Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medicine Year 2 > Scenario 31 > Flashcards

Scenario 31 Flashcards

(87 cards)

Start Studying
1
Q

Where is 5-HT released?

A

Alla round the brain incl cerebellum from raphe nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is 5-HT synthesised?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is 5-HT stored?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is 5-HT released?

A

Calcium dependent vesicular release at the end terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 5-HT receptors are there?

A

Ligand gates ion channels and GPCRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is 5-HT reuptaken?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is 5-HT degraded?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What drugs interfere with 5-HT synthesis and storage?

A

P–chlorophenyalanine and reserpine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What drugs interfere with 5-ht release?

A

MDMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What drugs interfere with 5-HT receptors?

A
  • Full agonists- 5-HT, sumitiptan
  • Partial agonists- buspirone
  • Antagonists- ondansetron, ketanserin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What drugs interfere with 5-HT reuptake?

A

SSRI (citalopram), TCAs, MDMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What drugs interfere with 5-HT degradation?

A

MAOI- Phenelzine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What recreational drugs interfere with 5-HT?

A

MDMA, LSD, mescaline, magic muschrooms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What diseases are related to 5-ht?

A

Depression, anxiety, migraine, hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is NA synthesised?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is NA stored?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is NA released?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What NA receptors are there?

A

All GPCRs (ligand gated so no fast firing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is NA degraded?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What drugs interfere with NA synthesis?

A

alpha-methyltyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What drugs interfere with NA storage?

A

resepine, tyramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What drugs interfere with NA release?

A

guanethidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What drugs interfere with NA receptors?
* Full agonists- NA, adrenaline, salbutamol * Parial Agonists- clonidine, ergotamine * Antagonists- propanolo, atenolol, prazosin, yohimbine
26
What drugs interfere with NA reuptake?
NSRI (reboxetine), TCAs (imipramine), amphetamine, cocaine
27
What drugs interfere with NA degradation?
MAO inhibitors- phenelzine
28
What recreational drugs intefere with NA?
cocaine, amphetamines
29
What diseases are related to NA?
Drug dependence, depression, hypertension
30
What is drug dependence defined as?
Repeated compulsive use of a drug to receive its chemical rewarding effect or to avoid withdrawal
31
What is the molecular target of opiods?
opiod receptors
32
What is the molecular target of amphetamines?
Dopamine transporter
33
What is the molecular target of cocaine
Dopamine transporter
34
What is the molecular target of nicotine?
Ach receptors
35
What is the molecular target of alcohol?
GABA receptors?
36
What is the molecular target of ecstasy?
5-HT transporter
37
What is psychological dependence?
Taking the drug primarily for the pleasurable rewarding effects
38
How do drugs produce pleasurable effcts?
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
What is the development of psychological dependence affected by?
Pharmacokinetics- more rapid onset more rewarding | Ritual and environment- can positively reinforce further
40
What is physiological dependence?
Taking the drug to avoid unpleasant effects
41
Why do we become tolerant of drugs?
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
Why does pharmacodynamic tolerance happen?
Receptors are upregulated and homeostatic changes- when stopped left upregulated and withdrawal response
43
How is drug dependence treated?
Reducing withdrawal discomfort, reduce rewarding effects of the drug, treat co-morbidities, diminish cravings
44
What are typical symptoms of psychoses?
Dellusions, halluinations
45
What is organic psychosis?
Caused by almost any physical disturbance to the brain and its environment (sometimes impaired consciousness) eg. dementias, endocrine, toxic (drugs), traumatic injury, neoplastic
46
What is functional psychosis?
No functional distrubance to the brain, happens in clear consciousness eg. schizophrenia, delusional disorder, acute and transient disorders, depression, manic
47
What is the life time risk of schizophrenia (SC)
0.9%
48
What is the world wide prevalence of SC
1%
49
What is the annual incidence of SC
10-15 pr 100,0000 adults
50
What is the ave age of onset of SC?
28 in men, 32 in women
51
What are the biological causes of SC?
MZ twins- 40-50% First degree relatives 10% Brain lesions during neurodevelopment Cannabis use
52
What are the social causes of SC?
Lower socio economic group
53
What are the psychological causes of SC?
Cognitive decline? critical comments (relapse) stress
54
What is the pathogenesis in SC?
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
What neurotransmitter changes take place in SC?
Serotonin- sleep disturbance NA Increased limbic dopamine- positive symptoms, thought disorder Ach/ GABA- cognitive impairment
56
What drugs are used to manage SC?
Antipsychotic- highly effective against positive symptoms but s/e such as extrapyramidal syndrome and hyperprolactinaemia, metabolic syndrome, sexual dysfunction
57
WHat other therapies can be used?
Psychological (family therapy, cognitive)
58
What are the common outcomes of SC patients
20% highly dependent, 50% relatively independent 30% fully independent
59
What are some common symptoms of anxiety?
sleep disturbance, muscle tension, sweating, tachycardia
60
What is the pathology of anxiety?
reduced GABA- agonists reduce anxiety (benzodiazipines), antagonists produce anxiety reduced 5-ht- agonists reduce anxiety (buspirone) NA- overactivity in locus coeruleus
61
How do you diagnose depression?
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
What is the genetic factor in depression?
60% concordance in MZ twins
63
What is the biolofical factor in depression?
HPA axis overactivity
64
What is the psychological factor in depression?
Negative bias, loss/ abuse in childhood
65
WHat is the social factor in depression?
Vulnerability- lack of support, life event onset brought forward
66
What are the NT changes in depression?
Decreased 5-HT (low mood, sleep disturbance), NA (decreased motivation), DA (anhedonia), increased cholinergic activity (memory and sleep)
67
What are the neuroendocrine changes in depression?
Increased CRH secretion (HPA activity, hypercortisolaemia), TRH/TSH (sub-clinial hypothyroid), GH/somatostatin (increased day time GH, reduced SST)
68
What is the lifetime risk of suicide?
1%
69
What is ETC?
Generate seizure activity in brain- unilateral electric shock
70
What drugs are available to treat depression?
Enzyme inhibitors- MAOI, RIMA Uptake inhibiroes- TCA, SNRI, SSRI, NSRI Presynaptic receptor antagonists- atypical
71
What enzymes do MAOIs and RIMAs inhibit? and what adverse reactions do they have?
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
What is an example of a MAOI?
Phenelzine
73
What is an example of a RIMA?
Moclobemide
74
What is an example of TCAs?
amitriptyline, clomipramine, imipramine
75
What is the function of TCAs?
Block 5-HT and NA reuptake
76
What is the cons of TCAs?
Many s/e and toxic in OD
77
How do SSRIs work and example?
Citalopram and block 5-HT reuptake
78
What is an exaple of a NSRI and what do they do?
Reboxetine and block NA reuptake
79
What is a s/e of NSRI
insomnia
80
What do atypicals so and example?
Mitrazapine and block NA or 5-HT presynaptic receptors
81
Adverse effect of atypicals?
Weight gain
82
What is the monoamine hypothesis?
Depression is caused by a functional defecit of MA transmitters, mania is a functional excess
83
What evidence is there to support the MAH?
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
What evidence is there against the MAH?
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
What drugs are used anxiolytics?
CNS acting or PNS acting
86
What CNS anxiolytics are there?
Benzodiazepines, GABAa receptor agonists (sedation, impaired coordination), buspirone (5-HT partial agonist), Autoreceptor modualtion (nausea, lag, restlessness)
87
What PNS anxiolytics are there?
Beta blockers for anxiety symptoms (bronchospasm, baradycardia, fatigue)

Medicine Year 2 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions