Pathology Chapter 9

Apertognathia

Anterior open bite

Bleeding: Hemophilia

Blood coagulation disorder, severely prolonged clotting time. Deficiency of one plasma proteins involved in coagulation Types: Type A and Type B- inherited Xlinked recessive, passed by unaffected carrier in males and in homozygous females, mom may have mildly prolonged coagulation time. Type A is classic and more common type caused by a deficiency of clotting factore called plasma thromboplastinogen (Factor VIII), severe hemorrhage Type B-Christmas Tree, less commong defects in plasma thromboplastin or factor IX ORAL: spontaneous gingival bleeding and exxhymoses DIAG and TX: Pt in pts are normal, and PTT is prolonged, missing factor and replace it for tx

Purpura

Blood disorders characterized by purplish or brownish-red discolorations caused by bleeding into the skin or tissues

Gestational Diabetes

Can occur during pregnancy (2-10% of cases) and disappears afterwards Screening is recommended and part of prenatal care Resistance likely from antagonistic effects of progesterone and cortisol Baby birth weight typically greater than normal Mothers much higher risk of developing Type 2

Receptor

Cell surfaceprotein to which a specific molecule (eg a hormone) can bind; such binding leads to biochemical events

Bleeding: Hemostasis

Cessation of bleeding Necessary to procduce fibrin, tightly binds platelets to form a clot Plasma proteins that that are made almost exclusively in liver called clotting factors or coagulation factors to change fibrinogen to fibrin. Successful hemostasis depends on the walls of the blood vessels, adequate numbers of functioning platelets, and adequate levels of properly functioning clotting factors. Defects in hemostasis are caused by abnormalities of either platelets or coagulation factors.

Diabetes Mellitus

Chronic and incurable disorder of carbohydrate (glucose) metabolism and is characterized by abnormal hyperglycemia from lack of insulin hormone due to obesity. Considered a syndrome Leads to disorders of protein and fat metabolism Insulin is then secreted directly into the bloodstream to facilitate uptake of glucose into fat and skeletal muscle cells (can use as energy when there is insulin, where no insulin cells are starved) Without insulin to meet demand for carbs, tissues broken down through catabolism w/weight loss, severe hyperglycemia leading to diabetic coma. Excess production of ketone bodies from catabolism of fat tissue is life threatening and common in TYPE 1. (Ketone bodies, acetone, lower pH of blood and lead to ketoacidosis, leading to coma and death) Phagocytic of macrophages reduced, chemotaxis of neutrophils delayed, lymphocyte function affected. Increase susceptible to infection, abnormal collagen production affecting healing. AGEs impair healing and contributes to perio progression.

WBC: Celiac Disease

Chronic disorder w/ sensitivity to dietary gluten. When ingested injury to intestinal mucosa. Malabsorption of other vitamins and nutrients Anemia develops CLINICAL AND ORAL: Diarrhea, nervousness, paresthesia of extremities, painful burning tongue, atrophy of papillae, ulcers on gingiva DIAG and TX: Gluten-free diet

Polydipsia

Chronic excessive thirst and intake of fluid

RBC: Aplastic Anemia

Dramatic decrease in all types of circulating blood cells (Pancytopenia) Severe depression of bone marrow activity All blood cells are produced from stem cells in bone marrow= life threatening blood disorder Primary- Cause unknown, most frequent in young adults Secondary- drug or chemical agent caused; chemotherapy, radioactive isotopes, radium, and radiant energy known causes System and Oral: infection, spontaneous bleeding, petechiae, purpuric spots Fatigue, weakness, tachycardia, significant bruising, ecchymoses, retinal and cerebral hemorrhages LOW WHITE BLOOD CELL COUNTS (NEUTROPENIA) PREDISPOSE THE PATIENT TO INFECTIONS THAT ARE OFTEN THE CAUSE OF DEATH Diag and Tx: Leukopenia, thrombocytopenia occur Primary is progressive and fatal, Secondary tx remove the cause

Xerostomia

Dry Mouth

WBC

3 groups: Granulocytes (3 types polymorphonuclear leukocytes (neutrophils), eosinophils, and basophils), lymphocytes, and monocytes Neutrophils primary function defend the body against foreign invaders such as bacteria, viruses, and fungi Response to infection is inflammatory response

Pancytopenia

A dramatic decrease in all types of circulating blood cells

RBC: Thalassemia

AKA Mediterranean or Cooley anemia Group of inherited disorders of hemoglobin synthesis Heterozygous form (one gene): Thalassemia minor; asymptomatic, mildly symptomatic Homozygous form (two gene): Thalassemia major; severe hemolytic anemia, from damage to the rbc membranes and destruction of rbc Clinical and Oral: Severe form begins early in life, yellowish skin pallor, fever, malaise, weakness, enlarged liver and spleen, prominent cheek bones, depression of brg of nose, unusual prominence of the premaxilla, protrusion or flaring of max ant teeth THERE IS A PROMINENCE OF SOME TRABECULAE AND A BLURRING AND DISAPPEARANCE OF OTHERS, RESULTING IN A "SALT AND PEPPER" EFFECT Thinning of lamina dura, circular radiolucencies in alveolar bone, lateral skull xrays "hair on end" appearance. TX: T Major is experimental w/ blood transfusions and splenectomy, poor prognosis, have extended life from early childhood to 20s, multiple blood transfusion lead to death by hemochromatosis (excessive iron in body)

Osteoporosis

Abnormal rarefaction of bone

Ketoacidosis

Accumulation of acid in the body resulting from the accumulation of ketone bodies

Exophthalmos

An abnormal protrusion (bulging) of one or both eyes

Bleeding Time

An assessment of the adequacy of platelet function, NOT platelet number How long it takes a standardized skin incision to stop bleeding by forming temporary clot. Usually between 1-6 mins 5-10 mins with platelet abnormalities Aspirin can affect bleeding time

Blood Disorders

Anemia Iron Deficiency Anemia Pernicious Anemia Folic Acid and Vitamin B12 Deficiency Anemia Thalassemia Sickle Cell Anemia Aplastic Anemia Polycythemia Agranulocytosis Cyclic Neutropenia Leukemia Celiac Disease Hemostasis Purpura Hemophilia

Hepatomegaly

Enlargement of the liver

Splenomegaly

Enlargement of the spleen

Hypercalcemia

Excess calcium in the blood

Hyperglycemia

Excess glucose in the blood

Hyperpituitarism

Excess hormone production by the anterior pituitary gland. It is caused most often by a benign tumor (pituitary adenoma) that produces growth hormone. Gigantism-during development before long bones close, 20% of gigantism cases, excessive growth of full skeleton, 8+ ft tall headaches, chronic, fatigue, and muscle & joint pain as adults. Acromegaly- rare, occurs in adult life after long bones close, 65 pts per million, both men and women, in 40s, slow and insidious onset, poor vision, sensitive to light, large hands, feet, ribs, max/mand, frontal bossing, large nasal bones w/ max sinus causing deep voice, thickened lips, macroglossia Diagnosis & Tx- Lab tests for serum growth via oral glucose dose, ususally hormone levels decrease, w/acromegaly no decrease. Tx surgical removal of pituitary adenoma, possible radiation

Hyperthyroidism (Thyrotoxicosis, Graves Disease)

Excessive production of thyroid hormone, 10 x more common in women, in 30s or 40s, most common cause is Graves Disease-autoimmune disorder in which antibodies called thyroid-simulating immunoglobulins (THIs) stimulate thyroid cells and thyroid gland enlarges too much w/ too much hormone produced; increase in metabolism, hyperplasia of gland, benign and malignant tumors, pituitary gland disease, metastatic tumors also causes FEATURES-goiter, rosy complex, erythema of palms, excessive sweating, fine hair, softened nails, exophthalmos, weight loss, anxiety, weakness, restlessness, cardiac problems ORAL MANIFESTATIONS-In children early tooth loss and perm tooth eruption; in adults osteoporosis that affects alveolar bone, caries & perio may develop and progress rapidly, burning tongue TX- surgery, meds to suppress thyroid, radioactive iodine, TX of hyper is most common cause of hypo and is iatrogenic or clinician caused disease

Hyperparathyroidism

Excessive secretion of PTH-Parathyroid hormone PTH important in calcium and phosphorus metabolism Hypercalcemia and hypophosphatemia w/ abnormal bone metabolism are PRIMARY HYPERPARATHYROIDISM: result of hyperplasia of parathyroid glands, benign/malignant (less common) tumor, elevated serum calcium= kidney stones, in adults over 60 more common in women Overproduction of PTH to long-term decreased levels of serum calcium associated w/ chronic renal disease-SECONDARY HYPERPARATHYROIDISM: calcium abnormally excreted by kdineys and parathyroid glands increase PTH to maintaint adequate blood levels of calcium, most common cause kidney failure malabsorption of nutrients and fat soluble vitamins (Vit D) through the gut or small intestine CLINICAL FEATURES: can be asymptomatic, joint pain/stifness, affects kidneys, skeletal system, GI system; severe shows lethargy, dementia, and coma ORAL: well-defined unilocular/multilocular radiolucencies, micrcro appear indistinguishable from central giant cell granulomas, rare peripheral giant cell granulomas, ground glass appearance, loss of lamina dura, loose teeth DIAG/TX: Measure PTH levels, correction of the cause, bone lesions resolve with control of hyperPT

Insulin Pump

External, size of a pager Delivers insulin through plastic tubing placed under the skin Small amounts of rapid-acting insulin on the hour over 24 hour period according to metabolic needs Insulin dose lower than individual injections Pt must deliver insulin because pump has no brain Should carry bag w/syringes in case pump fails Failure for insulin can lead to rapid development of hyperglycemia & ketoacidosis: nausea, abdominal cramps, disorientation, fatigue

WBC: Cyclic Neutropenia

Form of agranulocytosis Severe depression of granulocytes in periodic intervals, mutation of gene ELA-2 Cycles every 21-27 days when sharp decrease in neutrophilsfor 2-3 days Gingival inflammation, ulceration of tongue and mucosal tissues, Ulcers vary in size, painful and become infected

Coagulation

Formation of a clot

Insulin

Hormone produced in the pancreas by beta cells in the islets of Langerhans; insulin regulates glucose metabolism and is the major fuel-regulating hormone

Endocrine Disorders

Hyperpituitarism Hyperthyroidism (Thyrotoxicosis, Graves Disease) Hypothyroidism Hyperparatyroidism Diabetes Mellitus (1 and 2) Gestational Diabetes Addison Disease

Autoimmunity

Immune mediated destruction of the body's own cells and tissues; immunity against self

RBC: Polycythemia

Increase in number of circulating RBC, can be absolute or relative RBC production carefully regulated by both precusor cells in the bone marrow and hormone erythropoietin which produced in the kidney Polycythemia Vera-High number of circulating RBC, production is uncontrolled, cause is unknown, onset in 40-60s, more in men, Whites and RARE in blacks. Headaches, dizziness, pruritus. Impaired blood flow, vascular stasis, poor circulation. Thrombi can cause disruption of blood supply to brain, heart, or peripheral vessels. Thrombocytopenia occurs because of disruption of the marrow from which they are derived. Secondary Polycythemia- increase in rbc due to physiologic response to decreased oxygen which triggers increase in erythropoietin by kidneys, which increases rbc production. Oxygen decrease can be caused by pulmonary disease, heart disease, living at high altitudes and elevation in carbon monoxide (ie: smoking) Relative Polycythemia-decreased plasma volume and not an increase in rbc. Acute caused by diuretic use, vomiting, diarrhea, excessive sweating. Chronic form called stress polycythemia. Mostly middle age white men under physiologic stress, mildly overweight, hypertensive, heavy smokers with increase in cerebrovascular accidents and myocardial infarction. Oral: mucosa appears deep red to purple, gingiva may be edematous, bleed easily, submucosal petechia, ecchymoses, hermatoma formation, excessive bleeding after OS Diag and Tx: Lab testing and measurement of hemoglobin and hematocrit. TX may include removal of causative factors, chemo, and phlebotomy removing up to 500 ml of blood each day

Polycythemia

Increase in the total red blood cell mass in the blood

RBC: Sickle Cell Anemia

Inherited significant disorder predominantly in blacks, mediterranean or Asian orgin. Persons heterozygous are generally asymptomatic, called sickle cell trait Homozygous are more severly affected, presents before 30 years and mostly in women Abnormal type of hemoglobin in rbc, cells develop a sickle shape in presence of decreased oxygen. Triggered by exercise, exertion, admin of gen anesthetic, pregnancy, or sleep. Sickle shape is unable to pass through small blood vessels and are destroyed more rapidly than normal Clinical and Oral: Weakness, shortness of breath, fatigue, joint pain, nausea, abnormal kidney functions, eyes, and cardiovascular system, and CNS. 2 severe characteristics: Sickle cell crisis (severe sickling of erythrocytes) and Acute chest syndrome (Pulmonary involvement). All organs and tissues can be affected. Loss of trabeculation, large irregular narrow spaces on xrays CHANGES IN THE SKULL HAVE BEEN DESCRIBED AS A HAIR ON END PATTERN BECAUSE THE TRABECULAE RADIATE OUTWARD Diag and Tx: Sickle shaped blood cells on blood smear, RBCs and hemoglobin usually low Admin of Oxygen, IV and oral fluids, can cause enlargement of the heart, cardiac failure

Fibrin

Insoluble protein that is essential to the clotting of blood

RBC: Iron Deficiency

Insufficient amount of iron is supplied to the bone marrow for rbc development. MOST COMMON CAUSE OF ANEMIA IN US. Insufficient intake of iron, excess blood loss during menstruation, Chronic GI Bleeding, poor absorption, pregnancy or infancy. Plummer-Vinson Syndrome-Rare, develop as result of long standing iron deficiency anemia, dysphagia, glossitis, angular cheilitis, atrophy of papilla, atrophy of upper alimentart tract, predisposition to the development of esophageal and oral cancer. IN PLUMMER-VINSON SYNDROME, EVALUATION OF THE ESOPHAGUS IS PERFORMED BY ENDOSCOPY OR ESOPHAGEAL BARIUM, WHICH WILL HELP TO IDENTIFY ESOPHAGEAL WEBS. Clinical and Oral: Most often asymptomatic Severe: weakness, fatigue, low energy, shortness of breath, sometimes cardiac palpitations Diag and Tx: Lab tests that show low hemoglobin content of rbc and reduced hematocrit (volume of rbc) --->Iron is needed for hemoglobin synthesis: iron deficiency anemia the rbc appear smaller than normal and hypochromic (lighter in color)

Oral Manifestations of Therapy for Oral Cancer

Radiation Therapy Chemotherapy Effects of drugs on the Oral Cavity

Microcyte

Red blood cell that is smaller than normal

Bleeding: Purpura

Reddish blue or purplish discoloration of skin or mucosa that results in spontaneous extravasation of blood. Defect or deficiency in platelets or increase in fragility. Oral: oozing of blood at the gingival margins w/out presence of ggvts or inflammation, petechiae, ecchymoses, hemorrhagic blisters possible

WBC: Agranulocytosis

Reduction in circulating neutrophils (neutropenia) Any white blood cells can be involved, leukopenia most commonly involves neutrophils Results in problem of development or accelerated destruction of neutrophils Primary form: Cause unknown, may be immunologic disorder Secondary form: most commonly produced by chemo drugs and other immunologic reactions, most common in women Clinical and Oral: after ingesting offending drugs, sudden onset of high fever, chills, jaundice (icterus), weakness, sore throat. Oral ulcerations and infection. NUG excessive bleeding from gingiva, rapid destruction of supporting tissue of teeth, regional lymphadenopathy Diag and TX: Lab testing, WBC (normal 4,500 - 10, 000 cells/ml) reduced to less than 1,000 cells/ml. TX transfusions, antibiotics, secondary form removal of causative agent. infections can cause death, all surgical procedures including dental are contraindication

RBC: Anemia

Reduction in oxygen carrying capacity of the blood that in most cases is related to a decrease in the number of circulating red blood cells. Most common deficiencies: Iron, folic acid, B12 Occur when suppression of the bone marrow stem cells take place ORAL: manifestations are similar for all types of anemia; skin and mucosa pallor, angular cheilitis, erythema and atrophy of oral mucosa, loss of filiform and fungiform papillae on dorsum of the tongue

Anemia

Reduction of the number of Red Blood Cells, quantity of hemoglobin, or volume of packed red blood cells to less than normal

hemolysis

Release of hemoglobin from red blood cells by destruction of the cells

Bleeding: Platelet Count

Requested with CBC Normal platelet 200,000 to 400,000/mm3 Less than 100,000/mm3 is thrombocytopenia Spontaneous gingiva bleeding w/ count less than 20,000/mm3

Hormone

Secreted molecules produced in the body that have a specific regulatory action on target cells that are distant from their sites of synthesis; an endocrine hormone is frequently carried by the blood from its site of release to its target

Atherosclerosis

The process by which lipid accumulates within the walls of large and medium sized arteries. It leads to reduced blood flow to and death of vital organs

Aplasia

Lack of development

WBC: Leukemia

MALIGNANT NEOPLASMS OF THE HEMATOPOIETIC STEM CELLS Originate in stem cells of bone marrow EXCESSIVE NUMBER OF ABNORMAL WBS IN CIRCULATING BLOOD PATHOGENISIS IS UNKNOWN. HOWEVER, CURRENT INVESTIGATIONS ARE FOCUSING ON ONCOGENIC VIRUSES Many leukemias exist, classified on cells involved and maturity of neoplastic cells oral lesions more common in acute but can happen in chronic Acute: very immature cells, immature lymphocytes or granulocytes. Acute lymphoblastic leukemia affects children and young adults with good prognosis. Acute myeloblastic leukemia involves adolescents and young adults (15-39 yrs) w/ poor prognosis. Sudden and dramatic onset CLINICAL: weakness, fever, enlargement of lymph nodes, bleeding, cervical lymphs seen early on. Loss of cells produced by bone marrow, fatigue from anemia, fever from infection, bleeding from thrombocytopenia, advanced disease enlargement of spleen (splenomegaly) and liver (hepatomegaly) when infiltrated by leukemic cells. ORAL: gingival enlargement, oral infections (NUG), bleeding gums, petechie, ecchymoses may be present. Some report toothache. DIAG & TX: Lab tests include elevated WBC w/presence of many immature cells, anemia, and low platelet count. In children: prognosis is very good, in adolescents and young adults prognosis is poor. Remissions occur with chemo w/relapse and bone marrow transplant is tx. Chronic: Slow onset and primarily in adults. Present for months before diagnosed, sometimes made during a routine physical based on labs. CHRONIC MYELOID LEUKEMIA, IS ASSOCIATED WITH A DISTINCTIVE CHROMOSOMAL ABNORMALITY, THE PHILADELPHIA CHROMOSOME. CHRONIC LYMPHOCYTIC LEUKEMIA IS THE MOST COMMON FORM AND ACCOUNTS FOR ABOUT 25% OF THE TOTAL CASES OF LEUKEMIA. May be asymptomatic and about 50% of pts have abnormal karyotypes, but abnormality is different from Philadelphia Chromosome CLINICAL AND ORAL: easy fatigability, weakness, weight loss, anorexia, pallor of the lips and gingiva, gingiva enlargement, petechiae, ecchymosos, gingival bleeding, atypical perio DIAG and TX: Normal WBC (4,000 to 11,000 mm3) increases to 500,000 mm3. Remission with chemo, high doses in short time is induction chemo. Cryotherapy decreases oral ulceration. Once in remission, low doses of chemo over long periods, maintenance chemo. may use bone marrow transplantaion

Agranulocytosis

Marked decrease in the number of granulocytes, particularly neutrophils

Partial Thromboplastin Time

Measures effectiveness of clot formation, time it takes for a clot to form after the addition of kaolin, surface activating factor, cephalin a substitute platelet factor. A NORMAL PTT IS USUALLY 25 TO 40 SECONDS Used to monitor heparin therapy, commonly used for kidney hemodialysis in pts with renal failure.

Petechia

Minute red spot on the skin or mucous membrane caused by escaped of a small amount of blood

Oral Manifestations of Therapy for Oral Cancer: Radiation

Mucositis-painful, erythematous, ulcerated mucosa, difficulty eating, pain on swallowing, loss of taste, irreversible salivary gland destruction can occur from damage to major salivary glands, resulting in xerostomia. Mucosa easily irritated and prone to rampant caries and oral candidiasis Pilocarpine Hydrochloride-reduces severity of radiation induced xerostomia Risk for osteoradionecrosis

Myalgia

Muscle pain

Prothrombin Time

PT pts ability to form a clot Measure time it takes to form a clot when calcium and tissue factor are added to pts plasma. Normal PT is between 11 and 16 seconds Used to monitor anticoagulant therapy (coumarin or warfarin sodium) for preventing myocardial infarction. More accurate determination of PT is the international normalized ratio (INR), an expression of the ration of PT to thromboplastin activity; standard from lab to lab. Less than 3 are normal range, anticoagulants such as warfarin may have INR of 4-5.

Parathormone

Parathyroid hormone

Thrombocyte

Platelet

Bleeding: Nonthrombocytopenic Purpura

Bleeding disorders that result from either a defect in the capillary walls or platelet function. Vitamin C deficiency, chemicals and allergy Most common reason for prolonged bleeding is ingestion of drugs that affect platelet function. Small doses of aspirin produces an impairment of platelet function. NSAIDS adversely affect platelet function von Willebrand disease- Most common inherited human bleeding disorders, autosomal-dominant disorder, affects both genders ORAL: spontaneous gingival bleeding, petechiae, ecchymoses, hemorrhagic DIAG and TX: Normal platelet count, prolonged bleeding time, systemic corticosteroids, spenectomy, perm or temp discontinuation of causative agent

RBC: Folic Acid and Vit B12 Deficiency Anemia

Associated with malnutrition and increased metabolic requirements Malnutrition with alcoholism, pregnant women Folic Acid and Vit B12 are essential for DNA synthesis ORAL: indistinguishable from those of pernicious anemia Diag and TX: Lab tests that include serum assays of folic acid and vit B12. Megaloblastic anemias. Tx is dietary supplements.

Macrovascular Disease

Atherosclerosis of large and medium size blood vessels

Oral Manifestations of Therapy for Oral Cancer: Chemotheraphy

Complications predictable and differ for various types Mucositis and oral ulceration are frequent Epithelium becomes atrophic and ulcerated w/minor irritation Cells of bone marrow-decrease in all blood cells w/ increased risk for oportunistic infections and bleeding problems due to less WBC and platelets

Catabolism

Component of metabolism that involves the breakdown of tissues

Microvascular

Damage to small blood vessels

Thrombocytopenia

Decrease in the number of platelets in circulating blood

Neutropenia

Decreased number of neutrophils in the blood

Hypothyroidism (Cretinism, Myxedema)

Decreased output of thyroid hormone In infancy-Cretinism, Thickened lips, glossitis, delayed eruption of teeth Older children and adults- Myxedema, dry skinswelling of face, weakness, fatigue, macroglossia Causes= Developmental disturbances, autoimmune destruction of thyroid gland (aka Hashimoto's thyroiditis), iodine deficiency, drugs, pituitary treatments for hyperthyroidism Lab Tests-T4 (free thyroxine) and TSH measured

Hypophosphatemia

Deficiency of phosphates in the blood

Dysphagia

Difficulty swallowing

Platelet

Disk shaped structure, also called a thrombocyte, found in the blood; it plays an important role in blood coagulation

Immunodeficiencies

Primary Secondary

Addison Disease

Primary adrenal cortical insufficiency; insufficient production of adrenal steroids Malignant tumor and infections may be responsible for destruction of the adrenal gland. Most cases of unknown cause Pituitary gland increases production of adrenocorticotropic hormone: similar to melanin stimulating hormone, causes stimulation of melanocytes BROWN PIGMENTATION (BRONZING) OF THE SKIN OCCURS. Melanotic macules can develop on oral mucosa TX: corticostreroid replacement therapy

Immunodeficiency

Primary: genetic origin and can involve B/T or both cells, extremely rare Bruton disease (x-linked congenital agammaglobulinemia- lack of immunoglobulins) B cells don't mature, plasma cells are deficient throughout the body, T cells normal. Autoimmune diseases are common in these patients. DiGeorge Syndrome (thymic hypoplasia)- thymus is deficient or lacking, T lymphocytes don't mature. Infance and children are extremely susceptible to fungal/viral/bacterial infections that require T and B cell cooperation, B lymphocytes and immunoglobulins not affected. Severe combined immunodeficiency: most infants die in 1st year, vulnerable to all form of infections Secondary: most result from underlying disorder, more common, have accompanying immunodeficiency, including malnutrition Occur with immunodeficient drugs; corticosteroids, radiation, suppress immune system, treat autoimmune disease

Insulin shock

Profound hypoglycemia, or low blood sugar, that necessitates emergency intervention

Bleeding: Thrombocytopenic Purpura

Severe reduction in circulating platelets. Normal level is 200,000 to 400,000/mm3 Spontaneous bleeding when levels less than 20,000/mm3 Idiopathic thrombocytopenic purpura: unknown cause, usually seen in young pts w/ greatest incidence before 10 years, no sex predilection Immune Thrombocytopenia: autoimmune type Secondary Thrombocytopenic Purpura: associated w/ drugs including chemo, no age, no sex predilection CLINIC and ORAL: spontaneous purpuric or hemorrhagic lesions of the skin, vary in size and severity, bruise easily, blood in urine (hematuria), frequent epistaxis (nosebleeds), spontaneous gingival bleeding, petechiae, clusters of petechiae, purpuric spots, ecchymoses possible. DIAG and TX: Lab tests show decrease in platelets. bleeding time prolonged to 1 hour or more, capillary fragility test positive. Tx depends on cause, transfusions, corticosteroids, splenectomy. Dental surgival procedure, including scaling is contraindicated until labs confirm sufficient improvement in pts bleeding problem.

Ecchymosis

Small, flat, hemorrhagic patch larger than a petechia on the skin or mucous membrane

Hypochromic

Stained less intensely than normal

Hemostasis

Stoppage or cessation of bleeding

Types of Diabetes- Insulin-dependent Diabetes Mellitus

Type 1- IDDM, Autoimmunity- destruction of insulin producing beta cells of pancreas and profound insulin deficiency. May be associated with other autoimmune diseases; Addison, Graves, and Pernicious Anemia ONLY 3% OF ALL DIABETIC PATIENTS HAVE TYPE1 Can happen at any age, usually before 20s, usually thing body build **Abrupt onset with 3Ps: Polydipsia, Polyuria, Polyphagia Complications due to damaged blood vessels-Vascular system takes greatest beating Complications with: Eyes (blindness), Kidneys (end-stage kidney failure), Nerves (numbness, paresthesia) Atherosclerosis of large and medium size blood vessels: Aorta, coronary, cerebral arteries, thrombi break off causing gangrene and amputation of legs or feet ATHEROSCLEROSIS OF THE CORONARY ARTERIES LEADS TO ISCHEMIA, REDUCED SUPPLY OF BLOOD TO HEART, AND ULTIMATELY MYOCARDIAL INFARCTION, MOST COMMON CAUSE OF DEATH IN PEOPE WITH DIABETES. LAST, DAMAGE TO THE CEREBRAL ARTERIS LEAD TO A STROKE OR CEREBROCASCULAR ACCIDENT. Must control blood pressure and cholesterol Management: insulin injections, proper diet, exercise, frequent determinations of blood glucose at home Multiple injections can cause hypoglycemia; Insulin shock in severe cases Dependent on Insulin for life

