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All 422 Flashcards

1
Q

When does autism develop

A

2 months - 2 years

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2
Q

What does autism spectrum disorder include?

A

Aspergers
PDD NOS
Autsistic disorder

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3
Q

What is pathological demand avoidance?

A

A newer term to describe features presented in many children diagnosed with ASD

Features include - resisting and avoiding everyday demands of life, mood swings, procrastinating, lacking social understanding

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4
Q

What is the non pharmacological treatment of tourettes?

A

Habit reversal therapy - trying to identify and stop feelings/ sensations that trigger a tic

Exposure with response prevention - involves increasing exposure to thge urge to tic, leads to suppression of the tic response for longer

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5
Q

What is pharmacological treatment for tourettes?

A
  • Antipsychotics/ neuroleptics: aripiprazole, sulpiride, risperidone, pimozide, olanzapine, quetiapine, haloperido. These have side effects. Pimozide has fewer side effects but risk of heart problems.
  • Clonidine: works by stimulating the alpha 2 adreneegic system which inhibits the release of noradrenaline/ norepinephrine but causes drowsiness/ depression/ dizziness
  • Topiramate

If co morbid with ADHD, atomoxetine should be used because ADHS meds exacerbate tics

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6
Q

What are the severity levels of OCD?

A

Mild - <1 hours
Moderate - 1-3 hours
Severe - > 3 hours

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7
Q

How much of the population has OCD?

A

1%

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8
Q

What is the treatment for children and young people with OCD?

A

sertraline / fluvoxamine

If significant co morbidity with depression then fluoxetine should be used.

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9
Q

What should be used to treat children and young people with body dysmorphia?

A

Fluoxetine

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10
Q

What is the SSRI warning for children?

A

Increase risk of suicidal thoughts/ attempts, particularly in immediate period after started medication

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11
Q

What is the treatment for eating disorders?

A
  • CBT
  • Interpersonal psychotherapy
  • Dietary counselling

Anorexia - medication usually cautioned due to weakedned heart beacsue of emaciation

Bulemia - fluoxetine at higher doses than depression

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12
Q

What does lamotrigine act on?

A

Sodium channels and HVA calcium channels

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13
Q

What does levitiracetam act on?

A

Synaptic vesicle release - reduces glutamate release

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14
Q

What does parampanel act on?

A

AMPA recepors - reduces glutamate release

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15
Q

What does felbamate act on?

A

Ca, Na, GABA and glutamate

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16
Q

What can be used to treat Status epulepticus and what is the route of administration for each?

A
  • Midazolam buccaly
  • Lorazepam IV
  • Diazepam rectally
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17
Q

What are the safest drugs that can be used during pregnancy?

A

Lamotrigine and levitiracetam

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18
Q

What is the valproate pregnancy prevention programme?

A

MHRA determined that the valproate medicines are contraindicated in females of child bearing age unless the conditions of tyhe pregancy prevention programme are met;
1. GP must identify and recall all relevant females, provide the patient guide and check they have been reviewed by a specialist in the last year and are on highly effective contraception
2. Specialist must undertake reviews annually with female as part of the pregnancy prevention programme and reevaluate treatment as necessary

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19
Q

When is valproate contraindicated?

A

In pregnancy and bipolar disorder. Must only be considered if there is no alternate

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20
Q

What is MHRA advice regarding preganancy and valproate?

A

Babies born to mothers who take valproate during pregnancy have a 30-40% risk of developmental disability and a 10% risk of birth defects

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21
Q

What are the exceptions for valproate use in pregnancy?

A
  • Emergancy situations
  • Those who make a fully informed decisian
  • Whose treating professionals agree that pregnancy prevention is not appropriate;
  • Those with impaired capacity (such as some people with intellectual disability), where a bests interest process has been followed supporting the continuation of valproate
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22
Q

What is the role of a pharmacist in valproate prescribing?

