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NLM2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where do opioids act to reduce pain?

A

In the brain and spinal cord

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2
Q

What does activation of opioid receptors cause?

A

inhibits the release of excitatory transmitters e.g. Substance P, NO and glutamate

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3
Q

Main areas in the midbrain involved in inhibiting pain?

A

Periaqueductal grey

Nucleus raphe magnus

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4
Q

Examples of places in the brain where opioids act?

A

Increases transmission to the nucleus accumbens (associated with euphoria)

Decreases transmission to locus coeruleus (anxiety)

Increases transmission from Periaqueductal grey and nucleus raphe magnus

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5
Q

Three main types of opioid receptors?

A

Mu (μ)

Kappa (κ)

Delta (δ)

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6
Q

Two main pathways for pain? (type of pain they transmit?)

A

Paleospinothalamic - Blunt visceral pain

Neospinothalamic - sharp somatic pain

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7
Q

What four opiates might you use for short pain (and their features)?

A

Alfentanil: very short acting (orthopaedics)

Morphine: Poorly absorbed orally, very potent

Codeine: Less potent, better oral absorption

Pethidine: Rapid acting, less effect on respiration and uterus

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8
Q

Three steps of the WHO analgesic ladder?

A

Step 1: simple analgesics e.g. paracetamol/NSAIDS

Step 2: Moderate opioid e.g. mixed action opiate, dihydrocodeine
+ simple analgesics

Step 3: Strong opioid e.g. morphine, codeine heroin
+ simple analgesics
+ other psychoactive drugs

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9
Q

Non-analgesic affects of opioids?

A

Sedation and respiratory depression

Nausea and vomiting

Cough suppression

Miosis

Constipation (decreased gut motility)

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10
Q

What do you use to combat the withdrawal symptoms of opioids?

A

Methadone

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11
Q

Why is there no upper limit to opioid prescription?

A

Tolerance will build up and this is natural, can be combatted by increasing the dose

Opioids are not toxic and so upping the dose has no draw-backs

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12
Q

Is dependence on opioids common or rare in pain patients?

A

Very rare

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13
Q

Why is loperamide used to treat diarrhoea?

A

Causes decreased gut motility

Can’t get into the brain

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14
Q

What do NSAIDS inhibit?

A

COX-1 and COX-2

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15
Q

What does COX go on to do?

A

Catalyse the reaction from arachidonic acid to prostaglandins and thromboxane

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16
Q

What do prostaglandins do?

A

Cause:

Pain

Inflammation

Fever

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17
Q

What are the roles of prostaglandins and thromboxane on platelet aggregation?

A

Prostacyclin (PGI2) inhibits

TxA2 promotes aggregation

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18
Q

What do prostaglandins do to increase pain?

A

Sensitise pain nerve endings inducing substance P

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19
Q

Difference in COX-1 and COX-2?

A

COX-1 is constitutively expressed

COX-2 is expressed in inflammation

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20
Q

Effects of COX-1?

A

GI protection: Less acid, more mucus

Increase renal blood flow

Platelet aggregation effects

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21
Q

Effects of COX-2?

A

Pain

Inflammation

Fever

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22
Q

The adverse effects of NSAIDS are usually due to what?

A

COX-1 inhibition

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23
Q

What GI side effects are particularly bad in NSAIDS?

A

Gastric ulceration/bleeding

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24
Q

What side-effects can NSAIDS have on renal function, who should not receive them due to this?

A

Reduced renal blood flow and GFR, due to constricted afferent arteriole at the glomerulus

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25
Q

Actions of local anaesthetics?

A

They prevent action potentials on all nerves through sodium channel blockade

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26
Q

Why do local anaesthetics, such as lidocaine need to have both a ionised and non-ionised form?

A

The non-ionised form needs to cross the membrane and work from within

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27
Q

Do myelinated or non-myelinated fibres get blocked by local anaesthetics more? why?

A

Myelinated fibres (as they only have to block the nodes of ranvier)

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28
Q

benefits to local anaesthetics?

A
  • reversible impairment of conduction
  • non-irritant
  • low toxicity
  • readily metabolised + eliminated
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29
Q

What 4 things does the duration of action of local anaesthetics depend on? will these things increase or decrease duration?

A

Structure - water soluble will decrease duration

Site - well perfused sited will decrease duration

Actions - Vasodilators will decrease duration (cocaine a vasoconstrictor)

Co-administration: administration of vasoconstrictors will increase duration

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30
Q

Most widely used local anaesthetic?

A

Lidocaine

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31
Q

3 routes to administer lidocaine?

A

Infiltration as injection

Epidural

Spinal

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32
Q

Differences/similarities in epidural and spinal administrations?

A

Epidural

  • Larger doses
  • outside dural membranes
  • very precise

Spinal

  • into subarachnoid
  • Small dose
  • High precision
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33
Q

Main systemic S/E of local anaesthetics?

A

Respiratory depression

CVS collapse

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34
Q

What nervous system innervates the radial and the circular muscles of the eye?

A

Radial muscles are sympathetic

Circular muscles are parasympathetic

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35
Q

What intrinsic muscles of the eye control the pupil size and what muscles control the lens size, what are they innervated by?

A

Pupil size - Radial and Circular muscles, both sympathetic and parasympathetic

Lens size - Ciliary muscles, only parasympathetic

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36
Q

Action of Tropicamide?

A

Muscarinic antagonist

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37
Q

Action of phenylephrine?

A

Alpha-1 adrenoreceptor agonist

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38
Q

Action of amethocaine?

A

Local anaesthetic (na+ channel blocker)

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39
Q

Action of cocaine?

A

Local anaesthetic and Nor Adrenaline reuptake inhibitor.

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40
Q

If the ciliary muscles contract they decrease or increase the size of the lens?

A

increase the size of the lens - make it bulge (near vision)

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41
Q

What effect will sympathetic and parasympathetic activation have on scleral blood vessels, if any?

A

Sympathetic - constrict them

Parasympathetic - no effect

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42
Q

What effects will tropicamide have on the eye?

A

Pupil will dilate (less PNS input)

Lens will relax and enlarge (less PNS input)

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43
Q

What effect will phenylephrine have on the eye?

A

Dilate pupil

Conjunctival vessels will constrict

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44
Q

What effect will amethocaine have on the eye?

A

less sensation

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45
Q

what effect will cocaine have on the eye?

A

Less corneal sensation

More constricted conjunctival vessels (NA reuptake inhibitor)

Larger pupil (NA re-uptake inhibitor)

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46
Q

What is pharmacological eye-patching?

A

When a drug such as cylclopentolate (muscarinic antagonist) is given to dilate the pupil and lens and cause a blur, this encourages the patient to use the other eye.

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47
Q

What is iritis?

A

Adhesions that formed between the lens and the iris, causing inflammation

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48
Q

What is glaucoma?

A

Syndrome with many causes that results in raised intraocular pressure, due to inadequate drainage of the aqueous humour which if left untreated results in optic nerve damage

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49
Q

What two areas are treated in glaucoma?

A

Reduce aqueous production

Improve drainage

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50
Q

What is open and closed angle glaucoma?

A

Open is when the angle between the iris and cornea is open (most cases)

Closed is when it is closed resulting in inadequate drainage

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51
Q

How do you treat closed angle glaucoma?

A

Stimulants such as pilocarpine/neostigmine constrict the sphincter pupillae and open the anterior angle

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52
Q

What’s the canal of schlemm?

A

The canal where aqueous humour in the eye is drained

53
Q

Where is aqueous humour formed?

A

Ciliary body

54
Q

What drugs can be used to reduce aqueous production in glaucoma?

A

CA inhibitors e.g. acetazolamide, reduce production in ciliary epithelium

B2 blockers e.g. acetazolamide, reduce production in ciliary epithelium

Selective a-2 agonists do the same

55
Q

What drugs can be used to improve aqueous drainage in glaucoma?

A

Cholinergic agonists e.g. pilocarpine, constrict the iris, increasing the anterior angle (mostly act on PNS)

Prostaglandins F2 agonists

56
Q

Drugs used in prophylaxis of headaches?

Examples?

A

B-blocker: propranolol

Anti-epileptic: gabapentin

TCA’s amitryptyline

5HT agonist pizotifen

57
Q

Drugs used to treat acute headaches?

