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Pharmacology Flashcards

1
Q

What are the dangers of drug use?

A

Allergies = death

Toxicity = death

Interactions with other drugs which can have an effect on absorption and metabolism of other drugs.

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2
Q

What do LA work on?

A

Block propagation of impulses on ion channels

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3
Q

What is a positive action of adrenaline (vasoconstrictor)?

A

Constricts the blood vessels and allows the drug to remain in the desired area for longer.

Allows lower volume of the drug to be used.

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4
Q

What are the negative actions of adrenaline (vasoconstrictor)?

A

Constricts vessels allows drug to remain in the area for longer which can be toxic to the nerve tissue.

People can also have a reaction.

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5
Q

Name examples of local anaesthetics.

A 
Lignocaine.
Prilocaine.
Articaine.
Bupivivaine.
Mepivicaine.
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6
Q

Name commonly prescribed antibiotics.

A

Amoxycillin
Metronidazole.

Doxycycline.
Clindamycin.

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7
Q

Name antiviral drugs and how they can be used.

A

Aciclovir: topical/systemic

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8
Q

What are the drugs used in treating pain and inflammation called?

A

Analgesics.

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9
Q

What type of analgesic reduces inflammatory mediators?

A

NSAIDs

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10
Q

What type of analgesics reduce he inflammation process?

A

Corticosteroids.

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11
Q

How do NSAID work?

A

inhibit prostaglandin synthesis.

Change balance of PGE1 and PGE2.

Inhibit COX 1 and 2 enzymes.

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12
Q

What effect can NSAIDs have on blood?

A

NSAID has an effect on thromboxanes which makes the platelets less adhesive = more bleeding.

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13
Q

Where is aspirin rapidly absorbed from?

A

The GIT

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14
Q

What kind of clearance does aspirin have?

A

Fast

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15
Q

What are the actions of aspirin (NSAID)?

A

Reduces synthesis of prostaglandins.

Reduces production of inflammatory mediators.

Anti-pyrexic. (Reduces fever)

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16
Q

What is an advantage of using aspirin (NSAID)?

A

It is a pre-emptive analgesic. Can be taken before the inflammatory process begins.

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17
Q

List the side effects of Aspirin (NSAID). (5)

A

Gastric irritation= ulcerations.

Inhibition of platelet function = enhanced bleeding.

Bronchospasm = Effect on asthma.

Drug interactions (protein binding)

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18
Q

How do corticosteroids reduce inflammation?

A

Inhibits capillary permeability.

Inhibits the formation of bradykinin.

Inhibits the migration of white blood cells.

Reduces eicosanoid synthesis.

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19
Q

What is the disadvantage of using corticosteroids?

A

They suppress the inflammation but do not address the cause.

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20
Q

What are the ways that corticosteroids can be administered?

A

Topically

Systemically

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21
Q

Give 2 examples of topical corticosteroids.

A 
Steroid inhalers.
Hydrocortisone cream (eczema)
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22
Q

List the 3 steroid treatments for mouth ulcers.

A

Beclomethasone inhalers.

Hydrocortisone adhesive tablets.

Betamethasone solutions.

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23
Q

Prednisolone tablets are systemic corticosteroids, what are the uses of these tablets?

A

Prevent transplant rejection.

Treat immunological diseases.

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24
Q

Dexamethasone injections are systemic corticosteroids, what are the uses of these injections?

A

Reduce swelling after surgery.

i.e wisdom tooth removal.

