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Applied Pharmacology Flashcards

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1
Q

What is analgesic?

A

Drug that relieves or reduces pain

Control of symptoms and improvement of patients quality of life.

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2
Q

What does the NSAIDs mean?

A

Non-steroid anti-inflammatory drug

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3
Q

What is the arachidonic acid cascade?

A

Mechanism explaining NSAID action (include side effects)
Main action is to block COX enumerated

  • Arachidonic acid -fatty deposit
  • Cyclooxyrgenase (COX) act on arachidonic acid
  • convert AA to intermediates NSAID - competitive inhibition of COX enzymes stop cascade
  • Other cell/tissue specific enzymes – convert intermediates to prostanoids
  • Prostanoids – product (examples prostaglandins (activate the nociceptive receptors) and thromboxane)
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4
Q

What does NSAID do in the arachidonic acid cascade?

A
  • intermediate NSAID
  • competitive inhibition of COX enzymes
  • attach to binding sites
  • stop cascade
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5
Q

What are the different types of COX enzymes?

A

COX 1
COX 2
COX 3

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6
Q

What does COX 1 enzyme do?

A

COX 1 – most tissue/ cell – mainly endoplasmic reticulum – gastric protection, blood flow and platelet aggregation.

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7
Q

What does COX 2 enzyme do?

A

COX 2 – mast cells, fibroblasts, macrophages 0 endothelial cells – more in nuclear membrane – inflammation, pain and fever

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8
Q

What does the COX 3 enzyme do?

A

COX 3 – Mainly found in CNS – animal models – poor understanding – may not be active in humans

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9
Q

Explain binding selectivity of NSAIDs?

A

Different NSAIDs more actively attach to the different COX enzymes

Ketoprofen – more COX 1 selective
Celecoxib – more COX 2 selective

Aspirin and Fenoprofen – equally selective

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10
Q

NSAID mechanism of action - 4 main therapeutic effects

A
  1. Anti-inflammatory
  2. Analgesic (reduce pain)
  3. Antipyretic (prevent or reduce a fever)
  4. Platelet aggregation
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11
Q

Whats Special about aspirin binding to arachidonic acid binding site?

A

Irreversible binding to arachidonic acid

Other NSAIDs are usually reversible

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12
Q

What are the anti-inflammatory effects of NSAIDs?

A

-Inhibit COX-2 derives prostaglandins (powerful vasodilators)
- reduced vasodilations
- reduced oedema
- reduced swelling
- reduced redness
- reduced neurogenic inflammation
Promote release of other vasodilators (substance P and histamine)

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13
Q

What is the analgesic effects of NSAIDs?

A
  • Inhibit COX-2 derived prostaglandins
  • Reduced peripheral and central sensitisation of free nerve endings

So – reduce prostaglandin production, reduced transmitter release, reduced 2nd order neuron sensitivity

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14
Q

What are the antipyretic effects of NSAIDs?

A

-Pyrogens – stimulate PGE2 in hypothalamus
- PGE2 – inhibits temperature sensitive neurons
- NSAIDS – reduce PGE2 production by binding to COX-2

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15
Q

What are the platelet aggregation effects of NSAIDs?

A

-Good COX-1 selectivity – covalent binding (non reversible as covalent
binding)
- COX-1 inhibition reduces thromboxane A2 production (a prostanoids end of Arachidonic acid cascade)
- Platelet never recover =ability to aggregate
- New platelet production required

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16
Q

State the side effects of NSAIDs

A
  1. Gastrointestinal prostaglandins promote production of alkali mucus – NSAID blocks prostaglandin production, aspirin induced gastritis and alteration side effects)
  2. Respiratory
  3. Renal
    Liver
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17
Q

What are the effects of COX-2 enzyme?

A

More prevalent
- Inflammation, pain and fever
Less prevalent
Gastric protection, blood flow and platelet aggregation

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18
Q

Whats pros and cons of COX-2 selective NSAIDs?

A

pros
- Fewer gastric complications
- Reduced effects on platelet aggregation

cons
- Evidence of reduced analgesia
- Increased thrombin/ cardiovascular risks associated

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19
Q

Explain the Respiratory side effect of NSAID?

A
  • Aspirin induced asthma
  • When tissue injury and arachidonic acid produced lipoxygenase enzymes also act to produce leukotriene which is a bronchi constrictor
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20
Q

Whats the renal side effects of NSAIDs?

A
  • Block prostaglandin production reduces renal filtration and sodium retention.
  • Preventing the vasodilation which promotes glomerluar filtration – reduced filtration
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21
Q

What is the liver damaged caused by NSAIDs?

