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Nursing Year 1 > Applied Pharmacology > Flashcards

Applied Pharmacology Flashcards

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1
Q

What is an analgesic?

A

A drug that relives or reduces pain

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2
Q

What is an NSAID?

A

A non-steroidal anti-inflammatory drug which works in the hypothalamus of the brain, and blocks COX. They also help to reduce peripheral and central sensitisation.

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3
Q

What do NSAIDS do in the arachidonic acid cascade?

A

The normal cascade = Arachidonic acid is produced in damaged tissue, and is worked on by COX, and is converted to prostanoids and thromboxane. However, NSAIDs main action is to block COX enzymes, therefore this process cannot be carried out, as the COX is blocked.

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4
Q

What is COX 1?

A

COX 1 is in most tissues and cells, mainly in the endoplasmic reticulum. They get involved in regulating gastric protection, blood flow and platelet aggregation

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5
Q

What is COX 2?

A

COX 2 is in mast cells, fibroblasts, microphages, endothelial cells, and nuclear membrane. They get involved in inflammation, pain and fever. There is some degree of a functional overlap in many tissues in COX 1 and 2.

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6
Q

What is COX 3?

A

COX 3 is mainly found in the CNS, and is poorly understood, it may not be active in humans.

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7
Q

Why are COX important?

A

They have potentially different activity in different tissues.

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8
Q

What are some examples of NSAID’s?

A

Aspirin, ketoprofen, fenoprofen, and celecoxib

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9
Q

Which example of NSAID’s bind to which COX?

A

Ketoprofen is more COX1 selective, aspirin is equally selective and COX1 selective, fenoprofen is equally selective, celecoxib is COX2 selective.

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10
Q

What are the 4 main therapeutic effects of NSAID’s?

A

Anti-inflammatory, analgesic, antipyretic, platelet aggregation

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11
Q

Explain NSAID binding to COX

A

Binding to arachidonic acid binding site is blocking the COX. Aspirin irreversibly binds to the COX in covalent binding. Other NSAIDs usually reversibly bind to COX

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12
Q

Explain the anti-inflammatory effects in NSAID’s.

A

The NSAID’s inhibit COX2 which are derived of prostaglandins, which are powerful vasodilators. This promote the release of other vasodilators such as substance P and histamine. This reduced the production of prostaglandin, which therefore reduced swelling, redness, neurogenic inflammation, vasodilation and oedema.

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13
Q

Explain the analgesic effects of NSAID’s.

A

The NSAID’s inhibit COX2, which are derived of prostaglandins, and reduce the sensitisation of free nerve endings. The prostaglandins get involved in the sensitisation of the synapse of the 1st and 2nd order neuron, so the prostaglandin is reduced. Therefore, the NSAID’s reduce prostaglandin production due to the reduction of sensitisation of free endings, and they reduce 2nd order neuro sensitivity. They reduce peripheral and central sensitisation.

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14
Q

Explain antipyretic effects of NSAID’s.

A

The NSAID’s stimulate PGE2 in the hypothalamus which inhibits temperature sensitive neurons. Therefore, they reduce PGE2 production by binding COX2.

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15
Q

Explain platelet aggregation of NSAID’s.

A

The NSAID’s block COX1 to reduce the action of thromboxane and A2 production, this reduced the blood clotting response. The COX1 selectivity is good because the covalent binding means that platelets never recover the ability to aggregate, so new platelet production is required for this.

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16
Q

What are the gastrointestinal side effects of NSAID’s?

A

Prostaglandins promote production of alkali mucus, which protects the stomach wall, the barrier between the tissue of the stomach and its content is the alkali mucus. If you take aspirin, it blocks the prostaglandin production, which blocks the production of alkali mucus. This can lead to gastric complications like ulcers. This is why COX2 was made because they have fewer gastric complications.

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17
Q

What are the respiratory side effects of NSAID’s?

A

Aspirin can reduce asthma symptoms. Tissue injury can create arachidonic acid which can either work with COX which creates prostaglandin and thromboxane, or it can work with lipoxygenase which creates leukotriene which can start the overproduction of leukotrienes, which can occur due to aspirin. This overproduction can bring on asthmatic attacks.

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18
Q

What are the renal side effects of NSAID’S?

A

Prostaglandins promote vasodilation therefore glomerular filtration, however if they are blocked, there is reduced renal filtration which can lead to sodium retention in the blood.

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19
Q

What are the liver side effects of NSAID’s?

A

There is a relatively low incidence with the liver being affected, however if you take a large quantity of NSAID’s, it can cause a retention of bile, which can’t be transported out of the biliary system. Also, it can cause mitochondrial damage because NSAID’s can disrupt the pumps in mitochondria and reduce ATP production. Taking a large quantity can also cause the inhibition of prostaglandin E2 production, which can damage cells and loose liver cells, as well as the build-up of reactive metabolites in the liver which can become toxic.

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20
Q

What is paracetamol?

A

It is a pain relief and antipyretic effect. It is a non-opioid, which means it is not strictly an NSAID. It targets COX2 in the CNS and inhibits calcium channels. It’s usual dose is 1g 3-4 times a day, not exceeding 4g, this is because it could start damaging the liver. It is metabolised into NAPQI and then the NAPQI becomes a glutathione conjugate .

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21
Q

What is a mild opioid?

A

A compound resembling opium in its physiological effects.

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22
Q

How does a mild opioid work?

A

It binds to specific opioid receptors, and mimics the action of endogenous peptide neurotransmitters e.g. endorphins

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23
Q

Give an example of natural, semisynthetic and synthetic mild opioids.

A 
Natural = morphine and codeine
Semisynthetic = buprenorphine 
Synthetic = fentanyl
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24
Q

Explain opioid receptors.

A

The G-protein is coupled with receptors, so when you activate the new opioid receptors you down regulate nerve cell excitability

25
Q

Which voltage-gated channels are decreased and increased in mild opioids.

A

The voltage-gated Ca2+ channels activity is decreased, and the voltage-gated K+ channels activity is increased.

26
Q

What is the effect of mild opioids binding to their receptors?

A

The opiate drug binds to the opioid receptor in the 1st and 2nd order neuron, and makes them less sensitive, so it downgrades their excitability, which leads to a reduction in pain.

27
Q

Give examples of strong opioids.

A

Morphine, fentanyl, heroin, diamorphine

28
Q

What is a strong opioid?

A

They are strong agonists of opioid receptors, they have high potency and good efficacy.

29
Q

What are the side effects of strong opioids?

A

Constipation, depression of cough reflex, respiratory depression, nausea and vomiting, europhia, physical dependence, possible immune suppression, decreased sex hormone production, opiate induce hyperalgesia

30
Q

What are corticosteroids?

A

An anti-inflammatory medicine which provides pain relief and improves function/mobility. However, they are temporary.

31
Q

What is cortisol?

A

The principal human glucocorticoid (peak in the morning)

32
Q

How do glucocorticoids promote an anti-inflammatory action?

A

The corticosteroid inhibit arachidonic and acid production, and can be analgesics. They reduce the production of pro-inflammatory and inhibit mast cells.

33
Q

What is the general mechanism of corticosteroids?

A

They bind to cytoplasmic steroid receptors in the cell, which turns into a dimer and that enters the nucleus. Then there is regulation of gene transcription and regulation of key protein production.

34
Q

What is the mode of action of local anaesthetics?

A

To block the voltage-gated sodium ion channels.

35
Q

Explain how local anaesthetics block voltage-gated sodium ion channels.

A

When local anaesthetic is injected into the tissue around the nerve, the molecules diffuse into the tissue of the nerve and then into the axons, where the action begins, and they go into the voltage-gated sodium channels and it blocks it from the inside of the cell.

36
Q

Explain drug partitioning.

A

Lidocaine or bupivacaine sits in the extracellular space around the nerve cell, where part of it is ionised and part of it is not. Only the uncharged ones can pass through the plasma membrane, then the different environment in the cell as the uncharged particles go through causes drug partitioning. it ends up with mote of the local anaesthetic molecules charged, so they cannot get out of the cell and therefore they block the voltage-gate. This is why it takes time for the local anastatic block to develop.

37
Q

What are the complications of local anaesthetics?

A

Inflammatory acidosis affects drug partitioning. The decreasing pH facilitates ionisation, which compromises the blockade and can cause problems with anaesthesia.

38
Q

Define antibiotics.

A

Antibiotics destroys life and kills microorganisms and bacteria.

39
Q

What would an ideal antibiotic look like?

A

It would be selectively toxic, it does its jobs well and kills the bacteria, however it doesn’t affect the human

40
Q

What do antibiotics need to work?

A

They need drug targets that are dissimilar to eukaryotic cells

41
Q

Why is bacteria a prokaryote?

A

It has no nucleus, it has a structural/defensive cell wall, some have capsules, it has a plasma membrane, it has a genophore for DNA, there is ribosomal production, it has a plasmid DNA, it has a pila, and it has a flagellum.

42
Q

What is a gram-positive bacteria cell wall?

A

A cell wall that is on the outside of a cell, made of peptidoglycan. It is heavy and the peptidoglycans stain purple.

43
Q

What is a gram negative bacteria cell wall?

A

A cell wall that is in-between two membranes. The peptidoglycans are protected by the lipid membrane and barely stain.

44
Q

What is a petidoglycan?

A

A complex structural molecule which is part protein, part sugary substance

45
Q

Explain penicillin-like antibiotics.

A

They are known as beta lactam antibiotics and they block cell wall synthesis. The antibiotic grabs hold of the enzyme that connects the peptidoglycans and stops it from building the cell wall, this leads to it falling apart.

46
Q

Why might beta lactam antibiotics not be effective?

A

Some bacteria, such as mycoplasma have no cell wall, and therefore the beta lactam bacteria cannot do its job.

47
Q

What does erythromycin do?

A

It blocks protein synthesis, so it can be used for bacteria with no cell walls.

48
Q

What does rifampin do?

A

It uses RNA/DNA synthesis to kill bacteria.

49
Q

What is spontaneous mutations?

A

Repair mechanisms, which can lead to development of gene variants or gene mutations

50
Q

How does drug resistance develop?

A

Lots of germs and bacteria in the body, few are drug resistant. Antibiotics are then used to kill the bacteria causing the illness, but they also kill good bacteria which protects the body from illness. Therefore, the bacteria that is left is drug resistant and they now grow and take over, and can give their drug resistant’s to other bacteria

51
Q

Explain the transfer of resistance genes.

A

There is conjugation, contact with transfer of resistance genes. the F-pilli then connects two different bacterial cells, and plasmids with resistance factors are physically swapped.

52
Q

What is pharmacogenomics?

A

Genomics approach to personalised medicine. It helps medics and health care professionals target individual care

53
Q

How can gene variants occurring in a patient’s genome influence how they respond to medicines?

A

They can choose the best therapeutic choice, cost benefit predictions, decisions on drug dosing and decisions on drug choice

54
Q

How is genetic variants linked to pharmacokinetics and pharmacodynamics?

A

Gene variants can impact on one or more of the processes in pharmacokinetics and pharmacodynamics. People are different and can process, metabolise and respond to medicines differently.

55
Q

What is microarray technology?

A

A system for identifying different variants of interests that an individual carries. It is a genetic test.

56
Q

How is a microarray test conducted?

A

The participant spits into a tube, and it is tested and the DNA is extracted. The DNA is then put on a microarray and inserted into a reader, the probes of the DNA will bind with the probes in the microarray if they match. The chip then gives a readout of the variants an individual has. This can be used to test and see everyone’s different variants.

57
Q

Define potency of a drug

A

Revere to the concentration of a drug necessary to produce a given response

58
Q

Define efficacy of a drug

A

Refers to a drugs ability to produce the maximum possible effect when it binds to a receptor

Nursing Year 1 (8 decks)

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