CNS Final Exam Practice (Sem-2) Flashcards

These flashcards were produced by Dr Nikolas Dietis (Lecturer of Pharmacology, School of Pharmacy, University of Tasmania) as part of the Final Exam Revision of CSA231 students - October 2012. (100 cards)

1
Q

Amphetamines are structurally related to which neurotransmitter?

A

Noradrenaline

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2
Q

Which two types of proteins do amphetamines use as part of their main mechanism of action?

A

The monoamine re-uptake transporters and VMAT vesicle transporters

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3
Q

Amphetamine administration results in increase or decrease of neurotransmitter concentration?

A

Increase, both synaptically and intracellularly.

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4
Q

What are the sympathomimetic results of amphetamines in bronchial function and ventilation?

A

Bronchodilation causes hyperventilation,

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5
Q

Cocaine acts on which ion channels and what kind of effect does it have?

A

Na channel blocking

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6
Q

What is the main difference between amphetamine and cocaine effects?

A

Cocaine has an additional anaesthetic (= analgesic) action

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7
Q

Nicotine binds on nicotinic Ach receptors. What kind of receptors are these and what is their ionic role?

A

Ligand-gated ion channels: opening of the channel requires binding of a ligand, allowing ions (Na, Ka) to flow IN the cell.

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8
Q

What is the effect of nicotine on muscle?

A

Causes muscle contraction

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9
Q

Name three main types of diseases arising from nicotine-involved smoking.

A

Cancer, coronary heart disease, peripheral vascular diseases, obstractive pulmonary diseases

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10
Q

Caffeine is structurally similar to which purine?

A

Adenosine

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11
Q

What is the mechanism of action of caffeine?

A

Blocks adenosine receptors

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12
Q

Why caffeine is included in ergotamine formulations against migraine?

A

1) Cffeine increases ergotamine’s absorption and thus increases its therapeutic effect
2) Caffeine causes vasoconstriction, which has a direct effect on migraine

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13
Q

What is the nicotine cardiospecific effects?

A

Tachycardia by stimulation of autonomic ganglia

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14
Q

What is the effect of amphetamines in core body temperature and why is this important?

A

Hyperthermia, which is not easily detected due to increased activity and euphoria, resulting in permanent brain damage. Main cause of death in amphetamine users.

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15
Q

What is the common mechanism of action between amphetamines and cocaine?

A

They both block the re-uptake of NA and dopamine

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16
Q

Where is the anaesthetic action of cocaine based on?

A

Blocking the NA channels, resulting in inhibition of Na ions coming inside the cell, thus inhibiting the neuronal action potential, thus pain signals are not transmitted.

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17
Q

How fast does nicotine crosses the blood brain barrier?

A

Within 10 seconds

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18
Q

Name three withdrawal effects of nicotine dependence..

A

Irritability, impaired performance of psychomotor tasks, aggressiveness and sleep disturbances

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19
Q

Bupropion is used to treat nicotine dependence. What is its mechanism of action and side-effects?

A

It inhibits re-uptake of dopamine and noradrenaline (antidepressant activity, same as amphetamines) thus reduces cravings for nicotine.
Adverse effects include insomnia, nightmares, anxiety, agitation.

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20
Q

What are nicotine’s CNS effects?

A

Excitability of dopaminergic neurons cause a mild euphoric effect, which is very short.

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21
Q

Does cocaine produce muscle spasms or seizures?

A

Seizures

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22
Q

What is the cardiovascular effect of cocaine?

A

Its a potent vasoconstrictive thus causing hypertension

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23
Q

Which two main types of drugs will you consider for acute amphetamine overdose?

A

Potent vasodilators to reverse the vasoconstrictive effects.
Benzodiazepines to induce depressant effects and reverse over-activity, hyperventilation and anxiety.

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24
Q

Which two receptors does alcohol uses for its mechanism of action?