A
  • Low incidence – multiple mechanisms postulated
    1.retention of bile (cholestasis)
    2. Mitochondrial damage
    3. inhibition of prostaglandin E2 production
    4. Reactive metabolites
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22
Q

Whats the effect of paracetamol?

A

-Pain relief/ antipyretic effect
- non-opioid (Not really an NSAID)
- poor peripheral COX1/2 inhibition
- Target COX2 in CNS (maybe also COX3)
- Does not inhibit platelet aggregation
- Doesn’t damage gut mucosa

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23
Q

Whats the pros of paracetamol?

A

Does not inhibit platelet aggregation
- Doesn’t damage gut mucosa

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24
Q

Whats the pharmacokinetics of paracetamol?

A

Paracetamol effected on my cytochrome
Cytochrome P450 – NAPQ1 (very toxic to liver)
But almost immediately effected on by Glutathione (limited amount of production in body) to make Glutathione conjugate

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25
Q

How is paracetamol overdose easy?

A

Very toxic NAPQ1

Converted by glutathione which is limitedly produced in a day so must not exceed the supply other liver damage and down to DNA damage.

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26
Q

What is a mild opioid?

A

Compound resembling opium
Mainly work by weakly activating opioid receptors and have lower efficacy at the receptors

  1. Bind to specific opioid receptors
  2. Mimic action of endogenous peptide neurotransmitters
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27
Q

What are the three categories of opioids?

A
  1. Natural – occur biosphere
  2. Semisynthetic – chemical derivative
  3. Synthetic – noval man-made molecular structure
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28
Q

State the three different opioid receptors

A

Delta and mui receptors – supraspinal – spinal and peripheral – euphoric feelings

Kappa receptor – spinal

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29
Q

What are G-protein coupled receptors?

A

Cascade effect on these protein receptors

Down regulation of nerve cell excitability – reduce experience of pain

30
Q

What is the spinal cord molecular mechanism?

A
  1. Negatively adjust the voltage gated calcium channels in presynaptic – decrease activity
  2. Increase activity of voltage gated potassium channels in post-synaptic cell to reduce excitatory of 2nd order neurone

Reduction in nociceptive signals to the brain as pre and post synaptic cells are less excitatory.
Decrease neuronal excitability
Decreased sensitivity of synapses

31
Q

Peripheral general mechanisms of opioids?

A

-delta opioid receptor located in free nerve endings
- activated – reduces 1st order nociceptor sensibility
- reduce the magnitude of the signals to brain

32
Q

What is the central analgesia mechanism for opioids?>

A

Perception of signals that arrive in the brain distorted
The widespread effects on nociception and pain perception

-Spinal – inhibition of nociception
- supra spinal effects – lambic system and brain stem
- nociception receptors – descending control

33
Q

What is codeine?

A

Slow metabolisers of CYP2D6 or fast

Respiratory depression
GI motility

Codeine converts in liver by cytochrome into morphine

34
Q

What is a strong opioid?

A

Morphine analogues – morphine
Synthetic derivatives – fentanyl

String agonist of opioid receptors with high potency and good efficacy

35
Q

What are the side effects and complications of strong opioids?

A
  • Constipation
  • Depression of cough reflex
  • Respiratory depression
  • Nausea/vomiting
  • Tolerance effect – adapt 2nd messenger cascade
  • Euphoria
  • Physical dependency
36
Q

What are the long term side effects of strong opioids?

A
  • Possible immune suppression
  • Decreased sex hormone production
  • Opiate induce hyperalgesia
37
Q

What are some musculoskeletal uses of corticosteroids?

A

Intra articulation
Burial
Tendon sheath
Topical creams
Epidural
Soft tissue injection eg. Intramuscular
Oral/ inhaled

Very powerful drugs can cause depression

38
Q

What do corticosteroids do?

A

Pain relief
Improve function and mobility
Temporarily

39
Q

What is cortisol?

A

Principle human glucocorticoid

Diurnal production profile – peaks in early morning

40
Q

What are some adverse effects of glucocorticoid (cortisol)?

A
  1. Promote normal intermediary metabolism
  2. Promote gluconeogenesis – stress adaptation
  3. Redistribute immune cells – lymphoid tissue
  4. Regulate kidney filtration
  5. Potent ant-inflammatory and immunosuppressive actions
41
Q

How do corticosteroids effect prostaglandins?

