Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology and Pharmacology 2 > Drugs in the CNS: Lectures 21-24 > Flashcards

Drugs in the CNS: Lectures 21-24 Flashcards

1
Q

Where do drugs primarily act?

A

On neurons (bulk of the CNS)

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

How can therapeutic drugs affect us?

A

Neurologically (brain) - epilepsy, Parkinsons, Arlzheimers Psychotropic (mind/ emotions) - anaethetic, sedatives, antipsychotics and antidepressants.

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

Why do most drugs not act on the brain?

A

Have to cross the blood brain barrier - Only gaps are tight junctions - Must be either lipid soluble or use carrier-mediated transport

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

What are the different sites a drug can affect

A

Neurotransmission or Neuronal Function Ion channel excitability Receptors- pre and post synaptically Synthesis and delivery of peptide neurotransmitters

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

How can drugs affect neurotransmission?

A

Synthesis, removal, uptake, storage - Breakdown of neurotransmitter with MAO - Breakdown of neurotransmitter with COMT

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

How can drugs affect receptors?

A

Ionotropic- voltage or ligand gated ion channels - can affect membrane potential and signal transduction Metabotropic - GPCRs - Can affect the phospholipase C and cAMP pathways

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

What are the molecular targets of drug action?

A

Enzymes Transporters Receptors (incl ion channels, GPCRs, kinase linked)

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

What are anxiolytics?

A

Used to treat anxiety

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

What is the difference between being ‘normal’ and having ‘anxiety’?

A

Normal behaviour- defensive, fear, reflexes, alert, down Anxiety- these behaviour with no external cues –> interferes with normal activity

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

What are the different types of anxiety?

A

Generalised anxiety disorder, panic disorder, phobias, social anxiety, OCD, PTSD, separation anxiety.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do you treat anxiety?

A

Psychologically with benzodiazepines. Two types- sustained action e.g. diazepam, or short action e.g. lorazepam.

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

How do benzodiazepines treat anxiety?

A

Binds at top of GABA receptor between alpha 1 and gamma 2. Affects the GABAa receptor (selectively permeable to Cl- causing hyperpolarisation (inhibits depolarisation)) –> increased inhibition

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

What are the affects of benzodiazepines and possible side effects?

A

Reduced anxiety, reduced muscle tone and coordination, Sedation, Amnesia Develop tolerance over 1-2 weeks

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

What is the problem with the development of tolerance

A

Decreased effectiveness –> need more to have the same effects Builds up a dependence to the drug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are other anxiolytic options other than benzodiazepines?

A

Beta-blockers to treat the symptoms? Adrenoceptor-mediated activation

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

What is the purpose of hypnotic drugs?

A

Psychoactive drugs used to induce sleep in insomnia and anesthetics

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

What are some examples of hypnotics

A

Flurazepam, zalepon

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

What decides whether a drug such as a benzodiazepine is a hypnotic or anxiolytic.

A

Doseage as most of the drugs work at the same site.

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

Describe the basics of epilepsy.

A

Electrical disturbances in the brain causing breif, chronical, recurring and rapid onsetting seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do anti-epileptics work?

A

Use dependent block of sodium channels Acting on the GABAa receptor Inhibiting GABA breakdown

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

How does use dependently blocking sodium channels combat epilepsy?

A

Drug accumulates with the increased opening and activity of the channel. It therefore blocks depolarisation and excitation (inhibits channel) when rapid firing occurs - Phenytoin

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

How does the drug action on GABAa receptors combat epilepsy?

A

Potentiates the effects of GABA –> increased inhibition Inhbition leads to decreased chances of a seizure

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

How does inhibiting GABA breakdown combat epilepsy?

A

Decreased inhibition leads to increased GABA –> increased inhibition

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

Why are there different ways of combating epilepsy?

A

Different drugs with different mechanisms - a combination of drugs as no drug works for all patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What defines depression?

A

Intense or prologoned sadness often without external cues. Can display signs- pain, digestive or respiratory difficulties. –> high chance of suicide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the causes of depression?

A

Genetic and environmental - varies between people - Neurochemical imbalance - External factors : death, loss, separation - Biological amine theory - deficit of neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the different mechanisms of treatment for depression?

A

Increasing transmission of neurotransmitters - Inhibit re-uptake - Inhibit metabolism - Enhance release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does inhibiting re-uptake treat depression?

A

Generally either serotonin or Noradrenaline or both! - Use serotonin-noradrenaline-re-uptake inhibitors (SNRIs) Leads to an increase in the synaptic concentration - Not specific but selective –> side effects E.g.s tricylcic antidepressants, prozac, fluoxetine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does inhibiting metabolism of neurotransmitters treat depression?

A

Increase in the amount of MAO inhibitors –> NT taken up into vesicles and then recycled Can work reversibly or irreversibly Leads to a requirement for re-synthesis E.g. phenelzine

30
Q

How does enhancing the release of neurotransmitters treat depression?

A

Alpha-2 adrenoceptor antagonists e.g. mirtazapine –> inhibition of pre-synaptic receptors which produce inhibitory feedback mechanisms –> increased release / increased synaptic concentration

31
Q

Why does antidepressant treatment take a while to take effect?

A

Requires neuronal adaptation or neurogenesis

32
Q

What is neuronal adaptation?

A

Change in the number of receptors –> often a decrease with desensitisation –> takes longer for an effect to occur Can be triggered by antidepressants –> decrease in pre-synaptic auto-receptors and transports –> increased neurotransmission

33
Q

What is neurogenesis?

A

The creation of new neurons Produced due to antidepressant treatment –> increase in neurotrophins and neurotransmitters –> increase in growth factors –> increase in neurons

34
Q

How do you treat bipolar disorder?

A

Stabilised through acute and long-term control - Acute use drugs- benzodiazepines, antipsychotics - Long term: increase the amount of lithium i.e. lithium carbonate

35
Q

How does the increase in the amount of lithium increase stability in bipolar patients?

A

Stabilise the Galpha q PLC pathway - uncompetitive inhibition —> increased activity –> increased inhibition —> Lithium used by an enzyme that inhibitis inositol production.

36
Q

What are some examples of psychomotor stimulants?

A

Amphetamines, MDMA, Cocaine

37
Q

What are the effects of amphetamine?

A

Structurally realted to noradrenaline (targert specific) –> Both taken up by uptake 1 and have a weak affect on adrenoceptors.

38
Q

What mechanism does amphetamine work by?

A

In synapse –> uptake 1 –> exchanged by VMAT for the NA in vesicles –> increased NA release On uptake it causes the inhibition of MAO leading to decreased degradation of NA leading to increased concentrations Noradrenaline floods the synapses

39
Q

What are the clinical uses of amphetamines?

A

Narcolepsy - used in preventing excessive daytime sleeping and also Attention Deficit Hyperactive Disorder (ADHD).

40
Q

What are the recreational uses of amphetamines?

A

SPEED (snorted or injected) –> euphoria, confidence, hyperactivity Side effects: hypertension, insomnia, tremor

41
Q

What are the issues with taking MDMA / ectasy?

A

Cause sudden death due to feeling hot causing people to drink a lot. MDMA causes renal faliure and therefore the intake of liquid leads to death. Can also lead to long term CNS damage.

42
Q

What are the effects of taking cocaine?

A

Intense and immediate euphoria when snorted Smoked - side effects: cardiac problems, stroke like symptoms, foetal development issues

43
Q

How can cocaine be used clinically?

A

Local anaesthetic –> prevents action potentials

44
Q

By what mechanism does cocaine work?

A

Blocks re-uptake –> increased neurotransmitter in the synapse.

45
Q

What are psychoses?

A

Changed perception of reality, intellect, mood, motivation, motor ability.

46
Q

Psychoses can lead to schizophrenia, what are the positive and negative symptoms.

A

Positive: hallucinations, disorganised speech, behavioural changes Negative: change in normal behaviour Positive and negative symptoms must be treated differently - different antipsychotics.

47
Q

What are the ways of treating different parts of schizophrenia?

A

Postive and negative symptoms are treated with antipsychotics. Cognitive dysfunction - requires clinical treatment.

48
Q

What is aetiology?

A

A developmental brain disorder. Large amounts of changes in neuropathological pathways Changes in metabolism, blood flow, body chemistry

49
Q

What causes aetiology?

A

Over activity of dopaminergic systems –> changes in mesolimbic system. This in turn causes changes in cognition and emotions

50
Q

What are the different types of anti-psychotics drugs used?

A

Group 1 - chlorpromazine Group 2 Group 3 - haloperidol Less common- clozapine, olanzapine

51
Q

What is the basic mechanism for anti-psychotics?

A

All drugs are the antagonists of different GPC dopamine receptors - commonly D2 receptors (suggestive that schizophrenia caused by dopaminergic systems.

52
Q

How could dopaminergic systems be linked to the onset of schizophrenia?

A

Increased number of receptors –> increased activity.

53
Q

What does the effectiveness of drugs depend on?

A

Interactions with neurotransmitter systems. - affinity for other receptors. –> causes side-effects: stiffness, shakiness (parkinsons like).

54
Q

Why are less common drugs being used more frequently nowadays?

A

Reduced side effects but different side effects: weight gain, diabetes, sexual problems, saliva production. Reduce negative symptoms - suicidal and negative emotions, lack of emotions.

55
Q

Why could decreasing glutamate be an effective therapy?

A

Tackles both positive and negative symptoms.

56
Q

What are opoid analgesics used for?

A

Pain reduction - morphine and codeine Recreationally - opium –> euphoria, analgesia, sleep, diarrhoea relief, ADDICTION

57
Q

Define Opiod, Opiate and Endorphin

A

Opiod- any agonist with morphine like activity Opiate- any drug derived from the opium poppy Endorphin- endogenous substrate with morphine like properties

58
Q

What are the effects of opiods?

A

Analgesia and euphoria, nausea, sleepiness, mood change, reduced bowel movement, decrease HR and Respiration.

59
Q

What are the three types of opiod receptor?

A

All GPCRs distributed in grey matter Mu (where morphine acts), Kappa, and delta

60
Q

What opoid and precurosor proteins act on the different receptors?

A

Reproopiomelanocortin –> endorphin–> delta Preprokephalin –> met or leu encephalin –> kappa Preprodynorphin –> dynorphin –> mu or kappa

61
Q

How does opoid action link to GPCRs

A

Couple to Gi –> decreased production of cAMP Direction action of by (beta gamma) subunit -Increased K+ channel conductance –> hyperpolarisation, faster repolarisation, increases AP rate. - Decreased opening of VGCC —> decreased neurotransmission

62
Q

What is the difference between somatic and visceral pain?

A

Somatic pain - close to surface Visceral pain - deep tissue

63
Q

What are the affects of visceral pain (deep tissue damage)

A

Sweating, nausea, change in emotions

64
Q

Why is morphine often used in cancer treatment.

A

Stabilisation of emotions Treatment of visceral pain

65
Q

What mechanism does morphine work by?

A

Acts primarily on the mu receptor in the CNS Causes inhibition of primary afferent neurons —> INHIBITS post-synaptic excitability, neurotransmitter release, modulation of pre-synaptic AP firing

66
Q

Define tolerance:

A

The need to increase the drug doseage due to decreased effectiveness of response

67
Q

What are the possible mechanisms which can lead to tolerance?

A

-Increased metabolic tolerance - drugs broken down faster (up regulation of metabolism) - Cellular-adaptive - cellular response is altered –> often due to a change in receptor number - Behavioural conditioning- environment changes –> changes in effectiveness

68
Q

Define physical dependence:

A

adaptive state which leads to intense physical disturbance if drug removed

69
Q

Describe withdrawal or abstinence syndrome

A

Drug specific physiological and psychological symptoms - opposite of the drugs effects - pain, depression, anxiety Increases desire to take drug again Extent of dependence measured by severity of withdrawal

70
Q

Define psychological dependence:

A

cravings or desire to take a drug- feel like its necessary - neurochemical basis (reward) –> reward / desire may have an external cue —> predictive cue: taking any drug (placebo)–> effect

71
Q

What is the best way to combat an overdose?

A

A high affinity competitive antagonist is required - Naloxone removes agonist (heroin)

72
Q

How is opiod addiction often treated?

A

Partial agonists are used as a replacement - Buprenorphine Higher affinity than drug but lower efficacy –> wean off –> simultaneously prevent the use of opiods.

Physiology and Pharmacology 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions