Systemic Diseases

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Systemic Diseases by Mind Map: Systemic Diseases

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 Clinical features: Fatigue, pale, angular cheilitis, loss of filiform papilla, red/withering mucosa Iron Deficiency Anemia Sickle Cell Anemia Pernicious Anemia Aplastic Anemia

1.1.2. decreased O2 to brain- headache, dissiness

1.1.3. Polycythemia Vera (Primary) increase in RBCs etiology: uncontrolled production of bone marrow stem cells cause: unknown most common: white men >40 manifistations systemic oral

1.2. WBC Disorders

1.2.1. Agranulocytosis severe reduction in neurtophils production desruction type of Leukopenia oral symptoms cause unknown chemicals/drugs? immunologic? Hospital Dental Care Only

1.2.2. Cyclic Neutropenia hereditary symptoms similar but less severe than agranulocytosis- bone loss in children MD consult for pre-med.-- no tx during cycle

1.2.3. Leukopenia abnormal decrease in # WBCs (neutrophils)

1.2.4. Leukocytosis

1.2.5. abnormal increase in # WBCs (common in bacterial infections) cyclic depression in neutrophils (every 21-27 days for 2-3 days)

1.2.6. Leukemia malignant neoplasm: excess # of abnormal, immature WBCs unknown causes problems with dental care bleeding/brusing paleness/ fatiuge infections delayed healing oral manifestations gingival hyperplasia- infiltration of cancer cells into gingival tissues excessive gingival bleeding 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 decrease in circulating plateltes etiology <10 yrs= idiopathic AI clinical & oral manifestations spontaneous bleeding (ie nose bleeds, gingival bleeding w/out inflammation) clusters of petechiae, eccymosis, purpura brusing Dx Bleeding time- measures platelet function not count; >1 hour (normal: 1-6 min.) platelet count < 100,000 mm3 (normal: 150,000-400,000 mm3) MD consult necessary secondary to chemicals, radiation, leukemia, drugs, chemo

1.5.2. Hemophilia hereditary; sex-linked; occuring only in males; transmitted from daughter (carrier) to grandson Hemophilia A (classic)- most common- reduction in factor 8 Hemophilia B (christmas) reduction in factor 9 clotting disorder- severely prolonged clotting time Deficiency of one of the plasma proteins that convert fibrinogen to fibrin (necessary for permanent clot) Dx PTT- Partial Thromboblastin Time= prolonged > 50 sec. (normal 25-40 sec.) bleeding and PT- Prothrombin Time= normal involves identifying missing factor Tx missing factor replacement 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 men/women 40+ poor vision/ light sensitivity enlargement of hands, feet, rib cage, facial features

2.2. Hperthyroidism

2.2.1. Grave's Disease (Thyrotoxicosis) thyroid hormone AI disease cause: Thyroid-stimulating Immunoglobulins (THIs) [antibodies] stimulate thyroid cells thyroid enlarges too much TH is produced increase in metabolism clinical features goiter- elarged thyroid rosy complexion- increased body temp. exophthalmos (protruding eyes) nervousness, weakness, restlessness, anxiety cardiac problems- hypertension, tachycardia) weightloss oral manifestations kids- increased cavities; premature exfoliation adults

2.3. Hypothryroidism

2.3.1. Myxedema (adult) goiter slow metabolism weight gain edema fatigue bradycardia dry skin enlarged tongue

2.3.2. Cretinism (kids) thickened lips enlarged tongue delayed tooth eruption

2.3.3. causes: developmental disturbances Hashimoto's Disease- AI destruction of thyroid Iodine deficiency Drugs 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 Hypercalcemia= increased calcium blood lvls - calcium removed from bone into blood Hypophoshatemia- low lvl blood phosphorus Abnormal bone metabolism soft bones= bone pain fractures= demineralization Bone Lesions Brown's Tumors 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 ACTH is similar to melanin-stimulating hormone & causes stimulation of melanocytes bronzing of skin

2.6.4. causes of adrenal gland destruction AI disease malignant adrenal tumor infection 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 Diabetic Ketoacidosis breakdown of fatty tissue producing ketone acid which lowers blood pH coma/death insulin is severely lacking/ineffective acute manifestation of uncontrolled Type 1 diabetes impaired leukocyte function (immune response) insulin deficiency (not produced) collagen is abnormal = delayed healing

2.8.4. classifications Type I- insulin dependent- immune mediated AI disease? insulin-producing beta cells of pancreas are destroyed 3-5% of diabetic pts acute onset- 3 P insulin delivery most common endocrine metabolic disorder Type II- non-insulin dependent most common- 97% of diabetic pts insulin resistance Onset chronic complications acute complication defective insulin (doesn't effectively lower glucose lvl) symptoms oral complications Tx- control of insulin lvls MD referral/consult for uncontrolled diabetes; pre-med may be necessary for dental surgery Gestational- pregnancy induced- more susceptible to Type II later in life Secondary- caused by other diseases, meds. or surgery