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PHYSIOLOGY 2 > NEURO 2 - mental health > Flashcards

NEURO 2 - mental health Flashcards

1
Q

Types of depression

A

Unipolar

Bipolar

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2
Q

Bipolar depression

A

Oscillation between depression and mania
Type I = increase mania episodes with/without depression
Type II = Hypomania – episodes of major depression
Strong hereditary tendency

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3
Q

Mania

A

Excessive exuberance, enthusiasm, self-confidence, impulsive actions, aggression

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4
Q

Unipolar depression

A

Mood swings in 1 direction
Most common depressive illness
75% cases reactive – induced by environment
25% endogenous – genetic

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5
Q

Emotional symptoms of depression

A

Apathy, pessimism, negativity
low self-esteem, feeling guilty
low motivation
Indecisiveness

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6
Q

Biological symptoms of depression

A

decreased activity
decreased libido
Sleep disturbance
decreased appetite

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7
Q

Monoamine theory

A

Decrease activity of NA/5HT systems
Reserpine deplete NA and 5HT from brain
Decrease monoamines = decrease activity of noradrenergic system = increase post synaptic receptors - block reuptake = [NA+] plasme increase in depressed patients = increase anxiety and sympathetic activity

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8
Q

Neuroendocrine theory

A

If HP axis sensitive - in depressed people
Noradrenergic & 5HT neurones input to hypothalamus = release CRH to pituitary = release ACTH - cortisol released from adrenal cortex

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9
Q

Evidence for neurorendocrine theory

A

CRH mimics depression symptoms

Increased [cortisol] in plasma and saliva and increase [CRH] in CSH

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10
Q

Neuroplasticity and neurogenesis theory

A

Neuronal loss of hippocampus and pre-frontal cortex (decision making)
Antidepressents and ECT promote neurogenesis in regions
5HT promote neurogenesis during development.

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11
Q

Increased glutamate and neurogenesis

A

Lead to neuronal loss and depressison
Lots bind to NMDA = excitoxicity
Prevent with ketamine

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12
Q

Psychological treatments

A

Cognitive behavioural therapy

Interpersonal therapy

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13
Q

Cognitive behavioural therapy

A

helping depressed individuals recognise and change their negative cognitive processes and improve their mood and their counterproductive behaviours

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14
Q

Interpersonal therapy

A

assumes depression is multi-factorial but that interpersonal difficulties play a central role in maintain depressive symptoms

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15
Q

MAOIs - monoamine inhibitors mechanism

A

Increase [NA/5HT] cytoplasm - Increase [NA/5HT] cytoplasm leakage of amine - increase [NA/5HT] in synaptic cleft
MAOA break down 5HT more than NA
MAOI = Increase 5HT >NA > DA
Increase NA = Increase euphoria = increase motor activity
Inhibition of MAO A correlate with AD activity

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16
Q

Early drug examples of MAOIs

A

Phenelzine and isocarboxazid

Irreversible and non-selective inhibitors of MAO - down regulate post synaptic and pre-synaptic receptors

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17
Q

Problems with MAOI

Food and drug interactions

A

Tyramine in cheese and wine - indirect sympathomimentic - increase NA release - excess NA destroyed by MAO - if blocked NA accumulate

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18
Q

What happens if there is an accumulation of NA

A

Headache, intercranial haemorrhage leading to elevation in BP leading to severe hypertension

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19
Q

Reversible MAOI

counter the cheese and wine effect

A

Moclobemide
Accumulation of NA displaced RIMA allowing degradation of excess NA
RIMA safer and selective RIMA better tolerated

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20
Q

Tricyclic antidepressants TCAs examples

A

AMITRIPTYLLINE
IMIPRAMINE
IOFEBRAMINE

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21
Q

TCA therapeutic effects

A

NA and 5HT reuptake inhibitor - increase [NA] and [5HT] in synaptic cleft

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22
Q

SSRI examples

A

FLUOXETINE
PAROXETINE
CITALOPRAM
ESCITALOPRAM

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23
Q

SSRI therapeutic effects

A

5HT reuptake inhibitor
Increase [5HT] down regulation of 5HT1A/D autoreceptors, disinhibit 5HT neuron, increase 5HT release
Increase 5HT release = down regulate post synaptic 5HT receptors

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24
Q

Side effects of SSRI

A

5HT2 - insomnia, sexual dysfunction
5HT3 - Nausea, GI distress, headache, diarrhoea
May be associated with increase violence - 5HT3
Could overdose - serotonin syndrome

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25
Q

Serotonin syndrome

A

Surge in serotonin

Seizures, tremors, hyperthermia, CV collapse

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26
Q

Bipolar depression treatment

A

Lithium - mood stabiliser
Li+ in neuron depolarises - and inhibit enzymes invovled in signal transduction
Narrow therapeutic window - too little = no effect. Too high = toxicity
Side effects = drowsiness, confusion, seizures, coma, hypothyroidism

27
Q

Ion channel blockers for bipolar disorders

A

Valproate and gabapentin

Valproate can lead to liver damage

28
Q

Physiological symptoms of anxiety

A

Tachycardia, shortness of breath, excessive sweating, headache and dizziness, nausea, fatigue

29
Q

Alcohol and drugs effect on anxiety

A

Increase GABAergic neurotransmission - block glutamatergic neurotransmission
Balance between GABA and glutamate crucial for optimal brain function - alcohol disrupts balance
Brain adapts - counter imbalance - decrease levels of GABA and increase glutamate - trigger anxiety

30
Q

Amygdala and anxiety

A

Role in emotion and fear response
Stimulate HPA - promote cortisol release
Hyperactivity linked to anxiety disorder

31
Q

Hippocampus and anxiety

A

Role in learning and memory
Suppress HPA
Underactivity = anxiety

32
Q

Specific phobias

A

extreme fears/anxieties provoked by exposure to a particular situation or object – often lead to avoidance behaviour – Phobia object or situation provokes immediate fear or anxiety

33
Q

Social phobias

A

significant anxiety provoked by exposure to certain types of social or performance situations – Social situations provoke immediate fear/anxiety

34
Q

Panic disorder

A

recurring panic attacks without seemingly clear cause or trigger
An abrupt surge of intense fear/discomfort – peak within minutes
Includes increased HR, sweating, trembling, shortness of breath and fear of dying

35
Q

Obsessive compulsive disorder

A

characterised by compulsive ritualistic behaviour driven by irrational anxiety – time consuming
Obsessions – recurrent intrusive thoughts, images, ideas, or impulses
Compulsions – repetitive behaviours or mental acts performed to decrease anxiety associated with obsession

36
Q

PTSD

A

Distress triggered by the recall of past traumatic experiences
Include recurrent intrusive memories, nightmares, dissociative reactions, and psychological and physiological distress at exposure to cues

37
Q

Benzodiazepines

A

Bind to distinct regulatory site on GABAA receptors – stabilise the GABAA receptor binding site for GABA – Positive allosteric modulators
Increase GABA affinity for its binding site and produce a general enhancement of its neuroinhibitory actions
Suppress symtoms of anxiety

38
Q

Tolerance to benzodiazepines

A

Additional glutamate receptors to cell membrane - restore initial imbalance
Need higher dose

39
Q

Withdrawal to benozodiazepines

A

Sudden decrease in inhibitor GABA neurotransmission and increase excitatory glutamate neurotransmission
Lead to increase anziety and other side effects

40
Q

Busprione - 5HT1A receptor aganoist

A

Activates 5HT1A autoreceptors - inhibit 5HT release and activation of noradrenergic neurons - decrease arousal reactions

41
Q

Busprione mechanism

A

Induce desensitisation of auto inhibitory 5HT1A receptors - lead to down regulate 5HT1A receptors
Desensitisation lead to heightened excitation of serotonergic neurons and increase 5HT release
Suppress symptom of anxiety in GAD

42
Q

beta noradrenergic receptor antagonist - propranolol

A

Non-selective between beta 1 and 2 noradrenergic receptors - decrease some of peripheral manifestations of anxiety
tachycardia, sweating, tremor, GI problems

