Commonly Prescribed and OTC Medications and Clinical
Implications in Oral Healthcare
Elizabeth I. Pitts, RDH, MS
Adjunct Clinical Assistant Professor, Division of Dental Hygiene
University of Michigan School of Dentistry
1011 North University Avenue
Ann Arbor, MI 48109
Outline
Cardiovascular Pharmacology
Endocrine Pharmacology
NSAIDs
Objectives• Identify commonly prescribed and OTC
medications. • Describe the basic pathologic mechanism
of action for commonly prescribed and OTC medications.
• Discuss the clinical implications for the use of commonly prescribed and OTC medications.
Cardiovascular Pharmacology (Brief Overview)
Hypertension
• Blood pressure ≥130/80 mm Hg
• Genetic factors, psychological stress, and environmental and dietary factors (increased salt intake)
Blood pressure category
Complications of hypertension
• Untreated hypertension coronary artery disease and heart failure
Renin-angiotensin II-aldosterone system• Regulation of arterial pressure
Renin-angiotensin II-aldosterone system
• Kidneys sense decrease in arterial pressure and secretes enzyme renin to covert angiotensinogen into angiotensin I
• Angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II. Angiotensin II increases blood pressure and increases sodium re-absorption in the kidneys through the release of aldosterone
Common hypertension drugs• Inhibitors of the renin-angiotensin system
- ACE inhibitors (Lisinopril)- Angiotensin II receptor blockers (Losartan)
• Decrease sodium reabsorption (diuretics)• Calcium channel blockers
ACE inhibitors
• Interrupt the conversion of angiotensin I to angiotensin II
• Also increase bradykinin (inflammatory mediator)
- Side effects: coughing and angioedema
- Drug-induced angioedema: swelling of submucosal tissues, absence of itching or hives, commonly affects lips, tongue, face and upper airway
Angiotensin II receptor blockers (ARBs)
• ARBs bind to the angiotensin II receptor and inhibit secretion of aldosterone and vasopressin
Diuretics• Target sodium re-absorption at nephron
Diuretics
• Loop diuretics (Furosemide)• Inhibits sodium and chloride
resorption at loop of Henle• Thiazide diuretics
(Hydrochlorothiazide)• Inhibit sodium and chloride
resorption at distal convoluted tube
Vascular tone determines peripheral blood pressure
• Vascular tone: contraction of vascular smooth muscle oxygen level of peripheral tissue
Calcium channel blockers (CCBs)
• Block surface calcium channels (LTCC) to relax smooth muscle and heart muscle
• Heart: reduction of contractility• Artery: vasodilators
Side effect of CCBs
• Nifedipine is most frequently reported
• Clinical presentation:• Gingival overgrowth due to
the reduction of collagenase
• Poor oral hygiene may aggravate the symptoms
Endocrine Pharmacology
Pancreas Both exocrine and endocrine organ
Insulin and glucagon
• Insulin which promotes glucose uptake and utilization
• Glucagon which is released during fasting state and raises concentration of glucose in bloodstream
Diabetes mellitus (DM)
• Type 1 DM (5-10%): autoimmune destruction of beta cells in pancreas; affects children and adolescents
• Type 2 DM (90-95%): insulin resistance.
Diagnosis of Hyperglycemia
• HbA1c: glycated hemoglobin
Treatment of DM
• Alterations in diet and lifestyle, weight loss
Non-pharmacologic blood glucose control
• Metformin (Glucophage, Glumetza, Fortamet, Riomet) • Insulin (injection)
Pharmacologic management
Pharmacologic managementof DM
• Reduces post-meal and fasting glucose levels
• First line therapy, often given with other oral or injectable agent
Metformin
• Basal supplement (long-acting)• Pre-meal (short-acting or rapid
acting)
Insulin injection
ental considerations in DM
Periodontal disease
Xerostomia
Opportunistic infections• Increased oral candidiasis (median rhomboid glossitis,
denture stomatitis, candidiasis, and angular cheilitis)• Mucormycosis
ral complications in DM
Gingivitis Mucormycosis
Dental considerations n DM
• Medical history • Recent blood glucose levels, frequency
of hypoglycemic episodes, antidiabetic medications, dosage
• Appointment scheduling • Morning appointments• For pts who take insulin, avoid peaks
of insulin activity.
Dental considerations n DM
• Diet • Normal diet and medication
• Blood glucose monitoring• Low plasma glucose levels (< 70
mg/dL): oral carbohydrate before treatment to minimize the risk of hypoglycemia
• Increased blood glucose levels: referred for medical consultation prior to elective dental procedures
ental considerations in M
• Hypoglycemic episode• Most common complication in a dental office• Terminate dental treatment, immediately
administer 15 g fast-acting oral carbohydrate
ental management of the patient with DM
• Well-controlled type I DM• All dental procedures without modification
• Well-controlled type II DM• Take normal insulin and meals on appointment day, with glucose
source available• Acute oral infection in controlled DM
• Coordination with the physician• Aggressive management to control infection
reventing hypoglycemia
• When did you last eat?• What did you eat?• Little food, a long travel
time + sitting in a dental chair can cause hypoglycemia in a healthy patient!
Provider should ask
everypatient,
including diabetics two
questions before treating
NSAIDs
etaminophen and the nonsteroidal anti-inflammatory drugs (NSAIDs)
etaminophen and the nonsteroidal anti-inflammatory drugs (NSAIDs) continue to the most appropriate choices for the treatment of mild to moderate acute facial pain.
ether using these drugs alone or in combination, prescribers must be aware of potential safety concerns associated with all analgesic medications, especially
ght of new information promoting lower doses, shorter treatment durations, d decreased maximum recommended doses.
Autacoids are hormone-like substances that are rapidly synthesized in response to specific stimuli
Eicosanoids are types of autacoids that are mostly derived from arachidonic acid
Eicosanoids have roles in inflammation
• Blocking these pathways have lead to certain anti-inflammatory drugs NSAIDs
asthmarheumatoid arthritiscancerinflammatory bowel disease cardiovascular disease
• Arachidonic acid is derived from linoleic acid (omega 6).
• Arachidonic acid is released from the lipid membrane by enzyme called phospholipase A2.
• Phospholipase A2 is the enzyme that releases arachidonic acid.
• Eicosanoids are made from two pathways, the cyclooxygenase pathway and the lipooxygenasepathway.
• Cyclooxygenase converts arachidonic acid to formProstaglandinsProstacyclinThromboxanes
• There are two forms of cyclooxygenaseCOX 1COX 2
• COX-1• Expressed in almost
all tissues• Tissue protection
• COX-2• Found in inflamed
tissues• Proinflammatory
response
• Nonsteroidal anti inflammatory drugs block the activity of COX-1 and COX-2
• Prostaglandins are divided into four major types
• Note that prostaglandins help to protect the gastric mucosa through vasodilation
• Platelets produce thromboxane that stimulates activation of new platelets as well as increase platelet aggregation
• Figure B. Blood platelets adhere to site of injury and aggregate to each other, i.e. primary hemostasis
• Platelet activation involves change in shape and release of chemical mediators, thromboxane A2 and ADP which promote aggregation and formation of a plug.
Cyclooxygenase COX) inhibitors
onsteroidal antinflammatory drugs (NSAIDs) are important because their combined anti-inflammatory, antipyretic, and analgesic operties
oal of most NSAIDs is to block the generation of eicosanoids to limit e extent of inflammation, fever, and pain
icylates (Aspirin)
ks both COX -1 & -2, non specifice syndrome in children
Condition that causes brain swelling and liver damageChildren recovering from viral infection are most at risk, especially if they have been taking aspirin
tric or intestinal ulcerationCaution in patients struggling w alcoholismIron-deficiency anemia
rin has anti-thrombotic effects that prevents elets from forming thromboxane
used for management of atherosclerotic disease
profen
cks both COX -1 & -2, non specifictrointestinal bleeding, ulcerationRisk increased in patients with alcoholism
e: Ibuprofen was associated with er degree of damage to gastric cosa than aspirin
e all NSAIDs, may exacerbate ertension and congestive heart
ureFluid retention
proxen
cks both COX -1 & -2, non ecific times more potent than pirinated to ibuprofen and
milar adverse effects of GI eding, ulceration, and diovascular eventsough less GI adverse ects than aspirin
x-2 inhibitors
g-term NSAID therapy associated with dverse effects thought to be caused by
bition of cytoprotective COX-1
X-2 specific inhibitors May cause less GI bleeding as compared to nonselective COX inhibitorsDoes not inhibit platelet aggregationMany COX-2 specific inhibitors have been removed from the US market (Vioxx and Bextra) due to possible risk of MI and stroke
ecoxib (COX-2 ective) adverse • GI bleeding and ulceration
• Alcoholism• Lowest effective dose for shortest
possible duration
• Cardiovascular risk• Exacerbate hypertension and
congestive heart failure
Classified as NSAID (Sometimes)
etaminophen (APAP)
hough acetaminophen has lgesic and antipyretic effects ilar to aspirin, the anti-ammatory effect is insignificant ause of its weak inhibition of ooxygenases
Good for patients at risk for adverse effects of aspirin
taminophen is considered er than aspirin
etaminophen Adverse Effect
epatoxicity is an important adverse effect
FDA advised healthcare professionals to discontinue prescribing and dispensing combination prescription medications containing >325mg Leading cause of liver injury in United States 1998-2003Alcoholism
• The risk of developing hepatotoxicity appears to be increased in patients who regularly consume alcohol
• Hepatotoxicity possible even with standard doses
etaminophen Adverse Effect
epatotoxic metabolite of acetaminophen, N-acetyl-para-nzoquinoneimine (NAPQI), is hepatotoxic
cessive acetaminophen saturates the sulfation pathway (phase II etabolism)
Stores of glucuronide and sulfate are depletedExcess NAPQI binds to proteins in tissue
• Cellular necrosis of liver
Questions
erences
armacology for the Dental Hygienist (2nd Edition). M. Weinberg, C. Thiele, J. Fine. inciples of Pharmacology with Dental Hygiene Applications. F.A. Pickett, G.T. Terézhalmy.