate in tissues
  • capillaries become highly permeable (leaky) = lose fluid into the tissues = oedema, hives & itching

Antihistamine blocks H1 receptors

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38
Q

What does H2 receptor activation do?

A

Promotes secretion of HCL in stomach

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39
Q

What does vasopressin do?

A

It’s an ADH
If the blood becomes dehydrated, ADH is secreted to stop u seeing out. Also control BP (vascoconstrictor)
Works on V1 receptors (smooth muscle) & V2 receptors (distal tubule of kidney)

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40
Q

What are the 4 main types of receptors?

A
  1. Agonist (ligand)-gated ion channels
    • made up of protein sub-units that form a central pole (e.g.
      nicotinic, GABA receptors)
  2. G-protein coupled receptors
  3. Nuclear receptors
    • for steroid & thyroid hormones. They are present in cell nucleus &
      regulate transcription & protein synthesis
  4. Kinase-linked receptors
    • receptors for insulin, cytokines & growth factors
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41
Q

What are ion channels?

A

Selective pores in the membrane that allow for ready transfer of ions down their electrochemical gradient.

Either controlled by membrane potential (voltage-gated channels) or by NT substances (ligand-gated channels)

42
Q

What is the difference between tachyphylaxis and tolerance?

A

When a drug is given repeatedly, it’s effects often decrease with time. If the decrease occurs quickly called tachyphylaxis (desensitisation)

Tolerance refers to a slower decrease in response

43
Q

Which preganglionic nerve fibres are myelinated?

A

Both post sympathetic & parasympathetic are myelinated & release ACh from nerve terminals. ACh then depolarises ganglionic neurones by activating nicotinic receptors

44
Q

What are the effects when ACh binds to muscarinic receptors?

A

Mainly parasympathomimetic;

  • constriction if pupils
  • salivation
  • bronchiolar constriction
  • hypotension
45
Q

What are the effects when nicotinic receptors are stimulated?

A

Stimulation of all autonomic ganglia

46
Q

Which agent can block the effects of ACh or nicotine on nicotinic receptors?

A

Hexamethonium

47
Q

Drugs that mimic the effect of ACh are called?

A

Cholinomimetics

48
Q

What does anticholinesterases do?

A

Inhibit acetylcholinesterase, so act indirectly by allowing ACh to accumulate in synapse

49
Q

What are choline esters?

A

They are a group of cholinergic drugs that act at sites or organs where ACh is the NT
Musclarinic agonists e.g.
-bethanechol (used to stimulate bladder in urinary retention, doesn’t penetrate BBB, more prolonged action than ACh) now replaced with catheterisation
-pilocarpine (eyedrops, used to reduce intraocular pressure in pts with glaucoma

50
Q

Name 2 musclarinic antagonists & there clinical effects…

A

Atropine- weak central stimulant
hyoscine

Both reversible competitive antagonists

They block the effects of ACh released from postganglionic parasympathetic nerve terminals

Clinical effects;

  • tachycardia
  • inhibition of secretions
  • inhibition of sweating
  • dilates pupils
  • reduces GI motility
  • bronchial smooth muscle relaxation
  • urinary smooth muscle relaxation
  • antiemetic action
  • Excitatory effect on CNS
51
Q

Name a beta-adrenoceptor antagonist used in treatment of angina, cardiac arrhythmias & heart failure

A

Beta-blockers

52
Q

Which enzymes catabolise catecholamines?

A 
Monoamine oxidase (MAO)
Catechol-O-methyltransferase (COMT)
53
Q

Opiate receptors are what…?

A

G-proteins which cause hyperpolarisation of cell metabolism & reduce Ca2+ entry.

Opiates work by opening potassium channels
(Most of potassium is found inside cells (intracellular potassium) if cells are damaged/crushed e.g. crush injuries, potassium is leaked out into the circulation = cardiac toxin. Sudden rush in potassium can’t be filtered out by kidneys fast enough - give 1litre saline in crush injuries before they are released (this will flush out potassium through kidneys into bladder).

54
Q

what are the 4 opiate receptor sites?

A
  • mu (U)
  • Kappa (K)
  • Delta
  • sigma
55
Q

How is an action potential reached?

