Mid Semester Question Bank Flashcards

1
Q

What factor does not contribute to inter-individual variation?

A

Blood type

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2
Q

What is a peptide inhibitor?

A

A substrate that binds to the SH2 domain of proteins

–> Prevents dimerization with the intra-cellular part of the receptor

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3
Q

Kinase-linked receptors…

A

Have a very slow release

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4
Q

Name all types of antagonists:

A
  • Competitive
  • Non-competitive
  • Functional
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5
Q

The sequence of nuclear receptors:

A
  1. Drug binds to receptor
  2. Receptor homo-dimerizes
  3. Receptor activated gene transcription
  4. Protein is made
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6
Q

What determines the occupation of receptors during drug-receptor binding?

A

Affinity

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7
Q

What is a partial agonist?

A

A drug that produces a lowered maximal effect

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8
Q

How do receptors act as drug targets?

A

A drug can bind to a plasma membrane receptor to trigger signalling

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9
Q

What is potency?

A
  • The measure of affinity for the drug to receptor

- The x-shift on a dose-response curve

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10
Q

What is true about side effects and adverse effects of a drug?

A

Side effects are experienced within the therapeutic range.

Adverse effects are experienced beyond the therapeutic range

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11
Q

What does an agonist do?

A

An agonist binds to the active site

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12
Q

Through which routes are drugs eliminated?

A

Expired air

Feces and urine

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13
Q

How do dietary constituents inhibit metabolism?

A

Some molecules like cyclosporin –> hydroxyclyclosporin inhibit metabolism of other drugs

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14
Q

What governs the absorption in the intestine?

A

Weak acids and weak bases are well absorbed

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15
Q

How are drugs absorbed into the body?

A
  • Oral
  • Rectal
  • Percutaneous
  • Intramuscular
  • Intrathecal
  • Inhalation
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16
Q

What is the correct process for metabolism of aspirin?

A

Aspirin is hydrolized to salicylate and acetic acid by esterase in tissue and blood

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17
Q

Phase 2 reactions involve:

A
  • A cofactor donor group

- Transferases transfer water soluble groups to a receptor

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18
Q

K1 and K2 values are determined by…

A
  • Blood flow
  • Drug lipophilicity
  • Plasma
  • Tissue barriers
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19
Q

Absorbtion via the GI is dependant on:

A
  • Concentration gradient
  • Lipophilicity
  • Blood flow to site of absorption
  • Drug formulation
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20
Q

How does induction effect paracetamol?

A

Increased CYP metabolite –> toxicity

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21
Q

Principle points for protein binding:

A
  • Only unbound drugs can diffuse into peripheral tissue
  • Albumin is an important co-factor in drug binding
  • Plasma protein binding can be saturable for some drugs
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22
Q

Induction of CYP proteins leads to:

A

Increased metabolism of substrate and lower plasma drug levels

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23
Q

Oral bioavaliability:

A

The fraction of an oral dose that reaches systemic circulation

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24
Q

What determines the diffusion of drugs into peripheral tissue?

A
  • Drug size
  • Degree of ionization
  • Lipid solubility
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25
Q

What are the two different ACh receptors found in the parasympathetic division?

A
  • Nicotinic

- Muscarinic

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26
Q

Which neurotransmitter is released by preganglionic and postganglionic fibers in the parasympathetic division of the ANS?

A

Acetylcholine

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27
Q

What are the two different ACh receptors found on postsynaptic membranes in the parasympathetic division?

A

Nicotinic and musacarinic

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28
Q

Side effects of Mirtazapine:

A

Dry mouth
Weight gain
Sedation

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29
Q

Dopamine is degraded by MAO. T/F

A

True

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30
Q

MOA:

A

-> increased NA (and 5-HT)
levels in synaptic cleft due to
uptake inhibition

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31
Q

Direct acting agonists or antagonists can act at postsynaptic receptors. T/F

A

True

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32
Q

Indirect acting agonists release neurotransmitters from presynaptic nerve terminals to
produce a sympathomimetic effect, such as _____

A

amphetamines

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33
Q

Specific drugs can inhibit the Ca2+-dependent release of noradrenaline, thus having a
_____ effect

A

sympatholytic

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34
Q

Drugs such as reserpine cause the…

A

destruction of storage granules, and as a result,

depletion of the synaptic terminal of noradrenaline which is also a sympatholytic action.

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35
Q

Inhibition of the membrane uptake of catecholamines by drugs such as cocaine and
tricyclic antidepressants produce…

A

a sympathomimetic effect

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36
Q

Inhibition of monoamine oxidase by drugs such as some ____

A

antidepressants.

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37
Q

The IP3 and DAG pathway leads to:

A

Contraction

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38
Q

The cAMP pathway leads to:

A

Relaxation

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39
Q

What type of medication is given to decrease
sympathetic stimulation, resulting in decreased
heart rate?

A

Beta-blockers

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40
Q

Beta-blockers act by:

A

lowering your blood pressure by blocking the effect of hormones called adrenaline and noradrenaline

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41
Q

What are the functions of the ANS

A

Regulation of:

  • Body temp
  • Cardiovascular activity
  • Digestive functions
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42
Q

The 2 main colinergic receptors:

A

Nicotinic an muscarinic

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43
Q

What agonizes the nicotinic receptors?

A

Acetylcholine and nicotine

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44
Q

What symptoms would you expect if you ingested a muscarinic agonist?

A
Salvation
Lacrimation
Urination
Defecation
Gastro
Emisis
Bronchospasm
Bronchodilation
Bradycardia
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45
Q

Acetylcholinesterase inhibitors can:

A

Treat glucoma

Cause diarrhea

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46
Q

Side effects of nicotine:

A
Mydriasis
Tachycardia
Weakness
Hyperthermia
Fasciculation
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47
Q

Beta1-receptor activation leads to:

A

Contraction of the heart

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48
Q

Sympathomimetic drugs act to:

A

Agonise at a1, b1 and b2 receptors

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49
Q

Sympatholytic drugs act to:

A

Agonise at a1, b1 and b2 receptors
and;
antagonise at alpha2 receptors

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50
Q

Indirect sympathomimetic drugs:

A
  • NA uptake inhibitors
  • MAO-inhibitors
  • Amphetamine,
  • Ephedrine
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51
Q

Beta-blockers can be used to treat:

A

Hypertension

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52
Q

What is the adrenergic effect at target organs?

A

Vasodilation in skeletal muscle

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53
Q

Nicotine causes:

A

Mydriasis
Hyperthermia
Fasiculations
Weakness

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54
Q

Nicotine does not cause constipation. T/F

A

True

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55
Q

. Glaucoma can be treated by administration of muscarinic agonists and/or beta2-adrenoceptor antagonists. T/F

A

True

56
Q

Ganglionic blockers have a range of side effects including:

A
  • Tachycardia
  • Orthostatic hypotension,
  • Bronchodilation
  • Urinary retention
  • Constipation
  • Blurred vision
57
Q

The baroreceptor reflex is…

A

mediated by sensory nerve fibres relaying blood pressure information from the carotid sinus and aortic arch to the brainstem which then activates either parasympathetic or sympathetic nervous systems.

58
Q

Noradrenergic transmission can be reduced by drugs that block vesicular monoamine transporters e.g. _____

A

reserpine

59
Q

Adrenaline is used to treat anaphalactic shock because…

A

increase blood pressure by inducing increase in heart rate and contractility as well as peripheral vasoconstriction.
Also promotes bronchodilation

60
Q

a1 adrenergic receptor agonist side effects incl.

A

Hypertension
Constipation
Urinary retention
Decreased mucous

61
Q

Administration of a beta-blocker is likely to cause…

A

Bradycardia

62
Q

A patient presents with orthostatic hypotension. What drug might they have take?

A

VMAT blocker
a1 antagonist
Nicotinic anatgonist
a2 agonist

63
Q

Atropine can cause orthostatic hypotension. T/F

A

False

64
Q

Amphetamines are…

A

Taken up into vesicles synapses utilising NAT and VMAT

–> displacing noradrenaline and dopamine, causing non-vesicular noradrenaline and dopamine release

65
Q
  1. Which of the following would not be expected to be seen in a patient that ingests muscarine?
A

Dry mouth

66
Q

An antidote to a muscarinic antagonist is:

A

An ACHE inhibitor

67
Q

Effects of atropine incl.

A
  • Mydriasis, blurred vision
  • Tachycardia (80-90 bpm)
  • Bronchodilation
  • Dry mouth and skin (no sweating)
  • Urinary retention
  • Constipation
68
Q

Atropine can inhibit vagal reflexes. T/F

A

True, used during surgery

69
Q

Glaucoma:

A

Increased Intra-occular pressure within the Eye

Damaging of optic disc –> loss of peripheral vision

70
Q

Acetylcholinesterase inhibitors have…

A

“Agonistic” effects on neuromuscular

junction:

71
Q

Acetylcholinesterase inhibitors can be used to treat…

A

Parkinsons Disease

72
Q

High dose of ACHE:

Muscarinic effects:

A
  • Pinpoint pupils.
  • Blurred vision,
  • Hypersecretion by salivary, lacrimal, sweat, and bronchial
    glands.
  • Bowel and bladder incontinence
  • Nausea, vomiting, or diarrhea
  • Bradycardia, hypotension
  • Difficulties breathing
73
Q

High dose of ACHE:

Nicotinic effects:

A
  • Skeletal muscle twitching and cramping, followed by
  • Weakness and;
  • Flaccid paralysis
74
Q

High dose of ACHE:

CNS effects:

A
  • Seizures

- Respiratory depression

75
Q

An antidote of ACHE poisoning is…

A

Atropine

76
Q

Nicotine acts on the Postsynaptic skeletal

muscle cell to produce…

A

Muscle relaxants

77
Q

Nicotine acts on the postsynaptic

post-ganglionic cell to produce…

A

Ganglionic blockers.

78
Q

Nicotine overdose:

A
  • Nausea
  • Abdominal cramps - Sweating
  • Rapid breathing,
  • Convulsions
  • Coma
79
Q

Nicotine induces….

A
MTWT(H)F
Mydriasis
Tachycardia
Weakness
Hyperthermia
Fasciculations
80
Q

Ganglionic blockers will…

A
  • Block the sympathetic NS and its mediated vasoconstriction in skin and viscera.

–> vasodilation and the BP will drop.

81
Q

Use of muscle relaxants within surgery & ICU

A
  • Relax jaw muscle during intubation
  • Relaxed muscles are easier to cut
  • Less damage to relaxed muscles than contracted
    muscles when cut
  • Ensure immobility during surgery
  • To achieve muscle relaxation for endotracheal intubation
82
Q

Muscarinic receptors are 1000* more sensitive to ACh than nicotine. T/F

A

True

83
Q

Block of nARCHR in ganglions and adrenal medulla…

A

–> Decr. BP & Tachycardia

Leads to:

  • Apnea
  • Cardiovascular collapse
  • Post-operative respiratory failure
  • Histamine release –> bronchoconstriction
84
Q

Modern skeletal muscle relaxants…

A

Act peripherally at nAChR at the neuromuscular jct (not in the CNS) on striated skeletal muscle

85
Q

Skeletal muscle relaxants are administered…

A

Parentally

86
Q

Adverse effects of depolarising muscle relaxants:

A
  • Bradycardia
  • Muscle pain
  • Release of K+ from prolonged depolarization of muscle
87
Q

Atropine does not…

A

Relive constipation

88
Q

The administration of atropine may…

A
  • Induce mydriasis
  • Assist with asthma treatment
  • Reducing vagal reflexes to reduce bradycardia and bronchoconstriction during surgery
89
Q

Which of the following correctly explains why an acetylcholinesterase inhibitor may cause bradycardia, but at a VERY high dose may cause tachycardia?

A

Since acetylcholine has a greater affinity for muscarinic receptors than nicotinic receptors, it takes a greater dose of an AChEI before nicotinic effects are observed

–> Stimulating sympathetic post-ganglionic neurons that innervate the heart

90
Q

Deploarizing muscle relaxants rely on…

A

Overstimulation of nicotinic-acetylcholine receptors to cause flaccid paralysis

91
Q

An antidote to non-depolarising muscle relaxants:

A

Acetylcholinesterase

92
Q

Regarding Adrenaline, which of the following correctly pairs its use with its effect?

A
  • Binds to B2 receptors on the lungs to ease bronchoconstriction
  • Binds to a1 receptors to induce vasoconstriction of peripheral blood vessels
93
Q

A patient presents with diarrhoea, skeletal muscle paralysis, and is experiencing difficulty breathing, what type of drug has the patient taken and what is the correct antidote?

A

Acetylcholinesterase inhibitor; atropine

94
Q

You are treating a patient with hypertension that has a history of severe asthma, which of the following drugs should you NOT administer

A

Do NOT administer:

  • a1 agonist
  • B-blocker
  • VMAT blocker
95
Q

Select the correct pairing of drug action with a potential side-effect

A
  • Muscarinic agonist; seizures

- Ganglionic blocker; dysrhythmia

96
Q

Atropine is an antidote to acetylcholinesterase inhibitor. T/F

A

True

97
Q

A muscarininc antagonist is an antidote to a muscarinic agonist. T/F

A

True

98
Q

A muscarinic antagonist is an antidote to acetylcholinesterase inhibitor. T/F

A

True

99
Q

Am acetylcholinesterase inhibitor is an antidote to a depolarising skeletal muscle relaxant. T/F

A

False

100
Q
  1. A girl feeds her younger brother a bottle from the medicine cabinet, as he was annoying her one day. After dispensing the liquid into his mouth, the brother begins to experience increased salivation, bradycardia, sweating and his pupils constrict (miosis).
    A. What type of drug did the girls brother take?
    B. Are his symptoms likely?
    C. Are there any additional symptoms he would be expressing?
    D. What would this drug be used for normally?
    E. What would be an antidote?
A
  1. A – the little brother ingested a muscarinic agonist
    B – yes, these symptoms are likely, as they reflect enhanced muscarinic effects on the body, which would involve increase parasympathetic influence.
    C – bronchoconstriction, gastroemesis, increased urination, increased lacrimation, diarrhoea
    D – treating glaucoma or dry mouth
    E – an antidote would be atropine, as it acts against muscarinic effects
101
Q
  1. After wanting to improve his muscle power so he could impress the ladies, Pat went to the chemist and bought some pills. Not wanting to wait, he ingested a small handful hoping that his muscles would have enhanced contractile force. However, he then began to experience muscle paralysis, diarrhoea, nausea, and his vision blurred.
    A. What did pat take a very high dose of?
    B. What other effects/symptoms could he experience
    C. What is the drug normally used for?
    D. What is an antidote?
A
  1. A – Pat ingested an acetylcholinesterase inhibitor. These drugs enhance acetylcholine neurotransmission at the neuromuscular junction hence at low doses they can increase skeletal muscle contractile force
    B – other effects include enhance muscarinic effects (SLUDGE-BBB) such as bradycardia, hypotension, hypersecretion. These drugs also have nicotinic effects such as: tachycardia and hypertension
    C – ACHE inhibitors are usually used to increase muscle contractile force, treat glaucoma or GI Tract immobility.
    D – an antidote would be atropine
102
Q
  1. Wanting to be cool at a party, Helen decides to try a cool party trick that involves flicking a cigarette from her mouth. However, her trick horribly failed, and she ended up swallowing the unlit cigarette.
    A. What drug has Helen just ingested?
    B. What are the normal actions of this drug on the body’s nervous systems?
    C. What symptoms would Helen experience with an overdose?
    D. If delaying treatment, what symptoms would Helen experience with a toxic dose of this drug?
A
  1. A.- nicotine
    B – normally, nicotine acts as a non-selective agonist of nicotinic acetylcholine receptors on ganglionic neurons. Hence, it activates the dominant nervous systems for each area of the body, for example, the parasympathetic nervous system for the GIT or the heart, and the sympathetic nervous system for vasculature
    C – with a minor overdose, Helen would experience nausea, abdominal cramps, sweating, rapid breathing, and convulsions.
    D – a toxic dose of nicotine will result in a central block of respiration and a depolarising block of skeletal muscle.
    - Will also see: Mydriasis, Tachycardia, Weakness, Hypothermia, Fasciculations.
103
Q

Nicotine overdose:

A

Nausea, abdominal craps, sweating, rapid breathing, convulsions, coma

104
Q

An inverse agonist binds to…

A

The resting state of a receptor

105
Q

Biased signalling occurs when…

A

An agonist can activate different pathways by binding to the same receptor.
Different drugs can engage a receptor with different outcomes

106
Q

The 2-state receptor model:

A

explains why some agonists can decrease activity instead of increasing it

107
Q

A non-competitive antagonist….

A

Decreases the maximum effect

108
Q

Functional antagonists:

A

activate biological pathways that act in opposite directions

109
Q

The passive re-absorption occurs at….

A

the distal tubule

110
Q

Mutations in the multidrug resistance 1 (MDR1) gene that inactivate the p-glycoprotein
transporter can result in…

A

Increased drug-levels in the brain

111
Q

A patient shows the following symptoms and admits to having eaten a meal containing
mushrooms collected by her son. A doctor suspects muscarine poisoning. Which of these
symptoms can NOT be attributed to a high muscarine dose?

A

Mydriasis

112
Q

Which of the following drugs when given in small amounts will reduce signalling at nicotinic
acetylcholine receptors?

A

Acetylcholinesterase inhibitors

113
Q

A child shows the following symptoms and admits to having taken something from the
medicine box. A doctor suspects poisoning with a β-adrenoceptor antagonist. Which of these
symptoms can NOT be attributed to β-adrenoceptor blockade?

A

Urinary retention

114
Q

A non-competitive antagonist decreases…

A

Maximum effect

115
Q

Passive re-absorption occurs at the…

A

Distal tubule

116
Q

A decreased intestinal absorption of the drug…

A

increases drug levels in the brain –> mdr1 moves the drugs back to the lumen to protect brain barrier

117
Q

Which of the following drugs when given in small amounts will reduce signalling at nicotinic acetylcholine receptors?

A

Depolarising muscle relaxants

118
Q

Which of the following symptoms would you expect after an acetylcholinesterase inhibitor is given to a patient?

A

Muscle weakness

119
Q

A biased agonist is a drug that:

A

binds to a receptor that can signal along several pathways, but favours one pathway in particular

120
Q

A competitive antagonist decreases the maximum effect of an agonist. T/F

A

False

121
Q

Disadvantages of the intravenous route of administration of drugs include

A

Risk of introducing infectious organisms

122
Q

The blood-brain barrier is readily permeable to drugs that are…

A

hydrophobic

123
Q

Drugs metabolised by NAT2, such as isoniazid, show plasma concentrations that are normally distributed. T/F

A

False

124
Q

Rapid acetylators are more at risk of getting colon cancer if they are smokers. T/F

A

True

125
Q

Variation in NAT2 acetylation between individuals arises because of mutations that occur in the protein encoding region of the gene. T/F

A

True

126
Q

NAT2 can both bioactivate and detoxify arylamine carcinogens. T/F

A

True

127
Q

E NAT2 is found mainly in the liver and is responsible for most drug acetylation. T/F

A

True

128
Q

Ultra-rapid metabolisers of CYP2D6 substrates

A

carry multiple copies of the CYP2D6 gene.

129
Q

A patient shows the following symptoms and admits to having eaten a meal containing mushrooms collected by her son. A doctor suspects muscarine poisoning. Which of these symptoms can NOT be attributed to a high muscarine dose?
A bronchoconstriction

A

Tachycardia

130
Q

Which of the following symptoms would you expect after an acetylcholinesterase inhibitor is given to a patient?

A

Diarrhea

131
Q

Non-depolarising muscle relaxants are nicotinic acetylcholine receptor antagonists and are not active when taken orally. T/F

A

True

132
Q

Adrenaline and noradrenaline act on:

A

Alpha and beta receptors

133
Q

Acetylcholine acts on

A

Nicotine and muscarinic receptors

134
Q

MDR1 are selective. T/F

A

False. MDR1 genes are non-selective

135
Q

Carcinogens increase cytochrome P450 activity. T/F

A

True –> More rapid metabolism of substrates