A

Corticosteroids inhibit arachidonic acid production
Blocks the. Arachidonic acid cascade
(stop prostaglandins which play key role in nociception)

42
Q

How do corticosteroids effect inflammation?

A

Anti inflammatory action

  1. Blocks the arachidonic acid cascade
  2. Reduce availability of lymphocytes
  3. Inhibit macrophages/ lymphocyte excitatibility
  4. Decrease production of pro-inflammatory chemicals eg. Cytokines
  5. Inhibit mast cells - histamine
43
Q

General mechanism of action of corticosteroids?

A
  • Intracellular target
  • They are lipid soluble so can diffuse through cell membrane to bind to receptor
  • Specifically cytoplasmic steroid receptor (dimerisation) – receptor activated forms a ‘dimer’
  • Dimer enters the nucleus
  • Bind to glucose-corticosteroid response element – stimulate or in it activity of pro motor which:
    1. Regulation of gene transcription
    2. Regulation of key protein production
44
Q

What are the actions after corticosteroids bind?

A
  1. Regulation of gene transcription
  2. Regulation of key protein production
45
Q

Major side effects or complications of corticosteroids

A
  • Inhibit hypothalamic, pituitary, adrenal axis
  • Acute withdrawal
  • Adrenal insufficiency
  • Negative calcium balance – after long term – osteoporosis (increase osteoclast cells (break down in bone tissue) and inhibit osteocyte survival to manage bone tissue cell)
  • Increased risk of diabetes –due to increased gluconeogenesis in liver – increased glucose production – increased bone fracturing
  • Emotional disturbances – euphoria or depression
  • Increased risk of infection - impaired wound healing – down regulate the immune system
  • Gastro ulcer increased risk
46
Q

Pharmacokinetics of corticosteroids

A
  • Absorption/distribution – highly lipid soluble
  • Plasma binding – approx 90%
  • Metabolism – oxidation in liver, conjugated to glucuronic acid or sulphate
  • Excretion – predominantly renal, insignificant faecal route
47
Q

Adverse effects of local anaesthetics

A

to block voltage gated sodium channels
If hits a blood vessel goes to heart and blocks channels there and can inhibit its ability to pump

Especially bupivacaine – very dangerous and very active M

48
Q

Mode of action of local anaesthetics

A

Block voltage-gated sodium ion channels
- Block ability of nerve cells to carry action potentials – to stop activation of free nerve endings – stop pain response to brain
- Inject local anaesthetic around the nerve – as lipid soluble they diffuse into the axon cells to block the channels
- Local anaesthetic binding site to channel to inhibit movement of sodium

49
Q

Block ability of nerve cells to carry action potentials

what is the result?

A

– to stop activation of free nerve endings – stop pain response to brain

50
Q

what’s the result of injecting local anaesthetic around the nerve?

A

– as lipid soluble they diffuse into the axon cells to block the channels

51
Q

Explain Drug partitioning in case of local anaesthetics

A
  • Local anaesthetic diffuse into the cells over plasma membrane
  • Ph of tissue effects the proportion of the local anaesthetic that is ionised and so can still cross membrane – about 50% remain uncharged
  • pH means some become charged and so can’t diffuse
  • pH inside cell is also different and so charges some more particles of anaesthetic – 1:5 and are trapped inside the cell
  • overtime block the nerve concentration of local anaesthetic builds up in order to have a larger effect on channel as more can not leave every time
52
Q

Mechanism of action – complications of local anaesthetic

A

Decreasing pH facilitated ionisation
Leads to inflammatory acidosis – inflammation changes the pH of tissue
This facilitates the ionisation of anaesthetic
Stops more apathetic being able to diffuse into the axon cell
So can’t block the action potentials
Effects drug partitioning

Should inject anaesthetic into non inflamed areas.

53
Q

Define antibiotic

A

Killing of microorganisms and bacteria – inhibit growth of bacteria
No action on viruses

Not very unique – general action

54
Q

Explain the structure of prokaryotes cells eg. bacteria

A
  • no nuclear envelope
  • Structural/defensive cell wall
  • Some have a capsule
  • Have plasma membrane
  • Genophore. DNA – loose in cytoplasm
  • Ribosomal production of structural. Enzymatic and signalling protein
  • Plasmid DNA – circular transmissible elements – normally where resistance is found
  • Pila, cell recognition/ adhesion
  • Some have Flagellum – motility
55
Q

Explain the structure of Bacteria – cell walls – gram-positive bacteria

A
  • Preptidoglycan cell wall
    Heavy outer cell wall
56
Q

Explain the structure of Bacteria – cell wall – gram – negative bacteria

A
  • Outer membrane
  • Peptidoglycan cell wall
    Peptidoglycans protected by lipid membrane
    Not accessible to many antibiotics
57
Q

What is a peptiglycan?

A
  • Complex structural molecule
  • Part protein part sugary substance
  • Make up cell wall of. Gram-positive bacteria
    Antibiotics target the cell wall – peptidoglycan to destroy cell – eg. Penicillin
58
Q

What is the Mechanism of action – penicillin like antibiotics – gram positive?

A

-Drugs bind transpeptidase
Which disrupt cross-linking of peptidoglycans
Disrupts cell wall stability
Leads to cell lysis

Beta lactam – antibiotics block cell wall synthesis – act on bacteria cell wall – makes the bacteria cell burst as cell wall is broken down

59
Q

What are the Adverse reactions of antiobitic
Non specific effects – gram positive ?

A
  • Hypersensitivity – allergy eg. Penicillin agent
  • Diarrhea – due to changes in pH due to antibiotic
  • Nephritis – kidney – inflamed – change water absorptions
  • Neurotoxicity
60
Q

What antibiotics available for gram negative?

A

Not effected by non-specific as it has a lipid membrane so antibacteria can not effect it
Some bacteria also don’t have cell wall Eg. Mycoplasma or chlamydia – no cell wall – antibiotics not effective

61
Q

Whats the general action of erythromycin?

antibiotic

A

Different mechanism of action
Also useful if allergy to beta lactams eg. Penicillin
Useful against bacteria with no cell wall – eg. Mycoplasma, chlamydia

62
Q

What’s the mechanism of action for the antibiotic erythromycin?

A

Blocks protein synthesis
- Block crucial binding pore – ribosomes translate RNA – so leads to cell death
- As no proteins are made and cells die

63
Q

Whats the Alternative mechanisms of action for antibiotics?

A

Target RNA/DNA synthesis
Target metabolism
Target plasma membrane
Target cell wall – peptidoclycans
Target protein synthesis

64
Q

How does antibiotic resistance give bacteria an advantage?

A

Spontaneous mutations – genetic variability and reproduction in minutes
Acquisitions of new genes – acquire from other bacteria around them
Natural selection – survival of the fittest bacteria – mutations give advantage over other bacteria that is killed off
Main career of humans to spread

65
Q

What’s the process of antibiotic resistance?

A
  1. Lots of germs a few being resistant
  2. Antibiotics kill bacteria causing illness as well as good bacteria so protect body from infection
  3. Drug resistant bacteria now allowed to grow and take over – reproduction
  4. Some bacteria give drug resistance or other bacteria causing more problems
66
Q

Whats the key issue with antibiotic drug resistant?

A

Not controllable
Capitalise on selective advantage and spread uncontrollably
Must continue to use dose and duration – to prevent living of bacteria which reproduce and vary

67
Q

Explain the transfer of resistance genes between bacteria cells

A
  • Conjugation – cell to cell contact with transfer of resistance genes
  • F-pili connect two different bacterial cells
  • Plasmids with resistance factors physically swapped
  • Promiscuous plasmids – cross species
  • Bacterial viruses can transfer of resistance genes
  • Single nucleotide polymorphisms – evolution of bacterial genes to confer resistance
68
Q

How does gene variants lead to beneficial changes to protein function?

A
  • Alteration in anti microbial drug target site ;
  • Decreased uptake of drug due to changes in membrane permeability
  • Increased effluent of the drug
  • Antibiotic-inactivating enzymes – can destroy the antibiotic – eg, beta lactamase from penicillins
69
Q

Define- pharmacogenomics

A

Gene variants occurring in a patients genome can influence how they respond to medicines

As each individual processes, metabolises and responds to drugs and medicines in a different way.

70
Q

What are the factors benefited by pharmacogenomics?

A
  1. Best therapeutic choice
  2. Cost-benefit predictions for individual patients
  3. Decisions on drug dosing
  4. Decisions on drug choice
71
Q

What effects does genetic variability have on drug prescription?

A

Individual likely to drive differences in pharmacodynamics and pharmacokinetic processes.

Eg. Metabolism (gene variant SNPs affect rate of metabolism in CYP2D6 gene, vary in activity of metabolism eg. Ultra rapid, normal, poor), absorption differences

72
Q

What is arachidonic acid?

A

Arachidonic acid – a fatty substance released when cells/tissues are damaged

NSAID Stop this effect cascading

Applied Health Science (11 decks)

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