Mia Coliflores, Katie Jensen, Anja Thorson – EXAM 2 Collaboration

Chapter 71 Cyclooxygenase Inhibitors

· Review AMA 4 step approach for treatment of chronic pain

o Initiate nondrug measures
 PT, exercise, weight loss, orthotics, application of heat or cold
o Initiate drug therapy using Acetaminophen or Aspirin (these are Cyclooxygenase inhibitors)
o Initiate nonselective NSAIDs Therapy (ibuprofen, naproxen)
o Use selective COX2 inhibitors as last drug of choice
· Identify the therapeutic benefits and disadvantages of COX 1 and COX 2 inhibitors

COX 1 COX 2

 “housekeeping” chores · mediates fever/pain/inflammation

 Protect against gastric
mucosa/support renal function
 Prevent Platelet aggregation in all
tissues
 Considered the “good” COX
· Mediates renal function
· Vasodilation
· Contribution to colon cancer
(mediates harmful processes)
· Considered the “bad” COX

o Therapeutic Uses of inhibiting

 Suppress inflammation (COX2 inhibitor suppresses prostaglandin secretion)
 Relieve pain (COX2 inhibitor suppresses prostaglandin secretion)
 Reduce fever (COX2 inhibitor suppresses prostaglandin secretion)
 Protect against colorectal cancer (COX2 inhibitor can block tumor growth)
 Protection against MI/Stroke (COX1 inhibitor s/t reducing platelet aggregation)
o Adverse effects of inhibiting
 Gastric ulceration (COX1 inhibits production of mucosa)
 Bleeding (COX1 inhibiter suppresses platelet aggregation)
 Renal impairment (COX1 and COX2 inhibitor can cause fluid/Na retention)
 Promote MI/Stroke (COX2 inhibitor s/t to suppress vasodilation)
· Review the indications, therapeutic benefits and side effects of Aspirin and Acetaminophen
o Aspirin (irreversible nonselective)
 Therapeutic uses
 Anti-inflammatory (for RA, OA, Arthritis)
 Anti-pyretic (not children because Reye’s syndrome)
 Analgesic
 Relieve Dysmenorrhea (decreased number of cramps)
 Suppress platelet aggregation (prevent MI/Stroke)
 Prevent colorectal cancer at high doses
 Prevention of Alzheimer’s Disease (CNS effect)
 Adverse Effects
 Gastric ulcer
 Gastric Upset (take with food or glass of water)
 Bleeding
  Renal impairment
 Reye’s syndrome (head/liver swell) -- inc. With Aspirin use in children
 Pregnancy—anemia, postpartum hemorrhage, suppress contractions to increase labor
time
o Acetaminophen (reversible 1st gen NSAID) aka Tylenol/ Ofirmev
 COX1 and COX2 inhibitor
 Therapeutic uses
 Analgesic
 Antipyretic—inhibits prostaglandin in CNS only
 NOT anti-inflammatory
 Does not cause gastric ulcer or renal impairment
 Adverse Effects
 HTN
 SJS and TEN (Rash and blister)
 Acetaminophen overdose (leading cause of acute liver failure)
o Liver damage-- Hepatic necrosis/failure, coma, death (late s/s)
o n/v/d, sweating, abdominal discomfort (early s/s)
· Review signs/symptoms of Aspirin and Acetaminophen toxicity – include treatment option of overdose/toxicity
of Aspirin
o Acute Aspirin poisoning
 Like compensated respiratory alkalosis
 Respiratory depression
 Hyperthermia/sweating
 Dehydration
 Coma
o Acetaminophen overdose (leading cause of acute liver failure)
 Hepatic necrosis/failure, coma, death (late s/s)
 n/v/d, sweating, abdominal discomfort (early s/s)
 Antidote—Acetylcysteine-- provides cysteine for glutathione synthesis. Glutathione
subsequently acts as an antioxidant and facilitates conjugation to toxic metabolites.

