Autonomics Flashcards

1
Q
  1. Atropine is used to counteract:
    a) High sympathetic activity
    b) Excessively high parasympathetic activity
    c) Muscle contractions
    d) Neurotransmitter depletion
A

b) Excessively high parasympathetic activity
Rationale: Atropine is administered when parasympathetic activity is excessively high, such as in severe bradycardia, by blocking muscarinic receptors.

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2
Q
  1. Nicotinic receptors are primarily located in:
    a) The heart
    b) Smooth muscles
    c) Autonomic ganglia of the ANS and NMJ
    d) The liver
A

c) Autonomic ganglia of the ANS and NMJ
Rationale: Nicotinic receptors are located in the autonomic ganglia of the ANS, neuromuscular junctions (NMJ), and adrenal medulla.

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3
Q
  1. The action of muscarinic receptors in the heart is primarily:
    a) Excitatory
    b) Inhibitory
    c) Neutral
    d) Variable
A

b) Inhibitory
Rationale: In the heart, muscarinic receptors have an inhibitory effect, but they are excitatory in smooth muscle and glands.

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4
Q
  1. Ganglionic blockers such as hexamethonium act by blocking:
    a) Muscarinic receptors
    b) Nicotinic receptors
    c) Beta receptors
    d) Alpha receptors
A

b) Nicotinic receptors
Rationale: Ganglionic blockers like hexamethonium block nicotinic receptors, particularly at autonomic ganglia.

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5
Q
  1. Atropine’s mechanism of action involves:
    a) Exciting muscarinic receptors
    b) Blocking muscarinic receptors
    c) Increasing neurotransmitter release
    d) Blocking nicotinic receptors
A

b) Blocking muscarinic receptors
Rationale: Atropine acts by blocking muscarinic receptors, thus reducing parasympathetic activity.

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6
Q
  1. In smooth muscles and glands, muscarinic receptors cause:
    a) Inhibition
    b) Excitation
    c) No change in activity
    d) Stabilization
A

b) Excitation
Rationale: Muscarinic receptors are inhibitory in the heart but excitatory in smooth muscles and glands.

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7
Q
  1. The effect of activating nicotinic receptors at the NMJ is:
    a) Relaxation
    b) Excitation
    c) Inhibition
    d) Stabilization
A

b) Excitation
Rationale: Nicotinic receptors at the NMJ and in autonomic ganglia primarily cause excitation.

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8
Q
  1. Atropine is contraindicated in patients with:
    a) Low heart rate
    b) High heart rate
    c) Closed-angle glaucoma
    d) Open-angle glaucoma
A

c) Closed-angle glaucoma
Rationale: Atropine is contraindicated in closed-angle glaucoma due to the risk of increasing intraocular pressure.

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9
Q
  1. In the SA node, muscarinic receptors’ action leads to:
    a) Opening of sodium channels
    b) Inhibition of adenylate cyclase and opening of potassium channels
    c) Activation of calcium channels
    d) Excitation of the heart muscle
A

b) Inhibition of adenylate cyclase and opening of potassium channels
Rationale: Muscarinic receptors in the SA node inhibit adenylate cyclase, leading to the opening of potassium channels.

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10
Q
  1. The role of acetylcholine in the cholinergic system is to:
    a) Inhibit muscle contraction
    b) Act as a neurotransmitter
    c) Block receptor activity
    d) Decrease heart rate
A

b) Act as a neurotransmitter
Rationale: Acetylcholine is the primary neurotransmitter in the cholinergic system, playing a crucial role in various physiological functions.

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11
Q
  1. Hexamethonium’s primary action in the cholinergic system is to:
    a) Increase acetylcholine release
    b) Block nicotinic receptors at autonomic ganglia
    c) Stimulate muscarinic receptors
    d) Increase heart rate
A

b) Block nicotinic receptors at autonomic ganglia
Rationale: Hexamethonium acts as a ganglionic blocker by blocking nicotinic receptors at autonomic ganglia.

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12
Q
  1. In the treatment of bradycardia, atropine is effective because it:
    a) Decreases heart rate further
    b) Increases heart rate
    c) Has no effect on heart rate
    d) Stabilizes heart rate
A

b) Increases heart rate
Rationale: Atropine is used in severe bradycardia to increase heart rate by reducing parasympathetic activity.

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13
Q
  1. Muscarinic receptors in smooth muscles and glands are activated to cause:
    a) Decreased intracellular calcium
    b) Increased intracellular IP3 and calcium
    c) Stabilization of membrane potential
    d) Decrease in glandular secretions
A

b) Increased intracellular IP3 and calcium
Rationale: Activation of muscarinic receptors in smooth muscles and glands leads to increased IP3 and intracellular calcium levels.

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14
Q
  1. The primary effect of nicotinic receptors activation at the adrenal medulla is:
    a) Decreased adrenaline release
    b) Increased adrenaline release
    c) No effect on adrenaline release
    d) Stabilization of adrenaline levels
A

b) Increased adrenaline release
Rationale: Activation of nicotinic receptors at the adrenal medulla typically leads to increased adrenaline release.

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15
Q
  1. Atropine’s ability to increase sympathetic features is due to its action of:
    a) Stimulating muscarinic receptors
    b) Blocking muscarinic receptors
    c) Activating nicotinic receptors
    d) Inhibiting acetylcholine synthesis
A

b) Blocking muscarinic receptors
Rationale: Atropine increases sympathetic features by blocking muscarinic receptors, reducing parasympathetic activity.

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16
Q
  1. The use of hexamethonium in the cholinergic system primarily results in:
    a) Decreased sympathetic activity
    b) Increased parasympathetic activity
    c) Reduced neurotransmitter release
    d) Enhanced neurotransmitter release
A

c) Reduced neurotransmitter release
Rationale: Hexamethonium reduces neurotransmitter release by blocking nicotinic receptors at autonomic ganglia.

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17
Q
  1. In glaucoma treatment, the role of cholinergic drugs like Pilocarpine is to:
    a) Decrease intraocular pressure
    b) Increase intraocular pressure
    c) Dilate the pupil
    d) Improve vision clarity
A

a) Decrease intraocular pressure
Rationale: Cholinergic drugs like Pilocarpine decrease intraocular pressure by enhancing the drainage of aqueous humor.

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18
Q
  1. Atropine’s use in severe bradycardia works by:
    a) Decreasing cardiac output
    b) Increasing cardiac output
    c) Stabilizing heart rate
    d) Decreasing heart rate
A

b) Increasing cardiac output
Rationale: Atropine is used in severe bradycardia to increase heart rate and cardiac output by reducing parasympathetic activity.

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19
Q
  1. The action of muscarinic receptors in the heart primarily results in:
    a) Increased heart rate
    b) Decreased heart rate
    c) No change in heart rate
    d) Irregular heart rhythm
A

b) Decreased heart rate
Rationale: Muscarinic receptors in the heart primarily have an inhibitory effect, leading to a decreased heart rate.

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20
Q
  1. The therapeutic action of acetylcholine in the cholinergic system includes:
    a) Contracting smooth muscles
    b) Relaxing smooth muscles
    c) Blocking neurotransmitter release
    d) Increasing blood pressure
A

a) Contracting smooth muscles
Rationale: Acetylcholine in the cholinergic system plays a role in contracting smooth muscles, among other functions.

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21
Q
  1. What is the primary neurotransmitter of the parasympathetic nervous system?
    a) Dopamine
    b) Serotonin
    c) Acetylcholine
    d) Norepinephrine
A

c) Acetylcholine
Rationale: Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system, responsible for stimulating parasympathetic activities.

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22
Q
  1. Which type of drug would likely decrease heart rate?
    a) Cholinergic Agonist
    b) Cholinergic Antagonist
    c) Adrenergic Agonist
    d) Adrenergic Antagonist
A

a) Cholinergic Agonist
Rationale: Cholinergic agonists stimulate parasympathetic activity, leading to effects like decreased heart rate.

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23
Q
  1. Which drug category is known to dilate pupils?
    a) Cholinergic Agonist
    b) Cholinergic Antagonist
    c) Adrenergic Agonist
    d) Adrenergic Antagonist
A

c) Adrenergic Agonist

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24
Q
  1. Which medication type is used to manage asthma by expanding airways?
    a) Cholinergic Agonist
    b) Cholinergic Antagonist
    c) Adrenergic Agonist
    d) Adrenergic Antagonist
A

c) Adrenergic Agonist
Rationale: Adrenergic agonists increase sympathetic responses, such as expanded airways, useful in asthma management.

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25
Q
  1. What effect would an adrenergic antagonist have on blood pressure?
    a) Increase
    b) Decrease
    c) No change
    d) Variable
A

b) Decrease
Rationale: Adrenergic antagonists inhibit sympathetic activity, leading to effects like decreased blood pressure.

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26
Q
  1. Which type of drug would likely increase glandular secretions?
    a) Cholinergic Agonist
    b) Cholinergic Antagonist
    c) Adrenergic Agonist
    d) Adrenergic Antagonist
A

a) Cholinergic Agonist
Rationale: Cholinergic agonists stimulate parasympathetic activities, leading to increased glandular secretions.

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27
Q
  1. What is the primary action of adrenergic antagonists?
    a) Stimulate sympathetic activity
    b) Inhibit parasympathetic activity
    c) Inhibit sympathetic activity
    d) Stimulate parasympathetic activity
A

c) Inhibit sympathetic activity
Rationale: Adrenergic antagonists block the action of norepinephrine and adrenaline, reducing sympathetic activity.

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28
Q
  1. A drug that mimics the action of norepinephrine would be categorized as:
    a) Cholinergic Agonist
    b) Cholinergic Antagonist
    c) Adrenergic Agonist
    d) Adrenergic Antagonist
A

c) Adrenergic Agonist
Rationale: Adrenergic agonists enhance or mimic the effects of norepinephrine and adrenaline.

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29
Q
  1. Which medication class is primarily used in heart conditions to boost sympathetic activity?
    a) Cholinergic Agonist
    b) Cholinergic Antagonist
    c) Adrenergic Agonist
    d) Adrenergic Antagonist
A

c) Adrenergic Agonist
Rationale: Adrenergic agonists are often used in heart conditions to enhance sympathetic responses.

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30
Q
  1. What is the effect of cholinergic antagonists on digestion?
    a) Increase
    b) Decrease
    c) No change
    d) Variable
A

b) Decrease
Rationale: Cholinergic antagonists induce sympathetic-like effects, including decreased digestive activity.

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31
Q
  1. Which drugs mimic the effects of adrenaline?
    a) Cholinergic Agonist
    b) Cholinergic Antagonist
    c) Adrenergic Agonist
    d) Adrenergic Antagonist
A

c) Adrenergic Agonist
Rationale: Adrenergic agonists stimulate or enhance the effects of adrenaline.

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32
Q
  1. What is the primary effect of a cholinergic antagonist on the heart rate?
    a) Increase
    b) Decrease
    c) No change
    d) Variable
A

a) Increase
Rationale: By blocking the action of acetylcholine, cholinergic antagonists induce an increase in heart rate.

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33
Q
  1. What is the primary action of cholinergic agonists?
    a) Inhibit the parasympathetic nervous system
    b) Stimulate the sympathetic nervous system
    c) Mimic the actions of acetylcholine
    d) Block acetylcholine receptors
A

c) Mimic the actions of acetylcholine
Rationale: Cholinergic agonists stimulate the parasympathetic nervous system by mimicking the actions of acetylcholine.

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34
Q
  1. Which class of cholinergic agonists directly binds to acetylcholine receptors?
    a) Indirect Acting Cholinergic Agonists
    b) Direct Acting Cholinergic Agonists
    c) Organophosphates
    d) Myasthenia Gravis Treatments
A

b) Direct Acting Cholinergic Agonists
Rationale: Direct acting cholinergic agonists bind directly to and activate acetylcholine receptors.

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35
Q
  1. Pilocarpine, used to treat glaucoma, belongs to which category of cholinergic agonists?
    a) Direct Acting
    b) Indirect Acting
    c) Organophosphates
    d) Myasthenia Gravis Treatments
A

a) Direct Acting
Rationale: Pilocarpine is a direct-acting cholinergic agonist, used for glaucoma treatment.

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36
Q
  1. Which is an example of an indirect acting cholinergic agonist used in myasthenia gravis?
    a) Acetylcholine
    b) Carbachol
    c) Neostigmine
    d) Nicotine
A

c) Neostigmine

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37
Q
  1. Organophosphates, a category of cholinergic agonists, are primarily used as:
    a) Cardiac medications
    b) Pesticides
    c) Antidepressants
    d) Antihistamines
A

b) Pesticides
Rationale: Organophosphates, which are a type of indirect acting cholinergic agonist, are typically used as pesticides.

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38
Q
  1. What is the mechanism of action of indirect acting cholinergic agonists?
    a) Binding to acetylcholine receptors
    b) Inhibiting the breakdown of acetylcholine
    c) Blocking sympathetic neurotransmitters
    d) Enhancing the release of acetylcholine
A

b) Inhibiting the breakdown of acetylcholine
Rationale: Indirect acting cholinergic agonists increase acetylcholine levels by inhibiting its breakdown.

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39
Q
  1. Which of the following is a direct acting cholinergic agonist?
    a) Isoflurophate
    b) Bethanechol
    c) Edrophonium
    d) Parathion
A

b) Bethanechol
Rationale: Bethanechol is a direct acting cholinergic agonist.

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40
Q
  1. Neostigmine is used in the treatment of:
    a) Hypertension
    b) Myasthenia Gravis
    c) Glaucoma
    d) Depression
A

b) Myasthenia Gravis
Rationale: Neostigmine is an indirect acting cholinergic agonist used primarily in the management of myasthenia gravis.

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41
Q
  1. Drugs with names ending in “-chol” are generally:
    a) Indirect Acting Cholinergic Agonists
    b) Direct Acting Cholinergic Agonists
    c) Organophosphates
    d) Sympathetic Agonists
A

b) Direct Acting Cholinergic Agonists
Rationale: Drugs ending in “-chol” are typically direct acting cholinergic agonists, reflecting their relation to acetylcholine.

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42
Q
  1. Which drug is an organophosphate and an indirect acting cholinergic agonist?
    a) Carbachol
    b) Methacholine
    c) Ecothiophate
    d) Pilocarpine
A

c) Ecothiophate
Rationale: Ecothiophate/ Isoflurophate is an organophosphate and an indirect acting cholinergic agonist.

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43
Q
  1. Methacholine, a cholinergic agonist, is classified as:
    a) Direct Acting
    b) Indirect Acting
    c) Organophosphate
    d) Myasthenia Gravis Treatment
A

a) Direct Acting

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44
Q
  1. What is the primary reason pure acetylcholine is not used as a drug?
    a) It has a short half-life
    b) It is too expensive to synthesize
    c) It causes severe side effects
    d) It is ineffective in the human body
A

a) It has a short half-life
Rationale: Acetylcholine has a very short half-life, making it impractical to use in drug form. Analogues and derivatives are used instead.

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45
Q
  1. Which direct acting cholinergic agonist is the drug of choice for treating glaucoma?
    a) Bethanechol
    b) Pilocarpine
    c) Carbachol
    d) Methacholine
A

b) Pilocarpine
Rationale: Pilocarpine is primarily used for treating glaucoma due to its ability to stimulate miosis and facilitate the opening of the trabecular meshwork.

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46
Q
  1. What is the effect of acetylcholine on the cardiovascular system (CVS)?
    a) Increases heart rate and contractility
    b) Decreases heart rate and contractility
    c) Has no effect on heart rate
    d) Increases blood pressure
A

b) Decreases heart rate and contractility
Rationale: Acetylcholine affects the CVS by decreasing heart rate and contractility, and lowering blood pressure.

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47
Q
  1. Bethanechol is used to treat:
    a) Asthma
    b) Urinary retention
    c) Glaucoma
    d) High blood pressure
A

b) Urinary retention
Rationale: Bethanechol is used to treat urinary retention by activating smooth muscle in the bladder and bowel, facilitating voiding and bowel movements.

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48
Q
  1. What action does carbachol have on the eye?
    a) Decreases intraocular pressure
    b) Causes pupil dilation
    c) Reduces tear production
    d) Improves vision clarity
A

a) Decreases intraocular pressure
Rationale: Carbachol activates the ciliary muscle of the eye, which helps in the management of open-angle glaucoma, and the pupillary sphincter, used for narrow-angle glaucoma.

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49
Q
  1. What is a potential CNS effect of pilocarpine?
    a) Sedation
    b) Hallucinations and convulsions
    c) Memory enhancement
    d) Mood elevation
A

b) Hallucinations and convulsions
Rationale: Pilocarpine can penetrate the CNS and may cause hallucinations and convulsions; overdose can lead to severe hallucinations.

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50
Q
  1. The methacholine challenge test is used to diagnose:
    a) Urinary incontinence
    b) Asthma and bronchial hyperactivity
    c) Glaucoma
    d) Cardiac arrhythmias
A

b) Asthma and bronchial hyperactivity
Rationale: The methacholine challenge test, which provokes bronchoconstriction, is used to diagnose asthma and bronchial hyperactivity.

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51
Q
  1. Acetylcholine’s effect on the gastrointestinal (GI) system is to:
    a) Decrease motility
    b) Increase motility
    c) Cause constipation
    d) Reduce acid secretion
A

b) Increase motility
Rationale: Acetylcholine increases motility in the GI system.

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52
Q
  1. Which drug causes miosis (pupil constriction)?
    a) Bethanechol
    b) Pilocarpine
    c) Carbachol
    d) Methacholine
A

b) Pilocarpine
Rationale: Pilocarpine stimulates miosis, which is utilized in the treatment of glaucoma.

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53
Q
  1. The mnemonic “BBB” for Bethanechol stands for:
    a) Brain, Blood, Breath
    b) Bethanechol, Bladder, Bowel
    c) Bethanechol, Blood pressure, Bronchoconstriction
    d) Brain, Bladder, Bronchi
A

b) Bethanechol, Bladder, Bowel
Rationale: The mnemonic “BBB” for Bethanechol helps remember its use in treating conditions related to the bladder and bowel.

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54
Q
  1. Acetylcholine’s effect on the endocrine system is:
    a) Inhibiting insulin release
    b) Stimulating the release of epinephrine leading to sweating
    c) Decreasing cortisol levels
    d) Enhancing thyroid hormone secretion
A

b) Stimulating the release of epinephrine leading to sweating
Rationale: Acetylcholine stimulates the release of epinephrine, leading to sweating. This response is not purely sympathetic.

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55
Q
  1. The primary action of carbachol in the treatment of glaucoma is:
    a) Reducing redness and irritation
    b) Improving vision clarity
    c) Decreasing intraocular pressure
    d) Increasing tear production
A

c) Decreasing intraocular pressure
Rationale: Carbachol is used in glaucoma treatment primarily for its action in decreasing intraocular pressure.

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56
Q
  1. Acetylcholine’s effect on the pulmonary system is to:
    a) Decrease secretion in the bronchioles
    b) Increase secretion in the bronchioles
    c) Cause bronchodilation
    d) Reduce airway inflammation
A

b) Increase secretion in the bronchioles
Rationale: Acetylcholine increases secretion in the bronchioles as part of its effect on the pulmonary system.

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57
Q
  1. The effect of acetylcholine on the peripheral nervous system (PNS) is to:
    a) Induce muscle relaxation
    b) Induce muscle contraction
    c) Decrease nerve signal transmission
    d) Increase pain sensation
A

b) Induce muscle contraction
Rationale: In the PNS, acetylcholine induces muscle contraction.

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58
Q
  1. Carbachol’s use in eye surgery is due to its ability to:
    a) Improve vision clarity
    b) Induce miosis
    c) Prevent infection
    d) Reduce inflammation
A

b) Induce miosis
Rationale: Carbachol is used in eye surgery for its ability to induce miosis.

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59
Q
  1. Which of the following is a role of acetylcholine in the central nervous system (CNS)?
    a) Neurotransmission
    b) Blood-brain barrier protection
    c) Cognitive impairment
    d) Sleep induction
A

a) Neurotransmission
Rationale: Acetylcholine is involved in neurotransmission within the CNS.

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60
Q
  1. The usage of methacholine as a diagnostic tool is based on its ability to:
    a) Induce bronchodilation
    b) Provoke bronchoconstriction
    c) Stimulate the heart
    d) Relax smooth muscles
A

b) Provoke bronchoconstriction
Rationale: Methacholine is used to diagnose asthma and bronchial hyperactivity due to its ability to provoke bronchoconstriction.

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61
Q
  1. Pilocarpine’s mode of action in treating glaucoma involves:
    a) Reducing inflammation in the eye
    b) Stimulating miosis and facilitating the opening of the trabecular meshwork
    c) Lowering blood glucose levels
    d) Enhancing tear production
A

b) Stimulating miosis and facilitating the opening of the trabecular meshwork
Rationale: Pilocarpine treats glaucoma by stimulating miosis and facilitating the opening of the trabecular meshwork at the Canal of Schlemm.

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62
Q
  1. Bethanechol’s action on the bladder and bowel is to:
    a) Activate smooth muscle
    b) Inhibit smooth muscle
    c) Decrease secretions
    d) Increase pain sensation
A

a) Activate smooth muscle
Rationale: Bethanechol activates smooth muscle in the bladder and bowel, aiding in voiding and bowel movements.

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63
Q
  1. The primary reason for the limited use of carbachol is due to its:
    a) High cost
    b) Specific actions and side effects
    c) Lack of efficacy
    d) Drug interactions
A

b) Specific actions and side effects
Rationale: Carbachol’s limited use is attributed to its specific actions and side effects, making it less suitable for general use compared to other medications.

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64
Q
  1. What is the mechanism of action of organophosphates?
    a) They stimulate acetylcholine receptors directly.
    b) They reversibly inhibit acetylcholinesterase.
    c) They irreversibly inhibit acetylcholinesterase.
    d) They increase the breakdown of acetylcholine.
A

c) They irreversibly inhibit acetylcholinesterase.
Rationale: Organophosphates bind covalently to acetylcholinesterase, irreversibly inhibiting it and thus increasing acetylcholine levels.

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65
Q
  1. Which antidote is used to counteract organophosphate poisoning?
    a) Atropine
    b) Pralidoxime
    c) Epinephrine
    d) Naloxone
A

b) Pralidoxime
Rationale: Pralidoxime is used as an antidote to organophosphate poisoning.

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66
Q
  1. What is the duration of acetylcholinesterase inhibition by organophosphates?
    a) 24 hours
    b) About a week
    c) A month
    d) Indefinitely
A

b) About a week
Rationale: The inhibition of acetylcholinesterase by organophosphates typically lasts for about a week.

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67
Q
  1. Initial treatment steps for organophosphate poisoning include:
    a) Immediate administration of pralidoxime
    b) Washing the patient to remove any organophosphate from the skin
    c) Performing gastric lavage
    d) Administering activated charcoal
A

b) Washing the patient to remove any organophosphate from the skin
Rationale: The initial steps in real-world treatment of organophosphate poisoning include washing the patient to remove the chemical from the skin.

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68
Q
  1. Which of the following is an example of an organophosphate used in the treatment of glaucoma?
    a) Isoflurophate
    b) Neostigmine
    c) Bethanechol
    d) Pilocarpine
A

a) Isofluorophate
Rationale: Isofluorophate is an example of an organophosphate used occasionally in the treatment of glaucoma.

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69
Q
  1. The DUMBELS symptomatology in organophosphate poisoning includes:
    a) Dizziness, Urticaria, Muscle cramps
    b) Diarrhea, Urination, Miosis
    c) Drowsiness, Urinary retention, Mydriasis
    d) Dermatitis, Ulcers, Muscle weakness
A

b) Diarrhea, Urination, Miosis
Rationale: DUMBELS in organophosphate poisoning stands for Diarrhea, Urination, Miosis, Bronchoconstriction, Excitation of skeletal muscles, Lacrimation, Salivation and sweating.

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70
Q
  1. What is the effect of organophosphates on blood pressure?
    a) Increase
    b) Decrease
    c) No change
    d) Variable effects
A

b) Decrease
Rationale: Organophosphate poisoning can lead to decreased blood pressure as part of the DUMBELS symptomatology.

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71
Q
  1. What role does atropine play in the treatment of organophosphate poisoning?
    a) It serves as the primary antidote.
    b) It is used to counteract falling blood pressure and heart rate.
    c) It reverses the inhibition of acetylcholinesterase.
    d) It removes organophosphates from the body.
A

b) It is used to counteract falling blood pressure and heart rate.
Rationale: Atropine may be administered in organophosphate poisoning based on symptoms such as falling blood pressure and heart rate.

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72
Q
  1. Which organophosphate effect is considered a sympathetic response?
    a) Diarrhea
    b) Urination
    c) Sweating
    d) Miosis
A

c) Sweating (Not Purely SNS)
Rationale: While most effects of organophosphate poisoning are parasympathetic, sweating is a sympathetic response.

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73
Q
  1. In the context of examinations, what is important to remember about organophosphate poisoning?
    a) The immediate administration of atropine
    b) The use of pralidoxime as an antidote
    c) The necessity of immediate gastric lavage
    d) The application of activated charcoal
A

b) The use of pralidoxime as an antidote
Rationale: For exam purposes, it is important to remember that pralidoxime is the antidote for organophosphate poisoning.

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74
Q
  1. What is a symptom of organophosphate poisoning related to the pulmonary system?
    a) Increased lung capacity
    b) Bronchoconstriction
    c) Decreased mucus production
    d) Bronchodilation
A

b) Bronchoconstriction
Rationale: Bronchoconstriction is a symptom of organophosphate poisoning affecting the pulmonary system.

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75
Q
  1. Echothiophate, an organophosphate, is used in the treatment of:
    a) Myasthenia Gravis
    b) Glaucoma
    c) Urinary retention
    d) Asthma
A

b) Glaucoma
Rationale: Echothiophate is an organophosphate occasionally used in the treatment of glaucoma.

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76
Q
  1. What is the effect of organophosphates on salivation?
    a) Decrease
    b) Increase
    c) No change
    d) Variable
A

b) Increase
Rationale: Organophosphate poisoning leads to increased salivation as part of the DUMBELS symptomatology.

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77
Q
  1. Further management steps for organophosphate poisoning include:
    a) Administration of insulin
    b) Gastric lavage and activated charcoal
    c) Immediate surgery
    d) High doses of vitamin supplements
A

b) Gastric lavage and activated charcoal
Rationale: Gastric lavage and administration of activated charcoal are further steps in the treatment of organophosphate poisoning.

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78
Q
  1. What is the effect of organophosphates on the eyes?
    a) Causes mydriasis (pupil dilation)
    b) No effect
    c) Causes miosis (pupil constriction)
    d) Improves vision clarity
A

c) Causes miosis (pupil constriction)
Rationale: Organophosphates cause miosis, or pupil constriction, as part of their effect on the body.

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79
Q
  1. The main reason for performing gastric lavage in organophosphate poisoning is to:
    a) Relieve abdominal pain
    b) Remove the toxin from the stomach
    c) Alleviate nausea
    d) Counteract acidosis
A

b) Remove the toxin from the stomach
Rationale: Gastric lavage is performed to remove the organophosphate toxin from the stomach.

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80
Q
  1. The use of activated charcoal in organophosphate poisoning is primarily to:
    a) Neutralize the toxin
    b) Absorb the toxin from the gastrointestinal tract
    c) Induce vomiting
    d) Provide nutritional support
A

b) Absorb the toxin from the gastrointestinal tract
Rationale: Activated charcoal is used in organophosphate poisoning to absorb the toxin from the gastrointestinal tract.

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81
Q
  1. The excitation of skeletal muscles in organophosphate poisoning leads to:
    a) Increased strength and endurance
    b) Muscle spasms and twitching
    c) Muscle relaxation
    d) Decreased muscle tone
A

b) Muscle spasms and twitching
Rationale: Excitation of skeletal muscles in organophosphate poisoning can lead to muscle spasms and twitching.

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82
Q
  1. In organophosphate poisoning, the role of washing the patient (ligo) is to:
    a) Cool down the body temperature
    b) Remove any organophosphate from the skin
    c) Relieve itching and discomfort
    d) Stimulate blood circulation
A

b) Remove any organophosphate from the skin
Rationale: Washing the patient in organophosphate poisoning is crucial to remove the chemical from the skin and prevent its transfer to healthcare providers.

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83
Q
  1. Lacrimation (tearing) in organophosphate poisoning is due to:
    a) Irritation of the eye
    b) Increased parasympathetic activity
    c) An allergic reaction
    d) Dehydration
A

b) Increased parasympathetic activity
Rationale: Lacrimation or increased tearing in organophosphate poisoning is a result of increased parasympathetic activity.

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84
Q
  1. What is the primary mechanism of action of reversible indirect agonists?
    a) Decreasing acetylcholine synthesis
    b) Reversibly inhibiting acetylcholinesterase
    c) Blocking acetylcholine receptors
    d) Increasing the breakdown of acetylcholine
A

b) Reversibly inhibiting acetylcholinesterase
Rationale: These drugs increase acetylcholine levels by reversibly inhibiting acetylcholinesterase, leading to an accumulation of acetylcholine.

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85
Q
  1. Neostigmine is used primarily for the treatment of:
    a) Hypertension
    b) Myasthenia Gravis
    c) Glaucoma
    d) Depression
A

b) Myasthenia Gravis
Rationale: Neostigmine is the drug of choice for the treatment of myasthenia gravis.

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86
Q
  1. What is the duration of effect of Pyridostigmine?
    a) 30 minutes to 1 hour
    b) 1-2 hours
    c) 3-6 hours
    d) Over 6 hours
A

c) 3-6 hours
Rationale: Pyridostigmine has a long-lasting effect, typically 3-6 hours, and is used for long-term maintenance treatment of myasthenia gravis.

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87
Q
  1. Edrophonium is used diagnostically to:
    a) Confirm a diagnosis of hypertension
    b) Diagnose myasthenia gravis
    c) Diagnose glaucoma
    d) Evaluate liver function
A

b) Diagnose myasthenia gravis
Rationale: Edrophonium is administered to diagnose myasthenia gravis due to its brief increase in endogenous acetylcholine.

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88
Q
  1. Physostigmine is an effective antidote for overdoses of:
    a) Benzodiazepines
    b) Opioids
    c) Atropine, phenothiazines, and TCAs
    d) Beta-blockers
A

c) Atropine, phenothiazines, and TCAs
Rationale: Physostigmine can cross the blood-brain barrier and is effective for overdoses of atropine, phenothiazines, and tricyclic antidepressants (TCAs).

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89
Q
  1. A secondary use of Physostigmine is:
    a) Treating hypertension
    b) As a second-choice drug for glaucoma
    c) Managing diabetes
    d) Treating asthma
A

b) As a second-choice drug for glaucoma
Rationale: Physostigmine is used as a second-choice drug for glaucoma due to its ability to increase acetylcholine levels.

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90
Q
  1. Which drug is known for its brief increase in endogenous acetylcholine?
    a) Neostigmine
    b) Pyridostigmine
    c) Edrophonium
    d) Physostigmine
A

c) Edrophonium
Shortest T1/2 (Duration of action)
Rationale: Edrophonium causes a brief increase in endogenous acetylcholine and is used diagnostically for myasthenia gravis.

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91
Q
  1. The mnemonic “Neo the Cure” refers to:
    a) Neostigmine used for hypertension
    b) Neostigmine used for myasthenia gravis
    c) Neostigmine used for glaucoma
    d) Neostigmine used for diabetes
A

b) Neostigmine used for myasthenia gravis
Rationale: “Neo the Cure” is a mnemonic indicating that Neostigmine is the drug of choice for myasthenia gravis treatment.

