Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHYL2064 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

3 main drug targets

A

Receptors, transporters, enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 types of receptors that can be targeted by drugs

A

Ligand gated ion channels

  • Rapid action (milliseconds)
  • Nicotonic, AcH, glycine receptors

G protein coupled receptors

  • Slow signal transduction (seconds to mins)
  • Multiple parts meaning more time for effect
  • When drugs binds to receptor GDP becomes active (GTP) causing activation of downstream targets
  • Receptors can work in different way based on the second messenger pathways present → 1 receptors can couple to different G proteins with different alpha subunits

Kinase linked receptors

  • Very slow response (mins - hours)
  • Communicate to intracellular surface to activate enzyme cascade causing increase in certain output
  • Large signal amplification that will lead to changes at DNA level such as altered gene transcription

Nuclear receptors

  • Very slow response (hours)
  • In cytoplasm waiting for hormones
  • Hormones cross membrane and bind to receptors within cell targets. Migrate together to DNA within the nucleus binding to key sequences in DNA to cause transcription of desired proteins.
  • The resultant mRNA moves into cytoplasm for translation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Transporters as drug targets

A

Can block the reuptake transported on the pre synaptic terminal. Leading in increased time a neurotransmitter is present and thus improving signalling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Enzymes as drug targets

A

Enzymes can be blocked through either competitive inhibition (bind to active site) or non competitive inhibition (bind elsewhere and change shape of active site)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Agonists

A

Agonists bind to a receptor and activate it

Increased amount of agonist can lead to greater response with more receptors, however there will be a concentration at which the max number of receptors have been bound.

  • Full agonist - bind and have full physiological effect
  • low affinity agonist - may not fit as well into the receptor binding sit and comes off faster. Does not activate receptor to the same extent.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

4 types of antagonists

A

Competitive
- Binds to same site as agonist and blocks
- Countered by increasing agonist dose

Non competitive
-Binds somewhere elese and changes the receptor shape
-No change to EC50 (still same effect) but decrease in Rmax

Uncompetitive antagonists
-Receptors become permemently bound to antagonism

Functional/physiological antagonism
-Occurs in tissue due to 2nd messenger pathway
-2 drugs act on different receptors and antagonist the action NA/A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Components of graphical representation
EC50, Potency Efficacy, Therapeutic index

A

EC50 = concentration where drug has 50% of its effect
Potency = increase will mean less drug is needed for same effect
Efficacy = how effective a drug is at activating a receptor
Therapeutic index - when this is low the desired effects and toxic effects are close in concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is ADME

A

(administration)
Absorption
Distribution
Metabolism
Excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Parenteral and Enteral administration

A

Parenteral don’t use GIT (IV, intramuscular, inhalation, subcutaneous)

Enteral do (oral, sublingual, rectal (avoids first pass))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Factors that can effect absorption

A
  • Concentration gradient
  • Lipophilicity of drig
  • Blood flow at the site
  • SA
  • Gut motility (this may be decreased in illness)
  • Formulation/rate of drug release - coating to protect from stomach acid
  • GI tract content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is first pass effect and bioavailability

A

If a drug is taken orally (or enters blood stream) drug will pass through the liver at some point → main place for metabolism of drug

When this happens it will reduce the concentration of drug available to work

Bioavailability is between 100% and 0% (if 0 then cant take orally) → morphine has bioavailability of 20% this means that 80% will be metabolism in the liver before it can access circulation

Bioavailability = the fraction absorbed into the systemic circulation (how much actually makes it into the blood stream)

First pass metabolism effected by liver and gut wall

Can be avoided by administering drug rectally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is volume of distribution

A

Size and comp of patient need to be considered

Volume of distribution = amount in blood concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Distribution and protein binding

A

Once in the blood a drugs ability to work on receptors may depend on amount of proteins within the blood.

The less a drug binds to the proteins in blood the more available it is to work on receptors.

