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test > Case 12 > Flashcards

Case 12 Flashcards

1
Q

In the resting membrane, which area is more negative; the inside or outside of the neuron ?

A

Inside is more negative

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2
Q

In the resting membrane, what is the relative permeabilities to Na, K and potassium?

A

Na, poorly permeable
Proteins, yes
K, moderately in regulating balance

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3
Q

What values in mV are recorded if the membrane is said to be; polarised, at threshold, required for opening of K gates?

A

polarised = -70
Threshood = -55
K channels = 30

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4
Q

What is the difference between ion channels and G proteins ?

A

Ion channels = fast transmission

G proteins = slow

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5
Q

What do excitatory and inhibitory NTs induce in terms of polarisation ?

A 
Excitatory = Depolarisation 
Inhibitory = Hyperpolarisation
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6
Q

What is a major function of the choroid plexus ?

A

Produce CSF

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7
Q

What structure aids the formation of the basement membrane around the tight junctions between capillaries endothelial cells ?

A

Pericytes , secrete proteins

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8
Q

Apart from tight junctions, what other structures allow plasma to leave the cell but prevents larger structures from moving ?

A

Fenestrations between cells of the BVs

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9
Q

What is the HPA axis hypothesis ?

A

Hypothalamic pituitary adrenal axis. Elevated cortisol levels/non suppression in DST leads to degenerative changes/neuroplasticity abnormalities.

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10
Q

What is the glutamate hypothesis ?

A

Decreased levels of glutamate causes depression. Active at NMDA receptors.

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11
Q

What is neuroplasticity ?

A

Altered gene transcription

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12
Q

How can ketamine be used as treatment and what are its negative features ?

A

NMDA receptor antagonist. increases mood but only has short lived effects.

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13
Q

What is the monoamine hypothesis ?

A

All the monoamines show decreased levels in depression.

NA/DA show ^ in mania.

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14
Q

Where is serotonin produced ?

A

Raphe nuclei in the brain

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15
Q

How many receptors does Serotonin have?

A

13
12 are GPCR
5HT3 is inotropic

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16
Q

What causes the degrading of serotonin?

A

MAO (pref MAO-A) or reuptake.

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17
Q

What main characteristics does 5HT influence ? (4)

A

mood/emotion
sleep/wakefullness
feeding/sexual behaviour
Cognition

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18
Q

Which serotonin platelet binding sites show an increase in depression ?

A

5HT2 platelet and brain binding sites

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19
Q

What NT is produced in the Locus caerulus, pons and adrenal glands ?

A

Noradrenaline

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20
Q

What times during the day would NA be at it’s highest and lowest ?

A

Highest during stress/danger

Lowest during sleep

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21
Q

What colour would the Locus caerulus be under a microscope and why ?

A

Blue due to the melanin pigmentation

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22
Q

What behaviour is dopamine said to influence ?

A

Reward motivation behaviour

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23
Q

Where is dopamine produced ?

A

Adrenal medulla

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24
Q

What changes in seen for depression in relation to dopamine ?

A

Increase in D2 receptors, euphoriant effects of methamphatiamine (DA release)

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25
Q

What are SSRIs ?

A

Selective serotonin reuptake inhibitors.

First line of defence for depression or anxiety.

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26
Q

List some SSRIs ….

A

Sertraline, fluoxetine, Citalopram, paroxetine (prozac)

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27
Q

SSRIs…

Rate of absorption, where are they metabolised, by what ?

A

Rapid absorption, in the liver using CYP450.

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28
Q

How does the half life of an SSRI change its issue ? Which drugs have the shortest and longest half lives respectively ?

A

Shorter half life causes increases discontinuation.
Shortest = Paroxetine (prozac)
Longest = Fluoxetine

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29
Q

What type of drug are Venlafaxine and Duloxetine and when are they used ?

A

SNRIs - Serotonin noradrenaline reuptake inhibitors.

used in depressed px not responding to SSRIs

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30
Q

Where are SNRIs metabolised, what are they excreted by ?

A

CYP2D6 , excreted by the kidneys

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31
Q

A depressed px is on medication, starts experiencing does dependant ^ in BP, seizures and constant sweating. What type of medication are they on ?

A

SNRIs

Venlafaxine and Duloxetine

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32
Q

Apart from SNRIs, what other drug does CYP2D6 metabolise ?

A

TCAs, tricyclic antidepressants.

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33
Q

Why are TCAs difficult to issue and what severe SEs may be experienced ?

A

Thin therapeutic index, varied differential dose response.

Cardiac toxicity is the major con.

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34
Q

A px has just been switched from MAOIs to SSRIs. What changes are you likely to see in the first two weeks ?

A

None relating to SSRIs

there is a 2 week switching period of MAOI receptors so the new drug would take time to have an effect.

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35
Q

What is discontinuation syndrome ? What symptoms will be seen (5)

A

3-5 days after abrupt stop to a drug treatment.

Sleep disturbance, sense problems, GI upset, mood swings (mania) , psychosis (rare)

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36
Q

Serotonin syndrome is an ^ activity of 5HT in CNS. what are the two main causes ?

A

2 5HT enhancing drugs interacting with each other

Idiosyncratic to specific drug.

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37
Q

What does serotonin syndrome result in?

A

Autonomic instability, increased HR RR BP temp. altered conscious level, ^ tone.

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38
Q

At what age do antidepressants not result in an ^ in suicidal thoughts. Which drug doesn’t cause suicidal tendancies to ^ ?

A

Up to age 25

Fluoxetine

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39
Q

What effect do anxiety disorders have on these particular areas of the CNS ?
PAG , Medial hypothalamus, amygdala

A

PAG, brainstem hard wired fight or flight. Can induce pain attacks
Medial hypothalamus, autonomic/endocrine components of anxiety. HR changes, sweating
Amygdala, classical conditions chemoreceptors for CO2.

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40
Q

What system is responsible for feelings of avoidance/anticipatory anxiety and memory?

A

Hippocampal system

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41
Q

What do Yohimbine and Clonidime cause respectively ?

A

Yohimbine , ^ NA release - pain

Clonidime, decrease NA and sedation.

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42
Q

How is GABA formed ?

A

Decarboxylation of glutamate

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43
Q

What are the two types of receptor for GABA? Which one is coupled with Cl channels ?

A

GABA-A (ligand gated) and -B (G protein linked)

-A is coupled to Cl channels

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44
Q

Barbiturates can bind to GABA, causing what effect ?

A

Sleep inducing, ^ likelihood of channel opening creating inhibitory effect.

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45
Q

What is the difference between anxiolytic and anxiogenic effects ?

A

Anxiolytic, inhibits anxiety (NMDA, AMPA receptor antagonists are anxiolytic)
Anxiogenic, causes anxiety

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46
Q

Name two benzodiazepines

A

Diazepam or lorazepam

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47
Q

Lorazepam can produce active metabolites. What effect does this have ?

A

Longer half life, prolonged effect of drug action. May cause confusion in older px.

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48
Q

What is the effect of a Ca influx into presynaptic nerve terminal ?

A

Vesicles filled with NTs migrate to pre and release contents into cleft through exocytosis.

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49
Q

Which dopamine receptors are linked to depression ?

A

D1 and D2, D2 ^ in depression

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50
Q

How does transmission terminate in synapses?

A

active reuptake by pre/post terminals

enzymatic breakdown in synaptic cleft

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51
Q

For monoamines, what is the enzyme that breaks them down in the synaptic cleft ?

A

Monoamine oxidase

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52
Q

Why are DA, NA and 5HT sometimes referred to as ‘modulatory NTs’ ?

A

They have the potential to influence GABA and glutamate

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53
Q

Describe the process of DA synthesis ?

A

Tryosine across bbb. Hydroxylated (tyrosine hydroxylase) into L-DOPA
L-DOPA -> DA using L- amino acid decarboxylase (AADC)

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54
Q

What is required for the synthesis of DA other than Tyrosine ?

A

Fe, O2 and hydrogen donor for rate limiting step

Then Vit B6.

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55
Q

How is DA -> NA ?

A

Dopamine-B-hydroxylase inside synaptic vesicles using Vit C and Cu.

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56
Q

What is given in Parkinson’s treatment and why ?

A

L-DOPA is given because it avoids the rate limiting step of the reaction

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57
Q

What is serotonin converted to in the pineal gland ? What is this substance involved in?

A

Melatonin

Circadian rhythms and sleep

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58
Q

What is St John’s Wort and why does it have dangerous potentials ?

A

Herbel remedy intended for mild depression

Induces drug metabolising enzymes

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59
Q

What structures secrete proteins that contribute to the basement membrane ?

A

Pericytes, believed to be involved in production and maintenance of tight junctions between cerebral epithelial cells

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60
Q

Which area of the brain lacks the bbb?

A

Postrema

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61
Q

What effect does Fluoxetine have on 5HT regulation ?

A

Short term ^ in synaptic serotonin, long term down reg of postsynaptic 5HT receptors

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62
Q

What drug acts on GABA-A receptors in anxiety and sleep disorders ?

A

Lorazepam

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63
Q

What is Moclobemide ?

A

Selective (reversible) monoamine oxidase inhibitor. Used for depressive and anxiety disorders and psychosis

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64
Q

Name a TCA antidepressant that limits 5HT and NA reuptake but also blocks voltage gated cation channels in the CNS ?

A

Amitriptyline

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65
Q

What is personality ?

A

Combination of characteristics or qualities that form an individual’s distinctive character, patterns of thinking feeling and behaving.

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66
Q

What is the biological trait theory ?

A

Traits are heritable and can be described biologically. Personality is made of a number of distinct traits.

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67
Q

What is the behavioural theory?

A

Personality is result of interactions between the individuals and environment. Px responds to external stimulus

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68
Q

What theory is this; cognitive expectations about the world shape personality. Cognitive processes work in environmental influences

A

Social learning

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69
Q

What is the psychodynamic theory ?

A

Unconscious mind and childhood experience in development eg. motivations, sex, aggression, conflicts

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70
Q

What is the humanistic theory ?

A

Importance of freewill and individual experience on the development of personality

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71
Q

What are the 5 factors of the 5 factor model ?

A 
Openness 
Conscientiousness 
Extraversion 
Agreeableness 
Neuroticism
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72
Q

What traits would somebody have if they scored highly on the conscientiousness scale ? Where is the brain activity related to ?

A

Organised, thoughtful, meticulous, disciplined, dependable.

Dorsolateral PFC

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73
Q

What volume change is seen in the brain with a high score in agreeableness ?

A

Increased volume in the posterior cingulate cortex

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74
Q

For neuroticism; what traits would be common , what brain activity has changed, what disorders is it common in ?

A

Anxiety, emotional instability, tension, moodiness
5HT activity in thalamus and insular cortex
Anxiety/depressive disorders

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75
Q

What is the personality inventory measure and why is it limited ?

A

Most common personality measure, px does a questionnaire.

Response bias issues, px gives socially desirable answers

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76
Q

What is the dif between temperament and personality ?