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92
Q
  1. Pyridostigmine’s primary application is:
    a) Short-term relief of hypertension
    b) Long-term maintenance treatment of myasthenia gravis
    c) Emergency treatment of glaucoma
    d) Management of depression
A

b) Long-term maintenance treatment of myasthenia gravis
Rationale: Pyridostigmine is primarily used for the long-term maintenance treatment of myasthenia gravis.

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93
Q
  1. Which reversible indirect agonist is not recommended for myasthenia gravis?
    a) Neostigmine
    b) Pyridostigmine
    c) Edrophonium
    d) Physostigmine
A

d) Physostigmine
Rationale: Physostigmine is not recommended for myasthenia gravis treatment.

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94
Q
  1. One of the cautionary notes for Edrophonium is that it can:
    a) Cause hypertension
    b) Worsen a cholinergic crisis
    c) Lead to severe depression
    d) Increase blood sugar levels
A

b) Worsen a cholinergic crisis
Rationale: Edrophonium can worsen a cholinergic crisis if misused, particularly in the context of myasthenia gravis.

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95
Q
  1. What is a potential side effect of Physostigmine?
    a) Causing cataracts and muscle paralysis
    b) Inducing sleep
    c) Reducing heart rate
    d) Causing weight gain
A

a) Causing cataracts and muscle paralysis
Rationale: Physostigmine can cause side effects such as cataracts and muscle paralysis.

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96
Q
  1. Neostigmine is also used as an antidote for:
    a) Opioid overdose
    b) Benzodiazepine overdose
    c) Neuromuscular junction (NMJ) blockade post-operation
    d) Atropine overdose
A

c) Neuromuscular junction (NMJ) blockade post-operation
Rationale: Neostigmine is used for the reversal of neuromuscular junction blockade post-operation.

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97
Q
  1. The action of Pyridostigmine is to:
    a) Decrease muscle strength
    b) Increase endogenous acetylcholine, enhancing muscle strength
    c) Block acetylcholine receptors in the muscles
    d) Reduce blood pressure
A

b) Increase endogenous acetylcholine, enhancing muscle strength
Rationale: Pyridostigmine increases endogenous acetylcholine, which enhances muscle strength, particularly in the treatment of myasthenia gravis.

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98
Q
  1. Physostigmine’s ability to cross the Blood-Brain Barrier (BBB) can lead to:
    a) Improved cognitive function
    b) Reduced anxiety
    c) Seizures
    d) Enhanced mood
A

c) Seizures
Rationale: Due to its ability to cross the BBB, Physostigmine can lead to seizures as a side effect.

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99
Q
  1. “Dodong the Long Name” mnemonic is associated with:
    a) Neostigmine
    b) Pyridostigmine
    c) Edrophonium
    d) Physostigmine
A

b) Pyridostigmine
Rationale: The mnemonic “Dodong the Long Name” refers to Pyridostigmine, which is used for long-term maintenance therapy in myasthenia gravis.

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100
Q
  1. The primary role of Edrophonium in myasthenia gravis is:
    a) Long-term maintenance therapy
    b) Short-term symptomatic relief
    c) Diagnostic use
    d) As an antidote for NMJ blockade
A

c) Diagnostic use
Rationale: Edrophonium is used primarily for the diagnostic evaluation of myasthenia gravis.

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101
Q
  1. Neostigmine’s use in postoperative care is primarily for:
    a) Pain relief
    b) Treating hypertension
    c) Treating neurogenic ileus and urinary retention
    d) Accelerating wound healing
A

c) Treating neurogenic ileus and urinary retention
Rationale: Neostigmine is used in postoperative care for the treatment of neurogenic ileus and urinary retention.

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102
Q
  1. A caution with the use of Physostigmine is that it:
    a) Can lead to severe dehydration
    b) May cause irreversible muscle damage
    c) Can lead to seizures due to CNS penetration
    d) Causes chronic insomnia
A

c) Can lead to seizures due to CNS penetration
Rationale: Due to its ability to cross the blood-brain barrier, Physostigmine can lead to seizures.

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103
Q
  1. What is a common use of atropine in emergency medicine?
    a) To reduce high blood pressure
    b) To increase heart rate in bradycardia
    c) To manage hypertension
    d) As a pain reliever
A

b) To increase heart rate in bradycardia
Rationale: Atropine is administered in cases of bradycardia to increase heart rate.

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104
Q
  1. In ophthalmology, atropine is used for:
    a) Improving vision
    b) Reducing intraocular pressure
    c) Dilating pupils for eye examinations
    d) Treating infections
A

c) Dilating pupils for eye examinations
Rationale: Atropine is used in ophthalmology, particularly in fundoscopy, to dilate pupils.

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105
Q
  1. Atropine is an antidote for which type of poisoning?
    a) Benzodiazepine
    b) Opioid
    c) Organophosphate
    d) Alcohol
A

c) Organophosphate
Rationale: Atropine is used as an antidote for organophosphate poisoning.

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106
Q
  1. The plant from which atropine is derived is:
    a) Cannabis sativa
    b) Papaver somniferum
    c) Atropa belladonna
    d) Eucalyptus globulus
A

c) Atropa belladonna
Rationale: Atropine is derived from the plant Atropa belladonna.

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107
Q
  1. Atropine’s mechanism of action involves:
    a) Stimulating muscarinic receptors
    b) Blocking muscarinic receptors
    c) Inhibiting acetylcholinesterase
    d) Activating nicotinic receptors
A

b) Blocking muscarinic receptors
Rationale: Atropine works by blocking the effects of acetylcholine on muscarinic receptors.

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108
Q
  1. What is the duration of atropine’s effect in the body?
    a) 1 hour
    b) 2-3 hours
    c) About 4 hours
    d) Over 6 hours
A

c) About 4 hours
Rationale: Atropine lasts about 4 hours in the body, but its effect can persist for up to 72 hours in the eyes.

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109
Q
  1. Atropine is contraindicated in individuals with:
    a) Hypertension
    b) Diabetes
    c) Narrow-angle glaucoma
    d) Asthma
A

c) Narrow-angle glaucoma
Rationale: Atropine is not recommended for individuals with narrow-angle glaucoma due to the risk of acute crisis.

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110
Q
  1. One of the toxicity symptoms of atropine is:
    a) Excessive salivation
    b) Dry mouth
    c) Increased urination
    d) Excessive sweating
A

b) Dry mouth
Rationale: “Dry as a Bone” refers to the symptom of dry mouth in atropine toxicity.

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111
Q
  1. Atropine can cause which central nervous system effect in overdose?
    a) Sedation
    b) Tachycardia
    c) Paralysis
    d) Reduced reflexes
A

b) Tachycardia
Rationale: In overdose, atropine CANNOT cross the blood-brain barrier BUT can cause tachycardia.

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112
Q
  1. What is the effect of atropine on gastrointestinal procedures?
    a) Increases secretions
    b) Reduces secretions
    c) Stimulates digestion
    d) Causes constipation
A

b) Reduces secretions
Rationale: Atropine is used in gastrointestinal procedures to reduce secretions.

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113
Q
  1. “Mad as a Hatter” refers to which side effect of atropine?
    a) Hypertension
    b) Hallucinations or delirium
    c) Insomnia
    d) Anxiety
A

b) Hallucinations or delirium
Rationale: “Mad as a Hatter” describes the potential for hallucinations or delirium in atropine toxicity.

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114
Q
  1. The symptomatic effect of atropine on the bladder is:
    a) Increased urination
    b) Urinary retention
    c) Reducing urinary urgency
    d) Causing incontinence
A

c) Reducing urinary urgency
Rationale: Atropine reduces urinary urgency by alleviating bladder spasms.

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115
Q
  1. Which of the following is another muscarinic antagonist used in the treatment of Parkinson’s disease?
    a) Benztropine
    b) Thorazine (Chlorpromazine)
    c) Diphenhydramine
    d) Ipratropium
A

a) Benztropine
Rationale: Benztropine is a muscarinic antagonist used in the treatment of Parkinson’s disease.

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116
Q
  1. Which medication is a muscarinic antagonist used as an antipsychotic?
    a) Benztropine
    b) Thorazine (Chlorpromazine)
    c) Diphenhydramine
    d) Ipratropium
A

b) Thorazine (Chlorpromazine)
Rationale: Thorazine (Chlorpromazine) is an antipsychotic medication that also acts as a muscarinic antagonist.

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117
Q
  1. Diphenhydramine, a muscarinic antagonist, is commonly used for:
    a) Asthma
    b) Allergies
    c) Parkinson’s disease
    d) Glaucoma
A

b) Allergies
Rationale: Diphenhydramine is an antihistamine commonly used for allergies.

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118
Q
  1. Ipratropium, as a muscarinic antagonist, is used primarily for:
    a) Treating hypertension
    b) Managing diabetes
    c) As a bronchodilator in asthma
    d) Treating narcolepsy
A

c) As a bronchodilator in asthma
Rationale: Ipratropium is used as a bronchodilator in the treatment of asthma.

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119
Q
  1. The term “Red as a Beet” in atropine toxicity refers to:
    a) Skin irritation
    b) Tachycardia and cutaneous vasodilation
    c) Allergic reactions
    d) Elevated body temperature
A

b) Tachycardia and cutaneous vasodilation
Rationale: “Red as a Beet” describes tachycardia and cutaneous vasodilation seen in atropine toxicity.

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120
Q
  1. “Blind as a Bat” in the context of atropine toxicity refers to:
    a) Permanent vision loss
    b) Blurred vision
    c) Night blindness
    d) Color blindness
A

b) Blurred vision
Rationale: “Blind as a Bat” in atropine toxicity refers to the side effect of blurred vision.

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121
Q
  1. “Hot as a Hare” in atropine toxicity indicates:
    a) Fever
    b) Absence of sweating
    c) Skin redness
    d) Increased body temperature
A

b) Absence of sweating
Rationale: “Hot as a Hare” signifies the absence of sweating in atropine toxicity.

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122
Q
  1. Atropine’s effect on salivation is to:
    a) Increase
    b) Decrease
    c) No change
    d) Vary depending on dosage
A

b) Decrease
Rationale: Atropine decreases salivation as part of its muscarinic antagonist action.

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123
Q
  1. What makes succinylcholine unique among neuromuscular junction (NMJ) blockers?
    a) It is the only non-depolarizing NMJ blocker
    b) It has the longest duration of action
    c) It is the only depolarizing NMJ blocker currently in use
    d) It has no adverse drug reactions
A

c) It is the only depolarizing NMJ blocker currently in use
Rationale: Succinylcholine is unique because it is the only depolarizing neuromuscular junction blocker being used clinically.

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124
Q
  1. Succinylcholine is primarily used for:
    a) Managing chronic pain
    b) Reducing blood pressure
    c) Inducing paralysis during surgery
    d) Treating muscle spasms
A

c) Inducing paralysis during surgery
Rationale: Succinylcholine is commonly used to induce paralysis during surgery or facilitate mechanical ventilation.

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125
Q
  1. The typical duration of succinylcholine’s action is:
    a) 1-2 minutes
    b) 3-6 minutes
    c) 10-15 minutes
    d) Over 20 minutes
A

b) 3-6 minutes
Rationale: The effects of succinylcholine usually last between 3 to 6 minutes, making it suitable for short procedures.

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126
Q
  1. The most severe adverse drug reaction to succinylcholine is:
    a) Hypotension
    b) Malignant Hyperthermia
    c) Allergic reactions
    d) Nausea and vomiting
A

b) Malignant Hyperthermia
Rationale: Malignant Hyperthermia is the most common and severe adverse reaction to succinylcholine.

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127
Q
  1. The antidote used to treat Malignant Hyperthermia caused by succinylcholine is:
    a) Epinephrine
    b) Dantrolene
    c) Atropine
    d) Naloxone
A

b) Dantrolene
Rationale: Dantrolene is the antidote used to treat Malignant Hyperthermia, a severe reaction to succinylcholine.

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128
Q
  1. During the Phase I block of succinylcholine’s action, what occurs at the muscle cell?
    a) Repolarization
    b) Prolonged depolarization
    c) Sensitization to acetylcholine
    d) Inhibition of sodium channels
A

b) Prolonged depolarization
Rationale: In Phase I block, succinylcholine causes prolonged depolarization of the muscle cell, opening sodium channels.

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129
Q
  1. What is the effect of cholinesterase inhibitors during the Phase I block of succinylcholine?
    a) They reverse the block
    b) They potentiate the block
    c) They have no effect
    d) They shorten the duration of action
A

b) They potentiate the block
Rationale: During Phase I block of succinylcholine, cholinesterase inhibitors actually potentiate the effect, rather than reversing it.

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130
Q
  1. What characterizes the Phase II block in succinylcholine’s action?
    a) The muscle cell remains depolarized
    b) The muscle cell repolarizes but remains blocked
    c) Immediate muscle contraction
    d) Sensitization to acetylcholine
A

b) The muscle cell repolarizes but remains blocked
Rationale: In Phase II block, the muscle cell repolarizes but becomes desensitized to acetylcholine, preventing further action potential generation.

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131
Q
  1. What is the antidote for Phase II block caused by succinylcholine?
    a) Dantrolene
    b) Epinephrine
    c) Neostigmine
    d) Atropine
A

c) Neostigmine
Rationale: Neostigmine, a cholinesterase inhibitor, can be used to reverse the Phase II block caused by succinylcholine.

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132
Q
  1. Which clinical application is NOT a use for succinylcholine?
    a) Treating hypertension
    b) Facilitating mechanical ventilation
    c) Acting as an adjuvant to general anesthesia
    d) Inducing short-term paralysis
A

a) Treating hypertension
Rationale: Succinylcholine is not used for treating hypertension; it is used to induce paralysis during surgery and facilitate mechanical ventilation.

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133
Q
  1. What happens during succinylcholine-induced paralysis?
    a) Voluntary muscle control is enhanced
    b) There is a decrease in muscle tone
    c) Rapid muscle contractions occur
    d) Muscles are unable to contract
A

d) Muscles are unable to contract
Rationale: Succinylcholine causes paralysis by preventing muscle contraction through prolonged depolarization and subsequent desensitization.

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134
Q
  1. What is a key feature of succinylcholine’s mechanism of action?
    a) It blocks the release of acetylcholine
    b) It mimics acetylcholine at the NMJ
    c) It inhibits cholinesterase
    d) It activates nicotinic receptors
A

b) It mimics acetylcholine at the NMJ
Rationale: Succinylcholine mimics acetylcholine at the neuromuscular junction, leading to depolarization and paralysis.

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135
Q
  1. The reason succinylcholine is used as an adjuvant to general anesthesia is to:
    a) Enhance pain relief
    b) Reduce anxiety
    c) Induce muscle relaxation
    d) Prevent nausea
A

c) Induce muscle relaxation
Rationale: Succinylcholine is used alongside general anesthesia to induce muscle relaxation and facilitate surgical procedures.

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136
Q
  1. Which phase of succinylcholine’s action is reversible with cholinesterase inhibitors?
    a) Phase I
    b) Phase II
    c) Both phases
    d) Neither phase
A

b) Phase II
Rationale: Cholinesterase inhibitors like neostigmine can reverse the Phase II block of succinylcholine but not the Phase I block.

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137
Q
  1. The duration of succinylcholine’s effect is particularly suitable for:
    a) Long surgical procedures
    b) Short surgical procedures
    c) Chronic pain management
    d) Long-term mechanical ventilation
A

b) Short surgical procedures
Rationale: The short duration of action (3-6 minutes) makes succinylcholine suitable for short surgical procedures and rapid sequence intubation.

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138
Q
  1. Tubocurarine and Atracurium are examples of:
    a) Depolarizing neuromuscular blockers
    b) Nondepolarizing neuromuscular blockers
    c) Cholinesterase inhibitors
    d) Calcium channel blockers
A

b) Nondepolarizing neuromuscular blockers
Rationale: Tubocurarine and Atracurium are prominent nondepolarizing neuromuscular blockers used as muscle relaxants during surgery.

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139
Q
  1. The primary function of nondepolarizing neuromuscular blockers is to:
    a) Increase muscle tone
    b) Relax muscles during surgical procedures
    c) Induce muscle contraction
    d) Stimulate the central nervous system
A

b) Relax muscles during surgical procedures
Rationale: Nondepolarizing neuromuscular blockers are used to relax muscles in preparation for or during surgical procedures.

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140
Q
  1. The first muscles typically affected by nondepolarizing neuromuscular blockers are:
    a) Limb muscles
    b) Respiratory muscles
    c) Muscles of the eyes and face
    d) Abdominal muscles
A

c) Muscles of the eyes and face
Rationale: The initial effect of nondepolarizing neuromuscular blockers is usually observed in the muscles of the eyes and face.

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141
Q
  1. Which drug is used to reverse the effects of nondepolarizing neuromuscular blockers?
    a) Dantrolene
    b) Epinephrine
    c) Neostigmine
    d) Atropine
A

c) Neostigmine
Rationale: Neostigmine, a cholinesterase inhibitor, is commonly used to reverse the blockade caused by nondepolarizing neuromuscular blockers.

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142
Q
  1. Dantrolene is primarily used in the treatment of:
    a) Parkinson’s disease
    b) Malignant hyperthermia
    c) Chronic pain
    d) Hypertension
A

b) Malignant hyperthermia
Rationale: Dantrolene is used to treat malignant hyperthermia, particularly associated with the use of succinylcholine and halothane.

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143
Q
  1. The mechanism of action of dantrolene involves:
    a) Stimulating calcium release in muscles
    b) Preventing the release of calcium from the sarcoplasmic reticulum
    c) Inhibiting acetylcholinesterase
    d) Blocking sodium channels
A

b) Preventing the release of calcium from the sarcoplasmic reticulum
Rationale: Dantrolene works by inhibiting the release of calcium from the sarcoplasmic reticulum of skeletal muscle cells, reducing muscle contraction.

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144
Q
  1. Which condition is dantrolene also effective in treating?
    a) Neuroleptic malignant syndrome
    b) Glaucoma
    c) Asthma
    d) Diabetes
A

a) Neuroleptic malignant syndrome
Rationale: Dantrolene is effective in treating neuroleptic malignant syndrome, a severe reaction to antipsychotic drugs.

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145
Q
  1. Edrophonium is used to reverse the effects of:
    a) Depolarizing neuromuscular blockers
    b) Nondepolarizing neuromuscular blockers
    c) Antipsychotic drugs
    d) Calcium channel blockers
A

b) Nondepolarizing neuromuscular blockers
Rationale: Edrophonium, a cholinesterase inhibitor, can be used to reverse the effects of nondepolarizing neuromuscular blockers.

146
Q
  1. The last effect of nondepolarizing neuromuscular blockers is typically on the:
    a) Heart
    b) Limb muscles
    c) Respiratory system
    d) Central nervous system
A

c) Respiratory system
Rationale: The last effect of nondepolarizing neuromuscular blockers is generally observed on the respiratory system.

147
Q
  1. The blockade caused by nondepolarizing neuromuscular blockers can be reversed with:
    a) Calcium supplements
    b) Antihistamines
    c) Cholinesterase inhibitors
    d) Corticosteroids
A

c) Cholinesterase inhibitors
Rationale: Cholinesterase inhibitors like neostigmine and edrophonium are used to reverse the blockade caused by nondepolarizing neuromuscular blockers.

148
Q
  1. The primary action of nondepolarizing neuromuscular blockers is to:
    a) Depolarize muscle cells
    b) Block acetylcholine at the NMJ
    c) Stimulate the release of acetylcholine
    d) Increase muscle contraction
A

b) Block acetylcholine at the NMJ
Rationale: Nondepolarizing neuromuscular blockers function by blocking the action of acetylcholine at the neuromuscular junction, preventing muscle contraction.

149
Q
  1. What is the main difference between depolarizing and nondepolarizing neuromuscular blockers?
    a) The duration of action
    b) Their source of derivation
    c) The mechanism of muscle relaxation
    d) The type of surgery they are used for
A

c) The mechanism of muscle relaxation
Rationale: The key difference lies in their mechanism of action; depolarizing blockers like succinylcholine mimic acetylcholine, while nondepolarizing blockers like tubocurarine block acetylcholine.

150
Q
  1. In the context of surgical procedures, nondepolarizing neuromuscular blockers are used to:
    a) Reduce bleeding
    b) Enhance patient comfort
    c) Facilitate intubation and surgical access
    d) Prevent post-operative pain
A

c) Facilitate intubation and surgical access
Rationale: These blockers are primarily used to relax muscles, thereby facilitating intubation and providing better surgical access.

151
Q
  1. The respiratory system’s vulnerability to nondepolarizing neuromuscular blockers is due to:
    a) High concentration of acetylcholine receptors
    b) Lower blood supply to the respiratory muscles
    c) The essential role of muscles in respiration
    d) Increased sensitivity of respiratory muscles
A

c) The essential role of muscles in respiration
Rationale: The respiratory system is particularly affected due to the essential role of muscles in breathing, making their relaxation critical.

152
Q
  1. Ganglionic blockers act by blocking:
    a) Muscarinic neuronal receptors
    b) Nicotinic neuronal receptors
    c) Acetylcholine synthesis
    d) Norepinephrine release
A

b) Nicotinic neuronal receptors
Rationale: Ganglionic blockers function by inhibiting nicotinic neuronal receptors present in both the sympathetic and parasympathetic ganglia of the autonomic nervous system.

153
Q
  1. Ganglionic blockers are currently used in the management of:
    a) Asthma
    b) Diabetes
    c) Hypertensive emergencies
    d) Chronic pain
A

c) Hypertensive emergencies
Rationale: One of the few remaining uses of ganglionic blockers is in the rapid decrease of blood pressure during hypertensive emergencies.

154
Q
  1. A common side effect of ganglionic blockers is:
    a) Bradycardia
    b) Tachycardia
    c) Hypoglycemia
    d) Muscle spasms
A

b) Tachycardia
Rationale: Tachycardia occurs due to the inhibition of parasympathetic influence on the heart by ganglionic blockers.

155
Q
  1. Vasodilation caused by ganglionic blockers results from:
    a) Increased sympathetic activity
    b) Blockade of sympathetic vasoconstrictive signals
    c) Stimulation of parasympathetic activity
    d) Direct action on blood vessels
A

b) Blockade of sympathetic vasoconstrictive signals
Rationale: Ganglionic blockers cause vasodilation by inhibiting sympathetic vasoconstrictive signals.

156
Q
  1. Mydriasis (pupil dilation) from ganglionic blockers occurs due to:
    a) Increased sympathetic activity in the eye
    b) Reduced parasympathetic activity in the eye
    c) Direct irritation of the eye muscles
    d) Enhancement of visual acuity
A

b) Reduced parasympathetic activity in the eye
Rationale: Mydriasis occurs as a result of decreased parasympathetic activity in the eye due to ganglionic blockers.

157
Q
  1. The effect of ganglionic blockers on gastrointestinal tract (GIT) motility is:
    a) Increase in motility
    b) No change in motility
    c) Reduction in motility
    d) Unpredictable changes in motility
A

c) Reduction in motility
Rationale: Reduced GIT motility is a side effect of ganglionic blockers as both sympathetic and parasympathetic influences are diminished.

158
Q
  1. Urinary retention as a side effect of ganglionic blockers occurs due to:
    a) Stimulation of the bladder muscle
    b) Relaxation of the bladder muscle
    c) Infection of the urinary tract
    d) Increased fluid intake
A

b) Relaxation of the bladder muscle
Rationale: Ganglionic blockers can lead to urinary retention as a result of the relaxation of the bladder muscle.

159
Q
  1. Decreased sweating from ganglionic blockers is a result of:
    a) Enhanced sympathetic stimulation of sweat glands
    b) Diminished sympathetic stimulation of sweat glands
    c) Direct effect on sweat gland receptors
    d) Dehydration
A

b) Diminished sympathetic stimulation of sweat glands
Rationale: Decreased sweating is due to reduced sympathetic stimulation of sweat glands when using ganglionic blockers.

160
Q
  1. The reason ganglionic blockers are rarely used in current medical practice is due to:
    a) Their high cost
    b) The development of more effective drugs
    c) Their broad and often unpredictable effects
    d) Lack of availability
A

c) Their broad and often unpredictable effects
Rationale: Ganglionic blockers are seldom used because of their wide-ranging and often unpredictable effects on the body.

161
Q
  1. When using ganglionic blockers, one should monitor for:
    a) Increased blood glucose levels
    b) Changes in blood pressure
    c) Signs of infection
    d) Skin rashes
A

b) Changes in blood pressure
Rationale: Due to their significant impact on blood pressure, monitoring for changes in blood pressure is crucial when using ganglionic blockers.

162
Q
  1. Epinephrine acts on which adrenergic receptors?
    a) α1 and α2 only
    b) β1 and β2 only
    c) α1, α2, β1, and β2
    d) D1 and D2
A

c) α1, α2, β1, and β2
Rationale: Epinephrine acts on α1, α2, β1, and β2 adrenergic receptors, causing a range of effects like increased heart rate, vasoconstriction, and bronchodilation.

163
Q
  1. The primary effect of norepinephrine is:
    a) Lowering blood pressure
    b) Causing vasoconstriction
    c) Reducing heart rate
    d) Inducing sleep
A

b) Causing vasoconstriction
Rationale: Norepinephrine primarily affects α1 receptors, causing vasoconstriction and thereby increasing blood pressure.

164
Q
  1. Isoproterenol predominantly affects:
    a) α receptors
    b) β1 and β2 receptors
    c) D1 and D2 receptors
    d) Muscarinic receptors
A

b) β1 and β2 receptors
Rationale: Isoproterenol has an equal affinity for β1 and β2 receptors, leading to increased heart rate and bronchodilation.

165
Q
  1. Dopamine’s effect at low doses is primarily:
    a) Vasoconstriction
    b) Vasodilation
    c) Decreasing heart rate
    d) Bronchoconstriction
A

b) Vasodilation
Rationale: At low doses, dopamine predominantly affects dopamine receptors, leading to vasodilation.

166
Q
  1. Dobutamine is mainly used for:
    a) Increasing vascular resistance
    b) Decreasing cardiac output
    c) Increasing heart rate and force of contraction
    d) Causing bronchodilation
A

c) Increasing heart rate and force of contraction
Rationale: Dobutamine primarily stimulates β1 receptors, increasing cardiac output by raising heart rate and the force of contraction.

167
Q
  1. Which sympathomimetic drug lacks significant action on α receptors?
    a) Epinephrine
    b) Norepinephrine
    c) Isoproterenol
    d) Dopamine
A

c) Isoproterenol
Rationale: Isoproterenol lacks significant vasoconstrictive or vasodilative effects as it does not act on α receptors.

168
Q
  1. The increase in cardiac output caused by epinephrine is due to its action on:
    a) α1 receptors
    b) α2 receptors
    c) β1 receptors
    d) D1 receptors
A

c) β1 receptors
Rationale: Epinephrine increases heart rate and cardiac output primarily through its action on β1 adrenergic receptors.

169
Q
  1. In the management of cardiac arrest, which drug is commonly used?
    a) Norepinephrine
    b) Epinephrine
    c) Dobutamine
    d) Isoproterenol
A

b) Epinephrine
Rationale: Epinephrine is commonly used in cardiac arrest due to its ability to increase heart rate and cardiac output.

170
Q
  1. Dopamine’s effects at higher doses are mainly due to stimulation of:
    a) β and α receptors
    b) Dopamine receptors only
    c) Muscarinic receptors
    d) Serotonin receptors
A

a) β and α receptors
Rationale: At higher doses, dopamine stimulates β and α receptors, increasing heart rate and blood pressure.

170
Q
  1. The effect of dobutamine on vascular resistance is:
    a) Significant increase
    b) Significant decrease
    c) Minimal
    d) Unpredictable
A

c) Minimal
Rationale: Dobutamine primarily stimulates β1 receptors and has minimal effects on vascular resistance.

171
Q
  1. Which drug is known for its bronchodilation effect?
    a) Epinephrine
    b) Norepinephrine
    c) Isoproterenol
    d) Dopamine
A

c) Isoproterenol
Rationale: Isoproterenol causes bronchodilation due to its action on β2 receptors.

172
Q
  1. For patients with shock, which catecholamine is often preferred?
    a) Dopamine
    b) Dobutamine
    c) Epinephrine
    d) Norepinephrine
A

d) Norepinephrine
Rationale: Norepinephrine is often preferred for treating shock due to its potent vasoconstrictive effects, which help to increase blood pressure.

173
Q
  1. The therapeutic use of epinephrine in anaphylaxis is primarily due to its action on:
    a) β2 receptors causing bronchodilation
    b) α1 receptors causing vasoconstriction
    c) D1 receptors causing vasodilation
    d) β1 receptors increasing heart rate
A

a) β2 receptors causing bronchodilation
Rationale: In anaphylaxis, epinephrine’s action on β2 receptors causing bronchodilation is crucial for opening airways.

174
Q
  1. Which catecholamine is most likely to cause tachycardia as a side effect?
    a) Epinephrine
    b) Norepinephrine
    c) Isoproterenol
    d) Dopamine
A

c) Isoproterenol
Rationale: Isoproterenol, due to its strong action on β1 receptors, is more likely to cause tachycardia as a side effect.

175
Q
  1. The primary therapeutic use of clonidine is to treat:
    a) Hypertension
    b) Diabetes
    c) Asthma
    d) High cholesterol
A

a) Hypertension
Rationale: Clonidine, an α2 agonist, is primarily used to treat hypertension.

175
Q
  1. The use of dobutamine in heart failure patients is primarily to:
    a) Decrease heart rate
    b) Increase cardiac contractility
    c) Induce vasodilation
    d) Reduce blood pressure
A

b) Increase cardiac contractility
Rationale: In heart failure, dobutamine is used to increase cardiac contractility and improve cardiac output.

176
Q
  1. Phenylephrine primarily acts on which type of adrenergic receptor?
    a) α1
    b) α2
    c) β1
    d) β2
A

a) α1
Rationale: Phenylephrine is an α1 agonist that causes vasoconstriction, leading to increased blood pressure.

177
Q
  1. What is a common use of phenylephrine?
    a) Asthma treatment
    b) Nasal decongestant
    c) Treating diabetes
    d) Managing high cholesterol
A

b) Nasal decongestant
Rationale: Phenylephrine is often used as a nasal decongestant.

178
Q
  1. A precaution for patients taking clonidine is the risk of:
    a) Liver toxicity
    b) Orthostatic hypotension
    c) Severe headache
    d) Kidney damage
A

b) Orthostatic hypotension
Rationale: Patients on clonidine should be cautious of orthostatic hypotension and change positions slowly.

178
Q
  1. Methoxamine is used to treat:
    a) Hypertension
    b) Hypotension
    c) Congestive heart failure
    d) Arrhythmias
A

b) Hypotension
Rationale: Methoxamine, an α1 agonist, is primarily used to treat hypotension.

179
Q
  1. What is an adverse drug reaction (ADR) of clonidine?
    a) Increased heart rate
    b) Sedation
    c) Muscle spasms
    d) Weight gain
A

b) Sedation
Rationale: Common adverse drug reactions of clonidine include sedation, dry mouth, sexual dysfunction, and orthostatic hypotension.

180
Q
  1. Which condition is NOT an off-label use of clonidine?
    a) Atrial fibrillation
    b) Growth delay in children
    c) Tourette’s Syndrome
    d) Myocardial infarction
A

d) Myocardial infarction
Rationale: Clonidine has been studied for various off-label uses, but myocardial infarction is not one of them.

181
Q
  1. What effect does phenylephrine have on blood pressure?
    a) Decreases it
    b) Increases it
    c) Has no effect
    d) Variable effect
A

b) Increases it
Rationale: Phenylephrine causes vasoconstriction, leading to an increase in blood pressure.