High protein binding will lead to a decrease in free drug. Low protein binding will mean that a drug can more easily traverse cell membranes of diffuse to tissue receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can multiple drugs effect distribution of each other

A

Doses of multiple drugs may need to be considered as decrease one may lead to an increase in available binding proteins and indirectly decrease the dose of another drug. This can also work in reverse were adding a drug may increase the concentration of another.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Importance of bound drugs

A

A bound drug is inactive and may act as a reservoir.

If a medication is extensively bound (99%) then even a small change can have massive effects. (1% → 2% free = doubling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Two types of reactions for metabolism

A
  • Phase 1 reactions - drug may still work (minor change to prepare for next phase)
    • Oxidations
    • Reduction
    • Hydrolysis
      • Each increase the water solubility of resulting metabolite
  • Phase 2 reactions - unable to bind to receptors
    • Glucuronide
    • Glutathione
    • Sulfate
    • Acetate
      • All are large water soluble molecules
      • Metabolites are more highly ionised, water soluble, more likely to be excreted by the liver and kidneys, less pharmacologically active and less toxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Factor that can effect drug metabolism

A
  • Genetics
  • Age
  • Gender
  • Other drugs being taken (induction of inhibition of P450s or other CYP enzymes)
  • Food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are pro drugs

A

Pro drugs = therapeutics that require metabolism to an active metabolite for activity. Codeine is an example

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can drugs effect metabolism of other drugs

A

Many drugs can affect the metabolism of other drugs by inhibiting or reducing CYP enzyme activity and this is a potential problem when drugs are given at the same time which are both metabolised by the same CYP enzymes. Other drugs may induce or stimulate CYP function which may stimulate breakdown of medication.

  • Most CYP enzymes are inducible by drugs and other compounds
  • Results in more rapid metabolism, increased elimination and decreased effect
  • Most common when 2 drugs are metabolised by same enzyme
  • Can result in increased plasma levels and drug toxicity
  • Only relevant for drugs primarily removed from the body by metabolism
  • Significant for drugs with small therapeutic windows
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How can renal disease effect drugs

A

Drugs that are mainly excreted by the kidneys renal disease can lead to increased plasma concentrations.

Drug metabolites are more likely excreted in urine as they are more water soluble and not as likely to be reabsorbed back into the blood stream.

Renal function decreases in elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe local inflammation response

A

Activated macrophages and mast cells at the site of injury release chemical signals causing vasodilation and increase permeability at injury site.

Chemokines release by various kinds of cells attract more phagocytic cells from blood to injury site

Neutrophils and macrophages phagocytose pathogens

Results in redness, heat, pain and swelling → possible loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What controls inflammation (two types of mediators), why is inflammation not instantaneous

A

Controlled by inflammatory mediators which are intracellular chemical messengers released by inflammatory cells. Major mediators include:

  • Eicosanoids - derived of arachidonic acid, include prostaglandins and leukotrienes
  • Histamine - stored in mast cells, mediates allergic reaction. Start initial pulse at time of injury

With the exception of histamine inflammatory mediators are not stored, instead they are synthesised and released in response to inflammatory stimuli. This is why inflammation takes time to occur. It also means that histamine is able to be released quickly and start initial actions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Arachidonic acid and how is it released

A

Arachidonic acid is just stored but in presence of inflammatory stimuli the enzyme Phospholipase A is activated which goes to the phospholipid bilayer to release Arachidonic acid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What two paths can Arachidonic acid take once release

A

Free cytosolic (available for enzymes) Arachidonic acid is then able to follow 2 paths, being acted on by:

  • Lipoxygenase → leukotrienes
  • COX 1 and COX 2 → Prostaglandins and thromboxane

These products are then exported from the cell and activate receptors (normally GPCRs) on nearby cells and/or itself to mediate their effects.

