Cholinergic/Adrenergic drugs

Cholinergic/Adrenergic drugs US Medical PG Question 1: In patients with chronic obstructive pulmonary disease, stimulation of muscarinic acetylcholine receptors results in an increase in mucus secretion, smooth muscle contraction and bronchoconstriction. The end result is an increase in airway resistance. Which of the following pharmacologic agents interferes directly with this pathway?

• A. Epinephrine
• B. Albuterol
• C. Theophylline
• D. Ipratropium (Correct Answer)
• E. Metoprolol

Cholinergic/Adrenergic drugs Explanation: ***Ipratropium*** - **Ipratropium** is an **anticholinergic** agent that blocks muscarinic acetylcholine receptors. - By blocking these receptors, it **reduces bronchoconstriction**, mucus secretion, and smooth muscle contraction, thus decreasing airway resistance. *Epinephrine* - **Epinephrine** is a non-selective **adrenergic agonist** that stimulates both alpha and beta receptors. - Its effects in the airways are primarily mediated through **beta-2 agonism**, leading to bronchodilation, but it does not directly interfere with muscarinic pathways. *Albuterol* - **Albuterol** is a **short-acting beta-2 adrenergic agonist (SABA)**. - It primarily causes bronchodilation by stimulating beta-2 receptors on airway smooth muscle, independent of the muscarinic pathway. *Theophylline* - **Theophylline** is a **methylxanthine** that primarily acts as a non-selective phosphodiesterase inhibitor. - This leads to increased intracellular **cAMP** and bronchodilation, but it does not directly block muscarinic acetylcholine receptors. *Metoprolol* - **Metoprolol** is a **selective beta-1 adrenergic blocker** (beta-blocker). - Its primary action is on the heart; it has minimal effect on airway beta-2 receptors at therapeutic doses due to its selectivity, and it does not interfere with the muscarinic pathway.

Cholinergic/Adrenergic drugs US Medical PG Question 2: A 32-year-old farmer is brought to the emergency department by his wife. The patient was reportedly anxious, sweaty, and complaining of a headache and chest tightness before losing consciousness on route to the hospital. Which of the following is mechanistically responsible for this patient's symptoms?

• A. Reversible inhibition of acetylcholinesterase
• B. Competitive inhibition of acetylcholine at post-junctional effector sites
• C. Binding of acetylcholine agonists to post-junctional receptors
• D. Irreversible inhibition of acetylcholinesterase (Correct Answer)
• E. Inhibition of presynaptic exocytosis of acetylcholine vesicles

Cholinergic/Adrenergic drugs Explanation: ***Irreversible inhibition of acetylcholinesterase*** - The farmer's symptoms (anxiety, sweating, headache, chest tightness, loss of consciousness) are characteristic of **organophosphate poisoning**, which causes a cholinergic crisis due to accumulation of acetylcholine. - Organophosphates are common in **pesticides** and act by irreversibly inhibiting **acetylcholinesterase**, leading to prolonged stimulation of cholinergic receptors. *Reversible inhibition of acetylcholinesterase* - Reversible acetylcholinesterase inhibitors, such as **physostigmine** or **neostigmine**, typically have a shorter duration of action and might cause similar symptoms but are less likely to lead to such severe, acute presentations in an accidental exposure scenario for a farmer. - These agents are often used therapeutically and would not typically cause prolonged loss of consciousness in this context unless in very high intentional doses. *Competitive inhibition of acetylcholine at post-junctional effector sites* - This mechanism describes the action of **anticholinergic drugs** (e.g., atropine), which would block acetylcholine's effects and cause symptoms like dry mouth, dilated pupils, and tachycardia, opposite to what is observed here. - Such agents would alleviate, not cause, the cholinergic symptoms seen in this patient. *Binding of acetylcholine agonists to post-junctional receptors* - While direct agonists (e.g., pilocarpine, methacholine) would mimic acetylcholine and cause cholinergic symptoms, organophosphate poisoning operates by preventing acetylcholine breakdown, rather than directly binding as an exogenous agonist. - The context of a farmer and sudden, severe symptoms points more strongly to pesticide exposure and acetylcholinesterase inhibition. *Inhibition of presynaptic exocytosis of acetylcholine vesicles* - This mechanism is characteristic of **botulinum toxin**, which blocks the release of acetylcholine from presynaptic terminals, leading to muscle paralysis and weakness. - The patient's symptoms are those of cholinergic excess, not cholinergic blockade or deficiency at the neuromuscular junction.

Cholinergic/Adrenergic drugs US Medical PG Question 3: A 43-year-old man is brought to the emergency department by his wife because of a 1-hour history of confusion and strange behavior. She reports that he started behaving in an agitated manner shortly after eating some wild berries that they had picked during their camping trip. His temperature is 38.7°C (101.7°F). Physical examination shows warm, dry skin and dry mucous membranes. His pupils are dilated and minimally reactive to light. His bowel sounds are decreased. The patient is admitted and pharmacotherapy is initiated with a drug that eventually results in complete resolution of all of his symptoms. This patient was most likely administered which of the following drugs?

• A. Rivastigmine
• B. Atropine
• C. Scopolamine
• D. Physostigmine (Correct Answer)
• E. Neostigmine

Cholinergic/Adrenergic drugs Explanation: ***Physostigmine*** - The patient's symptoms (confusion, agitation, dilated pupils, warm/dry skin, decreased bowel sounds, fever) are characteristic of **anticholinergic toxicity**, often caused by ingestion of plants like Jimson weed or deadly nightshade (containing atropine-like alkaloids). - **Physostigmine** is a **reversible acetylcholinesterase inhibitor** that can cross the **blood-brain barrier** and reverse both central (confusion, agitation) and peripheral (dilated pupils, dry skin, decreased bowel sounds) anticholinergic effects. *Rivastigmine* - **Rivastigmine** is an acetylcholinesterase inhibitor primarily used to treat **Alzheimer's disease** and Parkinson's disease dementia. - While it inhibits acetylcholinesterase, its primary clinical use and efficacy profile do not align with rapid reversal of acute, severe anticholinergic poisoning. *Atropine* - **Atropine** is a **muscarinic anticholinergic agent** that would *exacerbate* the patient's symptoms, as the presentation is consistent with anticholinergic poisoning. - It works by blocking acetylcholine receptors, leading to effects like dilated pupils, dry mouth, and decreased gastrointestinal motility. *Scopolamine* - **Scopolamine** is another potent **muscarinic anticholinergic agent** that causes similar symptoms to atropine, particularly confusion and delirium due to its central nervous system effects. - Administering scopolamine would worsen the patient's existing anticholinergic toxidrome. *Neostigmine* - **Neostigmine** is a **reversible acetylcholinesterase inhibitor** used for conditions like myasthenia gravis and reversal of neuromuscular blockade. - However, **neostigmine does not cross the blood-brain barrier** effectively, meaning it would not reverse the central nervous system symptoms (confusion, agitation) prominent in this anticholinergic poisoning case.

Cholinergic/Adrenergic drugs US Medical PG Question 4: A 34-year-old female presents to the emergency room with headache and palpitations. She is sweating profusely and appears tremulous on exam. Vital signs are as follows: HR 120, BP 190/110, RR 18, O2 99% on room air, and Temp 37C. Urinary metanephrines and catechols are positive. Which of the following medical regimens is contraindicated as a first-line therapy in this patient?

• A. Labetalol
• B. Propranolol (Correct Answer)
• C. Nitroprusside
• D. Lisinopril
• E. Phenoxybenzamine

Cholinergic/Adrenergic drugs Explanation: ***Propranolol*** - This patient's presentation with headache, palpitations, sweating, hypertension, and tachycardia, along with elevated urinary metanephrines and catechols, is highly suggestive of a **pheochromocytoma**. - **Pure beta-blockers** (like propranolol) are **absolutely contraindicated** as first-line therapy because blocking $\beta_2$ receptors without initial $\alpha$-blockade leads to unopposed $\alpha$-adrenergic stimulation, causing severe **vasoconstriction** and a dangerous **hypertensive crisis**. - This is the **most contraindicated** option among the choices listed. *Labetalol* - Labetalol is a **non-selective $\beta$-blocker with some $\alpha_1$-blocking activity** (β:α blockade ratio ~7:1). - While **not recommended** as first-line monotherapy in pheochromocytoma due to predominant beta-blockade, it has **some alpha-blocking properties** that distinguish it from pure beta-blockers. - In practice, it's typically avoided as initial therapy, but it carries **less risk** than pure beta-blockers because of its partial alpha-blockade. - Some sources consider it relatively contraindicated, but propranolol (pure beta-blocker) is more definitively contraindicated. *Nitroprusside* - **Nitroprusside** is a potent **vasodilator** that acts on both arterial and venous beds, making it effective for **rapid blood pressure reduction** in hypertensive emergencies. - It is **not contraindicated** and can be used in a pheochromocytoma crisis for acute blood pressure control, though it should ideally be combined with alpha-blockade. - It does not directly address catecholamine effects but provides symptomatic BP control. *Lisinopril* - **Lisinopril** is an **ACE inhibitor**, which works by preventing the conversion of angiotensin I to angiotensin II, leading to vasodilation and reduced aldosterone secretion. - It is **not contraindicated** but is **inappropriate** as first-line therapy in pheochromocytoma crisis because it does not directly counteract the massive catecholamine release. - It would be ineffective for managing the acute hypertensive emergency. *Phenoxybenzamine* - **Phenoxybenzamine** is an **irreversible, non-selective $\alpha$-adrenergic blocker** that is the **gold standard first-line therapy** for pheochromocytoma. - It effectively blocks the vasoconstrictive effects of catecholamines, allowing for adequate blood pressure control before any $\beta$-blockade is considered. - This is the **correct first-line medication**, not contraindicated.

Cholinergic/Adrenergic drugs US Medical PG Question 5: A 55-year-old woman comes to the physician because of involuntary hand movements that improve with alcohol consumption. Physical examination shows bilateral hand tremors that worsen when the patient is asked to extend her arms out in front of her. The physician prescribes a medication that is associated with an increased risk of bronchospasms. This drug has which of the following immediate effects on the cardiovascular system? Stroke volume | Heart rate | Peripheral vascular resistance

• A. ↓ ↓ ↓
• B. ↓ ↓ ↑ (Correct Answer)
• C. ↓ ↑ ↑
• D. ↑ ↑ ↑
• E. ↑ ↑ ↓

Cholinergic/Adrenergic drugs Explanation: ***↓ ↓ ↑*** - This patient likely has **essential tremor**, which is characterized by **bilateral hand tremors** that improve with alcohol and worsen with intention (postural tremor). The prescribed medication is a **beta-blocker** (e.g., propranolol), which is associated with an increased risk of bronchospasms due to blocking **beta-2 receptors** in the airways. - Beta-blockers **decrease heart rate** (negative chronotropic effect) and **stroke volume** (negative inotropic effect) by blocking beta-1 receptors in the heart, reducing cardiac output. - **Peripheral vascular resistance increases** acutely due to: (1) **unopposed alpha-1 adrenergic tone** in blood vessels (loss of beta-2 mediated vasodilation), and (2) baroreceptor-mediated reflex vasoconstriction in response to decreased cardiac output. This helps maintain blood pressure despite reduced cardiac output. *↓ ↓ ↓* - While beta-blockers decrease **heart rate** and **stroke volume**, peripheral vascular resistance does not decrease acutely. A decrease in all three parameters would cause severe hypotension. - The loss of beta-2 receptor-mediated vasodilation and baroreceptor reflexes lead to increased, not decreased, peripheral vascular resistance. *↓ ↑ ↑* - Beta-blockers **decrease heart rate** through beta-1 blockade, not increase it. This is their primary cardiac mechanism of action. - An increase in heart rate would be expected with sympathomimetic drugs or anticholinergics, not beta-blockers. *↑ ↑ ↑* - This combination indicates increased cardiovascular activity, which is the opposite effect of **beta-blockers**. - Beta-blockers reduce heart rate and stroke volume by blocking beta-1 receptors; they do not increase these parameters. - This pattern would suggest sympathetic activation or administration of an adrenergic agonist. *↑ ↑ ↓* - Beta-blockers **decrease** (not increase) both heart rate and stroke volume through beta-1 receptor blockade. - While decreased peripheral vascular resistance occurs with vasodilators, beta-blockers acutely **increase** PVR due to unopposed alpha-adrenergic tone.

Cholinergic/Adrenergic drugs US Medical PG Question 6: A 44-year-old male is brought to the emergency department by fire and rescue after he was the unrestrained driver in a motor vehicle accident. His wife notes that the patient’s only past medical history is recent development of severe episodes of headache accompanied by sweating and palpitations. She says that these episodes were diagnosed as atypical panic attacks by the patient’s primary care provider, and the patient was started on sertraline and alprazolam. In the trauma bay, the patient’s temperature is 97.6°F (36.4°C), blood pressure is 81/56 mmHg, pulse is 127/min, and respirations are 14/min. He has a Glascow Coma Score (GCS) of 10. He is extremely tender to palpation in the abdomen with rebound and guarding. His skin is cool and clammy, and he has thready peripheral pulses. The patient's Focused Assessment with Sonography for Trauma (FAST) exam reveals bleeding in the perisplenic space, and he is taken for emergency laparotomy. He is found to have a ruptured spleen, and his spleen is removed. During manipulation of the bowel, the patient’s temperature is 97.8°F (36.6°C), blood pressure is 246/124 mmHg, and pulse is 104/min. The patient is administered intravenous labetalol, but his blood pressure continues to worsen. The patient dies during the surgery. Which of the following medications would most likely have prevented this outcome?

• A. Lorazepam
• B. Propylthiouracil
• C. Phenoxybenzamine (Correct Answer)
• D. Dantrolene
• E. Phentolamine

Cholinergic/Adrenergic drugs Explanation: ***Phenoxybenzamine*** - This patient likely had an undiagnosed **pheochromocytoma**, which is a **catecholamine-secreting tumor**. The severe labile hypertension during surgery, unresponsive to labetalol, is a classic sign of a catecholamine surge. - **Phenoxybenzamine** is an **irreversible alpha-adrenergic blocker** that would have been used pre-operatively to control blood pressure and prevent such a hypertensive crisis by blocking the effects of excess catecholamines. *Lorazepam* - **Lorazepam** is a **benzodiazepine** used for anxiety and seizure control. While it might have helped to calm the patient or manage panic, it would not address the underlying physiological cause of the hypertensive crisis associated with an endocrine tumor. - Its effects on blood pressure are generally mild and would not counteract the massive catecholamine release seen in a pheochromocytoma. *Propylthiouracil* - **Propylthiouracil** is an **antithyroid medication** used to treat **hyperthyroidism**. There is no indication of thyroid dysfunction in this patient's presentation. - The symptoms of palpitations and sweating are common to both pheochromocytoma and hyperthyroidism, but the rapid, extreme hypertensive crisis points away from thyroid storm and towards a catecholamine-secreting tumor. *Dantrolene* - **Dantrolene** is a **skeletal muscle relaxant** primarily used to treat and prevent **malignant hyperthermia**. - There is no evidence in the clinical presentation to suggest malignant hyperthermia as the cause of this patient's deterioration; the extreme hypertension is the primary issue. *Phentolamine* - **Phentolamine** is a **reversible alpha-adrenergic blocker** used to manage hypertensive crises, particularly those due to pheochromocytoma or monoamine oxidase inhibitor interactions. - While phentolamine could be used during a crisis, **phenoxybenzamine** is preferred for *pre-operative preparation* due to its longer-acting and irreversible blockade, preventing the crisis more effectively when surgery is anticipated for pheochromocytoma.

Cholinergic/Adrenergic drugs US Medical PG Question 7: A researcher is studying receptors that respond to epinephrine in the body and discovers a particular subset that is expressed in presynaptic adrenergic nerve terminals. She discovers that upon activation, these receptors will lead to decreased sympathetic nervous system activity. She then studies the intracellular second messenger changes that occur when this receptor is activated. She records these changes and begins searching for analogous receptor pathways. Which of the following receptors would cause the most similar set of intracellular second messenger changes?

• A. Muscarinic cholinoreceptors in the gastrointestinal tract
• B. Growth hormone receptors in the musculoskeletal system
• C. Vasopressin receptors in the kidney
• D. Dopamine receptors in the brain (Correct Answer)
• E. Aldosterone receptors in the kidney

Cholinergic/Adrenergic drugs Explanation: ***Dopamine receptors in the brain*** - The described presynaptic receptors for epinephrine that decrease sympathetic activity are **alpha-2 adrenergic receptors**, which are **G inhibitory protein (Gi)-coupled receptors**. - Gi-coupled receptors **inhibit adenylyl cyclase**, leading to a **decrease in intracellular cAMP**, a signaling pathway shared by **D2 dopamine receptors**. *Muscarinic cholinoreceptors in the gastrointestinal tract* - Most muscarinic receptors (M1 and M3) in the GI tract are **Gq-coupled**, leading to an **increase in phospholipase C (PLC) activity**, ultimately increasing intracellular **IP3 and DAG** and promoting smooth muscle contraction. - This mechanism is distinct from the **Gi-mediated inhibition of cAMP** described for the presynaptic adrenergic receptor. *Growth hormone receptors in the musculoskeletal system* - Growth hormone receptors are **tyrosine kinase-associated receptors** (specifically, they are linked to **JAK/STAT pathways**), not G protein-coupled receptors. - Their intracellular signaling involves **protein phosphorylation cascades**, which are fundamentally different from second messenger changes involving cAMP. *Vasopressin receptors in the kidney* - Vasopressin (ADH) acts on **V2 receptors** in the kidney, which are **G stimulatory protein (Gs)-coupled receptors**. - Activation of V2 receptors leads to an **increase in adenylyl cyclase activity** and thus an **increase in intracellular cAMP**, the opposite effect of the described Gi-coupled receptor. *Aldosterone receptors in the kidney* - Aldosterone receptors are **intracellular steroid hormone receptors** that directly bind to DNA and regulate gene transcription. - They do not engage in rapid intracellular second messenger changes like G protein-coupled receptors, but rather alter **protein synthesis** over hours to days.

Cholinergic/Adrenergic drugs US Medical PG Question 8: A 50-year-old woman presents with altered taste and a gritty sensation in her eyes for the last month. She mentions that she needs to drink water frequently and often feels that her mouth and throat are dry. On physical examination, she has bilateral enlargement of the parotid glands and dry conjunctivae. Her physical examination and laboratory findings suggest a diagnosis of sicca syndrome. In addition to non-pharmacological measures, a drug is prescribed to improve symptoms related to dryness of mouth by increasing salivation. Which of the following is the mechanism of action of the drug that most likely is being prescribed to this patient?