A
  1. Sodium channels open
    When sodium influx into cell reaches certain threshold, the channels open wider. This makes membrane difference +
  2. Sodium channels shut & potassium channels open
    Potassium moves out of the cell to become negative (repolarisation) goes past resting potential, then back to resting potential (membrane becomes polarised).
56
Q

What happens in VT in regards to sodium channels?

A

There is an irritable foci, sodium channels are deranged (e.g. due to ischemia) & start opening randomly. This happens fast so there is no time for ventricular filing -heart pumps nothing

57
Q

What happens in VF in regards to sodium channels?

A

There are lots of irritable foci, sodium channels are opening in random ways

58
Q

What impact does shocking the heart have of sodium channels?

A

The electrical charge shuts sodium channels causing paralysis. This causes one focus e.g. SA node to take over again.

59
Q

How can you reduce the risk of an AP from occurring?

A
  • make the polarised state lower (makes it harder for an AP to occur - as a stronger stimulus would be needed).
  • interfere with NA+, K+, Ca2+, Cl-
60
Q

What is the most common opioid receptor?

A

Mu

Acts on potassium channels

It’s gets into tissue fluid around spinal cord, where most of the mu receptors are (spinal cord analgesic)

61
Q

How does opiates increase the threshold for depolarisation?

A
  1. Activated mu receptor bumps into G-protein
  2. Alpha subunit breaks off
  3. Bumps into K+ channels - opens
  4. K+ diffuses out of cell (stronger concentration inside cell)
  5. Cell becomes more negative = increasing threshold for depolarisation
62
Q

How does BZs increase the threshold for depolarisation?

A

It mimics a natural negative NT (GABA) in the brain which reduces AP threshold. It opens Cl- channels, allowing Cl- to enter cell = makes membrane potential more negative.

63
Q

How does Digoxin work?

A

Poisons the sodium potassium ATPase pumps

  • in AF can act as an antiarrhymic by increasing repolarise time
  • Interferes with AP
64
Q

What is the cell membrane impermeable too?

A

Ions e.g. Na+ & molecules e.g. glucose. It’s a phospholipid bylayer. Ions & farts don’t mix.

There are specific ion channels & transporters through the membrane. These are mostly proteins - can be pharmacological targets.

65
Q

How does Amiodarone work?

A

Works on both ventricles & atria (whereas lignocaine only works on ventricles)

  • prolongs the refractory period
  • Potassium channel agonist
  • has an affect on beta 1 cells & sodium channel activity (dirty drug, doesn’t just target 1 receptor).
66
Q

What ions does frusemide interfere with?

A

1 sodium, 1 potassium & 2 chloride ions out through cell memebrane

67
Q

How do BZs work?

A

Indirectly activate chloride channels in CNS, which are activated by inhibitor NT GABA this

  • hyperpolarises the membranes - prevent neurones from firing
  • suppresses brain activity so resp activity is suppressed esp if other depressants e.g. opiates used.

E.g. diazepam, lorazepam, oxazepam

68
Q

Why can’t you give diazepam straight?

A

Causes thrombophlebitis (inflammation in wall of vein, associated with thrombus) you can reduce this effect by giving an emulsion (drug bound to fat molecules, makes it less hypotonic)= diazamals

69
Q

What drug is an antagonist at the BZ binding site?

A

Flumanzenil - it blows BZs from binding, more toxic then diazapam

ANTIDOTE

70
Q

What are the 3 places you find nicotinic ACh receptors?

A

-SNS 1st synapse
(The NT released at post-ganglionic neurone is NA)

-PNS 1st synapse
(NT released at the post ganglionic neurone is ACh)
(Receptors on glands & organs of PNS are muscarinic)

-motor neurones 1st synapse
(NT released at post ganglionic neurone is ACh)

71
Q

How many ACh is needed to open nicotinic receptors?

A

2

72
Q

What happens when an action potential reaches an axon?