Large diversity of these GPCRs and the effects they may have.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Glucocorticoid MOA

A
  • Carried by transporter glucocorticoid binding protein
  • Binds to glucocorticoid receptor complex which is coupled to two proteins which are dissociated
  • The activated complexed can move into the nucleus and alter gene transcription
  • Increased Lipocortin and decreases COX 2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Anti inflammatory action of SAIDs

A

Lipocortin-1 inhibits phospholipase A2 AND reduces expression of COX enzymes (important for prostaglandins). Results in reduced production of prostaglandins and therefore decreased inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Indications and side effects of corticosteroids (SAIDs)

A

Indications of corticosteroids

  • Transplant rejection
  • Rheumatoid arthritis → injected into joints
  • Inflammatory bowel disease such as chronic or ulcerative colitis
  • Asthma or allergies

Side effects of corticosteroids

  • Immunosuppressive activity increases risk of infections. Plays with the bodies own response. Therefore, only used for short term responses.
  • Worsen diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Overview, 3 main functions of NSAIDs and how

A
  • Inhibit prostaglandin synthesis by inhibiting COX 1 and 2
  • All have the follow 3 effects → anti inflammatory, anti pyretic (lower body temp) and analgesic (reduce pain)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Two different COX enzymes and what they do

A

COX 1 (always active) → Produces protective prostaglandins

  • Coat the the stomach lining with mucus
  • Aid in platelet aggregation (prevent excessive bleeding)
  • Regulate renal blood flow

COX 2 (only in inflammation) → Produce inflammatory prostaglandins

  • Sensitise skin nociceptors
  • Increase body tekp by acting on hypothalamus
  • Recruit inflammatory cells towards injured parts of body
  • Also plays a role in prostacyclin production and renal homeostasis meaning it is also protective
30
Q

How do NSAIDs have an anti pyretic effect

A
  • Body temp controlled by hypothalamus
  • Fever occurs when hypothalamic interleukin-1 (IL-1) generates E type PGs that elevate set point
  • NSAIDs act by interrupting the synthesis of PGE
  • The body then adjust dilation of blood vessel, sweating ect to restore normal temp
31
Q

How do NSAIDs cause pain relief

A
  • It is an indirect effect
  • Reduced inflammation leads to decreased firing of nerves due to less activity
32
Q

Common side effects of NSAIDs (GI, Renal, CV, other)

A

Majority come from inhibition of COX 1

  • GI
    • Inhibition of gastric mucosal production by PGs
    • Blockage of the acid secreting inhibitory effects of PGs
    • Direct irritation of gastric mucosa
  • Renal
    • Reduce renal blood flow, increases toxic effects of drugs
      • Inhibition of PG production that maintains high renal blood flow
  • CV
    • Anticoagulant effects of some NSAIDs can prolong bleeding time
  • Uncommon
    • Skin reaction
33
Q

Aspirin MOA

A

Irreversibly inhibits COX 1 and COX 2 through acetylation

Favours COX 1 (10:1)

34
Q

Aspirin effects on pain, fever and clot

A

Effects on pain and fever:

  • Decrease hyperalgesia after tissue injury → analgesic
  • Anti inflammatory in arthritis
  • PGs in hypothalamus change the set point for body temp to decrease fever

Effects on blood clotting via antiplatelet activity. Inhibits platelet thromboxane synthesis which slows clotting.

Thromboxane is a vasoconstrictor and aids platelet aggregation. By inactivating it, there is a marked
reduction in blood clotting

35
Q

Aspirin consideration

A
  • Aspirin’s preference for COX 1 at low concentration leads to permanent acetylation of COX 1 (inactivation of thromboxane production), may take body some time to replace COX 1.
  • Limited effects on venous clotting
  • Used to prevent arterial clotting in at risk patients (elderly)
  • Don’t use 1 week before surgery.
36
Q

Major side effects of Aspirin

A
  • Blood clotting → risk of internal or excessive bleeding
  • Nephrotoxicity → slow renal blood flow and urine flow
  • Gastric irritation → cam cause gastric ulceration (Major side effect of NSAIDs)
  • Can delay labour in pregnancy (stop taking)
  • CNS effects → tinnitus, confusion, delirium
  • Reye’s syndrome is why its contraindicated in <12 year old and <20 with viral fever
37
Q

Ibuprofen MOA

A

Competitive reversible inhibitor of COX 1 2 ~1:2

38
Q

Ibuprofen effects

A
  • More anti inflammatory effect than aspirin and same thermoregulatory
  • More effect against menstrual pain than other NSAIDs
  • Commonly used to treat rheumatoid arthritis
39
Q

2 pain pathways that are rich with opioid receptors

A

Afferent signalling
- DRG then uses spinothalamic pathway

Descending inhibitory
-Brain to dorsal horn

40
Q

Opioid receptors

A

Present on both pre an post synaptic
Family of GPCRs
3 receptor types but most common are mu (U) which are mostly found pre synaptically

41
Q

Effects of opioid receptors

A

Activation results in decreased AC enzyme function and/or decrease neurotransmitter release it also effects ion channels resulting in hyperpolarisation from increased K efflux and reduced neurotransmitter released (increase intracellular calcium)

Presynaptic activation - inhibition of presynaptic Ca ion channels which reduces neurotransmitter release (remember most are presynaptic)

Post - opening of post synaptic K ion channels causing hyperpolarisation making the receiving neuron less responsive.

Reduced signalling of pain in ascending spinothalamic tract and enhanced functionality of the descending inhibitory tract

42
Q

Spinal cord and supra spinal areas action of opioids

A
  • Spinal cord (ascending) - prevents pain transmission by binding presynaptic u receptors which will decrease CA influx and prevent vesicle release, also binds post synoptically to u receptors increasing K inflex and hyperpolarises post synaptic neuron
  • Supraspinal sites (descending) - activates u receptors on descending GABA releasing neurons in PAG in midbrain inhibiting them. Spinal block of pain.
43
Q

Major side effects of opioids

A

Most come from the U receptor

Respiratory depression
-decreases tidal volume and resp rate
due to decreased stim of resp centers

Pupil
-Miosis (small constricted pupil)
- Little tolerance so useful in diagnosing OD
Occur due to stim of nucleus of CN3

GI
-N/V, tolerance develops to this
-Constipation from increase tone and decreased motility

CV
-Hypotension and vasodilation

44
Q

ADME for codeine and morphine

A
  • Codeine undergoes less first pass metabolism therefore has greater bioavailability
  • Morphine well absorbed in gut and undergoes extensive first pass metabolism in liver
  • Codeine is converted to morphine by CYP2D6 which has large genetic variation
45
Q

Why use codeine

A
  • Codeine doesn’t have an effect until metabolised
  • Codeine in combination with morphine is used to treat moderately sever pain while morphine alone is used to treat severe pain
  • Codeine is used as it is much harder to abuse it also has an Emax meaning after taking a certain amount the effects will not increase as the dose increases
  • As morphine is far more potent is it harder to make small increases → morphine is much easier to monitor levels by using codeine
46
Q

Strong and moderate agonists in relation to pain

A
  • Strong agonists in humans are well tolerated which given in a dosage that is aimed at relieving sever pain
  • Moderate agonists have intolerable side effects which given at a dose aim at sever pain
  • Lower concentrations of moderate agonists are often coupled with NSAIDs for treatment of pain
47
Q

Morphine

A
  • Partial agonist on u receptors
  • Tolerance is a key factor in long term use
  • Used for server pain
48
Q

Fentalyn

A

Made into a patch to provide continuous pain relief → this is possible due to high potency and lipid solubility

50 - 100 times more potent than morphine

49
Q

Methadone

A

Used to treat opioid or heroin addiction or chronic pain

Does not cause euphoric effects

Delivered orally to limit needle sharing and transmission

Given once a day to control withdrawal → postpones withdrawal effects

50
Q

Pethidine - synthetic moderate

A

Tends to cause restlessness, euphoria but no miosis

Preferred to morphine during labour as it does not affect uterine smooth muscle function

