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NURS 6521 Midterm Exam Study-100% Verified -
- 100-question Exam which will assess your knowledge on the Learning Resources from Weeks 1-6.
- Time limit of 2 hours.
- Multiple choice or multiple selection.
Pharmacodynamics: how the drug effects the body
Pharmacokinetics: how the body effects the drug
❒ Understand the implications of changing renal function on creatinine & drug dosing.
Kidney/Renal functions :
- Filters blood = Remove Waste, Toxins, and Extra Fluid from the body
- Returns needed substances to the blood – & the remainder becomes urine
- Removes acid produced by cells of the body to maintain balanced water, salts; minerals
- Makes hormones that control BP, make RBCs; keeps bones strong
Creatinine : Measures kidney function - byproduct of muscle metabolism (creatinine phosphate)
Normal Serum Creatinine levels: 0.6-1.3 mg/dL - healthy kidney (Easily filters & excretes creatinine)
More Reliable than BUN. Creatinine is Not Absorbed by the kidneys.
Rises indicate renal damage or failure = Kidney is unable to properly filter & excrete waste (creatinine) = Lab
Value rises in the serum.
Creatinine = Kidney Function = Requires a decreased dose of medication or different dosing schedule
= Renal Dosing
❒ What is the impact of the following on drug levels and dosing:
➢ Cirrhosis : a disease in which normal liver cells are replaced by scar tissue.
As liver cells die, the organ makes less of the proteins that regulate fluid retention & blood clotting
and the liver loses its ability to metabolize the pigment bilirubin.
Liver/Hepatic functions :
- Produces proteins that help clot blood
- Removes / neutralizes poisons, drugs and alcohol
- Manufactures bile that helps the body absorb fats & cholesterol
- Helps maintain normal blood sugar levels
- Regulates hormones
With Cirrhosis - the liver fails to detoxify the blood & it becomes less able to metabolize medications , which
magnifies their effects. Eventually toxins build up in the brain & can produce:
- Increased sensitivity to drugs
- Levels of medication will be higher d/t decreased metabolism
- Requires decreased dose of medication
Liver/Hepatic Function = Ability to metabolize medication = Requires a decreased dose of
medication or different dosing schedule = Hepatic Dosing
- No matter what the amount of drug in the body may be, half (50%) will leave during a specified time period
(the half-life).
- The actual amount of drug that is lost during one half-life depends on just how much drug is present: the
more drug in the body, the larger the amount lost during 1 half-life.
Routes of Administration and Dosage Forms:
❒ Understand when it is OK to crush (or not crush) certain dosage forms & why.
▪ OK to Crush : Immediate Release
▪ Not OK to Crush : Sustained Release/ Enteric Coated
- Immediate Release : Rapid absorption of a drug after ingestion ( < 30 minutes )
- Extended-Release : Released over a period of time ( 8, 12, 24 hours)
o Sustained Release : Maintains drug release over a sustained period but not at a constant rate
o Controlled Release : Maintains drug release over a sustained period at a nearly constant rate
*prolongs actions but also attempt to maintain therapeutic drug levels
- Delayed Release : Releases the dose after a set time. Usually enteric coated to prevent release in the
stomach – it releases the dose in the intestinal track.
❒ Which Routes of administration have the fastest and slowest rates of absorption?
o Fastest to Slowest: IV, IM, SC, Oral
o IV, Inhaling, Snorting, Smoking, Swallowing, Rectal
o IV, IM, Intranasal, Intradermal, Subcutaneous, Oral, Rectal
Oral forms: Time until a pill/capsule is broken down enough to release the medication in the stomach:
Crushed/Chewed Tablet = under 10 mins
Chalk tablet = 10 mins & Solid tablet = 10
mins Time-release capsule = 45 minutes
Gel capsule = > 60 mins
ENTERAL ROUTE : to the GI/ Intestinal Tract
- Oral : By Mouth: PO: Easiest & most economical way. Avoid if pt is lethargic, has N/V, or unable
to swallow/NPO [Involves 1
st
pass effect – decreasing concentration rapidly before hits target]
- Sublingual : Under Tongue to dissolve. Absorbed through the mucous membranes of the gums, Not to
be Swallowed. No water until dissolved fully.