181
Q
  1. Clonidine can be used off-label to manage:
    a) High cholesterol
    b) Restless leg syndrome
    c) Bone fractures
    d) Skin infections
A

b) Restless leg syndrome
Rationale: Clonidine has off-label use in managing conditions like restless leg syndrome and Tourette’s Syndrome.

182
Q
  1. Phenylephrine’s use during the COVID season was noted for causing:
    a) Decreased heart rate
    b) Increased blood pressure
    c) Lowered blood sugar
    d) Improved lung function
A

b) Increased blood pressure
Rationale: Excessive use of phenylephrine in over-the-counter cold and allergy medications during the COVID season led to significant increases in blood pressure in some cases.

183
Q
  1. Clonidine’s mechanism of action in treating hypertension involves:
    a) Vasodilation
    b) Vasoconstriction
    c) Diuretic effect
    d) Blocking calcium channels
A

a) Vasodilation
Rationale: Clonidine, an α2 agonist, reduces blood pressure primarily through vasodilation.

184
Q
  1. One of the adverse effects of methoxamine is:
    a) Hypotension
    b) Reflex bradycardia
    c) Tachycardia
    d) Hypoglycemia
A

b) Reflex bradycardia
Rationale: Methoxamine can cause reflex bradycardia as a result of its vasoconstrictive action on α1 receptors.

185
Q
  1. The use of clonidine in benzodiazepine withdrawal is due to its ability to:
    a) Increase alertness
    b) Reduce anxiety
    c) Stimulate the central nervous system
    d) Increase heart rate
A

b) Reduce anxiety
Rationale: Clonidine is effective in managing benzodiazepine and opiate withdrawal, likely due to its sedative and anxiolytic effects.

186
Q
  1. A side effect of clonidine that patients need to be cautious about is:
    a) Excessive sweating
    b) Dry mouth
    c) Increased urination
    d) Insomnia
A

b) Dry mouth
Rationale: Dry mouth is a common side effect of clonidine, along with sedation and sexual dysfunction.

187
Q
  1. Phenylephrine’s reflex bradycardia is a result of:
    a) Direct stimulation of the heart
    b) Decreased cardiac output
    c) Baroreceptor reflex
    d) Blockade of β1 receptors
A

c) Baroreceptor reflex
Rationale: Reflex bradycardia from phenylephrine is caused by the baroreceptor reflex in response to increased blood pressure.

188
Q
  1. Which alpha agonist is known for its nasal decongestant properties?
    a) Clonidine
    b) Methoxamine
    c) Phenylephrine
    d) Epinephrine
A

c) Phenylephrine
Rationale: Phenylephrine is commonly used as a nasal decongestant due to its vasoconstrictive properties.

189
Q
  1. Clonidine’s off-label use in ADHD is due to its:
    a) Stimulant effect
    b) Sedative effect
    c) Effect on dopamine levels
    d) Vasoconstrictive properties
A

b) Sedative effect
Rationale: Clonidine is used off-label for ADHD, likely due to its sedative effects, which can help with hyperactivity and impulsivity.

190
Q
  1. The primary action of alpha agonists in hypertensive emergencies is to:
    a) Reduce heart rate
    b) Induce diuresis
    c) Increase blood pressure
    d) Lower blood sugar levels
A

a) Reduce heart rate

191
Q
  1. The common use of methoxamine is in the treatment of:
    a) Asthma
    b) Diabetes
    c) Hypotension
    d) High cholesterol
A

c) Hypotension
Rationale: Methoxamine is primarily used to treat hypotension due to its vasoconstrictive action on α1 receptors.

192
Q
  1. Dobutamine primarily acts on which beta receptors?
    a) β1 receptors
    b) β2 receptors
    c) Both β1 and β2 receptors equally
    d) Neither β1 nor β2 receptors
A

a) β1 receptors
Rationale: Dobutamine has a greater effect on β1 receptors, making it useful in increasing cardiac output, especially in congestive heart failure (CHF).

193
Q
  1. The primary clinical use of dobutamine is in the management of:
    a) Asthma
    b) Diabetes
    c) Congestive heart failure (CHF)
    d) High blood pressure
A

c) Congestive heart failure (CHF)
Rationale: Dobutamine is used primarily in the management of unstable congestive heart failure and shock situations due to its action on β1 receptors.

194
Q
  1. Isoproterenol exhibits equal action on:
    a) α1 and α2 receptors
    b) β1 and β2 receptors
    c) Muscarinic receptors
    d) Dopamine receptors
A

b) β1 and β2 receptors
Rationale: Isoproterenol has an equal affinity for both β1 and β2 receptors, affecting both cardiovascular and respiratory systems.

195
Q
  1. One of the cardiovascular effects of dobutamine is:
    a) Decreased heart rate
    b) Increased heart rate
    c) Lowered blood pressure
    d) Reduced cardiac output
A

b) Increased heart rate
Rationale: Dobutamine increases heart rate and cardiac output, which is beneficial in treating conditions like congestive heart failure.

196
Q
  1. The use of isoproterenol is beneficial in patients with:
    a) Heart block and bradycardia
    b) Hypertension
    c) Depression
    d) Chronic pain
A

a) Heart block and bradycardia
Rationale: Isoproterenol is used in patients with heart block and bradycardia to stimulate heart rate.

197
Q
  1. In addition to its cardiovascular effects, isoproterenol also has a significant impact on:
    a) Liver function
    b) Blood glucose levels
    c) Bronchodilation
    d) Gastrointestinal motility
A

c) Bronchodilation
Rationale: Isoproterenol causes bronchodilation due to its action on β2 receptors, making it beneficial in certain respiratory conditions.

198
Q
  1. Dobutamine’s action on β1 receptors results in:
    a) Decreased peripheral vascular resistance
    b) Lowered heart rate
    c) Increased cardiac output
    d) Bronchoconstriction
A

c) Increased cardiac output
Rationale: Dobutamine increases cardiac output by its action on β1 receptors, without significantly raising the heart rate.

199
Q
  1. The effect of isoproterenol on peripheral vascular resistance (PVR) is to:
    a) Increase it
    b) Decrease it
    c) Have no effect
    d) Variable effects
A

b) Decrease it
Rationale: Isoproterenol lowers peripheral vascular resistance, which can reduce blood pressure.

200
Q
  1. A common side effect of dobutamine related to its β1 activity is:
    a) Hypotension
    b) Tachycardia
    c) Hypoglycemia
    d) Dry mouth
A

b) Tachycardia
Rationale: As dobutamine stimulates β1 receptors in the heart, a common side effect is tachycardia.

201
Q
  1. Isoproterenol is used in respiratory conditions due to its effect on:
    a) α receptors
    b) β1 receptors
    c) β2 receptors
    d) Dopamine receptors
A

c) β2 receptors
Rationale: Isoproterenol’s action on β2 receptors in the lungs leads to bronchodilation, which is useful in treating certain respiratory conditions.

202
Q
  1. What differentiates the action of dobutamine from isoproterenol?
    a) Dobutamine causes more significant bronchodilation
    b) Isoproterenol has a more pronounced effect on heart rate
    c) Dobutamine has a greater effect on β1 receptors
    d) Isoproterenol is less effective in increasing cardiac output
A

c) Dobutamine has a greater effect on β1 receptors
Rationale: Dobutamine primarily acts on β1 receptors, whereas isoproterenol equally affects β1 and β2 receptors.

203
Q
  1. Isoproterenol’s lowering of blood pressure is primarily due to its action on:
    a) Heart rate
    b) Peripheral vascular resistance
    c) Blood volume
    d) Renal function
A

b) Peripheral vascular resistance
Rationale: Isoproterenol lowers peripheral vascular resistance, which can lead to a reduction in blood pressure.

204
Q
  1. The administration of dobutamine is particularly useful in:
    a) Shock situations
    b) Asthma attacks
    c) Diabetic emergencies
    d) Chronic hypertension
A

a) Shock situations
Rationale: Dobutamine is effective in shock situations due to its ability to increase cardiac output.

205
Q
  1. Which drug would be preferred in a patient with both respiratory distress and bradycardia?
    a) Dobutamine
    b) Isoproterenol
    c) Phenylephrine
    d) Clonidine
A

b) Isoproterenol
Rationale: Isoproterenol is beneficial in this scenario due to its bronchodilatory effect (β2 action) and ability to increase heart rate (β1 action).

206
Q
  1. In managing unstable congestive heart failure (CHF), the choice of dobutamine is due to its:
    a) Diuretic effect
    b) Ability to decrease heart rate
    c) Capacity to increase cardiac output
    d) Vasodilatory properties
A

c) Capacity to increase cardiac output
Rationale: In unstable CHF, dobutamine is chosen for its ability to effectively increase cardiac output without significantly raising heart rate.

207
Q
  1. The primary action of Beta2 selective agonists like Albuterol is to:
    a) Constrict bronchial smooth muscles
    b) Dilate bronchial smooth muscles
    c) Increase heart rate
    d) Decrease blood pressure
A

b) Dilate bronchial smooth muscles
Rationale: Beta2 selective agonists primarily act on beta2-adrenergic receptors in the bronchial smooth muscles, causing bronchodilation and easing breathing in conditions like asthma and COPD.

208
Q
  1. Terbutaline and Ritodrine are additionally used to:
    a) Lower blood sugar levels
    b) Relax the uterus during premature labor
    c) Treat high blood pressure
    d) Manage heart failure
A

b) Relax the uterus during premature labor
Rationale: Apart from their pulmonary applications, Terbutaline and Ritodrine can be used to relax the uterus, delaying delivery and reducing complications in premature birth.

209
Q
  1. One common adverse drug reaction (ADR) of Beta2 selective agonists is:
    a) Tachyphylaxis
    b) Bradycardia
    c) Hypoglycemia
    d) Muscle relaxation
A

a) Tachyphylaxis
Rationale: Tachyphylaxis, a rapidly diminishing response to successive doses of a drug, is a known adverse reaction of Beta2 selective agonists.

210
Q
  1. Metaproterenol is primarily used in the treatment of:
    a) Diabetes
    b) Asthma and COPD
    c) High cholesterol
    d) Renal disease
A

b) Asthma and COPD
Rationale: Metaproterenol is commonly used in the treatment of bronchial asthma and Chronic Obstructive Pulmonary Disease (COPD).

211
Q
  1. The mechanism of action of Albuterol involves:
    a) Blocking beta2 receptors
    b) Stimulating beta2 receptors
    c) Inhibiting cholinesterase
    d) Blocking alpha receptors
A

b) Stimulating beta2 receptors
Rationale: Albuterol works by stimulating beta2 receptors in bronchial smooth muscles, leading to bronchodilation.

212
Q
  1. In which condition would you most likely prescribe a Beta2 selective agonist like Terbutaline?
    a) Asthma
    b) Hypertension
    c) Gastric ulcer
    d) Anxiety disorder
A

a) Asthma
Rationale: Beta2 selective agonists like Terbutaline are most commonly prescribed for asthma due to their bronchodilatory effect.

213
Q
  1. The use of Ritodrine in premature labor is to:
    a) Induce labor
    b) Strengthen uterine contractions
    c) Relax the uterus
    d) Increase fetal heart rate
A

c) Relax the uterus
Rationale: Ritodrine is used in premature labor to relax the uterus, helping to delay delivery and reduce premature birth complications.

214
Q
  1. Which Beta2 selective agonist is commonly used for quick relief in asthma attacks?
    a) Metaproterenol
    b) Albuterol
    c) Terbutaline
    d) Ritodrine
A

b) Albuterol
Rationale: Albuterol is frequently used for quick relief during asthma attacks due to its fast-acting bronchodilatory effect.

215
Q
  1. The therapeutic effect of Beta2 selective agonists in COPD is primarily due to:
    a) Decreased mucus production
    b) Bronchodilation
    c) Reduced inflammation
    d) Strengthening respiratory muscles
A

b) Bronchodilation
Rationale: The therapeutic effect in COPD treatment with Beta2 selective agonists arises from bronchodilation, which improves airflow and breathing

216
Q
  1. An additional use of Terbutaline in clinical practice is:
    a) Treating heart arrhythmias
    b) Delaying premature labor
    c) Managing high blood pressure
    d) Reducing cholesterol levels
A

b) Delaying premature labor
Rationale: Besides its pulmonary applications, Terbutaline is also used to delay premature labor by relaxing the uterus.

217
Q
  1. Which Beta2 selective agonist is also used in managing premature labor?
    a) Albuterol
    b) Metaproterenol
    c) Terbutaline
    d) Dobutamine
A

c) Terbutaline
Rationale: Terbutaline, apart from its use in respiratory conditions, is also utilized to manage premature labor.

218
Q
  1. Tachyphylaxis to Beta2 selective agonists like Albuterol can lead to:
    a) Increased effectiveness over time
    b) Diminished response with successive doses
    c) Constant effectiveness regardless of dosage
    d) Spontaneous recovery of effectiveness
A

b) Diminished response with successive doses
Rationale: Tachyphylaxis is characterized by a rapidly diminishing response to successive doses of a drug like Albuterol, making it less effective over time.

219
Q
  1. The selection of Metaproterenol in asthma treatment is based on its ability to:
    a) Suppress immune responses
    b) Relieve bronchoconstriction
    c) Reduce allergic reactions
    d) Increase oxygen uptake
A

b) Relieve bronchoconstriction
Rationale: Metaproterenol is chosen for asthma treatment due to its bronchodilatory effect, which relieves bronchoconstriction and eases breathing.

220
Q
  1. In choosing a medication for acute asthma, a key factor favoring the use of Albuterol is its:
    a) Long-lasting effect
    b) Quick onset of action
    c) Impact on lowering blood pressure
    d) Sedative properties
A

b) Quick onset of action
Rationale: Albuterol’s quick onset of action makes it a preferred choice for immediate relief in acute asthma episodes.

221
Q
  1. The role of Terbutaline in COPD management is to:
    a) Increase lung capacity
    b) Enhance mucociliary clearance
    c) Relax bronchial smooth muscles
    d) Suppress cough reflex
A

c) Relax bronchial smooth muscles
Rationale: Terbutaline aids in COPD management by relaxing bronchial smooth muscles, thereby improving airflow and reducing breathing difficulties.

222
Q
  1. At low doses, epinephrine primarily acts on:
    a) Beta receptors
    b) Alpha receptors
    c) Dopamine receptors
    d) Muscarinic receptors
A

b) Alpha receptors
Rationale: At low doses, epinephrine predominantly acts on alpha receptors. Its action shifts towards beta receptors at higher doses.

223
Q
  1. A clinical use of epinephrine is in the treatment of:
    a) Diabetes
    b) Bronchial asthma
    c) Depression
    d) High blood pressure
A

b) Bronchial asthma
Rationale: Epinephrine is used in the treatment of bronchial asthma, anaphylaxis, and achieving hemostasis.`

224
Q
  1. Epinephrine reversal is observed when it is given after the blockade of:
    a) Beta-adrenergic receptors
    b) Alpha-adrenergic receptors
    c) Dopamine receptors
    d) Muscarinic receptors
A

b) Alpha-adrenergic receptors
Rationale: When epinephrine is administered following the blockade of alpha-adrenergic receptors, beta-receptor activation becomes more apparent, leading to a fall in blood pressure.

225
Q
  1. Norepinephrine lacks action on which type of receptor?
    a) Alpha1
    b) Alpha2
    c) Beta1
    d) Beta2
A

d) Beta2
Rationale: Norepinephrine does not act on beta2 receptors, differentiating it from other catecholamines.

226
Q
  1. The primary effect of norepinephrine is:
    a) Causing vasodilation
    b) Inducing reflex bradycardia
    c) Decreasing heart rate
    d) Bronchodilation
A

b) Inducing reflex bradycardia
Rationale: Norepinephrine primarily causes vasoconstriction and can induce reflex bradycardia.

227
Q
  1. Dopamine’s action at lower doses primarily involves:
    a) Stimulation of alpha receptors
    b) Activation of dopamine receptors
    c) Inhibition of beta receptors
    d) Blockade of muscarinic receptors
A

b) Activation of dopamine receptors
Rationale: At lower doses, dopamine predominantly acts on dopamine receptors, leading to vasodilation.

