Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharamacology, theraputics and prescribing > CNS and psychiatric drugs > Flashcards

CNS and psychiatric drugs Flashcards

1
Q

What is the difference between a partial and generalised seizure?

A 
Generalised= whole brain and loss of consciousness
Partial= part of brain and remains conscious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two types of partial seizure

A 
Simple= remains aware 
Complex= altered awareness and behaviour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give 3 secondary causes of seizures

A

Head injury, hypoxia, tumour, stroke, infection, hypoglycaemia, drugs, electrolyte imbalances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why can alcohol withdrawal cause seizures?

A

Alcohol stimulates GABA channels, therefor alcoholics have down regulated GABA channels, when alcohol is removed there is less GABA release leading to excitation and so seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name one class of drugs which inhibits seizures by stimulating GABA channels

A

Benzodiazepam (lorazepam and diazepam)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 3 drugs which inhibit seizures by inhibiting voltage gated sodium channels and so inhibit propagation of the seizure

A

carbemazepine, phenytoin, lamotrigine, also sodium valproate by secondary action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

State the 3 ways sodium valproate acts to inhibit seizures

A

voltage gated sodium channel inhibition, Ca2+ channel blocker (main) and weak GABA synthesis and activation stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why do voltage gated sodium channel blockers only affect the part of the brain having the seizure?

A

Because they move into and block the channel when it is open, therefor those which are open more (the depolarising neurones) will be affected more, so will reduce firing rate to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which seizures can carbamazepine be used on?

A

generalised tonic- clonic and partial seizures- not absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is significant about the drug interactions of carbemazepine?

A

It is a strong CYP450 inducer, so will decrease the effect of warfarin, oral contraceptives, steroid, phenytoin.
It will also reduce its own half life from 30hrs at the start of the regime to 15hrs with repeated use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give 3 ADRs of carbemazepine

A
  • GI upset/ vomiting
  • headache, dizziness, ataxia, motor disturbance, numbness, tingling
  • neutropenia (rare)
  • rashes (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When can phenytoin be used?

A

All partial seizures + generalised tonic clonic seizures NOT absent seizures. Also as loading dose + infusion if seizure not terminating after 10 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the interactions of phenytoin (2)

A
  • CYP450 inducer (warfarin, contraceptives, steroids) but doesnt affect its own metabolism
  • Highly protein bound (affects NSAIDs, valporate to increase both drugs free plasma conc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 3 ADRs of phenytoin

A
  • gingival hyperplasia (20%)
  • rashes (stevens johnsons syndrome in 2-5%)
  • ataxia, numbness, tingling, headache, dizziness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When is lamotrigine used and not used?

A

All types of seizures, but avoided in children due to ADRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe 2 important drug interactions with lamotrigine

A
  • oral contraceptives reduce its effect
  • valproate will increase its free plasma conc as its also protein bound
  • no CYP450 induction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 3 ADRs of lamotrigine

A
  • ataxia, diziness etc but less severe than other drugs

- nausea and skin rashes however more severe and more common in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When can sodium valproate be used?

A

all seizure types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give 3 interactions with sodium valproate

A
  • anti depressants will inhibit its action
  • anti psychotics will antagonise it
  • aspirin will compete with it in plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give 3 ADRs of sodium valproate

A
  • highly teratogenic
  • ataxia and weight gain
  • may elevate LFTs, but this will only lead to liver failure in minority of cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How can sodium valproate levels be monitored?

A

By saliva sample- concentration is the same as blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When are benzodiazepams used in epilepsy?

A

Generally reserved for status epilepticus/ emergencies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the administration of lorazepam, diazepam and midazolam

A 
lorazepam= IV bolus (1st choice)
Midazolam= Buccal or IV 
Diazepam= rectal or oral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give 3 ADRs of diazepam

A
  • sedation
  • tolerance and dependance with chronic use
  • confusion
  • aggression
  • resp and CNS depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the 5 steps to managing seizure emergencies and status epilepticus

A 
1st= ABCDE approach 
2nd= IV lorazepam or rectal diazepam
3rd= if no termination after 5 mins give more benzodiazepam 
4th= if no termination after 10-15 mins give loading dose of IV phenytoin, call ITU to get ready to sedate and intubate 
5th= send to ITU
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 3 rules to prescribing anti epileptic drugs

A
  • aim for monotherapy- if one drug doesnt work try a differnt one
  • if all dont work alone start combining them
  • start at low dose and slowly increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which drug is first choice for generalised seizures and which is for partial seizures?

