Final Exam Study Guide
Week 1: Intro to Pharmacotherapy
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What is the role of the Controlled Substance Act? The role of the controlled substance act is to provide
categories for drugs based on their abuse risk potential.
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What kinds of drugs are categorized as Schedule I? Schedule II? Schedule I drugs have a high risk
for abuse potential and no medical use. Schedule II drugs have a high risk for abuse potential and
some medical use.
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How do Schedule II drugs compare to Schedule V drugs? Schedule V drugs have the lowest risk for
abuse potential.
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Where can you find information about safe handling of hazardous drugs? Information about safe handling
for hazardous drugs can be found on the packaging, inserts and marketing literature, drug labels, boxed
warnings and Risk Evaluation and Mitigation Strategies (REMS).
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What does a pregnancy risk category of X indicate? Drugs that should NOT be used during pregnancy
because studies showed that they are teratogenic.
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What processes make up pharmacokinetics? Define each process. ADME, Absorption= drug administration
moving into the bloodstream, Distribution= drug moving from the bloodstream to body tissues,
Metabolism= change in the drug structure (on Liver) and Excretion= drug removal from the body (in
kidneys)
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What determines if a drug can move across membranes? Size of the drug, lipid solubility, structure
etc. Channels/Pores- for small enough drugs, Transport Systems depending on drug structure and
Direct Penetration of the drug if it is lipophilic.
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What pharmacokinetic process determines how quickly a drug will start working? Absorption, OOA
is determine based on the drugs bioavailability which is how much drug is absorbed.
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What happens when drugs are metabolized – are effects increased or decreased? Their effects are
increased, drugs are inactivated, accelerated renal clearance of the drugs, activating prodrugs, and
increased therapeutic actions.
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What are the pros and cons of the IV route? IM? Subcutaneous? Oral? IV Pro: instant absorption,
and precise dosage, IV Con: irreversible and expensive. IM/SC Pro: rapid absorption, poorly soluble
drugs, IM/SC Con: discomfort and inconvenient. PO Pro: convenient, cheap, and reversible PO Con:
absorptive barriers.
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What is an agonist? How does it have its effect? Activates receptors, mimics endogenous molecule effects
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What is a partial agonist? How does it have its effect? Agonist with moderate activity, max effect< agonist
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What is an antagonist? How does it have its effect? Inhibits receptor activation
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What is an adverse drug reaction? Noxious, unintended, and undesired effects with a normal drug dose.
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What are the Beers Criteria? RE: Which group of patients? List of potentially harmful drugs for Geriatrics.
Week 2: Autonomic & Adrenergic Nervous Systems
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Cholinesterase inhibitor (aka acetylcholinesterase inhibitor) -STIGMINE
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What is the mechanism of action? Indirectly activates the muscarinic receptors,
acetylcholinesterase is inhibited so there is an increase in AcH which activates the receptors
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What are the common reversible cholinesterase inhibitors and their indication? Neostigmine,
Pyridostigmine and Physostigmine. Neo and Pyrido= MG and Physo=Anticholinergic Toxicity
Neostigmine and pyridostigmine (drug of choice for myasthenia gravis– why?) Neo=IV and
Pryrido= Long Duration and low ADE’s. Pyridostigmine is the drug of choice for MG because it is
the only PO CI. MG= autoimmune disease that kills NicotinicM receptors in the neuromuscular
junctions.
Common anticholinergic medications- MOA: Block AcH by binding to M1, M2 and M3. (Muscarinic
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antagonist)
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Atropine – what are the common indications, therapeutic effects, and side effects. Used for
bradycardia, dry mouth, eye disorders, GI hypertonicity, and cholinergic crisis/muscarinic agonist
poisoning. The therapeutic effects of Atropine include tachycardia, decreased salivation, sweating
and lacrimation, decreased GI tone and motility and mydriasis. Side effects include dry mouth,
confusion, blurred vision, and tachycardia.
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What is the drug of choice for anaphylactic shock? Epinephrine
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Why? Epinephrine activates alpha 1, beta 1 and beta 2 receptors. It vasoconstricts, increases the
heart rate and force of contraction and bronchodilates.
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Which concentration of epinephrine is used for the IM administration? The stronger conc. of
1mg/mL of Epinephrine is used for Anaphylactic Shock.
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What are the response of activation of
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Alpha-1 receptor: vasoconstricts vasculature and dilates the pupils
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Beta-1 receptor: increases the HR and force of contraction of the heart
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Beta-2 receptor: bronchodilates, vasodilates and relaxes the uterus
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Dopamine receptor: vasodilates the kidneys
What are the adverse effects associated with activation of
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Alpha-1 receptor: HT, Bradycardia and Necrosis
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Beta-1 receptor: Tachycardia, Dysrhythmias and Angina
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Beta-2 receptor: hyperglycemia and tremor
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Dopamine receptor: minimal ADEs
Week 4: Antibiotics & Antivirals
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Define:
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Narrow-spectrum antibiotics are active against only a few microbes
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Broad-spectrum antibiotics are active against a wide range of microbes
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Bactericidal antibiotics kill the bacteria
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Bacteriostatic antibiotics slow the growth of the bacteria
How do we select antimicrobial agents? Based on the microbe, Match the Drug to the Bug, how susceptible
the microbe is to the drug and any other host factors.
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What is empiric therapy? When antimicrobials are started before the infecting organism is
identified, this is an “educated guess” to increase the odd of success.
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What are ways in which antibiotics are misused? When are they are not indicated? Why should we prevent
overuse? Antibiotics can be misused by giving the wrong drug, dose, or method. They are NOT indicated in
viral infections. We need to prevent misuse of antibiotics because it causes bacterial resistance to meds!
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What antibiotics are included in the beta-lactam class? Penicillin, Cephalosporins, Carbapenems and
Monobactams.
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How do beta-lactam antibiotics work? Are they bacteriostatic or bactericidal? Beta-Lactam antibiotics are
bactericidal, they bind to PBP’s, inhibit transpeptidase, stop peptidoglycan maintenance lysing the cell wall.
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Which antibiotics can be administered to a penicillin allergic patient? NOT other penicillin drugs can take
cephalosporins or Aztreonam (Monobactam).
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Which antibiotics cover MRSA infection? Cephalosporins, Linezolid, Vancomycin, Tigecycline and Mupirocin
can treat MRSA infections.
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What is the mechanism of action for acyclovir, valacyclovir and famciclovir? (Drugs for HSV and VZV) these
drugs inhibit DNA polymerase, blocking further DNA strand growth after being incorporated into the viral
DNA.
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How do acyclovir and valacyclovir differ from each other? Valacyclovir is the prodrug that is
converted into acyclovir, after absorption in the GI Tract.
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What is the mechanism of action of the neuraminidase inhibitors? Inhibit neuraminidase which is needed
for viral replication.
Which drugs fall into this class? Oseltamivir (Tamaflu), Zanamivir and Peramivir (-amivir)
What are common adverse effects of neuraminidase inhibitors? Nausea, delirium, and abnormal
behavior in children.
Name the five classes of medications used to treat HIV: 1) Reverse Transcriptase Inhibitors (Nucleoside
Reverse Transcriptase Inhibitors and Non-NRTIs), 2) Integrase Strand Transverse Inhibitors (ISTIs), 3)
Protease Inhibitors, 4) Fusion Inhibitors and 5) CCR5 Antagonists.
HIV therapy should always consist of multiple drugs from different drug classes. To combat resistance.
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Week 5: Heart Failure
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What are the mechanisms of action, common side effects and counseling points for thiazide diuretics, loop
diuretics, ACE-I, ARB, ARNI, DRI/K-sparing diuretic, beta blockers, and digoxin?
Thiazide Diuretics
Block Na/Cl reabsorption in the Distal
Convoluted Tubule
Loop Diuretics
Block Na/Cl reabsorption in the Loop of
Henle, ^Diuresis
ACE-I’s
Inhibit angiotensin converting enzyme to
make angiotensin 2 which increases BP by
vasoconstricting, stimulating aldosterone
and cardiac remodeling.
Block angiotensin 2 from binding to the
kidneys, causing vasodilation, decreased
aldosterone and cardiac remodeling.
Increases Na/water excretion with
increased glomerular filtration rate,
causing vasodilation and reduced renin
from the kidneys.
Bind to Renin and prevent it from cleaving
angiotensinogen to angiotensin 1. Causing
vasodilation, decreased aldosterone and
cardiac remodeling.
ARB’s
ARNI’s
Entresto aka
Valsartan/Sacubitril
DRI’s
K Sparing Diuretics
Beta Blockers
Metoprolol, Bisoprolol
and Carvedilol
Digoxin
(Class: Inotrope)
Aldosterone Antagonists and NonAldosterone Antagonists. Aldosterone
usually increases Na retention and K
excretion. So, these drugs decrease
potassium excretion, Increase Na excretion
and reduce cardiac remodeling.
Adrenergic Antagonists, block the effects
of epinephrine.
Inhibits the Na/K/ATPase Pump, increasing
intracellular Ca which increases force of
contraction. This drug increases cardiac
output and inhibits renin stopping RAAS.
Hyperglycemia,
Dehydration,
Hyperuricemia and
Electrolyte Imbalances.
Ototoxicity, Hypotension,
Dehydration,
Hyperuricemia and
Electrolyte imbalances.
Angioedema, Dry Cough,
Hyperkalemia and Renal
Failure.
Angioedema and Renal
Failure
Hypotension, Dry cough,
Renal Failure and
Hyperkalemia.
Angioedema, Dry cough,
Diarrhea, and
Hyperkalemia.
Hyperkalemia and
Endocrine effects like
Gynecomastia.
May experience fatigue,
dizziness, cold extremities,
Bradycardia and
Hypotension.
Nausea, vomiting,
anorexia, fatigue, blurred
vision, halos, yellow-tinged
vision, and cardiac
dysrhythmias.
Monitor for signs of
dehydration and electrolyte
levels. NOT at bedtime or with
SULFA ALLERGY.
Monitor for signs of
dehydration, NOT at bedtime
and slow IV. CATEGORY X
DRUGs.
First dose may cause
hypotension and CAN CAUSE
FETAL INJURY SO AVOID IN
PREGNANCY.
CAN CAUSE FETAL HARM SO
AVOID IN PREGNANCY.
Need a “wash out” period of
36 hours when switching from
ACEI’s to ARNI’s to avoid
angioedema.
MAY CAUSE FETAL INJURY SO
AVOID IN PREGNANCY!
(Alirisken can treat HT)
Avoid taking with other
diuretics and K increasing
agents.
Within the first 1-2 weeks pt
may experience adverse
effects.
Need a loading and
maintenance doses.
(Digifab reduces Digoxin
toxicity)
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What classes of medication can slow down cardiac remodeling? ARBs, DRIs, K-Sparing Diuretics, and
Aldosterone Inhibitors
Week 6: Hypertension & Antidysrhythmics
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How are the efficacy of antihypertensive medications monitored? By measuring the pt’s BP
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Loop diuretics
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Mechanism of action; indications; adverse effects; drug interactions. Loop Diuretics MOA is that
they block reabsorption of Na/Cl in the Loop of Henle which increases diuresis. They may cause
Dehydration, Electrolyte abnormalities, Ototoxicity, Hypotension and Hyperuricemia. Loop
Diuretics should not be taken with Digoxin, other Antihypertensives, K-sparing diuretics, Lithium,
NSAIDs and other ototoxic drugs.
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List the four loop diuretics: Furosemide, Torsemide, Bumetanide, Ethacrynic Acid
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Which one can be used in patients with a sulfa allergy? ONLY Ethacrynic Acid can be given
to pt’s with Sulfa Allergies.
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Thiazide diuretics
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Mechanism of action; indications; adverse effects; drug interactions. Thiazide Diuretics MOA is that
they block reabsorption of Na/Cl in the Distal Convoluted Tubules to increase diuresis. ADE’s
include Dehydration, Electrolyte Abnormalities, Hyperuricemia, and Hyperglycemia. Thiazide
Diuretics should not be taken with digoxin, K-sparing diuretics, NSAIDs, lithium and
Antihypertensives. (Should NOT take if allergic to sulfa!)
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List the four thiazide diuretics: Hydrochlorothiazide, Chlorothiazide, Chlorthalidone and
Metolazone
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Spironolactone
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Mechanism of action; indications; adverse effects; drug interactions (Hint! What drugs may have
additive effects?). Spironolactone is a K-sparing diuretic, more specifically it is an aldosterone
antagonist, therefore its MOA is that it blocks aldosterone in the DCT, causing increased Na
excretion and K retention. It is used to treat Acne, PCOS, HT, HF and Edema. It may cause
hyperkalemia and gynecomastia. It should not be given to pt’s taking thiazide diuretics and other K
raising agents.
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ACE Inhibitors
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Mechanism of action; indications; adverse effects; drug interactions. ACE-I’s MOA is that they
inhibit angiotensin converting enzyme from converting 1 to angiotensin 2. This causes increased BP
by vasoconstriction, stimulating aldosterone and cardiac remodeling. ACE-I’s are used to treat HT,
HF, edema, MI, Diabetic Nephropathy and Prophylaxis of MI/CVA and death in pt’s wit CV disease.
It may cause angioedema, renal failure, dry cough, hyperkalemia and first dose hypertension. This
is a Category X drug! NOT with diuretics, antihypertensives, Lithium, NSAIDs and K-raising agents.
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What is a rare but life-threatening ADE that can be seen with ACE inhibitors? Angioedema!
Recognize drugs in this class- ALL END IN -PRIL.
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Angiotensin II receptor blockers (ARBs)
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Mechanism of action; indications; adverse effects; drug interactions. ARB’s work by blocking
angiotensin 2 from binding in the kidneys, causing vasodilation, decreasing aldosterone and cardiac
remodeling. ARB’s are used to treat HT, HF, Diabetic Nephropathy, MI and prevention of MI/CVA
and death in pt’s with CV. Adverse effects of ARBs include angioedema, renal failure and can cause
fetal injury so do NOT take in Pregnancy! ARBs should NOT be taken with diuretics,
antihypertensives and K increasing agents.
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Recognize drugs in this class- ALL END IN -SARTAN
Calcium channel blockers (non-dihydropyridine vs. dihydropyridine)
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Mechanism of action; indications; adverse effects; drug interactions. Dihydropyridine: block the Ca
channels in smooth vascular muscle causing vasodilation which decreases BP, myocardial
perfusion, and reflex tachycardia. They are used to treat HT and angina pectoris. They may cause
dizziness, flushing, headache, peripheral edema, and reflex tachycardia. Do NOT take with beta
blockers. Non-dihydropyridines block Ca Channels in smooth vascular muscle and in the heart!
They vasodilate, causing decreased BP and myocardial perfusion, decrease HR and force of
contraction, making it easier for the heart to pump blood. They are used for HT, angina pectoris,
and dysrhythmias. They may cause dizziness, flushing, headache, peripheral edema, bradycardia,
AV block and constipation with Verapamil. Avoid with grapefruit juice, digoxin, and beta-blockers.
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Recognize drugs in this class. ALL DIHYDROPYRIDINE CCB’S END IN -DIPINE and Nondihydropyridines are Verapamil and Diltiazem.
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What are the mechanism of actions of class I, II, III, & IV antidysrhythmics. Class 1: Sodium Channel
Blockers, Class 2: Beta Blockers, Class 3: Potassium Channel Blockers, & Class 3: Calcium Channel Blockers.
Class 1: Sodium Channel Blockers
Class 2: Beta Blockers
Class 3: Potassium Channel Blockers
Decreases conduction velocity in the atria,
Disopyramide, Quinine,
ventricles, and His-Purkinje system. Similar in
Procainamide, Lidocaine,
action and structure to local anesthetics
Flecainide and Propafenone
Decrease automaticity in the SA node, Decrease
-OLOLs
conduction in the AV node and Decrease
Propranolol, Acebutolol, Esmolol,
myocardial contractility
and Sotalol
Delays repolarization of fast acting potential and
Amiodarone, Dronedarone
prolongs QTc interval.
(Category X) and Sotalol (Class 2
and 3)
Class 4: Calcium Channel Blockers
Block Ca Channels in smooth vascular muscle and
-DIPINE’s
heart, vasodilating and lowering BP. (in
Verapamil and Diltiazem also AV/SA blocks
Verapamil and Diltiazem
decreasing HR and decreases myocardial
contraction)
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What are the common side effects of Amiodarone- (PCB, Class 3) can cause toxicity of the lungs, liver, eyes
and thyroid, and photosensitivity. Should monitor for hypertension and use a 0.22-micron filter.
Week 7: Coronary Artery Disease, Hyperlipidemia, Antiplatelets, Anticoagulants & Thrombolytics
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Nitrates
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Mechanism of action; indications; adverse effects; drug interactions: Nitrates work by converting
nitric acid using sulfhydryl group to vasodilate/relax the vascular smooth muscle. They’re used to
treat Coronary Artery Disease and associated stable or variant angina. In stable angina they
vasodilate, decrease oxygen demand and in variant angina they relax the muscle spasm, increasing
oxygen supply. They may cause headache, orthostatic hypotension, and reflex tachycardia.
Tolerance can be developed as well. They interact with other drugs such as: antihypertensives,
PDE5 Inhibitors (ED Meds, end in -fil), Beta Blockers, and Verapamil/Diltiazem.
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Recognize drugs in this class: Nitroglycerin, Isosorbide Mononitrate, and Isosorbide Dinitrate
MONA-B= Morphine, Oxygen, Nitroglycerin, Aspirin and Beta-Blockers
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Components of mnemonic, their role in treatment (mechanism of action). Morphine: relieves pain,
vasodilates to decrease myocardial oxygen demand, Oxygen to increase O2 supply to myocardium,
Nitroglycerin: vasodilates, decreases preload, increases blood flow to heart and treats ischemic
pain, Aspirin suppresses platelet aggregation and should be given immediately, Beta Blockers
decrease HR, contractility and myocardial O2 demand.
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Indication: Immediate interventions for those with a suspected STEMI, to prevent necrosis.
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Which drug class is most effective in lowering LDL? HMG-CoA Reductase Inhibitors (-STATINS)
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Which drug class is most effective in lowering triglycerides? Fibric Acid Derivatives
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HMG-CoA reductase inhibitors
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Mechanism of action; indications; adverse effects. MOA of HMG-CoA Reductase Inhibitors is to
stop the synthesis of cholesterol which causes the hepatocytes to increase LDL Receptors, picking
up more LDL cholesterol from the blood. Decreases LDL’s, TG’s, increases HDL’s and plaque
stability. They are used in pt’s with high cholesterol, post MI therapy, Diabetes and
Primary/Secondary prevention of CV events. They may cause headache, rash, GI upset, myopathy,
hepatoxicity, memory loss and cataracts.
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Recognize drugs in this class- ALL END IN -STATIN
Bile Acid Sequestrants
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Mechanism of action; indications; adverse effects; drug interactions; counseling points regarding
co-administration with other medications. Bile Acid Sequestrants work to decrease LDLs by binding
to bile acids which prevent the reuptake of cholesterol in the blood. May also temporarily increase
TG’s. They’re used in adjunct therapy to lower LDL’s and may cause constipation, nausea, and
bloating. They must be given 1 hour before or 4 hours after other drugs. They must also be taken
with food and water.
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Recognize drugs in this class- ALL START WITH COL/CHOL- Colesevelam, Cholestyramine, Colestipol
Fibric Acid Derivatives
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Mechanism of action; indications. Fibric Acid Derivatives/Fibrates stimulate lipoprotein lipase via
activation of the PPAR-alpha in patients with significantly high LDL’s. They’re primary agents to
lower TG’s and are third line agents to lower LDL levels.
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Recognize drugs in this class- ALL CONTAIN FIB- Gemfibrozil, Fenofibrate, Fenobric Acid
What are the antidote/ reversals for heparin, enoxaparin, factor Xa inhibitors, and Vitamin K antagonist?
Heparin
UFH can be reversed with Protamine
Enoxaparin
Reversal with Protamine
Factor Xa Inhibitors
Reversal with Adexanet-alfa
Vitamin K Antagonists
Warfarin
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What medications are antiplatelet and anticoagulants? Antiplatelets are Aspirin, Clopidogrel, Prasugrel,
Ticagrelor, Tirofiban, Eptifibatide, Abciximab. Anticoagulants are Heparin, LMWH/Enoxaparin/Delteparin,
Fondaparinux, Warfarin, Direct Thrombin Inhibitors (Dabigatran, Bivalirudin, Argatroban), Factor Xa
Inhibitors (Rivaroxaban, Apixaban)
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How do we monitor efficacy and safety for warfarin? Monitor the International Normalized Ratio (INR)
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What should we monitor for after administration of fibrinolytics/thromboytics? Monitor these “clot busting
drugs” because there is a high risk of bleeding! (ALL END IN -PLASE)
Week 8: Peptic Ulcer Disease & Constipation
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What are the mechanism of action, adverse effects, and counseling points for proton pump inhibitors,
histamin2 receptor antagonists, antacid, sucralfate and misoprostol?
Proton Pump Inhibitors
Irreversibly inhibit the proton pump which
Increased risk of
Admin 60 mins before
stops the influx of H+ so the pH increases.
Pneumonia, Fractures,
meals and take on an
Hypomagnesemia and C.
empty stomach.
(-PRAZOLE)
diff infection.
Histamine2 Receptor
Block the H2RA receptors which are
Increased risk of
Should NOT be taken
Antagonists
essential in making the stomach acid so the
Pneumonia, and Cimetidine
with Antacids
pH increases, promoting gastric healing.
may cause
(-TIDINE)
dizziness/headache and
delirium/confusion in older
clients.
Antacids
Ants Make Children Scream
Alkaline products that raise GI pH, to inhibit
Separate Admin by 1
the action of Pepsin and increase PGE
hour with H2RAs,
(mucus/bicarb) synthesis.
Sucralfate and other
drugs by 2 hours.
Sucralfate
Polymerization and Cross-linking in the
Constipation and decreased
Give 1 hour before
stomach to create sticky-gel coating to
absorption of some
meals and 2 hours from
block acid and pepsin from reaching healthy
medications.
other meds.
Prostaglandin E1 Analog and promotes PGE
May cause diarrhea and
CATEGORY X DRUG!
(mucus/bicarb) synthesis as a prophylaxis
abdominal pain.
tissues.
Misoprostol
for ulcers with chronic NSAID use.
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What are the contraindication of using laxatives? The contraindications of using laxatives include
intraabdominal pain, surgical abdomen, fecal impaction/bowel obstruction, habitual use, and
Lactation/Pregnancy.
Week 9: Analgesics and Gout, Opioids
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COX Inhibitors (NSAIDs)
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Mechanism of action (difference between first and second generation); indications; ADE’s.
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List the first-generation COX inhibitors (HINT! Recognize common endings)
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List the second-generation COX inhibitors (HINT! There is only one)
First Generation
Ibuprofen, Fenoprofen and Ketoprofen,
Reversibly block
Mild Pain, Fever,
Nausea, Vomiting, GI
COX inhibitors
Naproxen,
the effects of
RA, OA, Closure of
Ulcers/Bleeding,
Diclofenac, Etodolac, Ketorolac,
COX-1 and COX-2
PDA in Neonates,
Increased bleeding time
Gout
and Renal Impairment.
Piroxicam and Meloxicam
(Indomethacin)
Second Generation
Celecoxib
COX inhibitors
Selectively
Pain, OA, RA,
GI Ulcers, CV events so
inhibits COX-2
Dysmenorrhea
taper dose and Renal
Impairment
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How does Aspirin differ from other first-generation COX inhibitors? Its MOA is irreversible and can
also suppress platelet aggregation. Aspirin should be avoided in children because may cause Reye’s
Syndrome. May cause salicylism with aspirin toxicity. Causing tinnitus, sweating,
dizziness/headache and respiratory alkalosis. It shouldn’t be taken with other NSAIDs.
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Gout
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When is acute management used vs. preventative therapy? Acute Management of Gout relieves
symptoms of infrequent flare-ups. Preventative Therapy for gout treats hyperuricemia to prevent
chronic gout attacks.
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What drugs are used for acute management (first line vs. second line)? When must they be
started? What is the goal of acute management? First Line agents for gouts are NSAIDs
including Indomethacin and Naproxen. They should be started at the first sign of the
attack! Second line agents for gout are glucocorticoids like Prednisone and Triamcinolone
Acetate. Colchine is used as the last line treatment and prevention of acute gout attacks
(but should not be taken during pregnancy or with grapefruit juice.)
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What drugs are used for preventative therapy? What is the goal of preventative therapy?
The goal of preventative therapy is to treat hyperuricemia by promoting the dissolution or
urate crystals, prevents new crystals, disease progression, reducing frequency of attacks
and improving the patient’s quality of life. Drugs that treat hyperuricemia include Xanthine
Oxidase Inhibitors like Allopurinol and Febuxostat. Additionally, Probenecid is used to
prevent hyperuricemia by excreting UA, this drug should NOT be started during an acute
attack.
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Headaches
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What is the difference between abortive therapy and preventative therapy? Which types of drugs
are used for each? Abortive Therapy stops headaches and uses Aspiring-Like Analgesics and Opioid
Analgesics like Meperidine and Butorphanol. Also, Acetaminophen (CNS COXi) Serotonin 1B/1D
Receptor Agonists and Ergot Alkaloids are also used in abortive therapy. Preventative Therapy
prevents headaches and uses Beta-Blockers (Propranolol/Metoprolol), Tricyclic Antidepressants
(Amitriptyline and Nortriptyline), Antiepileptic Drugs (Divalproex and Topiramate) and Estrogens.
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What should you counsel patient regarding medication use for headaches? How can medication
overuse headaches be prevented? Which drugs can cause it? How can we manage medication
overuse headache once it occurs? Medication Overuse Headaches are chronic headaches caused
by frequent use of HA meds and resolve after meds are stopped. ALL HA meds can lead to MOH’s.
Treatment includes stopping the HA meds and prevention includes limiting abortive therapy to 2-3
times/week and take the smallest dose necessary. Another way is to alternate abortive HA meds.
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Serotonin 1B/1D Receptor Agonists
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Mechanism of action; indications; adverse effects; counseling points. These migraine specific
medications are the first line abortive therapy for migraines. They vasoconstrict via selectively
binding 5-HT1B/1D to blood vessels and the trigeminal nerve leading to pain relief. THEY ALL END
IN -TRIPTAN. They may cause coronary vasospasm, heavy arms, chest pressure, vertigo, tingling
and fatigue. Shouldn’t take with other triptans, ergots, MAOis, SSRIs, and SNRIs. don’t take this
med if had previous MI, ischemic heart disease or uncontrolled HT. This is a Category X drug. PO
OOA is 30-120 mins, SQ OOA is 10-15 mins and IN OOA is 15-20 mins.
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Opioids
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Which medications are classified as:
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Opioid agonists: Morphine, Fentanyl, Hydromorphone, Methadone, Codeine. Oxycodone,
Hydrocodone, and Tepentadol.
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Opioid agonists/antagonists: Pentazocine, Nalbuphine, Butorphanol and Buprenorphine
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Opioid antagonists: Naloxone, Naltrexone, Methylnaltraxone, and Alvimopan.
What are the adverse effects associated with opioid agonists? Sedation, respiratory
arrest/depression, hypotension, and constipation.
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What is the difference between opioid tolerance and opioid dependence? Opioid Tolerance is
when a larger dose is needed to get the same response as a previously smaller dose, it develops to
analgesia, euphoria, sedation, and respiratory depression. It does NOT develop to constipation and
pupillary constriction. Opioid Dependence is when abstinence/withdrawal syndrome occurs when
the drug is abruptly removed, physiological adaptation.
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What are signs and symptoms of opioid withdrawal? Symptoms include yawning, sweating,
tremors, gooseflesh, runny-nose, and GI upset. They are uncomfortable but not life-threatening.
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Which opioid agonist can cause QTc prolongation? Methadone can cause QTC interval
prolongation so it should NOT be taken with other QTc prolonging drugs.
Week 10: Sedatives, Antidepressants & Antipsychotics
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Benzodiazepines
Mechanism of action; indications; adverse effects. Benzodiazepines bind to the GABA receptors and
make GABA work better and longer. So, because GABA is an inhibitory neurotransmitter, they prolong
CNS depression. They help treat short-term anxiety, insomnia, seizures, muscle spasms, alcohol
withdrawal and general anesthesia. They cause reduced anxiety, promote sleep, muscle relaxation,
confusion (specifically in elderly and children) and anterograde amnesia. They also can cause
hypotension when administered via IV and respiratory depression.
o List drugs in this category. Alprazolam, Clonazepam, Lorazepam, Midazolam, Temazepam and
Chlordiazepoxide. (END IN -AZOLAM and -AZEPAM)
o What is tolerance? When a patient becomes resistant to anti-seizure effects of the drug but NOT their
anxiolytic or hypnotic effects.
o What is dependence? How can we avoid it? Abstinence syndrome develops after long-term use; can be
avoided by tapering doses slowly over a period of several weeks.
o What drug can be used to reverse a benzodiazepine overdose? Flumazenil (IV)
Benzodiazepine-like Drugs
o Mechanism of action; indications; adverse effects. Bind to GABA receptors to potentiate the action of
GABA but are selective for subtype-1 GABA receptors. They are the first line therapy for insomnia. They
may cause daytime drowsiness, dizziness, sleep-driving and complex sleep related behaviors. Counsel
on sleep hygiene.
o List drugs in this category. Z Drugs, Zolpidem, Zaleplon and EsZopiclone.
o Other sleep inducers: Ramelteon, Trazodone, Doxepin, Diphenhydramine and Doxylamine.
First-Generation Antipsychotics-Chlorpromazine, Perphenazine, Fluphenazine and Haloperidol
o Mechanism of action; indications; adverse effects. They block dopamine2 receptors, AcH, Histamine
and NE. They are used to treat Schizophrenia. They may cause EPS and Haloperidol may cause QTc
prolonging.
Second-Generation Antipsychotics- Clozapine, Quetiapine, Olanzapine, Aripiprazole, Risperidone & Ziprasidone
o Mechanism of action; indications; adverse effects. They block D2, Serotonin/5-HT and sometimes
Histamine/AcH/NE. They’re used in not only Schizophrenia but Bipolar and MDD too. They may cause
weight gain, dyslipidemia and sometimes toxicity. Black Box Warning for risk of death.
o Which class has a higher rate of EPS? FGA’s have a higher rate of EPS than SGA’s.
o Which class has a higher rate of weight gain? Second Generation Antipsychotics (Clozapine and Olanzapin)
What are advantages of depot injections? They are long-acting injectable SGA’s, dosing intervals are every 2-4
weeks and show better adherence rates. These drugs prevent episodes and provide the highest level of
functioning.
Which medications are used as mood stabilizers? Lithium, Antiepileptic Drugs (Divalproex Sodium/Valproate and
Carbamazepine), Antipsychotics (Aripiprazole, Olanzapine and Ziprasidone.)
What factors can affect lithium levels? SODIUM, the excretion of Li is dependent on the body’s Na levels.
o When should lithium levels be obtained? Check levels 12 hours after previous dose.
What FDA warning has been issued for antidepressants? Black Box Warning: Risk of Suicide
What is the mechanism of action of SSRIs? Blocks the reuptake of serotonin, increasing serotonin in the
synapses and activating post-synaptic serotonin receptors.
o What are common and/or concerning adverse effects? Common- Nausea, insomnia and weight gain, ED
and Hyponatremia. Concerning- Serotonin Syndrome= accumulated Serotonin=hyperlexia, rigidity,
diaphoresis and agitation and Hyperthermia.
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Week 11: Asthma & COPDT
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What is the primary route of medication administration for asthma/COPD and what are the advantages of
this route of administration? Inhalation is the primary route of medication administration for Asthma/COPD
because they enhance the therapeutic effects, minimal systemic effects, and rapid relief for acute attacks.
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What are the pros and cons of different inhalation devices? Metered-Dose Inhalers require ‘hand-breath’
coordination and use of spacers to improve drug delivery to lungs. Respimat Inhalers deliver drugs as a
mist, increasing drug delivery to lungs. Dry-Powder Inhalers are breath activated but require long, strong
inhalation forces. Nebulizers mist the drugs through a facemask/mouthpiece and take several minutes.
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What medications are inhaled and oral corticosteroids. What are their adverse effects? What are the
counseling points for inhaled corticosteroids? Glucocorticoid Inhalers include Beclomethasone, Fluticasone
and Budesonide. Glucocorticoid Oral drugs include Prednisone, Prednisolone and Methylprednisolone.
Inhaled may cause slowed growth in children, dysphonia, oropharyngeal candidiasis. PO may cause
osteoporosis, adrenal suppression, hyperglycemia, and peptic ulcers. Patients should rinse/gargle with
water after use of inhaled glucocorticoids.
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What medications are leukotriene modifiers? Montelukast, decreases inflammation & bronchoconstriction.
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What is the mechanism of action of cromolyn? It is a mast cell stabilizer, preventing the release of
histamine/other mediators to decrease inflammation. Its less effective than other glucocorticoids.
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What medications are beta2 agonist? Which one are short-acting and long-acting? What are their specific
adverse effects and role in therapy in asthma/COPD? Beta2-Agonists: Short Acting= Albuterol and
Levalbuterol, they’re used for PRN asthma/COPD attack and may cause tachycardia, angina, and tremor.
Long Acting= Arformoterol, Formoterol and Salmeterol, used for COPD on a schedule, NOT PRN and second
line therapy for Asthma. They may cause increased risk of severe asthma/death, use with other meds, not
alone!
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What are the anticholinergic agents we can use in asthma/COPD? Which one can be used in combination
with albuterol for immediate symptom relief? What is the most common adverse effect? Ipratropium,
Tiotropium, Aclidinium and Umeclidinium block the muscarinic receptors in the bronchi to decrease
bronchoconstriction, they’re first line therapy for COPD and ‘off-label’ for asthma. They all cause dry
mouth- rinse the mouth out. ONLY Ipratropium can be used with Albuterol for immediate symptom relief.
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What are the treatment goals for asthma and COPD? Asthma treatment goals are to reduce impairment,
prevent chronic symptoms and reduce risk. COPD treatment goals are to reduce impairment, symptoms,
reduce risk and prevent progression.
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How do we manage severe exacerbation of asthma and COPD? In which condition would we consider
antibiotics?Asthma Severe Exacerbations: give O2, systemic glucocorticoid, high-dose nebulized SABA,
Nebulized Ipratropium and consider Magnesium IV. COPD Severe Exacerbations: give O2, high dose
nebulized SABA, systemic glucocorticoids, nebulized Ipratropium and antibiotics.
Last line therapy for Asthma/COPD= Methylxanthines- Theophylline/Aminophylline/Caffeine- bronchodilate
Week 12: Glucocorticoids, Thyroid Disorders and Diabetes
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What is the role of glucocorticoids (steroids) in metabolism? Central nervous system? Cardiovascular
system? Stress response? Neonatal respiratory system? Increase glucose levels, breakdown proteins to
produce glucose, breakdown fat, affect mood, CNS excitation, support skeletal muscle
perfusion/oxygenation, increased BP, increase RBC, Hb and WBCs, increased release in a Stress Response,
and help mature lungs in neonates.
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Glucocorticoid (Steroid) Replacement
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How long does treatment need to continue?
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What diseases are managed with glucocorticoid replacement? Mineralocorticoid replacement?
Addison’s Disease, Secondary and Tertiary Adrenal Hormone Deficiency, Congenital Adrenal
Hyperplasia, and Adrenal Crisis.
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How should clients be counseled take glucocorticoids? Clients should be advised that this is a lifelong treatment, it should mimic normal patterns so take a dose when they wake-up or 2/3 in the
morning and 1/3 in the afternoon.
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What changes should be made to the dose in the event of stress or illness? Dose should be
increased according to the 3-by-3 rule for stress/illness
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What are the drugs of choice for glucocorticoid replacement? Hydrocortisone, Prednisone and
Dexamethasone
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What is the drug of choice for mineralocorticoid replacement? Fludrocortisone
What are adverse effects associated with long-term glucocorticoid administration? Can any of these be
minimized, and if so how? How can we prevent adrenal suppression? ADE’s include adrenal suppression,
osteoporosis, glucose intolerance, infections, PUD, Myopathy and Psych disturbance. Adrenal Suppression
is when there is no CRH so the gland atrophies, to avoid this, doses should be tapered over 7 days or 50%
over 1 month.
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What are drug interactions/contraindications associated with glucocorticoid administration? NSAIDs,
Insulin, other anti-diabetics agents and Vaccines
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What is Cosyntropin used to test and diagnose? Cosyntopin test is used to measure the serum cortisol
levels, testes 3 times before the cosyntropin is administered, 30 mins after and 60 mins after. It is an ACTH
analog; a large dose is given and then cortisol levels are monitored. The levels should increase by 20mcg/dL
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Which test(s) is (are) preferred to diagnose hypothyroidism? Hyperthyroidism? To monitor hypothyroid
treatment? Serum TSH is used to diagnose hypothyroidism, monitor hypothyroid treatment, and
differentiate between primary and secondary hypothyroidism. Serum T4 is measured either total or free,
but free T4 is preferred to monitor treatment of hypothyroidism. Serum T3 measures total and free T3
levels while Free T3 is preferred to diagnose HypERthyroidsim.
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Why is management of hypothyroidism in infants and pregnant women especially important? Pregnant
patients present with pale, puffy, cold, and dry skin, who are lethargic and have goiter. Their fetus is at a
high risk for neurologic/mental impairment. The highest risk is during the 1st trimester but I difficult to
diagnose due to nonspecific symptoms. It is managed with thyroid hormone replacement therapy. Infants
present with protruding tongues, pot bellies, dwarf statures and delayed mental development. (If the
deficiency of thyroid hormone is mild, this condition is called hypothyroidism; however, if the deficiency is
severe this is categorized as myxedema. Patients with myxedema may experience a medical emergency
called myxedema coma which requires rapid repletion of thyroid hormone and steroids to reverse the
condition.)
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What medications are used to treat hypothyroidism? Synthetic T4= Levothyroxine and Liothyronine (PO and
IV), Synthetic Composite of T4+T3= Liotrix (PO), Animal= Armour Thyroid (PO, usually from pig and less reliable
potency)
o What are important counseling points for levothyroxine? (Hint! Think about administration
instructions, switching between brands) Take on an empty stomach, 30-60 mins before eating,
even small variations in does can dramatically impact patient, shouldn’t even switch brands, if
change then retest TSH in 6 weeks! Long half life, 7 days, so can miss a dose and be okay.
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Know how to convert from oral levothyroxine to IV levothyroxine and vice versa. For example, if a
patient is taking 50 mcg of oral levothyroxine, what would be the equivalent IV dose? IV dose is
~50% less than PO dose
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What medications are used to treat hyperthyroidism? Thionamides, Radioactive Iodine, Lugol’s and BB’s
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Thionamides- Methimazole and Propylthiouracil (PTU)
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Mechanism of action (what additional mechanism does PTU have?) Inhibits peroxidase, stopping
iodide from becoming iodine, which inhibits the coupling of iodine to tyrosine. PTU also blocks
T4->T4 conversion in the periphery.
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Adverse effects (which agent is associated with hepatotoxicity?) Generally well tolerated but may
cause agranulocytosis, symptoms of hypothyroidism and hepatotoxicity with PTU.
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Which agent is preferred in pregnancy? PTU
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Which agent has the shorter half-life, thus requiring more frequent dosing? Methimazole has a
longer half-life it is also dosed less frequently than PTU
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Which agent is considered a hazardous agent? What precautions must be taken by the nurse as
result? Methimazole, so wear gloves and be careful with pregnant/child-bearing age women
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Radioactive Iodine
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Mechanism of action: Iodine-131 is concentrated in the thyroid, beta particles destroy the thyroid
tissue but don’t leave the thyroid gland, maximal effects seen in 2-3 months.
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Advantages of this treatment option: cheap, no surgery, rare ADEs and no damage to non-thyroid
tissue
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Non-radioactive Iodine/Lugol’s Solution
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Mechanism of action: it’s taken up by the thyroid instead of iodine, preventing the thyroid’s ability
to make T3/T4. The larger the dose of Lugol’s, the less iodine the thyroid can pick up.
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Beta-blockers
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Mechanism of action in hyperthyroidism: prevents T4->T3 conversion ion the periphery
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Preferred beta-blocker for hyperthyroidism: Propanolol
Diabetes:
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Glycemic Goals: Tight vs Loose Glycemic Control. Tight=Intensive Insulin Therapy, its associated with higher
rates of hypoglycemia. The chosen approach should be based on the duration of DM, Age/Life Expectancy,
Comorbid conditions, Known CVD and Hypoglycemia unawareness. HgbA1c <7%, Premeal Glucose 80-130
mg/dL and Post-meal glucose <180 mg/dL.
How are insulins differentiated from one another? Insulins are grouped by onset of action and duration.
◦ The fastest onset is also the shortest duration. The slowest onset has the longest duration.
o Short Duration/Rapid-acting Insulins:
◦ Insulin aspart and insulin lispro
◦ Given with meals to control post-prandial rise in glucose
◦ OOA: 10-30 mins and Duration: 3-6 hours
o Short Duration/Slower-acting Insulin:
◦ Insulin Regular (like that produced in the body)
◦ Given before meals to control post-prandial rise in BG
◦ IV infusion for management of diabetic ketoacidosis
◦ OOA: 30 mins-1 hour and Duration: 6-10 hours
o Intermediate Duration Insulin:
◦ NPH Insulin
◦ Cloudy appearance (rest are clear)
◦ Used to control blood glucose between meals and overnight
◦ OOA: 60-120 mins and Duration: 16-24 hours
o Long Duration Insulins:
◦ Insulin glargine/U-100 and Insulin Detemir
◦ Used to control BG between meals and overnight
◦ OOA: 60-120 mins and Duration: 12-24 hours
◦ Tend to be longer acting than NPH insulin and they do not exhibit a ‘peak’ like NPH does. This
also decreases the risk of hypoglycemia.
◦ Administer at the same time every day.
o Ultra-long Duration Insulin:
◦ Insulin glargine (U-300) and Insulin degludec
◦ Used to control BG between meals and overnight
◦ OOA: 30-360 mins and Duration: >24 hours
Which blood glucose levels will each type of insulin decrease?
Which insulins can be mixed and what is the process for mixing?
o ONLY NPH and short-acting insulins can be mixed!
o Procedure for mixing insulins: first draw up short-acting insulin into the vial then draw NPH into the vial
second. CLEAR THEN CLOUDY.
How should insulin be stored? Refrigerate insulin never freeze!
o Open vials can be kept at room temp for 28 days max
o Avoid shaking the insulin
What are the adverse effects of insulin?
o HypOglycemia- BG<70, most important ADE!
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Signs and Symptoms: sweating, tiredness, dizziness, pale color, excessive hunger, tachycardia,
blurred vision, confusion and irritability
◦ Management: 15 g dextrose and recheck BG in 15 mins if conscious; if unconscious take
glucagon IM or IV dextrose 25-50 g if in hospital.
o Weight Gain
o HypOkalemia
o Allergic Reaction (NPH causes the most allergic reactions)
What counseling points should be included about insulin?
o How to administer the subcutaneous injection
o Make sure the appearance of the vial is normal for that type of insulin
o Keep the site consistent and use appropriately sized needle
o DDI’s with other hypoglycemic, hyperglycemic and beta blockers.
o Counsel pt on hypoglycemia signs/symptoms and management plus use of glucagon
Metformin:
o Drug of choice for type 2 DM, in the class Biguanides
o Avoid in pt’s with renal impairment
o What is the mechanism of action of metformin?
1. Inhibits glucose production in the liver
2. Sensitizes insulin receptors in skeletal and adipose tissue
3. Reduces glucose absorption in the gut
◦ *DOES NOT stimulate glucose release so has a LOW risk of hypoglycemia
o What are common and concerning adverse effects?
◦ ADE’s: Diarrhea, and other GI upset, decreased appetite, Vit B12 and folic acid deficientcy,
Lactic Acidosis- avoid use in pt’s with significant renal impairment.
◦ Monitor HbA1c, GI ADE’s and renal function.
◦ Counsel pt’s to not crush ER, take with food, start low dose and titrate up and GI upset is
common but should be temporary.
Sulfonylureas
o Second generation: Glipizide, Glyburide and Glimepiride
o First ORAL DM treatment
o Second gen are more potent, and fewer DDIs
o MOA: stimulates insulin release
o Highest risk for hypOglycemia
o ONLY FOR TYPE 2
o ADEs: hypoglycemia and weight gain
o Monitoring: HbA1c and BG
o DDI’s: alcohol- disulfiram reaction, hypoglycemic agents- like other insulins!!, beta-blockers: prevent
SU actions and mask hypoglycemic symptoms
o Counseling pts: signs/symptoms for hypoglycemia, management of hypoglycemia and to take the
medication BEFORE breakfast
Meglitinides:
o Repaglinide and Nateglinide
o MOA: stimulates insulin release (for type 2 DM)
o Admin: 3x a day WITH meals
ADE: hypOglycemia
Counseling pt’s: pt MUST eat within 30 mins of taking -glinides and signs/symptoms and management
of hypOglycemia
Thiazolidinediones: (TZDs)
o Pioglitazone and Rosiglitazone
o This class has been evaluated by the FDA for possible increase in CV events including MI, specifically
rosiglitazone so pioglitazone is preferred.
o MOA: sensitizes the body, makes the cells more responsive towards insulin
o Common ADE’s: upper respiratory infection
o Concerning ADE’s: exacerbation of existing heart failure and hepatotoxicity- so monitor the LFTs!
o (improves glucose control in type 2 DM)
o Do TZDs cause hypoglycemia? NOT TYPICALLY on its own.
o What disease states should not be combined with TZDs? Severe HF!
Alpha-glucosidase Inhibitors:
o Acarbose and Miglitol
o MOA: inhibits the enzyme that synthesizes monosaccharides from carbohydrates in the intestine, so by
inhibiting this enzyme the digestion of carbohydrates is slowed and post-prandial glucose decreases.
(improves glucose control in type 2 DM)
o ADEs: Flatulence, cramps, diarrhea and abdominal distension and bloating- counsel pt’s on these GI
ADEs
o Do AGIs cause hypoglycemia? NOT WHEN USED ALONE.
Dipeptidyl Peptidase-4’s/DPP-4 Inhibitors:
o Sitagliptin, Saxagliptin, Linagliptin and Alogliptin
o MOA: inhibits this enzyme which normally inactivates incretin hormones so these incretin hormones
now have a longer duration of action. (incretin=stimulate insulin/inhibit glucose) (improves glucose
control in type 2 DM)
o ADE’s: pancreatitis
o Monitor: BG when used with a sulfonylurea and signs/symptoms of pancreatitis
o Do DPP-4 inhibitors cause hypoglycemia? YES, when combined with sulfonylurea’s
Sodium-Glucose Co-Transporter 2/SGLT-2 Inhibitors:
o Canagliflozin, Dapagliflozin and Empagliflozin
o MOA: block reabsorption of glucose by the SGLT-2 transporter in the proximal convoluted tubules &
prevents glucose reabsorption in blood stream (type 2 DM)
o Concerning ADE’s: genital fungal infections, urinary tract infections
o Common ADE’s: dehydration, orthostatic hypotension
o Do SGLT-2 inhibitors cause hypoglycemia?
o Do SGLT-2 inhibitors affect weight? May cause weight loss!
o Monitor: signs/symptoms of dehydration, fungal infections and UTIs, DDIs with diuretics and how to
prevent orthostasis.
Glucagon-like GLP-1 Receptor Agonists/Incretin Mimetics
o Exenatie, Liraglutide, Lixisenatide, Albiglutide and Dulaglutide
o Subcutaneous Injections
o Indications: improving glucose control and promoting weight loss
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MOA: slows gastric emptying, suppresses appetite, stimulates glucose-dependent release of insulin,
and inhibits post-prandial release of glucagon
o ADE’s: GI upset, Pancreatitis, Renal Impairment, HypOglycemia, allergic reaction and thyroid cancer
(specifically with Liraglutide)
o Do GLP-1 receptor agonists cause hypoglycemia? Yes! With sulfonylureas or insulin use!
o Do GLP-1 receptor agonists affect weight? May cause weight loss!
o How are GLP-1 receptor agonists administered? Subcutaneously 1 hour before other oral medications!
o Counsel pt: on signs/symptoms of hypoglycemia and management, start lowest dose then titrate up to
void GI upset.
Identify 2 diabetic emergencies: Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar State (HHS)
What are the key components of therapy for each emergency?
o DKA: severe manifestation of absolute insulin deficiency
◦ Characterized hyperglycemia, ketoacid production, dehydration, acidosis and electrolyte
abnormalities.
◦ Usually occurs over hours to days with type 1 diabetics. It could lead to coma, shock and death.
◦ Treatment includes IV fluids for dehydration, Insulin and Potassium replacement (always given
together! Check K levels when admin insulin!)
◦ Caused by new type-1 DM, noncompliance to insulin therapy and stressful physiologic event
that requires more insulin that what is being administered
• Glucagon:
o MOA: promotes breakdown of glycogen to glucose, reduces conversion of glucose to glycogen and
stimulates gluconeogenesis
o Indicated in sever hypoglycemia when oral or IV dextrose cannot be administered
o OOA: 20 minutes (SQ)
What drugs can prevent detection of (mask the symptoms of) hypoglycemia? Beta-blockers because they mask the
symptoms like tachycardia
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