228
Q
  1. In clinical practice, dopamine is used in the management of:
    a) Asthma
    b) Shock
    c) Diabetes
    d) High cholesterol
A

b) Shock
Rationale: Dopamine is used in the management of shock, acute respiratory failure, and congestive heart failure.

229
Q
  1. The primary clinical application of norepinephrine is:
    a) Treating hypertension
    b) As a last resort in resuscitation efforts
    c) Managing diabetes
    d) Treating asthma
A

b) As a last resort in resuscitation efforts
Rationale: Norepinephrine is often used in resuscitation efforts, especially as a last resort to stimulate the heart.

230
Q
  1. At high doses, epinephrine’s action shifts towards:
    a) Alpha receptors
    b) Beta receptors
    c) Dopamine receptors
    d) Muscarinic receptors
A

b) Beta receptors
Rationale: At higher doses, epinephrine’s action predominantly affects beta receptors, leading to effects like bronchodilation and increased heart rate.

231
Q
  1. Dopamine’s activation of beta receptors (B1, B2) at higher doses results in:
    a) Decreased cardiac output
    b) Vasodilation
    c) Increased heart rate and cardiac output
    d) Vasoconstriction
A

c) Increased heart rate and cardiac output
Rationale: At higher doses, dopamine stimulates beta receptors, leading to increased heart rate and cardiac output.

232
Q
  1. In treating anaphylaxis, epinephrine is used due to its ability to:
    a) Lower blood pressure
    b) Increase blood glucose
    c) Cause bronchodilation
    d) Induce diuresis
A

c) Cause bronchodilation
Rationale: Epinephrine is crucial in treating anaphylaxis due to its bronchodilatory effect, along with its ability to increase heart rate and vasoconstriction.

233
Q
  1. Norepinephrine’s lack of action on beta2 receptors means it:
    a) Cannot induce bronchodilation
    b) Increases heart rate significantly
    c) Lowers blood pressure
    d) Causes muscle relaxation
A

a) Cannot induce bronchodilation
Rationale: Norepinephrine’s absence of action on beta2 receptors means it does not induce bronchodilation, unlike some other catecholamines.

234
Q
  1. The vasodilation effect of dopamine at lower doses is beneficial in treating:
    a) Hypertension
    b) Shock
    c) Diabetes
    d) High cholesterol
A

b) Shock
Rationale: Dopamine’s vasodilation effect at lower doses is particularly useful in the treatment of shock, where maintaining blood flow is crucial.

235
Q
  1. An important consideration when using epinephrine in a patient with pre-existing hypertension is its potential to:
    a) Lower blood pressure
    b) Further increase blood pressure
    c) Reduce heart rate
    d) Induce hypoglycemia
A

b) Further increase blood pressure
Rationale: Due to its vasoconstrictive effect, epinephrine can further increase blood pressure in patients with pre-existing hypertension.

236
Q
  1. In shock situations, dopamine is often preferred for its ability to:
    a) Lower heart rate
    b) Decrease cardiac output
    c) Provide renal protection
    d) Increase cardiac output
A

d) Increase cardiac output
Rationale: Dopamine is preferred in shock situations due to its ability to increase cardiac output and improve blood flow to vital organs.

237
Q
  1. Tyramine, when combined with MAOIs, can cause:
    a) Hypotensive crisis
    b) Hypertensive crisis
    c) Reduced heart rate
    d) Bronchodilation
A

b) Hypertensive crisis
Rationale: Tyramine can trigger a hypertensive crisis when ingested with monoamine oxidase inhibitors (MAOIs), due to excessive release of norepinephrine.

238
Q
  1. The primary clinical use of amphetamine is in the treatment of:
    a) Asthma
    b) Attention-Deficit/Hyperactivity Disorder (ADHD)
    c) Diabetes
    d) High blood pressure
A

b) Attention-Deficit/Hyperactivity Disorder (ADHD)
Rationale: Amphetamine is primarily prescribed for ADHD and appetite suppression, due to its ability to stimulate the release of norepinephrine and dopamine in the CNS.

239
Q
  1. Amphetamine exerts its effect by:
    a) Directly activating receptors
    b) Causing the release of neurotransmitters
    c) Inhibiting neurotransmitter breakdown
    d) Blocking neurotransmitter reuptake
A

b) Causing the release of neurotransmitters
Rationale: Amphetamines work indirectly by stimulating the release of neurotransmitters like norepinephrine and dopamine, rather than directly activating receptors.

240
Q
  1. Foods high in tyramine should be avoided when taking:
    a) Antibiotics
    b) NSAIDs
    c) Monoamine oxidase inhibitors (MAOIs)
    d) Beta-blockers
A

c) Monoamine oxidase inhibitors (MAOIs)
Rationale: Tyramine-rich foods like red wine, beer, and cheese can cause a hypertensive crisis when ingested with MAOIs.

241
Q
  1. Which system does amphetamine primarily affect?
    a) Digestive system
    b) Respiratory system
    c) Central nervous system (CNS)
    d) Cardiovascular system
A

c) Central nervous system (CNS)
Rationale: Amphetamine can enter the CNS and stimulate the release of neurotransmitters, affecting mood, attention, and alertness.

242
Q
  1. The interaction between tyramine and MAOIs is a significant concern due to:
    a) Decreased efficacy of MAOIs
    b) Risk of a hypertensive crisis
    c) Potential for allergic reactions
    d) Development of gastrointestinal issues
A

b) Risk of a hypertensive crisis
Rationale: The interaction between tyramine and MAOIs is dangerous due to the increased risk of a hypertensive crisis.

243
Q
  1. Apart from ADHD, another clinical use of amphetamine is for:
    a) Appetite suppression
    b) Treating hypertension
    c) Pain relief
    d) Sleep disorders
A

a) Appetite suppression
Rationale: Amphetamine is also used for appetite suppression due to its stimulant effects on the CNS.

244
Q
  1. Tyramine’s lack of therapeutic use is primarily because:
    a) It is ineffective as a drug
    b) It has a high potential for abuse
    c) It can cause serious interactions with certain medications
    d) It is naturally produced in the body
A

c) It can cause serious interactions with certain medications

Rationale: Tyramine is not used as a drug in medical treatments due to its potential to cause dangerous interactions, especially with MAOIs.

245
Q
  1. In individuals taking MAOIs, ingestion of tyramine can lead to:
    a) Lowered blood sugar levels
    b) Increased risk of infections
    c) Elevated blood pressure
    d) Decreased cognitive function
A

c) Elevated blood pressure
Rationale: Tyramine ingestion in individuals taking MAOIs can lead to elevated blood pressure, potentially resulting in a hypertensive crisis.

246
Q
  1. The effect of amphetamine on neurotransmitter release primarily leads to:
    a) Sedation
    b) Decreased attention span
    c) Increased alertness and energy
    d) Muscle relaxation
A

c) Increased alertness and energy
Rationale: Amphetamine increases alertness and energy by stimulating the release of norepinephrine and dopamine in the CNS.

247
Q
  1. Ephedrine’s primary mechanism of action involves:
    a) Blocking norepinephrine receptors
    b) Releasing norepinephrine from nerve terminals
    c) Inhibiting dopamine release
    d) Activating serotonin receptors
A

b) Releasing norepinephrine from nerve terminals
Rationale: Ephedrine primarily works by releasing norepin

248
Q
  1. One clinical use of ephedrine is in the treatment of:
    a) Urinary incontinence
    b) Diabetes
    c) High cholesterol
    d) Depression
A

a) Urinary incontinence
Rationale: Ephedrine is used in treating urinary incontinence due to its ability to increase urethral sphincter tone.

249
Q
  1. Ephedrine is effective in relieving bronchospasm due to its:
    a) Bronchoconstrictive effects
    b) Bronchodilatory effects
    c) Anti-inflammatory properties
    d) Mucolytic properties
A

b) Bronchodilatory effects
Rationale: Ephedrine has bronchodilatory effects, which make it effective in relieving bronchospasm.

250
Q
  1. The use of metaraminol is primarily indicated in:
    a) Treating hypertension
    b) Managing hypotension
    c) Reducing fever
    d) Alleviating pain
A

b) Managing hypotension
Rationale: Metaraminol is primarily used to manage hypotension, including in shock or during spinal anesthesia.

251
Q
  1. Like ephedrine, metaraminol’s mechanism of action involves:
    a) Stimulating serotonin release
    b) Releasing norepinephrine from nerve terminals
    c) Blocking dopamine receptors
    d) Inhibiting acetylcholine release
A

b) Releasing norepinephrine from nerve terminals
Rationale: Metaraminol, similar to ephedrine, works by releasing norepinephrine from nerve terminals, which affects blood pressure and other bodily functions.

252
Q
  1. Ephedrine can be used to treat hypotension primarily due to its:
    a) Diuretic effect
    b) Vasodilatory action
    c) Vasoconstrictive action
    d) Sedative properties
A

c) Vasoconstrictive action
Rationale: Ephedrine’s ability to release norepinephrine leads to vasoconstriction, making it useful in treating hypotension.

253
Q
  1. In the context of spinal anesthesia, metaraminol is used to counteract:
    a) Severe pain
    b) Infection risk
    c) Hypotension
    d) Nausea and vomiting
A

c) Hypotension
Rationale: Metaraminol is used during spinal anesthesia to counteract hypotension, a common side effect of this type of anesthesia.

254
Q
  1. Ephedrine’s use in bronchospasm is based on its ability to:
    a) Suppress cough reflex
    b) Relieve bronchial muscle constriction
    c) Enhance oxygen absorption
    d) Increase mucus production
A

b) Relieve bronchial muscle constriction
Rationale: Ephedrine relieves bronchospasm by causing bronchodilation, easing breathing difficulties in conditions like asthma.

255
Q
  1. In urinary incontinence, ephedrine helps by:
    a) Reducing bladder muscle contractions
    b) Increasing urethral sphincter tone
    c) Acting as a diuretic
    d) Decreasing urine production
A

b) Increasing urethral sphincter tone
Rationale: Ephedrine increases urethral sphincter tone, thereby reducing incontinence.

256
Q
  1. The similarity in the mechanism of action between ephedrine and metaraminol is their ability to:
    a) Increase heart rate
    b) Release norepinephrine from nerve terminals
    c) Decrease blood pressure
    d) Act as a sedative
A

b) Release norepinephrine from nerve terminals
Rationale: Both ephedrine and metaraminol act by releasing norepinephrine from nerve terminals, affecting cardiovascular and respiratory systems.

257
Q
  1. Phenoxybenzamine, a nonselective alpha blocker, is used primarily for:
    a) Treating asthma
    b) Controlling hypertension in pheochromocytoma
    c) Managing diabetes
    d) Treating heart failure
A

b) Controlling hypertension in pheochromocytoma
Rationale: Phenoxybenzamine is mainly used for pheochromocytoma, benign prostatic hyperplasia, and hypertension secondary to spinal cord injuries.

258
Q
  1. A characteristic feature of Phenoxybenzamine is that it is:
    a) Reversible
    b) Irreversible
    c) Selective for alpha1 receptors
    d) Selective for alpha2 receptors
A

b) Irreversible
Rationale: Phenoxybenzamine is an irreversible alpha blocker, leading to longer-lasting effects and requiring careful usage.

259
Q
  1. The first-dose phenomenon, commonly seen with alpha1 selective blockers, includes:
    a) Orthostatic hypotension
    b) Tachycardia
    c) Hypoglycemia
    d) Bradycardia
A

a) Orthostatic hypotension
Rationale: Common side effects of alpha1 selective blockers like Prazosin, Terazosin, and Doxazosin include the first-dose phenomenon of orthostatic hypotension.

260
Q
  1. Yohimbine, an alpha2 selective blocker, has been used in the treatment of:
    a) Asthma
    b) Diabetes
    c) Impotence
    d) Hypertension
A

c) Impotence
Rationale: Yohimbine has been controversially used for impotence, sometimes via direct penile injection, although its efficacy and safety are debated.

261
Q
  1. Phentolamine is a:
    a) Reversible alpha blocker
    b) Irreversible alpha blocker
    c) Beta blocker
    d) Calcium channel blocker
A

a) Reversible alpha blocker
Rationale: Phentolamine is a reversible alpha blocker, primarily used for the short-term control of pheochromocytoma.

262
Q
  1. Alpha1 selective blockers are commonly used in treating:
    a) Urinary retention in benign prostatic hyperplasia
    b) Asthma
    c) Diabetes
    d) Heart failure
A

a) Urinary retention in benign prostatic hyperplasia
Rationale: Alpha1 selective blockers are effective in reducing urinary retention in benign prostatic hyperplasia and managing hypertension.

263
Q
  1. One contraindication for using Phenoxybenzamine is:
    a) Diabetes
    b) Asthma
    c) Coronary artery disease
    d) Hypothyroidism
A

c) Coronary artery disease
Rationale: Phenoxybenzamine is not recommended for patients with coronary artery disease due to its cardiovascular effects.

264
Q
  1. A common side effect of both Phenoxybenzamine and Phentolamine is:
    a) Reflex tachycardia
    b) Increased insulin sensitivity
    c) Dry mouth
    d) Nausea
A

a) Reflex tachycardia
Rationale: Both Phenoxybenzamine and Phentolamine may cause orthostatic hypotension and reflex tachycardia.

265
Q
  1. The use of alpha1 selective blockers in hypertension is due to their ability to:
    a) Increase heart rate
    b) Decrease blood pressure
    c) Increase blood glucose
    d) Stimulate the central nervous system
A

b) Decrease blood pressure
Rationale: Alpha1 selective blockers decrease blood pressure by inhibiting the constriction of arterioles and veins.

266
Q
  1. An adverse effect of Yohimbine includes:
    a) Consistent efficacy in all patients
    b) Lack of significant side effects
    c) Limited use due to potential side effects
    d) Increased risk of heart failure
A

c) Limited use due to potential side effects
Rationale: Yohimbine’s use is limited because of inconsistent efficacy and potential side effects.

267
Q
  1. The primary action of Phentolamine in managing pheochromocytoma is to:
    a) Stimulate insulin release
    b) Control high blood pressure
    c) Increase heart rate
    d) Reduce cholesterol levels
A

b) Control high blood pressure
Rationale: Phentolamine is used in pheochromocytoma primarily to control high blood pressure associated with the condition.

268
Q
  1. One reason for the popularity of alpha1 selective blockers in benign prostatic hyperplasia is:
    a) Their sedative effect
    b) Their ability to reduce urinary retention
    c) Their impact on reducing prostate size
    d) Their ability to improve insulin sensitivity
A

b) Their ability to reduce urinary retention
Rationale: Alpha1 selective blockers are chosen for benign prostatic hyperplasia because they effectively reduce urinary retention.

269
Q
  1. Phenoxybenzamine’s toxicity can lead to:
    a) Hypertension
    b) Hypotension
    c) Hyperglycemia
    d) Hyperthyroidism
A

b) Hypotension
Rationale: Phenoxybenzamine can cause orthostatic hypotension, a significant concern in its toxicity profile.

270
Q
  1. The use of alpha blockers in the management of hypertension is primarily based on their ability to:
    a) Increase cardiac output
    b) Reduce heart rate
    c) Decrease peripheral vascular resistance
    d) Stimulate the parasympathetic nervous system
A

c) Decrease peripheral vascular resistance
Rationale: Alpha blockers decrease peripheral vascular resistance, leading to a reduction in blood pressure.

271
Q
  1. A patient with pheochromocytoma may be prescribed Phentolamine to:
    a) Lower blood glucose levels
    b) Manage thyroid function
    c) Control hypertension
    d) Treat cardiac arrhythmias
A

c) Control hypertension
Rationale: Phentolamine is used in pheochromocytoma to control the hypertension that often accompanies the condition.

272
Q
  1. The primary use of alpha blockers in spinal anesthesia is to:
    a) Relieve pain
    b) Prevent infection
    c) Treat hypotension
    d) Reduce spinal fluid leakage
A

c) Treat hypotension
Rationale: Alpha blockers can be used in spinal anesthesia to manage hypotension, a common complication of this procedure.

273
Q
  1. In treating benign prostatic hyperplasia (BPH), alpha1 selective blockers help by:
    a) Shrinking the prostate
    b) Improving urine flow
    c) Increasing urine production
    d) Reducing bladder infections
A

b) Improving urine flow
Rationale: Alpha1 selective blockers improve urine flow in BPH by relaxing muscles in the prostate and bladder neck.

274
Q
  1. The use of Phenoxybenzamine in hypertension secondary to spinal cord injuries is due to its effect on:
    a) Blood glucose levels
    b) Blood pressure
    c) Cholesterol levels
    d) Thyroid function
A

b) Blood pressure
Rationale: Phenoxybenzamine is used in hypertension secondary to spinal cord injuries primarily due to its blood pressure-lowering effects.

275
Q
  1. A patient with coronary artery disease should use Phenoxybenzamine with caution because of its potential to:
    a) Increase blood clotting
    b) Worsen heart function
    c) Cause significant blood pressure changes
    d) Increase blood glucose levels
A

c) Cause significant blood pressure changes
Rationale: Phenoxybenzamine can cause significant changes in blood pressure, which can be risky for patients with coronary artery disease.

276
Q
  1. The first-dose phenomenon in alpha1 selective blockers is characterized by:
    a) Rapid heart rate increase
    b) Severe headache
    c) Sudden drop in blood pressure upon standing
    d) Immediate relief of urinary symptoms
A

c) Sudden drop in blood pressure upon standing
Rationale: The first-dose phenomenon refers to a sudden drop in blood pressure upon standing, often experienced after the first dose of alpha1 selective blockers.

277
Q
  1. The primary mechanism of action of beta blockers in treating hypertension is:
    a) Increasing cardiac output
    b) Reducing renin secretion
    c) Increasing blood vessel tension
    d) Expanding blood vessels
A

b) Reducing renin secretion
Rationale: Beta blockers decrease cardiac output and reduce renin secretion, which leads to lower blood pressure.

278
Q
  1. In managing angina pectoris, beta blockers work by:
    a) Increasing heart rate
    b) Decreasing heart rate and contractility
    c) Expanding coronary arteries
    d) Increasing oxygen consumption
A

b) Decreasing heart rate and contractility
Rationale: Beta blockers reduce heart rate and contractility, decreasing oxygen consumption by the heart muscle and managing chest pain in angina.

279
Q
  1. Post-myocardial infarction, beta blockers are used to:
    a) Increase the workload on the heart
    b) Reduce mortality by decreasing heart workload
    c) Dilate coronary arteries
    d) Increase blood pressure
A

b) Reduce mortality by decreasing heart workload
Rationale: Beta blockers reduce the workload on the heart post-myocardial infarction, thereby reducing mortality.

280
Q
  1. Propranolol, a specific beta blocker, is used in treating:
    a) Diabetes
    b) Supraventricular Tachycardia (SVT)
    c) Asthma
    d) High cholesterol
A

b) Supraventricular Tachycardia (SVT)
Rationale: Propranolol is notably used in SVT as it slows AV conduction and velocity, helping control rapid heart rates.

281
Q
  1. In glaucoma, beta blockers are effective due to their ability to:
    a) Increase aqueous humor secretion
    b) Decrease aqueous humor secretion
    c) Improve vision
    d) Reduce eye inflammation
A

b) Decrease aqueous humor secretion
Rationale: Beta blockers decrease the secretion of aqueous humor in the eye, thereby reducing intraocular pressure in glaucoma.

282
Q
  1. Selective beta blockers are safer for patients with respiratory issues because they primarily block:
    a) Beta1 receptors
    b) Beta2 receptors
    c) Alpha receptors
    d) Dopamine receptors
A

a) Beta1 receptors
Rationale: Selective beta blockers (A-M “olols”) primarily block beta1 receptors and are safer for patients with respiratory issues.

283
Q
  1. Nonselective beta blockers act on:
    a) Only beta1 receptors
    b) Both beta1 and beta2 receptors
    c) Only alpha receptors
    d) Only dopamine receptors
A

b) Both beta1 and beta2 receptors
Rationale: Nonselective beta blockers (N-Z) act on both beta1 and beta2 receptors, having a broader range of effects.

284
Q
  1. Labetalol and Carvedilol are unique among beta blockers due to their:
    a) Beta-blocking and alpha-agonist properties
    b) Long-acting nature
    c) Specific action on the eyes
    d) Lack of side effects
A

a) Beta-blocking and alpha-agonist properties
Rationale: Labetalol and Carvedilol have both beta-blocking and alpha-agonist properties, making them useful in treating hypertension and heart failure.

285
Q
  1. Esmolol is known for being:
    a) The longest-acting beta blocker
    b) The shortest-acting beta blocker
    c) The most potent beta blocker
    d) The least used beta blocker
A

b) The shortest-acting beta blocker
Rationale: Esmolol is the shortest-acting beta blocker, often used in emergency settings or when rapid adjustments in dosage are needed.

286
Q
  1. The use of beta blockers in hypertension effectively:
    a) Increases heart rate
    b) Reduces heart rate and workload
    c) Stimulates the central nervous system
    d) Increases blood glucose levels
A

b) Reduces heart rate and workload
Rationale: Beta blockers are effective in hypertension as they reduce heart rate and workload, leading to lower blood pressure.

287
Q
  1. In the treatment of angina, beta blockers help by:
    a) Reducing the demand for oxygen by the heart
    b) Increasing blood flow to the heart
    c) Reducing cholesterol levels
    d) Thickening the heart muscle
A

a) Reducing the demand for oxygen by the heart
Rationale: Beta blockers manage chest pain associated with angina by reducing the heart’s demand for oxygen.

288
Q
  1. The first-line treatment for patients post-myocardial infarction often includes beta blockers to:
    a) Prevent further heart attacks
    b) Reduce the risk of arrhythmias
    c) Lower the risk of heart failure
    d) All of the above
A

d) All of the above
Rationale: Beta blockers are used post-myocardial infarction to reduce the workload on the heart, decreasing the risk of further heart attacks, arrhythmias, and heart failure.

289
Q
  1. The unique property of labetalol and carvedilol that makes them effective in heart failure is:
    a) Their diuretic effect
    b) Their dual action as beta blockers and alpha-agonists
    c) Their ability to increase heart rate
    d) Their action on cholesterol levels
A

b) Their dual action as beta blockers and alpha-agonists
Rationale: The combined beta-blocking and alpha-agonist properties of labetalol and carvedilol make them particularly effective in treating hypertension and heart failure.

290
Q
  1. Beta blockers are contraindicated in patients with:
    a) Hypertension
    b) Uncontrolled asthma
    c) Angina
    d) Myocardial infarction
A

b) Uncontrolled asthma
Rationale: Beta blockers, especially nonselective ones, are contraindicated in patients with uncontrolled asthma due to their potential to cause bronchoconstriction.

291
Q
  1. The “first-dose phenomenon” associated with alpha blockers is characterized by:
    a) Increased blood pressure
    b) Orthostatic hypotension
    c) Nausea
    d) Headache
A

b) Orthostatic hypotension
Rationale: The first-dose phenomenon with alpha blockers often includes orthostatic hypotension, causing dizziness and lightheadedness upon standing.

292
Q
  1. The use of beta blockers in glaucoma is primarily to:
    a) Increase intraocular pressure
    b) Decrease intraocular pressure
    c) Improve vision
    d) Alleviate pain
A

b) Decrease intraocular pressure
Rationale: In glaucoma, beta blockers are used to decrease intraocular pressure by reducing the secretion of aqueous humor.

293
Q
  1. Beta blockers can be particularly beneficial in treating angina by:
    a) Increasing oxygen supply to the heart
    b) Reducing the heart’s oxygen demand
    c) Increasing heart rate
    d) Expanding coronary arteries
A

b) Reducing the heart’s oxygen demand
Rationale: Beta blockers help manage angina by reducing heart rate and contractility, thereby decreasing the heart’s oxygen demand and preventing chest pain.

294
Q
  1. In treating supraventricular tachycardia (SVT), beta blockers like propranolol are used to:
    a) Speed up AV conduction
    b) Slow down AV conduction
    c) Increase heart contractility
    d) Dilate coronary arteries
A

b) Slow down AV conduction
Rationale: Propranolol is used in SVT to slow AV conduction and velocity, controlling rapid heart rates.

295
Q
  1. Carvedilol’s effectiveness in heart failure is due to its ability to:
    a) Increase heart rate
    b) Reduce blood pressure and heart workload
    c) Stimulate kidney function
    d) Increase fluid retention
A

b) Reduce blood pressure and heart workload
Rationale: Carvedilol’s beta-blocking and alpha-agonist properties reduce blood pressure and heart workload, improving heart failure symptoms.

296
Q
  1. The primary reason for beta blockers’ effectiveness in hypertension is their ability to:
    a) Decrease renin secretion
    b) Increase sodium excretion
    c) Dilate blood vessels
    d) Increase cardiac output
A

a) Decrease renin secretion
Rationale: Beta blockers decrease renin secretion, which reduces blood pressure by decreasing cardiac output and vascular resistance.

297
Q
  1. Beta1 blockers are primarily used to target receptors located in:
    a) The heart
    b) The lungs
    c) The liver
    d) The kidneys
A

a) The heart
Rationale: Beta1 blockers primarily affect beta1-adrenergic receptors, which are predominantly located in the heart.

298
Q
  1. In hypertension, cardioselective beta1 blockers are preferred because they:
    a) Do not affect blood glucose levels
    b) Avoid bronchoconstriction
    c) Increase cardiac output
    d) Reduce kidney function
A

b) Avoid bronchoconstriction
Rationale: For hypertensive patients with conditions like asthma, cardioselective beta1 blockers are preferred to avoid bronchoconstriction.

299
Q
  1. At high doses, some beta1 blockers may also block beta2 receptors, leading to:
    a) Increased heart rate
    b) Effects on the lungs and other tissues
    c) Decreased blood sugar levels
    d) Increased urine production
A

b) Effects on the lungs and other tissues
Rationale: At high doses, some beta1 blockers can block beta2 receptors, affecting the lungs and other tissues beyond the heart.

300
Q
  1. Propranolol, a nonselective beta blocker, is effective for:
    a) Only hypertension
    b) Angina, hypertension, thyroid storm, panic attacks, and migraines
    c) Asthma management
    d) Diabetes control
A

b) Angina, hypertension, thyroid storm, panic attacks, and migraines
Rationale: Nonselective beta blockers like Propranolol are effective for various conditions including angina, hypertension, thyroid storm, panic attacks, and migraines.

301
Q
  1. Beta blockers with agonistic properties, like Acebutolol, are indicated for patients with:
    a) Hypertension prone to bradycardia
    b) Asthma
    c) High cholesterol
    d) Kidney disease
A

a) Hypertension prone to bradycardia
Rationale: Beta blockers like Acebutolol, which possess agonistic properties, are suitable for patients with hypertension who are prone to bradycardia.

302
Q
  1. Labetalol and Carvedilol are unique among beta blockers due to their:
    a) Beta-only blocking properties
    b) Beta and alpha blocking properties
    c) Agonistic effects on beta receptors
    d) Direct vasodilatory action
A

b) Beta and alpha blocking properties
Rationale: Labetalol and Carvedilol have both beta and alpha blocking properties, making them effective in treating hypertension.

303
Q
  1. A contraindication for using beta blockers with alpha blocking properties is:
    a) Chronic asthma
    b) Acute congestive heart failure
    c) Hypothyroidism
    d) Mild hypertension
A

b) Acute congestive heart failure
Rationale: Beta blockers with alpha blocking properties, such as Labetalol and Carvedilol, should not be used in acute congestive heart failure.

304
Q
  1. A common side effect of beta blocker toxicity is:
    a) Hypertension
    b) Impotence
    c) Increased heart rate
    d) Hyperglycemia
A

b) Impotence
Rationale: Common side effects of beta blocker toxicity include impotence, exacerbation of asthma, bradycardia, AV block, congestive heart failure, sedation, and sleep alterations.

305
Q
  1. Nonselective beta blockers like Timolol can affect:
    a) Blood glucose and lipid metabolism
    b) Kidney function exclusively
    c) Thyroid hormone levels
    d) Bone density
A

a) Blood glucose and lipid metabolism
Rationale: Nonselective beta blockers can impact blood glucose and lipid metabolism, decreasing glycogenolysis and affecting VLDL and HDL levels.

306
Q
  1. Beta blockers are widely used in hypertension because they:
    a) Increase heart rate
    b) Increase blood vessel tension
    c) Reduce the workload of the heart
    d) Increase renal secretion
A

c) Reduce the workload of the heart
Rationale: Beta blockers are effective in reducing hypertension as they decrease the workload of the heart and blood vessel tension.

307
Q
  1. Beta blockers with agonistic properties are less likely to cause:
    a) Bronchoconstriction
    b) Bradycardia
    c) Hypertension
    d) Hyperglycemia
A

b) Bradycardia
Rationale: Beta blockers with agonistic properties, like Acebutolol, do not significantly lower heart rate due to their agonistic effects.

308
Q
  1. The use of nonselective beta blockers in patients with asthma is cautioned due to:
    a) The risk of bronchoconstriction
    b) The risk of increased heart rate
    c) Their diuretic effect
    d) Their effect on blood glucose levels
A

a) The risk of bronchoconstriction
Rationale: Nonselective beta blockers can cause bronchoconstriction, which is a concern for patients with asthma.

309
Q
  1. In treating glaucoma, beta blockers like Timolol work by:
    a) Increasing aqueous humor production
    b) Decreasing intraocular pressure
    c) Dilating the pupil
    d) Improving vision
A

b) Decreasing intraocular pressure
Rationale: Beta blockers are effective in glaucoma as they decrease intraocular pressure, often by reducing the production of aqueous humor.

310
Q
  1. The effectiveness of beta blockers in angina pectoris is mainly due to their ability to:
    a) Decrease oxygen consumption by the heart
    b) Increase blood flow to the heart
    c) Reduce cholesterol levels
    d) Decrease blood clotting
A

a) Decrease oxygen consumption by the heart
Rationale: Beta blockers help in managing angina by reducing heart rate and contractility, thereby decreasing oxygen consumption by the heart muscle.

311
Q
  1. Beta blockers are contraindicated in patients with uncontrolled heart failure because they:
    a) Increase cardiac output
    b) Reduce renal function
    c) Can exacerbate heart failure symptoms
    d) Increase blood glucose levels
A

c) Can exacerbate heart failure symptoms
Rationale: Beta blockers can exacerbate symptoms of uncontrolled heart failure due to their effect on decreasing cardiac output.

312
Q
  1. The use of beta blockers in myocardial infarction is to:
    a) Increase heart workload
    b) Decrease heart workload
    c) Dilate coronary arteries
    d) Increase cholesterol breakdown
A

b) Decrease heart workload
Rationale: Post-myocardial infarction, beta blockers are used to decrease the workload on the heart, reducing mortality.

313
Q
  1. Cardioselective beta1 blockers are preferred in hypertensive patients with:
    a) Diabetes
    b) Asthma
    c) Gastrointestinal issues
    d) Kidney disease
A

b) Asthma
Rationale: Cardioselective beta1 blockers are preferred in hypertensive patients with respiratory issues like asthma to avoid bronchoconstriction.

314
Q
  1. A side effect common to both selective and nonselective beta blockers is:
    a) Impotence
    b) Increased heart rate
    c) Increased blood glucose levels
    d) Bronchodilation
A

a) Impotence
Rationale: Impotence is a common side effect of both selective and nonselective beta blockers.