A

NSAIDS
Antiemetics
5HT agonists

58
Q

Two areas of the brainstem that contribute to vomiting and nausea?

A

Chemoreceptor Trigger Zone (CTZ)

Vomiting centre

59
Q

What sends fibres to the CTZ?

A

Vestibular apparatus

Toxins in blood

Irritants of the stomach

60
Q

What sends fibres to the vomiting centre in the brainstem?

A

Physical injury

Stomach irritants

61
Q

Drugs used to treat/prevent Nausea/Vomiting?

Examples?

A

Anti-muscarinics: Hyoscine

Anti-histamines: cyclizines

D2 agonists: domperidone

5-HT agonists: ondansetron

NK1 receptor agonists: aprepitant

62
Q

4 stages of anaesthesia?

A
  1. Analgesia
  2. Excitement
  3. Surgical anaesthesia
  4. Vital centre depression
63
Q

What are the two main types of administrating General anaesthetics?

A

IV

Inhaled

64
Q

2 examples of an IV general anaesthetic?

A

Thiopentone

Propofol

65
Q

2 examples of an inhaled general anaesthetic?

A 
Nitrous oxide (N2O)
Isoflurane
66
Q

What drugs are used to induce and maintain anaesthesia?

A

IV is used to induce anaesthesia

Inhalation is used to maintain anaesthesia

67
Q

Features of thiopentone?

A

IV general anaesthetic:

  • rapid onset
  • short duration
  • Cumulative (in muscle and fat)
  • Highly alkaline (tissue necrosis if injected outside of vein)
68
Q

Use of thiopentone

A

Induction of general anaesthesia

69
Q

Features of propofol?

Use?

A

IV general anaesthetic

  • Rapid onset
  • Short duration
  • Metabolised in the liver, so does not accumulate

Used for induction and maintenance in short procedures

70
Q

Nitrous oxide features?

Use?

A

Inhaled general anaesthetic

  • weak, so would require 95% to induce (would also asphyxiate)
  • 70% for maintenance (possible)
  • Can be used as a carrying agent
  • Analgesic and amnestic effects

Maintenance, normally with isoflurane

71
Q

Features of isoflurane?

Use?

A

Inhaled general anaesthetic

  • Strong (need 5% for induction)
  • Slow in onset

Maintenance (usually with N20)

72
Q

S/E of isoflurane?

A

Cardiac dysarrhythmias

Harmless ectopic ventricular beats

Small chance of Ventricular fibrillation

73
Q

S/E of opioids?

A

Constipation

Cough reflex reduced

Nausea and vomiting

74
Q

Main receptors in the CTZ?

A

D2

5-HT

75
Q

Main receptors in the vomiting centre?

A

Histamine

Muscarinic receptors

76
Q

What is epilepsy?

A

Abnormal discharge pattern in a group of neurones, resulting in paroxysmal discharges

77
Q

Main types of epilepsy?

A

Partial seizures - focal only, do not spread

Generalised seizures - spread from a focus:
2a) Tonic clonic (grand mal)

2b) Absences (petit mal)

78
Q

4 stages of an epileptic fit?

A
  1. Initiation
  2. Spread
  3. Maintenance
  4. Collapse
79
Q

What happens at each stage of an epileptic fit?

A

Initiation:

  • excitation is more than inhibition, excessive glutamate, loss of GABA inhibition

Spread:

  • by normal neuronal fibres
  • also by adjacent fibres by ephaptic transmission

Maintenance:

  • Positive feedback loops
  • post-tetanic potentiation

Collapse

  • Elevation of threshold
  • Metabolic factors
  • inhibition by other pathways
80
Q

The two stages of a tonic clonic seizure?

A

Tonic (not long):

  • intitial rigid extensor spasm
  • defecation, micturation, salivation
  • respiration stops

Clonic (longer, few minutes)

  • violent synchronous jerks
81
Q

4 Types of Na+ channel blockers used to treat epilepsy?

How do they treat the epilepsy?

A

Phenytoin
Lamotrigine
Carbamazide
Sodium valproate

stabilises Na+ channel in an inactivated state

82
Q

uses of phenytoin, what drug is it given as?