A
  • Ca2+ channels open - calcium enters -= causes vesicles to plant into cell membrane
  • NT released into synaptic cleft
  • NT binds to nicotinic receptor
  • nicotinic receptor opens, enabling sodium to enter muscle = initiates muscle AP
  • acetylcholinesterase (AChE) breaks ACh in half forming an Acetyl group & a choline group (no longer fits receptor) this causes it to fall off receptor & is re-uptakes into neurone where is put back together & repackaged in vesicles & recycled
73
Q

What happens if you chose to raise your arm?

A
  • motor cortex in conscious are of brain is activated
  • AP go through spinal cord & out to muscles of upper arm (triceps)
  • ACh is released all the time arm is raised & AChE breaking it down
  • AP released into muscle
  • stop producing ACh when you put your arm down
74
Q

How does the muscle relaxant atracurium work?

A

-It is a nondepolarising agent (nicotine competitive antagonist at nicotinic receptor of endplate)
-muscle cannot contract without stimulation of receptors = paralysis follows
-respiratory muscles are last to be affected + first to recover
-it can be reversed by giving AChE= raises the synaptic concentration of ACh as it’s no longer broken down = ACh accumulates in synapse + overcomes antagonist
Used to paralyse vocal cord for Intubation

75
Q

How does the muscle relaxant suxamethonium work?

A
  • It is a depolarising muscle relaxant.
  • It stimulates ACh receptor (opening sodium channels on muscle cell) producing muscular contractions
  • it is NOT destroyed by acetycholinesterase so its action is sustained
  • this prevents repolarisation at end plate = paralysis follows
  • rapid onset, but short acting (2-6min)
  • rapidly suppresses reflex gag for Intubation

Side effects;

  • Bradycardia + excessive salivation
  • painful muscle contractions
  • hyperkalemia (important in trauma + burns)
76
Q

What would make u suspect a tricyclic antidepressants overdose has occurred & why?

A

Tricyclic antidepressants e.g. amitriptyline block the re-uptake of NA = increases NA in synapse = sympathetic activation in brain.
NA receptors are also found e.g in beta 1 receptors in heart. Preventing Re uptake of NA in heart = increased HR, increased RR, hypertension & tachyarrhymias

77
Q

How do nasal decongestants work?

A

They are re-uptake inhibitors.

  • NA causes nasal constriction
  • nasal decongestants increase alpha 1 effect & reduces mucus secretion
  • it prevents the re-uptake of NA in those tissues
  • therefore more NA is in synapse - vasoconstriction in this area gets rid of oedema
78
Q

How does the bacteria cell wall divide?

A

Binary fusion

79
Q

What is GTN not affective in an MI?

A

GTN CANNOT vasodilation am artery filled with plaque
It causes blood to pool in periphery. Therefore if you rest, u reduce preload as the heart doesn’t have to work as hard, oxygen is repaid =lose chest pain

GTN is converted into nitric oxide

80
Q

Why can slodenafil (viagra) & GTN not be given together?

A

Slidenafil also acts on the nitric oxide pathway. They potentiate each other = this interaction causes hypotension

81
Q

What does NSAID stand for?

A

Non-steroid anti-inflammatory drugs

82
Q

Which intracellular enzyme do NSAIDs inhibit?

A

COX (cyclooxygenase)

83
Q

Why is aspirin the only NSAID used for an MI?

A

It also inhibits the enzyme thromboxane 2 (TXA2) synthesis = associated with clot formation

84
Q

Why does aspirin & ibuprofen cause ulcers?

A

They both inhibit COX 1 (housekeeping agent)- it’s responsible for producing mucus

85
Q

What are nuclear receptors?

A

-nuclear receptors exist within the cell unbound
-after binding with ligand, they become active
-causes changes in gene expression & protein synthesis
E.g. hormones e.g. testosterone or GCS e.g. hydrocortisone
They have an anti inflammatory action by working inside cell membrane of cell nucleus by altering gene transcription

86
Q

How do kinase-linked receptors work?

A
  • 2 molecules of drug e.g. insulin binds to the receptor to activate it
    -causes the 2 tyrosine-kinase receptor proteins (inactive monomers) to attach and become activated (phosphates added) = phosphorylated
    Needs ATP
87
Q

What happens if cells are starved of glucose?

