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Pharmacology Exam 2 > Pharm Exam 2 > Flashcards

Pharm Exam 2 Flashcards

1
Q

What are 6 muscarinic agonists?

A

acetylcholine, methacholine, carbachol, Bethanechol, muscarine, pilocarpine

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2
Q

What happens to Ach with the use of anticholinesterases?

A

Ach concentrations increase; these prevent the breakdown of Ach into choline and acetate

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3
Q

What are some reversible anticholinesterases?

A

edrophonium, neostigmine, pyridostigmine, rivastigmine, donepezil, galantamine

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4
Q

What are some irreversible anticholinesterases?

A

insecticides- malathion, diazinon, chlorpyrifos

nerve gases- sarin, tabun, soman

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5
Q

What are some therapeutic uses for anticholinesterases?

A

atonic bladder and GI tract, glaucoma, reversal of neuromuscular blockade, myasthenia gravis, Alzheimer’s disease

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6
Q

What is the preferred agent for paralytic ileus and atony of the urinary bladder?

A

neostigmine; peristalsis is fast when given subcutaneously

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7
Q

What is the mechanism of action of anticholinesterase when treating glaucoma?

A

there is contraction of ciliary muscle which allows aqueous humor to flow out -> decreasing intraocular pressure

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8
Q

Why is echothiophate not typically used in glaucoma?

A

it has been associated with the development of cataracts

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9
Q

What is myasthenia gravis?

A

autoimmune neuromuscular disorder characterized by significant skeletal muscle weakness; appears to result in decrease in ACh receptors

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10
Q

What is the tensilon test?

A

uses the drug tensilon to diagnose myasthenia gravis; tensilon is an anticholinesterase which helps prevent the break down of ACh which in turn helps stimulate the muscles; a patient has myasthenia gravis if muscles get stronger after being injected with Tensilon

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11
Q

What is the treatment for myasthenia gravis?

A

Physostigmine q2-4h; Neostigmine q3-6h; Ambenonium q3-8h

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12
Q

What is the pathophysiology behind Alzheimer’s Disease?

A

patients demonstrate a loss of neurons particularly cholinergic types

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13
Q

What is typically used to treat Alzheimer’s Disease?

A

donepezil, rivastigmine, galantamine; side effects include nausea, vomiting, diarrhea

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14
Q

What will be apparent in contact with organophosphates?

A

SLUDGE

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15
Q

How can one treat organophosphate poisoning?

A

administer atropine and pralidoxime STAT; remove all contaminated clothing immediately; wash skin with soap and water; rinse eyes with plain water for 10-15 min; maintain airway; do not induce vomitting

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16
Q

Where does acid production occur?

A

parietal cells

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17
Q

what receptors are on parietal cells?

A

gastrin, acetylcholine, histamine

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18
Q

Where does acetylcholine come from?

A

vagal stimulation of postganglionic enteric neurons

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19
Q

Where does gastrin come from?

A

G cells

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20
Q

Where does histamine come from?

A

ECL cells

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21
Q

What is a negative effect of antacids?

A

can impair absorption of iron and some antibiotics; decreases stomach acidity can impair the body’s ability to absorb protein, carbs, fats, vitamins A.E.C, folate, micro-trace elements, and minerals

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22
Q

What H2-receptor antagonist is not available IV?

A

nizatidine

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23
Q

What H2-receptor antagonist is most potent and most selective?

A

famotidine- with a duration of action of 10-12h

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24
Q

What excretes H2-Receptor Antagonists and why is this important?

A

the kidneys- must reduce the doses in people that have impaired renal functions

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25
Q

What side effects occur primarily with IV administration of H2-Recepto Antagonists?

A

mental status changes such as confusion

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26
Q

What are general side effects of H2-Receptor Antagonists?

A

diarrhea, headache, fatigue, constipation

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27
Q

What are the major therapeutic uses of H2-Receptor Antagonists?

A

promote healing of gastric and duodenal ulcers, treat GERD, and prevent occurrence of stress ulcers

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28
Q

What are the most potent suppressors of gastric acid secretion?

A

inhibitors of the gastric H+, K+-ATPase proton pump; proton pump inhibitors

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29
Q

What is the basic mechanism behind a PPI?

A

when activated the prodrug irreversibly binds to H+/K+-ATPase inactivating the pump molecule

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30
Q

After using a PPI what causes acid secretion to resume?

A

acid secretion can only resume after a new pump molecule has been synthesized and inserted into the luminal membrane

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31
Q

What is a downfall of a PPI?

A

they are highly sensitive to degradation by acid- therefore they are supplied in delayed release acid-resistant capsules or enteric-coated tablets

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32
Q

What happens to a PPI when given with food?

A

the bioavailability is decreased by 50%; should be given 1 hour prior to meal

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33
Q

What cytochromes are used by PPIs?

A

CYP3A4 and CYP2C19

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34
Q

Why is CYP2C19 a concern in PPIs?

A

Asians are more likely to have the CYP2C19 genotype that correlates with slow metabolism of PPIs

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35
Q

Are all PPIs equally protective?

A

Yes, when using equal doses

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36
Q

What are some general adverse effects of PPIs?

A

diarrhea, headache, stomach pain; these things occur only in a low percentage of patients

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37
Q

What is a adverse effect concerning the clearance of a PPI?

A

PPIs are metabolized and cleared by hepatic CYPs- therefore may interfere with other drugs cleared by this route

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38
Q

What is Clopidogrel?

A

Plavix- decreases platelet aggregation in people who have had a stroke, MI, recent CABG, or stent replacement; it is a prodrug that requires CYP2C19 to be converted to its active form

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39
Q

What is the drug interaction between a PPI and Clopidogrel?

A

PPIs have been shown to decrease the conversion of Clopidogrel to its active form therefore when taken with the use of PPIs Clopidogrel does not convert to its active anticoagulating form

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40
Q

What PPIs may be taken with Clopidogrel, but only if absolutely necessary?

A

rabeprazole or pantoprazole

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41
Q

What infection is a person at a higher risk of acquiring with the use of a PPI?

A

increased risk of nosocomial pneumonia; also increased risk of C.Diff infection; this is because gastric acid is an important barrier to intestinal infection

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42
Q

When should sucralfate be administered?

A

on an empty stomach an hour before food

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43
Q

How does sucralfate work?

A

binds selectively to ulcers and erosions like a bandage

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44
Q

How does misoprostol work?

A

it is a prostaglandin E1 analog; stimulates mucus and bicarbonate secretion and increases mucosal blood flow; modestly decreases acid secretion (not a major effect)

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45
Q

How many times a day is misoprostol give?

A

3-4 times a day because of a short half life

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46
Q

How is misoprostol excreted?

A

renally but does not require a dose adjustment

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47
Q

What are the adverse effects of misoprostol?

A

diarrhea, cramping in 10-20% of patients, can cause miscarriage, no drug interactions

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48
Q

How does bismuth subsalicylate work?

A

it coats erosions and ulcers but does not adhere like sucralfate; may increase productions of prostaglandins, bicarbonate, and mucous

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49
Q

What are the adverse effects of bismuth subsalicylate?

A

blackening of the stool, darkening of the tongue; high deses over long periods could cause salicylate toxicity; caution in renal impairment

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50
Q

What is another use of bismuth subsalicylate?

A

it decreases stool frequency and liquidity in acute infectious diarrhea; antimicrobial effects of bismuth beneficial in H. pylori infection and travelers diarrhea

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51
Q

What should be given if GERD symptoms are 3 or less times a week?

A

an antacid or H2-blocker prn

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52
Q

What should patients with severe symptoms of GERD (asthma, chronic couch, laryngitis, noncardiac chest pain) use?

A

a PPI bid for 3 months

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53
Q

What should be given with frequent symptoms of GERD?

A

H2-blocker bid; PPIs are superior particularly in more severs cases with erosion

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54
Q

In peptic ulcer disease what are the benefits of an H2-blocker?

A

provide nocturnal coverage which helps in healing; can give qhs for 6-8 weeks and healing typically occurs with 80-90% of patients

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55
Q

When are PPIs the drug of choice?

A

when you want to achieve rapid healing, 90% of duodenal ulcers were healed in 4 weeks and gastric ulcers were healed in 6-8 weeks

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56
Q

How should ulcers caused by NSAIDs be treated?

A

discontinue NSAID use, and give a PPI qd (once a day)

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57
Q

How should H. pylori ulceration be treated?

A

only PPI is effective in treating these ulcers and eradicating the H. pylori

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58
Q

How should stress ulcers be treated in the critically ill?

A

H2-blockers are preferred IV (due to cost and proven efficacy); an exception is that if a patient has an NG tube you should use immediate release oral omeprazole (PPI)

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59
Q

What is an example of a D2 Receptor Antagonist?

A

metoclopramide (Reglan)

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60
Q

How is metoclopramide available?

A

orally and parenterally

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61
Q

What are the uses for metoclopramide?

A

minimally effective in gastroparesis; potent anti-nausea and anti-vomiting due to D2 receptor blockade in chemoreceptor trigger zone as well as some mild 5-HT3 activity; used in GERD as an adjunct only; used post-surgically to delay gastric emptying

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62
Q

How is a D2 Receptor Antagonist excreted?

A

urine; must dose adjust for renally impaired patients

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63
Q

What is the half life for D2 receptor antagonists?

A

4-6 hours with a duration of action 1-2 hours

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64
Q

What are some adverse effects of D2 receptor antagonists?

A

extrapyramidal side effects due to lack of dopamine; increase prolactin levels (galactorrhea, gynecomastia, impotence, menstrual irregularities), tolerance to treatment is common

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65
Q

What is erythromycin?

A

macrolide antibiotic; motilin is a potent contractile agent of the upper GI tract; effects of motilin can be mimicked by erythromycin

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66
Q

What are the adverse effects of erythromycin?

A

nausea, vomiting, abdominal pain, tolerance develops to treatment within a few weeks, possibility of C. diff infection, drug interactions,

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67
Q

What are the symptoms of constipation?

A

less than 3 stools a week, straining, hard, dry stools, feeling as though there is incomplete emptying of bowel

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68
Q

What are bulk forming laxatives composed of?

A

indigestible hydrophilic colloids that absorb water

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69
Q

What is the mechanism of a bulk forming laxative?

A

distension of colon triggering peristalsis

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70
Q

What are the side effects of bilk forming laxatives?

A

bloating and gas; may prevent absorption of other drugs

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71
Q

What are the functions of the thyroid gland?

A

oxygen consumption, heat production, carb fat and protein metabolism, growth and differentiation, stimulation of other hormones

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72
Q

What is the first step in biosynthesis of thyroid hormones?

A

uptake of iodine by NIS (sodium iodide symporter)

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73
Q

What is organification?

A

oxidation of iodide and iodination of thyroglobulin tyrosyl groups to form monoiodotyrosyl (MIT, T1) or diiodotyrosyl (DIT, T2)

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74
Q

What are some of the clinical effects of thyroid hormones on growth an development?

A

there is a significant role in neurogenesis and skeletal formation
cretinism- a congenital hypothyroidism (maternal hypothyroidism) resulting in severely stunted growth and mental retardation

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75
Q

What are the clinical effects of thyroid hormones on cardiovascular functions?

A

increases heart rate, contractility, cardiac output, myocardial O2 consumption, diastolic relaxation, vasodilation

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76
Q

What are the clinical effects of thyroid hormones associated with metabolic functions?

A

stimulates conversion of cholesterol to bile acids, enhances glucose uptake by cells and generation of free glucose

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77
Q

What are some general clinical effects associated with thyroid hormones?

A

mental acuity, reproduction, thermogenesis in warm-blooded species

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78
Q

What are the effects of excess thyroid hormone?

A

A-fib, CHF, Osteoporosis, vision loss in severe cases, thyrotoxic crisis

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79
Q

What are the effects of inadequate thyroid hormone?

A

goiter (constant increased levels of TSH result in hypertrophy), increased LDL, CHF, cardiovascular disease, depression, peripheral neuropathy, myxedema, infertility, birth defects

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80
Q

What are some of the causes of hypothyroidism?

A

hashimoto’s thyroiditis, drug-induced, dyshormonogenesis, radiation, x-ray, thyroidectomy, congenital (cretinism), secondary (TSH deficit)

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81
Q

Goiters are present in what causes of hypothyroidism?

A

in hashimoto’s thyroiditis they present early and absent later, drug-induced, dyshormonogenesis, congenital they can be absent or present

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82
Q

In hypothyroidism what are the patients complaints?

A

fatigue, dry skin, hair loss, depression, mental slowness, poor, memory, constipation, cold intolerance, weight gain, fluid retention, muscle aches, stiffness, menstrual irregularities, infertility

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83
Q

As a provider what do we find in our observations in hypothyroidism?

A

goiters, bradycardia, delayed refluxes, hypertension, edema, periorbital puffiness, abdominal distention, decreased systolic and increased diastolic, pale, dry skin

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84
Q

When do you expect to reach a steady state with levothyroxine?

A

4-6 weeks

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85
Q

What is levothyroxine?

A

a synthetic T4 for the treatment of hypothyroidism

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86
Q

What is the half life of levothyroxine?

A

7 days, dosing is once daily dosing

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87
Q

What are the aging fluctuations concerning Levothyroxine?

A

aging, large fluctuations in body weight, and pregnancy require reevaluation of dose; pregnant patients require increased doses, infants and children require more T4 than adults, adults over 65 may require even less, in patients who have unusually high requirements consider gastritis, H. Pylori, or celiac

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88
Q

What is Liothyronine?

A

synthetic T3, but do not pick this drug; T3 can lead to toxicity and there is no evidence that using T3 in hypothyroidism is beneficial

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89
Q

What is Dessicated thyroid?

A

not considered first line, there are problems in protein antigenicity, stability, variability in hormone levels, no long-term safety data

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90
Q

What is the most common cause of hyperthyroidism?

A

Graves disease

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91
Q

What are some of the causes of hyperthyroidism?

A

graves disease, toxic multinodular goiter, toxic adenoma, thyroiditis or inflammation of the thyroid gland, TSH secreting pituitary adenoma, metastatic tumors

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92
Q

What are patient complaints with hyperthyroidism?

A

weight loss, anxiety, sweating, diarrhea, heart palpitations, muscular weakness, heat intolerance, tremor

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93
Q

As a provider what would be our observations seeing someone with hyperthyroidism?

A

warm moist skin, Proptosis, conjunctival irritation, blepharospasm, tachypnea, goiter, tremor, hyperactive reflexes, tachycardia

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94
Q

What are some treatment options for someone with hyperthyroidism?

A

surgical thyroidectomy, destruction of gland with radioactive iodine, Antithyroid drugs-thioamides- methimazole or PTU

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95
Q

What are Antithyroid drugs?

A

used in young patients with mild disease, pregnancy category D, inhibit iodine organification, effects are seen in 4 weeks or more because you must deplete all T4 stores in the body due to inhibition of synthesis but not release

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96
Q

What is Propylthiouracil?

A

hyperthyroidism…used in pregnancy (more protein binding than methimazole, doesn’t cross placental barrier as easily), thyroid storm; half life is 1.5 hours but this doesn’t indicate therapeutic effect due to accumulation in thyroid gland; severe hepatitis may occur; given q8h; additional benefit of preventing T4 to T3 conversion in periphery, brings levels down faster than methimazole

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97
Q

What is methimazole?

A

hyperthyroidism… 1st choice except in pregnancy and thyroid storm; half life is 6 hours but doesn’t indicate therapeutic effect due to accumulation in thyroid gland; less risk of liver damage; cholestatic jaundice is more common than with PTU; often give tid until euthyroid then proceed with once daily dosing

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98
Q

What are the side effects of thioamides?

A

Common: nausea, GI disturbance, altered sense of taste or smell (methimazole), rash, fever
Rare: urticaria rash, Vasculitis, Polyserositis
Life threatening: agranulocytosis, hepatitis (PTU)

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99
Q

What are additional treatments for hyperthyroidism?

A

iodides- used to decrease gland size prior to surgery and treatment of thyroid storm
radioactive iodide- 131I is the only form used for destruction of thyroid, but dangerous is given to pregnant or nursing moms
propranolol- for treatment of symptoms in acute phase, diltiazem if beta blocker is contraindicated

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100
Q

What are Langerhans?

A

areas of endocrine tissue that secrete hormones into the blood: insulin, glucagon, islet amyloid polypeptide (APP amylin), somatostatin, gastrin, pancreatic peptide

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101
Q

What percent of the islets of Langerhans do B cells make up?

A

75%

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102
Q

What is diabetes mellitus?

A

condition of elevated glucose due to absent or impaired insulin secretion with or without impaired ability to utilize insulin

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103
Q

What is somatostatin?

A

universal secretory inhibitor

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104
Q

What is islet amyloid polypeptide?

A

modulates appetite, gastric emptying, glucagon/insulin release

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105
Q

What are the functions of insulin in the liver?

A

inhibits of glycongenolysis, inhibits of ketogenesis, promotes glycogenesis

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106
Q

What are the functions of insulin in the muscle?

A

increases protein synthesis, increases glycogen synthesis, increases uptake of glucose

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107
Q

What are the functions of insulin in the adipose tissue?

A

increases triglyceride storage, inhibits breakdown of fat, increases fat storage

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108
Q

What is type 1 diabetes?

A

characterized by beta cell destruction resulting in severe to absolute insulin deficiency; primarily autoimmune; patients require exogenous insulin to survive- lack of insulin will result in diabetic ketoacidosis; obesity is not a factor

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109
Q

What is type 2 diabetes?

A

characterized by insulin resistance- inability to suppress hepatic glucose production, peripheral glucose uptake is impaired; strong correlation with obesity; definite genetic component; ketosis is typically not a concern; does not require insulin initially; nonketotic hyperosmolar syndrome via dehydration in combination with poorly controlled diabetes is a life threatening emergency

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110
Q

What are some symptoms of diabetes?

A

polyuria, polydipsia, polyphagia, extreme fatigue, weight loss even with increased food intake (type 1)

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111
Q

What are some complications of uncontrolled DM?

A

cardiovascular disease including atherosclerosis, MI, and stroke; neuropathy from mild tingling to numbness and potential limb loss; neuropathy may progress to renal failure requiring dialysis; retinopathy leading to blindness; difficulty healing; UTI, yeast infections; ketoacidosis in type 1; nonketotic hyperosmolar syndrome type 2

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112
Q

How does insulin secretion work?

A

presence of glucose at the beta cell leads to ATP production resulting in closure of the potassium channel and cell depolarization; cell depolarization opens calcium channel; calcium influx stimulates insulin release via exocytosis

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113
Q

What are the available preparations for exogenous insulin?

A

rapid-acting, short-acting, intermediate-acting, long-acting

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114
Q

What is the goal of therapy with exogenous insulin?

A

simulate normal basal and stimulated insulin secretion

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115
Q

What are the rapid-acting insulin drugs?

A

insulin lispro, insulin aspart, and insulin glulisin

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116
Q

What is rapid-acting insulin?

A

it stimulates prandial endogenous insulin release; it has the lowest absorption variability of all insulin; given immediately before a meal; the duration of action is not more than 3-4 hours; preferred for use in insulin pumps

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117
Q

What are the short-acting insulin?

A

regular insulin (humulin R, novolin R); injected as hexamers which have slowest absorption then eventually dissociate to dimers and eventually monomers which have fastest uptake; onset is 30 min, peak is 2-3 hours, duration is 5-8 hours; given 30-45 minutes before a meal

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118
Q

What are intermediate-acting insulin drugs?

A

NPH (Humulin N, Novolin N); onset is 2-5 hours, peak is 6-10 hours, duration is 10-16; unpredictable action and variable absorption; seen mixed with rapid or short acting formulations and given 2-4 times a day

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119
Q

What is a long acting insulin drug?

A

glargine (lantus, toujeo); detemir (Levemir)

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120
Q

How does a glargine long acting insulin drug work?

A

forms crystalline depot in the skin where insulin molecules slowly leach out into circulation

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121
Q

Toujeo vs. Lantus

A

toujeo is 3 times more potent than lantus with a slower release of insulin to improve 24 hour coverage

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122
Q

What is a contraindication of Glargine?

A

it cannot be mixed with other insulins because it will precipitate out in less acidic formulations

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123
Q

What is detemir?

A

a long acting insulin drug that is formulated to self-aggregate in subcutaneous tissue for slow release as well as bind to albumin reversibly; onset is 1-2 hours, duration 12 hours; dosed bid to maintain steady background insulin

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124
Q

What is an insulin mixture?

A

NPH may be mixed in the same syringe with lispro, aspart, or glulisine immediately before injection to achieve short and longer term coverage

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125
Q

What is a complications of insulin therapy?

A

hypoglycemia
causes: mismatched carb:insulin ratio and increased physical exertion
warning signs: tachycardia, palpitation, sweating, tremor, nausea, hunger, may progress to seizures or coma
correction of hypoglycemia occurs with glucose administration

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126
Q

What is another complication of insulin therapy?

A

insulin allergy: rare, urticaria results from histamine release from mast cells sensitized by anti-insulin IgE antibodies ; allergy is due to protein contaminants; human and analog insulins have resulted in decreased allergy

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127
Q

What is another complication of insulin therapy?

A

immune insulin resistance: most insulin treated patients develop low IgG anti-insulin antibody titers over time that neutralize effects of insulin; occasionally antibodies lead to insulin resistance

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128
Q

When is continuous subcutaneous infusion delivery for insulin used?

A

used with rapid acting insulins

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129
Q

What are the Antidiabetic agents that stimulate insulin secretion from beta cells?

A

insulin secretagogues: sulfonylureas, meglitinides, D-phenylalanine derivatives

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130
Q

How does the termination of action of catecholamine metabolism occur?

A

1) diffusion away from terminal
2) reuptake by NET
3) uptake by other tissues

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131
Q

What are the effects of acetylcholine on the cardiovascular system?

A

vasodilation, negative chronotrope (rate), negative inotrope (force), negative domotrope (conduction velocity)

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132
Q

What are the effects of acetylcholine on the respiratory tract?

A

bronchoconstriction, increase secretion, stimulation of carotid and aortic bodies

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133
Q

What are the effects of acetylcholine on the urinary tract?

A

detrusor muscle contraction, increased voiding pressure, ureteral peristalsis

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134
Q

What are the effects of aetylcholine on the GI tract?

A

increased tone, increased amplitude of contractions, increased secretions in stomach and intestine

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135
Q

What are some additional effects of acetylcholine?

A

miosis, increased lacrimal, nasopharyngeal, salivary secretions, increased production of sweat

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136
Q

What does SLUDGE BBM stand for?

A

salivation, lacrimation, urination, defecation, gut pain/contraction, emesis, bronchospasm, bronchorrhea, miosis

137
Q

What is acetylcholine used for clinically?

A

used topically to produce miosis immediately after lens placement in cataract surgery; poor oral absorption; onset is rapid; duration is approximately 10 minutes; brand name is Miochal-E

138
Q

What is methacholine used for clinically?

A

administered by inhalation to diagnose bronchial airway hyperactivity in people who do not demonstrate clinically apparent asthma

139
Q

What are the contraindications of methacholine?

A

in patients using beta blockers or who have demonstrated asthma

140
Q

What is the onset and duration of methacholine?

A

rapid with peak of 1-4 minutes; duration is 15-75 minutes or 5 minutes if it is followed by a beta agonist

141
Q

What is Bethanechol used to treat?

A

urinary retention-> causes the person to urinate; dosed 3-4 times a day on an empty stomach

142
Q

What is carbachol used for clinically?

A

causes miosis during surgery; reduces intraocular pressure in glaucoma

143
Q

What is pilocarpine used for clinically?

A

its a non-selective muscarinic agonist (side effects); but is treats xerostomia (dryness of the mouth) due to radiation, also Sjogren’s (autoimmune disorder)

144
Q

What is Cevimeline used for clinically?

A

it has a high affinity for lacrimal and salivary M3 muscarinic receptors

145
Q

What are some general precautions when using muscarinic agonists?

A

asthma, COPD, urinary obstruction, GI obstruction, cardiovascular disease w/ hypotension, bradycardia, hyperthyroidism (precipitate atrial flutter), acid-peptic disease

146
Q

What are some muscarinic antagonists?

A

atropine, scopolamine, methoscopolamine bromide, homatropine, ipratropium, tiotropium, tiotropium, benzatropine, trihexylphenidyl

147
Q

What are the muscarinic antagonists that are urinary agents?

A

oxybutynin, trospium, tolterodine, solifenacin, darifenacin, Fesoterodine

148
Q

What are the dosages for atropine and the associated effects?

A

.5, 1, 2, 5, greater than or equal to 10… red as a beet, dry as a bone, blind as a bat, hot as firestone, and mad as a hatter

149
Q

What are the effects of muscarinic antagonists cardiovascularly?

A

positive chronotropy (blood pressure is unaffected)

150
Q

What are the effects of muscarinic antagonists on the respiratory system?

A

decreased bronchoconstriction, decrease secretions

151
Q

What are the muscarinic antagonist effects on the eyes?

A

mydriasis (dilation of the pupil of the eye)

152
Q

What are the effects of muscarinic antagonists on the GI tract?

A

antispasmodic, decrease acid secretion (do not use this due to other negative systemic effects), decrease tone, amp, and freq of peristalsis

153
Q

What are the effects of muscarinic antagonists on secretions?

A

decrease salivation at almost any dose, decrease nasal secretions

154
Q

What are the effects of muscarinic antagonists on the urinary tract?

A

decrease tone (side effects always an issue)

155
Q

What are therapeutic uses of muscarinic antagonists on the CNS?

A

motion sickness (scopolamine and methoscopolamine); decreases extrapyramidal side effects of Parkinson treatment

156
Q

What are the therapeutic uses of muscarinic antagonists on the cardiovascular system?

A

vasovagal syncope- causes heart to slow down which results in fainting
asystole- state of no cardiac electrical activity

157
Q

What are the preferred muscarinic antagonists in mydriasis?

A

cyclopentolate, homatropine, and tropicamide are preferred for shorter duration than atropine

158
Q

What are the therapeutic uses of muscarinic antagonists on the GI tract?

A

used primarily for spasticity- when muscles are always tight or stiff; hyoscyamine, atropine, dicyclomine (Bentyl-weak antagonist); not good for peptic ulcer disease; ulcerative colitis, Chron’s, food poisoning are unresponsive

159
Q

What are the muscarinic antagonists used when dealing with issues in the genitourinary tract?

A

oxybutynin, tolterodine, trospium

160
Q

What cytochrome pathway does oxybutynin use?

A

CYP3A4 substrate; lots of side effects

161
Q

What cytochrome pathway does tolterodine use?

A

CYP2D6 however it does not require a dose adjustment with drugs that inhibit this pathway

162
Q

Which muscarinic antagonist urinary agent is more specific for the bladder?

A

tolterodine

163
Q

What is the only muscarinic antagonist affecting the genitourinary tract that is eliminated significantly by the kidneys?

A

trospium

164
Q

What is the therapeutic effect of Ipratropium?

A

relieves bronchial spasms; is available as aerosol or solution for nebulizer

165
Q

How is tiotropium available?

A

as a dry powder inhalant and lasts up to 24 hours

166
Q

What are Ipratropium and Tiotropium?

A

relieve bronchial spasms such as in asthma; they have action in mouth and airway exclusively; do not inhibit mucociliary clearance as atropine does

167
Q

What are warnings and precautions of muscarinic antagonists?

A

side effects- xerostomia, constipation, blurred vision, cognitive impairment
caution in- benign prostatic hyperplasia, GI obstruction, urinary obstruction, angle-closure glaucoma

168
Q

What is pyridostigmine?

A

approved for troop prophylaxis against exposure to soman; rapidly aging agent; goal is to preserve some acetylcholinesterase function

169
Q

what are direct acting agonists?

A

act directly on adrenergic receptors (may be highly selective for their receptor)

170
Q

What is a indirect-acting agonist?

A

availability of NE is increased via forcing the release of NE storage vesicles or blocking uptake or metabolism; tachyphylaxis may occur with indirect-acting agents presumably due to depletion of NE stores

171
Q

What is a mixed-acting agonist?

A

will share features of both direct and indirect

172
Q

What are the selective direct acting adrenergic agonists?

A

phenylephrine, clonidine, Dobutamine, and terbutaline

173
Q

What are the non-selective direct acting adrenergic agonists?

A

oxymetazoline, isoproterenol, epinephrine, norepinephrine

174
Q

What is a mixed acting adrenergic agonist?

A

ephedrine

175
Q

What are the releasing agents indirect acting adrenergic agonists?

A

amphetamine and tyramine

176
Q

What are the uptake inhibitor indirect acting adrenergic agonists?

A

cocaine

177
Q

What is a MOA inhibitor indirect acting adrenergic agonist?

A

selegiline

178
Q

What is a COMT inhibitor indirect acting adrenergic agonist?

A

entacapone

179
Q

What are the two pathways of pain modulation?

A

afferent pathway transmits painful stimuli and effect pathway modulates pain

180
Q

Opiate

A

a compound structurally related to those found in opium

181
Q

Opioid

A

an agent with the same functional and pharmacological properties of opiates

182
Q

What is the primary analgesic opioid receptor?

A

u-receptor

183
Q

Which drug it a full agonist at a u-receptor?

A

morphine

184
Q

Which drug is a partial u-receptor agonist?

A

codeine

185
Q

Which drug is a strong u-receptor antagonist?

A

naloxone

186
Q

What are examples of endogenous opioids?

A

endorphins, enkephalin, and dynorphins

187
Q

Which receptor are endomorphins selective for?

A

u-receptor

188
Q

How are endogenous opioids released?

A

in response to noxious stimuli or nociception (the encoding and processing of harmful stimuli)

189
Q

What is an exception concerning endogenous opioids?

A

dynorphin-A is in the dorsal horn of the spinal cord and it increases sensitization to nociceptive neurotransmission

190
Q

What are the primary neurotransmitters responsible for pain signaling?

A

glutamate, substance P, NMDA (n-methyl-d-aspartate)

191
Q

What are the primary endogenous pain control substances?

A

endogenous opioids, serotonin, norepinephrine

192
Q

What are the 2 cellular mechanisms of opioids?

A

close presynaptic voltage-gated Ca2+ channels decreasing neurotransmitter release

193
Q

How does an opioid act on an afferent transmission?

A

decreases the release of pain neurotransmitters; there is interruption of pain transmission by direct action on damaged tissue, spinal inhibition, or possible action in thalamus

194
Q

How do opioids act on efferent transmission?

A

inhibit inhibitory interneurons in the descending pathways which increases endogenous opioid release and thus pain modulation

195
Q

What are the routes of administration for opioids?

A

oral, transdermal, parenteral, sublingual/buccal, subcutaneous, insufflation, epidural, Intrathecal, rectal

196
Q

What is an issue concerning routes of administration in opioids?

A

oral bioavailability is a problems and oral doses are often much high than other routes

197
Q

What is the distribution of most opioids?

A

highly lipophilic opioids will accumulate in fatty tissue; but all distribute out of the blood compartment quickly to highly perfused tissues

198
Q

What opioids use the cytochrome system?

A

meperidine, fentanyl, alfentanil, sufentanil

199
Q

What is the metabolism and excretion of opioids?

A

mostly undergo glucuronidation, while some use the cytochrome system but excretion is primarily renal

200
Q

What are the clinical effects in the CNS of opioids?

A

analgesia, euphoria/dysphoria, sedation without amnesia, disrupted sleep architecture, respiratory depression, cough suppression (but not mucus clearance), miosis (no tolerance develops, useful in identifying OD), truncal rigidity (may cause ventilation issues), nausea and vomiting

201
Q

What are clinical effects in the periphery because of opioids?

A

minor bradycardia, constipation (no tolerance), antidiuretic effects, urinary retention, itching, sweating, flushing

202
Q

What are the therapeutic uses of opioids?

A

analgesia, acute cardiogenic pulmonary edema (mechanism is assumed to be decreased anxiety), cough suppression, non-infectious diarrhea, shivering (especially meperidine due to alpha2 agonist properties), anesthesia

203
Q

Which opioid has greatest effect on shivering?

A

meperidine due to alpha 2 agonist properties

204
Q

What are the long term effects of opioid use?

A

tolerance- decreases in apparent effectiveness of a drug with continuous or repeated administration, reversible, surmountable, develop in different systems at different times
dependence- neuronal adaption to repeated drug exposure leading to a withdrawal syndrome upon cessation, inevitable consequence

205
Q

What are some symptoms of opiate withdrawal?

A

rhinorrhea, lacrimation, yawning, chills, Goosebumps, hyperventilation, hyperthermia, mydriasis, aching, comiting, diarrhea, anxiety, hostility
addiction- behavioral patter characterized by compulsive use of a drug and overwhelming involvement with its procurement and use

206
Q

What is opioid addiction characterized by?

A

addiction affects reward center in brain, avoidance or alleviation of withdrawal, this is not a end result for all patients and should not be mistaken for dependence, short acting opiates are more likely to foster addiction due to constant ups and downs

207
Q

What are some precautions when using opioids?

A

use of full agonist with partial agonist, patients with head injuries, pregnancy, patients with impaired lung function, patients with liver or renal dysfunction, patients with endocrine disease may show exaggerated responses

208
Q

Why should you take precautions when giving opioids to patients with head injuries?

A

CO2 retention from respiratory depression may lead to lethal effects in patients with increase intracranial pressure

209
Q

Why should you take precautions when giving opioids to a pregnant women?

A

fetal dependence leading to withdrawal at birth

210
Q

What are some drug interactions with opioids?

A

general opiates should not be given with sedative-hypnotics, antipsychotics, or MAOIs; must also watch for cytochrome interactions and patients who cannot glucuronidate compounds

211
Q

What are the strong opioid agonists?

A

morphine, hydromorphone, oxymorphone are the prototypical agents; fentanyl and its derivatives alfentanil, sufentanil, remifentanil; meperidine; methadone

212
Q

When is fentanyl used?

A

in chronic pain; the derivatives alfentanil, sufentanil, and remifentanil are short acting and used in surgery

213
Q

Why is meperidine difficult to use?

A

anticholinergic action as well as seizures make it difficult to use

214
Q

What is methadone?

A

not only active on u-receptors but also blocks NMDA receptor and monoamine reuptake transporters -> useful for neuropathic cancer pain

215
Q

How is methadone metabolized?

A

Metabolized by CYP3A4

216
Q

What is methadone used to treat?

A

opioid addiction; high dose methadone is used in repeat heroin addicts; high doses cause cross tolerance to heroin removing the drive to seek it out

217
Q

What are some mild to moderate opioid agonists?

A

diphenoxylate, loperamide, oxycodone, codeine, dihydrocodeine, hydrocodone

218
Q

What to mild to moderate agonists are used to treat diarrhea?

A

diphenoxylate and loperamide

219
Q

What is diphenoxylate?

A

a mild to moderate opioid agonist; it is used to treat diarrhea; it is a controlled substance; used in combination with atropine to limit its abuse

220
Q

What is loperamide?

A

a mild to moderate opioid agonist; used to treat diarrhea and is available over the counter

221
Q

What is oxycodone?

A

a mild to moderate opioid agonist; available as immediate release and extended release

222
Q

What is the difference between oxycodone and codeine, dihydrocodeine, hydrocodone?

A

codeine, dihydrocodeine, and hydrocodone are less potent than oxycodone

223
Q

What are the mixed opioid receptor agents?

A

nalbuphine and buprenorphine

224
Q

What is nalbuphine?

A

a opioid mixed receptor agent, it is a strong k receptor agonist and a u receptor antagonist; given parenterally

225
Q

What is buprenorphine?

A

partial u-receptor and k-receptor antagonist; studies show it is equally effective to morphine in detox and maintenance of heroin addicts; in high doses it acts as a u-receptor antagonist; used to treat opioid addiction

226
Q

What is tramadol?

A

blocks SERT and NET; weak u-receptor agonist; lowers seizure threshold; risk of serotonin syndrome in patients on SSRIs; due to low u receptor activity it is safe to use with pure agonists as adjunct for pain

227
Q

What is tapentadol?

A

modest u receptor agonism and inhibits NE uptake

228
Q

What opioid agents are used for cough?

A

codeine and dextromethorphan

229
Q

What are the clinical features of depression?

A

depressed mood, sadness, decreased appetite, weight loss, increased appetite, weight gain, insomnia, increased sleep, change in activity level, loss of interest in activities, negative thinking, guilt, worthlessness, mental slowing, decreased cognition, active or passive suicidal ideation

230
Q

What are clinical features of anxiety?

A

feelings of fear or dread without cause, panic, difficulty thinking of anything other than present worry, increased sympathetic symptoms (fight or flight seems engaged)

231
Q

What is serotonin?

A

(5-hydroxytryptamine, 5-HT)a neurotransmitter that plays a role in mood, blood pressure, and gut motility

232
Q

How is serotonin primarily metabolized?

A

by MAO-A

233
Q

What is serotonin synthesized from?

A

tryptophan

234
Q

Where is SERT located?

A

serotonergic axon terminals, reuptake of synaptic 5-HT; also the platelet membrane, uptake of 5-HT from the blood

235
Q

5-HT is converted to what in the brain?

A

nearly 100% of 5-HT is converted to 5-HIAA in the brain

236
Q

What does large amounts of 5-HIAA in the urine indicate?

A

carcinoid tumor

237
Q

What are the functions of serotonin?

A

platelets- assist in aggregation and local vasoconstriction
cardiovascular- vasoconstriction, some inotropic and chronotropic effects
GI tract functions and CNS functions

238
Q

What are the functions of serotonin in the GI tract?

A

over 90% of serotonin is produced and stored in enterochromaffin cells of the gastric mucosa; this is where circulating 5-HT comes from; release is mediated by stretch receptors and efferent vagal stimulation; involved in emesis and peristalsis

239
Q

What are the functions of serotonin in the CNS?

A

sleep wake cycle, mood stabilization through decreases anger, decreased anxiety, and decreased depressive symptoms

240
Q

What are the treatment options for depression?

A

MAOIs, TCAs, SSRIs, SNRIs, atypical antipsychotics

241
Q

What are the treatment options for anxiety?

A

SSRIs, SNRIs, benzodiazepines, buspirone, beta-antagonists

242
Q

What are some issues with treating people with anxiety with benzos?

A

they can cause problems with cognition and memory and are addictive

243
Q

What can happen when treating someone with anxiety? should be a clinical consideration

A

anxious symptoms will increase in first few weeks of treatment, may need to bridge patient with benzodiazepine for two weeks

244
Q

What are the actions of a benzodiazepine?

A

anxiolytic, anticonvulsant, muscle relaxant, sedative/hypnotic, amnestic

245
Q

What is the mechanism behind a benzodiazepine?

A

it potentiates the effects of GABA; GABA binds to postsynaptic GABA-A receptors -> increased influx of Cl- -> membrane hyperpolarization -> neuronal inhibition

246
Q

What is alprazolam?

A

Xanax, effective for panic/anxiety, half life is 12-15 hours, metabolism through CYP3A4

247
Q

What is Chlordiazepoxide?

A

Librium, alcohol withdrawal, half life is greater then 100 hours, metabolism through CYP1A2

248
Q

What is Lorazepam?

A

Ativan, alcohol withdrawal, and anxiety, half life is 10-20 hours, metabolism is glucuronidation

249
Q

What is diazepam?

A

Valium, alcohol withdrawal, low back pain, muscle relaxant, metabolism is CYP1A2, 2C9, 2C19, 3A4

250
Q

What drugs are useful as hypnotics?

A

ones with a short half life, however this increases risk of abuse and withdrawal issues

251
Q

What drugs are useful as anticonvulsants?

A

ones with long half life, also drugs with a long half life are preferred for chronic anxiety

252
Q

Which benzodiazepines are a risk for high abuse potential?

A

alprazolam and diazepam

253
Q

What are the adverse effects of benzodiazepines?

A

light headedness, increased reaction time, forgetfulness, hangover, changes in sleep architecture, worsening of sleep apnea, addiction and dependence, dangerous when consumed with alcohol?

254
Q

What are some clinical considerations when using BZD in the elderly?

A

these drugs are the greatest fall risk for the elderly, shorter half life agents are preferred in this group, start low and go slow

255
Q

What is lubiprostone?

A

a prokinetic drug approved from chronic idiopathic constipation, constipation predominant IBS, and opioid induced constipations in patient with non cancer pain

256
Q

What is the mechanism behind lubiprostone?

A

it stimulates type 2 chloride channels in the small intestine increasing chloride rich fluid secretion -> this results in increased motility; however there is very poor bioavailability and it is rapidly metabolized in the stomach and jejunum

257
Q

What decreases the efficacy of Lubiprostone?

A

methadone because methadone decreases the activity of type 2 chloride channels

258
Q

Is there cytochrome involvement in Lubiprostone?

A

there is no cytochrome involvement

259
Q

What are the adverse effects of Lubiprostone?

A

side effects are nausea, diarrhea, and dyspnea; pregnancy category C due to fetal loss in pregnant pigs; the elderly had less nausea than the study population; contraindicated in obstruction

260
Q

Are there any dose adjustment requirements with Lubiprostone?

A

no dose adjustment in renal impairment; however there is dose adjustment needed in moderate to sever hepatic failure

261
Q

What are two opioid receptor antagonists that are used to treat constipation?

A

methylnaltrexone (Relestor) and alvimopan (Entereg); these are u-receptor selective and they do not cross the blood brain barrier

262
Q

What is methylnaltrexone?

A

Relestor; a sub-q-injection for patients with advanced illness receiving palliative care, as well as opioid-induced constipation in patients with chronic non-cancer pain

263
Q

What is alvimopan?

A

Entereg; is a capsule approved for acceleration of gut transit time following surgery with partial bowel resection; restricted to hospital use only and only for 15 doses; increased risk of MI

264
Q

What decreases GI transit time and increases stool water?

A

fiber, magnesium, lactulose, lubriprostone, senna, bisacodyl, and PEG

265
Q

What drug has the longest time to action when decreases transit time and increasing stool water?

A

fiber, lactulose, docusate all have 1-3 days before any action

266
Q

What drug has the shortest time to action when decreases transit time and increasing stool water?

A

magnesium and PEG have 1-3 hours before time to action

267
Q

When should you treat someone with an antidiarrheal agent?

A

reserve treatment for patients with significant or persistent symptoms; do not treat a patient with an anti-diarrheal med if they present with high fever, bloody stool or presence of microorganisms

268
Q

What is the number one priority when treating someone with severe diarrhea?

A

oral rehydration with an electrolyte solution

269
Q

How is a bulk-forming agent and anti-diarrheal agent?

A

they modify stool texture and viscosity; patient perception of diarrhea is improved

270
Q

What is bismuth?

A

anti-secretory, anti-inflammatory, antimicrobial effects; works on abdominal cramping; useful in travelers diarrhea

271
Q

What drugs are bile acid sequestrants?

A

cholestyramine, colestipol, colesevalam

272
Q

What patients are good for using bile acid sequestrants?

A

patients with malabsorption of bile salts such as those with Crohn’s or surgical resection of the gut

273
Q

What are the side effects of bile acid sequestrants?

A

bloating, gas, fecal impaction

274
Q

What is a negative affect when taking bile acid sequestrants with other drugs?

A

they bind other drugs and require at least a 2 hour separation (except for colesevalam)

275
Q

What is loperamide?

A

Imodium, opioid agonist and is 50 times more potent than morphine as an anti-diarrheal; does not cross blood brain barrier; in there is no improvement in 48 hours loperamide should be discontinued; useful in travelers diarrhea and can be used in long term chronic diarrheal disease

276
Q

What is diphenoxylate and difenoxin?

A

lomotil and motofen; structurally similar to meperidine; antidiarrheal agent; potential for abuse and addiction in high doses but formulated with atropine to discourage abuse and overdose; constipation and toxic megacolon may result from excessive use

277
Q

What are other anti diarrheal agents?

A

codeine, paregoric, octreotide, clonidine

278
Q

What is octreotide?

A

IV or sub-q in select patients who have secretory malfunctioning

279
Q

What is clonidine?

A

inhibit gut secretions and increase transit time, used in diabetic patients with autonomic neuropathy leading to chronic diarrhea; side effects are hypotension, fatigue, and depression

280
Q

What is IBS?

A

idiopathic chronic disorder characterized by hypersensitivity and hyperactivity

281
Q

What do patients with IBS present with?

A

abdominal discomfort, bloating, distension, cramps, associated with constipation diarrhea or both

282
Q

What drug is predominantly used for diarrhea?

A

loperamide

283
Q

What is predominantly used for constipation?

A

milk of magnesia

284
Q

What does chronic abdominal pain respond well to?

A

TCAs

285
Q

Who is alosetron approved for?

A

approved for treatment of severe IBS-D in women only!

286
Q

What is severe IBS-D defined as having diarrhea with one or more of what?

A

frequent or severe abdominal pain and discomfort, frequent bowel urgency or fecal incontinence, disability or restriction of daily activities due to IBS

287
Q

What is alosetron?

A

Lotronex; potent, selective 5-HT3 receptor antagonist; blockade of 5-HT3 receptors reduces pin and exaggerated motor response in patients with IBS

288
Q

How is alosetron excreted?

A

renally but there is no dose adjustment needed

289
Q

Which cytochromes is alosetron metabolized by?

A

P450, 1A2, 3A4, 2C9

290
Q

What are some adverse effects of alosetron?

A

side effects are dose dependent, but there could be liver failure and drug interaction; constipation occurs in 30 percent of patient; ischemic colitis is rare but serious and may result in death

291
Q

What are other treatments for IBS other than alosetron?

A

lubiprostone, anticholinergic antispasmodics

292
Q

What anticholinergic antispasmodics are used to treat IBS?

A

dicyclomine (Bentyl) and hyoscyamine; at low doses there is minimal muscarinic effects but at high doses there are side effects; may help some patients but these are not the first choice

293
Q

What are some treatment options for IBS-D?

A

antibiotics, antidepressants, antidiarrheals, antispasmodics, 5-HT3 antagonists, probiotics

294
Q

What are some treatment options for IBS-C?

A

antibiotics, antidepressants, laxatives, antispasmodics, CIC-2 activator, probiotics

295
Q

What are some treatment options for mixed IBS?

A

antibiotics, antidepressants, antispasmodics, probiotics

296
Q

What is an antibiotic given for IBS treatment?

A

Rifaximin (Xifaxan) given for 14 days and showed improvement in symptoms suggests that there may have been some involvement in altered gut microflora

297
Q

What are the by afferent sources that trigger nausea and vomiting?

A

chemoreceptor trigger zone (CTZ), vestibular system, vagal and spinal afferent nerves in GI tract, CNS

298
Q

how does chemoreceptor trigger zone initiate nausea and vomiting?

A

located outside the BBB it can sense emetogenic stimuli in the blood as well as in the cerebrospinal fluid, are is rich in D2, opioid, %-HT3, and neurokinin 1 receptors

299
Q

How does the vestibular system initiate nausea and vomiting?

A

through motion sickness and M1 and H1 receptors

300
Q

How can vagal and spinal afferent nerve in the GI tract initiate nausea and vomiting?

A

5-HT3 receptor sense release of serotonin from GI tract due to irritation

301
Q

How does the CNS initiate nausea and vomiting?

A

sense stress, psychiatric disorders, anticipatory vomiting with chemotherapy

302
Q

Why are 5-HT3 antagonists effective in treating nausea and vomiting?

A

due to vagal stimulation or chemotherapy

303
Q

What are the 5-HT3 antagonists used to treat emesis?

A

ondansetron (Zofran), granisetron, dolasetron, palonsetron

304
Q

What are the 5-HT3 antagonists that are given oral or IV, have a half life of 4-9 hours, and are given once a day?

A

ondansetron, granisetron, and dolasetron

305
Q

What is the 5-HT3 antagonist that has a greater affinity for 5-HT3 receptor and has a half life of over 40 hours

A

palonsetron (Aloxi)

306
Q

Do 5-HT3 antagonists require dose adjustments?

A

don’t require dose adjustment in renal impairment or in geriatric patients; there in extensive hepatic metabolism but only ondansetron requires dose adjustment

307
Q

What are the adverse effects of 5-HT3 antagonists?

A

excellent safety profile, some headache, dizziness, or constipation; although these drugs go through the cytochrome system dose adjustment is not needed when given with inducers or inhibitors, serotonin syndrome may occur when given with other serotonergic drugs

308
Q

What 5-HT3 antagonist specifically used for nausea and vomiting can cause arrhythmias if given with medications known to increase QT interval?

A

dolasetron

309
Q

What is an corticosteroid that is used as an antiemetic?

A

Dexamethasone- most date and is given IV prior to chemo then orally for 2-4 days following chemo

310
Q

How is a corticosteroid used as an antiemetic?

A

given along with 5-HT3 antagonists to enhance prevention of N/V; mechanism of action is unknown

311
Q

What drugs are NK1 receptor antagonists?

A

aprepitant and fosaprepitant

312
Q

What are the adverse effects of NK1 receptor antagonists?

A

diarrhea, fatigue, dizziness

313
Q

How are NK1 receptor antagonists metabolized?

A

metabolized by and moderately inhibits CYP3A4; if given in conjunction with a strong inhibitor, aprepitant levels will be increased

314
Q

What is a side effect of the antiemetic NK1 receptor antagonist drugs?

A

they decrease the efficacy of oral contraceptives

315
Q

How are NK1 receptor antagonists administered as an antiemetic drug?

A

administered 1 hour prior to chemo and then continued for 2 days after chemo

316
Q

What are phenothiazine’s?

A

they inhibit dopamine and muscarinic receptors

317
Q

What are two examples of phenothiazine drugs?

A

prochlorperazine and promethazine

318
Q

What is a side effect of phenothiazines?

A

they also have antihistamine properties so main side effect is drowsiness

319
Q

What are other antiemetic agents?

A

metoclopramide, trimethobenzamide, antihistamines such as diphenhydramine, dimenhydrinate, and meclizine; muscarinic receptor antagonist such as scopolamine; benzodiazepines; phosphorated carbohydrate solutions

320
Q

Why are metoclopramide and trimethobenzamide believed to be effective as antiemetic agents?

A

because of heir dopamine antagonism; but watch extrapyramidal side effects

321
Q

Why are antihistamines such as diphenhydramine, dimenhydrinate, and meclizine used as antiemetic agents?

A

good for motion sickness, not potent enough for CINV alone but used as adjuncts; anticholinergic properties lead to side effects; meclizine is less sedating, used for motion sickness as well as labyrinth dysfunction

322
Q

What is scopolamine?

A

a muscarinic receptor antagonist; excellent for motion sickness; side effects are high with oral formulation so best tolerated as patch

323
Q

Why are benzodiazepines useful as an antiemetic agent?

A

they have anticipatory N?V because of CNS component; however they are not overly effective alone

324
Q

What are examples of cannabinoids?

A

dronabinol better known as THC and nabilone

325
Q

What is dronabinol?

A

synthesized from marijuana plant but unknown mechanism of action; there is 10-20% bioavailability with high first past; metabolites are excreted in feces with minimal renal excretion; highly protein bound; very large Vd so metabolites are detectable in blood for weeks from a single does

326
Q

What are the clinical applications of cannabinoids?

A

they are used in CINV when other options have failed; dronabinol has additionally been shown to stimulate appetite in AIDS patients and those with anorexia

327
Q

What are the adverse effects of cannabinoids?

A

palpitations, tachycardia, vasodilation, hypotension, conjunctival injection; may cause a high so abuse is potential, paranoia and mental perception may occur, withdrawal may occur, may displace other highly protein bound drugs, Cesamet (Nabilone) has intense CNS effects which may be exaggerated when given with other psychoactive drugs leading to hypomania, drowsiness, and CNS depression

328
Q

What drugs are in the hypnotic drug class referred to as Z compounds?

A

zolpidem (ambien), zaleplon (sonata), zopiclone (not marked in the US), eszopicolne (lunesta)

329
Q

How do hypnotics (sleep inducers) work?

A

they act as agonists on the benzodiazepine site of GABA receptor; they have replaced benzos for treatment of insomnia

330
Q

What is Flumazenil (Romazicon)?

A

a benzo receptor antagonist; has a high affinity for GABA receptor and is a competitive antagonist; it is given IV

331
Q

What is Ramelteon?

A

(Rozeren) a synthetic analog of melatonin and is used for difficulty of sleep onset

332
Q

What are barbiturates?

A

used for sedative/ hypnotic treatment but have been replaced by safer benzos

333
Q

When should you use benzos with a short half life?

A

use for sleep onset issues

334
Q

When should you use benzos with a longer half life?

A

for daytime anxiety; except these people will have longer residual effects after discontinuation

335
Q

What benzos are preferred in liver disease and the elderly?

A

LOT (Lorazepam, Oxazepam, and Temazeam)

336
Q

What are the six available PPIs?

A

omeprazole, esomeprazole, Lansoprazole, Dexlansoprazole, rabeprazole, and pantoprazole

337
Q

What are some examples of antacids?

A

sodium bicarbonate (baking soda), calcium carbonate (Tums), and magnesium hydroxide/aluminum hydroxide (Maalox, Mylanta)

338
Q

What are examples of some H2 receptor antagonists?

A

cimetidine, ranitidine, famotidine, and nizatidine

339
Q

What is a negative about giving the elderly an H2 receptor antagonists?

A

they have a 50% clearance and a low Vd

Pharmacology Exam 2 (2 decks)

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