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GRACE Phase 2a Medicine > ICS - Pharmacology and Prescribing > Flashcards

ICS - Pharmacology and Prescribing Flashcards

1
Q

Pharmacokinetics

A

How the body affects the drug - absorption, distribution, metabolism, excretion (ADME)

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2
Q

Drug interactions - synergy

A

interaction of drugs such that the total effect is GREATER than the individual effects

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3
Q

Drug interactions - antagonism

A

A substance that acts AGAINST and blocks an action (i.e. two drugs that oppose each other)

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4
Q

Drug interactions - summation

A

different drugs used together to have the same effect as a single drug would

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5
Q

Drug interactions - potentiation

A

enhancement of one drug by another so that the combined effect is greater than the sum of each one alone

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6
Q

Pharmacokinetics - absorption (variables of)

A
  1. Motility - if the gut has slowed digestion, the drugs won’t work a well
  2. Acidity
  3. Vascularity
  4. Surface area
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7
Q

Pharmacokinetics - distribution

A

Drugs reversibly leave the bloodstream and enter the ECF and tissues, factors affecting e.g. blood flow, capillary permeability

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8
Q

First order drug metabolism

A

Rate of metabolism of drugs is proportional to drug concentration, constant half-life of elimination

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9
Q

Zero order drug metabolism

A

Rate of metabolism is constant regardless of drug concentration

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10
Q

Phase 1 drug reactions

A

CYP450, oxidation, hydrolysis, etc.

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11
Q

Phase 2 drug reactions

A

Conjugation reactions, make the drug more hydrophilic, e.g. glucoronidation

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12
Q

Pharmacodynamics

A

What the drug DOES to the body

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13
Q

Potency

A

measure of how well a drug works

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14
Q

Agonist

A

Compound that binds to a receptor and activates it

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15
Q

Antagonist

A

Compound that reduces the effect of an agonist, do NOT activate receptors

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16
Q

Signal transduction (cell signalling)

A

Transmission of molecular signals from a cells exterior –> interior, initiated by binding of a molecule to a cells surface receptors

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17
Q

Cholinergic receptors

A

ACh binding, two types: muscarinic and nicotinic

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18
Q

Affinity describes how well a ligand

A

Binds to a receptor

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19
Q

Efficacy describes how well a ligand

A

activates a receptor

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20
Q

PK - ADME

A

absorption, distribution, metabolism and excretion

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21
Q

Drug targets

A

Receptors, enzymes, ion channels, transporters

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22
Q

Types of receptor

A
  1. Ligand-gated ion channels
  2. G protein coupled receptors
  3. Kinase-linked receptors
  4. Cystolic/ nuclear receptors
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23
Q

Nicotinic ACh receptors are of what type?

A

Ligand-gated ion channels

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24
Q

Beta-adrenoreceptors are of what type?

A

G-protein coupled receptors

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25
Q

Kinase-linked receptors are receptors for?

A

growth factors

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26
Q

Cystolic/ nuclear receptors

A

modify gene transcription

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27
Q

Steroid receptors are

A

cystolic/nuclear receptors

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28
Q

Two types of cholinergic receptors?

A

nicotinic and muscarinic

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29
Q

What is meant by EC50

A

concentration of a drug that gives half the maximal response

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30
Q

Signal amplification

A

To increase the strength of a signal

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31
Q

Allosteric modulation

A

When an allosteric ligand binds to a different site on the molecule and prevents the signal being transmitted

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32
Q

Tolerance

A

The reduction in drug (agonist) effect over time, seen with continuous repeated high concentration use

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33
Q

Enzyme inhibitor

A

Molecule that binds to an enzyme and decreases its activity, it prevents the substrate from entering the enzyme’s active site and prevents it from catalysing its reaction

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34
Q

Irreversible enzyme inhibitors

A

react with enzyme and change it chemically

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35
Q

reversible enzyme inhibitors

A

bind non-covalently and different types of inhibition are produced depending on whether these inhibitors bind to the enzyme, the enzyme-substrate complex, or both

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36
Q

NSAIDs inhibit which enzyme?

A

COX

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37
Q

COX is responsible for the

A

breakdown of arachidonic acid to prostaglandin H2

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38
Q

Two iso-forms of COX

A

COX-1 and COX-2

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39
Q

How do NSAIDs work?

A

Preventing arachidonic acid from reaching the active site of the COX enzyme and thus from being broken down into prostaglandin H2 - competitive inhibition

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40
Q

How does aspirin affect the COX enzyme?

A

Irreversibly blocks the active site

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41
Q

ACE inhibitor examples

A

captopril, enalapril

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42
Q

How do ACE inhibitors work as antihypertensives?

A

Inhibit ACE enzyme, thereby preventing the conversion of angiotensin I to angiotensin II, therefore less vasoconstriction and less aldosterone released by the adrenal cortex

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43
Q

Drugs that target transporters?

A

Proton-pump inhibitors (PPIs), diuretics, neuronal uptake inhibitors

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44
Q

Uniporters

A

transporters that use energy from ATP to pull molecules in

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45
Q

Symporters

A

transporters that use movement in of one molecule to pull in another molecule against its concentration gradient

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46
Q

Antiporters

A

transporters that moves one substance against its gradient, using energy from the second substance moving down its gradient

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47
Q

Examples of PPIs

A

omeprazole, lansoprazole

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48
Q

Where are PPIs all activated?

A

In the acidic stomach environment

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49
Q

Diuretics act to inhibit?

A

symporters, can inhibit the NKCC2 pump on the thick ascending part of the loop of Henle, therefore reducing the amount of Na+, Cl- and K+ ions able to move into the medullary interstitium, therefore less water is reabsorbed and more passes out via the urine

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50
Q

Ion channels as drug targets

A

Calcium channel blockers, local anaesthetics

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51
Q

Examples of CCBs

A

amlopidine, verapamil

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52
Q

CCBs are used to treat?

A

hypertension

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53
Q

How does amlopidine work?

A

blocks calcium channels found in cardiac and smooth muscle, thereby preventing an influx of Ca2+, less vasoconstriction

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54
Q

Simply, how do local anaesthetics work?

A

interrupt axonal transmission by blocking voltage gated sodium channels and preventing neurones from depolarising - do not meet threshold and therefore AP cannot propagate

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55
Q

Passage of drug across the membrane?

A

Passive diffusion through the lipid layer, diffusion through pores/ ion channels, carrier mediated processes, pinocytosis

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56
Q

Bioavailability

A

amount of drug taken up as a proportion of the amount administered

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57
Q

Drug absorption - oral

A

Large SA and high blood flow of small intestine can give rapid and complete absorption of oral drugs

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58
Q

Obstacles of oral drug absorption

A
  1. Drug structure - drugs need to be lipid soluble and stable at a low pH
  2. Drug formulation - must be able to disintegrate and dissolve for absorption
  3. Gastric emptying - rate of which determines how soon a drug taken orally is delivered to the small intestine
  4. First pass metabolism - drugs taken orally have to pass 4 major metabolic barriers to reach circulation: intestinal lumen, intestinal wall, liver, lungs
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59
Q

Intradermal and subcutaneous absorption

A
  • avoids barrier of stratum corneum
  • limited by blood flow
  • use for local effect
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60
Q

Intramuscular absorption

A
  • depends on blood flow and water solubility

- bioavailability close to 1

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61
Q

Inhalational absorption

A
  • Large SA and high blood flow
  • Limited by risk of toxicity to alveoli
  • Largely restricted to volatile drugs
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62
Q

Protein binding absorption

A
  • Many drugs can bind to plasma/tissue proteins
  • Common reversible binding to albumin
  • Binding lowers the free concentration of the drug and can release the drug when the plasma concentration is low
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63
Q

Half life

A

Time taken for concentration to reduce by half

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64
Q

Elimination of a drug is from which compartment?

A

Plasma

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65
Q

Elimination route for most drugs?

A

Renal/ hepatic

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66
Q

Define clearance

A

Volume of plasma that can be completely cleared of a drug per unit time or per unit plasma concentration

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67
Q

Formula for clearance

A

Rate of appearance in urine/ plasma concentration

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68
Q

Marker substance for measuring renal clearance

A

Creatinine

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69
Q

Problem with renal failure and drug elimination?

A

Patient will not be able to eliminate drug for weeks

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70
Q

Criteria for most drugs eliminated by the kidneys?

A

Water soluble and small

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71
Q

For patients with renal impairment you might choose drugs which are eliminated by the

A

liver

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72
Q

What is the hepatic extraction ratio (HER)?

A

Proportion of drug removed by one passage through the liver

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73
Q

What is meant by high HER?

A

high removal of drug by liver, so that clearance is only limited by the hepatic blood flow

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74
Q

What is meant by low HER?

A

low removal of drug so the process is slow and inefficient

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75
Q

How does the liver adapt when exposed to a low HER drug?

A

produce more enzymes to enable it to increase clearance

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76
Q

Where do most phase 1 drug metabolism reactions occur?

A

SER

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77
Q

CYP 450 is what type of enzyme? Found where? Involved in what reactions?

A

Microsomal, SER, phase 1

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78
Q

Minimal effect of drug metabolism by liver until at least what % of the liver is lost?

A

70

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79
Q

Why are IV infusions used?

A

Enables steady state plasma levels to be maintained (drug intake is in equilibrium with elimination) and highly accurate drug delivery, quickest administration, 100% bioavailability

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80
Q

Limitations of IV infusions?

A

Require monitoring, potential for calculation errors, dosage based on body mass (problematic with extreme body weights)

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81
Q

Pharmacokinetic considerations of a IV drug infusion with a high volume of distribution?

A

Means there will be a small fraction in the plasma and so it will take a long time to reach a steady state

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82
Q

Adherence

A

Extent to which a patient’s actions match agreed recommendations

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83
Q

What % of prescribed medicines are not taken per year? (Costing the NHS £12.9 billion a year)

A

30-50%

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84
Q

What is meant by compliance?

A

Assumes doctor knows best, passive patient, patient follows doctors instructions

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85
Q

What is meant by adherence?

A

Acknowledges the importance of the patient’s beliefs but recognises that the healthcare professional is still the expert in conveying their knowledge

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86
Q

Necessity beliefs

A

perceptions of personal need for treatment

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87
Q

Key points about patient-centered approach

A
  • Shift in focus from treatment to process of care (holistic approach)
  • Philosophy of care that encourages focus in the consultation on the patient as a whole person who has individual preferences, and also a shared control of the consultation, decisions about intervention
88
Q

Good doctor-patient communication outcomes? (4)

A
  1. better health outcomes
  2. higher adherence to therapeutic regimes in patients
  3. higher patient and doctor satisfaction
  4. decrease in risk of malpractise
89
Q

Improving communication

A
  • adapt consultation style to patient’s needs

- encourage patient to ask questions

90
Q

Increase patient involvement

A
  • Explain condition, pros and cons
  • Clarify what the patient hopes to achieve from treatment
  • Record the decision if the patient decides NOT to take the medicine
91
Q

Understand the patient’s perspective

A
  • Ask what they know and understand about their medicines

- Raise any concerns

92
Q

Provide information

A
  • Offer thorough and clear information on their condition and treatments
  • Offer individualised information that is easy to understand
93
Q

Assess adherence

A
  • Routinely assess adherence in a non-judgemental way whenever you prescribe
94
Q

Review medicines

A
  • Review patient’s knowledge, understanding and concerns about medicine
95
Q

Concordance

A

Thinking about patients as equals in care settings rather than just following doctor’s instructions, patients to take part in decisions

96
Q

Barriers to concordance - patients

A

Sometimes makes the patients more anxious, simply want their doctor to instruct where medical decisions are complex

97
Q

Barriers to concordance - doctors

A
  • Relevant communication skills

- Time constraints

98
Q

Steps in sharing the decision with the patient

A
  1. Define the problem
  2. Convey that professionals may not have one set opinion on the best treatment
  3. Outline the options - pros and cons of treatments
  4. Clarify patient’s understanding and explore any concerns
  5. Check the patient accepts the decision
  6. Review the needs and preferences after the patient has had time for consideration
  7. Review treatment decisions over time
99
Q

Morphine is a receptor a______

A

agonist

100
Q

Oral bioavailability of morphine? Why so low?

A

50% due to the liver metabolism

101
Q

Naturally occurring opioids from opium?

A

morphine and codeine

102
Q

Antagonists to opioids?

A

Naloxone (give tot reverse overdose)

103
Q

Routes of administration for opioids?

A

oral, subcutaneous, IV

104
Q

If morphine is given intravenously, how long does it take to reach the brain?

A

5 minutes

105
Q

Diamorphine =

A

heroin, more potent and faster acting (crosses BBB quickly)

106
Q

How do opioids work?

A

Use existing pain modulation systems - natural endorphins and enkephalins

107
Q

Opioid receptors are of which type?

A

G coupled protein

108
Q

Subunits of opioid receptors

A

G alpha, beta, gamma

109
Q

When an opioid binds to its receptor what happens to the G receptor subunits?

A

Alpha separates from beta and gamma

110
Q

G beta gamma subunits?

A

Inhibit Ca2+ voltage gated channels, and stimulate hyperpolarisation by opening of K+ channels, both making an AP more difficult to occur

111
Q

G alpha subunit?

A

Inhibits cAMP synthesis

112
Q

Opioids inhibit the

A

pain ascending pathway

113
Q

opioids activate the

A

pain descending pathway which blocks the pain ascending

114
Q

Opioid receptor for morphone?

A

mu

115
Q

Where are opioid receptors located?

A

Midbrain, spine, GI tract, breathing centre

116
Q

Morphine is metabolised into? Is this more or less potent than morphine?

A

morphine 6 glucoronide, more

117
Q

How is morphine 6 glucoronide normally excreted? What clinical problems does this present?

A

Renally, patients with decreased renal function may have problems removing

118
Q

Sustained activation of opioid receptors –>

A

Tolerance and addiction

119
Q

Side effects of opioids (receptors exist OUTSIDE the pain system –> GI tract and respiratory control centre)

A

respiratory depression, nausea, constipation, itching, etc

120
Q

What to administer if opioid induced respiratory depression

A

Naloxone

121
Q

Divisions of the autonomic nervous system? what neurotransmitters are used?

A

parasympathetic and sympathetic, ACh and noradrenaline

122
Q

somatic nervous system uses which NT?

A

ACh

123
Q

Two types of cholinergic receptors?

A

Nicotinic and muscarinic

124
Q

Nicotinic receptors (nAChR) are what type of receptors?

A

ion channels

125
Q

Muscarinic receptors (mAChR) are what type of receptors

A

G-protein coupled

126
Q

In the parasympathetic NS, ACh acts on which receptors?

A

Muscarinic ACh receptors (M1, M2, M3)

127
Q

In the sympathetic NS, what mediates the release of noradrenaline?

A

ACh

128
Q

Noradrenaline activates which type of receptors?

A

adrenergic (alpha and beta)

129
Q

In the somatic NS, ACh acts on which type of receptors at the neuromuscular junction

A

nicotinic

130
Q

Where are nicotinic ACh receptors found?

A

NMJ

131
Q

Enzymes that forms ACh from acetyl CoA and choline in the neurone?

A

choline acetyl transferase enzyme

132
Q

After ACh is formed in the neurone, what happens to it?

A

Stored in a vesicle ready for release

133
Q

ACh is broken down in the synaptic cleft after use by what enzyme? what are the products?

A

acetylcholinesterase, into choline and acetate

134
Q

where are M1 receptors found?

A

mainly brain

135
Q

where are M2 receptors found?

A

mainly in the heart, activation SLOWS the heart

136
Q

where are M3 receptors found?

A

glandular and smooth muscle, causes bronchoconstriction, etc.

137
Q

where are M4 receptors found?

A

mainly in the CNS

138
Q

Muscarinic agonist?

A

Pilocarpine

139
Q

PS agonistic action of pilocarpine

A
  1. Stimulates salivation
  2. Contracts iris smooth muscle - pupil constriction
  3. Side effects of slowing the heart
140
Q

Treatment of bronchoconstriction?

A

Drugs that do this in the airway block the M3 receptor and are called anti-cholinergics or anti-muscarinics

141
Q

Drugs such as solifenacin that treat overactive bladders?

A

Anticholinergics

142
Q

Anti-cholinergic side effects

A

In the brain may worsen memory and may cause confusion

Peripherally, may cause constipation, drying of the mouth, blurring of the vision

143
Q

Botulinum toxin (botox) has both cosmetic and anti-spasmodic uses - how does it work put simply?

A

Prevents ACh release

144
Q

Precursor of catecholamines

A

Dopamine

145
Q

Adverse effects of muscarinic agonists (DUMBELS)

A

Diarrhoea, urination, miosis (excessive pupil constriction), bradycardia, emesis (vomiting), lacrimation, salivation

146
Q

Noradrenaline is a __________, adrenaline is a ___________

A

neurotransmitter, hormone

147
Q

Synthesis of adrenaline beginning with tyrosine?

A

Tyrosine, DOPA, dopamin,e noradrenaline, adrenaline

148
Q

Classes of alpha adrenergic receptors?

A

alpha 1 and 2

149
Q

Classes of beta adrenergic receptors?

A

beta 1, 2 and 3

150
Q

Effect of alpha-1 adrenoreceptors?

A

vasoconstriction, pupil dilation, bladder contraction

151
Q

Effect of alpha-2 adrenoreceptors?

A

Presynaptic inhibition of noradrenaline

152
Q

Alpha-1 adrenoreceptor activators act to? whereas alpha-2 act to?

A

Raise BP, lower BP

153
Q

Why might you block alpha-1 receptors?

A

Lower BP (e.g. doxazosin)

154
Q

Alpha-1 blocker which lowers BP drug?

A

doxazosin

155
Q

Effect of beta-1 adrenoreceptors?

A

Increased cardiac effects

156
Q

Effect of beta-2 adrenoreceptors?

A

Bronchodilation

157
Q

Effect of beta-3 adrenoreceptors?

A
  • increased lipolysis

- relaxation of the bladder

158
Q

Key adrenergic agonist

A

adrenaline

159
Q

What is meant by adrenaline being a non-selective agonist?

A

Works on any alpha and beta adrenoreceptor

160
Q

Uses of adrenaline has an adrenergic agonist?

A

anaphylaxis, cardiac arrest, acute hypotension

161
Q

What happens when adrenaline binds to beta-2 receptors?

A

bronchodilation

162
Q

Activation of which adrenergic receptors can be life saving in asthma?

A

Beta-2

163
Q

Activating alpha-1 adrenergic receptors causes?

A

vasoconstriction

164
Q

Activating beta-1 adrenergic receptors causes?

A

increased force of heart contraction

165
Q

Beta-3 agonists reduce symptoms of an?

A

Over-active bladder

166
Q

Beta blockers

A

Lower BP, reduce cardiac work, treat arrhythmias

167
Q

What patients would you not prescribe beta blockers to? Why?

A

Asthmatics, since already on beta-2 agonists

168
Q

Side effects of beta blockers?

A

tiredness, bronchoconstriction, bradycardia, cardiac depression

169
Q

Clinical indications relating to allergy?

A
  1. Epithelial - eczema, itching, reddening
  2. Excessive mucus production
  3. Airway constriction
  4. Abdominal bloating
  5. Anaphylaxis
170
Q

Ab involved in allergic phenomena?

A

IgE

171
Q

Low affinity IgE receptor expressing cells

A

B cells, T cells, monocytes, platelets, neutrophils

172
Q

High affinity IgE receptor expressing cells

A

eosinophils, mast cells, basophils

173
Q

Mast cells

A
  • IgE mediated immunity
  • primary role in innate and acquired immunity
  • only circulate in their immature form
174
Q

What mAKES an allergen?

A

Particulate delivery of antigens, presence of weak PAMPs resulting in weak innate immunity activation

175
Q

Complications of anaphylaxis?

A
  • Mast cell/ basophil activation
  • Vasodilation
  • Increased vascular permeability
  • Lowered BP
  • Mucus production
  • Rash
  • Swelling
176
Q

Allergy treatments - immunotherapy

A

Increasing dose of antigen via sub-lingual or subcutaneous, usually only used for very serious conditions

177
Q

Allergy treatments - reducing mast cell products

A

Histamine receptor antagonists, prostaglandin antagonists

178
Q

What is meant by druggability?

A

Ability of a protein target to bind small molecules with high affinity

179
Q

Penicillin was developed using?

A

fermentation

180
Q

Stereoisomers of a molecule affect its biological activity, which form of the isomer do biological systems use?

A

L-amino acids (R form)

181
Q

Recombinant proteins in clinical use?

A

Insulin, EPO, growth hormone, interleukin 2, gamma interferon

182
Q

What is meant by rational drug design?

A

Process of finding new medications based on the knowledge of a biological target

183
Q

Evolution of insulin as a therapy:

A
  • Extracted from beef/ pork pancreas
  • engineering insulin
  • second generation insulin
184
Q

Gene therapy in drug development

A

Delivery of a nucleic acid polymer to the cell, DNA is delivered using a viral vector, therapeuric gene administered to treat effects of mutated gene, suppresses mutated gene gene expression

185
Q

Adverse drug reactions

A

response to a drug which is noxious and unintended

186
Q

Adverse drug reactions - facts

A
  • 5% of hospital admissions
  • 10-20% occur in hospital inpatients
  • 60% are preventable
  • 5th most common cause of hospital death
  • Patients lose confidence in their doctors
187
Q

Types of adverse drug reactions (ADRs)? - ABCDE

A

Augmented, bizarre, chronic, delayed, end of use

188
Q

Side effects (as opposed to ADRs)

A

an unintended effect of a drug related to its pharmacological properties and can include unexpected benefits of treatment

189
Q

adverse drug reactions - beta blockers

A

Bradycardia and heart block are primary adverse effects. Bronchospasm is a secondary pharmacological adverse effect

190
Q

ADR - augmented

A
  • commonest, extension of clinical effect
  • predictable
  • dose-related
191
Q

ADR - augmented examples

A

Diuretic causing dehydration, drug for hypertension causing hypotension, anticoagulant causing bleeding

192
Q

ADR - bizarre

A
  • unexpected and unpredictable
  • unrelated to dose
  • mostly immunological mechanisms
  • hypersensitivity
193
Q

ADR - chronic

A
  • occurs after long term therapy, e.g. osteoporosis and steroids
194
Q

ADR - delayed

A

after long term treatment, e.g. malignancies after immunosuppression

195
Q

ADR - end of treatment

A

After abrupt drug withdrawal

196
Q

Susceptibility to ADR?

A

elderly, female, pregnant, diseased (liver or renal), genetics

197
Q

Causes for ADRs

A
  • Pharmaceutical variation
  • Receptor abnormality
  • Drug-drug interactions
198
Q

When to suspect an ADR?

A

Symptoms after: a new drug, dosage increase

199
Q

Commons ADRs?

A

confusion, nausea, balance problems, diarrhoea, constipation, hypotension

200
Q

DoTS (ADR)

A
  1. Dose relatedness
  2. Timing
  3. Susceptibility
201
Q

Most common drugs to have ADRs?

A

antibiotics, CDV drugs, NSAIDs, anti-neoplastics

202
Q

Name for the ADR reporting scheme?

A

Yellow card scheme

203
Q

Advantages of the yellow card scheme?

A
  • identifies adverse reactions
  • readily accessible
  • cheap to operate
  • acts as an early warning system
204
Q

Information to include on a yellow card? (4)

A
  1. Suspected drug
  2. Suspect reaction
  3. Patient details
  4. Reporter details
205
Q

Weaknesses of yellow card?

A
  • Relies on ADR being recognised

- Bias due to promotion and publicity

206
Q

What does the black triangle mean?

A

Indicates a medicine is undergoing additional monitoring e.g. contains a new active substance

207
Q

clinical criteria for allergy to drug

A
  • no correlation to dosage
  • no correlation to pharmacological drug properties
  • disappearance on cessation
208
Q

Main features of anaphylaxis

A
  1. Exposure to drug - immediate rapid onset rash
  2. Swelling of the face, lips, oedema
  3. Hypotension
  4. Cardiac arrest
209
Q

First step in the management of anaphylaxis?

A

Commence basic life support - airway, breathing, circulation (ABC)

210
Q

Effect of adrenaline in management of anaphylaxis?

A
  1. vasoconstriction
  2. bronchodilation
  3. increased cardiac output
211
Q

Medicine risk factors for drug hypersensitivity

A
  1. Protein base macro molecules e.g. penicillin

2. Monoclonal antibodies can cause reactions

212
Q

How does adrenaline cause vasoconstriction in the treatment of anaphylaxis?

A

via alpha 1 adrenoreceptors

213
Q

How does adrenaline cause increased CO in the treatment of anaphylaxis?

A

stimulation of beta-1 adrenoreceptors - positive ionotropic and chronotropic effects on the heart

214
Q

How does adrenaline reduce oedema in the treatment of anaphylaxis?

A

stimulation of beta-2 adrenoreceptors

215
Q

What is non-immune anaphylaxis?

A

Type of anaphylaxis that does not involve the immune system, rather the direct stimulation of mast cell degranulation, some drugs are recognised to cause this

216
Q

Drug interaction of avocado

A

Reduces the effectiveness of warfarin, thus could increase the risk of blood clots

217
Q

Drug interaction of grapefruit juice

A

Increases effectiveness of calcium channel blockers

GRACE Phase 2a Medicine (20 decks)

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