1. Blood Disorders
1.1. RBCs & Hemoglobin (protein that caries O2 to body cells)
1.1.1. Anemia- decrease in O2 carryying capacity of the blood; related to decrease in # of circulating RBCs
1.1.1.1. Clinical features: Fatigue, pale, angular cheilitis, loss of filiform papilla, red/withering mucosa
1.1.1.1.1. Iron Deficiency Anemia
1.1.1.1.2. Sickle Cell Anemia
1.1.1.1.3. Pernicious Anemia
1.1.1.1.4. Aplastic Anemia
1.1.2. decreased O2 to brain- headache, dissiness
1.1.3. Polycythemia Vera (Primary)
1.1.3.1. increase in RBCs
1.1.3.2. etiology: uncontrolled production of bone marrow stem cells
1.1.3.3. cause: unknown
1.1.3.4. most common: white men >40
1.1.3.5. manifistations
1.1.3.5.1. systemic
1.1.3.5.2. oral
1.2. WBC Disorders
1.2.1. Agranulocytosis
1.2.1.1. severe reduction in neurtophils
1.2.1.1.1. production
1.2.1.1.2. desruction
1.2.1.2. type of Leukopenia
1.2.1.2.1. oral symptoms
1.2.1.3. cause unknown
1.2.1.3.1. chemicals/drugs?
1.2.1.3.2. immunologic?
1.2.1.4. Hospital Dental Care Only
1.2.2. Cyclic Neutropenia
1.2.2.1. hereditary
1.2.2.2. symptoms similar but less severe than agranulocytosis- bone loss in children
1.2.2.3. MD consult for pre-med.-- no tx during cycle
1.2.3. Leukopenia
1.2.3.1. abnormal decrease in # WBCs (neutrophils)
1.2.4. Leukocytosis
1.2.5. abnormal increase in # WBCs (common in bacterial infections)
1.2.5.1. cyclic depression in neutrophils (every 21-27 days for 2-3 days)
1.2.6. Leukemia
1.2.6.1. malignant neoplasm:
1.2.6.1.1. excess # of abnormal, immature WBCs
1.2.6.2. unknown causes
1.2.6.3. problems with dental care
1.2.6.3.1. bleeding/brusing
1.2.6.3.2. paleness/ fatiuge
1.2.6.3.3. infections
1.2.6.3.4. delayed healing
1.2.6.4. oral manifestations
1.2.6.4.1. gingival hyperplasia- infiltration of cancer cells into gingival tissues
1.2.6.4.2. excessive gingival bleeding
1.2.6.5. MD consult regarding platelet and bleeding; possible pre-med.
1.3. Terms
1.3.1. Hemostasis- cessation of bleeding
1.3.2. Platelets (thrombocytes)- adhere to a damaged surface & aggregate to form a temporary clot
1.3.3. Fibrin- insoluble protein essential to clotting; binds to platelets
1.3.4. Clotting (Coagulation) Factors convert fibriogen into fibrin to stop bleeding permanently
1.3.5. bleeding disorders are caused by a defect/deficiency of platelets or clotting factors; determined by lab test
1.3.6. purpura= reddish-blue/purple discoloration of skin/mucosa
1.4. insulin resistance (not used properly)
1.5. Platelet Disorder
1.5.1. Thrombocytopenia Pupura
1.5.1.1. decrease in circulating plateltes
1.5.1.2. etiology
1.5.1.2.1. <10 yrs= idiopathic
1.5.1.2.2. AI
1.5.1.3. clinical & oral manifestations
1.5.1.3.1. spontaneous bleeding (ie nose bleeds, gingival bleeding w/out inflammation)
1.5.1.3.2. clusters of petechiae, eccymosis, purpura
1.5.1.3.3. brusing
1.5.1.4. Dx
1.5.1.4.1. Bleeding time- measures platelet function not count; >1 hour (normal: 1-6 min.)
1.5.1.4.2. platelet count < 100,000 mm3 (normal: 150,000-400,000 mm3)
1.5.1.5. MD consult necessary
1.5.1.6. secondary to chemicals, radiation, leukemia, drugs, chemo
1.5.2. Hemophilia
1.5.2.1. hereditary; sex-linked; occuring only in males; transmitted from daughter (carrier) to grandson