A

sodium valproate is first choice for generalised, carbemazepine is for partial seizures, but can be used in generalised too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which anti- epileptic drug is favoured in pregnancy

A

lamotrigine- least teratogenic, best to stop all drugs if you can. If lamotrigine need to be given, supplement with folic acid and vit K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Which anti- epileptic drugs have most and least effect on contraceptives

A

Phenytoin and carbamazepine both decrease efficacy of oral contraceptives.
Oral contraceptives reduce the effect of lamotrigine.
Valproate and benzodiazepines both have no interaction with oral contraceptives.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the cardinal features of parkinsons

A

Bradykinesia, ridgity, resting tremour, postural instabilty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the signs of parkinsons plus syndromes

A

Early onset dementia, early onset instability, early onset hallucinations/ psychosis, early autonomic signs (instability, incontinence) and ocular signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Name 3 types of parkinsons plus syndromes

A
  • multiple systems atrophy
  • progressive suprenuclear palsy
  • lewy body dementia
  • parkinsonism dementia (amytrophic lateral sclerosis complex)
  • corticobasal ganglionic degeneration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the pathophysiology behind Parkinson’s

A
  • loss of dopaminergic neurones in the substantia nigra-> reduced inhibition of indirect pathway and more activation of direct pathway-> less stimulation of thalamus and cortex -> bradykinesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is parkinsons diagnosed (3)

A

Symptoms + normal CT/MRI + good response to trial of treatment.
Also other cause of parkinonsism need to be ruled out: drug induced, vascular, parkinsons plus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe the mode of action of levo- dopa as a treatment for parkinsons

A

Levo dopa passes the blood brain barrier (dopamine doesnt) and is then converted to dopamine by dopa carboxylase when it gets into neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What % of levodopa given reaches the CNS?

A

1%- most is activated in intestinal wall or peripheral dopaminergic neurones, this is increased w/ compt inhibitors and carbidopa

37
Q

Give 3 ADRs of levo dopa

A
  • dyskinesia+ dystonia+ freezing
  • psychosis
  • n+ v, hypotension
38
Q

When is levo dopa used and not used in parkinsons

A
  • it is first line treatment for parkinsons
  • however will not work if there are no dopaminergic cells left in the STN
  • it is not neuroprotective so no point rushing into treatment
39
Q

What are on off fluctuations in parkinons? how are they managed?

A

Over time, more dopaminergic neurones are lost so the effect of levo dopa reduces, so you get periods where it doesnt work leading to dystonia and freezing, which are painful and dangerous.
You can reverse them with dopamine agonists (ropinirole)

40
Q

What is carbidopa?

A

A peripheral dopa decarboxylase inhibitor, which prevents levo dopa breakdown in peripheries so increases levodopa reaching the CNS. It is given in combination with levo dopa.

41
Q

Name one COMT inhibitor

A

Entacapone

42
Q

How do COMPT inhibitors work?

A

Prevents peripheral breakdown of L- dopa into a metabolite which inhibits CNS absorbtion of L- dopa.

43
Q

When are COMPT inhibitors used?

A

In combination with L dopa (and sometimes carbidopa) to increase L dopas effect. It also reduces wearing off of symptoms

44
Q

Name 1 ergot derived and one non ergot derived dopamine receptor agonist

A

Ergot derived: bromocriptine

Non ergot dervied: apomorphine, ropinerole

45
Q

What is the therapeutic difference between ergot derived and non ergot derived DRAs?

A

non ergot derived have fewer side effects

46
Q

When are dopamine receptor agonists used in parkinsons

A

can help control on off fluctuations, not used as first line as less efficacious and more expensive

47
Q

Give 3 ADRs of dopamine receptor agonists

A
  • more sleep attacks (so cant drive with them)
  • impulse control disorders become more common (more gambling, shopping etc)
  • sedation, hallucinations, confusion, N+V, hypotension can all occur
48
Q

Name one MAOI type B inhibitor sometimes used in parkinsons and describe its mode of action

A

selegiline
MAOI type B metabolises dopamine so inhibition of it leads to less breakdown of dopamine. It smoothes out motor responses and may also be neuroprotective

49
Q

State one anti-muscarinic used to treat parkinsons and state which symptoms they treat the best

A

Procyclidine

Works well to reduce tremour, little effect on bradykinesia,

50
Q

When is surgery an option for treatment of parkinsons

A

When L dopa is poorly tolerated but the individual is still dopamine responsive and they have no psychiatric illness

51
Q

Describe the surgery options used to treat parkinsons (3)

A

Can create lesions on the thalamus to treat tremours, lesions on GPi to treat dyskinesia and also deep brain stimulation of the subthalamic nucleus, which improves all symptoms

52
Q

What is the most common initial presentation of myasthenia gravis

A

weakness of extra ocular muscles leading to ptosis and diplopia

53
Q

Describe how pyridostigmine works to treat myasthenia gravis

A

An acetylcholine esterase inhibitor- more Ach engages with receptor- better coordination of muscle

54
Q

Which acetylcholinesterase inhibitor is IV and fast acting- so used in ITU

A

Neostigmine

55
Q

Describe the time taken for maximal response of pyridostigmine and the implications of this

A

Peak response after 30 mins, so should be taken 30-60 mins before a meal to minimise aspiration risk

56
Q

Give one ADR of acetylcholine esterase inhibitors when dose is too high? How is this reversed?

A
  • SLUDGE syndrome as doses too high (esp with neostigmine)

- Reverse with atropine

57
Q

Other than acetyl cholinesterase inhibitors, name 3 other methods of treating myasthenia gravis

A
  • corticosteroids to decrease immune response
  • IV immunoglobulins in acute decline or crisis
  • Plasmaphersis to remove Achr antibodies (short term improvement)
  • biological therapies emerging
58
Q

Name the 4 classes of drugs used to treat depression

A
  • Serotonin and noradrenaline reuptake inhibitors (SNRIs)
  • SNRIs + other actions (TCAs)
  • Selective serotonin reuptake inhibitors (SSRIs)
  • noradrenaline reuptake inhibitors (NARIs)
59
Q

Give 2 examples of SSRIs

A

fluoxetine, citalopram sertraline

60
Q

What is first line treatment of moderate to severe depression

A

SSRI + CBT

61
Q

How long can SSRIs take to work and for how long after symptoms have gone should they be taken for?

A

Can take up to 6 weeks to work. Should keep take for a year after symptoms gone to avoid relapse

62
Q

What is serotonin syndrome?

A

Tachycardia, sweating, hyperthermia etc within a few weeks of starting an SSRI/ SNRI. It is an emergency as can lead to seizures, hyperthermia etc

63
Q

Give 3 ADRs of SSRIs?

A
  • Anorexia, N+V, diarrhoea
  • Sexual dysfunction, sweating tremor and insomnia rarer
  • dyspepsia
  • citalopram prolongs QT-> arrhythmias
  • Many increase bleeding and cause hyponaturaemia, esp if taken with NSAIDs.
64
Q

Describe the safety of SSRIs in overdose

A

safe enough if its the only drug taken

65
Q

Give 2 examples of tricyclic antidepressants (TCAs)

A

Amytriptyline, imipramine, lofepramine

66
Q

other than depression, what can TCAs be used to treat?

A

Neuropathic pain

67
Q

How do TCAs work?

A

Largely by inhibiting NA and serotonin reuptake but also affect a1 adrenoreceptors and muscarinic receptors

68
Q

give 3 ADRs of TCAs?

A
  • dry mouth, dry nose, blurred vision, constipation, urinary retention due to anti muscarinic effects
  • sedation and impairment of psychomotor performance, lower seizure threshold
  • fatigue, abdo pain, restlessness, palpitations
  • extrapyramidal syndromes
69
Q

Give 2 effects of TCA overdose and how you would reverse it

A
  • CVS effects: tachycardia, postual hypotension, impaired contractility
  • CNS effects: seizures, sedation, hallucinations
  • Acidosis
    Sodium bicarbonate can be given to help bind to drug and also helps reverse the acidosis.
    Overall pretty bad so avoid giving to those who’re suicidal
70
Q

Give two example of SNRIs

A

venlafaxine, duloxetine

71
Q

Give 3 ADRs of SNRIs

A
  • As with SSRIs (anorexia, N+V, diarrhoea, insomnia, sexual dysfunction
  • increased BP, dry mouth, hyponaturaemia
  • withdrawal on continuous use is common
72
Q

Give 2 typical and 2 atypical antipsychotics

A

Typical: haloperidol, chlorpromazine
Atypical: olanzapine, risperidone, clozapine, quetiapine

73
Q

What is the difference in mode of action and side effects between typical and atypical anti psychotics?