- Buccal : Between the gum and cheek. Rotate sides to avoid irritation.
- Rectal : Suppository or Enema: When unable to take oral meds. Avoids about 2/.3 of first-
pass metabolism.
- Tubes : NG/Duodenal/G-Tubes: Meds needs to be crushed, so confirm orders!
MUCOUS MEMBRANE ROUTE:
- Transdermal : Patch: Through the skin. Left for extended time, Extended release meds are used
for longer effect.
- Drops/Sprays : Via Eyes, Nose, or ears. Absorbed through Mucous Membranes, Can Cause
Systemic Effects. Confirm # of drops/sprays to be administered.
- Vaginal : Can cause irritation to the mucous membranes.
TOPICAL ROUTE:
- Eye/ Nasal Mucosa/ Skin : Usually less lipophilic to reduce systemic absorption.
INHALATION ROUTE:
- Inhaler : Absorption can be Very Rapid & Complete. System or Local.
Pulmonary alveoli represent a large surface w/ minimal barrier to
diffusion. Rapid relief of Respiratory problems, or for anesthesia.
Enters directly into bloodstream & can cause SEVERE Systemic Side Effects.
PARENTERAL ROUTE : Does Not involve drub absorption via the GI Tract
- IV : Most reliable method to the systemic circulation. Bypasses many absorption barriers.
Bioavailability of drugs is 100%. Delivered directly into vascular space.
- IM : Absorption depends on muscle blood flow.
▪ [Depot IM: slowly releases drug at site of injection]
- SC or SQ : For drugs with low bioavailability (ex. Insulin)
- Transdermal : Drug must be highly lipophilic. Slow absorption but long-lasting effects
❒ Know the relative onset, monitoring and appropriate use of various dosage forms:
▪ Sublingual tablets : ( Nitro/Subox ): Immediate Systemic Onset : 1-5 Mins Peak : 10 Mins
▪ (Capsule/Tab/Liquid) ORAL : VARY! Onset : 20 Mins- 1 Hr Peak : 30 Mins- 1 Hr Duration : 4-6 Hrs
▪ Patches :
Rivastigmine : (Alzheimer’s): Onset : 30-60 Mins Peak : 8-16 Hrs after 1
st
dose Duration : 10 Hrs
Fentanyl : Onset : Unknown/ Within 24 Hrs Peak : 20-72 Hrs Duration : 72 Hrs
▪ Suppositories : ( Acetaminophen ): Onset : 1 Hr Peak : Duration : 2-4 Hrs
▪ Elixir - Active ingredients are mixed with liquid – syrup or alcohol (concentrated)
▪ Suspension – Med is mixed with liquid – water - it can’t dissolve = remains intact (SHAKE)
Therapeutics: Gastrointestinal, Cardiac, Respiratory, Pscyh,
Neurology, Musculoskeletal
Specific: treat the underlying cause of diarrhea. (anti-infective drugs & drugs to correct
malabsorption syndromes.
Nonspecific: agents that act on or within the bowel to provide symptomatic relief; these drugs do not influence
the underlying cause.
Opioids : activate the opioid receptors in the GI tract to decrease intestinal motility & slow intestinal
transit = allows more time of absorption of fluids and electrolytes. Decreases secretion of fluid into the small
intestine & increases absorption of fluid and salt. = present the large intestine with less water = fluid &
volume of stools are reduced & defecation frequency is decreased.
*Diphenoxylate HCl w/ atropine sulfate (Lomotil) [atropine present to discourage abuse - would cause unpleasant S/Es]
-May require four times daily dosing
*Loperamide (Imodium)
o mechanism of action : slows the passage of stool through the intestines/ Suppresses bowel motility
& fluid secretion into the intestinal lumen.
*GERD: Reflux esophagitis is an inflammatory condition caused by reflux of gastric contents back into the
esophagus. Cimetidine is a drug of choice for relieving symptoms but does little to hasten healing.
Antibiotics: to eradicate H pylori
Antisecretory agents:
H2 receptor antagonists:
Cimetidine [Tagamet]: 1
st
H2RA.
o
mechanism of action: Blocks H 2
receptors = reduces volume of gastric juice & its hydrogen ion
concentration. Suppresses basal acid secretion & secretion stimulated by gastrin and
acetylcholine. Cannot suppress symptoms of allergy.
o
side effects: Low and usually benign. Binds to androgen receptors, producing receptor blockade = can
cause gynecomastia, reduced libido, and impotence—all reverse when med stops. CNS: if older w/
renal/hepatic impairment: Confusion, hallucinations, CNS depression/excitation. Pneu d/t elevated gastric pH
o
appropriate use: Ulcers or GERD
o
contraindications/ cautions: Renal impairment requires reduced dose. Cimetidine inhibits hepatic drug-
metabolizing enzymes and can cause levels of many other drugs to rise. Avoid Antacids within 1 Hr.
Famotidine ]Pepcid]
Nizatidine [Axid]
*Ranitidine [Zantac] : Similar to Cimetidine but is more potent, produces fewer adverse effects, and causes fewer
drug interactions.
o
mechanism of action: Suppress acid secretion by blocking H2 receptors on parietal cells. Does not
block H1 receptors and hence does not reduce symptoms of allergy.
o
side effects: Uncommon. But could cause Headache. Penetrates BBB poorly, Rare CNS
effects. Elevated gastric pH risk for Pneu.
o
appropriate use: Ulcers or GERD
o
contraindications/ cautions: Not for use w/ renal impairment. Wait 2 hours before taking an antacid.
*PPIs: Suppress acid secretion by inhibiting H+, K+-ATPase (proton pump), enzyme that makes gastric acid.
Acid suppression is greater than with H2Ras w/ minimal side effects.
Dexlansoprazole [Dexilant]
Esomeprazole [Nexium]
Lansoprazole [Prevacid]
*Omeprazole [Prilosec]: 1
st
PPI available. Prodrug that undergoes conversion to active form within parietal cells
of stomach.
Pantoprazole [Protonix]
Raberprazole [Aciphex]
o
mechanism of action: Irreversible inhibition of proton pump – blocks final common pathway of gastric
production, can inhibit basal and stimulate avid release.
o
side effects: Minimal <1% : H/A, diarrhea, N/V
o
appropriate use: Short-term therapy for gastric/duodenal ulcers, esophagitis & GERD. Limit to 4-
wks. Long-term therapy for hypersecretory conditions (Zollinger-Ellison syndrome).
Used in ICU as prophylaxis against stress ulcers.
o
Contraindications/cautions: Risk for Pneu d/t altered upper GI flora & impaired WBC function for 1
st
few days of treatment, Risk for fracture w/ long-term use d/t decreased absorption of calcium
w/reduces acid secretion. *Maintain adequate calcium & Vit D with use.
▪ expected effects: reduces acid production 97% within 2 Hrs. Effects persist until new enzyme
is synthesized. 1 Hr half-life.
▪ appropriate use: TAKE 30 Mins before a meal (because they inhibit only actively
secreting proton pumps, and meals are the main stimulus of proton pump activity)
▪ Must be protected from stomach acid d/t it being acid labile! Capsule is enteric-coated -
Dissolves in the stomach but the granules remain intact until reaching the duodenum.
Mucosal protectant : Forms a barrier over the ulcer crater that protects against acid and pepsin
Sucralfate [Carafate, Sulcrate]
Antisecretory agent that enhances mucosal defense : Protects against NSAID-induced ulcers by stimulating
secretion of mucus & bicarbonate, maintaining submucosal blood flow, & suppressing secretion of gastric
acid
Mesoprostol [Cytotec]
Antacids: React with gastric acid to form neutral salts
Aluminum hydroxide, calcium carbonate, magnesium hydroxide
*Irritable bowel syndrome (IBS) : crampy abdominal pain or discomfort r/t diarrhea, constipation, or
both. Defined by presence, for at least 12 wks in the past yr, that cannot be explained by structural or
chemical abnormalities.
- Can use nonspecific drugs groups—antispasmodics (e.g., hyoscyamine, dicyclomine), bulk-forming
agents (e.g., psyllium, polycarbophil), antidiarrheals (e.g., loperamide), and tricyclic antidepressants
(TCAs)— to provide symptomatic relief.
Eluxadoline [Viberzi]: for IBS-D in men & women. A mu- and kappa-opioid receptor agonist. By
triggering these receptors, motility in the bowel is slowed.
Adverse reactions: constipation, nausea, and abd pain.
Lubiprostone [Amitiza]: for IBS-C in Women to reduce abdominal discomfort.
Causes selective activation of chloride channels in epithelial cells of the intestine
to
(1) promotes secretion of chloride-rich fluid into the intestinal lumen
(2) enhances motility of the small intestine and
colon. Take w/ food & water to reduce nausea.
*Alosetron [Lotronex] : Approved & Withdrawn in 2000 d/t GI toxicity & deaths /approved again
in 2002 with strict risk mgmt. program!
o
mechanism of action: causes selective blockade of 5-HT3 receptor (found on neurons that innervate
the viscera. Can decrease abdominal pain, increase colonic transit time, reduce intestinal secretions,
and increase absorption of water and sodium
o
Pharmacokinetics: Oral admin, rapid absorption, but incomplete (50-60%). Plasma levels peak after 1
Hr. Half-time is 1.5 Hrs.
o
side effects: constipation (29%), which can be complicated by impaction, bowel obstruction,
and perforation. Abdominal discomfort, pain, nausea.
o
appropriate use: Women with severe diarrhea-predominant IBS
o
contraindications/ cautions: Not for constipation. Bioavailability is decreased by food. Extensive
metabolism by hepatic cytochrome P450 enzymes, so drugs that interfere w/ these enzymes may alter
alosetron level. (e.g., carbamazepine, phenobarbital, cimetidine, quinolone antibiotics, ketoconazole,
clarithromycin, voriconazole, and protease inhibitors)
o
expected effects: Increase stool firmness & decrease fecal urgency & frequency
- Immunomodulators
o Infliximab [Remicade]: a monoclonal antibody for moderate to severe. IBD or RA. Reduces
symptoms and produces remission.
- Antibiotics
o Metronidazole [Flagyl]: long-term therapy required to avoid relapse. Peripheral neuropathy risk.
o Ciprofloxacin [Cipro]: for mild to moderate crohn’s. Often combined with Infliximab.
- Cough, cold, and sinus therapies:
Histamine :
Present is all tissue.
Synthesized & Stored in mast cells (skin , soft tissues) & basophils
(blood). Varying effects.
Release of Histamine is produced by allergic & nonallergic mechanisms.
[Histamine 1 stimulation]
Vascular System = Vasodilation - dilates small blood vessels (arterioles & venules)
Increased capillary permeability (escape of fluid into interstitial space =edema,
loss of intravascular fluid – decreased BP)
Bronchi = Bronchoconstriction of smooth muscle
[Histamine 2 stimulation]
Stomach =stimulates secretion of acid
Antihistamines: Block histamine-1 receptors = decrease itching, sneezing, rhinorrhea.
Does not reduce congestion.