A

Temperament is a set of narrowing defined characteristics that appear early in infancy whereas personality takes time to develop

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77
Q

What 4 temperaments are commonly assessed in an TCI ?

A 
Temperament and character inventory 
Novelty seeking 
Harm avoidance 
Reward dependance 
Persistence
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78
Q

What are the characters assessed in TCI ?

A

Self directness, cooperativeness, self transcendence

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79
Q

Why might having a low conscientiousness score be bad for treatment ?

A

More likely to have poor adherence

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80
Q

What trait is emotional instability most linked to ?

A

Neuroticism. Vulnerable to stress, anger, depression.

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81
Q

What would high score on neuroticism and low on extraversion indicate ?

A

Harm avoidance tendencies.

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82
Q

What is ‘felt’ stigma ?

A

shame/fear that interferes with person seeking help. Px may avoid confronting their condition so that they’re not -ve viewed

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83
Q

What are the 5 dimensions of adherence ?

A 
Social/economic 
Health care system 
Condition related 
Therapy related
Patient related
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84
Q

What is the difference between compliance and adherence ?

A

Compliance, passive role of the px

Adherence, active/voluntary collaborative involvement of the px.

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85
Q

What is the word used to describe a shared agreement between HCP and a px of therapeutic goals.

A

Concordance

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86
Q

What is enacted stigma ?

A

First hand experience of stigma eg. health condition.

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87
Q

What are the 9 protected characteristics ?

A 
Sexual orientation 
Religious beliefs 
Sex equality 
Pregnancy/maternity 
Gender reassignment 
Age 
Disability 
Marriage/civil partnership 
Race
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88
Q

When is a mental impairment considered long term? (3)

A

Lasted over 12 months
Will last over 12 months
Likely to last for rest of px life

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89
Q

What is indirect discrimination ?

A

Practice that appears neutral but puts a person at disadvantage

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90
Q

What is the difference between associative and perceptive discrimination ?

A

Association, connection with a disabled person

Perception, belief they’re disabled even when they’re not.

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91
Q

What is the major +ve of diagnostic labelling ?

A

Px receives care from a specialist in that field. Helps manage condition now and I the future.

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92
Q

What are the potential -ve of diagnostic labelling.

A

Removes uniqueness of illness may affect self worth.
In mental health may be part of ‘self fulfilling prophecy’
Others perceive the px differently

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93
Q

What is labelling theory ?

A

Assertion that deviance and conformity result not from what people do but from how others respond to those actions

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94
Q

What is inverse care law ?

A

Good medical/social care tends to vary inversely with the need of the population served

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95
Q

How does risk taking behaviour vary throughout puberty ?

A

^ throughout puberty compared with infancy then decrease post pubertal

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96
Q

When does adrenarche take place in girls and boys ?

A 
Girls = 6-9 years onset 
Boys = roughly 7-10
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97
Q

What is adrenarche ?

A

Deviation of HPA axis for adrenal production (zona reticularis)

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98
Q

Name the two adrenal androgens involved in adrenarche ?

A

DHEA and DHEA-S.

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99
Q

A girl is 11 yo , what development stage of puberty is she likely to be going through ?

A

Gonadarche.

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100
Q

What is the age range in boys for gonadarche ?

A

9-15 mean 12.

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101
Q

How is gonadarche initiated and what key hormone is involved ?

A

Reactivation of the HPA axis

Pulsatile release of GnRH from hypothalamus during sleep

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102
Q

What is the effect of GnRH during gonadarche ?

A

Stimulates APG production of FSH/LH -> gonadal maturational changes -> ^ in oestrogen and testosterone

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103
Q

What are the ‘4Fs’ of the hypothalamus ?

A

Fight or flight
Feeding
Fucking

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104
Q

What effect does a hyperactive environment have on a person development ?

A

Prolonged HPA activation which leads to less GH. Causes a smaller growth spurt and can also lead to mental consequences

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105
Q

What effect does GH have on the liver ?

A

Produces IGF-1

Acts on pituitary and hypothalamus in a +ve feedback loop.

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106
Q

What are 4 major effects on the brain during adolescence ?

A

Amygdala and hippocampus volume increase
Synapse elimination
Axonal growth and myelination
Prefrontal activity increases.

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107
Q

What are the 3 main affects of sex steroid hormones ?

A

^ reproductive behaviours (via hypothalamus)
Reorganisation of sensory and association regions (visual cortex, amygdala, hippocampus) , motivation and reward based behaviour (NA, DA pathways to PFC)

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108
Q

What 3 substances are released during anxiety triggered by an early stress repose

A

Cortisol, CRH, ACTH

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109
Q

How can a poor antigenic environment pre and post natally hinder growth ?

A

Pre, placental transfer of antibodies

Post, antibodies in breast milk and ^ exposure to allergens

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110
Q

How do white and grey matter growth vary in adolescence ?

A

White shows steady linear growth

Grey is region specific non linear growth.

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111
Q

Why does grey matter volume decrease post pubertal ?

A

Synaptic overproduction results in pruning

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112
Q

What is synaptic pruning ?

A

when rarely used connections are eliminated making the brain more efficient. Allows greater change in response to environmental demand

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113
Q

What is neuroplasticity ?

A

Structural changes from exposure to environmental stimuli, both +ve and -ve.

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114
Q

What are the 3 main areas of cognitive development during adolescence ?

A

Cognition; attention, goal setting, info processing
Behaviour, less inappropriate
Emotionally, more impulse control

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115
Q

What two structures form the ventral striatum ?

A

Nucleus accumbens and olfactory tubercle

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116
Q

What part of the brain is responsible for reward anticipation ?

A

Nucleus accumbens

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117
Q

What are the two systems responsible for adolescent risk taking ?

A

Prefrontal cognitive control

Subcortical motivational drive network

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118
Q

How does the development of the ‘dual system’ influence risk taking behaviours ?

A

Prefrontal cognitive control develops linearly and slowly whereas subcortical motivation is rapid. Therefore in the period in between risk taking behaviour is not inhibited.

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119
Q

Why is adolescence a key developmental period for mental health issues ?

A

Suboptimal trajections have ^ chance of developing before executive function matures

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120
Q

What are 3 key factors for depression onset ?

A

Familial/genetic risk
Environmental (acute stress life events)
Gene environment (high risk groups at ^ sensitivity)

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121
Q

Which circuit shows ^ activity during depression ?

A

Circuit connecting amygdala, hippocampus and PFC

Linked to HPA (^ Cortisol)

122
Q

What changes are seen during depression in the circuit connecting the striatum to PFC and ventral dopamine reward system ?

A

Decreased activity of the circuit

123
Q

From a psychological basis what is Schizophrenia ?

A

Decrease in attention and general impairment of executive functions possibly due to abnormal brain development

124
Q

What 3 responses indicate why sleep is important ?

A

Emotional ; feeling, stress, overt behaviour
Cognitive; attention, memory, executive
Somatic; drowsiness, pain/cold, CV disease, cancer risk, metabolic problems etc.

125
Q

What are the common negative effects of sleep deprivation ? (7)

A

Circadian rhythm disruptions; body temp, RR, hormonal production
Brain effect; REM sleep down, fatigue
GI disorders; dyspepsia, heartburn
Cancer risk; breast and colorectal ^
CV disorders; angina pectoris, hypertension, MI
Mental health; stress, anxiety, depression etc.

126
Q

What happens when the brain ‘wakes’ ?

A

Neurons in the pons produce ACh which go and activate the thalamus (channels signals to cerebral cortex - consciousness)

127
Q

What NTs are produced in the pons and hypothalamus to prime the cerebral cortex during the ‘woke’ state ?

A

NA, 5HT, DA and histamine.

128
Q

What are orexins and what is their effect on the arousal system ?

A

Peptides produced in lateral hypothalamus to reinforce and increase the arousal system

129
Q

Why does the brain ‘tire’ ?

A

^ adenosine triggers neutron activity in ventrolateral preoptic nucleus

130
Q

What is circadian control influenced by ?

A

Retinal signals throughout the day and melatonin from pineal gland at night

131
Q

In the brain ‘sleeps’ stage, VLPO neurons are activated. What happens next ?

A

They release GABA and galanin which binds to hypothalamus and pons to inhibit arousal system and sleep.

132
Q

What is the MOA of sleep tablets?

A

Tablets increase binding of GABA to decrease arousal

133
Q

How do the stages of sleep vary from a newborn to an adult ?

A

Newborn; ^ REM to allow for ^ development

Adult; N3 down as grey matter down from medial prefrontal cortex.

134
Q

Why do adenosine levels effect sleep ?

A

Adenosine binds to receptors in brain -> tiredness. ^ due to ATP breakdown throughout the day.

135
Q

How does coffee effect wakefulness ?

A

Blocks the binding of adenosine so stops the tiredness feelings from being induced

136
Q

What are the common triggers of the SCN? (4)

A

Suprachiasmatic nucleus

Melatonin, stress hormones, core body temp, alertness

137
Q

What is the term given to environmental agents or events that act as stimuli to reset the biological clock of an organism?

A

Zeitgebers

138
Q

What is the primary Zeitgeber ? list some others …

A

Light

food, stress, travel, sport, temp

139
Q

Why does jet lag effect the body ?

A

Takes time for the peripheral clocks to re-sync.

140
Q

Why shouldn’t you remove the eyes of a blind px ?

A

Removing the eyes takes away the SCN so no melanopsin is produced -> depression etc.
Retinal ganglion still work even though eyes don’t

141
Q

When is the urge to sleep the largest ?

A

When the gap between the homeostatic sleep drive and circadian arousal drive is largest.

142
Q

What type of condition is narcolepsy and what are the common sx (4)

A

Hypersomnolence disorder

Sleep attacks, Cataplexy, sleep paralysis, hypnagogic.

143
Q

Name two sleep related breathing disorders

A

Central sleep apnea; lack of resp drive causes resp movement down.
Obstructive sleep apnea; upper airway blockage during sleep

144
Q

How would you treat CSA ?

A

CPAP, continuous positive airway pressure

145
Q

What is the Diff between delayed and advanced sleep phase disorder ?

A

Delayed; rarely sleepy until 6am, awake by 12

Advanced; can’t sleep past 7pm.

146
Q

What condition is involuntary hypnic jerk seen in ?

A

Periodic limb movement disorder

Repetitive movements, common in limbs every 20-40 seconds.

147
Q

When is insomnia classed as chronic ?

A

3 nights a week for 3 months.

148
Q

What are the causes of insomnia according to the 3P model ?

A

Predisposing fx; hyperactivity, NT abnormalities
Precipitating fx; lifes stress, illness
Perpetuating fx; not sleeping in bed, staying in bed whilst awake

149
Q

What are two common methods of treatment for acute insomnia ?

A

Sleeping tablets, BZD receptor agonist

Sleep hygiene, 10 lifestyle points

150
Q

Name a BZD receptor agonist used as a hypnotic

A

Sleeping tablet - Zolpidem

151
Q

When asking screening Q’s for insomnia, if px shows a circadian phase disorder, what would be your next step ?

A

Target sleep schedule, melatonin and light therapy

152
Q

What are 3 major groups of health problems that can arise with Insomnia ?

A

Sleep apnoeas eg. restless leg
Mental health eg. depression
Kids with neudevelopmental disorders eg. ADHD.

153
Q

What are the ‘stimulus control’ components of CBT? (5)

A 
Only sleep (or sex) in bed 
15 min rule for sleep 
Sleep schedule 
No naps 
only go to bed when physically sleepy
154
Q

What is the equation for sleep efficiency?

A

Total hours slept / total hours in bed (x100)

155
Q

What is the expected value for sleep efficiency in a normal person ?

A

> 90%

156
Q

Where is dopamine synthesised ?

A

Substantia nigra, adrenal medulla

157
Q

How do dopamine levels change during psychosis ? What other NTs are thought to be linked as a cause ?

A

^ DA in the nigrostriatal (indirect) pathway.

Glutamate/GABA imbalance thought to be more of an issue

158
Q

What receptor is commonly blocked in antipsychotic medication ?

A

D2 antagonism

159
Q

Drug use ^ DA in nucleus accumbens, what does this mediate ? Which group of drugs is the only one not to show an ^ ?

A

Mediates positive reinforcement

BZD only drug not to show ^

160
Q

What sedative effects do antipsychotics induce ?

A

Anti histamine, alpha adrenergic antagonism.

161
Q

What does the mesolimbic pathway transport ?

A

Transports DA from mental segmental (midbrain) to the nucleus accumbens

162
Q

What are the major negative effects of D2 blockage in the mesolimbic pathway ?

A

Blunting affect, poverty of speech, limited +ve emotion.

163
Q

Which pathway connects the substantia nigra to the striatum?

A

Nigrostriatal pathway

164
Q

What are the components of the striatum ?

A

caudate and putamen

165
Q

D2 antagonism produces some EPSEs, given the 4 common ones

A

Extra pyramidal side effects

Dystonia, Parkinsons, Akathasia, Tardive dsykinesia

166
Q

What is the pathway of the tuberofundibular gland ?

A

Hypothalamus to the pituitary gland

167
Q

What effect does blockage of D2 receptors have on the tuberofundibular pathway ?

A

Causes the pituitary to ^ prolactin. Leads to;

Amenorrhea, gynaecomastia, glactorrhoea, sexual dysfunction, hypogonadism.

168
Q

Name 3 of the atypical antipsychotic drugs

A

Clozapine, olanzapine, risperidione

169
Q

What are the advantages of the 2nd generation antipsychotics over Haolperidal ? (3)

A

^ efficacy for +/- sx. lower tendency to cause EPSE. Less likely to ^ prolactin

170
Q

What condition shows; central obesity, HTN, DM, hyperlipidaemia, ^ serum triglycerides

A

Metabolic syndrome

171
Q

What are the suggested methods of tx of metabolic syndrome ? (4)

A

5HT2C antagonism, H1 antagonism, hyperprolactinemia, ^ serum leptin (leads to leptin desensitisation).

172
Q

What are the 3 main antipsychotics associated with weight gain, which have the highest and lowest risk ?

A

Clozapine (high), Olanzapine, Aripiprazole (low)

173
Q

Antipsychotics block repolarisation of K channels in myocardium. What effect does this have?

A

Prolongs QT interval, ^ risk of sudden cardiac death

174
Q

Dystonia is caused by reciprocal actions of DA and MACh systems in the basal ganglia. When is dystonia more likely ?

A

More likely with antipsychotics with no intrinsic antagonism of MACh receptors.

175
Q

What is the normal Tx of Parkinsons ?

A

Decrease dosage of antiepsychatrics. Change to an atypical. Add MACh antagonist

176
Q

What is a common MACh antagonist used in Dystonia treatment ?

A

Procyclidine

177
Q

What is Akathasia ?

A

Unpleasant subjective inner restlessness, unknown cause. Difficult to treat

178
Q

What is the tx for Akathasia? why must the px be monitored whilst being treated ?

A

Decrease dosage. Use BDZ/beta blockers. Can cause depression/suicidal thoughts

179
Q

What drugs might be used in neuroleptic malignant syndrome and why ?

A

Dantrolene (reduce muscle spasm)

Bromocriptine (DA receptor antagonist)

180
Q

How are endothelial cells connected in the bbb, what structures are present in the surrounding spaces ?

A

Tight junctions

Pericytes, secrete proteins which contribute to the basement membrane

181
Q

How do CNS drugs cross the bbb ?

A

Transcellular route, go through vascular endothelial cells rather than between (paracellular) due to the complex tight junctions.

182
Q

What structures are present that are able to rapidly transport drugs out of the CNS ?

A

Transmembrane pumps, even if the drugs have penetrated the BBB.

183
Q

How do certain drugs affect brain function ?

A

Utilise transporters decreasing protein uptake.

184
Q

What are the 3 main causes of weight loss ?

A

Malignancy, GI conditions, psychiatric causes

185
Q

What are the two main areas of the hypothalamus that ^ food intake ?

A

Lateral nuclei

Dorsomedial nuclei

186
Q

What effect does the Paraventricular nuclei have on food intake ?

A

Decreases food intake, lesions lead to excessive eating

187
Q

What is the proper name for the ‘satiety centre’, what is the effect when it is stimulated ?

A

Ventromedial nuclei. Stimulation leads to satiety even with highly appetising food. Destruction causes continued eating.

188
Q

How does the arcute nuclei effect food intake ?

A

Both ^ and decrease. Site of convergence of multiple hormones released by GI tract and adipose tissue.

189
Q

List some inputs that inhibit food intake…

A

Stretch receptors in stomach via the vagus nerve, chemical signals from circulating macronutrients, hormones released by adipose and GI tract, cerebral cortex (site, smell and taste of food)

190
Q

What macronutrients give off chemical signals to decrease food intake ?

A

Glucose, amino acids, fatty acids

191
Q

Name two orexigenic substances

A

Stimulate appetite
Neuropeptide Y
Agouti related protein.

192
Q

What is the action of Neuropeptide Y in ^ appetite ?

A

Released when energy stores are low to stimulate appetite. Reduces firing of POMC neurons which decreases it’s anorexigenic effects.

193
Q

What is Alpha MSH and where is it released from ?

A

Alpha melanocyte stimulating hormone. Released by POMC neutrons.

194
Q

What receptors does a-MSH act on and what does it stimulate ?

A

melancortin receptors (MCR) in neutrons of the paraventricular nuclei to decrease appetite.

195
Q

What is the action of MCR subtypes 3 and 4 when stimulated and inhibited ?

A 
Stimulated = intake ^
Inhibited = Reduce
196
Q

What stimulates CCK release from the duodenum ?

A

Fat and proteins entering the duodenum.

197
Q

What is the action of CCK once released ?

A

Stimulates digestion via the gallbladder. Sends inhibitory messages via the vagus to ^ gut motility

198
Q

Where is peptide YY released ?

A

GIT but especially ileum and colon.

199
Q

What is the effect of GLY, where is it released?

A

Reduces appetite
Directly - via ^ insulin production
Indirectly via secretion from the pancreas
Released from GIT, nucleus of tracts solitaires.

200
Q

What hormone is released from oxyntic cells of the stomach ?

A

Ghrelin

201
Q

Where is leptin released ?

A

Adipocytes, regulates appetite over the long term.

202
Q

What does leptin bind to?

A

Binds to anorexigenic receptors (POMC neutrons of arcuate nuclei and neurons of paraventricular nuclei.

203
Q

What effect does leptin have when it binds to anorexigneic receptors ?

A

Decreases hypothalamic production of appetite stimulators. stimulates corticotropin releasing hormone and sympathetic NS.

204
Q

What main domains does the MSE assess ? (7)

A 
Appearance and behaviour 
Speech 
Mood and affect 
Thoughts 
Perceptions 
Cognition 
Insight
205
Q

What is the required threshold for depression diagnosis ?

A

Persistant depressed mood for 2 weeks - 1 month

206
Q

What is anhedonia ?

A

Doesn’t find pleasure in activates px used to enjoy

207
Q

What is a persistent and long standing depressed mood that isn’t severe enough for depressive disorder ?

A

Dysthymia

208
Q

What effect does stress have on a physiological level ? (3 up, 3 down)

A

^ IL-1, IL-6, TNF-a released from cells from macrophage or monocyte lineage. Reduces IL-2, IFN-y and MHC2.

209
Q

Most organ related carcinomas produce a high conc of TNF-a. What does this do ?

A

Inhibits tyrosine phosphatase so less MHC 1 on cell surface. This means malignant cells escape immune surveillance.

210
Q

What is the cause of persistent activation of HPA ?

A

Release of stress mediators (NTs - NA, 5HT) , neuroendocrine and stress hormones (cortisol) and cytokines.

211
Q

What inflammatory cytokines compromise effects of the immune system ?

A

IL-2, IFN-y and TNF-a by Th1 cells

212
Q

Metabolic syndrome is a blanket term that encompasses which 4 conditions ?

A

Abdomen obesity, insulin resistance, dyslipidemia, elevated BP

213
Q

Why is weight gain common in Clozapine and Olanzapine ?

A

Antagonism of the histamine H1 and 5HT2C receptors.

214
Q

What are the risk factors for metabolic syndrome ?

A

Large waistline, high triglyceride levels, low HDL levels, hypertension, high blood sugars

215
Q

Which diagnostic criteria is most commonly used in practice for metabolic syndrome ?

A 
International diabetes federation (IDF) 
Waist >94 and >80
BP >130/85
HDL <40 <50
Triglycerides >150
Glucose >100
216
Q

What is the next course of action if the px doesn’t respond to screening/monitoring post a MS diagnosis ?

A

Prescribe Aripiprazole , reduces Clozapine induced side effects (weight reduction and lowers serum cholesterol)

217
Q

What 3 factors should be considered in schizophrenia px ?

A

lifestyle fx eg. exercise, diet, smoking
Aspects of psychotic disorder
Antipsychotic medication; 1/2 gen ? risk of MS etc.

218
Q

Once px diagnosed with schizophrenia what 4 areas should you monitor when monitoring MS development ?

A

BMI
BP
fasting glucose
Fasting plasma lipids

219
Q

How do location and personal isolation factors effect Schizophrenia ?

A

^ Population density ^ psychosis risk. Greater social cohesion with specific ethnic groups is protective fx.

220
Q

What are the ‘5As’ , negative symptoms in Schizophrenia?

A 
Affective flattening 
Alogia, poverty of speech 
Avolition, lack of motivaiton 
Attention 
Anhedonia , no pleasure
221
Q

Name 4 +ve sx of schizophrenia

A

Auidotry hallucinations
Persecutory delusions
Referntial element
Disorganised thoughts

222
Q

Why is cig smoking important to monitor in Schizophrenia tx ?