A 
Typical= D2 receptor antagonists, extrapyramidal sie effects common
Atypical= Dopamine antagonists and also serotonin receptor antagonists, Side effects less common + better at reducing negative symptoms
74
Q

State and describe 3 extrapyramidal side effects?

A

Dystonia= abnormal posture due to muscle contraction
Akathesia= internal feeling of restlessness
Tardive dyskinesia= abnormal involuntary movements
Pseudo parkinsonism.
These occur due to inhibition of the nigrostriatal pathway

75
Q

Give 3 non extra pyramidal side effects of anti- psychotics

A
  • Anticholinergic: dry mouth, urinary retention, blurred vision
  • Serotonergic: N+V, sexual dysfunction, insomnia
  • Metabolic: increased blood glucose, weight gain, increased CVS risk
  • Anti- dopamine: extra pyramidal side effects + hyperprolactinaemia
  • clozapine also causes neutropenia so needs FBC monitoring
76
Q

Describe the effects of OD on antipsychotics?

A

CNS depression, cardiac toxicity, risk of sudden death (esp with high doses)

77
Q

Describe treatment of anxiety

A

1st line= CBT and treatment of any co- existing disorders
2nd= SSRIs and SNRIs
Acute declines can be treated with benzodiazepams (anxiolytic) but not suitable for long term use
3rd= pregablin if SSRIs and SNRIs dont work

78
Q

Give 3 ADRs of benzodiazepams

A
  • withdrawal and dependance
  • drowsiness, dizziness, psychomotor impairment, ataxia, headache
  • tolerance
  • dry mouth, blurred vision, GI upset,
  • amnesia, restlessness
  • rash
  • May be teratogenic
79
Q

Describe the effect of benzodiazepam overdose and how it is reversed

A
  • respiratory depression

Usually supportive treatment is fine but may need flumazenil to reverse (Benzodiazepam receptor antagonist)

80
Q

Name 2 mood stabilisers used to treat bipolar

A 
Sodium valproate (valproic acid) and lithium (lithum carbonate) 
Carbemazopine, lamotrigine and some antipsychotics can also be used
81
Q

Why is monitoring required for lithium treatment of mania?

A

It has narrow theraputic window. TFTs, LFTs and U&Es need checking every 6 months

82
Q

Give 3 ADRs of lithium

A

Thirst, memory problems, polyuria, tremors, drowsiness, weight gain

83
Q

Describe the effect of lithium OD and its treatment

A

N+V, diarrhoea, coarse tremor, dysarthria, cognitive impariment, restlessness, agitiation.
Treat supportively, with anti convulsants, IV fluids and haemodialysis if very severe

84
Q

What are the two classes of drugs used to treat dementia

A

Ach esterase inhibitors (for mild to moderate dementia) and NMDA blockers (for severe dementia)

85
Q

Name 2 Ach esterase inhibitors used in dementia

A

Donepezil, galantamine, rivastigmine

86
Q

Name one NMDA blocker used in dementia

A

Memantine

87
Q

Give 3 ADRs of NMDA blockers

A

hypertension, dizziness, headache, drowsiness

88
Q

Give 3 ADRs of Ach esterase inhibitors

A
  • N+V, anorexia, diarrhoea
  • Fatigue, insomnia, headache
  • bradycardia
  • COPD worsening
  • gastric/ duodenal ulcers
89
Q

Name 3 mode of actions of anti- N+V drugs and give 1 example of each

A
  • Histamine antagonist (cyclizine)
  • Dopamine (D2) antagonist (metoclopramide, domperidone)
  • Serotonin antagonist (ondansertron)
  • Also hyoscine (motion sickness)

Pharamacology, theraputics and prescribing (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions