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Principles Of Pharmacology > Week 11 > Flashcards

Week 11 Flashcards

1
Q

What is drug tolerance?

A

With chronic exposure, adaptive changes occur which means the dose of the drug will need to be increased to maintain its effects.

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2
Q

With is drug withdrawal?

A

Signs of withdrawal appear when the drug is no longer available.

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3
Q

What is drug dependence?

A

The presence of a withdrawal symptom as a physical dependence.

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4
Q

What is drug addiction?

A

Relapsing drug use despite negative consequences due to psychological dependence.

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5
Q

What is the drug reward pathway?

A

A dopamingeric pathway from the ventral tegmental area to the nucleus accumbens and prefrontal Cortex of the brain.

Drugs move through this pathway and increase release of dopamine into the nucleus accumbens and prefrontal cortex.

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6
Q

Using the drug reward pathway, what molecule is increased and where?

A

More dopamine is release into the nucleus accumbens and prefrontal cortex of the brain.

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7
Q

What causes animals to self-administer cocaine?

A

Animas self administer cocaine into the nucleus accumbens and the pleasure this causes reinforces self-administration.

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8
Q

On what type of receptors do Opioid drugs act?

A

Mu-opiod receptors in the CNS and peripheral mu-receptors.

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9
Q

What type of drugs are Opioids at mu-opioid receptors in the CNS?

A

Agonists

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10
Q

What effects do Opioids have due to acting on peripheral mu-receptors?

A

Reduce motility of the GI tract.

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11
Q

What molecules can be used to stop the effects of Opioids and how?

A

Specific antagonists such as Naloxone which bind to Opioid receptors.

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12
Q

What are some of the adverse effects of Opioids?

A 
Drowsiness, confusion memory loss, fatigue, hallucinations, convulsions. 
Dilation of blood vessels causing increased pressure in the brain. 
Respiratory depression. 
Pupil contraction. 
Slurred speech. 
Nausea, vomiting, weight loss. 
Sexual dysfunction. 
Constripation.
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13
Q

What are the central effects of morphine?

A 
Analgesia
Sedation
Euphoria
Respiratory Depression
Vasomotor Centre Depression
Miosis
Nausea and vomiting due to CTZ stimulation
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14
Q

What is analgesia?

A

The inability to cause pain.

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15
Q

What are the peripheral effects of Morphine?

A

Constipation.
Billiary Spasm.
Constrition of the sphincter of Oddi.
Histamine release.

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16
Q

What the of receptors does Ketamine work at and how?

A

It is an antagonist and NMDA receptors. Competes with N-methyl-D-aspartate for NMDA receptors

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17
Q

What type of receptors are NMDA receptors?

A

They are glutamate ion channel-linked receptors.

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18
Q

What type of anaesthesia does ketamine cause?

A

Dissociative

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19
Q

What are the effects of chronic ketamine use?

A

Bladder removal

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20
Q

When were Barbiturates introduced to medicine?

A

1904, first cynically used in 1912.

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21
Q

Describe the therapeutic window of Barbiturates

A

Narrow

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22
Q

What were Barbiturates initially used to treat?

A

Sedatives and hypnotics

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23
Q

What type of drug became used more than Barbiturates as sedatives and hypnotics?

A

Benzodiazepine group

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24
Q

What are Barbiturates now used to treat?

A

Epilepsy and for anaesthesia.

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25
Q

What type of receptor agonists or antagonists are barbiturates?

A

GABAa receptor agonists.

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26
Q

What is the difference in the mechanisms of action between Barbiturates and Benzodiazepines?

A

Bind to different GABAa receptor site

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27
Q

What are Benzodiazepines used to treat?

A

Used as sedatives, hypnotics, for insomnia, anxiety and epilepsy.

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28
Q

Outline the mechanism of Benzodiazepines to cause neuronal excitability.

A

In the CNS, GABA neurotransmitter binds to GABAa receptors and causes a Cl- ion channel to open. Benzodiazepines enhance the binding of GABA to GABAa receptors meaning more Cl- enter the channel and cause excitability.

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29
Q

Do drugs that act on adrengeric nerve terminals act in the centra or peripheral nervous system and why?

A

Both. Noradrenaline is released by neurones in both the brain and sympathetic nervous system.

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30
Q

What effect does cocaine have on noradrenaline?

A

Cocaine blocks neuronal uptake of noradrenaline meaning more is available in the synaptic cleft.

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31
Q

How does cocaine affect dopamine neurones?

A

Cocaine blocks dopamine transporter in dopamingeric neurones meaning more dopamine is available.

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32
Q

How does cocaine affect Seratonin transporter?

A

Cocaine blocks serotonin transporter meaning more is available as neurotransmitter.

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33
Q

What type of nervous reaction does cocaine mimic and why?

A

The sympathetic nervous system by increasing noradrenaline availability in peripheral tissues.

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34
Q

What are the sympathetic effects that cocaine has?

A

Rapid heart rate
Hypertension
Decreased GI motility and secretion

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35
Q

How does Amphetamine affect noradrenaline?

A

Amphetamine displaces noradrenaline from its storage vesicles and reverses the direction of the uptake pump. This increases the concentration of noradrenaline in the synaptic cleft.

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36
Q

How does Amphetamine affect dopamine ?

A

Displaces Dopamine from its storage vesicles and reverses the direction of the uptake of the pump. This increases the concentration of dopamine available.

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37
Q

Name some possible side effects caused by Amphetamine

A 
Insomnia. 
Restlessness. 
Night terrors.  
Euphoria. 
Dependence. 
Tolerance. 
Psychosis. 
Anorexia. 
GI symptoms. 
Growth retardation. 
Dry mouth. 
Sweating. 
Tachycardia. 
Increased blood pressure.
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38
Q

Outline the mechanism used by LSD

A

It is an agonist at 5=HT2A receptors.

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39
Q

Outline the mechanism used by MDMA

A

It releases 5-HT and blocks uptake

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40
Q

What type of receptors does Psilocybin act on?

A

Acts on 5-HT2A receptors

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41
Q

What class of drug is Psilocybin?

A

Class A

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42
Q

Outline the mechanism and clinical use of Tetrahydro-cannabinol?

A

Activates CB1 and CB2 receptors.

Has analgesic and antiemetic properties.

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43
Q

What are analgesic properties?

A

Pain relief

44
Q

What are Antiemetic properties?

A

A drug effective against nausea and vomiting.

45
Q

Outline the mechanism of Salvinorin A

A

K-opioid receptor agonist

46
Q

What are some of the effects that can be caused by activating CB1 receptors?

A

Basal ganglia movement.
Cerebellum movement.
High cognitive function in the cerebral cortex.
Alters appetite in the hypothalamus.
Alters learning, memory and stress in the hippocampus.
Alters the peripheral sensation of pain in the spinal cord.

47
Q

What is the full name for CB1 receptors?

A

Cannabinoid receptors.

48
Q

Where are CB1 receptors expressed?

A

CNS

49
Q

What are the overall effects of activated CB1 receptors known as?

A

Psychoactive effects

50
Q

Were are CB2 receptors expressed?

A

Immune system and hematopoeitic cells.

51
Q

What exogenous ligands act on CB1 and CB2 receptors?

A

Anandamide and 2-Archidonolygycerol

52
Q

Define adverse drug reactions.

A

Any response to a drug which is noxious, unintended and occurs at doses used in man for prophylaxis, diagnosis or therapy.

53
Q

What is meant by a drug being noxious?

A

Harmful or poisonous

54
Q

What is a prophylactic drug

A

It is intended to prevent disease.

55
Q

What are the possible predisposing factors of adverse drug effects?

A

Can relate to properties of the rug or characteristics of the patient:
Genetics
Age
Sex
Physiology (pregnancy)
Exogenous factors (other drugs and food)
Disease

56
Q

What are the different types of adverse drug reaction?

A 
A - Augmented (dose-related). 
B - Bizarre (Idiosyncratic). 
C - chronic
D - delayed
E - end of treatment 
F - failure of therapy
57
Q

What are the features of Type A (augmented) adverse drug reactions?

A

Common.
Related to pharmacological action of the drug.
Predictable.
Low mortality rate.

58
Q

How are Type A adverse drug reactions managed?

A

Reduce dose or withhold.

Consider effects of concomitant therapy.

59
Q

What are the issues caused by Type A adverse drug reactions?

A

Pharmaceutical variation.
Pharmacokinetic variation.
Pharmacodynamic variation.

60
Q

What pharmaceutical variations occur due to type A adverse drug reactions?

A

Changes in bioavailability, out of date formulations, contamination.

61
Q

What pharmacokinetic variations occur due to type A adverse drug reactions?

A

Liver disease
Renal disease
Cardiac disease
Drug interactions

62
Q

What pharmacodynamic variations occur due to type A adverse drug reactions?

A

Changes in fluid/ electrolyte balance.

Drug interactions.

63
Q

Outline the effects of a type A adverse drug reaction with Tetracycline.

A

Tetracycline breaks down into a toxic anhydrotetracycline produce which causes Fanconi’s syndrome.

64
Q

What is Fanconi’s syndrome?

A

An impairment of the proximal tubule function where substances which would normally be reabsorbed back into the blood are excreted and lost in the urine.
(Glucose, amino acids, phosphate, uric acid).

65
Q

How can cirrhosis causes type A drug adverse reactions?

A

Drugs cannot be cleared by the liver.

66
Q

What is cirrhosis?

A

Degeneration of the liver cells causing inflammation and fibrous thickening of tissue. Caused by hepatitis or alcohol.

67
Q

Explain the type A adverse drug effect that can occur when taking Digoxin.

A

Blocks Na+/K+ pump of cardiac muscle cells. Competes with binding sites for K+ in the pump.
When K+ levels are low, Digoxin binds to the Na+/K+ pump easily

68
Q

What is the clinical use of Digoxin?

A

Used to treat heart failure.

69
Q

What are the features of type B (Idiosyncratic) adverse drug reactions?

A 
Uncommon. 
Not related to the pharmacological action of the drug. 
Not dose-related. 
Unpredictable. 
High mortality.  
Low morbidity.
70
Q

How can type B adverse drug reactions be managed?

A

Withhold and avoid the drug in future.

71
Q

How does Penicillin cause a type B adverse drug reaction?

A

Degradation products of Penicillin can combine with body proteins and become antigenic and therefore produce an allergic response.

Anaphylactic shock can also occur.

72
Q

What are Pseudoallergic reactions ?

A

Reactions that resemble allergic reactions but for which no immunological basis has been found.

73
Q

Give examples of Pseudoallergic reactions.

A

Aspirin-sensitive asthmatics.

Ampicillin rash.

74
Q

What are the possible effects caused by type C adverse drug reactions?

A

Tolerance / physical dependence.
Adrenal suppression.
Tardive dyskinesia.

75
Q

What type of drugs are likely to cause tolerance or physical dependence?

A

Narcotic Analgesics such as morphine.

76
Q

What type of drugs are likely to cause adrenal suppression?

A

Corticosteroids such as hydrocortisone.

77
Q

What type of drugs are likely to cause tardive dyskinesia?

A

Antipsychotic drugs such as haloperidol.

78
Q

What is Tardive Dyskinesia?

A

Repetitive, involuntary jerking movements that occur in the face, neck and tongue.

79
Q

What are the causes of Tardive Dysinesia?

A

The use of long term antipsychotic drugs are used to treat schizophrenia can cause TD. Even if this drug stops being taken, symptoms can continue to occur.

80
Q

What type of feedback mechanism controls the production and secretion of glucocorticoid hormones?

A

Negative feedback

81
Q

What type of conditions are glucocorticoids used to treat?

A

Inflammatory conditions such a rheumatoid arthritis.

82
Q

Outline how adrenal suppression may occur due to type C adverse drug reaction.

A

Prolonged treatment with high doses can result in suppression of glucocorticoid synthesis by the adrenal cortex.

83
Q

How can adrenaline suppression due to type C adverse drug reactions be overcome?

A

Gradual withdrawal of exogenous glucocorticoids.

84
Q

What are the effects of type D (delayed) adverse drug reactions?

A

Uncommon.
Dose-related.
Becomes apparent after the use of the drug.

85
Q

Describe the management of type D adverse drug reactions?

A

Hard to control.

86
Q

How is Carcinogenesis caused by Type D adverse drug effects?

A

Long-term Oestrogen treatments such HRT and oral contraceptives can lead to risk of carcinogenesis.

87
Q

What effects can type D adverse drug reactions have on fertility?

A

Impaired fertility - cytotoxic drugs used in cancer therapy can cause this.
Teratogenesis - congenital malformations of an embryo or foetus.

88
Q

Give an example of a drug which causes Teratogenesis

A

Thalidomide

89
Q

What are the features of type E adverse drug reactions?

A

Uncommon

Occurs soon after withdrawal of the drug.

90
Q

Give examples of type E adverse drug reactions.

A 
Opiate withdrawal syndrome. 
Myocardial ischaemia (beta-blocker withdrawal).
91
Q

What is the technical term for beta-blocker withdrawal?

A

Myocardial Ischaemia

92
Q

What are the features of type F adverse drug reactions?

A

Common
Dose-related
Often caused by drug interactions.

93
Q

Give ad example of a type F adverse drug reaction.

A

Inadequate dosage of oral contraceptive, particularly when used with specific metabolic enzyme inducers such as Rifampicin.

94
Q

How are type F adverse drug reactions managed?

A

Increased dosage.

Consider effects of concomitant therapy.

95
Q

Define pharmacogenetics.

A

The study of the influence of hereditary on both the pharmacokinetics of drugs and the pharmacodynamic responses to them.

96
Q

How does Succinylcholine choline cause type F adverse drug reactions?

A

Succinylcholine is used as a muscle relaxant and can cause prolonged apnoea in patients who lack the pseudocholinesterase enzyme that normally breaks down Succinylcholine.

97
Q

What is apnoea?

A

Shallow breathing

98
Q

What enzyme breaks down succinylcholine ?

A

Pseudocholinesterase

99
Q

What are the possible effects of drug interactions in the body ?

A

Interference with absorption.
Competition for plasma protein binding.
Inhibition or induction of metabolic enzymes.
Competition for elimination pathways.

100
Q

Give an example of drug interactions causing issues with absorption.

A

Tetracycline binds to calcium and iron and reduces absorption in the GI tract.

101
Q

Give an example of drug interactions causing competition within plasma protein binding.

A

Warfarin Vs Aspirin in the blood vessels.

102
Q

Give an example of inhibition or induction of metabolic enzymes leading to an adverse drug reaction.

A

Cimetidine inhibits Rifampicin induces.

Occurs in the liver.

103
Q

Give an example of competition for elimination pathways caused by drug interactions in the body.

A

Probenecid slows excretion of penicillin from the liver.

NSAIDS inhibits excretion of lithium from the liver

104
Q

Give an example of pharmacodynamic interactions causing adverse drug reactions?

A

Propanolol, a beta-receptor agnosia, can reduce the effects of Salbutamol beta-receptor agonist

105
Q

What’s the purpose of Levodopa?

A

Increases synaptic dopamine levels in parkinsons disease.

106
Q

What effects do Antipshychotics have on Levodopa and how does this occur?

A

They block dopamine receptors and can therefore reduce the effects of Levodopa.

Principles Of Pharmacology (11 decks)

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