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Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
Outline
Endocrine Disorders
Blood Disorders
Immunodeficiency
Oral Manifestations of Therapy for Oral Cancer
Effects of Drugs on the Oral Cavity
Oral Manifestations of Systemic Diseases
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
(pg. 288)
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
Endocrine Disorders
Hyperpituitarism
Hyperthyroidism
Hypothyroidism
Hyperparathyroidism
Diabetes Mellitus
Addison Disease
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
Endocrine Disorders
(pg. 288)
Hyperpituitarism
(pgs. 288-289)
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
Facial changes
(pgs. 288-289)
Mucosal changes
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Hyperthyroidism (Thyrotoxicosis)
(pg. 289)
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Clinical Features of
Hyperthyroidism
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Oral Manifestations of
Hyperthyroidism
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Treatment of Hyperthyroidism
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Hypothyroidism
(pg. 289)
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Hypothyroidism (cont.)
Oral manifestations
In infants
Thickened lips, enlarged tongue, and delayed
eruption of teeth
In adults
Enlarged tongue
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Hyperparathyroidism
(pgs. 289-290)
Hyperparathyroidism is characterized by
elevated blood levels of calcium
(hypercalcemia) and low levels of blood
phosphorous (hypophosphatemia).
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Hyperparathyroidism (cont.)
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Hyperparathyroidism (cont.)
19
Clinical Features
of Hyperparathyroidism
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Oral Manifestations of
Hyperparathyroidism
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Diabetes Mellitus
(pgs. 290-294)
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Types of Diabetes
Type 1
Type 2
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Insulin-Dependent Diabetes
Mellitus
(pgs. 291-292)
Insulin-producing cells of the pancreas are
destroyed.
3% to 5% of all diabetic patients have this type.
28
Insulin-Dependent Diabetes
Mellitus (cont.)
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Insulin-Dependent Diabetes
Mellitus (cont.)
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NonInsulin-Dependent
Diabetes Mellitus
(pgs. 292-294)
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(pg. 293)
32
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(pgs. 293-294)
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Addison Disease
(pg. 294)
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Clinical features
Treatment
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Blood Disorders
Elsevier items and derived items 2009 by Saunders, an imprint of Elsevier Inc.
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Anemia
Iron Deficiency Anemia
Pernicious Anemia
Folic Acid and Vitamin B12 Deficiency
Anemia
Thalassemia
Sickle Cell Anemia
Celiac Sprue
Aplastic Anemia
Polycythemia
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Anemia
(pgs. 294-295)
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Anemia (cont.)
Clinical features
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(pg. 295)
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(pg. 295)
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Treatment
Dietary supplements
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Pernicious Anemia
(pgs. 295-296)
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(pgs. 295-296)
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Treatment
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(pg. 296)
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Thalassemia
(Mediterranean or Cooley Anemia)
(pg. 296)
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(pg. 296)
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Treatment of Thalassemia
Experimental
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(pg. 297)
When someone is heterozygous, it is called sickle cell
trait.
When someone is homozygous, they are much more
severely affected.
57
(pg. 297)
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(pg. 297)
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Celiac Sprue
A chronic disorder
(pgs. 297-298)
Sensitivity to wheat gluten
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Aplastic Anemia
(pgs. 298-299)
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(pgs. 298-299)
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(pg. 298)
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Polycythemia
Polycythemia Vera
Secondary Polycythemia
Relative Polycythemia
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Polycythemia (cont.)
(pg. 298)
Polycythemia Vera
Secondary Polycythemia
Relative Polycythemia
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Polycythemia Vera
(Primary Polycythemia)
(pg. 298)
Unknown cause
More common in men than in women
Age of onset usually between 40 and 60 years
of age
Clinical features
71
Secondary Polycythemia
(pg. 298)
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Relative Polycythemia
(pg. 298)
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Oral Manifestations of
Polycythemia
(pg. 299)
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(pg. 299)
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Agranulocytosis
Cyclic Neutropenia
Leukemia
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(pgs. 299-301)
Granulocytes
Neutrophils (PMNs), eosinophils, and basophils
Lymphocytes
Monocytes
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Agranulocytosis
(pg. 300)
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Agranulocytosis (cont.)
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(pg. 300)
Oral infection
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(pg. 300)
Laboratory testing
Marked reduction in WBC count
Treatment
Transfusions, antibiotics
Removal of the cause for the secondary form
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Cyclic Neutropenia
(pg. 300)
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Leukemia
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Acute Leukemias
(pgs. 300-301)
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(pg. 301)
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Gingival enlargement
Oral infection
Bleeding gums, petechiae and ecchymosis
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Chronic Leukemias
(pg. 301)
Slow onset
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Bleeding Disorders
Hemostasis
Purpura
Hemophilia
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Hemostasis (cont.)
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Hemostasis (cont.)
A cessation of bleeding
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Hemostasis (cont.)
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Platelet Count
(pgs. 301-302)
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Bleeding Time
(pg. 302)
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(pgs. 302-303)
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(pg. 303)
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Purpura
(pgs. 303-304)
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Thrombocytopenic Purpura
(pgs. 303-304)
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Nonthrombocytopenic Purpura
(pg. 304)
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Oral Manifestations of
Nonthrombocytopenic Purpura
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Hemophilia
(pg. 304)
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Types of Hemophilia
(pg. 304)
Type B
Christmas disease
Less common, the clotting defect is plasma
thromboplastin or factor IX
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Immunodeficiency
(pgs. 304-305)
Divided into
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Primary Immunodeficiencies
Of genetic origin
(pg. 305)
May involve B cells, T cells, or both
Very rare
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Secondary Immunodeficiencies
(Cont.)
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Secondary Immunodeficiencies
(Cont.)
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(pgs. 305-307)
Radiation Therapy
Chemotherapy
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(pg. 305)
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Radiation Therapy
(pgs. 305-306)
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(pgs. 305-306)
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Fluoride application
Patient education
Frequent follow-up appointments
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Chemotherapy
(pgs. 306-307)
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(pgs. 307-308)
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Discussion Questions
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