A

The glycine and GABA receptors

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25
Why alcohol is prohibited during pregnancy?
It correlates to fetal alcohol syndrome, associated with deranged facial features, retarded brain growth and ultimately with permanent brain damage.
26
What is the cardiovascular effect of cannabis?
Increased heart rate
27
What is the common effect of cannabis in memory, learning and motor coordination?
Impairment
28
What is the effect of cannabis in intraocular pressure?
Reduction
29
What is the main active ingredient of cannabis and where does it act on?
4-THC (Delta-4-tetrahydrocannabinol), binds to cannabinoid receptors
30
What are endocannabinoids?
Endogenous cannabinoids (i.e. anandamide) that bind to cannabinoid receptors.
31
Which antagonist can be used for treatment of alcoholism and alcohol dependence?
An opioid antagonist; i.e. naltrexone
32
What is the effect of alcohol on the cardiovascular system?
Produces alcoholic cardiomyopathy; toxicity of cardiac muscle, reducing pumping efficiency and leading to heart failure
33
What is the effect of alcohol on cholesterol?
Increase of HDL, decrease of LDL
34
How many receptors are there for endocannabinoids?
Two; CB1 and CB2
35
What is the mechanism of action of THC?
Binds to CB1 and inhibits the release of neurotransmitters
36
What is the effect of cannabis on testosterone levels?
Decreased
37
What is the effect of cannabis on the immune system?
Suppression
38
Which substance has higher degrees of addiction; nicotine or cannabis?
Nicotine. Cannabis has the lowest degree of addiction among substances of abuse (~9%)
39
What is the medical use of cannabis; provide the names of two drugs
Dronabinol and Marinol; they are used in glaukoma (treatment of intraocular pressure), chronic pain (effective in neuropathic element), control of nausea/vomiting during pregnancy, complimentary treatment of arthritis
40
What is the concentration-dependent effect of alcohol on its own metabolism?
Low doses decrease CYP-dependent metabolism, high doses induce CYP-dependent metabolism
41
What is the difference between addiction and dependence?
Addiction is the continuous use of a drug despite its harmful effects; dependence is the manifestation of withdrawal symptoms after discontinuation of a drug
42
What is tolerance and which forms are there?
Tolerance is the manifestation of decreased therapeutic effects after repeated administration. Pharmacodynamic tolerance (due to changes in receptor density & function) and Pharmacokinetic tolerance (due to changes in drug concentration at the site of action.
43
Which one from addiction and dependence can be characterized as a disease?
Addiction
44
Which one comes first upon ligand binding; receptor phosphorylation or receptor internalization?
Receptor phosphorylation
45
Which neuronal pathways or system is implicated in substance dependence?
The mesolimbic dopaminergic pathway (or reward system).
46
What is the difference of rebound and withdrawal effects?
Withdrawal effects are effects of drug discontinuation based on a dependence element. Rebound effects are a form of withdrawal effects, that manifest as being opposite from the drug's actions.
47
What is the main difference and main similarity of neuropathic and nociceptive pain?
Difference: neuropathic pain involves damage of neuronal tissue only. Similarity: they both involve tissue damage of some sort.
48
Which drugs are MOST effective for neuropathic pain?
Antidepressants and anticonvulsants (main mechanism unknown)
49
Which analgesics are most effective for neuropathic pain?
Opioids
50
What is the main biological difference between acute and chronic pain?
Chronic pain produces functional, structural, chemical changes in the brain, whereas acute doesn't.
51
Name the FOUR elements of pain signaling
Transduction (signal initiation), Transmission (signal transfer), Modulation (signal inhibition/facilitation), Perception (signal recognition)
52
Which is the most important anatomical area in the spinal cord for pain transmission?
Dorsal horn
53
Does the motor reflex involve central modulation from the brain?
No, its a direct effect of spinal modulation
54
What are the nociceptors?
Are pain fibers from the periphery to the spinal cord (alpha-delta and C fibers)
55
Which area of the brain processes pain?
Cortex
56
Which area of the brain relays information coming from the spinal cord and disseminates signals accordingly?
Thalamus
57
What is the role of the limbic system in pain signalling?
It regulates the pain threshold and controls the emotional response to pain
58
What is the role of the hypothalamus and pituitary gland in pain signalling?
Hypothalamus is responsible for receiving ascending signals and promotes endocrine response to pain by pituitary gland (i.e. endorphin release)
59
Is the descending pathway inhibitory or facilitatory?
Both
60
Which three neurotransmitters are mainly present in the descending pain pathway?
NA, 5-HT and endorphins
61
Name FIVE substances that are present in tissue inflammation and facilitate pain transmission