• A. Selective M2 muscarinic receptor agonist
• B. Selective M3 muscarinic receptor agonist (Correct Answer)
• C. Selective M2 muscarinic receptor antagonist
• D. Selective M3 muscarinic receptor antagonist
• E. Selective M1 muscarinic receptor antagonist

Cholinergic/Adrenergic drugs Explanation: ***Selective M3 muscarinic receptor agonist*** - **Pilocarpine** or **cevimeline**, M3 muscarinic receptor agonists, are commonly used for **sicca symptoms** in Sjögren's syndrome. - Activation of **M3 receptors** on salivary and lacrimal glands directly stimulates increased **saliva** and **tear production**. *Selective M2 muscarinic receptor agonist* - **M2 receptors** are primarily found in the **heart**, and their activation would primarily affect **cardiac function** (e.g., bradycardia), not salivary secretion. - While M2 receptors are G protein-coupled, their role in exocrine gland secretion is minimal compared to M3. *Selective M2 muscarinic receptor antagonist* - An **M2 antagonist** would primarily cause an **increase in heart rate** by blocking parasympathetic input to the heart. - Such a drug would have no direct positive effect on saliva production and could worsen dry mouth by its indirect effects. *Selective M3 muscarinic receptor antagonist* - An **M3 antagonist** would **block salivary and tear production**, exacerbating the patient's dry mouth and gritty eyes. - These drugs are typically used to treat conditions like overactive bladder (e.g., darifenacin) or chronic obstructive pulmonary disease (e.g., tiotropium). *Selective M1 muscarinic receptor antagonist* - **M1 receptors** are predominantly found in the **cerebral cortex** and **gastric glands**. - An M1 antagonist would primarily affect cognitive function or gastric acid secretion, which is not the therapeutic goal here.

Cholinergic/Adrenergic drugs US Medical PG Question 9: A 3-year-old girl swallowed a handful of pills after her grandmother dropped the bottle on the ground this afternoon. She presents to the ER in a very drowsy but agitated state. She is clutching her abdomen, as if in pain, her skin is dry and flushed, and she does not know her name or where she is. Her pupils are dilated. Her grandmother reports that she has not urinated in several hours. The grandmother's medical history is significant for allergic rhinitis and osteoarthritis, both of which are treated with over the counter medications. What is the appropriate treatment for this child?

• A. N-acetylcysteine
• B. Naloxone
• C. Physostigmine (Correct Answer)
• D. Deferoxamine
• E. Atropine

Cholinergic/Adrenergic drugs Explanation: ***Physostigmine*** is the correct answer. - The patient's presentation with **dry, flushed skin**, **dilated pupils**, agitation, drowsiness, abdominal pain, and urinary retention is highly suggestive of **anticholinergic toxicity**. - **Physostigmine** is a **cholinesterase inhibitor** that increases acetylcholine levels, directly reversing the effects of anticholinergic poisoning. *N-acetylcysteine* - **N-acetylcysteine** is the specific antidote for **acetaminophen overdose**, which is not indicated by the patient's symptoms. - The symptoms described do not match the typical presentation of acetaminophen toxicity (e.g., hepatic damage). *Naloxone* - **Naloxone** is used to reverse **opioid overdose**, which typically presents with respiratory depression and miosis (pinpoint pupils), contrary to this patient's dilated pupils and lack of respiratory compromise. - The clinical picture does not suggest opioid intoxication. *Deferoxamine* - **Deferoxamine** is a chelating agent used to treat **iron overdose**, which can cause gastrointestinal symptoms but does not typically present with the anticholinergic signs seen here. - There are no indications of iron toxicity in the patient's history or symptoms. *Atropine* - **Atropine** is an **anticholinergic agent** itself and would worsen the patient's symptoms by further blocking acetylcholine receptors. - It is used to treat cholinergic crises, not overdose of anticholinergic drugs.