1.5.2.1.1. Hemophilia A (classic)- most common- reduction in factor 8
1.5.2.1.2. Hemophilia B (christmas) reduction in factor 9
1.5.2.2. clotting disorder- severely prolonged clotting time
1.5.2.3. Deficiency of one of the plasma proteins that convert fibrinogen to fibrin (necessary for permanent clot)
1.5.2.4. Dx
1.5.2.4.1. PTT- Partial Thromboblastin Time= prolonged > 50 sec. (normal 25-40 sec.)
1.5.2.4.2. bleeding and PT- Prothrombin Time= normal
1.5.2.4.3. involves identifying missing factor
1.5.2.5. Tx
1.5.2.5.1. missing factor replacement
1.5.2.6. MD consult necessary; possibly Hospital Dentistry
2. Endocrine System Diseases
2.1. Hyperpituitarism
2.1.1. Growth hormone produced by anterior pituitary gland
2.1.2. cause: benign tumor (pituitary adenoma) that PRODUCES GH
2.1.3. Giantism- childhood- occurs before the closure of long bones
2.1.4. Acromegaly- adulthood
2.1.4.1. men/women 40+
2.1.4.2. poor vision/ light sensitivity
2.1.4.3. enlargement of hands, feet, rib cage, facial features
2.2. Hperthyroidism
2.2.1. Grave's Disease (Thyrotoxicosis)
2.2.1.1. thyroid hormone
2.2.1.2. AI disease
2.2.1.3. cause: Thyroid-stimulating Immunoglobulins (THIs) [antibodies] stimulate thyroid cells
2.2.1.3.1. thyroid enlarges
2.2.1.3.2. too much TH is produced
2.2.1.3.3. increase in metabolism
2.2.1.4. clinical features
2.2.1.4.1. goiter- elarged thyroid
2.2.1.4.2. rosy complexion- increased body temp.
2.2.1.4.3. exophthalmos (protruding eyes)
2.2.1.4.4. nervousness, weakness, restlessness, anxiety
2.2.1.4.5. cardiac problems- hypertension, tachycardia)
2.2.1.4.6. weightloss
2.2.1.5. oral manifestations
2.2.1.5.1. kids- increased cavities; premature exfoliation
2.2.1.5.2. adults
2.3. Hypothryroidism
2.3.1. Myxedema (adult)
2.3.1.1. goiter
2.3.1.2. slow metabolism
2.3.1.3. weight gain
2.3.1.4. edema
2.3.1.5. fatigue
2.3.1.6. bradycardia
2.3.1.7. dry skin
2.3.1.8. enlarged tongue
2.3.2. Cretinism (kids)
2.3.2.1. thickened lips
2.3.2.2. enlarged tongue
2.3.2.3. delayed tooth eruption
2.3.3. causes:
2.3.3.1. developmental disturbances
2.3.3.2. Hashimoto's Disease- AI destruction of thyroid
2.3.3.3. Iodine deficiency
2.3.3.4. Drugs
2.3.3.5. hyperthyroid tx
2.4. Hyperparathyroidism
2.4.1. secretion of parathyroid hormone (PTH)
2.4.2. cause: benign tumor of 1+ parathyroid glands
2.4.3. manifestations
2.4.3.1. Hypercalcemia= increased calcium blood lvls - calcium removed from bone into blood
2.4.3.2. Hypophoshatemia- low lvl blood phosphorus
2.4.3.3. Abnormal bone metabolism
2.4.3.3.1. soft bones= bone pain
2.4.3.3.2. fractures= demineralization
2.4.3.4. Bone Lesions
2.4.3.4.1. Brown's Tumors
2.4.3.4.2. Jaw lesions
2.5. ground glass appearance of trabeculae
2.6. Addison Disease
2.6.1. aka Adrenal Cortical Insufficiency
2.6.2. decreased production of adrenal steroids
2.6.3. pituitary gland increases the production of Adrenocorticotropic Hormone (ACTH) to increase production of adrenal steroids
2.6.3.1. ACTH is similar to melanin-stimulating hormone & causes stimulation of melanocytes
2.6.3.2. bronzing of skin
2.6.4. causes of adrenal gland destruction
2.6.4.1. AI disease
2.6.4.2. malignant adrenal tumor
2.6.4.3. infection
2.6.4.4. most common- unknown
2.6.5. melanotic macules on oral mucosa (similar to Peutz-Jeghers Syndrome)
2.6.6. Tx: steroid replacement therapy
2.7. Tx: chemo; bone marrow transplant
2.8. Diabetes Mellitus
2.8.1. chronic disorder of glucose metabolism
2.8.2. hyperglycemia- abnormally high BGL
2.8.3. complications
2.8.3.1. Diabetic Ketoacidosis
2.8.3.1.1. breakdown of fatty tissue producing ketone acid which lowers blood pH
2.8.3.1.2. coma/death
2.8.3.1.3. insulin is severely lacking/ineffective
2.8.3.1.4. acute manifestation of uncontrolled Type 1 diabetes
2.8.3.2. impaired leukocyte function (immune response)
2.8.3.2.1. insulin deficiency (not produced)
2.8.3.3. collagen is abnormal = delayed healing
2.8.4. classifications
2.8.4.1. Type I- insulin dependent- immune mediated
2.8.4.1.1. AI disease?
2.8.4.1.2. insulin-producing beta cells of pancreas are destroyed
2.8.4.1.3. 3-5% of diabetic pts
2.8.4.1.4. acute onset- 3 P
2.8.4.1.5. insulin delivery
2.8.4.2. most common endocrine metabolic disorder
2.8.4.3. Type II- non-insulin dependent
2.8.4.3.1. most common- 97% of diabetic pts
2.8.4.3.2. insulin resistance
2.8.4.3.3. Onset
2.8.4.3.4. chronic complications
2.8.4.3.5. acute complication
2.8.4.3.6. defective insulin (doesn't effectively lower glucose lvl)
2.8.4.3.7. symptoms
2.8.4.3.8. oral complications
2.8.4.3.9. Tx- control of insulin lvls
2.8.4.3.10. MD referral/consult for uncontrolled diabetes; pre-med may be necessary for dental surgery
2.8.4.4. Gestational- pregnancy induced- more susceptible to Type II later in life
2.8.4.5. Secondary- caused by other diseases, meds. or surgery