Histamine-1 Receptor Antagonists: Mild allergic disorders CLASSIC Antihistamines
st
Generation: Sedating
Brompheniramine, Chlorpheniramine, Dexchlorpheniramine, Clemastine, Diphenhydramine, Promethazine,
Hydroxyzine
nd
Generation: Non-Sedating
**Cetirizine, Levocetirizine, Fexofenadine, Loratadine, Desloratadine
o mechanism of action: H1 blockers bind selectively to H1-histaminic receptors, thereby blocking
the actions of histamine at these sites. 1
st
Generation – Highly Sedating 2
nd
Generation – Not.
o side effects: sedation w/ 1
st
Gen., dizziness, incoordination, confusion, fatigue
o appropriate use: treat mild allergic disorders, motion sickness, insomnia, N/V/D/C, loss of appetite
o contraindications/ cautions: atropine-like properties can cause dryness of membranes, cholinergic
blockade = urinary hesitancy, constipation, palpitations. Caution w/ Asthma d/t thickening of
bronchial secretions. Caution w/ conditions worsened by muscarinic blockade (urinary retention,
BPH, HTN)
o Drug Interactions: w/Pregnancy & Lactation – excreted in milk,
w/ alcohol, & other CNS depressants – Barbs, Benzos, Opioids
o appropriate use: With food to avoid GI effects
Sympathomimetics (Decongestants): Nasal decongestant Does not reduce sneezing, itching, rhinorrhea.
Phenylephrine [Neo-Synephrine, others]
Pseudoephedrine [Sudafed, others]
Naphazoline [Privine]
o Colestipol: Increased dig level – increased absorption or bioavailability
o expected effects: Positive inotropic action on heart = Increased the force of ventricular contraction
= increased cardiac output! **HR is reduced d/t decreased sympathetic tone/nerve traffic from the
increased output pressure. Complete ventricular filling.
o appropriate use: Food can alter/decrease absorption
Dosing : 0.25 mg/day or >
Target Plasma Digoxin Drug Level = 0.5 – 0.8ng/mL
TOXICITY = Altered HR or rhythm, Visual or GI
disturbances
‘Statins: Lipid-lowering:
o mechanism of action: Inhibit HMG-CoA reductase - Blocking the pathway for synthesizing
cholesterol in the liver & and LDL (lowering circulating LDL in the blood)
o side effects: muscle pain, increased risk of diabetes mellitus, and abnormal blood levels of liver
enzymes, Muscle Damage. Risk of DM, neuropathy, pancreatic and liver dysfunction, and
sexual dysfunction.
o expected effects: Lower cholesterol & LDL
Nitroglycerin: Nitrostat] (nitrate class)
o mechanism of action: Vasodilates to treat angina & elevated BP
o side effects: Hypotension, Headache, dizziness, Hypersensitivity, lightheadedness, nausea, and
flushing may occur as your body adjusts to this medication appropriate use
o expected effects: prevent chest pain (angina) in people with CAD {Pain occurs when the heart is
not getting enough blood} = Increase HR & Decrease BP
o appropriate use: For acute relief of an attack or acute prophylaxis for CAD. Can Take 5-15 Min
before exercise! Limit driving/heavy machinery. Avoid alcohol.
- Blood pressure medications
Calcium channel blockers: relax and open up narrowed blood vessels, reduce heart rate and lower blood
pressure. prevents calcium from entering the smooth muscle cells of the heart and arteries. When calcium
enters these cells, it causes a stronger and harder contraction, so by decreasing the calcium, the hearts'
contraction is not as forceful.
ACE Inhibitors: ACE inhibitors help the body produce less angiotensin, which helps the blood vessels
relax and open up, which, in turn, lowers blood pressure. (Angiotensin is a chemical that causes the arteries
to become narrow. ACE stands for Angiotensin-converting enzyme.)
Diuretics: help the body get rid of excess sodium (salt) and water and help control blood pressure.
Beta-blockers: Reduce the heart rate, the heart's workload and the heart's output of blood, which lowers blood
pressure. (Ex. Acebutolol)
Adrenergic Antagonist : blocks the sympathetic receptors in the sympathetic nervous system.
Nitroprusside [Nitropress]: creates a rapid, but controlled reduction in BP via IV (similar to Nitro.)
o mechanism of action: direct-acting vasodilator that relaxes smooth muscle of arterioles and veins
o side effects: Excessive Hypotension, Thiocyanate toxicity, Cyanide poisoning
o contraindications/cautions: Don’t mix with this IV solution. & Can trigger retention of sodium
and water; furosemide can help counteract this effect.
o expected effects: reflex tachycardia is minimal
- Diuretics (spironolactone, furosemide, hydrochlorothiazide)
▪ mechanism of action: help the body get rid of excess sodium (salt) and water / help control
blood pressure.
▪ side effects: some - decreased Potassium = leg cramps/ tiredness, Gout, increased blood
sugar, impotence.
▪ appropriate use: Eat foods with Potassium
- Sedative Hypnotics :
Barbiturates: 1
st
higher risk of Resp. Depression. Often for insomnia
*Zolpidem [Ambien]
*Zaleplon [Sonata]
Eszopiclone [Lunesta]
Ramelteon [Rozerem/Doxepin]
Benzodiazepines: 2
nd
: Anxiety, Insomnia. Sz disorder. Gen anesthesia, muscle spasm, Alcohol Withdrawal
Alprazolam [Xanax]; Anx
Chlordiazepoxide [Librium]: Anx, Alc
W Clonazepam [Klonopin]: Sz, Anx
Clorazepate: Anx, Sz, Alc W
Diazepam [Valium]: Sz
Lorazepam [Ativan]: Anx, Ins, Sz, Alc W,
Anesthesia Midazolam [Versed]: Anesthesia
Oxazepam: Anx, Alc W
Temazepam [Restoril]:
Ins
o mechanism of action: Depress CNS. Intensify the effects of GABA (not direct agonists)
o side effects: Occasional reactions include weakness, headache, blurred vision, vertigo, nausea,
vomiting, epigastric distress, and diarrhea. Neutropenia and jaundice occur rarely. Rarely,
benzodiazepines may cause severe allergic reactions, including angioedema and anaphylaxis.
o contraindications/cautions: Pregnancy & Lactation. Other CNS depressants. Dependence!
Anxiolytics: to treat Anxiety
Buspirone [Buspar] : Not a CNS depressant. No abuse potential. Slowly works – 1 wk before effects appear &
several more weeks for peak. Ideal for short-term (1 yr)
- Inhalers
For Asthma:
Anti-inflammatory Drugs: Glucocorticoids: suppress inflammation (Preventative use)
Beclomethasone
Prednisone
o appropriate use : Schizophrenia & Tourette’s Syndrome
o contraindications
o key patient education points:
▪ cautions:
▪ expected effects:
▪ appropriate use: (with food, empty stomach, etc.
What is neuroleptic malignant syndrome?: Rare but serious reaction:
“Lead pipe” muscle rigidity
Sudden high fever
Sweating
Autonomic instability: dysrhythmias & fluctuations in BP
Level of consciousness may rise & fall: Confused or mute, & seizures or coma may develop!
**Death can result from respiratory failure, cardiovascular collapse, dysrhythmias, and other causes.
Treatment : supportive measures, drug therapy, and immediate withdrawal of antipsychotic
medication. Hyperthermia should be controlled with cooling blankets & antipyretics (e.g., aspirin,
acetaminophen). Hydration should be maintained with fluids.
Benzodiazepines may relieve anxiety & help reduce BP & tachycardia.
Waiting at least 2 weeks before resuming antipsychotic treatment & use the lowest effective dosage
- Anti-neoplastic
etoposide
o mechanism of action: Inhibits Topoisomerase II (which is crucial for DNA replication/synthesis)
which leads to cancer cell apoptosis.
o side effects: myelosuppression (decreased WBC
o appropriate use: Small cell Lung CA or Testicular CA
o contraindications
o key patient education points:
▪ cautions:
▪ expected effects:
▪ appropriate use: (with food, empty stomach, etc.
5-FU
Monitor WBC nadir
Bicalutamide
Cisplatin (Platinol): destroys DNA & Prevents cellular replication
o mechanism of action: Alkylating agents prevent cancer cells from reproducing by attaching an alkyl
group to DNA. Binds to cell & forms cross-links witin strands of DNA to prevent DNA replication
& lead to cell death.
o side effects: D/T damage to normal cells = CANNOT differentiate between normal & cancerous
cells: N/V/myelosuppression, peripheral neuropathy, nephrotoxicity, ototoxicity.
o appropriate use: Testicular/ Ovarian CA (or lung, head; neck CA)
o contraindications
o key patient education points:
▪ cautions: will effect GI tract & bone marrow.
▪ expected effects:
▪ appropriate use: (with food, empty stomach, etc.) Can take w/antiemetic to minimize N/V.
Avoid Renal Damage with excessive hydration.
- Agents for thyroid disease:
Levothyroxine[Synthroid]: For Hypothyroidism regardless of cause
o mechanism of action: converted to T3 in the body to produce nearly normal levels of T3 and T
o side effects: Rare: Thyrotoxicosis - tachycardia, angina, tremor, nervousness, insomnia,
hyperthermia, heat intolerance, and sweating. Chronic OD: accelerated bone loss & Increased risk
for AFib
o contraindications/cautions: Separate use by 4 hours of certain meds & supplements:
(H 2 )receptorblockers(e.g.,cimetidine[Tagamet])
- Protonpumpinhibitors(e.g.,lansoprazole[Prevacid]
- Sucralfate[Carafate]
- Cholestyramine[Questran]
- Colestipol[Colestid]
- Aluminum-containingantacids(e.g.,Maalox,Mylanta)
- Calcium su p
lements(e.g.,Tums,Os-Cal)
lements(e.g.,fe r
oussulfate)
- Magnesium salts
- Orlistat[Xenical]
o appropriate use: On Empty Stomach in the morning 30-60m before breakfast (absorption is reduced
by food)
Methimazole [Tapazole]: {a thionamide}: For Hyperthyroidism
o mechanism of action: inhibits thyroid hormone secretion. Does not destroy existing stores of
hormone! Inhibits peroxidase =
Prevents oxidation of iodine. Inhibits incorporation of iodine into tyrosine. Prevents iodinated tyrosines
from coupling.
o side effects: Could cause Hypo if given in high doses.
o contraindications/cautions: Avoid w/ 1
st
Tri pregnancy
- Antidepressants – SSRIs (Ex. LEXAPRO)
o mechanism of action : Selectively inhibits the reuptake of Serotonin
(Depression stems from a deficiency of the neurotransmitter Serotonin)
o side effects: Sexual Dysfunction, CNS Stimulation, Weight gain, Serotonin Syndrome: HTN,
Autonomic instability, rigidity, myoclonus (from MAOIs-monoamine oxidase inhibitors)
o appropriate use: To treat depression
o contraindications: MAOIs = Serotonin Syndrome (d/t increased available pool of serotonin),
Anticoagulants/Antiplatelets = Bleed
o key patient education points:
▪ cautions: Suicide Risk Increased when first started & delayed onset (1-3 weeks to be therapeutic)
▪ expected effects: = Increases the available amount of serotonin (a Monoamine Neurotransmitter)
- Multiple sclerosis therapies
into neurons is inhibited, and hence action potentials are suppressed. Blockade of sodium entry is
limited to neurons that are hyperactive. As a result, the drug suppresses activity of seizure-generating
neurons while leaving healthy neurons unaffected.
o side effects:
o CNS: sedation at therapeutic level/ Nystagmus, ataxia (staggered gait), diplopia (double
vision), cognitive impairment w/ excessive dosage.
o Gigival hyperplasia (Excessive gum growth – swelling, tender, bleeding)
o Dermatological – morbilliform (measeles-like) rash = Steven-Johnson syndrome (SKS) or
toxic epidermis necrosis (TEN)
o Cardiovascular – via IV = dysrhythmias & HTN
o Hirsutism – Overgrowth of hair in unusual places
o Interference w/ Vit D metabolism = Rickets & Osteomalacia ( bone-softening)
o Interference w/ Vit K metabolism = can lower PT = bleeding in newborns
o appropriate use: Epilepsy & Cardiac dysrhythmia
o contraindications/cautions: Teratogen – Pregnancy = cleft palate, heart malformation, fetal deficiencies
ethosuximide [Zarontin]: to help eliminate absence seizures
o mechanism of action: suppresses neurons in the thalamus that are responsible for generating absence
seizures. The specific mechanism is inhibition of low-threshold calcium currents, known as T
currents. Ethosuximide does not block sodium channels and does not enhance GABA-mediated
neuronal inhibition.
o side effects: initial drowsiness, dizziness, lethargy
o appropriate use: Oral – Plasma level between 40-100 mcg/mL. Long half-life but dose twice daily
for better tolerance.
o appropriate use: With food to avoid N/V
- Osteoporosis: low bone mass, altered architecture; increased fragility
Calcium RDA: Male 1000 mg/day Female 1200 mg/day
Calcitonin-salmon: treatment not prevention of Osteo. Paget disease, hypercalcemia
o mechanism of action: inhibits the activity of osteoclasts & decreases bone resorption. & Inhibits
tubular resorption of calcium and thereby increases calcium excretion. As a result of decreasing bone
turnover, calcitonin decreases alkaline phosphatase in blood and increases hydroxyproline in urine.
o side effects: Nausea & inflamed insertion site w/ IM or SQ. Nasal dryness & irritation w/ intranasal.
o appropriate use: Take also with calcium and vit D
- Hypoglycemics: Lower blood glucose levels (for DM)
Biguanide: Decreases glucose production by the liver, increases tissue response to insulin
Metformin [Glucophage]
nd
Generation Sulfonylureas: Promote insulin secretion by the pancreas; may also increase tissue response to
insulin
Glyburide[DiaBeta]
Glipizide [Glucotrol]
Glimepiride [Amaryl]
insulin, etc.)
- Pain (opioids, muscle relaxants, NSAIDs, acetaminophen, topical lidocaine, etc.)
o mechanism of action
o side effects
o appropriate use
o contraindications/cautions:
o expected effects:
o appropriate use: (with food, empty stomach, etc.
- Orlistat: Lipase Inhibitor: for weight loss
o mechanism of action: Acts in the GI tract to reduce absorption of fat. In the stomach and small
intestine to cause irreversible inhibition of gastric and pancreatic lipases – enzymes that break down
Trig. into monoglycerides & free fatty acids.
o Additional effects: reduced Chol, LDL & raised HDL. Reduced glucose & BP
o Adverse Effects: GI – diarrhea/incontinence/leakage, possible Liver damage, kidney stones,
acute pancreatitis
o appropriate use: obese pt. > 12
o contraindications/cautions: Will reduce Levothyroxine Absorption
o expected effects: Reduction of absorbed dietary fat d/t triglycerides not being broken down & absorbed.
o appropriate use: (with food, empty stomach, etc.
- Adrenergic agonists
o mechanism of action: produce their effects by activating adrenergic receptors = responses similar to
stimulation of the sympathetic nervous system
Adrenergic Receptor Stimulation
- Direct: receptor activation through direct binding to adrenergic receptors & mimic actions of
natural transmitter (NE, Epinephrine, Dopamine)
o Dopamine
o Epinephrine
o Isoproterenol
o Ephedrine
- Indirect:
o Promotion of NE release: by acting on terminals of sympathetic nerves to cause NE release
▪ Amphetamine
▪ Ephedrine
o Inhibition of NE reuptake: can cause NE to accumulate within the synaptic gap &
can thereby increase receptor activation.
▪ Cocaine
▪ Tricyclic Antidepressants
o Inhibition of MAO: can increase the amount of NE available or release & enhance activation
