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INBDE Pharmacology Guide

Section #1 Antibiotics
Section 1: Antibiotics

There are two main ways antibiotics impact bacteria:

 The first is by killing bacteria - termed “bactericidal.”

 Classes of bactericidal drugs include:
o Penicillin
o Amoxicillin
o Augmentin
o Fluoroquinolones
o Cephalosporins
o Metronidazole
o Vancomycin
o Rifampin
 The other category is “bacteriostatic” drugs, which essentially stop bacteria
from reproducing/replicating, so they rely on the body’s immune system to
clear the infection.
 Examples of bacteriostatic drugs are:
o Macrolides
o Sulfonamides
o Lincosamides
o Tetracycline.
o Note: Bacteriostatic drugs should NOT be used in
immunocompromised patients because their body’s immune system is
not strong enough to fight infection.

It is essential to classify each antibiotic drug class one may see on the INBDE. We
will cover each class’s mechanisms of action and high-yield topics for the INBDE.

Penicillins

 Penicillins are by far the most common class of antibiotics prescribed in

dentistry.
  Mechanism of action:
o Block the formation of bacterial cell wall synthesis. More
importantly, they do this by inhibiting a transpeptidase that catalyzes
the last step in cell wall synthesis. Without a transpeptidase, bacterial
cell walls will lack integrity.
 The most significant side effect of penicillin is allergy to penicillin.
Penicillins will be the most commonly reported drug allergy for patients. It has
been estimated that up to 1 in 10 patients reports themselves as allergic. The
actual allergic number is much lower, but it is essential to pay attention when
one considers prescribing this drug.
 Penicillins are also the first-line drug to be prescribed for antibiotic
premedication for patients. Penicillin classes used in dentistry and ones that
commonly show up on the INBDE are listed below.
 Note: Sometimes, penicillins can also be called β-lactam antibiotics,
stemming from a functional group in its chemical structure. Do not get
confused by this terminology.

Source

Cephalosporins

 Mechanistically speaking, cephalosporins are similar to penicillins and will be

classified as β-lactams. Because they are so similar, it is worth noting that an
allergic cross-reaction is present, so if a patient reports being penicillin-
allergic, avoid prescribing cephalosporins as well. Any questions on the INBDE
 with a patient box that claims to have a penicillin-allergic patient,
automatically cross out cephalosporin.
 Cephalosporins are generally categorized into multiple classes based on
generation. Each generation differs in effectiveness and broadness of the
spectrum for bactericidal activity. It is easiest to view this in a table format
placed below.

Source

Lincosamides and Macrolides

Lincosamides and macrolides both inhibit the 50s subunit on a ribosome. When
ribosomes malfunction, protein synthesis stops. The critical difference is
that lincosamides are narrow-spectrum antibiotics, while macrolides are
moderate-spectrum antibiotics.

Clindamycin is perhaps the most important lincosamide.

For macrolides, the most important is azithromycin.

 In the new ADA recommendations for premedication, azithromycin is now

the second-line antibiotic when a patient is allergic to penicillin.
  In the past, clindamycin was prescribed as the second line antibiotic, but is no
longer recommended due to its high association with the risk of
developing Clostridium difficile.
 Due to the confusion on this topic and while we wait for the INBDE questions
to catch up to the new guidelines, below is how you might think through this
scenario.

1. If clindamycin is the only choice for a pen-allergic patient, choose it.

2. If clindamycin and azithromycin are possible answers, check the dosage.
1. If the doses are only correct for one or the other, pick the one with
the correct dose.
2. If the dosages for both drugs are correct, pick azithromycin.
3. Clindamycin dosage is 600mg 30–60 min prior to the
procedure. Azithromycin is 500mg 30–60 min prior to the procedure.

It can be unclear because the guidelines recently changed, yet old medications and
guidelines could still appear on the exam. Some other macrolides are used in
dentistry, such as clarithromycin and crythromycin. These are not typically
prescribed due to adverse reactions and ineffectiveness. Clarithromycin has been
linked to causing sudden cardiac toxicity and death. Erythromycin stimulates
motilin, which causes excessive gut motility. The takeaway from this section is to be
aware of clindamycin and azithromycin. See the table below for quick future
reference.

Source

Source

Fluoroquinolones

 These drugs are not commonly prescribed in dentistry; the most common
ones are ciprofloxacin and levofloxacin.
 Mechanism of action: Fluoroquinolones act by inhibiting enzymes involved
with DNA synthesis for bacteria. They specifically inhibit DNA gyrase and
topoisomerases.
  Be familiar with their black box warning or severe side effects — these drugs
have been linked to causing Achilles tendon ruptures.

Tetracyclines

 Tetracyclines inhibit the 30s subunit in ribosomal translation. This is not the
same as the 50s subunit that macrolides and lincosamides inhibit, so do not
get confused.
 The most commonly used tetracyclines in dentistry are minocycline and
doxycycline.
 An important note is that tetracyclines are used for patients with periodontitis.
These drugs build up in the gingival crevicular fluid and are effective in
targeting periodontal pockets.
 Another vital aspect of tetracyclines is that they can cause distinct banded
staining on the teeth during development. This staining appears as brownish-
green bands across the teeth (see image below). This pattern is a tell-tale
indicator of tetracycline use when the teeth were developing. Typically, this
discoloration would result from tetracycline use from the range of in-utero to
approximately age 8 from a tooth developmental standpoint.

Tetracycline staining example

Miscellaneous High-Yield Antibiotics

Metronidazole (Flagyl)
  Mechanism of action: Disruption of bacterial DNA. This drug is not effective
against aerobic bacteria.
 It is usually used to treat ANUG or ANUP in periodontal cases.
 Patients are strictly advised not to consume alcohol, which can produce a
disulfiram-like adverse reaction. Another unique effect is that it can cause a
metallic taste in the mouth.
 This drug also has a black box warning for being linked to carcinogenicity in
animal models.

Sulfa Drugs

 Sulfa drugs are not used frequently in dentistry, but it is important to

understand their mechanism of action just in case it randomly appears. It
inhibits PABA (para-aminobenzoic acid).

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 INBDE Pharmacology Guide
Section #2 Antibiotic Premedication Guidelines
Section #2 Antibiotic Premedication Guidelines

AAE 2017 Updated Guidelines for Antibiotic Premedication

Indications

 Prosthetic cardiac valves, including transcatheter-implanted prostheses and

homografts.
 Prosthetic material used for cardiac valve repairs, such as annuloplasty rings
and chords.
 Previous infective endocarditis.
 Unrepaired cyanotic congenital heart disease or repaired congenital heart
disease, with residual shunts or valvular regurgitation at the site of or
adjacent to the site of a prosthetic patch or prosthetic device.
 Cardiac transplant with valve regurgitation due to a structurally abnormal
valve.
 Patients with previous late artificial joint infection.
 Increased morbidity associated with joint surgery (wound
drainage/hematoma).
 Patients undergoing treatment for severe and spreading oral infections
(cellulitis).
 Patients with increased susceptibility to systemic infection.
 Congenital or acquired immunodeficiency.
 Patients on immunosuppressive medications (chemo treatment, radiation,
corticosteroids, organ transplant recipients/bone marrow recipients).
 Patients with diabetes with poor glycemic control (HbA1C greater than 8% or
blood glucose greater than 200 mg/dL).
 Patients with systemic immunocompromising disorders (rheumatoid arthritis,
lupus erythematosus).
 Patients for whom extensive and invasive procedures are planned.
 Before surgical procedures, patients are at significant risk for medication-
related osteonecrosis of the jaw.
 Vascular grafts less than six months old.
 Asplenic patients.
 Patients with Ventriculoatrial shunts (just this shunt; other shunts will not
require pre-med).

Contraindications

 Patients with uneventful healing from joint replacements (only patients that
have had infections on replaced joints require it).
 Any cardiac condition not listed above (mitral valve prolapse, rheumatic heart
disease, or stenosis) does not require it.
 Patients with a pacemaker.
 Breast implants.
  Cochlear devices.
 Dental implants.
 Intraocular lenses.
 Artificially implanted cardiac defibrillators.
 Hernia mesh repair.
 Cardiac stents.

Dental Procedures Where Premedications Would be Indicated

 Only dental procedures that create a potential for bacteremia require

antibiotic premedication.
 All procedures that involve manipulation of gingival tissue or the periapical
region of teeth or perforation of the oral tissue, including but not limited to:
o Scaling and root planing
o Extractions
o Flap elevation
o Taking a biopsy

Dental Procedures Exempt from Premedication

 Routine anesthetic injections through non-infected tissue.

 Making routine radiographs.
 Placement of removable prosthodontic or orthodontic appliances.
 Adjustment of orthodontic appliances, placement of orthodontic brackets.
 Shedding of deciduous teeth or bleeding from trauma to the lips or oral
mucosa.
 Placement of retraction cord.
 Suture removal.
 Rubber dam clamp isolation.
 Intracanal endodontic procedures.
 Routine restorative procedures.

Next, we discuss the most common first-line premedication drugs and their
recommended doses. In general, we start off using amoxicillin. If a patient is
allergic, the next best choice is azithromycin. The table below contains the new
2021 guidelines from the AHA.
Clindamycin is no longer recommended for antibiotic prophylaxis for dental
procedures.

IM indicates intramuscular; and IV, intravenous.

* Or other first- or second-generation oral cephalosporin in equivalent adult or

pediatric dosing.

† Cephalosporins should not be used in an individual with a history of anaphylaxis,

angioedema, or urticarial with penicillin or ampicillin.

Source

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 

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Section #3 Local Anesthetics
Section #3 Local Anesthetics

It is essential to classify dental local anesthetics into either amide or ester classes.
The INBDE loves to ask which drug is an ester or which drug is an amide.

Ester Local Anesthetics

 Esters were the first local anesthetics to be developed.

 Esters have a greater risk for allergic reaction than amides.
 Esters also generally cause more significant vasodilatory effects than amides,
which causes their duration of action to be shorter than amides.
 Pseudocholinesterase metabolizes esters in patient plasma.
 Examples of common ester local anesthetics are listed below:
o Procaine
o Tetracaine
o Cocaine: Causes vasoconstriction, no dilation! Contraindication to using
local anesthetics that contain epinephrine.
o Benzocaine - 20% benzocaine is commonly used as a topical
anesthetic.
The drugs listed above are not commonly used clinically, besides benzocaine, simply
due to their drawbacks. Amide local anesthetics have a better effect, duration of
action, and decrease allergic risk in patients.
Amide Local Anesthetics

 Amides are more newly developed than esters.

 They are the local anesthetic of choice used for dental treatment because
they are more effective at achieving intraoral anesthesia.
 One drawback is that they pose a greater risk of systemic toxicity than esters;
these toxic reactions are dose-related. We will discuss dose limitations for
adults, kids, and patients with heart diseases later.
 Amides are metabolized within patient liver by CYP450 enzyme (as opposed
to esters which are metabolized by pseudocholinesterase in plasma).
 Examples of amide local anesthetics include:
o Lidocaine (xylocaine)
o Articaine (septocaine): Metabolized by esterases
(pseudocholinesterase)*** exception to liver metabolism rule in the
amide class.
o Mepivacaine (Carbocaine)
o Bupivacaine (Maracaine): Long duration of action 6–9 hours.
o Prilocaine (Citanest): Can cause methemoglobinemia, treated with
methylene blue dye.
o Etidocaine (Durant)

Mechanism of Action

 Local anesthetics act on nerve membranes to prevent the generation and

conduction of action potentials. The brain cannot decipher any pain if an
action potential is not generated.
 Local anesthetics prevent action potentials by binding to voltage-gated Na+
ion channels. After they bind to the Na+ ion channels, they close the channel,
which prevents Na+ from flowing through the channel. When Na+ cannot
pass through the nerve, it cannot form an action potential, thus preventing
the brain from receiving the pain stimulus.

Local Anesthetics pH and Diffusion

 Local anesthetics are all weak bases combined with acids.

 This allows them to form water-soluble salts.
 The uncharged free base form will penetrate the lipid bilayer when local
anesthetics are first injected. Once it passes through, some molecules will
change into their charged acidic form and begin to equilibrate.
 It is important to note that only the acidic or charged form of local anesthetic
can bind to the voltage-gated Na+ channels.
 A clinical example of pH and diffusion can be shown through patients with
active dental infections. Since the infected tissue is more acidic (5–6 pH) than
normal tissue (7 pH), it changes the disassociation of the local anesthetic,
which impacts how quickly the local anesthetic will work. This is caused by
 more of the local anesthetic staying in its charged ionic form which cannot
cross the nerve membrane.

Allergies to Local Anesthetics

 True allergies are infrequent.

 Most reported complications of allergies are due to previous intravascular
injections, which can cause patient discomfort.
 Most true allergic reactions are caused by the ester group (PABA). Hydrolysis
of the ester group leads to the formation of PABA-like compounds. It is worth
noting that research has found that someone who is allergic to esters is not
also allergic to amides. So, just because patients may have an actual allergy
to an ester local anesthetic like benzocaine, it does not mean they will have a
true allergy to lidocaine.

Metabolism

 IMPORTANT RECAP:
o Esters: Metabolized (hydrolyzed) in the plasma by
pseudocholinesterase enzymes. Drugs with a high rate of hydrolysis
are the least toxic (since they break down fast). Tetracaine has the
lowest hydrolysis rate, making it the most toxic in the ester category.
o Amides: Primarily metabolized in the liver by CYP450. In general,
decreased blood flow to the liver causes slower biotransformation. This
leads to higher blood levels and more toxic reactions. Use caution
when giving amides to patients with hypotension, liver
disease/cirrhosis, and heart failure.
o Prilocaine: Also metabolized in the lung to some degree.

Vasoconstriction

 All local anesthetics have some degree of vasodilating activity in their raw
form. This leads to increased absorption rate, higher plasma levels (increased
risk of cardiovascular toxicity), faster clearance (decreased depth and
duration of action), and increased bleeding at the injection site. These are
typically undesirable properties.
 Thus, vasoconstrictors are usually added, such as epinephrine. They function
to prolong the duration of action of the local anesthetic by reducing blood
supply to the area and causing more local anesthetic to enter the nerve,
increasing the duration of action.
 Vasoconstrictors also limit bleeding during procedures, limit systemic
absorption of drugs, reduce systemic toxicity, and increase the depth of the
anesthesia.

Dosages

 Below are numbers that can easily be memorized to calculate any dosage
questions quickly.
 o mL in 1 carpule is 1.7 or 1.8 mL.
o 2% lidocaine has 34 mg or 36 mg per carp, depending on if 1.7 or 1.8
mL is the starting point.
o 4% articaine would then have 68 mg or 72 mg depending on starting
carp mL they give.
o These numbers can be used to quickly calculate how many mg of
lidocaine may be in 5 carps (e.g. 5 × 34 = 170 mg).
o For children, use the rule of 1 carp per 20 pounds. This is not the
textbook calculation, but for simplicity’s sake, it provides a very close
mathematical approximation.
o Vasoconstriction calculations: Know that 0.034 mg is in 1:100,000.
From there, figure out that 0.068 mg would be in 1:50,000 or that
0.017 mg would be in 1:200,000.
o Patients with cardiovascular disease: ALWAYS LIMIT EPI TO 0.04 mg!
This is about 2.3 carps per standard 1:100,000 epi in 2% lidocaine.
Never give more than two carps to a patient with severe cardiovascular
disease or when taking a non-selective beta-blocker.

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Section #4 Pain Management and Dental Analgesia
Section #4 Pain Management and Dental Analgesia

The image below provides an overview of Rx pain medications:

NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)

3 Classes and Mechanisms of Actions:

 Aspirin
o ASA (acetylsalicylic acid), also known as aspirin, acts to irreversibly
inhibit COX-1 and COX-2 enzymes. In general, these are not used
to control dental pain. They are less potent and cause more side
effects than non-aspirin NSAIDs.
o A key note is that aspirin will suppress platelet activity, which is why it
can cause bleeding when combined with other blood thinners. Again,
the effect is irreversible.
 Coxibs
o Selectively inhibiting COX-2, these avoid the GI side effects resulting
from the suppression of prostaglandins synthesized by COX-1. A key
note is that Coxibs increase cardiovascular events like MIs and strokes.
Again, not commonly used due to the increased risk of thrombosis,
myocardial infarction, and strokes.
 Non-Selective COX inhibitors
 o Most commonly used in dentistry, this class of NSAIDs
include ibuprofen and naproxen (Aleve).
o They have varying inhibitory effects against COX-1 and COX-2.
Remember: blocking COX leads to inhibition of prostaglandins (see
below).

Dosing of ibuprofen:

 The maximum prescribed dose for ibuprofen is 3,200 mg/day.

 The maximum OTC use of ibuprofen by patients is 1,200 mg/day.

Contraindications for NSAIDs:

 NEVER prescribe NSAIDs to patients with the following:

o Moderate renal failure or kidney disease.
o Already taking an NSAID; OTC or Rx by another doctor.
o Taking an anticoagulant like warfarin or apixaban.
o Patients with peptic ulcer disease or hiatal hernias.

Acetaminophen (Tylenol)
Mechanism of action:

 Acetaminophen is commonly used in the dental setting.

 The mechanism of action is not fully understood yet, but it is important to
remember that it inhibits a secondary step involved in prostanoid synthesis by
COX-1 and COX-2 enzymes.
 Another critical note is that because it impacts a secondary step, it has
minimal anti-platelet and anti-inflammatory effects (unlike NSAIDs).
 While Acetaminophen does not have anti-platelet or anti-inflammatory effects,
it does elicit antipyretic and analgesic effects.
  There are also no significant GI, renal, or cardiovascular risks (unlike
NSAIDs).

Dosing of acetaminophen:

 The maximum prescribed use is 4,000 mg/day.

 The maximum OTC use by patients is 3,000 mg/day.
 Maximum chronic use without monitoring is 2,600 mg/day.
 Doses greater than 2,765 mg/day will increase INR in anticoagulated warfarin
patients.

Toxicity:

 Severe liver injury is most concerning here because the liver is responsible
for metabolizing acetaminophen. If a patient overdoses, they will overload
and damage their liver.
 Due to this, be careful prescribing acetaminophen to patients with liver
impairment.

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Section #6 Cardiovascular Drugs
Section #6 Cardiovascular Drugs
Hypertension

 High blood pressure is very common, and many antihypertensives appear on

patient health history forms. Because the hypertension guidelines have
changed in recent years, we will see even more patients being prescribed
these drugs. (Refer to the reference ranges listed below)
 Hypertension diagnosis guideline:
o Normal
 Systolic < 120 mmHg
 Diastolic < 80 mmHg
o Elevated
 Systolic 120–129 mmHg
 Diastolic < 80 mmHg
o Hypertension stage 1
 Systolic 130–139 mmHg
 Diastolic 80–89
o Hypertension stage 2
 Systolic ≥ 140 mmHg
 Diastolic ≥ 90 mmHg
o Hypertensive urgency
 Systolic > 180 mmHg
 Diastolic > 120 mmHg
 If the patient’s blood pressure falls within the hypertensive
urgency category, it is advised to defer elective treatment.
 If the patient is symptomatic and has any chest
pains/discomfort, dizziness, or other symptoms, it is best to
refer them to the emergency room for evaluation ASAP.
 The patient should be referred to a physician for further
diagnosis.
Hypertension Drug Classes and Their Respective Drugs

 ACE inhibitors
o Drugs (“-pril”)
 Lisinopril (Prinivil, Zestril)
 Captopril (Capoten)
 Enalapril (Vasotec)
 Benazepril (Lotensin)
o Mechanism of action: Inhibit angiotensinogen converting
enzyme (ACE). It is essential to know that ACE works to convert
angiotensin I to angiotensin II. When angiotensin II formation
decreases or is blocked by ACE, blood pressure in the body decreases.
(See diagram below for the entire pathway)
 
o Adverse effects
 Chronic dry cough
 Angioedema
 Scalded mouth syndrome
 Orthostatic hypotension
 Oral lesions
 Angiotensin II receptor blockers
o Drugs (-sartan)
 Losartan
 Valsartan
o Mechanism of action
 Similar to ACE, inhibitors act on a different part of the pathway.
Angiotensin II is what signals the body to increase blood
pressure. These drugs will block the binding of Angiotensin II to
their AT1 receptors in the body.
o Adverse effects
 Similar to ACE inhibitors, the critical difference is that these do
not cause a chronic dry cough and are way more expensive.
 Diuretics
o All of these drugs reduce blood pressure by driving water out of the
bloodstream.
o Thiazide diuretics
 Drugs
 Chlorthalidone
 Chlorothiazide
 Chlorothiazide
 Mechanism of action:
  Thiazides inhibit sodium (Na+) and Chloride (Cl-)
reabsorption from the distal convoluted tubule in the
kidney. Remember, water follows sodium, so less sodium
being reabsorbed means the water will stay with it and
leave the body as well.
 Adverse effects
 Slight xerostomia
 Cause oral mucosal lesions
 Hypokalemia (may cause heart arrhythmias)
 Increased cholesterol and LDL numbers
 High uric acid (can cause gout)
 High blood sugar
 Hemolytic anemia
o Loop diuretics
 Drugs
 Furosemide (Lasix)
 Torsemide (Demadex)
 Bumetanide (Bumex)
 Mechanism of action
 Selectively inhibit Sodium (Na+) and chloride (Cl-)
reabsorption in the thick ascending limb of the kidney.
These drugs will also cause calcium loss. Note that this is
very similar to thiazides. The only difference is which part
of the nephron loop sodium reabsorption is blocked.
 Adverse reactions
 Dehydration
 Hypokalemia, hypomagnesemia, hyponatremia
 Oral lichenoid lesions
 Xerostomia (much more severe than thiazides)
 Ototoxicity
 High uric acid (can cause gout)
o Potassium sparing diuretics
 Drugs
 Spironolactone
 Amiloride
 Eplerenone
 Triamterene
 Mechanism of action
 Acts as an aldosterone antagonist. It will bind specifically
at the aldosterone-dependent sodium-potassium
exchange site in the distal convoluted renal tubule. This
causes sodium and water excretion and potassium
retention.
 Adverse reactions
 Gynecomastia (male breast development)
 Hyperkalemia (opposite of thiazides and loop diuretics)
 Beta-adrenergic blockers (beta-blockers, end in “-olol”)
o Types of beta-blockers
  Beta-1 receptors in the heart
 Blocking these will decrease heart rate and contractility.
 Beta-2 receptors in the smooth muscle of peripheral
vasculature
 Blocking these will cause vasodilation, decreasing
peripheral resistance and blood pressure.
 Nonselective beta-blockers (block both beta-1 and beta-2
receptors)
 Carteolol
 Propranolol
 Timolol
 Sotalol
 Nadolol
 Penbutolol
 Selective beta-blockers (block only beta-1 receptors)
 Acebutolol
 Atenolol
 Metoprolol
 Bisoprolol
 Betaxolol
o Mechanism of action: These drugs block beta receptors, which can be
found in the heart and the blood vessels. This promotes decreased
heart contractility and heart rate, and causes vasodilation.
o Adverse effects
 Cold fingers/toes
 Difficulty sleeping/nightmares
 Tired, dizzy, lightheadedness
 Nausea
o Local anesthetic administration with beta-blockers
 Patients that take nonselective beta-blockers: Limit epi to about
2.5 carpules of 1:100,000 epi every two hours.
 Patients who take a selective beta-blocker: Limit epi to about
five carpules of 1:100,000 epi every two hours.
 The reasoning is that since beta receptors are blocked, we have
unopposed α-1 receptors that are active. This causes a
significant increase in vagal tone, making the vessels constrict.
This will cause hypertension and bradycardia.
 Calcium channel blockers
o Drugs
 Amlodipine
 Diltiazem
 Felodipine
 Verapamil
 Nifedipine
 Isradipine
 Nisoldipine
 Nicardipine
 Nimodipine
 o Mechanism of action: These drugs block calcium from entering the
heart through their slow channels. Without calcium, the heart relaxes.
o Adverse effects
 GINGIVAL OVERGROWTH! (appears on INBDE time and time
again)
 Headache
 Dizziness
 Fast heartbeat (tachycardia)
 Edema
 Alpha receptor antagonists
o Drugs (-”zosin”)
 Doxazosin
 Prazosin
 Terazosin
o Mechanism of action: These drugs inhibit alpha receptors. Alpha
receptors, for cardiology purposes, cause vasoconstriction. Blocking
them decreases blood pressure.
 These drugs will also treat benign prostate hypertension (BPH).

Angina (Chest Pain)

 Types
o Stable angina
 Chest pain and symptoms occur upon physical exertion and
dissipate upon rest (when the patient runs they experience
chest pain). When they stop, the pain goes away.
o Unstable angina
 Spontaneous symptoms of chest pain that can occur at rest (the
patient was watching TV and experienced chest pain).
o There are two other types of angina; Nocturnal and variant. Do not
spend too much time studying these.
 Symptoms of angina
o Typically patients experience pressure, weight-bearing, and tightness
over the chest. People sometimes describe it as an elephant sitting on
their chest.
o The pressure, weight, or tightness usually occurs between the
epigastric region and the pharynx.
o Duration: Not specified; it can last from 1 to 30 minutes.
o Essential hints or descriptives that can help one lean towards an
angina episode. The above symptoms can also overlap with other non-
life threatening issues such as acid reflux (GERD) or even a panic
attack. A big difference is that chest pain associated with angina can
radiate to the left arm, shoulder, or jaw area. If the patient has chest
pain that starts to radiate in these areas, be very wary of the patient
having an anginal episode. This can be crucial when differentiating
from other diseases/issues.
 Pharmacologic management
 o The overall goal is to get more oxygen to the heart and prevent
ischemia from occurring.
o Drug
 Nitroglycerin
o Mechanism of action: Stimulates guanylyl cyclase; this activates a
cascade that causes relaxation of vascular smooth muscle and arterial
relaxation/dilation. This causes a decrease in myocardial wall tension
and dilates heart vessels, allowing the heart to have less oxygen
demand and increase oxygen flow to the heart.
o Dispensing nitroglycerin
 After giving nitroglycerin to a patient, wait 5 minutes and see if
symptoms subside.
 If they do not, give them another dose.
 If nothing happens after the second dose, give one more
nitroglycerin tablet, have them chew a baby aspirin (81 mg),
and call EMS/9-1-1.
o Adverse reactions
 Severe headache
 Orthostatic hypotension
 Palpitations

Cardiac Arrhythmias

 This is a difficult section, so if it is really frustrating, consider moving on and

coming back when time allows. Don’t spend all your time here.
 Classes of drugs: Drugs here are separated into classes. These classes
correspond to what part of the EKG phase impacts the heartbeat.
o Class 1A
 These prolong action potential duration by blocking SODIUM
channels.
 Drugs used
 Quinidine, procainamide, disopyramide
o Class 1B
 These block sodium channels and have RAPID dissociation.
 Drugs used
 Lidocaine, mexiletine
o Class 1C
 These block sodium channels and have SLOW dissociation.
 Drugs used
 Flecainide, propafenone
o Class II
 Beta-blockers
 Drugs used
 Propranolol, sotalol, esmolol
o Class III
 These prolong action potential duration by blocking POTASSIUM
channels.
 Drugs used
  Amiodarone, sotalol, ibutilide, dofetilide,
dronedarone
o Class IV
 Calcium channel blockers
 Drugs used
 Verapamil, diltiazem
 Miscellaneous drug
o Digoxin: for whatever reason, the boards sometimes ask about this
drug's mechanism of action. It is no longer used, but note that it is a
sodium/potassium ATPase inhibitor! It ultimately makes the heart
contract stronger.
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Section #7 Antifungals
Section #7 Antifungals
Fungal Infections

 Most fungal infections stem from compromised immune systems and/or

disruption of normal flora (they are typically opportunistic).
 Most antifungal drugs take advantage of one key feature of fungi:
o The sterol group critical to maintaining plasma membrane structure in
fungi is different from that of our mammalian cells.
o Our cells contain cholesterol, while fungal cells contain ergosterol.
o Remember
 Mammalian cells = Cholesterol
 Fungal cells = Ergosterol
 Note that their function is very similar in that they help maintain cell integrity
and normal cell membrane homeostasis through regulating fluids, ions, and
growth.

The following antifungals are important to be familiar with:

 Terbinafine (Lamisil)
o Not used in dentistry, but commonly used in general
o Mechanism of action
 Targets and inhibits squalene monooxygenase (also called
squalene epoxidase) which is involved in making ergosterol for
fungi cell membranes.
 Once squalene is inhibited, it will also accumulate within the cell
and will further act to weaken the fungal membrane.


o Adverse effects
 Can cause severe liver problems, including liver failure
 Rash
 Headache
 Fever
 Stomach pain

Polyenes
  Amphotericin-B
o Mechanism of action
 Binds to ergosterol in fungal membranes. Once bound, it forms
a pore within the membrane. This hole causes ion leakage and
cell death.
o Uses
 Only used for severe, life-threatening fungal infections.
 Not common for infections of the mouth, throat, or vagina.
o Adverse effects
 Nicknamed “ampho-the-terrible” from having an extensive list of
side effects
 Nephrotoxicity - decreases blood flow and causes ischemia
 Nausea
 Vomiting
 Stomach pain
 Hypotension
 Anemia
 Arrhythmias
 Fever and chills
 Nystatin
o Mechanism of action (same as amphotericin)
 Binds to ergosterol in fungal membranes. Once bound, it forms
a pore within the membrane. This hole causes ion leakage and
cell death.
o Unlike amphotericin, nystatin is used to treat mild-moderate fungal
infections of the mouth, throat, GI tract, vaginal mucosa, and angular
cheilitis candida infections.
o Adverse effects
 Mouth irritation
 Skin rash
 Upset stomach, nausea, vomiting
 Fast heart rate

Azoles (miconazole, clotrimazole, and fluconazole are common in dentistry)

 Note: All azoles are teratogenic***

 Mechanism of action
o Inhibit fungal cytochrome P450 enzymes. These enzymes convert
lanosterol to ergosterol. Again, if the fungi cannot produce ergosterol,
their cell membranes lack integrity.
 Imidazoles
o Drugs:
 Miconazole
 Ketoconazole
 Clotrimazole
o Great for angular cheilitis treatment.
o Troches 10mg 5x daily great for oral candidiasis.
 Triazoles
 o Fluconazole (Diflucan) - another common dental Rx
 Adverse reactions
 Abdominal pain
 QT prolongation and torsade de pointes
 Nausea
 vomiting
o Itraconazole (Sporanox)
o Voriconazole (Vfend)
o Posaconazole (Noxafil)
o Isavuconazonium (Cresemba)

Echinocandins

 Drugs:
o Caspofungin
o Anidulafungin
o Micafungin
 Mechanism of action
o Echinocandins target 1,3 β-d-glucan synthase enzymes. This enzyme
forms β-glucans, which are crucial for fungal cell membrane integrity.
 Adverse effects
 Bilirubinemia
 Nausea
 Vomiting
 Hepatotoxicity
 Histamine release (flushing, pruritus, rash, fever)

Flucytosine (5-FC)

 Oral synthetic pyrimidine antimetabolite

 Mechanism of action
o Inhibits fungal DNA synthesis and protein synthesis.
o It penetrates the cell wall and gets converted to 5-fluorouracil. Once
converted, it competes with uracil and gets incorporated into fungal
DNA and RNA, causing unbalanced growth and cell death.

Summary
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Section #8 Anticoagulants
Section #8 Anticoagulants
Anticoagulants are common in patients with the following indications:

 Venous thrombosis
 Atrial fibrillation
 Mechanical heart valve
 Pulmonary embolism
 Previous heart attack, acute myocardial infarction
 Cerebrovascular accident
 Valvular heart disease
 Stroke
The Clotting Pathway

 Drugs for anticoagulation act at various points on the clotting cascade

(below). Where or what factor they block leads to the different mechanisms
or categories of drug classes.
o Intrinsic and extrinsic pathways differ in where the blood clot begins.
 Intrinsic pathway - initiated by factors in the blood. Exposed
endothelial collagen will activate this pathway.
 Extrinsic pathway- initiated by tissue factor released from
endothelial cells after external damage.
 Both pathways converge on Factor X. Factor X is very
important for clotting, and some drugs will act directly on it.

Warfarin (Coumadin)

 A vital drug to know, key points below.

 Mechanism of action
o Inhibits vitamin K epoxide reductase.
o Vitamin K-dependent clotting factors are II, VII, IX, and X.
o Therefore, warfarin stops vitamin K formation and indirectly blocks all
those clotting factors from being able to form, which causes decreased
clotting.
 Adverse effects
o Bleeding
o Teratogenic
 Dental management
 o It is important to take an INR for patients on warfarin to assess their
bleeding risk. This is especially crucial for tooth extractions and all
other surgeries in dentistry.
o INR Ranges
 Greater than 3.5: P:atients are at significant risk for bleeding.
We want the number to be lower than 3.5 for surgery.
 3–3.5: Most routine extractions can proceed with some caution,
but there can be significant bleeding with major oral surgery
(alveoplasty, full arch extractions with flaps reflected, or surgical
extractions requiring bone removal).
 Less than 3: The “Green zone”. This is where we want the
patient to be for oral surgery.
o Avoid aspirin and NSAIDs when patients are on warfarin.
 When performing oral surgery, do not prescribe these to
manage pain. The reason is that aspirin and NSAIDs also have
some anticoagulation properties. The patient would have an
increased risk of bleeding by taking these while on Warfarin.

Heparin

 Mechanism of action
o Overall, clotting factors II (thrombin) and X.
o More specifically, heparin binds to antithrombin III, forms a complex,
and irreversibly inactivates factor II, and X.
o Note heparin is an indirect-thrombin inhibitor, not direct! The direct
inhibitors are below.

Factor Xa Direct inhibitors


o Drugs
Rivaroxaban (Xarelto)
Apixaban (Eliquis)
o Mechanism of action
 Blocks factor X formation.
 Recall this is where both intrinsic and extrinsic pathways
converge.
o Reversal agent
 Portola

Factor IIa Direct inhibitors (Factor II is also known as thrombin)

 Drugs
o Dabigatran (Pradaxa)
 Mechanism of action
o Blocks thrombin (factor II) formation
 Reversal agents
o Praxbind
Antiplatelet drugs

 These anticoagulants are direct and indirect factor inhibitors. Nonetheless,

they still have anticoagulative effects.
 Drugs
o Aspirin
 Mechanism of action
 Irreversibly blocks cyclooxygenase-1 in platelets. This
inhibits the formation of thromboxane, a vasoconstrictor,
and platelet aggregate.
 Note this is different from NSAIDs which REVERSIBLY
inhibit cyclooxygenase-1.
o Clopidogrel (Plavix), Ticagrelor (Brillinta), Prasugrel (Effient)
 Mechanism of action
 These three drugs above block a receptor on platelets
called P2Y12. This prevents ADP (adenosine diphosphate)
from activating platelets.
 Adverse reactions
 The biggest one for all of these is excessive bleeding!

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Section #9 Antivirals

Section #9 Antivirals

Pharmacotherapy of Viral Infections

 These drugs are only active against replicating viruses (they stop the virus
from creating more of itself and getting worse).
 Viral drugs are not curative in nature and largely have no remedy; they help
mitigate patient symptoms.

Retrovirus

Questions on HIV are common, so this retrovirus section is important.

 A retrovirus is any RNA virus that inserts a copy of their genome into the host
cell (genome) to replicate.
 Retroviruses transcribe their RNA into DNA once they infect or enter host
cells. They package with their material an enzyme called Reverse
transcriptase (RT).
o RT generates a complementary DNA strand from an RNA template.
o RT transcribes single-stranded RNA into double-stranded DNA.
 Once RT transcribes viral RNA to DNA, it will use an integrase enzyme that
fuses the viral-created DNA into our actual DNA, so the host cells now encode
information to create the virus.
HIV Drugs

 In the past, HIV was essentially non-treatable, and drugs were not very
effective.
 Today though, people can live a long life with HIV, and the drugs target many
areas of the HIV replication cycle. In some patients, the viral load may even
be undetectable, but these drugs will not cure the patient! The goal of HIV
treatment is to reduce the viral load to be as low as possible.
 Nucleos(t)ide reverse transcriptase inhibitors (NRTIs)
o Drugs
 Zidovudine (Retrovir)
 Lamivudine (Epivir)
 Abacavir sulfate (Ziagen)
 Emtricitabine (Emtriva)
 Tenofovir disoproxil fumarate (Viread)
o Mechanism of action
 These drugs interfere with reverse transcriptase from
converting RNA to DNA.
 Once the drugs enter the host cells, they are phosphorylated to
an active form and act as a chain terminator for DNA synthesis,
stopping DNA from becoming replicated to completion.
o Adverse effects
 Mitochondrial Toxicities
 Lactic acidosis
 Pancreatitis
 Peripheral neuropathy
 Hepatic steatosis
 Lipoatrophy
 Integrase Strand Inhibitors
o Drugs (all end in -gravir)
 Raltegravir (Isentress)
 Elvitegravir (Vitekta)
 Dolutegravir (Tivicay)
 Bictegravir (Biktarvy)
o Mechanism of action
 Block the HIV enzyme integrase.
 Without functional integrase, HIV cannot splice its viral-created
DNA into our human DNA.
o Adverse Effects
 Diarrhea
 Nausea
 Fatigue
 Dizziness
 Insomnia
 Protease inhibitors
o Drugs
 atazanavir sulfate (Reyataz)
 darunavir ethanolate (Prezista)
 fosamprenavir calcium (Lexiva)
 ritonavir (Norvir)
 saquinavir mesylate (Invirase)
 tipranavir (Aptivus)
 indinavir sulfate (Crixivan)
 nelfinavir mesylate (Viracept)
o Mechanism of action
 Bind to protease and block their ability to function.
 HIV depends on aspartate protease to assemble active virions.
If protease is inhibited, HIV is no longer infectious.
o Adverse effects
 Insulin resistance
 Development of gallstones and kidney stones
 Changes in the taste of food
 Insomnia
 Elevated cholesterol
 Hyperglycemia
Image Source

Antiherpes Drugs
Exam tip: Oral pathology images showing a herpetic infection on the lip or oral
cavity are common, along with a followup question on which drug should be
prescribed to treat the outbreak. Note that these drugs also work for shingles.

 Acyclovir (Zovirax)
o Mechanism of action
 Converted to a triphosphate form in the body, which then acts
to inhibit viral DNA polymerase from working. The triphosphate
form also incorporates itself into and terminates the growing
viral DNA chain.
o Adverse effects
 Joint pain
 Hair loss
 Upset stomach
 Nausea
 Vomiting
 tiredness
 Valacyclovir (Valtrex)
o Mechanism of action
 When Valacyclovir enters the body, it is converted to acyclovir,
so the mechanism of action is the same as listed above. A key
note is that valacyclovir is more orally bioavailable, so it is used
more frequently today.
o Adverse effects
 Headache
  Malaise
 Upset stomach
 Nausea
 vomiting
 Famciclovir (Famvir)
o Mechanism of action
 Like acyclovir, it gets phosphorylated upon entry to the cells
after it inhibits viral DNA polymerase, thus blocking DNA
synthesis of the virus. The only difference is that famciclovir
does not cause chain termination.
 Docosanol (Abreva)
o A cream you can apply to cold sores at earliest onset of symptoms.
o Mechanism of action
 Docosanol inhibits the fusion between the plasma membrane
and the viral envelope. If this can not happen, the virus can not
enter the cell and begin its replication process.
o Adverse effects
 Acne
 Burning
 Rash
 Dryness
 Redness
 Swelling of area

Anti-Influenza Drugs

 Drugs
o Zanamivir (Relenza)
o Oseltamivir (Tamiflu)
o Peramivir (Rapivab)
 Mechanism of Action
o Neuraminidase inhibitors act by blocking the active site of
neuraminidase on viral envelopes and uncleaved sialic acid residues on
the surface of host cells and viral envelopes.
Image Source

 Adverse effects
o Diarrhea
o Nausea
o Sinusitis
o Bronchitis
o Cough
o Headache
 Rare adverse reactions
o Toxic epidermal necrolysis
o Stevens-Johnson syndrome

Viral Hepatitis B

 Drugs
o Tenofovir disoproxil fumarate (Viread)
 Note this drug is also used to treat HIV
o Entecavir (Baraclude)
 Mechanism of action
o These are nucleoside reverse transcription inhibitors.
o Interfere with reverse transcriptase from converting RNA to DNA.
 o Once the drugs enter the host cells, they are phosphorylated to an
active form and act as a chain terminator for DNA synthesis, stopping
DNA from becoming replicated to completion.
 Adverse effects
o Can cause lactic acidosis
o Kidney problems
o Liver problems
o Fanconi syndrome (watch for this buzzword)
o Osteomalacia

Hepatitis C

 Quick facts
o HepC can be 100% cured by drugs, which is not typical of antivirals.
o Treatment usually lasts 3 to 4 months.
 Drugs used
o Ribavirin
 Side effects
 Decreases red blood cells and anemia
 Nausea and vomiting
 Changes in ability to taste
 Muscle pain
 Difficulty sleeping
 Memory loss
o Grazoprevir
o Sofosbuvir
o Dasabuvir
o Ledipasvir
o Elbasvir
o Interferons
 Note that these drugs treat Hep-C. These drugs are often combined with
others in treatment and are not always stand-alone drugs.

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Section #10 Parkinson Drugs
Section #10 Parkinson Drugs
What is Parkinson disease?

 Loss of dopamine neurons in the basal ganglia (more specifically in the

substantia nigra).
 Dopamine in the basal ganglia regulates motor tone and modulates
learning and memory.
 Symptoms of Parkinson
o Resting tremor
o Rigidity
o Bradykinesia
o Postural instability
o Cognitive impairment
o Autonomic dysfunction
o Sleep disorders
o Psychiatric manifestations
 Around 60–80% of cells are lost by the time symptoms appear.
 The average age of onset is 60 years old.

Drug Therapy

 Dopamine (DA) replacement

o DA replacement with levodopa/carbidopa is the primary drug given.
o Levodopa is a neutral amino acid precursor of dopamine and
norepinephrine.
 o Normal dopamine cannot cross the blood-brain barrier. Thus, Parkinson
patients are given levodopa which can cross the blood-brain barrier
and then becomes converted to dopamine once in the CNS.
o Levodopa is decarboxylated to dopamine by dopa-decarboxylase in the
brain and not in the periphery.
o Carbidopa inhibits dopa-decarboxylase in the periphery.
o This prevents it from getting metabolized prior to entering the brain,
which is why it is commonly given with levodopa.
o The efficacy of levodopa/carbidopa decreases over time for patients.
o Adverse effects
 Levodopa-induced dyskinesias are the most severe challenge
with long-term therapy, so clinicians often delay utilization of
carbidopa/levodopa as long as possible.
 Catechol-O-Methyltransferase inhibitors (COMT)
o COMT metabolizes dopamine/levodopa, which decreases its
effectiveness when taken to treat Parkinson.
o Tolcapone
 Tolcapone inhibits both central and peripheral COMT, but it is
hepatotoxic, thus not used often.
o Entacapone
 Inhibits peripheral COMT and is not hepatotoxic. Hence,
typically the drug of choice.
o Both drugs are reversible inhibitors of COMT. They will allow more
levodopa to reach the CNS.
 Monoamine oxidase type-B inhibitors
o Selegiline
 Converted to amphetamine metabolites during the first pass
through the liver.
o Rasagiline
 More potent than selegiline.
 Unlike selegiline, it is not metabolized to a toxic amphetamine
metabolite.
o These are selective irreversible inhibitors of MAO-B, the primary
enzyme in the striatum responsible for dopamine metabolism.
o Contraindications
 Meperidine/fentanyl derivatives
 Methadone
 Dextromethorphan
 Most antidepressants
 Indirect or mixed-acting sympathomimetics
 Direct dopamine receptor agonists
o Act directly on postsynaptic DA receptors.
o They elicit a separate but similar mechanism compared to levodopa.
o Drugs
 Ropinirole
 Pramipexole
 Rotigotine
o Advantages
 No metabolic conversion to an active compound
Less likely to generate damaging free radicals
Longer duration of action than levodopa with fewer "on-off"
changes
 More selective than levodopa
 Amantadine (can also be used to treat influenza A)
o Mechanism of action for Parkinson
 Prevents reuptake and facilitates release of dopamine
 Weak anticholinergic properties
 Blocks glutamate NMDA receptors which could contribute to
reducing excitation-induced neurotoxicity and dyskinesias
 Often used late in therapy to reduce the severity and extent of
levodopa dyskinesias

Dental Considerations of Parkinson's Disease

 Physical barriers
o Orofacial motor impairments
o Excess saliva
o Levodopa could be administered with acidic beverages
 Behavioral barriers
o Levodopa peak levels can cause too much movement
o Orthostatic hypotension is common in Parkinson patients using
levodopa
o No clinically significant interaction with epinephrine

Summary of Parkinson Drugs

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Section #11 Opioids
Section #11 Opioids
Mechanism of Action

 All opioid drugs bind to both presynaptic and postsynaptic nerve

sites, primarily in the CNS.
 The target receptor most commonly used is Mu (μ).
 Once bound, they cause an inhibitory effect which will inhibit
neurotransmitter release.
 They can act at cortical brain sites, influencing the interpretation and
emotional action to pain. This is how pain sensations are decreased for
patients taking these drugs.
Main Opioid Drug Categories Used in Dentistry

 Phenanthrenes (most commonly prescribed and abused category)

o Morphine
o Codeine
o Hydrocodone
o Hydromorphone
o Nalbuphine
o Oxycodone
 Note: If a patient is allergic to one of these drugs listed above,
they will have an allergy to all the others in this category.
 Many patients will report having false allergies to these drugs
because opioids cause histamine release in the peripheral
tissues. This can cause itchy, nausea, and sweating symptoms.
 Phenylpiperidines
o Meperidine
o Fentanyl
o Alfentanil
o Sufentanil
o Remifentanil
 The most commonly used here is fentanyl for anesthesia cases.
 Phenylpropanolamine
o Tramadol
 Diphenylheptane
o Methadone

Adverse Effects of Opioids

 Respiratory depression
o Opioids decrease the brainstem respiratory centers, making this
the most dangerous adverse effect.
  Pruritus
 Sedation
 Euphoric feeling
 Constipation
 Myoclonus
 Seizures
 Urticaria
 Nausea/vomiting
 Pupillary constriction (miosis)

Opioid Intoxication and Abuse

 Opioids pose a severe threat to addiction. Be aware of drugs that can be

administered when treating someone who is acutely intoxicated.
o Naloxone (Narcan)
 This is a true reversal agent and antagonist to the opioid
receptors, commonly referenced or asked about on the boards.
o Also due to addiction and abusive behavior, providers need a DEA
number to prescribe opioids. You may also need to check your
state’s prescription monitoring program (PMP) before prescribing.
o Opioids are mostly Class II and Class controlled substances.

Opioid Prescribing Guidelines and General Rules

 1st line is 5–10 mg hydrocodone with 325 mg of acetaminophen.

 General rule of thumb is to give 3 days of the opioid, with only 1
prescription, for only 1 dental procedure the “3-1-1 rule”
 Remember hydrocodone is usually 1st line for opioid in pain control because it
is less euphorigenic than oxycodone and releases more histamine thus is less
pleasant to take for patients.
 Rarely consider oxycodone; usually reserved for major surgery (major oral
maxillofacial surgical cases).
 Also avoid tramadol because it is a partial agonist thus less helpful for
pain, has a similar chance to elicit drug abuse and dependency, and is
a stronger CYP2D6 inducer in liver, causing more chances for drug-drug
interactions

Know Morphine Equivalents

 These are used to determine how potent a specific opioid drug is (compared
to morphine) and may be important to know for the boards.
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Section #12 Tuberculosis, Cancer, and Immune Drugs
Section #12 Tuberculosis, Cancer, and Immune Drugs
Tuberculosis

 With a focus on pharmacology, the physiology of tuberculosis is beyond the

scope of this guide, but one should know how to manage situations where
staff come into contact with an actively infected patient. Additionally,
know whether a patient can be treated that is actively infected or how long to
wait to treat them. For the drugs, recognize the significant adverse effects,
with a focus on isoniazid and rifampin!
 Drugs
o Isoniazid
 Mechanism of action: Inhibits mycolic acid synthesis.
 Adverse effects: Numbness, hepatitis, vision changes, seizures,
blood dyscrasias.
 Blood dyscrasias are the most important side-effects to
be aware of.
o Rifampin
 Mechanism of action: inhibits DNA-dependent RNA polymerase
activity
 Adverse effects: Elevated liver function test, vomiting, epigastric
distress, nausea, diarrhea, pseudomembranous colitis
o Rifabutin
o Rifapentine
o Pyrazinamide
o Ethambutol

Cancer

 Cancer is a very prevalent disease in our patients. As dentists, we need to be

aware of how anticancer drugs work in general and what repercussions these
medications can cause to the oral cavity.
 Alkylating agents
o Drugs
  Cisplatin
 Carboplatin
 Cyclophosphamide
 Busulfan
o Mechanism of action: These agents alkylate DNA, which causes
the DNA to cross-link. This leads to replication inhibition,
transcription inhibition, cell cycle arrest, and ultimately cell death.
o Adverse effects
 Mucositis!
 Neurotoxicity
 Alopecia
 Pulmonary fibrosis and infertility (if taken long-term)
 Nausea and vomiting
 Nephrotoxicity
 Ototoxicity
 Antimetabolites
o Drugs
 Methotrexate
 5-Fluorouracil
 Gemcitabine
 Fludarabine
o Mechanism of action: These drugs block the metabolites needed for
cell growth. They specifically block the S (synthesis) phase of DNA
replication. Without these essential metabolites, DNA cannot be
synthesized.
o Adverse effects
 Folate antagonists
 Thrombocytopenia
 Pulmonary pneumonitis
 Alopecia
 Hepatotoxicity
 Mucositis
 Nephropathy
 Proteasome inhibitors
o Drugs
 Bortezomib
 Carfilzomib
o Mechanism of action: Block proteasome function. Both are used to
treat multiple myeloma.
o Adverse effects
 Thrombocytopenia
 Fatigue
 Neutropenia
 Anemia
 Antitumor antibiotics
o Drugs
 Bleomycin
 Doxorubicin
  Dactinomycin
 Can cause Stevens-Johnson syndrome, hepatotoxicity,
thrombocytopenia
o Mechanism of action: These generate oxygen-free radicals, which will
cause breaks in DNA strands. They also inhibit topoisomerase II.
o Adverse reactions
 Mucositis
 Myelosuppression
 Alopecia
 Cardiotoxicity
 GI issues
 Tyrosine kinase inhibitors
o Drugs (“-NIB”)
 There are too many to list, so remember, if a drug ends in -nib,
that is it.
o E.g. sunitinib, gefitinib, ruxolitinib. No, they are not made up. The
names are just plain crazy!
 Angiogenesis inhibitors
o Drugs
 Bevacizumab
 Ziv-aflibercept
o Mechanism of action: These block VEGF (vascular endothelial growth
factor). This prevents cancer from creating more blood vessels to help
its growth. Without this, it cannot keep growing to a large size.

Dentistry and Cancer

 There are many anticancer drugs, but a few true and key concepts for most
of these drugs shine through.
 Mucositis
o Up to 40–75% of chemo and cancer drug-used patients will experience
some mucositis.
o Management of mucositis:
 Pain control
 Can give topical anesthetics, mucosal coating agents, or
sometimes systemic pain medications.
 Stress great oral hygiene
 Recommend soft toothbrushes, flossing, and non-
medicated rinses. This can decrease the incidence and
duration of mucositis.
 Increased incidence of viral, bacterial, fungal infections
o Remember, many cancer drugs inhibit the immune system, so expect
to see an increased incidence of these infections during appointments.
  Dry mouth
o Cancer drugs and treatments also many times decrease salivary flow.
It is imperative to be aware of this because the patient's caries risk
may skyrocket even though they previously had excellent oral hygiene.
o Recommend dry mouth products like Biotene, for example, if a patient
reports dry mouth.

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Section #13 Anxiolytics / Sedative Hypnotics
Section #13 Anxiolytics / Sedative Hypnotics
Benzodiazepines

 These drugs are commonly prescribed for patients with moderate-severe

anxiety.
 Therapeutic uses
o Anxiety
o Epilepsy
o Skeletal muscle relaxants
o Alcohol withdrawal
o Sedative-hypnotic
o Sedation and general anesthesia
 Benzodiazepines induce an anterograde amnesia effect in
patients (causes them to lose the memory of events after the
drug is given), which is beneficial before a stressful
surgery/procedure.
 Drugs (-pams and -lams)
o Alprazolam (Xanax)
o Diazepam
 This is the only benzodiazepine approved for treating skeletal
muscle spasms of CNS origin
o Lorazepam
 Eliminated rapidly, great for patients with compromised CYP450
activity
o Oxazepam
 Eliminated rapidly, great for patients with compromised CYP450
activity
o Midazolam
 Commonly used in dental anesthesia
 o Clonazepam
 Most commonly used is benzodiazepine as an
anticonvulsant/seizure medication
o Clorazepate
o Flurazepam
 Mechanism of Action
o Benzodiazepines work by enhancing GABA neurotransmitters.
o Specifically, they bind to GABA receptor subunits to facilitate Cl-
channel opening.
o Remember that GABA is an inhibitory neurotransmitter. Thus,
benzodiazepines will cause a sedative, hypnotic (sleep-inducing),
anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant effect.
 Adverse effects
o Drowsiness
o Ataxia
o Incoordination
o Confusion
o Apathy
o Muscle weakness
o Nightmares
o Hyperactivity
o Insomnia
o Irritability
o Agitation
 Other adverse reaction notes
o IV Diazepam can cause pain, phlebitis, and thrombosis. It is not water-
soluble, and the propylene glycol and benzyl alcohol can cause the
symptoms above.
o Benzodiazepines are teratogenic. Never give a pregnant patient these
drugs!
o Also, remember that patients can become addicted to
benzodiazepines. This can lead to tolerance and physical dependence.
That is why these are controlled substances.
 Drug interactions
o Because benzodiazepines induce CYP enzymes in the liver, drugs like
macrolides antibiotic, azole antifungal, grapefruit, and rifampin can
dramatically increase the blood concentration of benzodiazepines.
o Opioid use with benzodiazepine can also be a concern because the
depressant nature of both drugs can stack up. The same can be said
for abusive alcohol usage.
 Reversal agents
o Flumazenil
 This will reverse benzodiazepine sedation if the patient is
pushed into too deep of a sedation state.

Barbiturates
  Barbiturates are not included in this section because they are not commonly
used anymore. They were an older drug of choice until benzodiazepine use
became more widespread and popular.

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Section #14 Statins (Drugs for High Cholesterol)
Section #14 Statins
Introduction

 High cholesterol and lipid profiles are prevalent in Western society, so a

significant number of patients are taking one form or another of these drugs.
While many drugs are used to control high cholesterol, we will concentrate on
the most common ones.
Drugs

HMG-CoA reductase inhibitors (-statin drugs)

 Drugs
o Atorvastatin
o Fluvastatin
o Rosuvastatin
o Simvastatin
o Pravastatin
 Mechanism of action:
o Inhibit HMG-CoA reductase (hence the name)
o This is the rate-limiting step in cholesterol synthesis, thus cholesterol
and LDL levels decrease dramatically.
o They also are known to have anti-atherosclerotic and anti-inflammatory
effects on the body, and can also prevent bone loss. In other words,
doctors love prescribing these drugs.
 Adverse reactions
o Elevations of serum aminotransferases (liver failure)
o Headache
o GI issues
o Elevation of creatine kinase
 This gets released from skeletal muscle and can cause muscle
pain and rhabdomyolysis.
o Teratogenic: Remember, a baby will need cholesterol to live.

PCSK9 inhibitors

 Drugs
o Alirocumab
o Evolocumab
 Mechanism of action: Inhibit proprotein convertase subtilisin/Kexin 9 (PCSK9),
as the name suggests. Inhibition of PCSK9 prevents degradation of LDL
receptors, promoting greater clearance of LDL.
  Adverse Effects
o Flu-like symptoms
o Injection site reactions

Ezetimibe

 Mechanism of action: Inhibits cholesterol uptake by binding to its GI

transporter to prevent it from uptaking cholesterol.
 Adverse effects: When combined with a statin drug can increase the risk of
liver toxicity.

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Section #15 Asthma
Section #15 Asthma
Pathophysiology

 Reversible narrowing of bronchioles. Unlike COPD, this is a REVERSIBLE

process. Asthma is not a progressive disease like COPD.
 Asthma is also an inflammatory disease. Bronchospasm, mucosal swelling,
and increased mucus production can make it hard to breathe effectively.
 Due to asthma being both an airway constriction and an inflammatory issue,
antiasthmatic drugs target both the airway and inflammation.

Beta 2 Agonists

 Rapid onset, short-acting drugs (all asthma patients should have one of
these, as they are used to treat acute asthma episodes)
 Drugs
o Albuterol
o Levalbuterol
o Terbutaline
o Metaproterenol
o Pirbuterol
 Long-acting drugs (used for maintenance therapy only! If prolonged use,
they can lead to receptor desensitization.)
o Salmeterol
o Formoterol
 Mechanism of action: These drugs activate β-2 receptors in the airway. This
relaxes smooth muscles in the bronchioles, causing dilation and allowing more
air to pass into the lungs.

Antimuscarinic Agents
  Used for patients that cannot tolerate β-2 agonists.
 Drugs
o Ipratropium bromide
 Mechanism of action: Inhibits acetylcholine at muscarinic receptors. This leads
to airway dilation and decreased secretion of mucus. Both are great for
asthmatic patients.

Corticosteroids

 These will target the inflammation associated with asthma.

 Drugs
o Prednisone
o Fluticasone
o Mometasone
o Beclomethasone dipropionate
o Budesonide
 Mechanism of action: These agents act as broad-spectrum anti-inflammatory
agents. They primarily inhibit the infiltration of inflammatory cells in the
airway like mast cells, eosinophils, and lymphocytes.

Leukotriene Antagonists

 Drugs
o Montelukast
o Zafirlukast
 Mechanism of action: Block synthesis and action of leukotrienes. They
antagonize the LTD receptor.

Dental Management of Asthma

 Dental procedures can trigger asthma. Chemicals or dust from drilling

teeth may trigger a response, or even the stress of the procedure itself can
bring out an episode.
 Thorough health history. Ask if patients have had an asthmatic episode in
a dental office before.
 Make sure they bring their inhaler to the appointment if they use one!
 Patients taking corticosteroids are at an increased risk of candidiasis
(may see white plaques in the posterior airway). Educate patients and remind
them to rinse their mouths after usage.

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Section #16 Bisphosphonates
Section #16 Bisphosphonates
It is crucial to recognize bisphosphonate drugs because they can cause
medication-related osteonecrosis of the jaw (MRONJ). Although rare, it can
be debilitating when it occurs and something we want to avoid at all costs.

 Indications for bisphosphonate therapy

o Osteoporosis, patients with low bone density
o Paget disease
o Multiple myeloma
o Bone diseases or cancer that metastasized to the bone
 Drugs
o Alendronate (Fosamax)
o Etidronate (Didronel)
o Zoledronate (Reclast)
o Ibandronate (Boniva)
o Risedronate (Actonel)
o Pamidronate (Aredia)
o Denosumab (Prolia)
  Note: this is a RANKL inhibitor which is different from the ones
above. These inhibit RANKL but still elicit the same effects listed
below.

 Mechanism of action: Bind to bone surfaces and inhibit farnesyl diphosphate

synthase. These effects will increase bone density but impair bone healing
because it will not remodel efficiently. Overall, they impair osteoclast function,
cause them to undergo apoptosis, and allow osteoblasts to produce more
bone.
 Adverse effects
o MRONJ (medication-related osteonecrosis of the jaw)
o This is the biggest effect we are concerned with and must manage. It
is defined clinically as exposed bone in the oral cavity that fails to
heal in 8 weeks in a patient that has taken a bisphosphonate and
has received no radiation therapy to the jaw.
o Why does MRONJ occur in the jaw? The jaw has a high turnover
of bone, and the jaw is in an intense trauma environment. Think about
every time you chew and how much you use your jaw. It occurs in
the mandible more frequently than in the maxilla. It also occurs more
in the posterior area of the mandible than anterior.
o Most cases of MRONJ follow tooth extractions. Thus we want to
avoid this procedure if possible.
o Most patients that have MRONJ are cancer patients with IV
bisphosphonate therapy.
o The half-life of bisphosphonates can last decades!
o Stages of MRONJ
 Stage 0: Patients are at risk
 Stage 1: Bone exposure, no pain, no evidence of infection
 Stage 2: Bone exposure, evidence of infection by pain or
redness of the area
 Stage 3: Bone exposure, with pain, infection, and exposed and
necrotic bone extending beyond the region of alveolar bone
 Dental management:
o Before bisphosphonate treatment
 Oral hygiene education.
 Prophylaxis, exam, and stabilization of any decay.
 Make panoramic radiograph.
  Remove any infected, abscessed, or diseased teeth.
 If a patient is in dentures, ensure a proper fit and that is not
damaging to tissues or causing ulcerations.
o After bisphosphonate treatment
 Manage dental infections nonsurgically with endo or as minimal
surgery as possible.
 If surgery cannot be avoided, consider referring to an oral
surgeon or specialist.
 The ADA does not recommend a drug holiday prior to surgical
treatments.
 If edentulous, continue to monitor denture fit and avoid as
much soft tissue injury as possible.
o If suspected MRONJ occurs for a patient with a history of
bisphosphonate, refer to an oral surgeon for treatment.

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 INBDE Pharmacology Guide
Section #17 Corticosteroids
Section #17 Corticosteroids

Because these drugs are very common, we will only review the drugs and dental
management topics.

Drug Classes

 Mineralocorticoids
o Aldosterone
 Stimulates renal tubule to reabsorb sodium and excrete
potassium.
 Glucocorticoids
o Cortisol
 Regulates protein, carbohydrate, and fat metabolism.
 The body will naturally secrete this in response to stress.
 Cortisol will inhibit the immune system!
 Adrenal androgens
o Dehydroepiandrosterone
 A precursor to female and male sex hormones.

The Hypothalamic-Pituitary-Adrenal (HPA) Axis

 Remember, the body naturally secretes corticosteroids, so when a patient is

prescribed them, they could have suppression of the HPA axis.
 The body cannot respond to stressful situations if we entirely suppress the
body’s cortisol response.
 This will occur with long-term (> 3 weeks) steroid use.

Essential Diseases to Know

 Addison disease
o An autoimmune reaction that causes primary adrenal insufficiency
o Symptoms:
 Chronic fatigue
 Muscle weakness
 Hyperpigmentation of skin
 Postural hypotension
 Weight loss
 Dehydration
 Low salt and high potassium
 Elevated blood urea nitrogen
 Cushing disease
o Secondary adrenocortical insufficiency
o ACTH is usually overproduced from an adenoma
 o This drives cortisol levels to be very high - the opposite of Addison,
where cortisol is low.
o Symptoms:
 Moon face, central obesity, and buffalo hump!
 The INBDE loves asking about these
 Hypertension
 High calcium levels

Corticosteroid Therapy

 Indications
o Replacement therapy for Addison disease
o Nephrotic syndrome
o Acute lymphocytic leukemia
o Lymphoma
o Shock
 o Severe asthma
o Allergic responses
o Rheumatoid arthritis
o Crohn's disease
o Organ transplant recipients
o Skin conditions and oral conditions: lichen planus
o Ocular conditions
 Drugs commonly used
o Prednisone
o Dexamethasone
o Hydrocortisone
 Adverse effects
o Cushing syndrome
o Myopathy
o Osteoporosis
o Growth suppression
 can prematurely fuse long bones to their epiphyseal plates
o GI irritation
o Abnormal fat distribution
o Hyperglycemia
o Insomnia
o Can trigger depressive or manic episodes
o Decreased immune function can compromise host defense
 Think about how patients taking oral corticosteroids develop
thrush/candidiasis
 Acute adrenal crisis
o Occurs from very low corticosteroids. Usually caused by infections that
cause the body severe stress.
 Signs and symptoms
 Hypotension
 Cardiovascular collapse
 Hypoglycemia
 Loss of consciousness
 Nausea and vomiting
 Hypoglycemia
 High potassium
o This is a medical emergency, so contact EMS.
o Treatment starts with IV 100–300 mg hydrocortisone + saline.
 Dental management
o The key point here is that we need to pay attention to how much
and how long patients have been taking corticosteroids. We
need to know because if they undergo a stressful procedure, we may
want Rx corticoids to cover patients for systemic stress.
o If patients have taken 5–15mg daily of prednisone for at least
three weeks, we can assume there is some suppression. The
suppression can come from another drug of similar equivalency
(prednisone is listed because it is most commonly used)
 o 5 mg of Prednisone = 20 mg hydrocortisone = 0.75 mg of
dexamethasone
 Suppose this patient is anxious or scheduled for a traumatic
procedure like surgical tooth extraction.
 We will manage this by doubling the daily dose to a maximum
of 20 mg of prednisone for 2–3 days starting the day of the
procedure.
o If the patient takes less than 5 mg prednisone daily, no
supplementation is needed.
o Also no supplementation is needed if a patient takes more than 15
mg of daily prednisone.
 Unless a patient has extreme anxiety or a procedure is very
traumatic.

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Section #18 Antidepressants, Antiepileptics, & Antipsychotics
Section #18 Antidepressants, Antiepileptics, & Antipsychotics
Antidepressants

 Monoamine oxidase inhibitors (MAOIs)

o Drugs
 Rasagiline (remember this was a Parkinson drug)
 Phenelzine
 Tranylcypromine
 *These are predominantly used for migraine treatment
o Mechanism of action: Irreversibly bind to monoamine oxidase. This
prevents the inactivation of amines like norepinephrine, serotonin, and
dopamine.
o Adverse effects
 Weight gain
 Sexual dysfunction
 Sleep disturbance
 Orthostatic hypotension
 Nausea
 Dizziness
o The problem with MAOIs
 A hypertensive crisis can occur if food is consumed with
tyramine.
 Serotonin syndrome can occur if taken with meds that
increase serotonin or have sympathomimetic actions.
 Serotonin syndrome causes
 Abdominal pain
 Myoclonus
 Delirium
 Hypertension
 Can lead to cardiovascular shock and death.
 
o Drug interactions with many drugs
 SSRIs
 TCAs
 Buspirone
 Meperidine/fentanyl (lethal if combined)
 Methadone
 Tramadol
 Vasoconstrictors (like epi, levonordefrin)
 This can result in hypertension, headache, and hypertensive
crisis!
 Tricyclic antidepressants (TCAs)
o Drugs
 Amitriptyline
 Imipramine
 Desipramine
 Nortriptyline
 Clomipramine
 Desipramine
 Doxepin
 Protriptyline
o Mechanism of action: Primarily inhibit the reuptake of serotonin and
norepinephrine, thus elevating the levels of these neurotransmitters in
the brain.
o Adverse effects
 Can cause QT lengthening
 Sedation
 Weight gain
  Dry mouth*** These are very drying agents.
 Dry eyes
 Constipation
 Memory deficits/delirium
 Sexual dysfunction
 Orthostatic hypotension
 Lithium
o An old-school drug used as the only medication that reduces the
suicide rate.
o Used to treat bipolar disorder
o Side effects
 Weight gain
 Tremor
 Hypothyroidism
 Tremor
 Nausea
 Diarrhea
 Increased thirst, water retention
 Increased urination
 Congenital disabilities!
o Dental-related questions the INBDE likes:
 Lithium can cause a metallic taste in the oral cavity
 Lithium can cause tardive dyskinesia/orofacial movements
 NSAIDs increase lithium levels drastically if given
 Selective serotonin reuptake inhibitors (SSRIs)
o These are very commonly used drugs
o Drugs
 Fluoxetine (Prozac)
 Escitalopram (Lexapro)
 Citalopram (Celexa)
 Sertraline (Zoloft)
 Paroxetine (Paxil)
o Mechanism of action: Block reuptake of serotonin in the CNS.
o Adverse effects
 May cause bruxism in patients! If this occurs, the patient may
discuss with physician about changing meds.
 They usually add buspirone to try and treat.
 Dry mouth (lesser extent than TCAs)
 Sexual issues, dysfunction
 Feeling agitated, shaky, nervousness
o Drug interaction:
 Avoid giving patients tramadol. This can cause serotonin
syndrome.
 Serotonin-norepinephrine reuptake inhibitors (SNRIs)
o Drugs
 Duloxetine (Cymbalta)
 Venlafaxine (Effexor)
 Can cause QT prolongation
 Desvenlafaxine (Pristiq)
 Dose-related increase in LDL, triglycerides, and
cholesterol
 Levomilnacipran (Fetzima)
o Mechanism of action: Inhibit both serotonin and norepinephrine
uptake. They are similar to TCA drugs but do not have large
antihistamine, antiadrenergic, or anticholinergic side effects. This is
why they are more commonly used.
o Adverse effects
 Nausea
 Hypertension at high doses
 Sexual dysfunction
 GI distress
 Alpha-2 receptor antagonist
o Drug
 Mirtazapine
o Mechanism of action: Antagonizes adrenergic α2-autoreceptors and α2-
heteroreceptors and blocking 5-HT2 and 5-HT3 receptors, causing
enhanced norepinephrine release.
o Adverse reactions
 Dry mouth
 Drowsiness
Weight gain (most patients do not like this drug because of this)
Sedation
o Increases serum cholesterol and triglycerides
o It caused less bruxism than other antidepressants.
o It also causes fewer sexual dysfunction symptoms.
 Aminoketone antidepressant
o Drug
 Bupropion (Wellbutrin)
o Mechanism of action: Inhibits both the reuptake of norepinephrine and
dopamine. This is unique! Bupropion is the only agent that will do
this!
o Adverse effects
 Can increase seizure risk if taking high doses.
 Can cause anxiety, agitation, and insomnia
 High abuse potential
o This drug, oddly enough, can be used to treat smoking cessation.
o Also, bupropion will increase sexual dysfunction because it enhances
dopamine. If someone takes an SSRI and has sexual dysfunction, they
may take this as an adjunct.

Antiepileptic (Antiseizure) Drugs

 Drugs
o Lamotrigine
o Topiramate
o Phenytoin
 ***Causes gingival overgrowth***
 They love asking about this!
o Tiagabine
o Sodium valproate
 Can cause platelet dysfunction
o Carbamazepine
 Adverse effects
o CNS depression
o Dermatologic
o Mucosal toxicity!
o Blood dyscrasias, thrombocytopenia
o Drowsiness
o Ataxia

Antipsychotic Drugs

 Drugs
o Haloperidol
o Risperidone
o Clozapine
o Chlorpromazine
 o Aripiprazole
o Iloperidone
o Lurasidone
 Adverse effects
o QT prolongation
o Sedation
o It can cause tardive dyskinesia!

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Section #19 Cholinergics
Section #19 Cholinergics

Because there will be many drugs for this section, we will not be going into details
on the physiology of the receptors they activate (see the table for a quick
reference). Do not spend a ton of time memorizing these drugs, but do be able to
recognize and determine their category.
Direct-Acting Muscarinic Agonists Drugs

 Pilocarpine
o Used to treat Sjögren syndrome
o Increases salivation
 Bethanechol
 Methacholine
o Adverse effects are parasympathomimetic effects***
 Cyclospasm
 Diarrhea
 Urinary urgency
 Vasodilation
 Reflex tachycardia
 Sweating
 Bronchoconstriction

Indirect-Acting Muscarinic Agonists

 Neostigmine
 Pyridostigmine
 Physostigmine
 Edrophonium
 Rivastigmine
 Parathion
 Malathion
o Adverse effects are parasympathomimetic effects***
 Cyclospasm
 Diarrhea
  Urinary urgency
 Vasodilation
 Reflex tachycardia
 sweating

Muscarinic Antagonists

 Atropine
 Oxybutynin
 Scopolamine
 Darifenacin
 Benztropine
 Dicyclomine
 Tolterodine
 Aclidinium
 Ipratropium
 Tiotropium
o Adverse effects are parasympatholytic effects***
 Drying of mouth and eyes
 Abdominal pain
 Palpitations
 Tachycardia
 Flushing
 Urinary retention

Nicotinic Antagonists

 Tubocurarine
 Succinylcholine
o These act to block nicotinic receptors.
o They will cause paralysis.

Adrenergic Agonist Drugs

 Mixed alpha and beta-agonists

o Norepinephrine
o Epinephrine
 Alpha agonists
o Phenylephrine (Sudafed)
 Vasoconstriction reduces nasal congestion/swelling when sick
o Clonidine
o Methoxamine
 Beta-agonists
o Dobutamine
 Used for shock victims, spikes heart action
o Isoproterenol
o Albuterol
 We know this one, a bronchodilator for asthma patients
  Dopamine agonists
o Dopamine
o Fenoldopam

Adrenergic Antagonists

 Alpha-blockers
o These are used mainly for BPH treatment
o “-sin” drugs are also used for hypertension (they lower blood pressure)
 Prazosin
 Doxazosin
 Terazosin
 Tamsulosin
 Only used for BPH treatment
 Phentolamine
 Phenoxybenzamine
 Beta-blockers (we already know these)
o These drugs lower heart rate and blood pressure.
o Beta-blockers are all “LOL” drugs
 Propranolol
 Nadolol
 Timolol
 Metoprolol
 Atenolol

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Section #20 Allergy and GI Drugs
Section #20 Allergy and GI Drugs
Antihistamines for Allergies

 Remember: Histamine release from mast cells is a big part of the allergic
response.
 Effects of histamine:
o Lung bronchoconstriction
o The stomach increases gastric acid secretion
o Vascular smooth muscles dilation
o Sensitization of peripheral nerves causing itchiness and pain
 There are four histamine receptors, whereas we will focus on 1 and 2.
o Histamine H1 receptor causes
 Smooth muscle contraction, increased capillary permeability,
vasodilation, and sensory nerve endings causing pain and
itching.
 This is what most of our allergy medications will antagonize.
o Histamine H2 receptor causes
 Increased gastric acid secretion, blood vessel vasodilation, and
increased capillary permeability.
 Drugs targeting H2 receptors will be mainly used for acid reflux,
which many people take.
Allergy Drugs (H1 blockers)

 Diphenhydramine
 Hydroxyzine
o Both of these are first generation. They have not used as much
anymore because they make patients very drowsy.
 Cetirizine (Zyrtec)
 Fexofenadine (Allegra)
 Loratadine (Claritin)
o These are second generation, used more because they have a
significant effect without causing drowsiness.
 Mechanism of action: They all block histamine H1 receptors. Refer to the
picture above if you need to remember the H1 receptor's physiologic effect.

Antacids (H2 blockers)

 Cimetidine
o Can cause gynecomastia, impotence, galactorrhea
 Famotidine
 Ranitidine (Zantic)
 Nizatidine
o Anxiety, pruritus, nasopharyngitis
 Mechanism of action: Block H2 receptors and decrease gastric acid
secretion.
Proton Pump Inhibitors

 Omeprazole
 Esomeprazole
 Mechanism of action: These are different as they do not block histamine
H2 receptors like the others listed above! They suppress stomach acid
secretion by specific inhibition of the H+/K+-ATPase system found at the
secretory surface of gastric parietal cells.
 Adverse effects
o Headaches
o Stomach pain
o Constipation
o Nausea

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