Adrenergic receptor subtypes US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Adrenergic receptor subtypes. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Adrenergic receptor subtypes US Medical PG Question 1: Which receptor type mediates the slow phase of synaptic transmission in autonomic ganglia?
- A. Muscarinic (M3)
- B. Muscarinic (M2)
- C. Muscarinic (M1) (Correct Answer)
- D. Nicotinic (N2)
Adrenergic receptor subtypes Explanation: ***Muscarinic (M1)***
- **M1 receptors** are **Gq-protein coupled receptors** that activate phospholipase C, leading to increased intracellular calcium and diacylglycerol, which mediates the slow excitatory postsynaptic potential in autonomic ganglia.
- This activation results in a **slow depolarization** that prolongs the excitability of ganglionic neurons after the initial fast synaptic transmission.
*Muscarinic (M3)*
- **M3 receptors** are primarily found on **smooth muscle**, glands, and endothelium, mediating contraction, secretion, and vasodilation, respectively.
- While also **Gq-protein coupled**, their role in autonomic ganglia is not the main mediator of the slow phase of synaptic transmission.
*Muscarinic (M2)*
- **M2 receptors** are **Gi-protein coupled receptors** mainly found in the heart, mediating decreased heart rate and contractility.
- In autonomic ganglia, M2 receptors could have a modulatory role, but they are not responsible for the slow excitatory phase of synaptic transmission.
*Nicotinic (N2)*
- **Nicotinic N2 receptors** (also known as **NN or neuronal nicotinic receptors**) mediate the **fast excitatory postsynaptic potential** (EPSP) in autonomic ganglia by opening ion channels.
- This leads to rapid depolarization and action potential generation, which is distinct from the **slower, prolonged phase** of transmission.
Adrenergic receptor subtypes US Medical PG Question 2: A 23-year-old woman presents to the emergency department with acute onset of shortness of breath, wheezing, and chest tightness. This is her 4th visit for these symptoms in the last 5 years. She tells you she recently ran out of her normal "controller" medication. Concerned for an asthma exacerbation, you begin therapy with a short-acting beta2-agonist. What is the expected cellular response to your therapy?
- A. Gs protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP (Correct Answer)
- B. Gq protein coupled receptor activates phospholipase C and increases intracellular calcium
- C. Gq protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP
- D. Gs protein coupled receptor activates phospholipase C and increases intracellular calcium
- E. Gi protein coupled receptor inhibits adenylyl cyclase and decreases cAMP
Adrenergic receptor subtypes Explanation: ***Gs protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP***
- **Short-acting beta2-agonists (SABAs)** like **albuterol** bind to **beta2-adrenergic receptors** on airway smooth muscle cells, which are **Gs protein-coupled receptors**.
- Activation of **Gs protein** stimulates **adenylyl cyclase**, leading to an increase in intracellular **cyclic AMP (cAMP)**, which triggers downstream relaxation of bronchial smooth muscle.
*Gq protein coupled receptor activates phospholipase C and increases intracellular calcium*
- **Gq protein-coupled receptors** are typically associated with **alpha1-adrenergic receptors** or **muscarinic M1/M3 receptors**, which, when activated, cause **bronchoconstriction** not bronchodilation.
- Activation of **Gq protein** leads to activation of **phospholipase C**, which generates **IP3** and **DAG**, ultimately increasing intracellular **calcium** and promoting contraction.
*Gq protein coupled receptor activates adenylyl cyclase and increases intracellular cAMP*
- This option incorrectly pairs **Gq protein** with the activation of **adenylyl cyclase** and an increase in **cAMP**.
- **Gq protein** signaling primarily involves the **phospholipase C pathway** and **calcium** mobilization, not direct adenylyl cyclase activation.
*Gs protein coupled receptor activates phospholipase C and increases intracellular calcium*
- This option incorrectly pairs **Gs protein** with the activation of **phospholipase C** and an increase in intracellular **calcium**.
- **Gs protein** is specifically coupled to the **adenylyl cyclase/cAMP pathway**, while **phospholipase C** and **calcium** are associated with **Gq protein** signaling.
*Gi protein coupled receptor inhibits adenylyl cyclase and decreases cAMP*
- **Gi protein-coupled receptors** inhibit **adenylyl cyclase** and decrease intracellular **cAMP**, which would lead to **bronchoconstriction**, not bronchodilation.
- This mechanism is associated with **M2 muscarinic receptors** on presynaptic terminals, which regulate acetylcholine release, or alpha2-adrenergic receptors, which are not the primary target for bronchodilation in asthma exacerbations.
Adrenergic receptor subtypes US Medical PG Question 3: A 60-year-old man presents to the office for a scheduled follow-up visit. He has had hypertension for the past 30 years and his current anti-hypertensive medications include lisinopril (40 mg/day) and hydrochlorothiazide (50 mg/day). He follows most of the lifestyle modifications recommended by his physician, but is concerned about his occasional occipital headaches in the morning. His blood pressure is 160/98 mm Hg. The physician adds another drug to his regimen that acts centrally as an α2-adrenergic agonist. Which of the following second messengers is involved in the mechanism of action of this new drug?
- A. Calcium ions
- B. Inositol triphosphate
- C. Cyclic guanosine monophosphate
- D. Cyclic adenosine monophosphate (Correct Answer)
- E. Diacylglycerol
Adrenergic receptor subtypes Explanation: ***Cyclic adenosine monophosphate***
- The physician likely added **clonidine or methyldopa**, both of which are **central α2-adrenergic agonists** used to treat hypertension.
- Activation of **α2-adrenergic receptors** leads to the **inhibition of adenylyl cyclase** and a decrease in **intracellular cyclic AMP (cAMP) levels**, which is the second messenger.
*Calcium ions*
- While calcium ions are crucial second messengers in many cellular processes, they are primarily involved in the mechanism of action of **α1-adrenergic receptors** and **voltage-gated calcium channels**, not directly inhibited by α2-agonists.
- **α2-adrenergic agonism** primarily acts to *reduce* neuronal excitability, which can indirectly affect calcium flux but does not directly involve calcium as the primary second messenger.
*Inositol triphosphate*
- **Inositol triphosphate (IP3)** is a second messenger primarily associated with the activation of **Gq protein-coupled receptors**, leading to the release of intracellular calcium.
- This pathway is characteristic of **α1-adrenergic receptors**, which cause vasoconstriction, and is antagonistic to the α2-agonist mechanism.
*Cyclic guanosine monophosphate*
- **Cyclic GMP (cGMP)** is a key second messenger in processes such as **vasodilation mediated by nitric oxide** and the action of ANP/BNP.
- **α2-adrenergic agonists** do not directly modulate cGMP levels as their primary mechanism of action.
*Diacylglycerol*
- **Diacylglycerol (DAG)** is a second messenger, along with IP3, produced from the hydrolysis of **PIP2** by phospholipase C, following activation of **Gq protein-coupled receptors**.
- This pathway is associated with **α1-adrenergic receptor activation**, not the inhibitory pathway initiated by central α2-adrenergic agonists.
Adrenergic receptor subtypes US Medical PG Question 4: A 72-year-old man with coronary artery disease comes to the physician because of intermittent episodes of substernal chest pain and shortness of breath. The episodes occur only when walking up stairs and resolves after resting for a few minutes. He is a delivery man and is concerned because the chest pain has impacted his ability to work. His pulse is 98/min and blood pressure is 132/77 mm Hg. Physical examination is unremarkable. An ECG shows no abnormalities. A drug that blocks which of the following receptors is most likely to prevent future episodes of chest pain from occurring?
- A. Angiotensin II receptors
- B. M2 muscarinic receptors
- C. Aldosterone receptors
- D. Beta-1 adrenergic receptors (Correct Answer)
- E. Alpha-2 adrenergic receptors
Adrenergic receptor subtypes Explanation: ***Beta-1 adrenergic receptors***
- The patient's symptoms are classic for **stable angina**, triggered by exertion and relieved by rest, which indicates myocardial oxygen demand exceeding supply. Blocking **beta-1 adrenergic receptors** with a beta-blocker **reduces heart rate** and **contractility**, thereby decreasing myocardial oxygen consumption.
- Beta-blockers are a cornerstone in the treatment of stable angina to prevent future episodes of chest pain by **reducing cardiac workload**.
*Angiotensin II receptors*
- Blocking **Angiotensin II receptors** (e.g., with ARBs) is primarily used for **hypertension**, **heart failure**, and **renal protection**, not as a first-line treatment for acute angina prevention by reducing myocardial oxygen demand.
- While beneficial for overall cardiovascular risk reduction, ARBs do not directly lower heart rate or contractility to the same extent as beta-blockers for immediate angina symptom control.
*M2 muscarinic receptors*
- Blocking **M2 muscarinic receptors** would primarily **increase heart rate** and contractility by inhibiting parasympathetic tone, which would worsen, not prevent, angina by increasing myocardial oxygen demand.
- This is the opposite effect desired for angina management.
*Aldosterone receptors*
- Aldosterone receptor blockade (e.g., with spironolactone) is mainly used in **heart failure** and **hypertension** to reduce fluid retention and remodeling, but it does not directly impact myocardial oxygen demand or supply to prevent exertional angina.
- It does not have a direct anti-anginal effect on heart rate or contractility.
*Alpha-2 adrenergic receptors*
- Alpha-2 adrenergic receptor agonists (e.g., clonidine) are centrally acting sympatholytics that **decrease sympathetic outflow**, leading to vasodilation and reduced heart rate and blood pressure. However, they are not first-line agents for stable angina due to potential side effects and less direct impact on myocardial oxygen demand compared to beta-blockers.
- Their primary role is in **hypertension management**, and sudden discontinuation can lead to **rebound hypertension**.
Adrenergic receptor subtypes US Medical PG Question 5: A 53-year-old man presents to the office for a routine examination. The medical history is significant for diabetes mellitus, for which he is taking metformin. The medical records show blood pressure readings from three separate visits to fall in the 130–160 mm Hg range for systolic and 90–100 mm Hg range for diastolic. Prazosin is prescribed. Which of the following are effects of this drug?
- A. Vasodilation, decreased heart rate, bronchial constriction
- B. Vasodilation, increased peristalsis, bronchial dilation
- C. Vasoconstriction, bladder sphincter constriction, mydriasis
- D. Vasoconstriction, increase in AV conduction rate, bronchial dilation
- E. Vasodilation, bladder sphincter relaxation (Correct Answer)
Adrenergic receptor subtypes Explanation: ***Vasodilation, bladder sphincter relaxation***
- **Prazosin** is an **alpha-1 adrenergic receptor antagonist**, which blocks the effects of norepinephrine on vascular smooth muscle, leading to **vasodilation** and decreased blood pressure.
- Blocking alpha-1 receptors in the bladder neck and prostate causes **bladder sphincter relaxation**, which can improve urine flow and is also useful in benign prostatic hyperplasia (BPH).
- These are the two primary clinically relevant effects of alpha-1 blockade with prazosin.
*Vasodilation, decreased heart rate, bronchial constriction*
- While prazosin causes **vasodilation**, it does not typically decrease heart rate directly; alpha-1 blockade can lead to **reflex tachycardia** due to decreased blood pressure.
- Prazosin has no significant effect on bronchial smooth muscle and does not cause **bronchial constriction**; bronchial effects are primarily mediated by beta-2 receptors or muscarinic (M3) receptors.
*Vasodilation, increased peristalsis, bronchial dilation*
- Prazosin does cause **vasodilation** but does not directly cause **increased peristalsis**; gastrointestinal motility is mainly regulated by the autonomic nervous system via muscarinic receptors and the enteric nervous system.
- Prazosin does not cause **bronchial dilation**; this effect is mediated by beta-2 adrenergic receptor stimulation.
*Vasoconstriction, bladder sphincter constriction, mydriasis*
- Prazosin is an alpha-1 antagonist, meaning it *blocks* **vasoconstriction** and instead causes vasodilation.
- Similarly, it causes **bladder sphincter relaxation**, not constriction.
- Prazosin has minimal effects on pupil size; mydriasis would be caused by alpha-1 agonists or muscarinic antagonists, not alpha-1 antagonists.
*Vasoconstriction, increase in AV conduction rate, bronchial dilation*
- Prazosin causes **vasodilation**, not vasoconstriction.