A

They start metabolising fats = ketoacidosis

88
Q

What is ketamine an antagonist of?

A

NMDA receptors = causes hyper-salivation (keep pt on there side & cardiac monitor)

89
Q

what it competitive inhibition?

A

Drug may be structured similar to a substrate of an enzyme. It will then compete for the enzyme & slow down the normal reaction that the enzyme catalyses.

90
Q

What is non-competitive inhibition?

A

The drug combines with the enzyme & disables it permanently e.g. aspirin prevents formation of thromboxane

91
Q

What mechanisms can cause desensitisation?

A
  • loss of receptors
  • extrusion of the cell actively
  • increased drug metabolism
  • change in receptor shape
92
Q

What are the effects of muscarinic agonists?

A
  • slow HR
  • decrease CO
  • vasodilation (indirect effect due to release of NO by endothelium of blood vessels)
  • fall in BP
  • smooth muscle contraction (increases peristalsis)
  • increased secretions
  • pupil constriction
93
Q

What are the clinical applications of musclarinic agonists?

A
  • pilocarpine (constricts pupil, allows drainage of aqueous humour in glaucoma)
  • bethabechol (assists bladder emptying)
94
Q

What are the clinical applications of musclarinic antagonists?

A

Cardiac
-atropine used in sinus bradycardia

Respiratory

  • ipratropium reduces bronchospasm +secretions in chronic obstructive pulmonary disease + asthma
  • atropine used in anaesthesia to reduce secretions from resp tract +reduce reflex bronchoconstriction

GI + urinary tract

  • hyoscine relaxes smooth muscle
  • urinary incontinence (reduce involuntary contractions of detrusor muscle)

Motion sickness
-hyoscine

Parkinsonism
-reduce effects of too much ACh in brain which occurs as a result of deficiency of dopamine e.g. benzatropine

The eye
-dilate pupil + paralyse ciliary muscle for eye examination

95
Q

Drugs acting on nicotinic receptors- both agonists + antagonists can produce neuromuscular block. How do nondepolarising + depolarising agents work?

A

Nondepolarising agents - block ACh receptors. They are competitive antagonists + block nicotinic receptor

Depolarising agents (agonists) stimulate receptor then remain in receptor so it’s not free to be stimulated again

Used as paralytic agents

96
Q

What are ganglion-blocking agents?

A

They block the transmission at both sympathetic + parasympathetic ganglia. Cause;

  • fall in BP
  • postural hypotension + fainting

Hexamrthonium first used - no trimetaphan used

97
Q

What is the effect of drugs that enhance acetylcholine transmission?

A

Act by inhibiting acetylcholinesterase (AChE) - prevents destruction of ACh. used to treat Alzheimer’s + dementia
Effects;
-enhances ACh activity in PNS = increased secretions, peristalsis, bronchoconstriction, bradycardia + hypotension
-effects at neuromuscular junction - repetitive firing of muscle fibres used to counteract blocking agents
-effects on CNS if drug is lipid soluble = depression of CNS

98
Q

What are the clinical applications for drugs that inhibit acetylcholinesterase?

A

To treat myasthenia gravis

  • autoimmune condition where there is destruction of ACh receptor on skeletal muscle = weakness + muscle fatigue
  • used to restore movement

To improve memory of AD
-loss of cholinergic neurones in brain =cognitive impairment + memory loss

99
Q

What is an irreversible anticholinesterases?

A

Inhibit action of acetylcholinesterase often for life of enzyme. Most are organophosphate compounds, used as pesticides + war gases.

  • highly lipid soluble
  • rapidly absorbed through mucus membranes
  • pass through broken skin
100
Q

What are the effects of organophosphate poisoning?

A

ACh accumulates at synapse in both central + peripheral nervous systems = overstimulation at both neuromuscular + autonomic synapses

DUMBBELS
Diarrhoea
Urination
Mioisis/muscle weakness 
Bradycardia 
Bronchospasm + bronchorrhoea
Emisis 
Lacrimation
Salivation/sweating

Stimulation of nicotinic receptors at neuromuscular junction causes muscle weakness, fasciculations + paralysis

Pralidoxime only antidote

Pharmacology (11 decks)

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