A
  1. Ensure the patient card is provided every time
  2. Check patient is on contraception
  3. Remind the patient for the need for annual specialist review
  4. Dispense valproate in original package due to warning
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23
Q

What are the novel treatments for drug resistant epilepsy?

A
  1. Cannabidiol
  2. Ketogenic diet
  3. Vagal nerve stimulation
  4. Trans cranial stimulation
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23
Q

What are the causes of sudden unexpected death in epilepsy?

A

Proposed pathophysiology mechanism includes seizure induced cardiac and respiratory arrest

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24
Q

What are the numbers for sudden unexpected death in epilepsy?

A

1/1000 adults every year
1/4500 children every year
34% of all childrens deaths

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25
Q

What are the risk factors for sudden unexpected death in epilepsy?

A

Severity of seizures, increased refractoriness of epilepsy, decrease frequency tonic–clonic seizures.
Poor compliance with meds- decreased therapeutic levels of anti-epileptic drugs,
Young age, and early age of seizures onset.
Male gender
Being asleep during a seizure

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26
Q

How are most drugs used in child pschiatry?

A

Off label manner

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27
Q

What are typical antipschotics used for?

A

Psychosis, bipolar disorder, ASD associated steotypes, compulsions, aggression and self injerous behavious

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28
Q

What are atypical antipsychotics used for?

A

Symptoms of delusions, paranoia, disorganised thinking and used to deal with agrression and irratability

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29
Q

What are the side effects associated with blocked dopamine receptors?

A

Extrapyramidal side effects - inability to sit still, involuntary muscel contractions, tremours, stiff muscles involuntary facial movements

Hyperprolactinaemia

Sexual dysfunction

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30
Q

What are the side effects associated with 2nd gen antipsychotics?

A

Cardiotoxic, weight gain/ hypoglycaemia leading to metabolic syndrome

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31
Q

What are the monitoring requirements of antipshycotics?

A

Physicl health parameters need to be monitored on a regular basis to identify/ manage/ treat the metabolic side effects of second gen antipshyctics

  • Weight/ BMI intially and every 3 months
  • Us and Es - baseline & yearly
  • Blood glucose and lipids - initially and every 3 months
  • Prolactin - if symptoms of prolactinaemia present
  • ECG - initially if a cardiac risk patient
  • LFTS - baseline and yearly
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32
Q

What is hyperkinetic disorder?

A

A narrower restritive term tequiring more pervasive and impairing symptoms. In the UK 5% adhd, 1% hyperkinetic disorder

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33
Q

How is ADHD diagnosed?

A

By clinical interviews using reports and standerdised scales

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34
Q

What is the pathophysiology of ADHD?

A

Defective inhibitatory response, the compromised pre frontal cortex cant filter incoming stimuli

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35
Q

What is clonidines use in ADHD?

A

Mainly to augment therapy, is unlicensed

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36
Q

Methylphenidates effect is due to which enantiomer?

A

D enantiomer

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37
Q

What is atomoxetine?

A

A inhibitor of norepinephrine

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38
Q

What is guanfacine?

A

Sustained release preparation. Takes a long time to get therapeutic effects. Has a calming effect - may be useful in aggressive/ challanging behaviour and in reducing tics.

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39
Q

What is clonidine?

A

Unliscned for ADHD, 2-3 times a day dosing. Drop in bp a major side effect

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40
Q

What monitoring is required for stimulants?

A

increase monitoring of physical health parameters
- Baseline heart rate and blood pressure - repeat every dose adjustment and every 6 months
- Pre treatment height and weight on growth chart and evry 6 monts

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41
Q

What antidepressants are used for OCD?

A

Sertraline 150mg daily
Clomipramine 300mg daily

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42
Q

What are the antidepressants for depression in children?

A
  1. Fluoxetine 10mg a day
  2. Sertraline/ citalopram

Dont use TCA, venlafaxine, paroxetine
Must supply written information to parents
Decrease by 25% a week
Behavioiral adverse effects liekly ie agitation and restlessness
SSRIs p450 metabolism so absorbed and metabolised faster so may need higher doses

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43
Q

What are the numbers for seizures?

A

1/20 people will have a seziur ein there life

Epilepsy is a collection of 40 diseases which give rise to sezures

More prelevant in men

affects 1/100 people in the UK

70% successfully controlled by meds

25% of cases are preventable

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44
Q

What are the types of generalised seizures?

A

Tonic clonic - combines
Tonic - Increase tone in limbs
Clonic - rhythmic jerking
Absense - altered awaremess
Myoclonic - muscle contraction
Atonic - sudden loss of muscel tone

45
Q

What are the causes of epilepsy?

A

Genetics - dravets syndrome
immune - rasmussen syndrome
infection - bacterial or viral encephalotics
unknown - 1/3 of cases are unknown
structural - acquired or geentic
metabolic - glut1 deficiency

46
Q

What is the carrier protein that transports l dopa?

A

Large neutral amino acid transporter

47
Q

What is used to treat late stage of PD?

A

Transdermal patch/ SC administration

48
Q

What carrier transport is used for sodium valproate?

A

Monocarboxylase transporter

49
Q

What enteric coating is used for gastroresistant tablets?

A

diethyl pthalate
Polyvinyl acetate pthalate

50
Q

Where are chewable tablets dissolved?

A

Stomach or intestine

51
Q

What flavouring is used for chewable tablets?

A

Mannitol or sorbitol

52
Q

What matrix is used for erosion controlled matrix system?

A

Lipid, wax, polymers

53
Q

What are erosion controlled matrix systems?

A

The rate of drug released is controlled by the erosion of a matrix in which the drug is released

Eroding matrix: lipids, waxes, polymers (hydroxyethylcellulose)

54
Q

What is a diffusion controlled matrix system?

A

Drug dispersed as solid particles within a porous matrix formed of a water-insoluble polymer (polyvinyl chloride). Dissolution of drug particles located close to the surface. Diffusion of the drug through pores

Eg ropinerole ReQuip XL

Advantage:
-Prevention of in vitro burst effect, in vivo dose dumping

Disadvantages:
Sophisticated trilayer tablet compression machine needed
More labour-intensive process

55
Q

What is diffusion and erosion controlled matrix system?

A

Penetration of GI fluids in the matrix cvause dissolution of the drug and diffusion
Erosion is separation of the matrix surface from the core, leading to drug release

56
Q

How do extended release tablets work?

A

In the morning:
Dissolution of the drug overcoat - Immediate release of 22 % of the dose within 1 h

1 h later:
- Permeation of water through the membrane into the tablet core
- Expansion of the osmotically active polymer excipients in the push compartment, acting as an osmotic pump
- Regular release of the drug through the orifice
-Regular delivery of the drug for the rest of the morning

In the afternoon:
- The push mechanism continues to expand
- Increase of the drug release rate from the system with time, due to the drug concentration gradient incorporated into the two drug layers of the tablet

57
Q

How do modified release capsules work?

A

Gelatine capsule contains a matrix - hydrophillic polymers - erosion of the matrix - release of the drug by diffusion eg madopar CR - co beneldopa

58
Q

What are the limitations of rotigotine patches?

A

No exposure to external heat source - risk of increasing the rate and extent of drug absorption - may cause overdose

No exposure to water - can affect patch adherance

The backing layer of neupro contains aluminium so need to remove patch if having MRI or cardioversion to avoid skin burns

59
Q

How does a rotigotine patch work?

A

Apply patch once a day, same time everday.

Patch remains on skin for 24 hours

Replace with a new patch at a different site - abdomen, thigh, hip, flank, shoulder, upper arm

60
Q

When is IV injection used?

A

Urgent treatment if seizures last longer than 5 mins - use lorazepam - repeat once after 10 mins if seizure fails to repsond

61
Q

When is IM injection used?

A

Procyclidine hydrochloride - for acute dystonia

62
Q

When is SC injection used

A

Apomorphine hydrochloride: treatment of disabling motor fluctuations (“on-off” phenomena) in PD which persist despite treatment with levodopa
- Subcutaneous use by intermittent bolus injection.
- Continuous subcutaneous infusion by minipump and/or syringe driver
- Mini-pump for patients who require many and frequent injections (more than 10 per day)

63
Q

What are the primary headaches?

A

Migraine with/ without aura
Cluster headache
Trigeminal autonomic cephalgia

64
Q

What is a migraine without aura?

A

Headache attacks lasting 4-72 h (untreated or unsuccessfully treated)

Headache has 2 of the following characteristics:
1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
aggravation by or causing avoidance of routine physical activity (eg, walking, climbing stairs)

Headache 1 of the following:
1. nausea and/or vomiting
2. photophobia and phonophobia

65
Q

What are the triggers for migraines without aura?

A

Stress and other emotions
Biological and environmental conditions, such as hormonal shifts or exposure to light or smells
Fatigue and changes in one’s sleep pattern
Glaring or flickering lights
Weather changes
Certain foods and drinks

66
Q

What is a migraine with aura?

A

Headache ≥1 of the following fully reversible aura symptoms:
1. visual; 2. sensory; 3. speech and/or language; 4. motor; 5. brainstem; 6. retinal
Headache≥3 of the following 6 characteristics:
1. aura symptom spreads gradually over ≥5 min
2. ≥2 symptoms occur in succession
3. each individual aura symptom lasts 5-60 min
4. ≥1 aura symptom is unilateral
5. ≥1 aura symptom is positive
6. aura accompanied, or followed in <60 min, by headache
If Suspected , should be referred

67
Q

What are the treatment options for primary headaches?

A

Paracetamol - acts in inhibition of prostaglandin production in pain pathway. Also in activation of descending serotonergic pathways

Ibuprofen – act on COX -1 and COX-2 receptors to inhibit production pf prostaglandins in pain pathway

Codeine – acts centrally, has limited effectiveness on its own and works better in combination products – but has issues

Buclizine – antihistamine with anti-emetic properties, also sedating

Triptans - selective 5-HT Serotonin receptor agonists causes cranial vasoconstriction.Sumatriptan is P med with restrictions

Pizitofen – acts on serotonin, histamine and tryptamine reducing blood flow and alters pain threshold in migraine POM

Propranolol – B-blocker reduces blood flow POM

Other – Ergotamine POM, Menthol, Oral ContraceptivesPOM (CI for migraine with Aura), non Pharmocological

68
Q

What aches in secondary headaches?

A

A network of nerves that extends over the scalp
Certain nerves in the face, mouth, and throat
Muscles of the head, neck, and shoulders
Blood vessels found along the surface and at the base of the brain (these contain delicate nerve fibres)

69
Q

What is a tension headcahe?

A

Tension headaches.Tension headaches are the most common type of headache. Stress and muscle tension are often factors in tension-type headaches. Common features are:
Slow onset of the headache
Bilateral -Head usually hurts on both sides
Pain is dull or feels like a band or vice around the head
Pain may involve the back (posterior) part of the head or neck
Pain is mild to moderate,
but not severe

70
Q

What are the treatment options for secondary headaches

A

Painkillers – Paracetamol, Ibuprofen, codeine
Muscle relaxants – Non Pharm, Diazepam (Rx)
Anti-bacterial – Rx dependant on causative organism
Decongestants – Pseudoephedrine, Xylometazoline,
Anxiolytics – POM and watch out for herbals eg St John’s Wort
Amitryptyline – POM (Neuralgias)
Gabapentin/Pregabalin/Carbamazepine – POM (Neuralgias)

71
Q

What are the 2 diagnostic systems for depression?

A

ICD 10/ 11 & DSM5

72
Q

When is bipolar disorder usually diagnosed?

A

In late teens

73
Q

What are the mechanism of action of lithium?