- It does not significantly affect **AV conduction rate** or directly cause **bronchial dilation**.
Adrenergic receptor subtypes US Medical PG Question 6: A 72-year-old male presents to his primary care physician complaining of increased urinary frequency and a weakened urinary stream. He has a history of gout, obesity, diabetes mellitus, and hyperlipidemia. He currently takes allopurinol, metformin, glyburide, and rosuvastatin. His temperature is 98.6°F (37°C), blood pressure is 130/85 mmHg, pulse is 90/min, and respirations are 18/min. Physical examination reveals an enlarged, non-tender prostate without nodules or masses. An ultrasound reveals a uniformly enlarged prostate that is 40mL in size. His physician starts him on a new medication. After taking the first dose, the patient experiences lightheadedness upon standing and has a syncopal event. Which of the following mechanisms of action is most consistent with the medication in question?
- A. Dihydropyridine calcium channel blocker
- B. Selective muscarinic agonist
- C. Alpha-2-adrenergic receptor agonist
- D. Alpha-1-adrenergic receptor antagonist (Correct Answer)
- E. Non-selective alpha receptor antagonist
Adrenergic receptor subtypes Explanation: ***Alpha-1-adrenergic receptor antagonist***
- The patient's symptoms of **increased urinary frequency** and **weakened urinary stream** are consistent with **benign prostatic hyperplasia (BPH)**. The physical exam and ultrasound findings of an **enlarged, non-tender prostate** confirm this.
- The medication caused **lightheadedness upon standing** and a **syncopal event** after the first dose, which is indicative of **first-dose orthostatic hypotension**. This adverse effect is characteristic of **alpha-1-adrenergic receptor antagonists**, which relax smooth muscles in the prostate and bladder neck but can also cause vasodilation.
*Dihydropyridine calcium channel blocker*
- These drugs primarily relax **vascular smooth muscle**, leading to vasodilation and can cause **hypotension**, but **orthostatic hypotension** and syncope as a "first-dose effect" are less common compared to alpha-1 blockers.
- They are used to treat **hypertension** and **angina**, not directly for BPH symptoms.
*Selective muscarinic agonist*
- **Muscarinic agonists** (e.g., bethanechol) would **increase bladder contraction** and could worsen urinary outflow obstruction in BPH, not improve it.
- Their primary side effects include **diarrhea**, **nausea**, and **bradycardia**, not orthostatic hypotension and syncope.
*Alpha-2-adrenergic receptor agonist*
- **Alpha-2 agonists** (e.g., clonidine) typically **lower blood pressure** by reducing sympathetic outflow from the central nervous system, but they primarily cause **sedation** and **dry mouth**, and are not used for BPH.
- While they can cause hypotension, the specific presentation of first-dose syncope in the context of BPH treatment points away from this class.
*Non-selective alpha receptor antagonist*
- Although non-selective alpha antagonists can also cause **orthostatic hypotension** due to vasodilation, **selective alpha-1 antagonists** are the preferred choice for BPH due to their more targeted action on the prostate and bladder neck, and the question describes a direct therapy for BPH.
- Alpha-2 blockade is less relevant to BPH and can cause additional side effects.
Adrenergic receptor subtypes US Medical PG Question 7: A 75-year-old male arrives by ambulance to the emergency room severely confused. His vitals are T 40 C, HR 120 bpm, BP 80/55 mmHg, RR 25. His wife explains that he injured himself about a week ago while cooking, and several days later his finger became infected, oozing with pus. He ignored her warning to see a doctor and even refused after he developed fever, chills, and severe fatigue yesterday. After being seen by the emergency physician, he was given antibiotics and IV fluids. Following initial resuscitation with IV fluids, he remains hypotensive. The ED physicians place a central venous catheter and begin infusing norepinephrine. Which of the following receptors are activated by norepinephrine?
- A. Alpha 1, Alpha 2, Beta 1, Beta 2
- B. Alpha 1, Alpha 2, Beta 1 (Correct Answer)
- C. Alpha 2
- D. Alpha 1, Beta 1, Dopamine 1
- E. Alpha 1, Beta 1
Adrenergic receptor subtypes Explanation: ***Alpha 1, Alpha 2, Beta 1***
- **Norepinephrine** primarily activates **alpha-1** (peripheral vasoconstriction), **alpha-2** (presynaptic inhibition and some vasoconstriction), and **beta-1** (increased heart rate and contractility) adrenergic receptors.
- These are the **primary receptors** responsible for norepinephrine's clinical effects: vasoconstriction (alpha-1, alpha-2) and positive inotropic/chronotropic effects (beta-1).
- This receptor profile makes norepinephrine an ideal **vasopressor** in septic shock, as seen in this patient.
*Alpha 1, Alpha 2, Beta 1, Beta 2*
- While **norepinephrine** does activate alpha-1, alpha-2, and beta-1 receptors, it has **negligible affinity for beta-2 receptors**.
- **Epinephrine** (not norepinephrine) is the catecholamine with significant **beta-2 activity**, causing bronchodilation and vasodilation in skeletal muscle.
- Including beta-2 is a common mistake when confusing norepinephrine with epinephrine.
*Alpha 2*
- This option is far too incomplete as **norepinephrine** has significant action on **alpha-1** and **beta-1** receptors, which are crucial for its vasoconstrictive and inotropic effects.
- Activating only alpha-2 receptors would primarily lead to presynaptic inhibition and limited vasoconstriction, not the broad cardiovascular support required in septic shock.
*Alpha 1, Beta 1, Dopamine 1*
- While **norepinephrine** does activate **alpha-1** and **beta-1** receptors, it does **not** activate **dopamine 1 (D1) receptors**.
- Only **dopamine** itself or specific **dopamine agonists** stimulate D1 receptors, leading to renal and mesenteric vasodilation.
- This option incorrectly attributes dopaminergic activity to norepinephrine.
*Alpha 1, Beta 1*
- This option correctly identifies two of the main receptors activated by **norepinephrine**: alpha-1 (vasoconstriction) and beta-1 (positive inotropy and chronotropy).
- However, it **omits alpha-2 receptors**, which norepinephrine also activates, contributing to both presynaptic feedback inhibition and additional vasoconstriction.
- While not completely wrong, this is an incomplete answer.
Adrenergic receptor subtypes US Medical PG Question 8: Which neurotransmitter is primarily responsible for parasympathetic effects on heart rate?
- A. Norepinephrine
- B. Dopamine
- C. Acetylcholine (Correct Answer)
- D. Epinephrine
Adrenergic receptor subtypes Explanation: ***Acetylcholine***
- **Acetylcholine** is the primary neurotransmitter released by postganglionic parasympathetic neurons.
- It acts on **muscarinic receptors** (M2 receptors) in the heart to decrease heart rate.
*Norepinephrine*
- **Norepinephrine** is primarily associated with the **sympathetic nervous system**, increasing heart rate and contractility.
- It acts on **beta-1 adrenergic receptors** in the heart.
*Dopamine*
- **Dopamine** is a precursor to norepinephrine and epinephrine, and primarily functions as a neurotransmitter in the **central nervous system** and in regulating renal blood flow.
- While it can have cardiac effects, it is not the primary neurotransmitter for parasympathetic actions on heart rate.
*Epinephrine*
- **Epinephrine** (adrenaline) is a hormone released by the adrenal medulla and a neurotransmitter in the sympathetic nervous system, causing an **increase in heart rate** and contractility.
- It works through **beta-1 adrenergic receptors**, antagonistic to parasympathetic effects.
Adrenergic receptor subtypes US Medical PG Question 9: A 58-year-old woman presents to her physician complaining of a headache in the occipital region for 1 week. Past medical history is significant for essential hypertension, managed with lifestyle modifications and 2 antihypertensives for the previous 6 months. Her blood pressure is 150/90 mm Hg. Neurological examination is normal. A third antihypertensive drug is added that acts as a selective α2 adrenergic receptor agonist. On follow-up, she reports that she does not have any symptoms and her blood pressure is 124/82 mm Hg. Which of the following mechanisms best explains the therapeutic effect of this new drug in this patient?
