front 1 What are the basic steps of cholinergic synaptic transmission? | back 1 Synthesis of ACh → Storage/Release of ACh → Receptor binding (Muscarinic & Nicotinic) → Degradation of ACh. |
front 2 What physiological functions do cholinergic synapses control? | back 2 They mediate EPSPs or IPSPs and are involved in autonomic and somatic motor functions. |
front 3 What happens if ACh synthesis or AChE is inhibited? | back 3 Inhibition of ACh synthesis reduces ACh levels; inhibition of AChE increases ACh activity at synapses. |
front 4 Difference between nicotinic and muscarinic receptor agonists? | back 4 Nicotinic agonists: stimulate skeletal muscle and autonomic ganglia Muscarinic agonists: affect parasympathetic organs. |
front 5 Depolarizing vs non-depolarizing blockade? | back 5 Depolarizing (e.g., succinylcholine): Persistent activation of receptor → paralysis. Non-depolarizing (e.g., pancuronium): Competitive antagonist that blocks the receptor without activating it. |
front 6 What are parasympathomimetic drugs? | back 6 Drugs that mimic parasympathetic activity by stimulating muscarinic receptors or inhibiting acetylcholinesterase (AChE). |
front 7 What are the subtypes of muscarinic receptors and their general functions? | back 7
"Mind’s Memory Makes Muscles Move More."
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front 8 Basic steps in adrenergic synaptic transmission? | back 8 Synthesis of Norepinephrine/ Epinephrine→ Storage/Release → Receptor binding (α and β) → Reuptake/metabolism (e.g., MAO, COMT). |
front 9 What is a sympathomimetic vs sympatholytic drug? | back 9 Sympathomimetic: Mimics sympathetic nervous system activity. Sympatholytic: Blocks or reduces sympathetic nervous system activity. |
front 10 What are the types and mechanisms of adrenergic receptors? | back 10 Alpha-1: Vasoconstriction (↑ BP), mydriasis (Dilated pupils) and bladder sphincter contraction via Gq Alpha-2: Inhibits Norepinephrine (NE) release (negative feedback), insulin secretion, and lipolysis via Gi Beta-1: Increases heart rate, contractility and Renin release via Gs Beta-2: Bronchodilation, vasodilation and smooth muscle (uterine) relaxation via Gs |
front 11 How are adrenergic receptors regulated? | back 11 Through desensitization and downregulation via GRKs and β-arrestins (homologous and heterologous regulation). |
front 12 Examples of indirect-acting sympathomimetic drugs? | back 12 Amphetamines and ephedrines — they increase NE release or block its reuptake. |
front 13 What is the effect of inhibiting norepinephrine reuptake (NET inhibition)? | back 13 Mechanism: Inhibits reuptake of NE from the synaptic cleft → prolonged stimulation Example: Cocaine. Organ Effects:
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front 14 What is the effect of inhibiting catecholamine metabolism (MAO inhibitors)? | back 14 Mechanism: Blocks breakdown of NE, E, and dopamine by MAO → ↑ catecholamines. Organ Effects:
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front 15 What are sympathomimetic drugs and their general effects? | back 15 Mechanism: Mimic sympathetic nervous system activity by stimulating α or β adrenergic receptors. Organ Effects:
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front 16 Compare specific, mixed-action, and indirect-acting sympathomimetics. | back 16 Specific: Direct receptor binding (e.g., phenylephrine → α1) Mixed: Receptor stimulation + ↑ NE release (e.g., ephedrine) Indirect: Only ↑ NE release or inhibit reuptake (e.g., amphetamine, tyramine) Organ Effects: Similar to general adrenergic stimulation depending on receptor target |
front 17 What are the 3 main types of sympathomimetic drugs based on mechanism? | back 17 1. Direct-Acting: Bind directly to adrenergic receptors (e.g., phenylephrine, albuterol). 2. Indirect-Acting: Increase NE availability by enhancing release or inhibiting reuptake (e.g., amphetamines, cocaine). 3. Mixed-Acting: Both bind receptors and increase NE release (e.g., ephedrine). |
front 18 What is a Direct-Acting Sympathomimetic drug? | back 18 Mechanism: Directly activates α or β adrenergic receptors. Examples:
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front 19 What is an Indirect-Acting Sympathomimetic drug? | back 19 Mechanism: Increases levels of NE/E by:
Examples:
Key Sign: No receptor binding; effect depends on endogenous NE. |
front 20 What is a Mixed-Acting Sympathomimetic drug? | back 20 Mechanism: Directly stimulates receptors and increases NE release. Example: Ephedrine Effects:
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front 21 How can you identify a drug’s class based on its mechanism? | back 21 Direct-Acting: Known receptor affinity; effect persists without NE stores. Indirect-Acting: Ineffective if NE stores are depleted (e.g., after reserpine). Mixed-Acting: Retains partial effect even if NE is depleted. |
front 22 What class is amphetamine and how does it work? | back 22 Class: Indirect-acting sympathomimetic Mechanism: Increases NE release from nerve terminals. Effect: ↑ HR, BP, CNS stimulation |
front 23 What class is ephedrine and how does it work? | back 23 Class: Mixed-acting sympathomimetic Mechanism: Direct α/β receptor stimulation + increases NE release. Effect: ↑ BP, bronchodilation, decongestion |
front 24 How would you classify a drug that increases NE release but has no direct receptor activity? | back 24 Indirect-acting sympathomimetic (e.g., amphetamine, tyramine) |
front 25 How would you classify a drug that stimulates β2 receptors and causes bronchodilation? | back 25 Direct-acting sympathomimetic (e.g., albuterol) |
front 26 How would you classify a drug that causes vasoconstriction and also increases NE release? | back 26 Mixed-acting sympathomimetic (e.g., ephedrine) |
front 27 Alpha receptor agonists – MOA and organ effects | back 27 α1 agonists (e.g., phenylephrine): Vasoconstriction → ↑ BP, Mydriasis (pupil dilation), and Urinary retention (bladder sphincter contraction) α2 agonists (e.g., clonidine): ↓ NE release → ↓ BP and HR (centrally acting) |
front 28 Beta receptor agonists – MOA and organ effects | back 28 β1 agonists (e.g., dobutamine): ↑ Heart rate and contractility → used in heart failure β2 agonists (e.g., albuterol): Bronchodilation → used in asthma, Uterine relaxation → prevents premature labor, and Vasodilation → mild ↓ BP |
front 29 Alpha receptor antagonists – MOA and organ effects | back 29 Mechanism: Block α receptors → vasodilation Examples: Prazosin (α1), Phentolamine (non-selective) Organ Effects:
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front 30 Beta receptor antagonists (Beta blockers) – MOA and organ effects | back 30 Mechanism: Block β1 and/or β2 receptors Examples: Propranolol (non-selective), Atenolol (β1-selective), Labetalol (mixed α/β) Organ Effects:
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front 31 Receptor desensitization and downregulation – what is it and what organs are affected? | back 31 Mechanism:
Organ Impact: All adrenergic target tissues (heart, vessels, lungs) may show reduced response to chronic drug use |