Neuropharm - lets do this

Question 1

Allyglycine

Answer 1

inhibits Glutamic acid dehydrogenase

Question 2

Vigabatrin

Answer 2

Inhibits GABA transaminase

Question 3

Tiagabine

Answer 3

Inhibits GAT

Question 4

baclofen

Answer 4

GABA(B) agonist

Question 5

saclofen

Answer 5

GABA(B) antagonist

Question 6

what causes a stroke?

Answer 6

interrupted blood flow to the brain either by haemorrhage - high BP, weakened blood vessels, amphetamine/cocaine (15%) or by occlusion - atheroscloerisis, thrombosis, embolism (85%).

Question 7

what happens during a stroke to cause brain damage?

Answer 7

hypo perfusion, electric failure, ionic pump failure, Na influx, K efflux, depolarisation - huge Ca influx. Oxidative stress - free radicals, degrade membranes and proteins. cell death and cerebral damage. also bbb dysfunction

Question 8

what are the 7 main treatments/preventions for stroke?

Answer 8

treatments (4): Aptiganel - GluR antagonist, Nicardipine - Ca channel blocker, Lamotrignine - Na channel blocker, Clot busters - Alteplase (desmoteplase still in trials) - must be thrombotic. preventatives (3); antihypertensives, statins or aspirin

Question 9

why are there different symptoms of epilepsy and which brain area is responsible for each?

Answer 9

The symptoms depend on the location of the epileptic foci in the brain. Motor cortex - convulsions. Reticular formation - unconsciousness. Temporal lobe - psychomotor epilepsy. Hypothalamus - peripheral autonomic discharge.

Question 10

what can trigger epilepsy?

Answer 10

stress, drop in pH, drop in blood glucose, fatigue, infection, gaming, antihistamines

Question 11

what is a proposed mechanism for epilepsy?

Answer 11

mismatch between GABA and Glut that causes a paroxysmal depol shift. AP spreads from focus - synchronous wave of depol.

Question 12

what are the 4 main targets for epilepsy treatment?

Answer 12

enhancement of GABAergic transmission. inhibition of na channels. inhibition of ca channels. inhibition of glutamate receptors.

Question 13

gluR antagonist?

Answer 13

perampanel

Question 14

enhancement of GABAergic transmission?

Answer 14

Vigabatrin - inhibits Gaba transaminase, tiagabine - inhibits GAT, valproate - SSADH inhibitor, barbiturates - GABAa receptor enhancement, may also prevent seizures at the initial site e.g. phenobarbital.

Question 15

na channel inhibitors?

Answer 15

valproate, lamotrigine

Question 16

ca channel inhibitors

Answer 16

mainly used in absence seizures, t-type ca channels - ethosuximide, gabapentin

Question 17

What is anxiety?

Answer 17

fear is a physiological response to fearful stimuli - anticipation of these events

Question 18

What is the correlation between anxiety and GABA?

Answer 18

People with anxiety have reduced GABAa receptors.

Question 19

What are the five main categories of anxiety?

Answer 19

General anxiety disorder. Panic disorder - sudden attacks of terror. Phobias - irrational fear of object/situation. PTSD - anxiety caused by recall of previous stressful event. OCD - recurrent and persistent thoughts in which the individual responds by performing ritualised excessive actions.

Question 20

What are the main treatments for each type?

Answer 20

GAD - benzodiazepines and buspirone. Panic disorder - benzodiazepines and antidepressants. Phobias - benzodiazepines. PTSD - antidepressants and b-blockers. OCD - antidepressants.

Question 21

How do we study fear and anxiety?

Answer 21

Innate (movement from dark to light) or learnt (e.g. electric shock in response to stimulus). apply stimulus or give environment and observe. elevated plus maze.

Question 22

How does the HPA axis regulate anxiety?

Answer 22

Hippocampus and amygdala. Amygdala is the on signal and stimulates PVN in hypothalamus. Causes release of CRF. Stimulates release of adrenocorticotropic factor. Stimulates adrenal medulla to release glucocorticoids. glucocorticoids inhibit all but amygdala and ACTF.

Question 23

What are the four main treatments for anxiety?

Answer 23

Benzodiazepines, buspirone, beta-blockers and antidepressants.

Question 24

Diazepines

Answer 24

allosteric modulators of GABAa receptor. require gamma2 for binding. increase affinity for gaba so only potentiate gaba already released. ideally would be selective for alpha2.

Question 25

give two examples of benzodiazepines

Answer 25

valium, diazepam

Question 26

beta-blockers used for anxiety?

Answer 26

e.g. propanolol. used to reduce peripheral effects of panic attacks

Question 27

buspirone?

Answer 27

used to treat anxiety - dirty pharm - 5-HT1a, D2, D3 etc. can take weeks to take effect

Question 28

4 main treatments for insomnia?

Answer 28

benzodiazepines, antihistamines, tricyclic antidepressants and zolpidem

Question 29

define depression

Answer 29

inability to cope

Question 30

what are the two main types of depression?

Answer 30

unipolar - 90% - mood swings always down. bipolar (10%) - alternating periods of manic and depressive behaviour

Question 31

what are other categories of depression?

Answer 31

reactive (75%) - in response to a stressful life, unipolar. endogenous (25%) - unipolar and most bipolar, often familial susceptibility.

Question 32

how does functional imbalance in the limbic system correlate with depression?

Answer 32

Amygdala - increased dendritic growth and spine formation - hyper-responsive. Hippocampus - dendritic atrophy and decrease in neurogenes - reduction in volume. medial pre-frontal cortex - dendritic atrophy and spine loss - hyporesponsive

Question 33

how does stress affect depression? how do antidepressants counter act this?

Answer 33

stress stimulates release of glucocorticoids which reduces BDNF secretion. this increases atrophy and decreases survival causing an increase in vulnerability. antidepressants increase NA and 5-HT secretion, increasing BDNF secretion and stimulating survival and growth.

Question 34

evidence for/against monoaminergic hypothesis

Answer 34

reserpine - irreversible VMAT inhibitor induces depression. drugs that reduce NA and 5-HT storage depress mood and drugs that inhibit NA and 5-HT uptake elevate mood. some effective antidepressants have no effect on monoamines - monoamines are perhaps the symptoms but not the cause

Question 35

what are the 3 main pathways influenced by dopamine?

Answer 35

niagrostriatal pathway - control of movement. mesolimbic/mesocortical pathway - cognition, memory, attention etc. tubers-infundibular system - endocrine.

Question 36

what are the different classes of 5-HT receptor?

Answer 36

5-HT1, 2, 4, 6 and 7 are GPCRs. 1 - Gi, 2 - Gq, 4, 6, 7 - Gs. 5-HT3 is a LGIC.

Question 37

types of ssri?

Answer 37

reserpine - blocks VMAT. fluoxetine - inhibits SERT. busprione - 5-HT1A agonist.

Question 38

what does serotonin do in the brain?

Answer 38

mood, wakefulness, sleep, feeding

Question 39

give examples of maoi and explain how they work

Answer 39

selegiline - inhibit mao-b and iproniazid - non-selective. prevent breakdown of monoamines. side effects such as urinary retention and tremor due to inhibition of tyramine breakdown. irreversible

Question 40

name 6 tricyclic antidepressants and their moa

Answer 40

amitriptyline and imipramine - non-selective NET/SERT inhibitors. citalopram, sertraline and fluoxetine - SERT selective. disipramine - NET selective

Question 41

what are side effects of tricyclic antidepressants?

Answer 41

sedation and fatigue, postural hypotension

Question 42

what are the three main symptom types for schizophrenia?

Answer 42

positive, negative and cognitive

Question 43

what are the 4 main things shown in brain imaging studies for people with schizophrenia?

Answer 43

thinner prefrontal and temporal cortex. enlarged ventricles. increased activity in the subcortical areas. decreased activity in the prefrontal areas.

Question 44

what is the glutamate hypothesis?

Answer 44

decreased glutamate and decreased glutamate receptors in schizophrenics. (PCP and amphetamine, NMDA receptor antagonists precipitate psychosis)