43
Q

Positive symptoms of SCZ

A

Hallucinations
Delusions
Disorganised thought/speeech
Movement disorders

44
Q

Negative symptoms of SCZ

A 
Social withdrawal
Anhedonia
Lack motivation
Poverty of speech
Emotional flatness
45
Q

Cognitive symptoms of SCZ

A

Impaired working memory
Impaired attention
Impaired comprehension

46
Q

Hallucinations

A

Perceptions experienced without stimulus - commonly auditory

47
Q

Delusions

A

Fixed/unshakeable belief

Not consistent with social norms. Often paranoid or persecutory

48
Q

Motor, volitional, and behavioural disorders

A

Peculiar forms of motility, stupor, mutism, stereotypy
Stereotypies - repetitive acts - tics
Bizzare postures - strange mannerisms - altered facial expression
Bouts of hyperactivity - destructiveness

49
Q

Formal thought disorder

A

Conceptual thinking reflected in speech that is difficult to understand - rapid shift in topics
Disturbance in thinking - derailment of speech.
Fail to follow through to conclusions

50
Q

Phases of SCZ

A
  1. Prodrome - late teens/early 20s - can be triggered by stress
  2. Active/acute phase - onset of + symptoms - difficulty differentiating real and fake
  3. Remission - treatment to normal
  4. Relapse
51
Q

Nigrostriatal pathway - Dopaminergic neurons project from:

A

Dopaminergic neurons from:

Substantia nigra to the striatum - movement

52
Q

Mesolimbic pathway -

Dopaminergic neurons project from:

A

VTA to nucleus accumbens and to the amygdala and hippocampus - reward

53
Q

Mesocortical pathway -

Dopaminergic neurons project from:

A

VTA to frontal cortex - cognition and motivation

54
Q

Hypophyseal pathway - Dopaminergic neuron project from:

A

Dopamine to hypothalamus to anterior pituitary and on D2 receptors = release prolactin

55
Q

Dopamine hypothesis

A

Hyperactivity mesolimbic pathway - + symptoms - hallucinations and illusions
Mesocortical pathway - VTA to frontal cortex - hypoactivity associated with decrease cognitive symptom - loss memory

56
Q

Evidence for dopamine hypothesis

A

Amphetamine increase dopamine in mesolimbic pathway - psychotic episodes.
Dopamine activate D2 receptors - block D2 = antipsychotic effect
Reserpine deplete monoamine - antipsychotic effect

57
Q

Brain structure differences in SCZ

A

Brain slightly smaller - decrease grey matter

Enlarged lateral ventricles - smaller hippocampus

58
Q

Hypofrontality SCZ

A

Decrease blood flow to frontal cortex - decrease activity in frontal cortex - affect decision making

59
Q

NMDA receptor hypofunction

A

Antagonists
Decrease [glutamate] and glutamate receptors in prefrontal cortex - stereotyped behaviour and decrease social interaction

60
Q

Serotonin evidence of SCZ

A

LSD partial agonist 5HT receptors
Overstimulation of mesolimbic D2 receptors - hypoactivity of frontal cortical D1 receptors - decrease prefrontal glutaminergic activity

61
Q

Treatment for SCZ

A

Suppress hyperactivity of DA neurons - block D2 receptors - but D2 in striatum = decrease movement - side effects like parkinson’s

62
Q

Typical antipsychotics

A

1st generation
Antagonise D2
Motor impairment

63
Q

Atypical antipsychotics

A

2nd generation
Antagonise D2 and 5HT2A receptors
Limit side effects from typical antipsychotics

64
Q

Anticholinergic effects of antipsychotics

A

Antagonise mAChR
Blockade of mAChRs at NMJ - alleviate EPSE - but thought to impact cognition
Unblocked = parasympathetic reactions. Blocked = sympathetic reactions
Salivary secretion - dry mouth
Pupillary muscles - blurred vision
Smooth muscle contraction - constipation and urinary retention

PHYSIOLOGY 2 (5 decks)

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