A
  • modulation of glutamate, GABA & DA neurotransmission
    -inhibition of inositol triphosphate formation
  • interference of cAMP formation
  • accumulation of Li+ in cell, leading to sustained depolarisation
74
Q

What are the side effects of lithium?

A

Long half life leads to common side effects such as nausea, thirst, tremor, mental confusion

75
Q

What are the symptoms of major depressive disorder?

A

Key symptoms:
persistent sadness or low mood
loss of interests or pleasure
fatigue or low energy

Associated symptoms:
disturbed sleep
poor concentration or indecisiveness
low self-confidence
poor or increased appetite
suicidal thoughts or acts
agitation or slowing of movements
guilt or self-blame

76
Q

What are the neural pathways involved in affective disorders?

A

Glutaminergic
Dopaminergic
GABAergic

77
Q

How do monoamines modulate through the brain?

A

Noradrenergic system - local coerulus
Seratonergic system - raphe nucleus
Dopaminergic system - VTA & SN

78
Q

What are the psychotherapies for depression?

A
  • Behavioural therapy
  • Interpersonal psychotherapy
  • Group therapy
  • CBT
  • Mindfulness based cognitive therapy
79
Q

What are the brain stimulation methods for depression?

A
  • Electroconvulsive therapy
  • Vagus nerve stimulation
  • Transcranial megnetic stimulation
  • Deep brain stimulation
80
Q

What are SSRIs associated with?

A

Increased risk of bleeding especially in older patients and those taking anticoagulants

81
Q

What are the side effects of TCAs?

A

dry mouth, urinary retention, blurred vision, cardiotoxicity, sedation , weight gain

Risk of overdose - increased risk of coma/ seizure and potentially fatal cardiac arrythmia/ arrest

82
Q

What are the novel treatments for depression?

A

Ketamine and psilocybin

A single dose of these NMDA inhibitors can cause a rapid (next day) antidepressant effect in patients with major depression.

Primarily used in treatment-resistant depression (resistant to 2 or more other antidepressants).

83
Q

what are the key clinical points for diagnosing Genarilised anxiety disorders?

A

Generalized anxiety disorder is characterized by persistent anxiety and uncontrollable worry that occurs consistently for at least 6 months.

This disorder is commonly associated with depression, alcohol and substance abuse, physical health problems, or all these factors.

In primary care, patients with this disorder often present with physical symptoms such as headaches, muscle tension, gastrointestinal symptoms, back pain, and insomnia.

Brief validated screening tools such as the Generalized Anxiety Disorder 7 (GAD-7) scale should be used to assess the severity of symptoms and response to treatment.

84
Q

What are the social signs of anxiety disorder?

A
  • Fear of leaving the house/ social withdrawal
  • Compulsive/ repetitive behaviours
  • Frequent emotional and physical health issues
  • Extreme, unwanted fear of particular situations/ things
85
Q

What is included in DSM 5 classification?

A

Social Anxiety Disorder (Social Phobia)

Specific Phobia

Panic Disorder

Agoraphobia

Generalized Anxiety Disorder

Anxiety Disorder Due To Another
Medical Condition

Substance/Medication-Induced Anxiety Disorder

Selective Mutism

Separation Anxiety Disorder

Other Specified Anxiety Disorder

Unspecified Anxiety Disorder

86
Q

What are ICD10 classifications?

A

F40 Phobic anxiety disorders
F41 Other anxiety disorders
F42 Obsessive-compulsive disorder
F43 Reaction to severe stress, and adjustment disorders
F44 Dissociative and conversion disorders
F45 Somatoform disorders
F48 Other nonpsychotic mental disorders

87
Q

What is the pathophysiology of anxiety?

A

Brain regions: The limbic system is thought to play central role in anxiety disorders (evidence form animal and human models).

Neurotransmitter systems: Altered sensitivity of the GABA system is implicated.

In addition, some evidence exists for the serotoninergic (5-HT) system to be involved.

88
Q

What are the anxiolytics?

A

benzodiazepines
SSRIs
TCAs
5-HT agonists

89
Q

What is the elimination and metabolism of benzodiazapenes?

