4. Guidelines
American Diabetes Association (ADA).
Updated yearly in the January supplement of
Diabetes Care
American College of Endocrinology/AACE
Canadian Diabetes Association
Various European groups
5.
6. Type 1 Diabetes
• Attributable to cellular-mediated β-cell destruction leading
to insulin deficiency (insulin needed for survival)
• Accounts for 5%–10% of DM
• Formerly known as insulin-dependent diabetes and
juvenile-onset diabetes
• Usually presents in childhood or early adulthood but can
present in any stage of life
• Usually symptomatic with a rapid onset in childhood, but a
slower onset can occur in older adults
7. Type 2
Diabetes
• Results primarily from insulin resistance in muscle and liver,
with subsequent defect in pancreatic insulin secretion, though
GI, brain, liver, and kidneys are all involved in the
pathophysiology
• Accounts for 90%–95% of diabetes mellitus
• Formerly known as non–insulin-dependent diabetes or adult-
onset diabetes
• Often asymptomatic, with a slow onset over 5–10 years.
Rationale for early, frequent screening of those at risk (see
text that follows) and initial assessment for complications at
diagnosis
• Disturbing increased trends in T2D in children and adolescents
attributed to rise in obesity
14. α-
Glucosidase
Inhibitor
Mechanism:
Inhibitors α-Glucosidase, which helps
breaks down sugar in the intestine
Example:
Acarbose, miglitol
Indications:
Diabetes (type 2)
Common
Adverse
Reactions:
Diarrhea, flatulence, abdominal
cramping
Dental
Concerns:
May inhibit the treatment of
hypoglycemia
15. /
Sodium/Glucose Co-Transporter-2 Inhibitor
Mechanism:
• Inhibits the
reabsorption of
glucose in the
urine, thereby
excreting
glucose
Example:
• Canagliflozin,
Empagliflozin (-
glifozin)
Indications:
• Diabetes (type
2)
Common Adverse
Reactions:
• Urinary track
infections,
hypotension
Dental Concerns:
• Orthostatic
hypotension
25. Hyperthyroid
• Toxic diffuse goiter (Graves disease): Most common hyperthyroid
disorder
◦ Autoimmune disorder
◦ Thyroid-stimulating antibodies directed at thyrotropin receptors
mimic TSH and stimulate triiodothyronine (T3) and T4 production.
• Pituitary adenomas: Produce excessive TSH secretion that does not
respond to normal T3 negative feedback
• Toxic adenoma: Nodule in thyroid, autonomous of pituitary, and TSH
• Toxic multinodular goiter (Plummer disease): Several autonomous
follicles that, if large enough, cause excessive thyroid hormone
secretion
• Painful subacute thyroiditis: Self-limiting inflammation of the thyroid
gland caused by viral invasion of the parenchyma, resulting in the
release of stored hormone
• Drug induced (e.g., excessive exogenous thyroid hormone dosages,
amiodarone therapy)
26. Treating
Hyperthyroidism
Mechanism:
Inhibits coupling and
organification steps of thyroid
hormone synthesis
Example: Proplthiouracil, methimazole
Indications: Hyperthyroidism
Common Adverse Reactions:
Aplastic anemia,
agranulocytosis, rash,
symptoms of hyperthyroidism
Dental Concerns: N/A
27. Hypothyroidism
• Hashimoto disease: Most common hypothyroid disorder in
areas with iodine sufficiency
◦ Autoimmune-induced thyroid injury resulting in decreased
thyroid secretion
◦ Disproportionately affects women
• Iatrogenic: Thyroid resection or radioiodine ablative therapy
for hyperthyroidism
• Iodine deficiency most common cause worldwide
• Secondary causes
◦ Pituitary insufficiency (failure to produce adequate TSH
secretion, called by some a central or secondary
hypothyroidism)
◦ Drug induced (e.g., amiodarone, lithium)
28. Treating
Hypothyroidism
• Hormone replacement for T4 or T3 (active)
Mechanism:
• Levothyroxine, Armor Thyroid
Example:
• Hypothyroidism
Indications:
• Symptoms of hypothyroidism/hyperthyroidism (if
too high a dose, aka HTN)
Common Adverse
Reactions:
• May have drug-drug interactions
Dental Concerns:
37. Asthma
• Asthma is a chronic inflammatory disorder of the airways
causing recurrent episodes of wheezing, breathlessness,
cough, and chest tightness, particularly at night or early in the
morning. During episodes, there is variable airway
obstruction, often reversible spontaneously or with
treatment. There is also increased bronchial
hyperresponsiveness to a variety of stimuli.
• Guidelines: Global Initiative for Asthma (GINA): Global
Strategy for Asthma Management and Prevention 2018.
Available at www.ginasthma.org/.
42. Inhaled
glucocorticoids
•Decreases production of leukotrienes and
prostaglandins by inhibits phospholipase A2 to reduce
inflammation in airways
Mechanism:
•Fluticasone, budesonide
Example:
•Asthma (in combination, never monotherapy), COPD
Indications:
•Fatigue, headache, arthralgia, sinus infections
Common Adverse
Reactions:
•Oral candidiasis
Dental Concerns:
43. Inhaled
antimuscarinic
Mechanism:
Blocks muscarinic receptors in
bronchi, leading to
bronchodilation.
Example:
tiotropium (long acting),
ipratropium (short acting)
Indications: Asthma, COPD
Common Adverse Reactions:
Upper respiratory track
infection, sinusitis, edema
Dental Concerns: Xerostoma (common SE)
45. COPD
• Definition: COPD is a common, preventable, and treatable
syndrome of persistent limitation in expiratory airflow
encompassing both small airway disease (obstructive
bronchiolitis) and parenchymal destruction (emphysema).
Airflow obstruction may be accompanied by airway
hyperresponsiveness and may not be fully reversible. Airway
and alveolar abnormalities are usually caused by significant
exposure to noxious particles.
◦ Chronic bronchitis consists of persistent cough plus sputum
production for most days of 3 months in at least 2 consecutive years
and is an independent disease entity that may occur before or after
the development of airflow limitation.
◦ Emphysema is abnormal permanent enlargement of the airspaces
distal to the terminal bronchioles, accompanied by destruction of
their walls and without obvious fibrosis. Emphysema is only one of
several structural abnormalities in patients with COPD.
46.
47. COPD
Pharmacotherapy
Patient
Group
Recommended 1st line Alternative Other Possible
Treatments
A SA anticholinergic prn
OR
SA beta2-agonist prn
LA anticholinergic
OR
LA beta2-agonist
OR
SA beta2-agonist + SA
anticholinergic
Theophylline
B LA anticholinergic
OR
LA beta2-agonist
LA anticholinergic + LA beta2-
agonist
SA beta2-agonist
and/or
SA anticholinergic
Theophylline
C ICS + LA beta2-agonist
OR
LA anticholinergic
LA anticholinergic + LA beta2-
agonist
OR
LA anticholinergic + PDE-4 Inhibitor
OR
LA beta2-agonist + PDE-4 Inhibitor
SA beta2-agonist
and/or
SA anticholinergic
Theophylline
D ICS + LA beta2-agonist
AND/OR
LA anticholinergic
ICS + LA beta2-agonist + LA
anticholinergic
OR
ICS+ LA beta2-agonist + PDE-4
Inhibitor
OR
LA anticholinergic + LA beta2-
agonist
OR
LA anticholinergic + PDE-4 Inhibitor
Carbocysteine
N-acetylcysteine
SA beta2-agonist
and/or
SA anticholinergic
Theophylline
51. Epidemiology
A systemic disease characterized by a bilateral
inflammatory arthritis that usually affects the small
joints of the hands, wrists, and feet
The prevalence is estimated to be 1%–2%, with
women predominating until after age 60, when
prevalence becomes equal.
RA can occur at any age but has an increasing
prevalence up to age 70.
RA is an autoimmune disease with a strong genetic
predisposition.
52. Treatment Goals
• The treatment goal is to control the inflammatory process so
that disease remission occurs. This leads to relief of pain,
maintenance of function, and improved quality of life.
Treatment response can be measured by:
◦ Reduction in the number of affected joints and in joint tenderness
and swelling
◦ Improvement in pain
◦ Decreased amount of morning stiffness
◦ Reduction in serologic markers such as RF
◦ Improvement in quality-of-life scales
53. Agents for
treating RA
• Nonbiologic DMARDs are first line.
◦ Methotrexate has the most long-term data and better outcomes.
◦ Hydroxychloroquine has slow onset of action.
◦ Sulfasalazine is the drug of choice in pregnancy but also has slow
onset.
◦ Leflunomide substitutes, with efficacy comparable with
methotrexate.
• Biologic DMARDs are used in combination with
methotrexate for severe disease or as alternatives if
nonbiologic DMARDs are ineffective or contraindicated.
◦ Tumor necrosis factor (TNF) inhibitors: Etanercept, infliximab,
adalimumab, certolizumab, golimumab
◦ Non-TNF biologics: Abatacept, anakinra, rituximab, tocilizumab
◦ Biologic kinase inhibitor: Tofacitinib
◦ Etanercept, infliximab, abatacept, or rituximab is most often
used.
54. Disease Modifying Anti-Rheumatic Drugs
(DMARD)
• Mechanism:
◦ The immunosuppressive drugs act by a variety of mechanisms. In general, the precise
mechanisms responsible for most therapeutic benefits observed with these agents are
understood only partially. Unlike biologic agents that selectively inhibit a proinflammatory
cytokine and/or block its receptor, conventional immunosuppressive drugs interfere with
combinations of critical pathways in the inflammatory cascade (next slide)
• Example:
◦ Methotrexate, Sulfasalazine
• Indications:
◦ Various, Rheumatoid Arthritis
• Common Adverse Reactions:
◦ See next slide
• Dental Concerns:
◦ RA predisposes to xerostomia, increased risk of infection
55. Disease Modifying
Anti-Rheumatic Drugs
(DMARD): Biologic
• Mechanism:
◦ Biologic agents that selectively inhibit a
proinflammatory cytokine and/or block its
receptor
• Example:
◦ Abatacept, Etanercept
• Indications:
◦ Various, Rheumatoid Arthritis
• Common Adverse Reactions:
◦ See next slide
• Dental Concerns:
◦ RA predisposes to xerostomia, increased risk of
infection