A

When taking SGAs eg. Clozapine/Olanzapine, any drastic reductions in smoking can produce toxic effects at previously tolerated doses. Nicotine is an enzyme inhibitor.

223
Q

Px presents with rapid onset muscle rigidity, hypertension and ^ HR. What rare condition does he have ?

A

Neuroleptic malignant syndrome.

224
Q

What bone lies directly posterior to the cerebellum, medulla and pons ?

A

Occipital bone

225
Q

What does ‘electrochemical’ mean in terms of nerve stimulation ?

A

Electro; involves changes in conductivity of cell membrane

Chemical; releases Its at a synapse

226
Q

How is ACh used by the spinal cord and brain respectively ?

A

Spinal cord, to control muscle

Brain, to regulate memory

227
Q

What do low and high levels of dopamine lead to ?

A 
High = Schizophrenia 
Low = Parkinsons
228
Q

5HT is involved in mood, appetite and sensory perception. What is its action in the spinal cord ?

A

Inhibits pain pathways -> depression, migraine, ADHD, anxiety

229
Q

What is the function of the spino/paracerebellum ?

A

Regulate body and limb movements

230
Q

What is the function of the lateral norocerebullum

A

Regulates planning, sensory movement for action.

231
Q

Where is serotonin produced ?

A

Serotogenic nuclei in the raphe nuclei

232
Q

Where are dopaminergic nuclei found?

A

Ventral tegmental and substantia nigra

233
Q

Where is NA synthesised ?

A

Locus coeruleus

234
Q

What is produced in the tuberomammiliary nucleus ?

A

Histamine

235
Q

What are the 3 primary divisions of the brain?

A

Prosencephalon (fore) Mesencephalon (mid) and rhombocephalon (Hind)

236
Q

What is the function of the superior Colliculus ?

A

Visual processing and eye movement control.

237
Q

What structure is involved in auditory processing ?

A

Inferior Colliculus

238
Q

How does Parkinsons affect the substantial nigra ?

A

Decreased DA neurons in substantial nigra

239
Q

The dicephalon contains the lateral and medial geniculate nuclei. What two things do they control ?

A 
Lat = visual pathway 
Med = auditory pathway
240
Q

What is secreted from the pineal body ?

A

Melonatonin

241
Q

What structures are damaged in Wernicke Korsakoff syndrome, due to what vitamin deficiency ?

A

Mammilary bodies

B1 (Thiamine)

242
Q

Where is the amygdala located and what is it responsible for ?

A

Deep in the temporal lobe

Emotional response

243
Q

What structures do the mammilary bodies connect ?

A

Part of hypothalamus, receives input from hippocampus via the fornix and projects them onto the thalamus

244
Q

What is the cerebellum responsible for ?

A

association (intelligence)

245
Q

What sort of memory is the hippocampus involved in, what happens in atrophy ?

A

Short to long term memory conversion.

Atrophy leads to Alzeihmers/memory dementia

246
Q

What are the folds and grooves called in the cortex ?

A 
Fold = gyrus 
Groove = sulcus
247
Q

What is the function of the inferior frontal gyrus ?

A

Language processing. Broca’s area, expressive aphasia impedes language processing.

248
Q

What is Pick’s disease and where does it occur ?

A

Accumulation of Tau proteins at frontotemporal regions. Along with associated symptoms give diagnosis

249
Q

Which area of the brain is responsible for planning and executive function ?

A

Prefrontal cortex

250
Q

What do the temporal lobe and superior temporal gyrus form ?

A

Auditory cortex, processes sound and apply comprehension

251
Q

What pathologies are associated with posterior superior temporal gyrus ?

A

(Wernicke’s area) aphasia. px knows what to say but words don’t come out (gibberish)

252
Q

What is the fusiform gyrus responsible form?

A

Facial recognition, synaesthesia, dyslexia

253
Q

What tract links Broca’s to Wernicke’s area ?

A

Arcuate fasciculus

254
Q

What are the 4 drug free interventions to target abnormal brain function ?

A

Vagal nerve stimulatin
Deep brain stimulation
Electroconvulsive therapy
Repetitive transcranial magnetic stimulation

255
Q

What is GWAS ?

A

Genomic wide association studies

Systemic search fro common alleles.

256
Q

What are CNVs ?

A

Copy number variants

Small regions of genome that have been deleted/duplicated. Hinders developing brain/cells

257
Q

What is the difference between mutation and polymorphism ?

A

Mutation - minor allele is rarer than 1%
Polymorphism - Allele is more common
The same change is involved in both

258
Q

What has Pleiotropy shown relative to Schizophrenia ?

A

Genetic correlation between Schizophrenia and selected psych disorder, also with autism and ID

259
Q

What is anosognosia ?

A

Non dominant parietal lobe and motor cortex disfunction in which px is unaware in ‘delusional denial’. Occurs in head injury or stroke

260
Q

What are the 7 areas to assess in MSE ?

A 
Appearance/behaviour 
Speech 
Mood 
Thoughts 
Perceptions 
Cognition 
Insight
261
Q

What are the 4 major abnormal positive sx of schizophrenia ?

A

Thoughts (delusions)
Perceptions (hallucinations)
Movement/behaviour
Thought process/cognition

262
Q

What are ; low mood, anhedonia and anergia the 3 core sx of ?

A

Unipolar depression

263
Q

How do you class different types of BPAD?

A

Bipolar affective disorder
1; one episode must be mania
2; can never have had mania.

264
Q

What is the most inhibitory NT in the CNS ?

A

GABA

265
Q

Antidepressant tx can reverse abnormal patterns of glucose metabolism in which parts of the brain ?

