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Adrenal insufficiency & diabetes mellitus /certified fixed orthodontic courses by Indian dental academy
1. ADRENAL INSUFFICIENCY
Leader in continuing dental education
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INDIAN DENTAL ACADEMY
2. ADRENAL INSUFFICIENCY
Adrenal Insufficiency is a true
medical emergency in which victim is in
immediate danger because of
Glucocorticoid deficiency
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Acute
3. CORTISOL
A Glucocrticoid
Secreted – Adrenal Cortex
Helps the body adapt to stress
Hypersecretion – Cushing’s Syndrome
Deficiency – Addison’s Disease
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5. In primary Adrenal Insufficiency
Clinical manifestation do not develop until at least
70% - 80% of adrenal cortex is destroyed
Patient is capable of maintaining endogenous
cortisol for day to day living
In stress full situation ( Dental appointments )
Adrenal cortex is unable to produce additional
quantity of cortisol needed to adapt to stress .
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6. SECONDARY ADRENAL INSUFFICIENCY
Glucocorticoids drugs are widely prescribed for
variety of disorders
It produces diffuse atrophy of adrenal cortex
diminishing the ability to increase corticosteroid
levels in respose to stressful situation
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7. PRE DISPOSING FACTORS
Sudden withdrawal of steroid harmones
Physiologic or Psychological Stress
Bilateral adrenelectomy
Injury to Adrenal gland due to Trauma, infection
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8. CLINICAL MANIFESTATION
If a patient with Addison's disease is challenged by
stress (e.g., illness, infection, surgery), an adrenal crisis
may be precipitated.
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The most common complaints are
weakness, fatigue, and abnormal pigmentation of the
skin and mucous membranes
Hypotension, anorexia, and weight loss are additional
common findings.
9.
This medical emergency manifests as severe
exacerbation of the patient's condition, including
If not treated rapidly, the patient may develop
hypothermia, severe hypotension, hypoglycemia, and
circulatory collapse that can result in death.
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sunken eyes, profuse sweating, hypotension, weak pulse,
cyanosis, nausea, vomiting, weakness, headache,
dehydration, fever, dyspnea, myalgias, arthralgia,
hyponatremia, and eosinophilia.
10. PATIENT PAST HISTORY OF SYSTEMIC
CORTICOSTEROID USE
Evaluate the patient.
Determine whether systemic corticosteroid was taken
within the past 2 weeks and the reason for
discontinuing usage.
Identify signs and symptoms of possible adrenal
insufficiency.
If major invasive oral procedure is planned and
corticosteroid was taken within the past 2 weeks,
consult with the physician regarding status and stability
If adrenal insufficient, implement steroid
supplementation protocol.
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11. PATIENT CURRENTLY TAKING SYSTEMIC
CORTICOSTEROIDS
Identify signs and symptoms of possible adrenal
insufficiency.
For diagnostic and minimally invasive procedures,
have patient take the usual daily dose, and perform oral
procedure in the morning, shortly after the
corticosteroid is taken.
Stress reduction measures should be implemented,
blood pressure recorded during the procedure.
For major invasive oral procedures, consult with the
physician
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12. PATIENT NOT TAKING SYSTEMIC CORTICOSTEROIDS,
BUT MAY HAVE ADRENAL INSUFFICIENCY
Evaluate the patient for historical findings associated
with risk for adrenal insufficiency.
Identify signs and symptoms of adrenal insufficiency.
Refer to the physician for ACTH testing.
If the patient is found to be adrenally insufficient, defer
dental treatment until stabilized with corticosteroid
treatment.
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13. STEROID SUPPLEMENTATION PROTOCOL FOR
MAJOR SURGICAL PROCEDURE:
Discontinue drugs that decrease cortisol levels (e.g.,
ketoconazole, metyrapone) at least 24 hours before
surgery with the consent of the patient's physician.
Have patient take usual morning dose and provide
supplemental hydrocortisone preoperatively and
intraoperatively to achieve 100 mg within first hour of
surgery.
Give hydrocortisone 25 mg every 8 hours subsequent to
surgery for 24 to 48 hours.
Provide adequate operative and postoperative
analgesia.
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14.
Communicate with the patient at the end of the
appointment and within 4 hours postoperatively to
determine whether features of weak pulse,
hypotension, dyspnea, myalgias, arthralgia,
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Monitor blood pressure (BP) and blood loss
throughout the procedure.
If BP drops to below 100/60 mm Hg and the patient is
unresponsive to fluid replacement and vasopressive
measures, administer supplemental steroids.
15. MANAGEMENT
ASSESS CONSCIOUSNESS
TERMINATE DENTAL TREATMENT
POSITION – FEET ELEVATED
PROVIDE BLS
DEFINITIVE CARE:
Monitor Vital Signs
Emergency kit & O & Medical Assisstance
Administer Glucocorticosteroid
2
ADDITIONAL MANAGEMENT
TRANSFER TO HOSPITAL IF UNCONSCIOUS
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19.
TYPE 1:
TYPE 2:
Result from impaired insulin function. (insulin resistance)
GDM:
Defined as any degree of glucose intolerance with onset or
first recognition during pregnancy
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Autoimmune destruction of the insulin-producing beta cells of
pancreas.
20. PATHOPHYSIOLOGY
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Healthy people blood glucose level maintained within 60 to
150 mg/dL.
Insulin synthesized in beta cells of pancreas and secreted
rapidly into blood in response to elevations in blood sugar.
Promoting uptake of glucose from blood into cells and its
storage as glycogen
Fatty acid and amino acids converted to triglyceride and
protein stores.
21. Lack of insulin or insulin resistance, result in inability of
insulin-dependent cells to use glucose.
Triglycerides broken down to fatty acids blood ketones↑
diabelic ketoacidosis.
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22. As blood sugar levels became elevated (hyperglycemia),
glucose is excreted in the urine and excessive of urination
occurs due to osmotic diuresis (polyuria).
Increased fluid loss leads to dehydration and excess thirst
(polydipsia).
Since cells are starved of glucose, the patient experiences
increased hunger (polyphagia).
Paradoxically, the diabetic patient often loss weight, since
the cells are unable to take up glucose.
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25. MEDICAL MANAGEMENT
Sulfonyl ureas
Bigaunides
Meglitidines
Thiazoledinediones
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Exercise and diet control
Insulin : rapid, short, intermediate, long acting.
Oral antidiabetic agents
26. MANAGEMENT:
• Lifestyle
intervention
(HbA1c ↓1–2%)
• Metformin
(HbA1c ↓1.5%)
STEP 2
After 2–3 months select
1 additional agent
STEP 3
Adjust therapy
• Basal insulin
HbA1c
≥ 7%
(HbA1c ↓1.5–2.5%)
• Sulfonylureas
(HbA1c ↓1.5%)
• Thiazolidinedione
(HbA1c ↓0.5–1.4%)
HbA1c
≥ 7%
•Start or intensify
insulin therapy
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STEP 1
Initial therapy
• Add a third oral
agent if cost-effective
•
Adapted from Nathan DM, et al. Diabetologia 2006;49:1711–21
27. ORAL MANIFESTATIONS
Periodontal disease
Salivary glands
Xerostomia is common, but reason is unclear.
Tenderness, pain and burning sensation of tongue.
Dental caries
Increase caries prevalence in adult with diabetes.
(xerostomia, increase saliva glucose)
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Microangiopathy altering antigenic challenge.
Altered cell-mediated immune response and impaired of
neutrophil chemotaxis.
Increased Ca+ and glucose lead to plaque formation.
Increased collagen breakdown.
28.
Increased risk of infection:
Delayed wound healing:
Due to microangiopathy and ultilisation of protein for
energy, may retard the repair of tissues.
Increase prevalence of dry socket.
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advanced glycation end- products (AGE) synthesized due
to hyperglycemia,
can convert macrophages into cells with a destructive
phenotype,
producing high levels of interleukin-1β, interleukin 6(IL-6)
and tumour necrosis factor- α (TNF-α).
29. DENTAL MANAGEMENT
CONSIDERATIONS
Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times.
Consultation
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To minimize the risk of an intraoperative emergency,
clinicians need to consider some issues before
initiating dental treatment
Medical history : take hx and assess glycemic
control at initial appt.
30. DENTAL MANAGEMENT
CONSIDERATIONS
Scheduling of visits
Morning appt. (endogeneous cortisol)
Do not coincide with peak activity.
Diet
Blood glucose monitoring
Ensure that the patient has eaten normally and taken medications
as usual.
Measured before beginning.
Prophylactic antibiotics
Established infection
Pre-operation contamination wound
Major surgery
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31. DENTAL MANAGEMENT
CONSIDERATIONS
During treatment
After treatment
Infection control
Dietary intake
Medications : salicylates increase insulin secretion and
sensitivity avoid aspirin.
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The most complication of DM occur is hypoglycemia
episode.
Hyperglycemia