- A. Vasodilation of peripheral arteries
- B. Vasodilation of peripheral arteries and peripheral veins
- C. Decreased peripheral sympathetic outflow (Correct Answer)
- D. Negative inotropic effect on the heart
- E. Vasodilation of peripheral veins
Adrenergic receptor subtypes Explanation: ***Decreased peripheral sympathetic outflow***
- Selective **α2 adrenergic receptor agonists** (e.g., clonidine, guanfacine, methyldopa) act **centrally in the brainstem** (nucleus tractus solitarius and rostral ventrolateral medulla) to reduce **sympathetic nervous system activity**.
- This **central action** leads to a **decrease in peripheral sympathetic outflow**, resulting in reduced heart rate, decreased cardiac output, and peripheral vasodilation, all contributing to lower blood pressure.
- This is the **primary mechanism** of antihypertensive action for central α2 agonists.
*Vasodilation of peripheral arteries*
- While central α2 agonists do cause some peripheral vasodilation, this is an **indirect effect** of **reduced sympathetic tone**, not a primary direct action on peripheral arteries.
- Their main mechanism of action is **central**, decreasing the overall sympathetic drive to the vasculature.
*Vasodilation of peripheral arteries and peripheral veins*
- This option describes a broader effect, and while some vasodilation occurs, it doesn't pinpoint the **primary mechanism of action** of central α2 agonists.
- Drugs like alpha-1 blockers (prazosin, doxazosin) or direct vasodilators (hydralazine, minoxidil) would have a more pronounced direct effect on both arterial and venous smooth muscle.
*Negative inotropic effect on the heart*
- While central α2 agonists can **reduce heart rate** (bradycardia) and cardiac output due to decreased sympathetic stimulation, a **negative inotropic effect** (decreased myocardial contractility) is not their primary or most significant mechanism.
- **Beta-blockers** are primarily known for their negative inotropic and chronotropic effects on the heart.
*Vasodilation of peripheral veins*
- Similar to arterial vasodilation, this is an **indirect effect** of **reduced sympathetic tone**, not the primary mechanism of action of central α2 agonists.
- Direct venodilators like **nitrates** would primarily target peripheral veins to reduce preload.
Adrenergic receptor subtypes US Medical PG Question 10: You have been asked to deliver a lecture to medical students about the effects of various body hormones and neurotransmitters on the metabolism of glucose. Which of the following statements best describes the effects of sympathetic stimulation on glucose metabolism?
- A. Norepinephrine causes increased glucose absorption within the intestines.
- B. Without epinephrine, insulin cannot act on the liver.
- C. Peripheral tissues require epinephrine to take up glucose.
- D. Epinephrine increases liver glycogenolysis. (Correct Answer)
- E. Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.
Adrenergic receptor subtypes Explanation: ***Epinephrine increases liver glycogenolysis.***
- **Epinephrine**, released during sympathetic stimulation, primarily acts to increase **glucose availability** for immediate energy.
- It achieves this by stimulating **glycogenolysis** (breakdown of glycogen into glucose) in the liver via **beta-adrenergic receptors**.
*Norepinephrine causes increased glucose absorption within the intestines.*
- **Norepinephrine** primarily causes **vasoconstriction** and can *decrease* **intestinal motility** and nutrient absorption due to shunting blood away from the digestive tract during stress.
- Glucose absorption is mainly regulated by digestive enzymes and transport proteins, not directly increased by norepinephrine.
*Without epinephrine, insulin cannot act on the liver.*
- **Insulin** acts on the liver independent of epinephrine to promote **glucose uptake**, **glycogenesis**, and **lipid synthesis**.
- Epinephrine and insulin have **antagonistic effects** on liver glucose metabolism; epinephrine increases glucose output, while insulin decreases it.
*Peripheral tissues require epinephrine to take up glucose.*
- **Insulin** is the primary hormone required for **glucose uptake** by most peripheral tissues, especially **muscle** and **adipose tissue**, via **GLUT4 transporters**.
- Epinephrine generally *reduces* glucose uptake by peripheral tissues to preserve glucose for the brain during stress.
*Sympathetic stimulation to alpha receptors of the pancreas increases insulin release.*
- Sympathetic stimulation, primarily acting through **alpha-2 adrenergic receptors** on pancreatic beta cells, actually **inhibits** **insulin secretion**.
- This inhibition helps to increase blood glucose levels by reducing insulin's glucose-lowering effects.
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