Histamine, prostaglandins, bradykinin, substance P, neurokinin A,
62
Name three opioid receptors
MOP (or mu), KOP (or kappa), DOP (or delta)
63
What is the cAMP effect of opioid binding on an opioid receptor?
Activation of opioid receptor produces reduction in intracellular cAMP
64
What is the effect of morphine binding on MOP receptors, in terms of Ca and K?
Reduction of cAMP leads to reduction in intracellular Ca and outflow of cellular K
65
Morphine produces pain analgesia by which main two mechanisms?
Hyperpolarization of the post-synaptic neuron and pre-synaptic reduction of neurotransmitter release.
66
Which endogenous opioid binds selectively to MOP receptors?
Endomorphins
67
Which two serotonin receptors are coupled to inhibitory G proteins?
5-HT1 and 5-HT5
68
Which two adrenergic receptors are coupled to inhibitory G proteins?
alpha-2
69
Which opioid has particularly potent cough suppression effect?
Codeine
70
What is the opioid effect on ventilation?
Respiratory depression, hypoventilation
71
Why euphoria is an important opioid effect of analgesia?
Because stress is an emotional aspect of pain, therefore the ideal analgesic should also have a euphoric or anxiolytic effect
72
Where does morphine's itching effect come from?
Due to promotion of histamine release from mast cells
73
Morphine produces pupil contraction or dilation?
Contraction
74
Name as many opioid drugs as you can..
Morphine, fentanyl, oxycodone, codeine, pentazocine, meperidine, methadone, propoxyphene, remifentanil
75
What is the effect of morphine on GI motility?
Reduction = constipation
76
Where do we use opioid antagonists?
Treatment of addiction (naltrexone) and opioid overdose (naloxone),
77
What is the most common side-effect of opioid antagonists?
They might cause hyperalgesia
78
What are the symptoms of opioid toxicity (overdose)?
Slow/shallow breathing, hypoxia/hypoventilation, bradycardia, hypotension, muscle spasms, lethargy
79
When is opioid tolerance detected?
Within 24 hours of repeated administration
80
Is opioid cross-tolerance, complete or incomplete?
Incomplete; this is why opioid medication rotation has some use
81
What kind of pharmacological treatment is used for opioid dependence?
Treatment of dependence symptoms by using non-opioid analgesics, antiemetics, antidiarrhoeals, benzodiazepines, alpha-2 receptor agonists
82
Which are the TWO most common drugs used for treatment of opioid dependence?
methadone and buprenorphine
83
What is the mechanism of action of NSAIDs?
Inhibition of COX (cyclo-oxygenase) enzyme, COX-1 and COX-2
84
Name THREE roles of COX-1 enzyme function
Gastric protection, renal blood flow homeostasis and platelet adhesion
85
COX enzyme produces prostaglandins from which substance?
Arachidonic acid
86
Name a similarity between aspirin and ibuprofen with respect to COX
They are both non-selective
87
Name a difference between naproxen and meloxicam with respect to COX
Meloxicam is a COX-2 selective, naproxen is non-selective
88
The inhibition of which prostaflandin is responsible for the antipyretic activity of NSAIDs and where is it produced?
PGE-2, produced by the hypothalamus
89
Which activity of aspirin provides cardiovascular protection?
antiplatelet action (inhibition of platelet adhesion & aggregation)
90
Describe three mechanisms of NSAID GI effects
1. Irritation of gastric mucosa 2. Risk of GI bleeding by inhibition of platelet aggregation 3. Inhibition of gastroprotective prostaglandins
91
What is the connection between PGI-2 and COX-2 selective NSADs' cardiovascular risk?
COX-2 is responsible for producing PGI-2 (prostacyclin), which is cardioprotective. COX-2 selective NSAIDs will inhibit COX-2 and thus produce a cardiovascular risk.
92
Are paracetamol's actions central or peripheral?
Central
93
What kind of two effects does paracetamol have?
Analgesic and antipyretic
94
Which drugs can be used for treating paracetamol overdose?
Activated charcoal and N-acetylcysteine
95
What is aura in migraine vascular theory?
A phase of reduced cerebral blood flow which starts in visual cortex and is responsible for the visuoneurological symptoms of migraine
96
What is the relationship of serotonin concentration and migraine?
In vasoconstriction phase prior to migraine attack, serotonin is increased. In vasodilation phase during migraine attack, serotonin is decreased.
97
Name three type of drugs for acute treatment of migraine attacks
Analgesics (NSAIDs or paracetamol), antiemetic drugs and anti-migraine drugs (ergot alkaloids and triptans)
98
Name the different drug types that are effective in the prophylaxis of migraine attacks
Beta-blockers (propranolol, atenolol), 5-HT2 antagonists (pizotifen, cyproheptadine), tricyclic antidepressants (amitriptyline), anticonvulsants (valproate, topiramate), Ca channel blocker (verapamil), α-2 agonist (clonidine)
99
What is the mechanism of action of ergotamine?
5-HT1B/1D partial agonists, causing cerebral vasoconstriction
100
What is the mechanism of action of methysergide?
Its a 5-HT2 receptor antagonist