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Year 2 > People and illness Week 1 > Flashcards

People and illness Week 1 Flashcards

1
Q

What is growth?

A

A programmed sequence of development that is reversed towards the end of life

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2
Q

Describe how the brain changes as it grows in utero:

A
  • initially to gyral/sulcal pattern
  • 26 weeks -> very immature (danger if born premature)
  • some neuroblasts remain undifferentiated for plasticity
  • term brain formed by 40 weeks
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3
Q

What 3 overlapping processes are involved in developments of the cerebral cortex?

A

1) Neuroblast proliferation where the cells divide
2) Migration of immature neurons from ventricular zone to cortical plate
3) Organisation into 6 layered cortex and connections form throughout the brain

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4
Q

What is holoprosencephaly?

A

Prosencephalon fails to develop into two halfs

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5
Q

What is lissencephaly?

A

Smooth brain with lack of gyri and sulci as neural crest cells fail to migrate

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6
Q

What are congenital causes of neurodisability?

A
  • genes
  • chromosomes
  • intrauterine infections
  • prematurity
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7
Q

What are environmental causes of neurodisability?

A
  • toxins (cocaine)
  • FAS (foetal alcohol syndrome)
  • infection (rubella)
  • anti-epileptic drugs
  • general anaesthetics
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8
Q

What is focal cortical dysplasia?

A
  • where there is poorly differentiated grey matter, areas of FCD is the brain are common in children/adults with epilepsy
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9
Q

What is periventricular leukomalacia?

A
  • type of white matter necrosis that can occur as a result of ischemia during premature birth or from hypotension during a caesarean section
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10
Q

Describe non-accidental brain injuries:

A
  • classed as “shaken baby syndrome”
  • triad of symptoms that some medical professionals use to infer child abuse:
  • > subdural haematoma
  • > retinal haemorrhage
  • > encephalopathy
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11
Q

What is neuroplasticity?

A
  • the brains ability to grow and change and reorganise new connections throughout life
  • after a brain injury you may need more brain volume to carry out a simple function -> the brain can reorganise and some neural cells can change their function
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12
Q

What is the Kennard principle?

A

There is a linear relationship between the age you are when you have a brain injury and the outcome expectancy (i.e. the older you are the worse you recover)

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13
Q

What are some of the relationships between eduction attainment and upbringing?

A
  • children with quiet homes and how have a predictable routine tend to do better at school
  • children with confusion/unpredictable home life tend to withdraw from challenge
  • family chaos = poor early reading level and poor sleep cycles
  • maternal IQ is most predictive of a child’s IQ
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14
Q

Why is attachment important for child development?

A
  • rely and thrive on family

- needed for mother-child relationships

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15
Q

What effects can neglect/deprivation have on child development?

A
  • children raised in institutions are at increased risk for many social and behavioural problems
  • as the age of entry into foster care increases, the IQ of the child is reduced
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16
Q

What NORMAL social/cognitive/behavioural changes occur during adolescence?

A
  • starts around 9-12 years (earlier for girls and older for boys)
  • brain changes continue into 20’s
  • metabolic changes
  • rapid period of physical growth
  • new sex drives
  • identity
  • relationships develop
  • intimacy
  • emotional regulation
  • social skills
  • risk taking
  • peacock displays
  • remained attachments to parents and family as well as growing friend groups
  • become more independent
  • gain strong peer identification
  • committed
  • develop morals
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17
Q

What brain changes occur in adolescence?

A
  • decreased grey matter volume after adolescence
  • major prefrontal cortex changes (initially there is increased neuronal growth in the prefrontal cortex but then synaptic pruning occurs for fine tuning and strengthening of important connections)
  • limbic system changes (is hypersensitive during adolescence)
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18
Q

Define normal adolescence:

A
  • transition from child to adult
  • WHO = 10-19 years
  • ends when an adult has an accepted behaviour and identity
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19
Q

What changes occur in behaviour during adolescence:

A
  • more exploratory behaviour: smoking, violence, risk taking
  • relationship interests and sexual identity
  • maturation
  • later on reduction in risk-taking tendancies
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20
Q

What factors increase risk taking tendency?

A
  • low socioeconomic status
  • peer pressure
  • lack of parental monitoring
  • lack of future ambition
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21
Q

What factors decrease risk taking tendency?

A
  • close trusting parental relationships
  • good self-esteem
  • good future ambition
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22
Q

What is the prefrontal area of the brain involved in?

A

High level cognitive functioning:

  • decision making
  • planning
  • inhibiting inappropriate behaviour
  • self-awareness
  • social interaction
  • understanding other people
  • stops us taking excessive risks, but is still developing in adolescence
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23
Q

What is the function of the limbic system?

A
  • involved in emotion and reward processing

- in adolescence it is hypersensitive to the reward feeling and ‘rush’ of risk taking

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24
Q

What makes up the limbic system?

A
  • cingulate gyrus (medial part of cerebral cortex)
  • temporal lobe
  • amygdala
  • nucleus accumbens
  • hippocampus
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25
Q

What hormonal changes occur in adolescence?

A
  • noradrenaline, dopamine and serotonin changes

- sex hormone changes

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26
Q

What is the function of dopamine?

A

pleasure, reward, motivation, drive

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27
Q

What is the function of noradrenaline?

A

alertness, concentration, energy

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28
Q

What is the function of serotonin?

A

emotion, memory, obsession and compulsion

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29
Q

Define ADHD and its aetiology:

A
  • attention deficit hyperactivity disorder
  • group of behavioural symptoms that include inattentiveness, hyperactivity and impulsiveness
  • various genetic and environmental factors are thought to cause the disorder
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30
Q

What genetic factors can predispose to ADHD?

A
  • no single gene identified by various susceptibility gene mutations
  • > dopamine receptor D4 (causes impulsivity and overactivity)
  • > dopamine receptor transporter genes
  • > serotonin transporter genes
  • > serotonin receptor gene
  • 3-4 males to every 1 female
  • genes can increase/decrease the impact an environment has
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31
Q

What environmental factors can predispose to ADHD?

A
  • maternal smoking
  • alcohol consumption
  • heroin use in pregnancy
  • epilepsy
  • foetal hypoxia
  • brain injury
  • dietary factors (additives, E-numbers)
  • disruptive family life and being in care
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32
Q

What are signs/symptoms of ADHD?

A
  • inattention and lack of persistence in activities that require concentration
  • impulsivity (running across road without checking)
  • excessive activity
  • restless and fidgety
  • poor peer relationships
  • social disinhibition
  • talking excessively and using inner voice
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33
Q

What co-morbidities are associated with ADHD?

A
  • sleep disorders
  • OCD
  • learning disabilities
  • co-ordination disorders
  • anxiety
  • social and communication difficulties
  • below average IQ
34
Q

What brain changes are seen on a fMRI in ADHD?

A
  • smaller volume frontal and parietal cortexes
  • smaller basal ganglia
  • deficits in the fronto-striatal network
35
Q

How do you diagnose ADHD using ICD10?

A

1 - symptoms apparent before the age of 7 in a child
2 - behaviours are excessive for the child’s age
3 - evidence of behaviours in 1+ environment
4 - symptoms worsen in the afternoon

3 principle features:

  • inattentiveness
  • impulsivity
  • excessive activity
36
Q

How do you diagnose ADHD?

A
  • history
  • questionnaires (SNAP-4 = 18Q for parents and teachers and rate answers 0-3 / Conner’s parent rating scale)
  • PMH -> birth, trauma
  • observe in school and at home
  • develop a formulation: look for predisposing and perpetuating factors
37
Q

How can ADHD be treated non-pharmacologically?

A

1) psychostimulants
2) non-stimulants
3) supplementary therapy

38
Q

How can ADHD be treated non-pharmacologically?

A
  • manage the environment (remove stimuli, avoid long quiet situations)
  • behaviour training programmes
  • reward programmes
  • praise children for short periods they are calm and well behaved
  • praise parents too
  • routine and reinforcements with rewards
  • specialised school teaching
  • regular reassessments
39
Q

Describe common psychostimulants, how they work and some common side effects:

A

DEXAMFETAMINE
- increases dopamine release from presynaptic terminal
- prevents dopamine re-uptake by blocking the transporter protein
- very potent, careful prescribing (abuse)
ELVANSE (lisdexamfetamine) = pro drug converted to dexamfetamine that has more sustained release effect

METHYLPHENIDATE

  • sustained release tablet taken in morning with ‘immediate’ release top ups
  • only has 1 action acting on dopamine transporter preventing re-uptake
  • have side effects of growth retardation, anorexia, BP/HR irregularities, headaches
  • may cause anxiety, suicidal tendencies
  • can develop tolerance with long term use
40
Q

Describe common non-stimulant drugs, how they work and some common side effects:

A

ATOMOXETINE

  • noradrenaline reuptake inhibitor
  • enhances NA transmission in the PFC
  • binds to NA transporter in the synapse to stop NA being reuptaken into the presynaptic terminal so it remains in the synapse and has potentiated action
  • takes 6 weeks to work so beneficial if dose missed
  • GOOD for depression and anxiety
  • side effects of nausea, vomiting, insomnia, hepatic impairment
41
Q

Describe common supplementary drugs, how they work and some common side effects:

A
  • NA antagonists = CLONIDINE/GUANFACINE
  • guanfacine is substrate for CYP enzyme so avoid enzyme inducers
  • can cause sedation/dizziness
  • anti-depressants (MAOI, SSRI) - increase the amount of monoamines in the synapses
  • dopaminergic drugs (MODAFINOL)
  • weak psychostimulants that decreases GABA and increase glutamate
  • side effects of dry mouth, GI upset and tachycardia
42
Q

What is CAMHS and its role?

A
  • child and adolescent mental health services
  • umbrella term for all the services involved in working with children and adolescents with emotional and behavioural difficulties
  • many MDT’s involved (psychiatrists, social workers, nurses, support workers, OT’s, psychotherapists, psychologists)
  • treat many mental health disorders like schizophrenia, anxiety, anorexia etc.
  • works with and supports entire family
43
Q

What are the risks for an ADHD child later in life:

A
  • 20% cases progress into adulthood
  • difficulty holding down job
  • delayed writing and reading
  • poor academic attainment
  • relationship issues
  • 4x increased risk of dying in RTA
  • 3x increased risk of illegitimate child
  • 10% prisoners have ADHD
44
Q

How is dopamine synthesised?

A

tyrosine -(tyrosine hydroxylase)-> dopa -(dopa decarboxylase)-> dopamine

45
Q

How is NA synthesised from dopamine?

A

dopamine -(dopamine Beta hydroxylase)-> NA

46
Q

How is NA converted to A?

A

NA -(PNMT)-> A

PNMT = phenylethanolamine-N-methyltransferase

47
Q

Describe the two main arousal changes that can occur in the brain in ADHD:

A
  • hypoarousal

- hyperarousal

48
Q

Describe hypoarousal in ADHD:

A
  • brain under-active (low dopamine and NA firing)
  • does not react enough to stimuli
  • to improve this type of ADHD you must increase the signal to noise detection ratio
  • even though this seems counter-intuitive as you are giving someone a stimulant who already is stimulated, you are stimulating certain under-active brain areas
49
Q

Describe hyperarousal in ADHD:

A
  • too much arousal and XS dopamine and noradrenaline firing
  • the signal to noise detection ratio is deteriorated (so a small signal results in a large response)
  • to treat this you have to desensitise post-synaptic NA/dopamine receptors to down-regulate neuronal activity to return NA/dopamine neurons to normal phasic firing
50
Q

What are the three legal classes of drugs?

A

1) GSL: general sales list
2) P: pharmacy
3) POM: prescription only medication

51
Q

What is pharmacokinetics?

A

What your body does to a drug (what happens to the drug from ingestion to secretion)

52
Q

What is pharmacodynamics?

A

What the drug does to your body (how a drug actually exerts its effect and any side effects it may have)

53
Q

What is bioavailability and why is it important?

A
  • F = the fraction of the administered drug that reaches the systemic circulation
  • it can be affected by other factors like:
  • > drug factors
  • > absorption and 1st pass metabolism
  • > grapefruit juice (increase F)
  • > phenytoin (reduce F)
54
Q

What is volume of distribution?

A
  • volume into which a drug must be uniformly distributed to produce the desired blood concentration
55
Q

What is the relationship between VOD and half life?

A
  • drugs with high VOD have a much longer half life and are harder to excrete therefore takes longer time for toxic side effects to pass
56
Q

What is clearance?

A

The volume of plasma cleared of drug per unit time

57
Q

How can poor renal function affect clearance?

A
  • can impair clearance, so less dosing of drug required (less top ups needed as drug remains in body for longer time)
58
Q

What is the relationship between clearance and half life?

A

When clearance is halves, the half life is doubled

59
Q

What is half life and how is it calculated?

A
  • half life = time taken for serum plasma concentration to decrease by half
  • loading doses often used for drugs with a long half life
  • t(.5) = -0.693 x V/Cl
60
Q

How much active drug will be left in your body after 4-5 half lives?

A

3-6% of the active drug

61
Q

Describe linear pharmacokinetics in terms of concentration and dose:

A

As you double the dose you double the concentration = they are proportional

62
Q

Describe non-linear pharmacokinetics in terms of concentration and dose:

A

When you give a dose of a drug and then the resulting drug is not proportional to the dose
- as the dose gradually increases, the concentration suddenly peaks

63
Q

Name a non-linear drug:

A

There are very few but one is PHENYTOIN

64
Q

What can changing drug route of administration do?

A

Can alter bioavailability as oral drugs have much lower F than IV drugs

65
Q

How do you calculate loading dose?

A

Target concentration (mg/L) x V(L/kg)

the L’s cancel out

66
Q

Describe 6 different types of receptor proteins:

A

1 - regulatory protein that changes activity of cellular enzymes
2 - enzyme linked receptor that can be inhibited or activated by drugs
3 - transport proteins (ATPases)
4 - structural proteins that form cell parts
5 - ion channel linked
6 - nuclear (gene) linked

67
Q

What is affinity?

A

The attractiveness of a drug and receptor - the propensity of a drug to bind to its receptor

68
Q

What is efficacy?

A

= intrinsic activity

- the ability of a bound drug to change the receptor and cause an effect

69
Q

What is potency?

A

The strength of a drug

- a drug which is more potent is not necessarily clinically superior

70
Q 
Describe the following in terms of affinity and efficacy:
1 - agonist
2 - antagonist
3 - full agonist
4 - partial agonist
A

1 - affinity and efficacy
2 - affinity but not efficacy
3 - has affinity and maximal efficacy
4 - has affinity but less than maximal efficacy

71
Q

How does a competitive agonist work?

A

Competes with agonist for receptor and can be overcome as agonist concentration increases

72
Q

How does a non-competitive agonist work?

A

Changes shape of receptor so that normal agonist cannot bind, cannot be overcome

73
Q

What is therapeutic index and how can you calculate it?

A

TI = TD or LD / ED

74
Q

What is LD?

A

lethal dose = the dose at which a drug is lethal for 50% of the population

75
Q

What is TD?

A

toxic dose = the amount of substance taken that is expected to produce a toxic dose

76
Q

What is ED?

A

effective dose = the dose that produces the desired effect

77
Q

Is high TI good or bad?

A

The higher the TI the better the drug, but their use has to be monitored carefully

78
Q

What two factors increase dosing interval?

A

Hepatic disease and renal disease

79
Q

What condition reduces dosing interval?

A

CF - it increases drug metabolism and clearance and so reduces the dosing interval, overall more drug is needed

80
Q

What drugs should be avoided in renal disease?

A

NSAID’s and metformin

81
Q

What drugs should be reduced in dose in renal disease?

A

Digoxin, antibiotics phenytoin and LMWH

Year 2 (22 decks)

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