week 1 Flashcards

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1
Q

psychotic

A

out of touch from reality

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2
Q

hallucination

A

experience something without an external stimulus

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3
Q

delusions

A

false unshakeable idea or belief is out keeping with the patients educational , cultural and social background; it is held with extraordinary conviction and subjective certainty

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4
Q

different types of delusions

A

grandiose

hypochondriacal

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5
Q

pharmacodynamics

A

what the drug does to your body

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6
Q

bioavailability

A

expressed as F
affected by many factors
fraction of the administered does of the drug that reaches the systemic circulation
enzyme enhancers/inhibitors affect F

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7
Q

apparent vol of drug distribution

A

total amount of the drug in the body/ drug blood plasma conc.
the amount of the drug would need to be uniformly distributed to produce observed blood conc

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8
Q

half life

A

timre required for serum plasma conc to decrease by half

determined by clearance and vol of distribution

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9
Q

elimination half life

A

time for conc to fall by half

-time to eliminate the drug

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10
Q

linear pharmoco

A

double the dose double the conc

50% of the drug will be eliminated in a given time frame

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11
Q

non linear oharmaco

A

concentration that results is not proportional to dose

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12
Q

how to avoid morphone over dose going from oral to subcut

A

when converting oral to parenteral morphine we prescribe 1/3 of the oral dose
there is a difference in bioavailability

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13
Q

loading does

A

A loading dose is an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose.
volume of distribution needs to be considered here

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14
Q

phenytoin has what feature

A

non linear pharmacokinetics

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15
Q

loading dose depends on…

A

the concentration you wish to achieve and the volume of distribution

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16
Q

IV loading dose? how to calculate

A

target conc (mg/L)x volume of distribution (L/kg) = target c x (mg/kg)

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17
Q

pharmacodynamics

A

what the drug does t0 you

e.g.efficacy

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18
Q

different drug receptors

A
enzyme linked (multiple actions)
ion channel linked (speedy)
g protein linked (amplifier)
nuclear (gene) linked (long lasting)
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19
Q

Affinity

A

measure of the propensity of a drug to bind wiht receptor , the attractiveness of drug and receptor

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20
Q

efficacy?

A

ability of a bound drug to change the receptor in a way

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21
Q

core features in ADHD

A
excessive activity 
impulsivity
inattention 
inattention 
impact on family and child
worse in the afternoon
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22
Q

pervasive

A

evident in more than one in enviroment , look for 3 environments

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23
Q

comrobid associations with adhd

A
sleep disorders 
behavioural difficulties 
specific learning disabilities 
developmental coordination disorders
social communication difficulties 
anxiety symptoms 
tic disorders
mood difficulties
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24
Q

diagnosis for adhd

A

assessments

  • direct observation in more than one setting
  • psychoeducation assessment - schools, school staff
  • structured questionnaires , full developmental history
  • identifying co-morbid mental health problems
  • multi diciplinary team used
25
Q

what neurotransmitter is responsible for alertness , concentration, and energy

A

Noradrenaline

26
Q

what emotions is serotinin responsible for

A

obsessions and compulsions memory

27
Q

what emptions is dopamine responsible for?

A

pleasure reward , motivation

28
Q

ADHD characteristics

A
Attention deficit (selected attention and sustained attention )
motor hyperactivity / psychomotor agitation 
Impulsivity- inappropriate /defective filtering of info
29
Q

Dopamine neurotransmission relative to ADHD

A

enhances signal

improves attention - focus , on task behaviour , on task recognition

30
Q

NA neurotransmission relative to ADHD

A

Dampens noise
executive operations
increases inhibition

31
Q

A defective inhibitory response in a compromised prefrontal cortex leads to

A

insufficient info processing - symptoms of inattention , hyper activity and impulsivity . neurons in the prefrontal cortex are out of tune and unable to distinguish between important signals and background noise

32
Q

what is hypo-arousal

A

need to improve the signal to noise detection ratio - to relieve adhd symptoms - increase the drive of the arousal network to improve efficiency of info processing . Hypoarousal is associated with low tonic firing of dopamine and noradrenaline neurons.

33
Q

Stimulants enhance …

A

arousal neurotransmitters - amplify tonic firing rates.

34
Q

hyper arousal

A

Too much ‘arousal’ i.e excess norad/dop stimulates some receptors and causes the signal to noise detection to deteriorate (poor attention and impulsivity)
Hyper-arousal is associated with increased phasic firing of dop / norad neurons
Need to desensitize postsynaptic norad / dop receptors & down regulate neuronal activity to return norad/dop neurons to normal phasic firing

35
Q

first line treatment of ADHD

A

Psychostimulants - methylphenidate and dexamphetamine

36
Q

2nd line for ADHD

A

When stimulants ineffective/ not tolerated/ co morbidity - atomoxetine

37
Q

3rd line ADHD

A

augment therapy

38
Q

example of a dopaminergic drug

A

modafinal

39
Q

co morbidities of ADHD

A
Tics -11%
CD - 14%
mood -4%
anxiety -40%
ODD - 40%
Oppositional defiant disorder (ODD) - 40%
40
Q

psychostimulants

A

Since tonic firing rates are low – need drugs which boost norad / dop signalling
Effective in majority of cases (75%)
Improve attention span,  hyperactivity & impulsivity ,  aggression
Rapid onset of action (within an hour)

41
Q

Dexamfetamine

A

facilitates release of dopamine from presynaptic cytoplasmic storage vesicles in synapse & blocks dopamine transporter protein (inhibits reuptake) – NET RESULT IS INCREASE IN DOPAMINE

42
Q

Methylphenidate

A

acts primarily on the dopamine transporter & has little effect on synaptic release – INCREASE IN DOPAMINE

43
Q

prep for dexamfetamine

A

dexedrine 5 mg
Rapid onset of action, lasts 13 hours
Can be dissolved in water (ease of administration)

44
Q

prep for methylphenidate

A

MPH immediate releasing tabs 3-4 x a day

modified release and sustained release - duration of 8-12 hours

rapid action of onset
usually give long acting in the morning with IR tablet slate in afternoon before 5

45
Q

Psychostimulant side effects

A

Potential for growth retardation (clinically insignificant effect on height, weight)
Anorexia (give with meals, dose  or omission)
BP and HR irregularities (monitor after every dose increase)
Insomnia / sleep difficulties (good sleep hygiene or melatonin)
Other: sadness, irritability, abdominal pain & headaches

46
Q

what kind of monitoring is required for ADHD

A

 monitoring of physical health parameters
Baseline HP & BP. Repeat at every dose adjustment & every 6 months
Pre- treatment height & weight on growth chart & every 6 months
Complete history documenting concomitant medicines, past, present medical & psychiatric disorders, family history of sudden cardiac death & unexplained death
 in contra indications including history of depression, anorexia, suicidal tendencies, psychosis, pre-existing cardio vascular disorders

47
Q

legal status of ritilin

A

has 28 days validity
30 days supply and more can be requested
must be signed on collection to prove identity

48
Q

Prescription requirements

A

the form and strength
total quantity to be supplied in words and figures
the dose to be administered
must be signed and dated by prescriber

49
Q

Atomoxetine

A
noradrenaline reuptake inhibitor 
enhances NA transmission in the PFC area
once daily or twice a day.
monitoring on BP pulse weight , LFTs , mood
No recorded abuse 
effective for co morbidity 
SIX weeks for onset .
NA is released into the synapse , NA reversibly attaches to receptors , atomoxetine blocks the reabsorption of NA from the synapse .
50
Q

side effects of atomoxetine

A

Nausea / vomiting
Excessive tiredness
Insomnia
Abdominal pain, appetite suppression, weight loss
Constipation
Headaches
Mood swings / Rage
Hepatic impairment (monitor LFTs, recognise symptoms)
Increased heart rate / blood pressure
Suicidal ideation (raised awareness amongst parents/carers)

51
Q

example of alpha adrenergic

A

clonidine and guanfacine

52
Q

mechanism of alpha adrenergic

A

Central & peripheral adrenergic agonists - inhibit norad at the synapse .
clinical effect takes 4-6 weeks .
Children metabolise faster so require frequent dosing (clonidine may be Rx TDS)

53
Q

alpha adrenergic side effects

A

SE’s: Sedation, dizziness, hypotension (monitor BP &HR)
Precaution with psychostims- case reports of sudden death
.
Caution- Guanfacine is a CYP 3A4 substrate

54
Q

Antidepressants- not used in CAMHS

A

Enhance amount of monoamines at the synapse.
Rarely used in children (mostly adults)
Nortriptyline, Imipramine most common.
SE’s: anticholinergic, cardiac, seizures

55
Q

modafinil

A

not used in CAMHS
-Weak psychostimulant - weak affinity for dopamine uptake carrier sites ; may work by decreased GABA and increased release of glutamate also contolling the degreee of hypothalmic control

56
Q

susceptibility ADHD genes

A

DRD4 Receptor 7-Repeat Alleles
associated with overactivity & impulsivity

SLC6A3/DAT1 – Dopamine Transporter gene

DRD5 - Dopamine receptor gene

SLC6A4/5HTT – Serotonin Transporter gene
associated with emotional volatility

HTR1B - Serotonin receptor gene
associated with emotional volatility

57
Q

brain anatomy in people with ADHD

A

smaller brain volume – frontal & parietal cortex

smaller basal ganglia

right dorso-lateral prefrontal lobe reduced

smaller cerebellar vermis

58
Q

assessments for ADHD

A

Direct Observations in ≥ 1 setting

Psychoeducational Assessment

Structured Questionnaires

Identifying co-morbid (mental) health problem

Developmental history

Develop a formulation

59
Q

additional test when assessing for ADHD

A

hearing and vision screening checks (low threshold)
If appropriate to previous health problems, e.g. cardiac or epilepsy
screening for neurological signs & physical anomalies

Baseline height & weight (record on growth chart)
Baseline blood pressure & heart sounds