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25
What is the danger with taking systemic steroids for a prolonged period of time?
If you take the steroids for a prolonged period of time side effects WILL occur. ``` The longer u take the steroid the more serious the side effects will become. High BP Weight gain Change is fat distribution (centripetal obesity) Gastric ulcers Adrenal suppression Osteoporosis Diabetes ```
26
What are the side effects of systemic steroids?
``` High BP Weight gain Change is fat distribution (centripetal obesity) Gastric ulcers Adrenal suppression Osteoporosis Diabetes ```
27
Name anxiolytic drugs.
Benzodiazepines: | Diazepam, midazolam.
28
What is the action of benzodiazepines?
Have an effect on the gamma receptor in membranes.
29
What are the dangers of using benzodiazepines?
The drug is helpful whilst in use but problems occur once the medication is removed.
30
Name an anxiolytic gas.
Nitrous oxide
31
What are the advantages of nitrous oxide?
The amount of effect can be adjusted during the procedure. No issues with organ metabolism, is excreted unchanged.
32
When can nitrous oxide not be used and why?
In pregnancy. | Interferes with folic acid metabolism which is required for the formation of the brain and spinal cord in an embryo.
33
What are the functions of the thyroid hormone?
Balance bodys metabolism
34
What messengers (2) does thyroxine replace?
T3 and T4
35
How must the dosage of the thyroxine tablets be altered?
Gradually
36
How do thyroxine tablets act?
Directly upon the tissues - no effect on the gland.
37
Name the 2 types of nerve communication.
Sympathetic | Parasympathetic
38
What drug acts on the sympathetic NS? What is this stimulation called?
Adrenaline | Adrenergic stimulation
39
What drug acts on the parasympathetic NS?What is this stimulation called?
Acetylecholine | Cholinergic stimulation
40
What is the effect of the sympathetic NS? How does this occur?
Speeds up heart rate via beta-receptors.
41
What is the effect of the parasympathetic NS? How does this occur?
Slows the heart via cholinergic receptors.
42
What autonomic drug is a beta agonist?
Adrenaline
43
What autonomic drug is a beta blocker?
Atenolol
44
What autonomic drug is a cholinergic agonist?
Pilocarpine
45
What autonomic drug is a cholinergic blocker?
Atropine
46
In terms of drug/receptor interaction, what happens if the drug does not find the receptor?
No effect
47
In terms of drug/receptor interaction, what happens if the drug binds to the receptor yet the fit isn't ideal?
Shape of protein remains unaltered so no effect occurs. However, the binding site is blocked.
48
In terms of drug/receptor interaction, what happens if the drug (agonist) binds and the fits the shape of the binding site?
Causes a shape change which has an effect with the cell.
49
What are the 2 components in drug-receptor activity?
Drug-receptor interaction. Drug induced response.
50
What are the 2 main points components of drug receptor interaction?
AFFINITY | OCCUPANCY
51
In drug-receptor interaction what is the definition of affinity?
How well the drug and receptor bind.
52
n drug-receptor interaction what is the definition of occupancy?
How long the drug and receptor are bound together.
53
What is the main component in the drug induced response?
How effective the drug is in producing a change within the cell.
54
Define AGonist.
Binds to a receptor and causes and effect.
55
Define partial AGonists.
A drug that is more difficult to produce an effect. Some of the effect is produced but not all.
56
How can the effect of partial AGonists be increased?
Increasing the concentration of the partial agonist. DOESN'T WORK FOR ALL PARTIAL AGONISTS.
57
Name the 2 types of ANTagonists.
Competitive | Non-competitive.
58
How can the effect of a reversible antagonist be reduced?
By increasing the concentration of the AGonist
59
What is the effect of irreversible ANTagonists?
Binds and reduces the availability of receptors for the AGonist.
60
Name an example of a reversible ANTagonist.
Atenolol
61
Name an example of an irreversible ANTagonist.
Phenoxybenzamine
62
Define ANTagonist.
Drug that binds to the binding site and blocks it. No effect produced.
63
Name 5 routes of administration.
``` Oral Intravenous Intramuscular Subcutaneous Inhalation ```
64
What type of administration does and inhaler fall into?
Topical. | Once inhaled the drug doesn't reach the alveoli and is absorbed via the surface of airways. = topical
65
What are the advantages of oral administration?
Socially acceptable, more people likely to take drugs via oral method.
66
What are the disadvantages of oral administration?
Slow onset Variable absorption: some of the drug is lost on route, never know exactly how much is being directly absorbed. Drug can be destroyed by gastric acid. First pass metabolism: drug passes through the portal vein into the liver where is it partially metabolised. Only a portion of the drug actually reaches circulation.
67
List other factors that can affect oral absorption.
Lipid solubility- can only be absorbed if the drug is soluble in lipids. Drug formulation- Drugs can be coated which allows absorption at different stages in the route. Problems with GI motility- drug can't be passed through the GI tract. Drug can interact with other substances in the gut. Disease of the GI tract- some patients may not have enough bowel to allow absorption.
68
(First pass metabolism) All blood from the GI tract drains into the hepatic portal vein. Which 2 veins do not?
Sublingual | Rectal
69
In terms of managing FPM what do some drugs have the ability to do?
Some drugs can become activated after being metabolised in the liver.
70
What is a disadvantage of FPM?
More drug needs to be administered orally so the desired amount can reach the circulation- have desired clinical effect. e.g. Glyceryl Trinitrate.
71
Before administering an oral drug, what is important to consider?
If the patient has normal liver function. Cant give high dosages of drugs since the liver cannot metabolise it efficiently.
72
When does abnormal liver function occur?
In extremes of life. | Those with liver disease.
73
What are the advantages of non-oral drug administration?
Predictable plasma levels | No first pass metabolism.
74
What are the disadvantages of non-oral drug administration?
Reactions are more severe: occur all over body not localised. Difficult to self-medicate. Drug cost higher.
75
Define bioavailability.
Proportion of an administered drug that is available for clinical effect. e.g. IV = 100% Oral = variable
76
In terms of drug distribution what determines where the drug will travel to?
Circulation. | Areas with higher blood flow receive more of the drug.
77
Define the 2 phases in drug elimination.
Phase 1: Inactivating the drug via oxidation, reduction, hydrolysis etc. Reactions make changes to the drugs which inactivate them. Phase 2: Conjugation. A molecule is bound to the drug which helps the drug be filtered and excreted by the kidney. i.e glucuronidation, sulphation, methylation etc
78
How can drugs be excreted?
Renal-urine, liver-bile, lungs-gas, sweat, saliva.
79
What is the main way drugs are excreted?
Kidney-urine.
80
Define single compartment models.
Drug behaves as if it is evenly distributed throughout the body.
81
Define two compartment models.
Drug behaves as if it is in equilibrium with different tissues in the body.
82
How do you work out drug clearance?
Plasma half life. (t 0.5) First order kinetics Zero order kinetics
83
Define 1st order kinetics.
Most common. Drug elimination/absorption by PASSIVE DIFFUSION. Proportional to the drug concentration. The higher the concentration the faster the removal. Logarithmic graph is a straight line. Constant half life.
84
Define Zero order kinetics.
Elimination is and ACTIVE process can be saturated by high drug concentrations. Linear graph of drug elimination. Constant amount of drug us eliminated per unit time.
85
What are the consequences of a dosing schedule that is too frequent?
Toxic plasma levels depends on drugs therapeutic index.
86
What are the consequences of a dosing schedule that is too infrequent?
No clinical effect
87
Define pharmacodynamics.
The interactions between the drug and the body.
88
Define Pharmacokinetics.
How the body processes the drug.
89
Define bioavailability.
The amount of drug present in the circulation that is able to produce an effect.
90
What information do you need to know before creating a dosing schedule?
The half life of the drug. The drug clearance time. The function of the liver/kidney.
91
What are the 2 classes of local anaesthetic?
Amides (most common) and esters.
92
How can you tell what LA are amides? (Hack)
Amides have an i in the prefix of the name, not the 'caine' bit. i.e. Lidocaine.
93
In 1% LA how many milligrams are in 1 millilitre?
10 miligrams to 1 millilitre.
94
What drugs should you avoid interacting with warfrin?
Antifungals
95
What drugs should you avoid interacting with statins (for lowering cholesterol)?
Antifungals.
96
Name anti fungal drugs and how they are administered.
Nystatin: Topical Fluconazole: oral

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