A

Rapid (t 1/2 < 5 hrs): midazolam

Short (t1/2 = 5-20 hrs): lorazepam, temazepam

Intermediate (t 1/2 = 20-40 hrs): nitrazepam.

Slow (t1/2 > 40 hrs): diazepam, chlordiazepoxide

Long half-lives usually means the generation of active metabolites.

Side effects: overdose, drug interaction, tolerance & dependence.

90
Q

What are the benefits of SSRI?

A

Can be helpful for depression, panic disorder and social phobia.

Safe in overdose.

No tolerance and no withdrawal unless patient stops abruptly.

No weight gain.

91
Q

What are the disadvantages of SSRI?

A

4-6 weeks to see effects, full benefit develops in up to 12 weeks.

Patients often experience a temporary worsening of symptoms.

Side effects such as nausea, insomnia, headaches, sexual dysfunction, initial agitation.

92
Q

What SSRI are prescribed for anxiety?

A

fluoxetine (prozac), sertraline, paroxetine, citalopram.

93
Q

What is buspirone?

A

5HT1a partial agonist. A mild tranquiliser. Used to treat generalied anxiety and social phobias

94
Q

What are the benefits of buspirone?

A

No sedation or impairment of performance
No cross-tolerance with BZs
No tolerance or withdrawal
No abuse potential

95
Q

What are the disadvantages of buspirone?

A

Nausea, headache, insomnia, nervousness, restlessness. dizziness, light headedness. Might requires extended treatment to see beneficial effects.

96
Q

Give examples of neurosis

A

Anxiety, mild depression

97
Q

Give examples of pschosis

A

Severe depression, schizphrenia

98
Q

What type of dosage form is usually used for neurosis?

A

oral/ patches

99
Q

What type of dosage form is usually used for psychosis

A

IM/ IV

100
Q

When may benzodiazapene depndance occus?

A

after 4-6 weeks of treatment

101
Q

How do you wean off benzodiazapenes?

A

decrease by 1/6 - 1/8 every fortnight

102
Q

What are extended release capsules?

A

Equsym XL - contain 70% slow release tablets and 30% fast releasing tablets. Effective for 8 hours

103
Q

What is a matrix type patch?

A

Eg daytrana - methylphenidate. Appky to hip 2 hours before effect is needed. Remive patch 9 hours after use.

104
Q

What are the warnings assocuated with methylphenidate use?

A
  • Sudden death reported in association with methylphenidate treatment at usual dose in children and adolesncets with structural cradiac abnormalities or other serious heart problems

Long term suspension of growth - if using long term - 7 days for 1 year. Have a temporary slowing in growth rate - about 2 cm less height and 2.7kg less in weight over 3 years.

105
Q

When are parenteral injections preferred?

A
  • When a schizophrenic patient needs long term maintenence
  • Acutely psychotic patient - need of prompt drug therapy, prevent self harm or harm to others
106
Q

What are injections?

A

Sterile solutions, emulsions, or suspensions in water or non aqauous liquid

107
Q

What are the advantaged of lipophillic diazepam?

A

higher drug payload, less pain on injection, protection of the drug by the oily environment

108
Q

Describe depot therapy

A

Effective plasma therapeautic level reached within one week, maintained fir 14 - 28 days. Injection every 2-4 weeks.

109
Q

What are advantages of depot therapy?

A
  • lower total dose of drug than oral form
  • Facilitation of community care
  • Regular contact with pateint by carer
  • Supervised administration
  • no accumulation or abuse of unused tablets
  • No issue of compliance§
110
Q

What are the disadvantages of depot therapy?

A
  • Pain on injcetion site
  • No rapid elimination from the body if adverse effects
111
Q

What are other stratergies of depot therapy?

A

Enxapsulation of the drug in PLG microsphere. 381mg of risperidone per gram of microsphere. Lag phase of 4 weeks, during which oral therapy must be continued

422 Exam prep (1 decks)

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