Cholinergic/Adrenergic drugs US Medical PG Question 10: A 50-year-old man comes to the physician because of gradually worsening rhythmic movements of his right hand for the past 5 months. His symptoms worsen when he is in a meeting and he is concerned that people are noticing it more frequently. There is no personal or family history of serious illness, but the patient recalls that his father developed bobbing of the head in older age. He takes no medications. Neurological examination shows a tremor of the right hand when the limbs are relaxed. When the patient is asked to move his arm the tremor decreases. He has reduced arm swing while walking. Which of the following is the most appropriate pharmacotherapy?

• A. Trihexyphenidyl
• B. Propranolol
• C. Clonazepam
• D. Donepezil
• E. Levodopa/carbidopa (Correct Answer)

Cholinergic/Adrenergic drugs Explanation: ***Levodopa/carbidopa*** - The patient's symptoms (gradually worsening rhythmic movements, **resting tremor** which improves with action, reduced arm swing, and possible family history of head bobbing/tremor) are highly suggestive of **Parkinson's disease**. - **Levodopa/carbidopa** is the most effective medication for symptomatic treatment of Parkinson's disease, particularly for motor symptoms like tremor, bradykinesia, and rigidity. *Trihexyphenidyl* - This is an **anticholinergic** medication that can be used to treat tremor in Parkinson's disease, but it is generally less effective than levodopa and has more side effects, especially in older patients (e.g., confusion, dry mouth, blurred vision). - It is typically considered for younger patients with prominent tremor rather than older individuals or those with a broader range of motor symptoms. *Propranolol* - **Propranolol** is a beta-blocker primarily used to treat **essential tremor**, a condition characterized by an action or postural tremor that improves with alcohol and often has a strong family history. - The patient's tremor is a **resting tremor** that decreases with action, making essential tremor less likely. *Clonazepam* - **Clonazepam** is a benzodiazepine that is used to treat various conditions, including anxiety, seizures, and some movement disorders (e.g., restless legs syndrome, clonus). - It is not a primary treatment for Parkinson's disease tremor and would not address the other motor symptoms like reduced arm swing. *Donepezil* - **Donepezil** is an **acetylcholinesterase inhibitor** used to treat the cognitive symptoms of Alzheimer's disease and other dementias. - It has no role in the treatment of the motor symptoms of Parkinson's disease.

Cholinergic/Adrenergic drugs Flashcard 1 of 10

Question: Which adrenergic receptor is sympatholytic? _____

Answer: 2

Cholinergic/Adrenergic drugs Flashcard 2 of 10

Question: Terazosin is a _____ receptor antagonist used to treat BPH in patients with hypertension

Answer: non-selective 1

Cholinergic/Adrenergic drugs Flashcard 3 of 10

Question: What drug class does methacholine belong to? _____

Answer: Cholinomimetics (muscarinic agonists)

Cholinergic/Adrenergic drugs Flashcard 4 of 10

Question: What G-protein is the M2 muscarinic receptor coupled to? _____

Answer: Gi

Cholinergic/Adrenergic drugs Flashcard 5 of 10

Question: The vestibular system contains _____ muscarinic receptors

Answer: M1

Cholinergic/Adrenergic drugs Flashcard 6 of 10

Question: One adverse effect of anti-muscarinics (e.g. atropine) is _____ (HR)

Answer: tachycardia

Cholinergic/Adrenergic drugs Flashcard 7 of 10

Question: Trazodone is an _____-adrenergic antagonist

Answer: 1

Cholinergic/Adrenergic drugs Flashcard 8 of 10

Question: Which cholinesterase inhibitor poisoning antidote reverses the central muscarinic effects?_____

Answer: Atropine

Cholinergic/Adrenergic drugs Flashcard 9 of 10

Question: terbutaline

Answer:

Extra Information: relaxation of premature uterine contractionsβ2 - agonist

Cholinergic/Adrenergic drugs Flashcard 10 of 10

Question: tamsulosin

Answer:

Extra Information: BPHα1-antagonist, inhibits smooth muscle contraction, selective for prostatic receptors