Non-insulin Dependent Diabetes Mellitus

Type 2, insulin resistant NOT deficiency 97% of diabetics have Type 2 Gradual onset, diagnosed in 35-40 yrs Weight gain- obesity is common Epidemic among children especially minorities, social, cultural, and ethical dimensions. Poor High-crime neighborhoods with restricted free space. Western Diet is Obesogenic Obesity decreases # of receptors for insulin binding in sensitive tissues like fat and muscle May be controlled with diet and weight loss Byetta-NOT insulin

Clinical and Oral features of Diabetes

Vascular system most severely affected Decreased resistance to infection Skin infections: boils, UTI, and TB Acanthosis Nigricans: hyperpigmented, velvety textured plaques on neck and hands Increase in candida albicans w/ increase in prevalence of oral candidiasis, mucormycosis: rare fungal infection Bilateral, asymptomatic parotid gland enlargement Xerostomia Altered subgingival flora; change in taste, burning mouth or tongue Accentuated response to plaque Hyperplastic and erythematous gingiva, acute and fulminating gingival abscesses, excessive perio bone loss, tooth mobility, early tooth loss Perio aggravates control of diabetes If pt is undiagnosed and diabetes out of control, the perio will never be controlled

RBC: Pernicious Anemia

Vit B12 deficiency caused by deficiency of intrinsic factor (substance secreted by parietal cells of the stomach) which is necessary for absorption of B12. B12 is needed for DNA synthesis, when lacking, development of rapidly dividing cells such as bone marrow cells and epithelial cells is affected. Clinical and Oral: Weakness, pallor, fatigue, shortness of breath on exertion, nausea, dizziness, diarrhea, abdominal pain, loss of appetite, weight loss, severe paresthesia may occur, angular cheilitis, mucosal pallor, painful, atrophic erythematous mucosa, mucosal ulceration, loss of papillae, burning painful tongue. Diag and Tx: Lab tests features low serum vitamin B12 levels and gastric achlorhydria (lack of hydrochloric acid) Megaloblastic anemia characterized by red blood cells that are immature, abnormally large and have nuclei (megaloblasts) SCHILLING TEST WHICH DETECTS AN INABILITY TO ABSORB AN ORAL DOSE OF VIT B12 (CYANOCOBALAMIN) Tx is injections of vit B12

Hematocrit

Volume percentage of red blood cells in whole blood

Oral Manifestations of Therapy for Oral Cancer: Drugs

Xerostomia can be caused by drugs for blood pressure, antianxiety, antipsychotic, antihistamines Prednisone and antibiotics increase risk of candidiasis Tetracyline tooth discoloration Phenytoin, nifedipine, cyclosporine- Gingiva enlargement Osteonecrosis of max and mand is a complication with bisphosphonate therapy. Used in pts with multiple myeloma, mastatic carcinoma or breast and prostate to preven tumor associated bone destruction. May act against tumor cells. Bisphosphonate is used experimentally in pts with paget disease, orally to treat osteoporosis. Bisphosphonate-associated osteonecrosis (BON) as exposed necrotic bone in the maxillofacial region that has persisted for more than 8 weeks in a pt with current or previous tx w/ bisphosphonate and no hx of radiation therapy to the jaws. Intravenous has higher risk that oral therapy. No clear risk factors. Local risks include dentoalveolar surgery, hx of inflammatory dental disease, trauma to areas such as tori and exostoses are minimum. No tx, meds stay in bone for many years