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Medicine Year 2 > Scenario 31 > Flashcards

Scenario 31 Flashcards

1
Q

Where is 5-HT released?

A

Alla round the brain incl cerebellum from raphe nuclei

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2
Q

How is 5-HT synthesised?

A

Tryptophan (diet)→5-hydroxytryptophan→ 5-hydroxytryptamine

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3
Q

How is 5-HT stored?

A

Vesicle in presynaptic terminal, uses proton gradient- requires ATP (VMAT)

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4
Q

How is 5-HT released?

A

Calcium dependent vesicular release at the end terminal

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5
Q

What 5-HT receptors are there?

A

Ligand gates ion channels and GPCRs

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6
Q

How is 5-HT reuptaken?

A

Diffuses round end terminal and is reutaken by SERT co transporting with Cl and Na

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7
Q

How is 5-HT degraded?

A

5-hydroxytryptamine→ 5-hydroxyinolealdehyde→5-hydroxyindeoleacetic acid

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8
Q

What drugs interfere with 5-HT synthesis and storage?

A

P–chlorophenyalanine and reserpine

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9
Q

What drugs interfere with 5-ht release?

A

MDMA

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10
Q

What drugs interfere with 5-HT receptors?

A
  • Full agonists- 5-HT, sumitiptan
  • Partial agonists- buspirone
  • Antagonists- ondansetron, ketanserin
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11
Q

What drugs interfere with 5-HT reuptake?

A

SSRI (citalopram), TCAs, MDMA

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12
Q

What drugs interfere with 5-HT degradation?

A

MAOI- Phenelzine

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13
Q

What recreational drugs interfere with 5-HT?

A

MDMA, LSD, mescaline, magic muschrooms

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14
Q

What diseases are related to 5-ht?

A

Depression, anxiety, migraine, hallucinations

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15
Q

Where is NA released?

A

Very few neurons, post ganglionic symp nerves, retina and almost everywhere in brain (incl cerebellum)- associated with mood

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16
Q

How is NA synthesised?

A

Tyrosine–>DOPA–>Dopamine–>NA (by beta-hydroxylase)

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17
Q

How is NA stored?

A

In vesicles filled using a proton pump using ATP (transported in as dopamine then converted)

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18
Q

How is NA released?

A

Calcium dependent vesicular release at end teminal and en passant varicosities (Co-released with ATP)

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19
Q

What NA receptors are there?

A

All GPCRs (ligand gated so no fast firing)

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20
Q

How is NA reuptaken?

A

Diffuses round end teminal and taken up by NET whihc requires Cl and Na -uptake 1
Also taken up by glia also using NET

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21
Q

How is NA degraded?

A

Diff pathways involving MAO and COMT resulting in VMA which can be measured in urine

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22
Q

What drugs interfere with NA synthesis?

A

alpha-methyltyrosine

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23
Q

What drugs interfere with NA storage?

A

resepine, tyramine

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24
Q

What drugs interfere with NA release?

A

guanethidine

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25
Q

What drugs interfere with NA receptors?

A
  • Full agonists- NA, adrenaline, salbutamol
  • Parial Agonists- clonidine, ergotamine
  • Antagonists- propanolo, atenolol, prazosin, yohimbine
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26
Q

What drugs interfere with NA reuptake?

A

NSRI (reboxetine), TCAs (imipramine), amphetamine, cocaine

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27
Q

What drugs interfere with NA degradation?

A

MAO inhibitors- phenelzine

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28
Q

What recreational drugs intefere with NA?

A

cocaine, amphetamines

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29
Q

What diseases are related to NA?

A

Drug dependence, depression, hypertension

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30
Q

What is drug dependence defined as?

A

Repeated compulsive use of a drug to receive its chemical rewarding effect or to avoid withdrawal

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31
Q

What is the molecular target of opiods?

A

opiod receptors

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32
Q

What is the molecular target of amphetamines?

A

Dopamine transporter

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33
Q

What is the molecular target of cocaine

A

Dopamine transporter

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34
Q

What is the molecular target of nicotine?

A

Ach receptors

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35
Q

What is the molecular target of alcohol?

A

GABA receptors?

36
Q

What is the molecular target of ecstasy?

A

5-HT transporter

37
Q

What is psychological dependence?

A

Taking the drug primarily for the pleasurable rewarding effects

38
Q

How do drugs produce pleasurable effcts?

A

Reward pathways in the brain are hijacked by the drug causing DA transmission in mesolimbic DA pathway (particulary nucleus accumbens- strenthens association between stimuli and response)

39
Q

What is the development of psychological dependence affected by?

A

Pharmacokinetics- more rapid onset more rewarding

Ritual and environment- can positively reinforce further

40
Q

What is physiological dependence?

A

Taking the drug to avoid unpleasant effects

41
Q

Why do we become tolerant of drugs?

A

Pharmacokinetics- blood levels not maintained (new enzymes)
Pharmacodynamics- reduced effect of drug despite maintained blood levels (eg opiod tolerance- can tolerate a dose usually lethal)

42
Q

Why does pharmacodynamic tolerance happen?

A

Receptors are upregulated and homeostatic changes- when stopped left upregulated and withdrawal response

43
Q

How is drug dependence treated?

A

Reducing withdrawal discomfort, reduce rewarding effects of the drug, treat co-morbidities, diminish cravings

44
Q

What are typical symptoms of psychoses?

A

Dellusions, halluinations

45
Q

What is organic psychosis?

A

Caused by almost any physical disturbance to the brain and its environment (sometimes impaired consciousness) eg. dementias, endocrine, toxic (drugs), traumatic injury, neoplastic

46
Q

What is functional psychosis?

A

No functional distrubance to the brain, happens in clear consciousness eg. schizophrenia, delusional disorder, acute and transient disorders, depression, manic

47
Q

What is the life time risk of schizophrenia (SC)

A

0.9%

48
Q

What is the world wide prevalence of SC

A

1%

49
Q

What is the annual incidence of SC

A

10-15 pr 100,0000 adults

50
Q

What is the ave age of onset of SC?

A

28 in men, 32 in women

51
Q

What are the biological causes of SC?

A

MZ twins- 40-50%
First degree relatives 10%
Brain lesions during neurodevelopment
Cannabis use

52
Q

What are the social causes of SC?

A

Lower socio economic group

53
Q

What are the psychological causes of SC?

A

Cognitive decline? critical comments (relapse) stress

54
Q

What is the pathogenesis in SC?

A

increased ventricle:brain ratio
disruption of hippocampal pyramidal cells and cell loss in amygdala and enterohinal corted
Smaller neurons and reduced density in prefrontal cortex

55
Q

What neurotransmitter changes take place in SC?

A

Serotonin- sleep disturbance
NA
Increased limbic dopamine- positive symptoms, thought disorder
Ach/ GABA- cognitive impairment

56
Q

What drugs are used to manage SC?

A

Antipsychotic- highly effective against positive symptoms but s/e such as extrapyramidal syndrome and hyperprolactinaemia, metabolic syndrome, sexual dysfunction

57
Q

WHat other therapies can be used?

A

Psychological (family therapy, cognitive)

58
Q

What are the common outcomes of SC patients

A

20% highly dependent, 50% relatively independent 30% fully independent

59
Q

What are some common symptoms of anxiety?

A

sleep disturbance, muscle tension, sweating, tachycardia

60
Q

What is the pathology of anxiety?

A

reduced GABA- agonists reduce anxiety (benzodiazipines), antagonists produce anxiety
reduced 5-ht- agonists reduce anxiety (buspirone)
NA- overactivity in locus coeruleus

61
Q

How do you diagnose depression?

A

Need 2 of- low mood, low interest and enjoyment, reduced energy
Need 3 of- reduced self-esteem, guilty, pessimism, self-harm, reduced concentration, seep disturbance, reduced appetite
For 2 weeks

62
Q

What is the genetic factor in depression?

A

60% concordance in MZ twins

63
Q

What is the biolofical factor in depression?

A

HPA axis overactivity

64
Q

What is the psychological factor in depression?

A

Negative bias, loss/ abuse in childhood

65
Q

WHat is the social factor in depression?

A

Vulnerability- lack of support, life event onset brought forward

66
Q

What are the NT changes in depression?

A

Decreased 5-HT (low mood, sleep disturbance), NA (decreased motivation), DA (anhedonia), increased cholinergic activity (memory and sleep)

67
Q

What are the neuroendocrine changes in depression?

A

Increased CRH secretion (HPA activity, hypercortisolaemia), TRH/TSH (sub-clinial hypothyroid), GH/somatostatin (increased day time GH, reduced SST)

68
Q

What is the lifetime risk of suicide?

A

1%

69
Q

What is ETC?

A

Generate seizure activity in brain- unilateral electric shock

70
Q

What drugs are available to treat depression?

A

Enzyme inhibitors- MAOI, RIMA
Uptake inhibiroes- TCA, SNRI, SSRI, NSRI
Presynaptic receptor antagonists- atypical

71
Q

What enzymes do MAOIs and RIMAs inhibit? and what adverse reactions do they have?

A

Degrative enzynes for 5-HT and NA- diet interactions (more for MAOIs) because tyramine from diet can displace NA and increase symp drive to the heart increasing BP

72
Q

What is an example of a MAOI?

A

Phenelzine

73
Q

What is an example of a RIMA?

A

Moclobemide

74
Q

What is an example of TCAs?

A

amitriptyline, clomipramine, imipramine

75
Q

What is the function of TCAs?

A

Block 5-HT and NA reuptake

76
Q

What is the cons of TCAs?

A

Many s/e and toxic in OD

77
Q

How do SSRIs work and example?

A

Citalopram and block 5-HT reuptake

78
Q

What is an exaple of a NSRI and what do they do?

A

Reboxetine and block NA reuptake

79
Q

What is a s/e of NSRI

A

insomnia

80
Q

What do atypicals so and example?

A

Mitrazapine and block NA or 5-HT presynaptic receptors

81
Q

Adverse effect of atypicals?

A

Weight gain

82
Q

What is the monoamine hypothesis?

A

Depression is caused by a functional defecit of MA transmitters, mania is a functional excess

83
Q

What evidence is there to support the MAH?

A

Show genetic linkage- biochemical basis
Drugs that increase functional availability treat and opposite causes depression
Some drugs that reduce NA synthesis can mimic depression

84
Q

What evidence is there against the MAH?

A

Therapeutic lag, no clear evidence of mechanism of ECT and psychology, cocain and amphetamine increase NA but nnot anti depressant
Some people dont respond to drug treatment and other systems involved

85
Q

What drugs are used anxiolytics?

A

CNS acting or PNS acting

86
Q

What CNS anxiolytics are there?

A

Benzodiazepines, GABAa receptor agonists (sedation, impaired coordination), buspirone (5-HT partial agonist), Autoreceptor modualtion (nausea, lag, restlessness)

87
Q

What PNS anxiolytics are there?

A

Beta blockers for anxiety symptoms (bronchospasm, baradycardia, fatigue)

Medicine Year 2 (19 decks)

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