51
Q

Buprenorphine

A

Partial agonist for u

Ceiling effect exists for respiratory depression making it safer as addicts are less likely to overdose

Combined with naloxone (poorley absorbed sublingually and orally but well absorbed when injected IV) meaning that addicts wont inject the table otherwise they will get withdrawal symptoms

52
Q

Antagonists - naloxone and naltrexone

A

Competitive antagonists competing with opioid for opioid receptor binding sites

naltrexone is longer lasting

53
Q

Risk factors for parkinson’s

A

Risk factors:

  • Age is most important risk factor >60
  • Family history
  • Male gender

Smoking and caffeine have been associated with lower rats of Parkinson’s

54
Q

Presentation of parkinsons

A

TRAP is a good way to remember presentation:

  • Tremor at rest
  • Rigidity of limbs
  • Akinesia (harder to start movement)
  • Postural problems

Rigidity → excess weight to every muscle
Normally one side of the body is affected first

Without treatment it can progress over 5-10 years where the patient will end up in a rigid akinetic state → death may result from immobility, aspiration, pneumonia or embolism

Symptoms → swallowing problem, indistinct speech (muscle), weight loss (lots of energy to move)

55
Q

CNS changes with parkinson’s

A
  • Degeneration in neural tract that goes from substantia nigra to the basal ganglia (putamen and caduate)
  • Death of neurons means that there is a loss of pigmentation in the region
  • Substantia nigra is major origin of dopaminergic innervation of striatum → regulate posture and muscle tone
  • About 60-80% loss of dopaminergic neurons before motor symptoms are seen
  • The end result is decreased inhibition of striatum resulting in increased AcH and therefore GABA release causing the rigidity
56
Q

4 drug types for Parkinson’s

A

Drugs that form DA
Drugs that inhibit metabolism
DA receptor agonists
Other

57
Q

Drugs used that form DA

A

L-DOPA
- Can cross BBB
- Converted to DA by dopaminergic neruon
- MOstly converted in GI tractn
Carbidopa prevents L-DOPA conversion by inhibiting Decarboxylase enzyme

Adverse effects: depression, nausea, vomiting, mood changes, low blood pressure, constipation, sleepiness

Some patient also experience very noticeable on/off states meaning they have very good control in the on state but once the drug wears off they have severe motor features → this can be due to variable drug absorption and transit across the BBB.

58
Q

Why cant dopamine be used for treatment

A

Dopamine cant cross the BBB when its given orally

59
Q

What are dyskineasas

A

Dyskinesia’s which are involuntary twisting hyperkinetic movements occur when L-dopa is at its peak dose → the brain is unable to cope with the increase in L-dopa at points. Meaning there is a balance between adverse effects and optimal control

60
Q

Drugs that inhibit metabolism of DA and their side effects

A

MOA - B inhibitors

Slow normal degradation of dopamine in the brain and preserve it for recycling into vesicle

Rasagiline

Adverse effects:

  • GI side effects, Aching joints, Depression, Dry mouth, Insomnia, Dizziness, Hallucinations, Indigestion, Headaches

COMT inhibitors

May counteract fluctuation of L-DOPA

Entacapone

Adverse effects

  • may increase dyskinesias seen with L-DOPA, sleepiness, nausea, loss of appetite, diarrhea, dizziness, dry mouth, headaches.
61
Q

Dopamine receptor agonists

A

These drugs are less powerful than L-DOPA in controlling symptoms of PD but they’re also less likley to cause dyskinesias. However if patient already has dyskinesia’s, agonists can make them worse.