Chapter 72 Glucocorticoids in Nonendocrine Disorders

· Review indication of glucocorticoids therapeutic use and potential side effects

o Physiologic effects (low doses):
 (Long term use) Modulation of glucose metabolism in pt w/ adrenocortical insufficiency
o Pharmacologic, therapeutic effects (high doses)
 Anti-inflammatory (produce greater effect than NSAIDS) + suppress immune responses
(autoimmune, asthma, allograft rejection)
 Mobility
 Rheumatoid Arthritis (anti-inflammatory; analgesic but not for long-term uses)
 Bursitis, tendonitis, OA
 Respiratory
 Most effective anti-asthma medication
 Prevent pre-term respiratory distress syndrome (premature babies do not have enough
glucocorticoids for lung maturation, so need drugs)
  Cancer
 ALL, Hodgkins, non-Hodgkins/ (glucocorticoids toxic to malignant lymphocytes)
 Increased WBC because of steroids
 Treats dermatologic disorders (psoriasis)
 Suppression of SLE symptoms
o Adverse Effects (increases with dosage size and treatment duration)
 Adrenal insufficiency--> suppress natural glucocorticoids in adrenal gland
 Osteoporosis (suppress bone formation—compression fractures!)
 Susceptible to infections! (Because immune system suppression)
 Inc. Plasma glucose = hyperglycemia (you become glucose intolerant)
 Check diabetics for sugar levels
 Myopathy (muscle injury) --> muscle weakness and skin thinning
 Electrolyte/fluid imbalances
 Na/H2O retention = HTN and Edema
 Potassium loss = dysrhythmias
 Iatrogenic Cushing's disease
 PUD
 Cataracts/glaucoma
· Identify the appropriate prevention and treatments for glucocorticoids side effects
o Withdraw drugs slowly to avoid withdrawal or adrenal suppression --> do over 7 days
o Admin dose low and slow when no threat
o Admin dose high and decrease, if possible, with immediate threat
o Dose in the morning to mimic normal body production
o Check bone density and give Calcium and Vitamin D
o Check diabetics for sugar levels before
· Review patient education related to glucocorticoids treatment and what drugs should be avoided while on
glucocorticoids
o Don’t give with Digoxin/ loop-diuretics and thiazide (because potassium loss)
o Don’t give with NSAIDS (inc. Risk of GI bleeding/ulcers
o Don’t give with live virus vaccines (can dec. Antibody response to vaccines)
o Don’t get pregnant within 6 months after treatment because it can cause infertility, fertility
issues/defects
· Identify reason for discontinuation of glucocorticoid therapy
o If you see signs of infection, yellow eyes, mouth ulcers, bleeding, SOB—report immediately

Chapter 73 Drug Therapy of Rheumatoid Arthritis

· Review the classification of antiarthritic drugs – include side effects

o NSAIDs
 Rapid relief of symptoms and safer
 Does not prevent joint damage or slow disease progression
o Glucocorticoids
 Although effective, long term, therapy causes toxicity
o DMARDs (disease-modifying antirheumatic drugs)
  Nonbiologic DMARDs
 Biologic DMARDs
 Decrease progression of RA
· Review Methotrexate, therapeutic use, important lab values to monitor and why?
o Most rapid-acting DMARD; nonbiologic
o Therapeutic uses: immunosuppression s/t reducing the activity of B and T lymphocytes
o Adverse effects:
 Hepatic fibrosis
 Bone marrow suppression
 GI Ulcers
 Pneumonitis (inflam of lung)
 Can cause fetal death and congenital abnormalities
o Monitor labs:
 Platelet count--> thrombocytopenia
 WBC--> leukopenia
 Hematocrit and Hemoglobin --> Anemia
 Lier enzymes (ALT + AST) --> elevated
· What is the priority of treatment and patient teaching when a patient is receiving both methotrexate as well as a
glucocorticoid?
o Make sure the patient is aware that both medications suppress immune system function so patient
should be aware of risk of infection

Chapter 74 Drug Therapy of Gout

· Review gout and what contributes to development of gout

o Gout: recurrent inflammatory disorder characterized by hyperuricemia and joint pain (esp. in big toe
because it’s cold), usually seen in men
 Caused by excess in production of uric acid or impaired excretion of uric acid
o Key point of inflammatory process: crystallization of sodium urate in synovial space and large gritty
deposits, tophi, form in effected joint or it may cause renal damage (kidney stones)
· Review first-line therapy for gouty flare-up
o NSAIDs (1st choice) -- Naprosyn, indomethacin, voltaren
 Better toleration and more predictable side effects
 Anti-inflammatory
 Used to treat short-term Acute Gouty Attacks (<3 times per year)
 Marked relief within 24 hours and swelling subsides over few days
 Adverse effects: GI ulcer, impaired renal function, fluid retention, inc. Risk for cardiovasc.
Problems
o Glucocorticoids—Prednisone + triamcinolone
 Can be used to treat acute gouty attacks
 Avoid using in patients prone to hyperglycemia
 Used when patients are hypersensitive to NSAIDS or contraindicated for use
· Review Allopurinol and how it works and patient education
o Mechanism of action: inhibits xanthine oxidase, which is required for uric acid formation--> reduce
blood levels of uric acid
 o Oral dosing, eliminated via renal excretion, prolonged half-life (25 hours), once-a-day dosing is adequate
o Lack analgesic/anti-inflammatory effects (not for Acute attacks)
o Therapeutic uses
 Drug of choice for CHRONIC gout (prevent tophi formation and tophi regression s/t reducing uric
acid levels)
 Can be used for treating hyperuricemia s/t cancer chemotherapy (must be administered before
chemotherapy starts)
o Adverse effects
 Fatal hypersensitivity syndrome (rare)-- rash, fever, eosinophilia, liver/kidney dysfunction
 Stop medication immediately if rash occurs
 GI upset—n/v/d, abdominal discomfort
 Neurological effects—drowsiness, headache, metallic taste
 Cataracts with prolonged use
 Drug accumulation risk with patient with renal impairment
o Patient Teaching
 Initial therapy may cause an acute gouty attack within the 1 st month of use. This can be
prevented by giving low-dose NSAID or colchicine.
 Drink water for kidney preservation (2L)

Chapter 20 Intro to CNS

 Review blood brain barrier and how it works

o BBB—keeps harmful AND therapeutic substances out
o Only lipid soluble drugs can pass through BBB
o Protein bound drugs and highly ionized drugs cannot pass
o BBB not developed at birth, infants more sensitive
 Review how tolerance and physical dependence works
o Tolerance: decreased response over time; need higher dose
 CNS can adapt to prolonged drug exposure
 Certain drugs used in psychiatry must be taken for several weeks before full therapeutic
effect effects develop
 Beneficial responses may be delayed because they result from adaptive changes and to
the direct effects of the drug
 Full CNS effects not seen until CNS has had time to modify itself in response to
prolonged drug exposure
o Physical dependence: withdrawal syndrome if stopped abruptly

Chapter 21 Drugs for Parkinson’s Disease

 Identify the initial drug of choice for treatment of Parkinson's and what symptoms are corrected
o Levodopa
o Highly effective but benefits diminish over time (2 years fully effective, end of 5 years symptoms may
return to pre-medicated levels)
o Converted to dopamine in brain by decarboxylase enzyme (can cross BBB!)
o Helps restore active balance between dopamine and ACh
o Levodopa patient education
 Do not take medication with high protein meals
  Spread your protein intake out over the whole day – do not eat a lot at once
 Do not take anticholinergics with this medication (dyskinesia can occur)
 Review the loss of drug effect and how it is treated/correct --> “acute loss of effect syndrome”
o Gradual loss— “wearing off”—develops near the end of the dosing interval and indicates that drug levels
have declined to a subtherapeutic value
o Wearing off can be minimized in three ways:
 Shortening the dosing interval
 Giving a drug that prolongs levodopa’s plasma half-life (for example, entacapone)
 Giving a direct-acting dopamine agonist
 Review patient education related to drug treatment of levodopa/carbidopa Identify how levodopa/carbidopa
improves patient’s condition
o Carbidopa enhances levodopa effects
 Has no effect on its own
o Prevents decarboxylation of levodopa in intestine/peripheral tissues (more available to the brain)
 Ex: 10% left for brain after body metabolism vs 2% left without carbidopa
 Prevents conversion to dopamine in tissues = more available to brain
o Carbidopa cannot cross BBB
 No effect on decarboxylation in brain
o Drug interaction: Combination more effective than levodopa alone
o Levodopa dose can be lower (decreasing side effects)
o Disadvantages
 Carbidopa has no adverse effects on its own
 Abnormal movements and psychiatric disturbances can occur sooner
 Review carbidopa and how it works in the body and its effect on the brain – what its function when combined
with levodopa How does entacapone work (mechanism of action), and when is it used?
o Entacapone
 Selective and reversible inhibitor of COMT
 Indicated for use with levodopa
 Inhibits metabolism of levodopa in the intestines and the peripheral tissues
 Prolongs time that levodopa is available to the brain
 Stops metabolism in periphery
 Increases levodopa availability by inhibiting COMT, which decreases the production of levodopa
metabolites that compete with levodopa for transport