A

Amygdala

266
Q

Schizophrenia is said to link the limbic system and what ?

A

PFC

267
Q

What region of the brain is associated in processing, reward, motivation and pleasure seeking ?

A

Nucleus accumbens

268
Q

You prescribe MOAs to a px. What should they avoid eating and drinking ?

A

Red wine, strong cheese, broad beans

269
Q

What receptor does Citalopram target ?

A

5HT

270
Q

Which receptor do antipsychotic drugs target to reduce Sx of Schizophrenia ?

A

D2

271
Q

px gets weight gain after starting antipsychotics meds 3 months ago. What receptor is this side effect responsible for ?

A

Antagonism of the H1 histamine receptor. Also occurs with antagonism of specific 5HT2 receptor

272
Q

What sx are characteristics of Panic disorder ?

A

Sudden attacks of palpations, sweating, dizziness, fear of losing control in variety of situations often without cause.

273
Q

Large, rare CNVs shown to ^ risk for which psych disorder?

A

Schizophrenia

274
Q

What is the difference between Hypnopompic and Hypnogogic

A

Hypnopompic is hallucinations during or after sleep

Hypnogogic is hallucinations before or immediately at the start of sleep

275
Q

High scores in which dimension of personality is associated with decreased risk of physical and mental illness ?

A

Conscientiousness

276
Q

What is the effect of NPY on appetite?

A

Neuropeptide Y

Released when energy stores are low ^ appetite.

277
Q

What foods should be avoided whilst on MOAs and why ?

A

Red wine, strong cheese, broad beans

Contain tyromine which can cause hypertensive crisis

278
Q

What is the cause of the antidepressant side effect postural hypotension ?

A

Antiadrenergic

279
Q

What antidepressant side effects are caused by antihistamines ?

A

Weight gain, drowsiness

280
Q

What is circumstantialily in a schizophrenia px ?

A

Px goes into unneeded detail and makes irrelevant remarks however in time returns to Q asked.

281
Q

when px speaks goes from one topic to another mid sentence without returning to original stem, what is this ?

A

Derailment

282
Q

What does the ventromedial PFC control ?

A

Pain, aggression, libido, appetite moderation

283
Q

What area of the brain controls executive function, attention and working memory ?

A

Dorsolateral PFC

284
Q

How is the lateral orbital PFC different in depression ?

A

Hyperactive, enhanced sensitivity to stress, anger, anxiety.

285
Q

What is the monoamine hypothesis ?

A

Low levels of monoamines cause depression eg. dopamine

286
Q

What hypothesis is linked to cortisol ?

A

Glucocorticoid receptor. Cortisol -> stress hormone -> damage to neurons in hippocampus

287
Q

What is the neutrophic hypothesis ?

A

Stress and genetic vulnerability linked to overactive glucocorticoids mediated by glutamate lead to cellular atrophy.

288
Q

How does the neutrophic hypothesis view BDNF?

A

Rapid ^ in brain derived neurotrophic factor especially in hippocampus.

289
Q

What is the MOSPAD-C ?

A

cognitive disorders about the self, others and the world
Magnification/minimisation , overgeneralisation, selective abstraction, personalisation, arbitrary interference, dichotomous thinking, catastrophisation

290
Q

Why are changes in appetite typical in depression ?

A

^ Corticotropin releasing fx causes an aroused stress response

291
Q

What receptor is involved in satiety ?

A

5HT2c, less 5HT at receptor linked to decreased satiety and carb craving

292
Q

What effect does ketamine/pcp have on healthy volunteers ?

A

Induces Schizophrenic +/- sx through antagonism of the NMDA receptor.

293
Q

What is the general function of antipsychotics ?

A

Block dopamine, higher affinity for DA blockade = ^ clinical potency

294
Q

What causes EPSEs and what are a few examples ?

A

Caused by striatal DA antagonism

acute dystonia, akathisia (subjective/psychomotor restlessness).

295
Q

How would you use the confidence interval to calculate the mean ?

A

The CI is the value around the mean eg. +/- 1.04 therefore half the CI is the mean. So in this case the mean is 0.52

296
Q

What is the MHI-5?

A

Mental health inventory, asks 5 questions:
Have you been ; very nervous ? happy?
Have you felt ; down in the dumps that nothing could cheer you up ? calm and peaceful ? downhearted and depressed ?

297
Q

How is the MHI-5 scored and what does a lower score indicate ?

A

scored between 0-100 , lower scores indicate poorer mental health

298
Q

What is the P value of a test ? What does a smaller P value show ?

A

The probability of a difference is greater than the observed difference (chance) if null hypothesis were true. Smaller P value = stronger evidence against hypothesis (shows results not due to chance)

299
Q

If the P < 0.05 for a test, what would this tell you ?

A

Evidence to reject the hypothesis at 5% level because a difference exists. 5% means 1/20 chance the difference has occurred by chance

300
Q

What is the student’s t test , when can it not be used ?

A

Compares distinct groups in an ‘unpaired comparison’. Assumes data is normally distributed with equal SDs in 2 groups. Can’t be used if more than 2 groups.

301
Q

If the ANOVA score for a test was F(2,15) = 4.76 … what would the ‘(2,15)’ section mean?

A 
2= group degrees of freedom (so 3 groups in the study) 
15 = total observations degrees of freedom (so 18 people total divided into 3 groups of 6)
302
Q

How do you calculate the variation between groups in ANOVA ?

A

‘Mean of the group means’. So calculate mean of each group, then the mean of those eg. 3 values. Then calculate sum of squares. Finally times by no in each group and add together.

test (14 decks)

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