315
Q
  1. Beta blockers are beneficial in supraventricular tachycardia because they:
    a) Increase AV conduction
    b) Decrease AV conduction
    c) Increase heart contractility
    d) Dilate the coronary arteries
A

b) Decrease AV conduction
Rationale: In supraventricular tachycardia, beta blockers like Propranolol are used to decrease AV conduction, controlling rapid heart rates.

316
Q
  1. In addition to treating hypertension, nonselective beta blockers like Propranolol are also effective for:
    a) Only thyroid storm
    b) Thyroid storm, panic attacks, and migraines
    c) Only panic attacks
    d) Only migraines
A

b) Thyroid storm, panic attacks, and migraines
Rationale: Nonselective beta blockers like Propranolol are effective in treating various conditions including thyroid storm, panic attacks, and migraines.

317
Q
  1. The primary mechanism of action of indirect adrenergic antagonists is:
    a) Blocking alpha receptors
    b) Inhibiting the release of norepinephrine
    c) Stimulating the release of norepinephrine
    d) Blocking beta receptors
A

b) Inhibiting the release of norepinephrine
Rationale: Indirect adrenergic antagonists work by reducing the release of norepinephrine from nerve endings or depleting its stores, thereby diminishing sympathetic activity.

318
Q
  1. Guanethidine is primarily used in the treatment of:
    a) Diabetes
    b) Hypertension
    c) Asthma
    d) High cholesterol
A

b) Hypertension
Rationale: Guanethidine is primarily used to treat hypertension by reducing sympathetic tone, leading to decreased blood pressure.

319
Q
  1. A common side effect of Guanethidine is:
    a) Tachycardia
    b) Orthostatic hypotension
    c) Increased heart rate
    d) Bronchodilation
A

b) Orthostatic hypotension
Rationale: Common side effects of Guanethidine include orthostatic hypotension and sexual dysfunction.

320
Q
  1. Reserpine’s mechanism of action involves:
    a) Depleting norepinephrine from nerve endings
    b) Increasing norepinephrine synthesis
    c) Blocking dopamine receptors
    d) Stimulating serotonin release
A

a) Depleting norepinephrine from nerve endings
Rationale: Reserpine works by depleting norepinephrine (and other monoamines like serotonin and dopamine) from nerve endings.

321
Q
  1. Reserpine is sometimes used in psychiatric settings due to its effect on:
    a) Blood pressure
    b) Central nervous system
    c) Lung function
A

b) Central nervous system
Rationale: While its use for cardiac or autonomic nervous system problems has decreased, Reserpine is sometimes used in psychiatric settings due to its CNS effects.

322
Q
  1. Guanethidine lowers blood pressure by:
    a) Dilating blood vessels
    b) Inhibiting the release of norepinephrine
    c) Increasing heart rate
    d) Stimulating the parasympathetic nervous system
A

b) Inhibiting the release of norepinephrine
Rationale: Guanethidine lowers blood pressure by inhibiting the release of norepinephrine from sympathetic nerve endings.

323
Q
  1. A significant side effect associated with Reserpine is:
    a) Bradycardia
    b) Hypoglycemia
    c) Bronchospasm
    d) Increased libido
A

a) Bradycardia
Rationale: Reserpine can cause bradycardia and central nervous system depression.

324
Q
  1. The use of indirect adrenergic antagonists in hypertension is based on their ability to:
    a) Increase renal excretion of sodium
    b) Decrease sympathetic tone
    c) Block calcium channels
    d) Increase vasodilation
A

b) Decrease sympathetic tone
Rationale: Indirect adrenergic antagonists treat hypertension by reducing the sympathetic tone, thereby lowering blood pressure.

325
Q
  1. Guanethidine’s effect on sexual function is primarily due to:
    a) Its stimulating effect on testosterone
    b) Its vasodilatory action
    c) Inhibition of sympathetic nervous system
    d) Increased blood flow to reproductive organs
A

c) Inhibition of sympathetic nervous system
Rationale: Guanethidine commonly causes sexual dysfunction as a side effect due to its inhibitory effect on the sympathetic nervous system.

326
Q
  1. In treating hypertension, Reserpine’s unique mechanism is:
    a) Blocking beta1 receptors
    b) Depleting monoamines from nerve endings
    c) Increasing norepinephrine storage
    d) Dilating coronary arteries
A

b) Depleting monoamines from nerve endings
Rationale: Reserpine’s unique mechanism in treating hypertension involves depleting monoamines like norepinephrine from nerve endings.

327
Q
  1. The effect of indirect adrenergic antagonists on the CNS can lead to:
    a) Stimulation and increased alertness
    b) Depression and sedation
    c) Memory enhancement
    d) Increased cognitive function
A

b) Depression and sedation
Rationale: Indirect adrenergic antagonists, like Reserpine, can cause CNS depression and bradycardia.

328
Q
  1. Guanethidine’s action in the sympathetic nervous system results in:
    a) Increased norepinephrine release
    b) Decreased norepinephrine release
    c) Stimulation of alpha receptors
    d) Blockade of beta receptors
A

b) Decreased norepinephrine release
Rationale: Guanethidine inhibits the release of norepinephrine from sympathetic nerve endings, leading to decreased blood pressure.

329
Q
  1. Reserpine’s role in psychiatric treatment is primarily due to its influence on:
    a) Serotonin and dopamine levels
    b) Blood pressure regulation
    c) Increasing norepinephrine levels
    d) Stimulating the immune system
A

a) Serotonin and dopamine levels
Rationale: Reserpine’s use in psychiatric settings is due to its effect on central neurotransmitters like serotonin and dopamine.

330
Q
  1. The primary reason for the decreased use of Reserpine in treating cardiac problems is its:
    a) High cost
    b) Side effects on the central nervous system
    c) Lack of effectiveness
    d) Interaction with other cardiac medications
A

b) Side effects on the central nervous system
Rationale: Reserpine’s use in cardiac or autonomic nervous system problems has decreased due to its side effects on the CNS.

331
Q
  1. In managing hypertension, indirect adrenergic antagonists like Guanethidine are effective due to their:
    a) Diuretic properties
    b) Beta-blocking properties
    c) Ability to decrease sympathetic nervous system activity
    d) Vasodilatory effects
A

c) Ability to decrease sympathetic nervous system activity
Rationale: Indirect adrenergic antagonists manage hypertension by reducing sympathetic nervous system activity, leading to decreased blood pressure.

332
Q
  1. One of the primary challenges in using Guanethidine for hypertension is managing its side effect of:
    a) Orthostatic hypotension
    b) Increased heart rate
    c) Weight gain
    d) Hyperglycemia
A

a) Orthostatic hypotension
Rationale: A common challenge with Guanethidine is managing its side effect of orthostatic hypotension, a drop in blood pressure upon standing.

333
Q
  1. The mechanism of action of Reserpine in lowering blood pressure involves:
    a) Increasing heart rate
    b) Blocking calcium channels
    c) Depleting norepinephrine stores
    d) Dilating peripheral blood vessels
A

c) Depleting norepinephrine stores
Rationale: Reserpine lowers blood pressure by depleting norepinephrine (and other monoamines) from nerve endings.

334
Q
  1. Guanethidine’s inhibitory effect on the sympathetic nervous system can lead to:
    a) Increased alertness
    b) Heightened reflexes
    c) Sexual dysfunction
    d) Increased energy levels
A

c) Sexual dysfunction
Rationale: Guanethidine can cause sexual dysfunction due to its inhibitory effect on the sympathetic nervous system.

335
Q
  1. The choice of using Reserpine in psychiatric treatment is influenced by its:
    a) Rapid onset of action
    b) Lack of side effects
    c) Effect on central neurotransmitters
    d) Ability to regulate blood sugar
A

c) Effect on central neurotransmitters
Rationale: Reserpine is sometimes used in psychiatric settings due to its effect on central neurotransmitters, leading to CNS depression.

336
Q
  1. Guanethidine’s mechanism in reducing blood pressure is primarily through:
    a) Increased renal excretion
    b) Vasodilation of blood vessels
    c) Decreasing norepinephrine release
    d) Stimulating the parasympathetic nervous system
A

c) Decreasing norepinephrine release
Rationale: Guanethidine reduces blood pressure primarily by decreasing norepinephrine release from sympathetic nerve endings.

337
Q
  1. Epinephrine, used in glaucoma, primarily works by:
    a) Increasing the outflow of aqueous humor
    b) Decreasing the outflow of aqueous humor
    c) Reducing aqueous humor synthesis
    d) Contracting the ciliary muscle
A

a) Increasing the outflow of aqueous humor
Rationale: Epinephrine works in glaucoma by increasing the outflow of aqueous humor, thereby reducing intraocular pressure.

338
Q
  1. A potential side effect of using Epinephrine in glaucoma treatment is:
    a) Mydriasis
    b) Miosis
    c) Decreased intraocular pressure
    d) Improved vision
A

a) Mydriasis
Rationale: Epinephrine may cause mydriasis (pupil dilation) and stinging; it is not recommended for closed-angle glaucoma.

339
Q
  1. Brimonidine, an alpha agonist, reduces intraocular pressure by:
    a) Contracting the ciliary muscle
    b) Increasing aqueous humor outflow
    c) Reducing aqueous humor synthesis
    d) Dilating the pupil
A

c) Reducing aqueous humor synthesis
Rationale: Brimonidine primarily works by reducing aqueous humor synthesis, making it effective in lowering intraocular pressure.

340
Q
  1. The mechanism of action of beta blockers like Timolol in glaucoma is to:
    a) Decrease aqueous humor secretion
    b) Increase aqueous humor secretion
    c) Dilate the pupil
    d) Contract the ciliary muscle
A

a) Decrease aqueous humor secretion
Rationale: Beta blockers such as Timolol decrease aqueous humor secretion, which helps in reducing intraocular pressure.

341
Q
  1. Pilocarpine, a cholinomimetic, treats glaucoma by:
    a) Enhancing the drainage of aqueous humor
    b) Increasing aqueous humor production
    c) Reducing blood flow to the eye
    d) Decreasing the size of the pupil
A

a) Enhancing the drainage of aqueous humor
Rationale: Pilocarpine contracts the ciliary muscle, leading to the opening of the trabecular meshwork and enhancing the drainage of aqueous humor.

342
Q
  1. A common side effect of cholinomimetics like Carbachol in glaucoma treatment is:
    a) Mydriasis
    b) Miosis
    c) Dry eyes
    d) Increased intraocular pressure
A

b) Miosis
Rationale: Cholinomimetics can cause miosis (pupil constriction) and potentially decrease vision quality due to the ‘pinhole effect.’

343
Q
  1. Timolol, used in glaucoma, is classified as a:
    a) Alpha agonist
    b) Beta blocker
    c) Cholinomimetic
    d) Carbonic anhydrase inhibitor
A

b) Beta blocker
Rationale: Timolol is a beta blocker that decreases aqueous humor secretion, widely used in glaucoma treatment.

344
Q
  1. In treating glaucoma, Echothiophate’s action is to:
    a) Dilate the pupil
    b) Decrease aqueous humor production
    c) Contract the ciliary muscle
    d) Block alpha receptors
A

c) Contract the ciliary muscle
Rationale: Echothiophate contracts the ciliary muscle, enhancing the drainage of aqueous humor.

345
Q
  1. Betaxolol, as a beta blocker in glaucoma therapy, is known for:
    a) Causing significant pupillary changes
    b) Not causing significant pupillary or vision changes
    c) Increasing the risk of closed-angle glaucoma
    d) Reducing blood flow to the optic nerve
A

b) Not causing significant pupillary or vision changes
Rationale: Betaxolol generally does not cause significant pupillary or vision changes, making it a mainstay in glaucoma treatment.

346
Q
  1. Brimonidine’s selectivity in glaucoma treatment means it typically:
    a) Does not cause pupillary or vision changes
    b) Causes significant vision improvement
    c) Increases intraocular pressure
    d) Dilates the pupil
A

a) Does not cause pupillary or vision changes
Rationale: Brimonidine is more selective in its action, typically not causing pupillary or vision changes.

347
Q
  1. The use of cholinomimetics in glaucoma may lead to a decrease in vision quality due to:
    a) Blurred vision
    b) The ‘pinhole effect’
    c) Dry eye syndrome
    d) Optic nerve damage
A

b) The ‘pinhole effect’
Rationale: Cholinomimetics like Pilocarpine can cause the ‘pinhole effect,’ a reduced field of vision, due to pupil constriction.

348
Q
  1. The use of Epinephrine in closed-angle glaucoma is contraindicated due to the risk of:
    a) Decreasing intraocular pressure
    b) Increasing intraocular pressure
    c) Causing cataracts
    d) Reducing vision quality
A

b) Increasing intraocular pressure
Rationale: Epinephrine is not recommended for closed-angle glaucoma as it may increase intraocular pressure.

349
Q
  1. In managing glaucoma, Carteolol as a beta blocker primarily:
    a) Increases the outflow of aqueous humor
    b) Decreases aqueous humor production
    c) Contracts the ciliary muscle
    d) Dilates the pupil
A

b) Decreases aqueous humor production
Rationale: Carteolol, like other beta blockers, decreases aqueous humor production, thereby reducing intraocular pressure.

350
Q
  1. Physostigmine’s effect in glaucoma treatment is similar to:
    a) Beta blockers
    b) Alpha agonists
    c) Cholinomimetics
    d) Carbonic anhydrase inhibitors
A

c) Cholinomimetics
Rationale: Physostigmine, as a cholinomimetic, contracts the ciliary muscle, enhancing aqueous humor drainage.

351
Q
  1. The primary reason for the efficacy of beta blockers in glaucoma treatment is their ability to:
    a) Reduce intraocular pressure by decreasing aqueous humor secretion
    b) Increase intraocular pressure by increasing aqueous humor secretion
    c) Contract the ciliary muscle
    d) Dilate the pupil
A

a) Reduce intraocular pressure by decreasing aqueous humor secretion
Rationale: Beta blockers like Timolol are effective in glaucoma due to their ability to decrease aqueous humor secretion, reducing intraocular pressure.

352
Q
  1. Cholinomimetics are used in glaucoma due to their ability to:
    a) Decrease aqueous humor production
    b) Increase aqueous humor production
    c) Enhance aqueous humor outflow
    d) Block alpha receptors
A

c) Enhance aqueous humor outflow
Rationale: Cholinomimetics increase the outflow of aqueous humor by contracting the ciliary muscle, thereby lowering intraocular pressure.

353
Q
  1. When using alpha agonists like Brimonidine in glaucoma, a notable advantage is:
    a) The absence of systemic side effects
    b) The lack of effect on pupil size and vision
    c) The rapid onset of action
    d) The long-term improvement in vision
A

b) The lack of effect on pupil size and vision
Rationale: Brimonidine, as an alpha agonist, is more selective and typically does not cause significant changes in pupil size or vision.

354
Q
  1. Beta blockers like Betaxolol are considered a mainstay in glaucoma treatment due to:
    a) Their limited effect on intraocular pressure
    b) Their minimal impact on pupillary or vision changes
    c) Their ability to improve vision clarity
    d) Their role in reversing glaucoma damage
A

b) Their minimal impact on pupillary or vision changes
Rationale: Beta blockers are widely used in glaucoma treatment due to their efficacy and fewer visual side effects.

355
Q
  1. In glaucoma therapy, the contraindication of using Epinephrine in certain types highlights the importance of:
    a) Assessing the type of glaucoma before drug selection
    b) The rapid action of the drug
    c) The universal applicability of glaucoma drugs
    d) The cost-effectiveness of treatment
A

a) Assessing the type of glaucoma before drug selection
Rationale: Choosing the right glaucoma medication, such as avoiding Epinephrine in closed-angle glaucoma, underscores the need for careful assessment of the type of glaucoma.

356
Q
  1. The ‘pinhole effect’ caused by cholinomimetics like Pilocarpine in glaucoma treatment refers to:
    a) Enhanced peripheral vision
    b) Reduced field of vision
    c) Improved night vision
    d) Increased visual acuity
A

b) Reduced field of vision
Rationale: The ‘pinhole effect’ from cholinomimetics results in a reduced field of vision due to pupil constriction, which can impact vision quality.