Chapter 22 Drugs for Alzheimer’s Disease

 Review cholinesterase inhibitors used in early diagnosis of AD, what drugs should be avoided when patient is
taking cholinesterase inhibitors and outline the patient education
o Indicated for mild to moderate AD
o Prevent breakdown of acetylcholine
 Elevate Ach concentration in cerebral cortex
o May help to slow progression of disease
o Only three drugs are recommended for use and have equivalent benefits:
 Donepezil
 Galantamine
 Rivastigmine
 o Do not mix cholinesterase drug therapy with:
 Drugs that block cholinergic receptors
 First-generation antihistamines
 Tricyclic antidepressants
 Conventional antipsychotics
 Because they can reduce an individual’s responses to cholinesterase inhibitors
 Review side effects of cholinesterase inhibitors highlighting the concerning side effects
o Cholinergic side effects
o Gastrointestinal effects (common)
o Dizziness
o Headache
o Bronchoconstriction
 Review memantine outline, how it works (mechanism of action), indication of use, effects on the receptors, and
the side effects
o Blocks neuronal receptors for N-methyl-d-aspartate
o MMDA receptor blocker
o Should be given without food but with small meals to reduce GI problems
o Better tolerated than cholinesterase inhibitors
o May be on psych medications while on this drug
o Adverse effects
 Dizziness
 Headache
 Confusion
 Constipation

Chapter 24 Drugs for Seizure Disorder

 Review priority nursing actions in management of status epilepticus

o Maintain ventilation, correct hypoglycemia, and terminate the seizure
o Establish IV to draw blood for analysis of glucose levels, electrolyte levels, and drug levels
 Line also used to administer glucose and AEDs
o Lorazepam (a benzodiazepine) is recommended for first-line management, terminate the seizure
 Effects can last up to 72 hours, 4mg IV at 2mg/min
o Once seizures controlled- phenytoin given for long-term suppression
 If patient cannot take hydantoin AEDs, valproic acid to be used
 Review patient education related to phenytoin and valproic acid also review the side effects
o Phenytoin
 Side/adverse effects: nystagmus, sedations, ataxia, diplopia, cognitive impairment, gingival
hyperplasia, skin rash, teratogenic effects, cardiovascular: decreased automaticity, increased AV
conduction, hypotension, dysrhythmias
 Patient education: take exactly as prescribed and w/ food to decrease gastric discomfort, may
need to switch to different birth control method, no alcohol consumption, awareness of
depressant effects, stopping the medication abruptly can cause rebound seizures, good oral
hygiene to prevent gum irritation, inform the health care provider of adverse reactions, patients
with diabetes to monitor serum glucose levels more closely than usual, blood levels will need to
be monitored on a regular basis
 o Valproic acid
 Side/adverse effects: nausea, vomiting, indigestion, hepatotoxicity-liver failure, pancreatitis,
teratogenic effects
 Patient education: awareness of depressant effects, no drug-drug interactions, take with food to
decrease GI disturbances, importance of taking the medication as directed, do not crush or
chew tablets and capsules, call provider if noticing signs of liver injury (jaundice, malaise) or
pancreatitis (abdominal pain, nausea, vomiting)
 Review drug-drug and drug-food interactions of phenytoin, valproic acid and Tegretol
o Phenytoin:
 Decreases the effects of oral contraceptives, warfarin, and glucocorticoids- due to induction of
hepatic drug-metabolizing enzymes
 Increased level of phenytoin in blood if combined with diazepam, isoniazid, cimetidine, and
alcohol (acute use) by reducing the metabolism rate of phenytoin
 Valproic acid elevates free phenytoin by displacing phenytoin from binding sites on
protein
 Decreased level of phenytoin in blood if combined with carbamazepine, phenobarbital, and
alcohol (chronic use) since they accelerate metabolism
 CNS depressants (alcohol, barbiturates) will add to depressant effects of phenytoin
o Valproic acid:
 Increased levels of phenobarbital and phenytoin
 ASA, NSAIDS, and warfarin lead to increased risk of bleeding
 CNS depressants have an additive effect
o Tegretol (carbamazepine)
 Accelerates inactivation of oral contraceptives and warfarin since it induces hepatic drug-
metabolizing enzymes
 Phenytoin and phenobarbital have same effect on liver enzymes, accelerated
metabolism decreases effects
 Grapefruit juice: can inhibit metabolism, causes plasma levels to rise, increases peak and
trough levels by 40%
 Review how antiepileptic drugs work and how to monitor the effectiveness of the drug
o Hydantoins, carbamazepine, and valproic acid: suppress sodium influx, drug binds to sodium channel
when it is inactivated, prolongs the channel in activation , preventing neuron firing
o Valproic acid and succinimides: suppress the calcium influx, prevents electric current generated by
calcium ions to T-type calcium channel
o Benzodiazepines, barbiturates, valproic acid: increase action of gamma-aminobutyric acid (GABA) which
inhibits NT throughout the brain
o Monitoring Effectiveness
 Monitor closely for signs and symptoms of seizure activity, depression, suicidal tendencies, and
unusual behavior
 Monitor CBC with differential, renal function, liver function test, and (BP)
 Observe frequently for recurrence of seizure activity. Assess for clinical improvement (decrease
in intensity/frequency of seizures).

Chapter 70 Antihistamines
  Understand the role of histamine? What causes its release and where is it stored?
o Dilates small blood vessels, increases capillary permeability, constriction of smooth muscle in bronchi,
stimulates secretion of acid in stomach, acts as a neurotransmitter in the CNS
o Release is prompted by
 Allergic mechanism- presence of allergen in body, cascade promotes release
 Nonallergic mechanism- certain drugs, radiocontrast media, plasma expanders, etc act directly
on mast cells to trigger release
o Located in practically all tissues, especially high levels in skin, lungs, GI tract
 Review patient education and who should avoid taking antihistamine
o Patient education: take w/ food to avoid GI upset, do not crush or chew enteric-coated preparations, be
aware of sedative effects- no driving or hazardous activity, use hard sugarless candy and sips of liquid to
reduce dry mouth, no drinking alcohol
o Contraindications: children younger than 2 years old due to risk of fatal respiratory depression
 Review serious side effects of antihistamine
o Sedation, dizziness, incoordination, confusion, fatigue, nausea, vomiting, loss of appetite, diarrhea,
constipation, anticholinergic effects (SNS symptoms) like dry mucous membranes, urinary hesitancy,
palpitations, IV- extravasation
 Review the differences between H1 & H2 receptors are found and what are the effects of each one when
stimulated
o H1 receptors: vasodilation, increased capillary permeability, bronchoconstriction, modulation of
neurotransmitter release, produces itching and pain, secretion of mucus, found in CNS organs
o H2 receptors: secretion of gastric acid, found in stomach
 Review the therapeutic use of H1 & H2 blockers
o H1 blockers: mild allergy, severe allergy, motion sickness, insomnia, common cold,
o H2 blockers: treat and prevent return of duodenal ulcers
 Review first and second generation H1 blockers
o First generation: varying levels of CNS depression, significant anticholinergic properties- dry mouth,
urinary hesitancy
o Second generation: less sedation, cross BBB poorly, devoid of anticholinergic actions, OTC
 List signs and symptoms of H1 blocker toxicity and the appropriate treatment
o Similar to atropine poisoning- dilated pupils. Flushed face, hyperpyrexia, tachycardia, dry mouth, urinary
retention
o No specific antidote, treatment directed at drug removal and managing symptoms, minimize absorption
by giving activated charcoal, then a cathartic to speed up export from GI, treat convulsions w/ IV
benzodiazepines, reduce hyperthermia w/ ice packs

Chapter 76 Drugs for Asthma and Chronic Obstructive Pulmonary

 Review pathophysiology of asthma, chronic bronchitis, and emphysema, include causes and signs/ symptoms
o Asthma: chronic inflammatory disorder of airways, immune response triggered by allergen,
bronchoconstriction, infiltration and activation of inflammatory cells, airway inflammation accompanied
by edema, mucus plugging, and smooth muscle hypertrophy
o Chronic bronchitis: type of COPD, chronic cough and excessive sputum production, from hypertrophy of
mucus-secreting glands in large airways, bronchial edema, increased mucus secretions
o Emphysema: type of COPD, enlargement of air space within bronchioles and alveoli brought on by
deterioration of walls of air spaces, decrease in elastic recoil of alveolar walls
  Review two major drug classes used to treat asthma and COPD (Chronic Obstructive Pulmonary Disorder)
o Anti-inflammatory agents: glucocorticoids, administered on fixed schedule by inhalation for
chronic/stable conditions
o Bronchodilators: beta2 agonists, administered on fixed schedule for long term control or PRN to manage
an acute attack, usually inhaled
 Review drug therapy for acute management (short-term) and maintenance therapy (long-term) for asthma and
COPD
o Acute management: short-acting beta2 agonists, act promptly to reverse bronchoconstriction and
provide rapid relief from cough, chest tightness, wheezing, albuterol
o Maintenance therapy: inhaled glucocorticoids, regular dosing, reduce frequency and severity of attacks,
less need for quick relief medications
o COPD: anticholinergics
o Asthma: leukotriene modifiers
 Identify benefits of drugs taken in inhalation verses taken orally
o Inhaled drugs: result in less bone density loss, less growth suppression, localized effects, not systemic
effects= fewer side effects

Chapter 77 Drugs for Allergic Rhinitis, Cough, and Colds

 Review pathophysiology and clinical signs/symptoms of allergic rhinitis

o Inflammatory disorder affecting upper airway, sneezing, rhinorrhea, pruritus, nasal congestion, caused
by dilation and increased permeability of nasal blood vessels, conjunctivitis, sinusitis, asthma, symptoms
triggered by airborne allergens
 Review three classes of drug therapy for allergic rhinitis, how they work and which class is first line drug?
o Glucocorticoids: intranasal, most effective drugs for prevention and treatment of seasonal and perennial
rhinitis, prevent or suppress major symptoms- congestion, rhinorrhea, sneezing, nasal itching, erythema,
suppress immune response
o Antihistamines: oral, H1 receptor antagonists, most effective when taken as prevention, can relieve
sneezing, rhinorrhea, nasal itching, prevent blood vessel dilation and bronchoconstriction
o Sympathomimetics: reduce nasal congestion by activating alpha1 adrenergic receptors on nasal blood
vessels, vasoconstriction causes shrinkage of swollen membranes and nasal drainage
 List the benefits and drawbacks of drugs given orally or via nasal route
o Nasal route: most effective, systemic absorption can cause drowsiness, nosebleeds, headaches, bad
taste, drying of nasal mucosa, burning/itching, sore throat, nose bleed, systemic effects rare, can't blow
nose after, simple administration, at site of action
o Oral route: systemic effects, first pass effect, decreased half life, not localized
 Review mechanism of action and side effects of antitussives, mucolytics and expectorants
o Antitussives: suppress cough, opioid class: act in the CNS to elevate cough threshold, nonopioid class:
acts in CNS, does no produce opioid euphoria or physical dependence, reduce pain, unclear mechanism
o Mucolytics: reacts directly with mucus to make it less viscous, makes cough more productive, can trigger
bronchospasm, smells like rotten eggs
o Expectorants: renders cough more productive by stimulating flow of respiratory tract secretions,
2/25 - Week 6

Chapter 78 Drugs for Peptic Ulcer Disease

 Review the two most common causes of PUD

o Helicobacter pylori infection
 Gram-negative bacillus that colonizes stomach and duodenum (in between epithelial cells +
mucus barrier)
 Can remain in GI tract for decades
 Mechanism that makes ulcers is unknown, but some possibilities are...
 Enzymatic degradation of mucus layer
 Cytotoxin that injures mucosal cells
 Infiltration of neutrophils + other inflammatory cells
 Production of urease
o Long-term use of NSAIDs (+ high doses)
 Inhibit biosynthesis of prostaglandins
 Decrease submucosal blood flow
 Suppress secretion of mucus + bicarb
 Promote secretion of gastric acid
 Irritate mucosa directly
o Can both weaken defenses including
 Mucus secretion, bicarbonate secretion (neutralize H+), blood flow to mucosa, prostaglandins
 Describe the rational for combined drug therapy to treat H-Pylori and what drugs are used and how they work
o Antibiotics (clarithromycin, amoxicillin, bismuth, metronidazole, tetracycline)
 None are effective alone – risk of developing resistance increases
o Clarithromycin
 Suppresses growth of H. pylori by inhibiting protein synthesis
 Rate of resistance is rising
 Side effects: nausea, diarrhea, taste distortion
o Amoxicillin
 Disrupts cell wall of H. pylori
 Works best in neutral pH (use with antisecretory agent)
 Rate of resistance low
 Side effects: diarrhea
o Bismuth
 Disrupt cell wall of H. pylori --> lysis + cell death
 Inhibit urease activity to prevent bacteria from sticking to GI surface
 Side effects: black colored tongue / stool (harmless); long-term use risk of neurologic injury
o Metronidazole (and Tinidazole)
 Almost half of strains are resistant
 Side effects: nausea + HA
 Avoid alcohol, do not take in pregnancy
o Tetracycline
 Inhibits protein synthesis in bacteria
  Resistance is rare
 Side effects: can stain developing teeth
 Avoid in pregnancy/young children
 Review nonpharmacological treatments for PUD
o Diet: 5-6 small meals / day instead of big ones can help in healing (reduce flux in acid levels)
 No ‘ulcer diet’ accelerates healing
o Avoid smoking
o Avoid NSAIDs (aspirin!!)
 Exception: use of Aspirin in cardiovasc disease prevention
o Reduce stress + anxiety
o May need to avoid alcohol if they notice a relationship to worse S/S
 Review patient education related to H2 blockers, PPI, Antacid (TUMS)
o H2 blockers – first choice in treatment
 Promotes healing by suppressing gastric acid secretion
 4 drugs equally effective – Ranitidine, Famotidine, Cimetidine, Nizatidine
 Serious side effects uncommon
 BUT using this in conjunction w/ PPIs = kidney damage
o Proton Pump Inhibitors – best to suppress GA secretion
 Used for gastric/duodenal ulcers, GERD, GI bleed + erosive esophagitis
 Acts directly on proton pump (inhibit release of H+ that forms acid)
 Can increase risk of serious adverse events (fracture, pneumonia, acid rebound) (HA, GI effects)
 Deplete magnesium – advise them to eat Mg rich foods
 Omeprazole, Esomeprazole, Lansoprazole, Pantoprazole
o Antacid
 Neutralize acid – react w/ GA to make neutral salts/salts of low acidity
 Adverse effects: constipation (Ca, Al), diarrhea (Mg)
 Use with caution in pts with renal impairment
 Review dietary recommendations for individuals taking PPI (Omeprazole)
o Take on an empty stomach
o Sensible to not eat foods that ‘overstimulate’ GA secretion after taking it (or in general) - spicy/fatty
foods, pop, alcohol, coffee

Chapter 79 Laxatives

 Define a cathartic effect versus a laxative effect

o Cathartic effect
 A fluid evacuation of the bowel
 Relatively fast and intense
 Watery and unformed
o Laxative effect
 Production of a soft, formed stool over a period of 1 or more days
 Slower and relatively mild
 Review the action and side effects of commonly used bowel preps
o Sodium Phosphate
 Hypertonic with body fluids
 Mechanism of action: osmotic laxative that brings water into intestinal lumen --> softens and
swells the fecal mass, which stretches the wall to stimulate peristalsis
 Swallow with large amount of water
  Side Effects: nausea, bloating, abd. Discomfort
 Adverse effects: dehydration and electrolyte disturbances, possible renal damage
o Polyethylene glycol (PEG) + electrolytes (ELS)
 Isotonic with body fluids
 Requires ingestion of large volume of bad-tasting liquid
 Combination of sodium picosulfate (stimulant laxative) + magnesium oxide /citric acid (osmotic
laxative)
 Used in individuals w/ kidney disease to avoid further kidney damage
o CoLyte, GoLYTELY
 HUGE VOL administered (4L)
 Patients must ingest 250-300mL every 10 minutes for 2-3 hours.
 With HalfLytely and MoviPrep = ½ of volume
 Adverse effects: bloating, nausea, abdominal discomfort
 Not frequently used
 Identify 3 contraindications to laxative use
1. Abdominal pain, nausea, cramps; s/s of appendicitis, regional enteritis, diverticulitis, ulcerative colitis
2. Acute surgical abdomen
3. Fecal impaction or bowel obstruction—b/c inc. Peristalsis could cause bowel perforation
4. Habitual use—Laxative Abuse (dec. Defactory reflexes = more reliance on laxatives, electrolyte
imbalance, dehydration, colitis)
5. Use with caution in pregnancy (could induce labor) and lactation (laxative excrete with breast milk)
 Review which laxative commonly used to promote the excretion of ammonia
o Lactulose
 Metabolized to lactic acid, formic acid, an acetic acid--> exert osmotic action to produce a soft
formed stool in 1-3 days
 More expensive than other laxatives
 More unpleasant side effects (flatulence and cramping)
 Inc excretion of ammonia!
 Benefits: lowers blood ammonia content in pts with portal HTN + Hepatic
encephalopathy s/t chronic liver disease (disease causes pH change that retains ammonia)

Chapter 80 Other Gastrointestinal Drugs

 Review the clinical indications and beneficial effects of Ondansetron (Zofran)

o Used to treat chemotherapy induced nausea and vomiting, prevent nausea and vomiting associated with
radiotherapy and anesthesia
o Used off-label to treat nausea and vomiting from childhood viral gastritis and morning sickness from
pregnancy
 Identify the side effects of Ondansetron including the important life-threatening side effect
o Headache, diarrhea, dizziness
o Prolonged QT interval- risk of torsades de pointes
 Describe the clinical indications and beneficial effects of Metoclopramide
o IV administration: can suppress postoperative nausea and vomiting, as well as emesis caused by
anticancer drugs, opioids, toxins, and radiation therapy
o Increases upper GI motility (enhances action of acetylcholine) in the case of diabetic gastroparesis
o Used for suppression of gastroesophageal reflux
o IV administration: suppress post-op nausea + vomiting, suppression of CINV, facilitation of small bowel
intubation, facilitation of radiologic examination of GI tract
 o Off-label uses: hiccups, nausea + vomiting of early pregnancy

Chapter 57 Drugs for Diabetes Mellitus

 Review the importance of monitoring Hg A1C, including normal level / abnormal values and what Hg A1C is
reflecting.
o Importance of monitoring Hg A1C:
 Normal levels: 4-6.5
 Abnormal levels: 6.5+ = diabetes diagnostic
 What it reflects: average plasma glucose for the previous 2-3 months
 Monitor to see how well controlled blood glucose has been
 Review the following insulins, include therapeutic use, onset of action, patient education, dose frequency and
when should they be administered (dosing frequency & special consideration related to time of administration)
o Regular: (SA)
 Therapeutic use: used to combat DKA
 Onset of action: 30-60m
 Patient education:
 Dose frequency: duration up to 10h
 Time of admin:
o NPH: (ID)
 Therapeutic use: provide glycemic control between meals / during night
 Onset of action: 60-120 m
 Patient education:
 Must mix before drawing up (roll btwn palms to mix) – only cloudy solution
 Only administer subQ
 If mixing with SA, draw that up first then this
o Can be mixed with: Regular, Aspart, Glulisine
 Dose frequency: 2/3x a day
 Time of admin:
o Glargine (LD)
 Therapeutic use:
 Onset of action: 70m
 Patient education:
 Cannot be mixed, cannot be given IV
 Less risk of hypo/hyperglycemia - constant, has no peak
 Dose frequency: once daily; duration up to 24h
 Time of admin: daily at the same time
 Normally at bedtime
o Levemir:
 Therapeutic use:
  Onset of action:
 Patient education:
 Dose frequency:
 Time of admin:
o Insulin Lispro/Humalog: (RA)
 Therapeutic use: acts fast to increase insulin levels and stimulate glucose uptake
 Use with long-acting insulin for T1 DM
 Onset of action: 15-30 minutes post-injection subQ
 Patient education:
 Usual route subQ injection / use of insulin pump
 Shorter duration of action than regular insulin
 Dose frequency: duration 3-6h
 Time of admin: 5-10 m before meals
o General Teaching / Pt Education:
 All but NPH are solutions + ready to use
 Mixing: double check that you can, draw up short acting first, then NPH
 Storage:
 In unopened, store in fridge
 Opened in fridge = good for 3mo
 Opened room temp = good for 1mo
 Teach what it looks like + to dispose if it looks abnormal
 Review the oral antidiabetics focusing on mechanism of action, the serious adverse effects, and patient education
o *all used in conjunction with lifestyle changes
o Biguanides: Metformin
 Mechanism of action:
 Inhibits glucose production from liver
 Slows absorption of glucose from intestines
 Sensitizes insulin receptors in fat + muscle --> increases glucose uptake
 Adverse effects:
 Anorexia, N/D
 Toxic dose – lactic acidosis – rare + fatal – concern in renal failure pts
 Patient education:
 Alcohol can increase risk of lactic acidosis
 May be combines with sulfonylureas
 Bonus info:
 Drug of choice for T2DM in step 1 (w/diet/exercise)
 Low risk of hypoglycemic (doesn’t stimulate release from pancreas)
 Prevention / treatment of T2 + gestational
o Sulfonylureas: Glipizide, glyburide, glimepiride
 Mechanism of action:
 Stimulates release of insulin from pancreatic islets – beta cells
 Long term use: may increase insulin receptor sensitivity
 Adverse effects:
 Hypoglycemia – increased risk in pts with liver/kidney damage
 Weight gain
 Patient education:
 Do not use during pregnancy
  Do not use if you have sulfa allergy
o Thiazolidinediones (aka Glitazones or TZDs): Pioglitazone (Actos)
 Mechanism of action:
 Decreases insulin resistance
 Increases response of cells to insulin
 May decrease glucose production in liver
 Adverse effects:
 Well tolerated
 Upper respiratory infections, HA, sinusitis, myalgia, fluid retention
 Patient education:
 Do not use in severe HF / liver failure / with bladder CA

Chapter 58 Drugs for Thyroid Disorders

 Review the difference between the signs and symptoms & diagnostic test for hypo & hyperthyroidism
 Review the commonly used medications for both hypo/hyperthyroidism and what are important drug admin
considerations. Also review the side effects of these medications