Term
| What does acetylcholine do to the nicotinic acetylcholine receptor? |
|
Definition
| Acetylcholine opens up the sodium ion channel, sodium rushes into the nerve, depolarizes and neuron fires |
|
|
Term
| How does the steroid interact with the receptor and how does it bring about a hormone response? |
|
Definition
| steroid is usually bound by corticosteroid-binding globulin in blood but enters the cell as free molecule (uncharged), bind to intracellular receptor, enters nucleus, turns on transcription by binding to glucocorticoid response element on regulatory region, protein makes hormone response |
|
|
Term
| True or false: A single cell may only have 1 receptor and signaling system. |
|
Definition
| False-A single cell may have multiple receptors and signaling systems |
|
|
Term
| What is it called when continuous stimulation of a receptor often results in loss of response and down-regulation of receptors? |
|
Definition
| tachyphylaxis (ex: type II diabetes-insulin receptors become insensitive) |
|
|
Term
| Receptor sensitivity can be (increased or decreased) as a result of withdrawal of the agonist |
|
Definition
| Receptor sensitivity can be increased as a result of withdrawal of the agonist. (rebound effect) |
|
|
Term
| How do antihistamines work in terms of a binding to a receptor? |
|
Definition
| Antihistamines as an example of a class of drugs that bind to a receptor and inhibit normal ligand action |
|
|
Term
| What type of antagonists must be taken every few hours because they are only effective if they are present at an effective concentration? |
|
Definition
| Reversible competitive antagonists (H1 receptors) |
|
|
Term
Are reversible competitive antagonists of (H1 or H2) receptors used as decongestants?
Is (H1 or H2) used to treat excess stomach acid? |
|
Definition
Reversible competitive antagonists of H1 receptors are used as decongestants
Reversible competitive antagonists of H2 receptors are used to treat excess stomach acid |
|
|
Term
| Where does histamine come from? |
|
Definition
| Mast cells (contains mediators that cause inflammation: histamine, enzymes, prostaglandins, leukotrienes, platelet activating factor, cytokines) in the tissue and basophils in the blood |
|
|
Term
| What factors activate mast cells? |
|
Definition
IgE-mediated (allergies) - vasodilation, recruits WBCs
Anaphylatoxins (C5a, C3a)
Direct release by certain drugs (opiates)
Physical stimuli (heat, cold, trauma)
Autoimmune (chronic urticaria) |
|
|
Term
| Does histamine have any clinical application in the treatment of disease? |
|
Definition
| Histamine has no clinical application in the treatment of disease |
|
|
Term
| What are the 3 different histamine receptors? |
|
Definition
|
|
Term
| What are the 3 ways you can reduce histamine effects? |
|
Definition
Epinephrine
Mast cell stabilizers
Antihistamines |
|
|
Term
| What is the physiological antagonist that causes smooth muscle actions (vasoconstriction) opposite of histamine, and is used for anaphylaxis and severe urticaria? |
|
Definition
|
|
Term
| What is used in asthma that cause mast cells to not release as much histamine but the mechanism is unknown |
|
Definition
|
|
Term
| What is the reversible competitive antagonists of H1 receptors in nasal mucosal tissues? |
|
Definition
|
|
Term
What is the difference between 1st and 2nd generation antihistamines?
Why does one cause drowsiness while the other doesn't? How do stop the drowsiness? |
|
Definition
1st generation-Penetrates CNS (side effect=causes drowsiness), older, cheaper, generic
2nd- better, more expensive, 1/2 life or ability to enter CNS is changed
Make the drug charged so it won't go across the blood brain barrier and cause drowsiness |
|
|
Term
Is (H1 or H2) Gq-protein-mediated activation of phospholipase C to make IP3 and diacyglycerol?
Is (H1 or H2) Gs-protein-mediated activation of adenylyl cyclase to make cAMP? |
|
Definition
|
|
Term
Is (H1 or H2) found in the stomach, heart, some smooth muscles (uterus), CNS?
Is (H1 or H2) found in smooth muscles (especially in intestine, blood vessels, bladder, trachea), heart, adrenal medulla, vascular endothelium, CNS |
|
Definition
|
|
Term
| How many transmembrane domains are there in histamine receptors (both H1 and H2)? |
|
Definition
|
|
Term
Do (H1 or H2) receptor antagonists Commonly cause sedation, blurred vision, nervousness, dryness of mouth/respiratory passages, urinary retention
Paradoxical effect in some children
Prevent motion sickness
Prevent nausea and vomiting
Suppress effects of tremors associated with antipsychotics |
|
Definition
|
|
Term
| Are (1st or 2nd) generation antihistamines Rapidly absorbed, Long duration of action (12-24 hrs), Poor distribution to the CNS, Little to no sedation, Older agents metabolized by CYP450 enzyme system, Combined with pseudoephedrine (vasoconstriction) in some products |
|
Definition
|
|
Term
Identify whether these drugs are 1st or 2nd generation drugs of H1 receptors
Chlorpheniramine
Cyclazine
Cetirizine
Cyproheptadine
Dimenhydrinate
Diphenhydramine
Fexofenadine
Hydroxyzine
Loratadine
Promethazine |
|
Definition
Chlorpheniramine-1
Cyclazine-1
Cetirizine-2
Cyproheptadine-1
Dimenhydrinate-1
Diphenhydramine-1
Fexofenadine-2
Hydroxyzine-1
Loratadine-2
Promethazine-1
(cetirizine, loratadine, and fexofenadine-2nd generation! can't enter CNS) |
|
|
Term
| How would you treat allergic conjunctivitis? |
|
Definition
Treatment with a **mast-cell stabilizer and antihistamine
(may attempt to avoid allergens) |
|
|
Term
| Olopatadine (Patanol) drops, Alcaftadine, azelastin, bepotastin, epinastine, are what types of histamine reducers? |
|
Definition
| combines both anti-histamine and mast cell stabilizer effects (anti-histamine effects occur rapidly, mast cell stabilizer effects take longer) to treat allergic conjunctivitis |
|
|
Term
| Cimetidine, Ranitine, Famotidine and Nizatidine are (H1 or H2) Receptor Antagonist and what do they treat? |
|
Definition
Histamine H2 Receptor Antagonists
Orally effective, competitive inhibitors of H2 receptors on gastric parietal cells, treats acid reflux, decreases amount of acid secreted into the stomach |
|
|
Term
Which of the following drugs is least likely to cause sedation?
Diphenhydramine
Hydroxyzine
Cetirizine
Promethazine |
|
Definition
| Cetirizine - 2nd generation |
|
|
Term
Which of the following mediators causes the immediate symptoms observed after IgE is cross-linked by allergens?
Histamine
Prostaglandins
Leukotrienes
Interleukins |
|
Definition
| Histamine - causes immediate effect- prompts vasodilation, swelling |
|
|
Term
Which of the following is not a systemic effect of histamine?
Gastric acid secretion
Constriction of small blood vessels
Bronchoconstriction of bronchiolar smooth muscle
Formation of edema |
|
Definition
| Constriction of small blood vessels |
|
|
Term
What receptors do acetylcholine bind to?
Which one is couple to ion channels on the neurons, very quick?
Which one is coupled to G proteins that increase the formation of diacylglycerol and inositol triphosphate (IP3) by activating phospholipase C (muscles, slower, increases release of calcium)? |
|
Definition
Nicotinic Receptor-coupled to ion channels
Muscarinic Receptors-coupled to G proteins that increase the formation of diacylglycerol and inositol triphosphate (IP3) by activating phospholipase C |
|
|
Term
| What receptors does norepinephrine bind to? |
|
Definition
|
|
Term
| Which adrenergic receptor is coupled to Gs proteins that increase cAMP and is found primarily in the heart? |
|
Definition
|
|
Term
| Which adrenergic receptor is coupled to Gs proteins that increase cAMP levels found in the lungs? |
|
Definition
| B2 (B2 agonist given to treat asthma) |
|
|
Term
| Which adrenergic receptor is coupled to G proteins that increase the formation of diacylglycerol and inositol triphosphate (IP3) by activating phospholipase C |
|
Definition
|
|
Term
| Which adrenergic receptor is coupled to G proteins but is located on the neuron itself (other ones located on target cell) and decreases cAMP level by feedback inhibition? |
|
Definition
| A2 (slows down heart rate) |
|
|
Term
Does acetylcholine have an enzyme that degrades it at the synaptic cleft? Why?
Does norepinephrine? |
|
Definition
Yes-acetylcholinesterase has to clear acetylcholine out to depolarize quickly. Acetylcholinesterase inhibitors causes acetylcholine action duration to increase
No |
|
|
Term
| **What does norepinephrine bind to versus what does epinephrine bind to? |
|
Definition
Epinephrine binds to all adrenergic receptors (A1, A2, B1, B2)
Norepinephrine does NOT bind to B2 (found in lungs and cause to dilate-why we don't give NE for asthmatic attack) but binds to A1, A2, B1 |
|
|
Term
Drugs that mimic the actions of the sympathoadrenal system are called?
Drugs that block or reduce these actions are called? |
|
Definition
Sympathomimetics, Adrenomimetics, Sympathetic Agonists
Sympatholytics, Sympathoplegic, Sympathetic Antagonists |
|
|
Term
What is biosynthesis of neurotransmitters pathway?
What is in the storage vesicles?
How are the contents released? |
|
Definition
Tyrosine -> DOPA -> Dopamine -> NE -> EPI
norepinephrine, ATP, and dopamine beta-hydroxylase (converts dopamine to norepinephrine)
Ca2+ dependent (nerve depolarizes, sodium rushes in, calcium rushes in, vesicles release contents into cleft) |
|
|
Term
What breaks down norepinephrine?
How is norepinephrine taken up? |
|
Definition
monoamine oxidase and COMT (found in liver)
monoamine transporters (NET), cocaine-sensitive, binds to A2 |
|
|
Term
What does NOT happen when you see a bear enter the room?
you immediately open your eyes wide to find an escape route (mydriasis)
increase your heart rate
redistribute blood flow from your intestines to your skeletal muscles
open your pulmonary bronchioles
decrease your blood glucose |
|
Definition
| decrease your blood glucose |
|
|
Term
*What type of agonist would you use during an eye exam to cause mydriasis?
What type of agonist would you use if you want to increase aqueous humor? |
|
Definition
alpha agonist (mydriatic agent), NE, phenylephrine
beta agonist (use beta-blocker to decrease fluid/treat glaucoma) |
|
|
Term
Adrenergic innervation of the eye innervates?
What receptors predominate? |
|
Definition
Innervates iris dilator muscle, Mueller’s muscle (upper eyelid), conjunctival vasculature
A1 receptors predominate |
|
|
Term
Cholinergic innervation of the eye innervates?
What receptors predominate |
|
Definition
Innervates iris sphincter muscle, ciliary body
Muscarinic receptors predominate |
|
|
Term
| What agonist activity constricts pupil (miosis), contracts ciliary muscle, and lowers intraocular pressure |
|
Definition
| muscarinic agonist activity (muscarinic antagonist cause midriasis) |
|
|
Term
In the cardiovascular, what causes vasoconstriction (increase resistance and pressure)?
What causes vasodilation?
What causes increased heart rate, increased force of contraction? |
|
Definition
|
|
Term
| True or False: During a bear attack, alpha 1 is stimulated and beta 2 is not |
|
Definition
False
alpha 1 (vasoconstriction) decreases blood flow to the intestine
beta 2 (vasodilation) increases blood to the skeletal muscle at the same time |
|
|
Term
| At low dose of epinephrine, the affinity for which receptors dominate? At high doses of epinephrine what receptors dominate? |
|
Definition
| Low doses of Epinephrine - beta1 (cardiac) and beta2 (vasodilation) High doses of Epinephrine - alpha1 (vasoconstriction) |
|
|
Term
**Which G-protein Couple Receptor activates adenylyl cyclase?
Inhibits adenylyl cyclase?
Activates phospholipase C? |
|
Definition
Gs activates adenylyl cyclase
B1, B2, D1
Gi inhibits adenylyl cyclase
M2, A2, D2
Gq activates phospholipase C
M1, M3, A1 |
|
|
Term
Alpha and beta receptors are sympathetic or parasympathetic?
Muscarinic receptors are sympathetic or parasympathetic? |
|
Definition
sympathetic
Parasympathetic |
|
|
Term
| *What adrenergenic agonist causes vasoconstriction in most vessels except skeletal muscles, increase BP, nasal decongestion, mydriasis: contract radial muscle of iris, receptors located at the post-junctional membrane |
|
Definition
|
|
Term
| What adrenergenic agonist causes feedback inhibition of NE release, receptors located at the pre-junctional membrane, decreases BP |
|
Definition
|
|
Term
| What is the alpha 2 agonist drug that decreases BP? |
|
Definition
|
|
Term
| What adrenergic agonist causes cardiac effects: increase heart rate, conduction velocity & force of contraction receptors located at post-junctional membrane |
|
Definition
|
|
Term
| What adrenergic agonist causes pulmonary effect: dilate bronchioles receptors located on post-junctional membranes |
|
Definition
|
|
Term
What are the 3 adrenergic transmitters?
What are the three amine collectively called? |
|
Definition
norepinephrine (NE)
dopamine (DA)
epinephrine (EPI)
catecholamines - bind to several distinct adrenergic receptors in different cell types |
|
|
Term
What does monoamine oxidase work on?
What does it NOT work on? |
|
Definition
sympathomimetic Amines
Amphetamine (lasts longer in synaptic cleft than NE)
Isoproterenol |
|
|
Term
How does amphetamine effect the mechanism of reuptake of NE back into the noradrenergic neuron?
Cocaine?
Are these direct or indirect blockers? |
|
Definition
Amphetamine can get into the neuron and vesicles and decrease amount of NE released and can bind to receptors and cause release of NE
Cocaine blocks norepinephrine transporter and inhibits reuptake (massive effect at first, and then diminished effect later)
Indirect blockers |
|
|
Term
What does dopamine bind to?
Isoproterenol?
Dobutamine?
Phenylephrine?
Clonidine?
Terbutaline & Albuterol? |
|
Definition
Dopamine (A1, A2, B1, D1, D2)
Isoproterenol (B1, B2)
Dobutamine (B1)
Phenylephrine (A1)
Clonidine (A2)
Terbutaline & Albuterol (B2) |
|
|
Term
Is Amphetamine and Tyramine direct or indirect acting?
Is Ephedrine? |
|
Definition
Amphetamine & Tyramine (indirect)
Ephedrine (mixed agonist and indirect) |
|
|
Term
| What are the advantages of synthetic compounds as therapeutic agents? |
|
Definition
1. Increased selectivity for particular adrenergic receptors
2. Improved oral bioavailability
3. Prolonged duration of action |
|
|
Term
| What agonist would you use to treat nasal congestion, treat hypotension, cause mydriasis (dilation of the pupil for eye exam.), or mix with injected local anesthetic drugs to cause vasoconstriction at the site of injection and slow the rate at which the local anesthetic is removed to not get to the heart? |
|
Definition
|
|
Term
| What agonist would you use to treat hypertension (not used much because of rebound effect), is highly lipid soluble, crosses blood-brain barrier, activates receptors in hypothalamus and medulla to decrease NE release, decrease sympathetic action in the heart, but may cause xerostomia, drowsiness, constipation? |
|
Definition
| Alpha 2 adrenoceptor agonist |
|
|
Term
| What agonist is used for short term treatment of cardiac decompensation (heart failure), Not recommended for chronic use because of receptor desensitization and down-regulation, and cause undesirable side effects (tachycardia, hypertension and arrhythmias) - used in hospital setting |
|
Definition
|
|
Term
| What agonist treats asthma by aerosol spray to lungs to minimize systemic side-effects (tachycardia, hypertension, arrhythmias) and often combined with glucocorticoid therapy |
|
Definition
| B2 agonists (too much B2 causes tachycardia because it gets to the heart and interacts with B1 receptors) |
|
|
Term
What B2 agonists are Fast-acting agents for immediate effect (rescue inhaler) ?
Which is long-acting agents for once/twice daily prophylactic effects ? |
|
Definition
salmeterol
albuterol, terbutaline |
|
|
Term
| Is terbutaline (B1 or B2) selective? Is dobutamine (B1 or B2) selective? |
|
Definition
|
|
Term
| What is an A2 selective agonist that acts centrally to reduce sympathetic outflow to the periphery. Used for mild to moderate hypertension. Xerostomia, sedation, and constipation are major side effects |
|
Definition
|
|
Term
| What is B1 selective, used for short term therapy of cardia decompensation; chronic use and/or high doses result in tachycardia and arrhythmias |
|
Definition
|
|
Term
| What is B2 selective, administered as aerosols, first-line therapy for asthma, bronchospasm, and emphysema. Nervousness, headache, tachycardia, palpitations, and skeletal muscle tremors are side effects |
|
Definition
| albuterol and terbutaline |
|
|
Term
| What has high A1 selectivity? |
|
Definition
| Phenylephrine (mydriasis eye drops) and metaraminol |
|
|
Term
What does phentolamine block and what would that cause?
What does prazosin block and what would that cause? |
|
Definition
phentolamine- blocks A1 (big cardiac effect) and A2 (lots of NE release)=tachycardia
prazosin- blocks A1 (not A2), so feedback inhibition for A2 is still in place but still big effect on beta 1 receptors = increase heart rate |
|
|
Term
What does propanolol, Timolol block?
What does it do? |
|
Definition
blocks B1 and B2
decrease aqueous humor production by the ciliary body
(good for stage fright) |
|
|
Term
What does Atenolol, metoprolol (taken orally) block?
What does it do? |
|
Definition
Blocks B1
brings heart rate down |
|
|
Term
What does Reserpine block?
Is it a direct blocker or indirect? |
|
Definition
Reserpine blocks Norepi storage & release from neurons
Indirect |
|
|
Term
| What antagonist is good for reducing hypertension (blocks NE) and helping with benign prostatic hyperplasia and urinary obstruction as a side effect? |
|
Definition
|
|
Term
What 3 antagonist drugs have been shown to reverse prostate smooth muscle contraction (alpha1A) and improve urinary flow?
Which one is less potent, but more selective for alpha1 and has a longer duration of action?
Which one has greatest selectivity for alpha1A |
|
Definition
Prazosin
Terazosin is less potent, but more selective for alpha1 and has a longer duration of action
Tamsulosin has greater selectivity for alpha1A than prazosin and terazosin |
|
|
Term
| What drug is a a good antidote for clonidine toxicity? |
|
Definition
| Yohimbine blocks clonidine and norepinephrine binding to the alpha2 receptor |
|
|
Term
Liver metabolism (First-pass metabolism) is most important for (lipophilic or non-lipophilic drugs)?
Renal excretion is most important for (lipophilic or non-lipophilic drugs)? |
|
Definition
Liver metabolism (First-pass metabolism) : (most important for lipophilic drugs)
*Have to be careful about drug-drug interactions that are metabolized by CYP450
Renal excretion : (most important for non-lipophilic drugs) bad if reduced renal function |
|
|
Term
Plasma half-life of most beta blockers is? (hours)
What are the once a day beta blockers?
*What is the one beta blocker that has rapid onset and short duration (half-life=9 minutes)? |
|
Definition
3-6 hrs
Bentaxolol (eye drop for glaucoma) and Nadolol
Esmolol |
|
|
Term
| Why is the list of beta blockers so long with so many different ones?? |
|
Definition
| Because of the way they are metabolized |
|
|
Term
| List the clinical uses of Beta-blockers |
|
Definition
Antihypertensive
Antiarrhythmic (slows heart rate)
antianginal
hyperthyroidism
open-angle glaucoma
anxiety
migraine |
|
|
Term
| How do beta blockers help with hypertension? |
|
Definition
short term : no change in BP
long term : decrease renin release from kidneys -> decrease angiotensin -> decrease angiotensin 2 ->sodium reabsorption |
|
|
Term
| How do beta blockers help with angina? |
|
Definition
| Decreases heart rate (like arrhythmia and hyperthyroid) to alleviate pain but doesn't help the occlusion of the vessels that causes pain, just the symptoms |
|
|
Term
| How do beta blockers help with hyperthyroid? |
|
Definition
| decreases heart rate, but doesn't cure it |
|
|
Term
| What beta blocker helps with open-angle glaucoma and how does it help? |
|
Definition
Timolol
- decreases aqueous humor production
- decreases ocular pressure |
|
|
Term
What is NOT a major adverse side effect of Beta-blockers
Bradycardia, heart block, congestive heart failure
Bronchospasms
Tiredness
Diarrhea
Heartburn
hyperglycemia
hallucinations |
|
Definition
hyperglycemia
- potentiates hypoglycemia, especially in patients with insulin-dependent diabetes |
|
|
Term
What is only condition that you WOULD give a beta-blocker to?
sinus bradycardia
heart block
cardiogenic shock
overt cardiac failure
diabetes
hypertensive
asthma
emphysema |
|
Definition
hypertensive
Any heart condition-don't give
diabetes, asthma, emphysema-might block B2 (bad) |
|
|
Term
| What drug blocks A1 (decreases vasoconstriction=lowers blood pressure), B1 (slows heart rate), and B2(bronchoconstriction) |
|
Definition
|
|
Term
| What drug blocks A1, B1, and B2 and has antioxidant activity (decreases O2 radicals) |
|
Definition
|
|
Term
Metoprolol, Atenolol, and Esmolol are ___ generation beta blockers. What do they block?
Propranolol, Timolol, and Nadolol are ___ generation beta blockers. What do they block? |
|
Definition
2nd (B1 selective)
1st (B1 and B2)
(as generations go on, the more selective the drugs become) |
|
|
Term
Does adrenergic (agonist or antagonist) and cholinergic (agonist or antagonist) cause mydriasis?
Does adrenergic (agonist or antagonist) and cholinergic (agonist or antagonist) cause miosis? |
|
Definition
adrenergic agonist and cholinergic antagonist
adrenergic antagonist and cholinergic agonist |
|
|
Term
| What drug is a competitive inhibition of A1 receptors in iris dilator muscle, Used clinically to reverse iatrogenically dilated pupils, Reverses phenylephrine-induced dilation in ~ 30-45 min, Reverses tropicamide (cholinergic receptor)-induced dilation in ~ 2-3 hr |
|
Definition
| Dapiprazole HCl (causes red eyes) |
|
|
Term
If you were given acetylcholine, what would be the effects?
If you were to block acetylcholine action, what would the effect be? |
|
Definition
miosis, low heart rate, increase secretions
heart rate goes up, midriasis |
|
|
Term
| What toxin prevents proteins found in vesicle membrane and cell membrane from hooking up so inhibits ACh release from vesicles --> paralyzes muscles |
|
Definition
|
|
Term
| What happens after choline gets taken up? |
|
Definition
binds with acetyl-Coa to form acetylcholine and gets taken up into vesicle.
Cell depolarizes -> vesicles goes into synaptic cleft
It can bind to muscarinic or nicotinic receptors (you can block=paralyze muscles), or broken down by acetylcholinesterases to be taken back up, or bind to acetylcholine auto receptor to turn off release |
|
|
Term
| How can you treat myasthenia gravis? |
|
Definition
| blocke acetylcholinesterase so acetylcholine will be around longer because they have fewer acetylcholine receptors (indirect agonists) |
|
|
Term
What are drugs that look like acetylcholine that bind to the receptor?
What are drugs that look like acetylcholine that bind to the receptor and block acetylcholine binding?
What are drugs that are acetylcholinesterase inhibitors? |
|
Definition
cholinergic agonists
antagonist
indirect agonists |
|
|
Term
| Which muscarinic receptor is found in the CNS neurons, sympathetic postganglionic neurons and forms IP3 and DAG that increases intracellular calcium? |
|
Definition
|
|
Term
| Which muscarinic receptor is found in the myocardium, smooth muscle, CNS and opens potassium channels and inhibits adenylyl cyclase (slows down heart) |
|
Definition
|
|
Term
| Which muscarinic receptor is found on exocrine glands, vessels, CNS and forms IP3 and DAG that increases intracellular calcium? |
|
Definition
|
|
Term
| Which muscarinic receptor is found in the CNS neurons, possibly vagal nerve endings that opens potassium channels and inhibits adenylyl cyclase? |
|
Definition
|
|
Term
| Which muscarinic receptor is found in vascular endothelium, especiall cerebral vessels and CNS neurons and forms IP3 and DAG that increases intracellular calcium? |
|
Definition
|
|
Term
| Where are nicotinic receptors found and what is the result of ligand binding? |
|
Definition
Found in postganglionic neurons and skeletal muscles
2 molecules of ACH bind to open Na+/K+ channels and cause depolarization (sends signal to target cell=excitatory) |
|
|
Term
| which muscarinic receptors are excitatory, increase phospholipase C? |
|
Definition
|
|
Term
| Which muscarinic receptors are inhibitory, inhibits adenylyl cyclase activity? |
|
Definition
|
|
Term
2 ways drugs activate Cholinergic responses:
(Direct or indirect) resemble acetylcholine in structure but it is a false substrate for acetylcholinesterase (inhibits) and causes ACh levels to increase above normal?
(Direct or indirect) resembles ACh in structure, binds to ACh receptors to activate ACh signalling pathways |
|
Definition
Indirect cholinomimetic drugs (binds BOTH muscarinic and nicotinic receptors)
Direct cholinomimetic drugs |
|
|
Term
What are the acetyl choline derivatives (cholinergic agonists)?
What is good about the derivatives? |
|
Definition
Methacholine (Muscarinic)
Bethanecol (Muscarinic)
Carbachol (Muscarinic and Nicotinic)
They have longer half-lifes than acetyl choline |
|
|
Term
What are the muscarinic plant alkaloids
What are the nicotinic plant alkaloids |
|
Definition
Muscarinic: Muscarine, Pilocarpine
Nicotinic: Nicotine, Lobeline |
|
|
Term
| What happens when the vagus nerves releases ACh onto organs like GI tract and heart? |
|
Definition
it binds to M2 receptors (linked to Gi protein) so it decreases cAMP and decreases protein kinase A (opposite effect of NE binding to B1)
opens up K+ channel, K+ leaks out and causes hyperpolarization so more difficult to fire |
|
|
Term
| What does ACh do at a nicotinic receptor? |
|
Definition
opens up Na channel and allow Na to enter --> depolarization gets an action potential
(muscarinic receptor decreases firing (K+ flow outs), Nicotinic receptor increases firing) |
|
|
Term
| What enzyme normally reduces ACh in synaptic cleft, responsible for termination of ACh action, allows nerve terminal to recover after depolarization, is necessary for normal nerve function, and is localized on post-synaptic membrane |
|
Definition
|
|
Term
| Acetylcholinesterase is transiently acetylated as _____ is hydrolyzed. |
|
Definition
| Enzyme is transiently acetylated as ACh is hydrolyzed |
|
|
Term
| *List the Acetylcholinesterase inhibitors (indirect cholinergic mimetics) |
|
Definition
Neostigmine (charged)
Physostigmine (uncharged)
Edrophonium (used to diagnose Myasthenia Gravis)
Insecticides (irreversible)
Neurotoxins |
|
|
Term
| If given Neostigmine, what effects does it have on your eye, intraocular pressure, heart rate? |
|
Definition
| Miosis, lower IOP, lower heart rate (Neostigmine=acetylcholinesterase inhibitor, elevates acetyl choline) |
|
|
Term
| What kind of chemical would inhibit Acetylcholinesterase? |
|
Definition
| One that looks like acetyl choline (binds to acetylcholinesterase and doesn't let go as quickly) |
|
|
Term
| What effect would an Acetylcholinesterase inhibitor have on different organs? |
|
Definition
| if we gave someone ACh we would get same effects |
|
|
Term
| Would an Acetylcholinesterase inhibitor gain access to the Central Nervous System? |
|
Definition
| Depends if charged (doesn't get in in CNS) or uncharged (gets in CNS) |
|
|
Term
| What is the best type of drug we have to slow down Alzheimer's Disease? |
|
Definition
| Oral Acetyl cholinesterase inhibitors |
|
|
Term
| *A farmer accidentally gets an organophospahte insectide on his clothing. It penetrates his skin. He collapses and is brought to the emergency room. What happened and how do you treat it? |
|
Definition
Insecticide poisoning (irreversible inhibition)- excessive sweating, lungs fill up with fluid, heart stops beating, diaphragm stops contracting
Treat with pralidoxime (PAM) within 24 hrs - prevents irreversible inhibition of acetylcholinesterase (aging)
Atropine to relieve symptoms of excess ACh (acetylcholine antagonist) |
|
|
Term
| What is the drug that inhibits choline reuptake (looks like 2 acetylcholine molecules put together) to deplete acetylcholine? |
|
Definition
|
|
Term
| What is the drug that inhibit ACh uptake into vesicles to deplete acetylcholine released? |
|
Definition
|
|
Term
| What anticholinergic drug blocks ACh binding to Muscarinic drugs (ex:bella donna plant)? |
|
Definition
|
|
Term
Atropine analogs with (shorter or longer) half-lives have been developed.
(short or long) duration of effect makes it less attractive for routine use. |
|
Definition
|
|
Term
| What are the atropine analogs? Are they cholinergic activators or inhibitors? |
|
Definition
Tropicamide: Mydriasis & Cycloplegia
Ipratropium: Bronchodilator
Benztropine: Parkinson’s disease therapy
Scopolamine: Motion sickness relief
Cholinergic inhibitors |
|
|
Term
Which atropine analog causes mydriasis and cycloplegia (paralysis of the lens)
Tropicamide:
Ipratropium:
Benztropine:
Scopolamine |
|
Definition
|
|
Term
Which atropine analog is bronchodilator?
Tropicamide:
Ipratropium:
Benztropine:
Scopolamine |
|
Definition
|
|
Term
Which atropine analong is given orally for Parkinson's disease therapy?
Tropicamide:
Ipratropium:
Benztropine:
Scopolamine |
|
Definition
|
|
Term
Which atropine analog is used for motion sickness relief (goes to stomach, not the CNS)?
Tropicamide:
Ipratropium:
Benztropine:
Scopolamine |
|
Definition
|
|