A

Tonic clonic/partial

Given as fosphenytoin

83
Q

S/E of phenytoin?

A

CNS:

  • Diplopia
  • Nystagmus
  • Ataxia
  • Sedation

Induction of p450
Allergies

84
Q

Uses for carbmazepine? advantages?

A

Tonic clonic/partial seizures

Little sedation

85
Q

Lamotrigine uses? advantages?

A

Tonic clonic

Long half life

Does not affect p450

Rare S/E

86
Q

Sodium valproate uses? advantages/disadvantages?

A

Tonic clonic, partial and petit mal

  • Best choice for petit mal
  • Hepatotoxicity
87
Q

Anti-epileptics that act on GABA pathways?

A

Phenobarbitone - only barbituate used, very long half-life

Benzodiazepines - diazepam (IV for staus epilepticus), or clonezepam (marked sedation)

Also sodium valproate

88
Q

How does sodium valproate work?

A

Acts on Na+ channels and Ca2+ channels in the thalamus and GABA pathways

Enhances the production of GABA and inhibits its breakdown

89
Q

What causes parkinsons?

A

Degeneration of dopaminergic neurones in nigrostriatal pathways

90
Q

Symptoms of parkinsons?

A

Tremor, rigidity, bardykinesia, postural instability

91
Q

The three dopaminergic pathways of the brain?

A

Nigrostriatal: Control of movement

Mesolimbic: Mood, emotion

Pituitary hormones

92
Q

What parts of the nigrostriatal pathway are there?

A

Globus pallidus, striatum and substantia nigra

93
Q

What do COMT and MAO do?

A

Breakdown L-dopa and Dopamine

94
Q

What is levodopa, how’s it work and what are the disadvantages, how are these solved?

A

A prodrug to treat parkinsons

Crosses the BBB and is converted to dopamine in dopminergic neurones by DOPA decarboxylase

Only 1% taken up by brain, means there is lots of dopamine in the periphery, given with a PDI (peripheral decarboxylase inhibitor)

Only works effectively for 2-5 years, bad in 50% of patients after 5 years (give other drugs)

95
Q

An example of a PDI?

A

Carbidopa

96
Q

Because Levodopa only works effectively for 2-5 years, what other drugs can be given?

A

COMT inhibitors e.g. entacapone

MAO-b inhibitors e.g selegiline

D2 receptor agonists e.g. ropinirole

Antimuscarinics e.g. benzehexol

97
Q

red flags for parkinsons?

A

Early falls

Wheelchair

Postural hypotension

abnormal eye-movements

98
Q

How do COMT inhibitors work to reduce parkinsons? e.g?

A

Entacapone

Inhibit peripheral COMT so there is more Levodopa to get into the brain

Can combine with l-dope and a PDI

99
Q

How do MAO-b inhibitors work to reduce parkinsons? e.g?

A

Selegiline

Inhibit the breakdown of dopamine in the CNS, prolonging dopamine survival in the CNS

allows less L-dopa dose

100
Q

How do D2 receptor agonists work to reduce parkinsons? e.g?

A

Ropinirole

agonise dopamine receptors in the CNS, can be used in combination with l-dopa + PDI

101
Q

How do antimuscarinics work to reduce parkinsons? e.g?

A

Useful in treating symptoms e.g. tremor/rigidity

102
Q

What’s the monoamine theory for depression?

A

The theory that depression is associated with decreased activity in central NA and/or 5HT synthesis

103
Q

All antidepressant drugs? examples?

A

MAIN

SSRI’s - citalopram

SNRIs - venlafaxine

TCAs - clomipramine

MAO inhibitors - pheneteine

OTHERS

antipsychotics - quetiapine

anticonvulsants - lamotrigine

Lithium

104
Q

What advantage do SSRI’s and SNRI’s have over older TCAs?

A

TCAs are unsafe in overdose and have troublesome S/E’s

105
Q

What do MAO inhibitors do?

What can’t you do on MAOIs?

A

Inhibit both MAO-B and A

Can’t eat tyramine rich foods e.g. cheese/game/wine

106
Q

Issues with SSRIs?

A

Increased nervousness in 1st week

worsened sexual function (40%)

107
Q

S/E of TCAs?

A

weight gain/drowsiness

108
Q

What are the two categories of sleep disorder?

A

Dyssomnias: interruption to timing/quality or amount of sleep

Parasomnias: abnormalities during sleep

109
Q

Drugs to treat anxiety (anxiolytics)?

A

SSRIs - citalopram

SNRI’s - venlafaxine

Pregabalin

Benzodiazepine - diazepam

TCAs - clomipramine

MAOIs - phenelzine

Antipsychotic - quetiapine

B-Blockers - propranolol

5-HT partial agonists - buspirone

110
Q

What drugs are used to insomnias? (hypnotics)

A

Barbituates - phenobarbitol

Benzodiazepines - diazepam

Z drugs - zaleplon

111
Q

Positives/negatives of barbituates? Mechanism?

A

Increase the duration of Cl- channel opening

significant risk of dependence

Highly dangerous in overdose and in combination with alcohol

Used only in severe insomnia

112
Q

Positives/negatives of benzodiazepines? Mechanism?

A

Safer alternative to barbituates

increase in the frequency of Cl- channel opening

will only bind to site if GABA has already bound to the site

Metobolites will accumulate

Risk of dependence

Dangerous if combined with alcohol

Only recommended for short term treatment (4 weeks)

113
Q

How does pregabalin work, what is it good for?

A

Reduces release of excitatory neurotransmitters e.g. glutamate

Good in GAD/SAD (generalised and social anxiety disorder)

114
Q

What is mania and hypomania?

A

Mania - highly elevated mood/irritable mood/quickness of thought

Hypomania - less severe elations, lower levels of disturbances

115
Q

What is bipolar I and II?

A

Bipolar I - mania

Bipolar II - hypomania

116
Q

When is bipolar diagnosed (conditions for diagnosis)?

A

Two or more episodes in which the patients mood/activity levels are significantly altered for a significant length of time

117
Q

pharmacological treatment for bipolar?

A

Lithium

Sodium valproate

Carbamazepine

Lamotrigine

118
Q

Cause of schizophrenia?

A

Increased dopaminergic activity in mesolimbic system, and mesocortical system

119
Q

What is the main class of drugs used in antipsychotic treatment? main receptors?

A

Dopamine receptor antagonists

D2 is main receptor

some drugs also block D3/4 and 5-HT receptors

120
Q

S/E of Dopamine receptor antagonist antipsychotics?

A

Blockade of dopamine in the nigrostriatal pathway:

  • Parkinsonian symptoms

Hypothalamus blockade (Dopamine receptors)

  • decreased Growth Hormone in children
  • Increased cortisol leading to cushings

Muscarinic receptors:

  • Dry mouth
  • Constipation
  • blurred vision

Histamine receptors:

  • Sedation

a-adrenoceptors

  • hypotension
  • hypothermia
121
Q

Three main classes of antipsychotic?

A

Phenothiazine (classical)

non-phenothaizine (classical)

Atypical

122
Q

Newer classical antipsychotics effects, example?

A

Fluphenazine

less antihistamine/antimuscarinic effects

More movement affects

123
Q

Older classical antipsychotics effects, example?

A

Chlorpromazine

less movement effects

more antimuscarinic/antihitsmine effects

124
Q

When might you use an atypical drug, example of two?

A

In treatment of negative symptoms

In non-responders to classical drugs

Clozapine: no movement disorders but risk of agranulocytosis (named basis only)

Remoxipride: little sedation but risk of aplastic anaemia

125
Q

Will phenylephrine have an effect on accommodation of the eye?

A

No, this is controlled by the lens which is parasympathetically innervated only

126
Q

What is horners syndrome caused by?

A

Lack of sympathetic outflow to the face

127
Q

What drugs will reduce aqueous humour production?

A

Alpa 2 adrenoceptor agonists

128
Q

What enzymes mostly break down L-dopa in the gut and in the brain?

A

COMT in the gut

MAO-B in the brain

129
Q

What is domperidone, why does it have an antiemetic effect?

A

A peripheral dopamine antagonist, exerts it’s affect on the CTZ (technically outside the BBB)

NLM2 (14 decks)

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