Aimed at specific D receptors

Side effects: drowsiness, nausea, vomiting, dry mouth, dizziness, hallucinations – should resolve in a few days

62
Q

What is brain stim and its advantages

A

Brain stimulation targeted at subthalamic nucleus or globulus pallidus interna → suppress the disabling dyskinesia of L-DOPA treatment in latter stage PD

The electrical current inhibits cell bodies and excites axons. It also promotes astrocytes to release Ca2+, which leads to the release of glutamate and adenosine

Advantages:

  • Adjustable stimulation parameters make it patient specific
  • an be activate 24hr a day
  • Surgery on both side of brain
63
Q

Types of ADRs

A
  • Type A - acute, predictable, related to MOA or ADME
    • Concentration dependent!!! (which is why they’re predictable) → dealt with by reducing the dose
    • Drug metabolism is also a significant factor for TA → taking other medications at the same time can create competition for metabolising enzymes leading to increased concentrations → drugs competitively inhibit the metabolism of each other
    • Drugs can also induce the metabolism of other drugs
  • Type B - Bizarre, unpredictable, not necessarily related to MOA but may involve patient qualities
    • Rarely seen in trials
    • Factors contributing to these ADRs include receptor or metabolic abnormalities or drug allergy
  • Type C - Chronic or continuous effects
    • These occur as a response to long term (chronic) use
    • May be due to drug tolerance or receptor changes due to physical dependence
  • Type D - Delayed
    • Delayed until after pregnancy
  • Type E - End of treatment effects
    • Rebound effect → normally the opposite of the drug effects. This is due to the re-sensitisation and re-regulation of receptors of CNS and PNS
64
Q

What is hepatotoxicity

A

Hepatocytes are a predominant site for cytochrome P450 (CYP) enzymes which metabolise drugs to reactive metabolites. Drug metabolites may become concentrated in the kidney renal tubules which may be toxic.

Hepatotoxicity

Paracetamol can cause this. After a night of alcohol consumption CYP enzymes are induced which convert paracetamol to the reactive metabolite NAPBQI. This metabolite then initiates the mechanisms of cell damage/death

Symptoms of this:

Phase 1 (0-24h): nausea and vomiting
Phase 2 (24-72h): right upper quadrant Pain, elevated liver enzymes
Phase 3 (72-96h): Vomiting, symptoms of liver failure, renal failure, pancreatitis
Phase 4 (>4 days): resolution of symptoms or progression to fatality

65
Q

Two mechanisms for drug tolerance

A

Prolonged exposure of receptors to an agonist drug can lead to decrease in effect or response as receptor numbers and signalling can change

Good example is opioids

Two major mechanisms in which this occurs:

  • Receptor uncoupling (desensitisation)
  • Receptor loss (down regulation)

Meaning that over time increasing the dose to counter this may also increase risk of unwanted effects.

66
Q

Anti inflam on SAIDs

A

Lipocortin-1 inhibits phospholipase A2 AND reduces expression of COX enzymes (important for prostaglandins). Results in reduced production of prostaglandins and therefore decreased inflammation

67
Q

Side effects of SAIDs

A
  • Immunosuppressive activity increases risk of infections. Plays with the bodies own response. Therefore, only used for short term responses.
  • Worsen diabetes
68
Q

Action of COX 1

A

COX 1 (always active) → Produces protective prostaglandins

  • Coat the the stomach lining with mucus
  • Aid in platelet aggregation (prevent excessive bleeding)
  • Regulate renal blood flow
69
Q

Action of COX 2

A

COX 2 (only in inflammation) → Produce inflammatory prostaglandins

  • Sensitise skin nociceptors
  • Increase body tekp by acting on hypothalamus
  • Recruit inflammatory cells towards injured parts of body
  • Also plays a role in prostacyclin production and renal homeostasis meaning it is also protective
70
Q

Side effects of NSAIDs

A

Majority come from inhibition of COX 1

  • GI
    • Inhibition of gastric mucosal production by PGs
    • Blockage of the acid secreting inhibitory effects of PGs
    • Direct irritation of gastric mucosa
  • Renal
    • Reduce renal blood flow, increases toxic effects of drugs
      • Inhibition of PG production that maintains high renal blood flow
  • CV
    • Anticoagulant effects of some NSAIDs can prolong bleeding time
  • Uncommon
    • Skin reaction

PHYL2064 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions