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.