Exam 2 Flashcards
1
Q
Where are muscarinic receptors located?
A
Heart muscle, sphincters of bladder and gi tract, bronchioles of lungs, sweat glands, iris constrictor
2
Q
Name the prototype drug that represents the muscarinic agonists. This drug works by reversibly binding directly to and activating muscarinic receptors. It has no effect on nicotinic receptors.
A
Bethanechol (Urechol)
3
Q
What 4 areas does bethanechol effect that can cause adverse reactions?
A
heart, exocrine glands, smooth muscle, and eye
4
Q
There are three therapeutic uses for bethanechol, one approved one and two invesitgational or off label ones, what are they?
A
treating urinary retention postoperatively is the approved one, it is also used investigationally for treating GERD and GI paralysis.
5
Q
Name some of the adverse effects of bethanechol.
A
cardiovascular effects such as hypotension and bradycardia, alimentary effects such as increased salivation, secretions, diarrhea and involuntary defecation, bronchoconstriction, dysrhythmia in hyperthyroid patients.
6
Q
Name three sources of toxicology due to muscarinic agonists.
A
ingestion of inocybe an clitocybe mushrooms, overdose on direct acting musarinic agonists such as bethanechol and pilocarpine, and overdose on cholinesterase inhibitors
7
Q
What is the treatment for overdose on muscarinic agonists?
A
atropine - a muscarinic blocking agent
8
Q
Name the prototype muscarinic antagonist which competitively blocks Acetylcholine action. It can be extracted from plants.
A
Atropine
9
Q
Name the seven things that atropine does.
A
increases heart rate, decreases secretions, relaxes bronchi, decreases bladder tone, decreases GI motility and tone, dilates the pupil and relaxes the ciliary muscle, CNS excitation.
10
Q
From low to high doses, what areas and in what order does atropine effect?
A
secretions, heart, eye, urinary tract, intestine, lung, stomach
11
Q
Name some therapeutic uses for atropine.
A
preanesthesia to block the baroreceptor reflex and keep heart rate from dropping, eye disorders and exams to cause mydriasis (pupil enlargement) and paralysis of ciliary muscle, bradycardia, intestinal hypertonicity and hypermotility, muscarinic agonist poisoning, peptic ulcer disease, asthma, gall stones (relaxes biliary tract smooth muscle)
12
Q
Name some adverse effects of atropine.
A
xerostomia (dry mouth), blurred vision, elevated intraocular pressure, urinary retention, constipation, anhidrosis (low or absent sweat), tachycardia, thickening and drying of bronchial secretions.
13
Q
What are some sources of antimuscarinic poisoning?
A
natural products like atropa belladonna and datura stramonium, overdose of atropine or scopolamine, other drugs with pronounced antimuscarinic properties like antihistamines, phenothiazines, antipsychotics, and tricyclic antidepressants.
14
Q
What are some drugs that atropine interacts with?
A
any drug that causes muscarinic block - antihistamines, phenothiazine, antipsychotics, tricyclic antidepressants.
15
Q
What is the treatment for toxicology to muscarinic antagonists?
A
physostigmine which is a cholinesterase inhibitor, syrup of ipecac and activated charcoal can also be used.
16
Q
Urinary frequency, urgency, nocturia, and urge incontinence are all symptoms of what pathology?
A
overactive bladder (OAB)
17
Q
What class of drugs is used to treat overactive bladder and what is the mechanism of action?
A
Anticholinergic drugs are used, they work by blocking muscarinic receptors on the bladder detrusor muscle and inhibit bladder contractions and voiding. They block specific M3 receptors (bladder, GI, eye, and salivary glands)
18
Q
Name some of the anticholinergic drugs used to treat OAB.
A
oxybutynin (ditropan, oxytrol), darifenacin/enablex (highly M3 selective), solifenacin/vesicare (primarily M3 selective), tolterodone/detrol (nonselective), trospium (sanctura)
19
Q
Cholinesterase inhibitors are used to treat what condition?
A
myasthenia gravis
20
Q
What are the two basic categories of cholinesterase inhibitors?
A
reversible and irreversible
21
Q
Name the prototype reversible cholinesterase inhibitor and discuss its mechanism of action.
A
Neostigmine. It intensifies neurotransmitters action and causes muscarinic responses similar to muscarinic agonists. At the neuromuscular junction it causes increased force of contraction and at toxic levels can cause constant depolarization. Can cause some mild CNS stimulation and CNS depression can result with toxic levels.
22
Q
Name two therapeutic uses for neostigmine.
A
myasthenia gravis and reversal of nondepolarizing neuromuscular blockade. (postoperative or OD on muscle relaxant)
23
Q
What are some adverse reactions of neostigmine?
A
excessive muscarinic stimulation, neuromuscular blockade - too much Ach at the receptor leads to constant stimulation and paralysis.
24
Q
Name the only irreversible cholinesterase inhibitor that is used medicinally and what condition is it used to treat?
A
echothiophate and it is used for glaucoma. It’s pharmacologic effects are exactly like the reversible cholinesterase inhibitors but produces a state of cholinergic crisis.
25
Name the only irreversible cholinesterase inhibitor that is used medicinally and what condition is it used to treat?
echothiophate and it is used for glaucoma
26
What is cholinergic crisis?
It is caused by overdose on a cholinesterase inhibitor and results in muscle weakness and paralysis due to constant Ach stimulation. There is excessive muscarinic stimulation and medical treatment such as atropine and respiratory support is needed.
27
How can you differentiate between myasthenia crisis and cholinergic crisis?
A challenge dose of an ultrashort acting cholinesterase inhibitor (edrophonium) can be given, if symptoms improve then it is a myasthenia crisis, it they worse it is a cholinergic crisis.
28
How can you differentiate between myasthenia crisis and cholinergic crisis?
A challenge dose of an ultrashort acting cholinesterase inhibitor (edrophonium) can be given, if symptoms improve then it is a myasthenia crisis, it they worse it is a cholinergic crisis.
29
What are the 4 cholinesterase inhibitors used to treat alzheimer's disease?
doneprazil, galantamine, rivastigamine, tacrine
30
What are the 4 cholinesterase inhibitors used to treat alzheimer's disease?
doneprazil, galantamine, rivastigamine, tacrine
31
What is the different between polarizing and depolarizing nicotinic blocking agents?
Depolarizing agents don't let the depolarization and repolarization process happen. The muscle contracts and then relaxes. Nonpolarizing agents compete with ACh and bind to NicotinicM receptors and block ACh action.
32
What is the prototype drug that is given for nondepolarizing neuromuscular blockers and what is its mechanism of action?
Tubocurarine is the drug and it works by competing with ACh at the neuromuscular junction and not activating the receptor. It works like an antagonist.
33
What are the therapeutic uses of tubocurarine and similiar acting drugs?
muscle relaxation for surgery mechanical ventilation and other diagnostic procedures, as well as the diagnosis of myasthenia gravis.
34
What are the therapeutic uses of tubocurarine and similiar acting drugs?
muscle relaxation for surgery mechanical ventilation and other diagnostic procedures, as well as the diagnosis of myasthenia gravis.
35
What are some adverse effects of tubocurarine?
respiratory arrest due to respiratory muscle relaxation and cardiovascular effects such as hypotension, bradycardia, dysrhythmias, and cardiac failure due to sympathetic blockade, histamine release and other unknown mechanisms.
36
What is the prototype drug for depolarizing neuromuscular blcokers and what is its mechanism of action?
succinyl choline and it is structurally similar to acetylcholine and causes depolarization of them muscles followed by a depolarizing blockade. Thus there is muscle contraction followed by relaxation.
37
What is the prototype drug for depolarizing neuromuscular blcokers and what is its mechanism of action?
succinyl choline and it is structurally similar to acetylcholine and causes depolarization of them muscles followed by a depolarizing blockade. Thus there is muscle contraction followed by relaxation.
38
What are the pharmacologic effects of succinyl choline?
muscle relaxation, contraction before paralysis which is ultrashort, muscle cramps following administration due to initial contraction, no effect on the CNS.
39
What are some adverse effects of succinyl choline?
the most unique one is malignant hyperthermia characterized by muscle rigidity and high temperatures and is genetically determine. Others include prolonged apnea in people with low pseudocholinesterase activity, postoperative muscle pain due to contraction, hyperkalemia can occur because the drug promotes release of potassium from tissues and so is contraindicate din burn victims.
40
What are the problems with and treatment options for succinyl choline toxicity?
Toxicity causes prolonged apnea with no antidote, treatment is purely support based.
41
What are the problems with and treatment options for succinyl choline toxicity?
Toxicity causes prolonged apnea with no antidote, treatment is purely support based.
42
How long do long-acting nondepolarizing agents work and what are three such agents?
They last 25-100 minutes and three of these drugs would be doxacurium, metocurine, pipecuronium.
43
How long do short-acting nondepolarizing agents work and what is one such agent?
They last 10-15 minutes and the medication is mivacurium.
44
Name two ganglionic blockers and discuss their mechanism of action.
The two drugs are trimetaphan and mecamylamine (inversine). They work by competing with ACh at nictotinicN receptors in the autonomic ganglia. This occurs nondiscriminately and can affect both sympathetic and parasympathetic ganglia.
45
Name two ganglionic blockers and discuss their mechanism of action.
The two drugs are trimetaphan and mecamylamine (inversine). They work by competing with ACh at nictotinicN receptors in the autonomic ganglia. This occurs nondiscriminately and can affect both sympathetic and parasympathetic ganglia.
46
What are the adverse effects of ganglionic blockers?
antimuscarinic effects such as parasympathetic blockade, hypotension due to sympathetic blockade, CNS effects since it crosses the BBB -tremor and convulsions.
47
What are the adverse effects of ganglionic blockers?
antimuscarinic effects such as parasympathetic blockade, hypotension due to sympathetic blockade, CNS effects since it crosses the BBB -tremor and convulsions.
48
Where are alpha1 receptors found and what do they do?
in blood vessels - they cause vasoconstriction and increased blood pressure.
49
Where are alpha2 receptors found and what do they do?
they are located presynaptically and their activation inhibits NE release.
50
Where are beta2 receptors found and what do they do?
smooth muscle of lungs and uterus, skeletal muscle, liver, bronchodilation due to smooth muscle relaxation in lungs, delay of preterm labor. Hyperglycemia and tremor are also possible.
51
Where are beta2 receptors found and what do they do?
smooth muscle of lungs and uterus, skeletal muscle, liver, bronchodilation due to smooth muscle relaxation in lungs, delay of preterm labor. Hyperglycemia and tremor are also possible.
52
The neurotransmitter epinephrine acts at which receptor sites?
alpha 1, alpha 2, beta 1, beta 2
53
The neurotransmitter dopamine acts at which receptor sites?
alpha 1, beta 1, and dopamine
54
The neurotransmitter dopamine acts at which receptor sites?
alpha 1, beta 1, and dopamine
55
Name the two drugs that are noncatecholamines.
phenylephrine and albuterol
56
Name the two drugs that are noncatecholamines.
phenylephrine and albuterol
57
What are the clinical consequences of alpha 1 activation?
think vasoconstriction and eyes. hemostasis due to vasoconstriction, nasal decongestion, adjunct to local anesthesia because it prolongs anesthetic absorption and causes mydriasis (dilation of the pupil).
58
What are the clinical consequences of alpha 2 activation?
they are located presynaptically and activation inhibits NE release, little to no significance in the periphery. In the CNS it causes decreased sympathetic outflow and vasodilation - used for HTN.
59
What are the clinical consequences of alpha 2 activation?
they are located presynaptically and activation inhibits NE release, little to no significance in the periphery. In the CNS it causes decreased sympathetic outflow and vasodilation - used for HTN.
60
What are the clinical consequences of beta 1 activation?
limited to the heart. for cardiac arrest epinephrine injected directly will help. With heart failure there is a positive inotropic effect that improves cardiac performance. For shock it can be used to increase cardiac performance and tissue perfusion. It can also be used for AV block to temporarily overcome it.
61
What are the adverse effects of beta 1 activation?
Overstimulation can produce tachycardia and dysrhythmias. Angina pectoris can also be caused - substernal pain in the region of the heart. Blocked coronary arteries will get worse.
62
What are the clinical consequences of beta 2 activation?
bronchodilation and it is utilized to treat asthma patients and relaxes uterine smooth muscle thus delaying preterm labor.
63
What are the clinical consequences of dopamine receptor activation?
activation of peripheral dopamine receptor cause dilation of the vasculature of the kidneys which is exploited to increase kidney perfusion during shock, and it also enhances cardiac performance due to beta 1 activation.
64
What are the clinical consequences of dopamine receptor activation?
activation of peripheral dopamine receptor cause dilation of the vasculature of the kidneys which is exploited to increase kidney perfusion during shock, and it also enhances cardiac performance due to beta 1 activation.
65
Epinephrine is administered as either adrenalin or an epipen, what are its therapeutic uses?
It activates A1 A2 B1 and B2 receptors. With the alpha 1 activation it can be used to delay anesthetic absorption, control bleeding, elevate BP, relieve nasal congestion, and dilate the pupils (mydriasis). With Beta 1 activation it can be used to overcome AV block and restore cardiac function, and with Beta 2 activation it can be used for bronchodilation.
66
What are some adverse effects of epinephrine administration?
hypertensive crisis, disrrhythmias, angina pectoris, necrosis (extravasation), hyperglycemia in diabetics
67
Why can't norepinephrine/Levophed be used to treat anaphylaxis?
Because it doesn't activate beta 2 receptors.
68
What are the characteristics of anaphylaxis that can be overcome by epinephrine and how does this happen?
During anaphylaxis hypotension happens due to vasodilation, bronchoconstriction and edema of the glottis happen in a severe response to an allergen. Epinephrine treats all of these by activating alpha 1, and beta 1 and 2 receptors.
69
What are the characteristics of anaphylaxis that can be overcome by epinephrine and how does this happen?
During anaphylaxis hypotension happens due to vasodilation, bronchoconstriction and edema of the glottis happen in a severe response to an allergen. Epinephrine treats all of these by activating alpha 1, and beta 1 and 2 receptors.
70
What are the therapeutic uses of the adrenergic agonist dopamine?
it is used in shock and heart failure because the activation of beta 1 receptors increases cardiac output and thus perfusion. It used to be used in acute renal failure to increase renal bloodflow but that has been found ineffective.
71
What are some drug-drug interaction problems with dopamine?
MAO inhibitors intensify its effects as can tricyclic antidepressants, general anesthetics can sensitize the myocardium to DA and cause dysrythmias) and diuretics can compliment the affects of DA on the kidneys.
72
What are the therapeutic uses, adverse effects and drug drug interactions of the adrenergic agonist dobutamine (dobutrex)?
It is used to treat heart failure and works on beta 1 receptors primarily in the heart. The major adverse effect is tachycardia. MAO inhibitors (intensified effect), TCAs (increased CV effects), and Anesthesia (sensitized myocardium - dysrhytmia) should be avoided.
73
What are the therapeutic uses of the adrenergic agonist Phenylephrine (neo-synephrine)?
It acts on alpha 1 receptors. It can be used locally as a nasal decongestant, it can increase Bp when used parenterally, when used as eye drops it an dilate the pupil, and it can be coadministered with local anesthesia to prolong absorption.
74
Why is ephedrine considered a mixed acting drug? What are its therapeutic uses and adverse effects?
It is considered a mixed acting drug because it acts directly on alpha and beta receptors and releases norepinephrine indirectly. Therapeutically it is used for nasal congestion (alpha 1 - vasoconstriction/topical), asthma (beta-2 - bronchodilation) and shock (alpha and beta improve hemodynamics). The adverse effects are similiar to epinephrine plus insomnia due to it crossing the BBB and having CNS effects.
75
What are the therapeutic effects of alpha 1 blockade as would be caused by alpha 1 adrenergic antagonists?
think vasodilation. essential HTN due to vasodilation. Reversal of toxicity from alpha 1 agonists (also extravasation - phentolamine), benign prostatic hyperplasia (reduces trigone and sphincter contraction in bladder neck), pheochromocytoma (CA secreting tumor of the adrenal glands), Raynaud's disease (peripheral vascular disorder that causes vasospasm in toes/fingers and local sensation of cold/pain - relieves symptoms)
76
What are the therapeutic effects of alpha 1 blockade as would be caused by alpha 1 adrenergic antagonists?
think vasodilation. essential HTN due to vasodilation. Reversal of toxicity from alpha 1 agonists (also extravasation - phentolamine), benign prostatic hyperplasia (reduces trigone and sphincter contraction in bladder neck), pheochromocytoma (CA secreting tumor of the adrenal glands), Raynaud's disease (peripheral vascular disorder that causes vasospasm in toes/fingers and local sensation of cold/pain - relieves symptoms)
77
What are some therapeutic effects of beta blockade?
angina pectoris (decreases cardiac work and is a mainstay therapy), HTN (reduces peripheral resistance and is used as a long term therapy), cardiac dysrhythmias (decrease SA node discharge and AV node conduction), myocardial infarction (reduce pain, infarct size - give immediately), heart failure (new tx. carvedilol, bisoprolol, metaprolol), hyperthyroidism (associated with sensitivity of heart to catecholamines), migraines (prophylactic - reduce frequency unknown mechanism), stage freight (tachycardia and sweating), pheochromocytoma (prevents cardiac stimulation), glaucoma (reduce intraocular pressure (betoxolol and timolol).
78
What are some therapeutic effects of beta blockade?
angina pectoris (decreases cardiac work and is a mainstay therapy), HTN (reduces peripheral resistance and is used as a long term therapy), cardiac dysrhythmias (decrease SA node discharge and AV node conduction), myocardial infarction (reduce pain, infarct size - give immediately), heart failure (new tx. carvedilol, bisoprolol, metaprolol), hyperthyroidism (associated with sensitivity of heart to catecholamines), migraines (prophylactic - reduce frequency unknown mechanism), stage freight (tachycardia and sweating), pheochromocytoma (prevents cardiac stimulation), glaucoma (reduce intraocular pressure (betoxolol and timolol).
79
What are some adverse effects of Beta 2 blockade?
bronchoconstriction in the lung (don't use with asthma patients, use a beta 1 selective drug like metaprolol), inhibition of glycogenolysis (beta 2 block in the liver - in diabetic patients you have to adjust insulin, but preferably should choose a beta 1 specific drug instead).
80
Name the prototype nonselective alpha adrenergic antagonist (alpha blocker) and list its actions and uses as well as adverse effects and contraindications.
The drug is Phentolamine (Regitine) and it acts on both alpha 1 and 2 receptors (nonselective) and is used specifically to treat pheochromocytoma and to prevent tissue necrosis when drugs that produce alpha 1 mediated vasoconstriction are extravasated. The adverse effects are the same as all alpha adrenergic antagonists with greater reflex tachycardia due to alpha 2 block as well. It is contraindicated in patients with angina and MI.
81
Name the prototype selective alpha adrenergic antagonist (alpha blocker) and discuss its actions and uses as well as adverse effects.
The drug is Prazosin (Minipress) and it is alpha 1 selective. It is a competitive alpha 1 blocker that causes dilation of arterioles and veins and also relaxes smooth muscle in the neck of the bladder and prostatic capsule, it is approved for HTN only but has investigational uses related to BPH. Adverse effects include orthostatic hypotension, reflex tachycardia, inhibition of ejaculation, and nasal congestion. Also 1% lose consciousness after first dose so it should be given in small doses at HS initially.
82
Name the prototype selective alpha adrenergic antagonist (alpha blocker) and discuss its actions and uses as well as adverse effects.
The drug is Prazosin (Minipress) and it is alpha 1 selective. It is a competitive alpha 1 blocker that causes dilation of arterioles and veins and also relaxes smooth muscle in the neck of the bladder and prostatic capsule, it is approved for HTN only but has investigational uses related to BPH. Adverse effects include orthostatic hypotension, reflex tachycardia, inhibition of ejaculation, and nasal congestion. Also 1% lose consciousness after first dose so it should be given in small doses at HS initially.
83
What is the prototype drug for nonselective beta blockers and what are its therapeutic uses?
Propanolol (inderal) is the drug and it is a beta 1 and 2 blocker (nonselective). It is used to treat hypertension, angina pectoris, dysrythmias, and myocardial infarction. It can also be used to treat migraines and stage freight.
84
What are the adverse effects of propanolol (inderal)?
bradycardia, AV heart block, heart failure (warn patients of early signs like edema), rebound cardiac excitation (d/t abrupt withdrawal), bronchconstriction (d/t beta 2 blockade), inhibition of glycogenolysis (adjust insulin for diabetics), BBB can be crossed so there can be CNS effects like depression, insomnia, nightmares, and hallucinations.
85
What are the contraindications, warnings, and precautions for propanolol?
It shouldn't be used in patients with severe allergic reactions because it will render an epipen useless. Diabetics probably shouldn't be on it because it inhibits glycogenolysis and suppresses tachycardia which efficiently masks hypoglycemia. Patients with cardiac, respiratory, and psychiatric disorders also shouldn't take it due to adverse effects.
86
What are the contraindications, warnings, and precautions for propanolol?
It shouldn't be used in patients with severe allergic reactions because it will render an epipen useless. Diabetics probably shouldn't be on it because it inhibits glycogenolysis and suppresses tachycardia which efficiently masks hypoglycemia. Patients with cardiac, respiratory, and psychiatric disorders also shouldn't take it due to adverse effects.
87
What are some drug drug interactions that are problematic for propanolol?
calcium channel blockers (verapamil) should be avoided d/t excessive cardiac suppression. Insulin also needs to be adjusted d/t suppressed tachycardia and blocked glycogenolysis.
88
What is the prototype drug for selective beta adrenergic antagonists and what is its pharmacologic effect?
Metaprolol (Lopressor) is the drug and it is beta 1 selective at therapeutic doses. (at high doses it can block beta 2). The pharmacologic effect is that it reduces heart rate, force of contraction, and conduction velocity through the AV node. It also reduces secretion of renin by the kidney.
89
What are the adverse effects and precautions and warnings associated with metaprolol?
Adverse effects include bradycardia, reduced cardiac output, AV heart block, and rebound cardiac excitation following abrupt withdrawal. It is contraindicated for patients with sinus bradycardia, AV block greater than first degree, and patients with heart failure.
90
What are the two types of indirect acting antiadrenergic agents and how do they work?
The first group is adrenergic neuron blocking agents which decrese norepinephrine release. Reserpine, Guanethidine and Guanadrel are in this group. The second group is centrally acting alpha 2 agonists (work in the CNS) which reduce impulses along the sympathetic nerves.
91
What are the two types of indirect acting antiadrenergic agents and how do they work?
The first group is adrenergic neuron blocking agents which decrese norepinephrine release. Reserpine, Guanethidine and Guanadrel are in this group. The second group is centrally acting alpha 2 agonists (work in the CNS) which reduce impulses along the sympathetic nerves.
92
What is the prototype drug for adrenergic neuron blocking agents? What are its pharmacological effects?
Reserpine is the drug. Its effects are depletion of norepinephrine at the synapses, which decreases the beta and alpha receptor activation, causing the heart rate to slow and reducing cardiac output respectively. There are also CNS effects such as sedation, depression, and state of indifference to the environment causes by depletion of serotonin and catecholamines.
93
What are some therapeutic uses for reserpine?
It is used to treat HTN but its effects take a week, and it can rarely be used for tx. of psychotic states.
94
What are some adverse effects of reserpine?
severe depression and possible suicide d/t NE depletion in the CNS, cardiovascular effects like bradycardia and hypotension, GI effects like increased gastric secretions (possible ulcers may result), increased gastric tone and motility causing cramps and diarrhea.
95
What are some adverse effects of reserpine?
severe depression and possible suicide d/t NE depletion in the CNS, cardiovascular effects like bradycardia and hypotension, GI effects like increased gastric secretions (possible ulcers may result), increased gastric tone and motility causing cramps and diarrhea.
96
What is the prototype drug for centrally acting alpha 2 agonists? What are its pharmacological effects?
Clonidine (Catapres) is the drug. It causes selective stimulation of alpha 2 receptors in the CNS. It reduces sympathetic outflow to blood vessels and the heart. It is primarily indicated for the treatment of HTN.
97
What are some adverse effects of Clonidine?
drowsiness d/t CNS depression, rebound HTN upon rapid withdrawal, xerostomia (dry mouth), It is embryotoxic potentially and so is contraindicated for pregnant women. It can also cause constipation, impotence and other CNS effects.
98
What are some adverse effects of Clonidine?
drowsiness d/t CNS depression, rebound HTN upon rapid withdrawal, xerostomia (dry mouth), It is embryotoxic potentially and so is contraindicated for pregnant women. It can also cause constipation, impotence and other CNs effects.
99
What is the therapeutic use of methyldopa and methyldopate
It is used primarily to treat HTN. Adverse effects include a 10-20% chance of a positive Coomb's test, which tests for hemolytic anemia. If this occurs the patient should be taken off the drug to prevent the development of hemolytic anemia which happens in 5% of patients who have a positive Coomb's test. Other adverse effects include xerostomia, sexual dysfunction, orthostatic hypotension, and CNS effects.
100
What is the therapeutic use of methyldopa and methyldopate
It is used primarily to treat HTN. Adverse effects include a 10-20% chance of a positive Coomb's test, which tests for hemolytic anemia. If this occurs the patient should be taken off the drug to prevent the development of hemolytic anemia which happens in 5% of patients who have a positive Coomb's test. Other adverse effects include xerostomia, sexual dysfunction, orthostatic hypotension, and CNS effects.
101
How is asthma induced?
An allergen triggers mast cells to react, which then cause bronchospasm and then activate other inflammatory cells and chemical mediators of inflammation. All of this combined leads to inflammation and bronchospasm which causes airflow limitations.
102
How is asthma induced?
An allergen triggers mast cells to react, which then cause bronchospasm and then activate other inflammatory cells and chemical mediators of inflammation. All of this combined leads to inflammation and bronchospasm which causes airflow limitations.
103
What are the two main classifications of drugs for asthma and what are they used for?
Anti-inflammatory agents are one class and they are used for prophylaxis, bronchodilators are the other class and they are used for immediate relief.
104
Name some bronchodilator drugs for asthma.
Beta 2 agonists (albuterol), methylxanthines (theophylline), antocholinergics (ipratopium - muscarinic receptors in the lungs cause bronchoconstriction)
105
Name some bronchodilator drugs for asthma.
Beta 2 agonists (albuterol), methylxanthines (theophylline), antocholinergics (ipratopium - muscarinic receptors in the lungs cause bronchoconstriction)
106
What are the three types of inhalers and what are some of their characteristics?
metered dose inhalers (MDIs) require coordination to use, dry powder inhalers (DPIs) utilize micronized powders and are breath activated with no propellents, nebulizers utilize mist delivery and take a long tiem to deliver but are good for children.
107
What is the mechanism of action of inhaled glucocorticoids?
They work to suppress the immune system. They suppress inflammation by causing decreased synthesis and release of anti-inflammatory mediators, decreased infiltration and activity of inflammatory cells, and decreased edema of airway mucosa. They also increase the number of beta 2 receptors and their response to beta agonists.
108
What is the mechanism of action of inhaled glucocorticoids?
They work to suppress the immune system. They suppress inflammation by causing decreased synthesis and release of anti-inflammatory mediators, decreased infiltration and activity of inflammatory cells, and decreased edema of airway mucosa. They also increase the number of beta 2 receptors and their response to beta agonists.
109
Name two inhaled glucocorticoids and what are they used for?
Beclomethasone (QVAR) and Budenoside (pulmicort). They are used for prophylaxis of chronic asthma and are administered on a fixed schedule. They are a first like of defense for moderate to severe asthma and are safe and highly effective.
110
What is the oral glucocorticoid that is used for asthma treatment?
prednisone and it is only used for severe asthma due to toxicity. It is used when other treatments aren't working.
111
What are some adverse effects of inhaled glucocorticoids?
dysphonia (hoarseness/difficulty speaking), oropharyngeal candidiasis (fungal infection of throat). Both of these can be helped somewhat by gargling after administration and use of a spacer. Long term effects (generally low) include adrenal suppression (stop making glucocorticoids), bone loss (premenopausal women) and slow growth (less bone formation in children and young adults).
112
What are some adverse effects of oral glucocorticoids?
adrenal suppression, bone loss, slow growth, hyperglycemia, and peptic ulcer disease
113
What is the drug cromolyn (intal) used for and what is it's mechanism of action?
It is used for the prophylaxis of moderate asthma, it can also be used for exercise induced asthma or allergic rhinitis. It is a safe treatment on a fixed schedule. It works by suppressing inflammation and stabilizing mast cell membranes which decreases histamine release. It also inhibits other inflammatory cells.
114
What is the drug cromolyn (intal) used for and what is it's mechanism of action?
It is used for the prophylaxis of moderate asthma, it can also be used for exercise induced asthma or allergic rhinitis. It is a safe treatment on a fixed schedule. It works by suppressing inflammation and stabilizing mast cell membranes which decreases histamine release. It also inhibits other inflammatory cells.
115
What are some adverse effects of cromolyn (intal)?
It is the safest of all asthma medications for children. Rare side effects include chest tightening, wheezing, difficulty swallowing/breathing (FDA warning for this), low BP and hives. Also cough and bronchospasm on inhalation.
116
What are some adverse effects of cromolyn (intal)?
It is the safest of all asthma medications for children. Rare side effects include chest tightening, wheezing, difficulty swallowing/breathing (FDA warning for this), low BP and hives. Also cough and bronchospasm on inhalation.
117
What is the mechanism of action in general for leukotriene modifiers?
They suppress leukotrienes which cause bronchoconstriction, eosinophil infiltration, mucus production, and airway edema.
118
Zafirlukast (Accolate) was the first leukotriene receptor antagonist on the market (1996), what is its mechanism of action, major side effect, and appropriate age for usage?
It is a leukotriene antagonist, so it blocks leukotriene receptors and is used for the prophylaxis and treatment of asthma in children ages 5 and up. The major side effect is liver toxicity, mainly in females.
119
Montelukast (Singulair) is another asthma medication. What is it's mechanism of action, what makes it unique and what does it treat? What is it's mechanism of action?
This drug is well tolerated in most individuals and van be used by patients 1 year and up. It comes in 4 different formulations and which is used is based on age. It can be used for the prophylaxis and maintenance in asthma patients, as well as exercise induced bronchospasms and allergic rhinitis. It works by blocking leukotriene receptors.
