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Diabetes Mellitus
 

Diabetes Mellitus

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    Diabetes Mellitus Diabetes Mellitus Presentation Transcript

    • Endocrine System (2) Ema A. Dragoescu, M.D. June 11, 2009
    • Adrenal Gland
      • Cortex
        • Zona glomerulosa  aldosterone
        • Zona fasciculata  cortisol
        • Zona reticularis  sex hormones
      • Medulla  cathecolamines (epinephrine)
    • Adrenocortical Hyperfunction
      • Hormones produced by adrenal cortex:
        • Cortisol
        • Aldosterone
        • Sex hormones (androgens)
      • Syndromes:
        • Cushing Syndrome
        • Hyperaldosteronism (Conn syndrome)
        • Adrenogenital (or virilizing) syndromes
    • Cushing Syndrome
      • Endogenous
      • Pituitary hypersecretion of ACTH
      • Adrenal hypersecretion of cortisol (adenoma, carcinoma, nodular hyperplasia)
      • Ectopic ACTH (small cell lung cancer)
      • Exogenous
      • 4. Adm. of exogenous glucocorticoids
    • Cushing Syndrome
    • Adrenal cortical adenoma. Single, bright yellow nodule. Morphology is identical to that of a nonfunctional adenoma or adenoma from Conn syndrome. The yellow color is due to increased lipid content of the adrenal cortical cells. Adrenal cortical hyperplasia. The cortex is diffusely thickened and yellow.
    • Adrenal cortical adenoma
      • Functional
        • Cortisol: Cushing syndrome
        • Aldosterone: Conn’s syndrome (primary hyperaldosteronism)
      • Nonfunctional
    • Cushing Syndrome – Clinical Features
      • Hypertension
      • Weight gain:
        • Truncal obesity
        • “ moon” face
        • “ buffalo hump”
      • Decreased muscle mass
      • Hyperglycemia
      • Catabolic effect on proteins with loss of collagen: cutaneous striae, easy brusing, osteoporosis
      • Hirsutism, amenorrhea
      • Increased risk of infections (because of decreased immune response)
    • Cushing syndrome. Round face, red cheeks, hirsutism. Cushing syndrome. Truncal obesity and abdominal striae.
    • Oral candidasis in a patient taking inhaler steroids for asthma
    • Dental Management of the Patient Taking Corticosteroids
      • Routine procedures (excluding surgery)
      • a. Good local anesthesia & postoperative
      • pain control if necessary
      • b. Monitor blood pressure during procedure
      • Dental extractions or surgery
      • a. Corticosteroid dose generally will need to be increased, consult patient’s MD prior to the procedure
    • Hyperaldosteronism
      • Na retention and K excretion  HTN, hypokalemia
      • Primary (Conn syndrome)
        • Adrenal cortical adenoma
        • Suppression of RAA: plasma renin = low
      • Secondary
        • Due to decreased renal perfusion (renal artery stenosis, arteriolar nephrosclerosis, CHF)
        • Activation of RAA: plasma renin = high
    • Adrenocortical insufficiency
      • Acute
        • Massive adrenal hemorrhage (DIC, sepsis = Waterhouse-Friderichsen sdr.)
        • Sudden withdrawal of long-term corticosteroid therapy
        • Stress in patients with chronic adrenocortical insufficiency
      • Chronic (Addison disease)
        • Autoimmune, infections (TB, fungal), AIDS, metastatic cancers
    • Addison disease
      • Progressive weakness
      • GI symptoms: anorexia, vomiting, weight loss
      • Hyperpigmentation
      • Low aldosterone: hyponatremia, hypotension
      • Low cortisol: hypoglycemia
      • Death if untreated
    •  
    • Addison disease. Heavy pigmentation of the skin and blothcy pigmentation of the tongue. Oral pigmentation in Addison disease is most common in areas subject to masticatory trauma (cheeks), but can involve any part of the oral mucosa. Oral pigmentation can be the initial presentation of adrenal insufficiency.
    • Pheochromocytoma
      • Tumor of adrenal medulla in adults
      • Paroxysmal episodes of hypertension
      • Urinary excretion of of free cathecolamines and their metabolites (VMA)
      • 10% tumor (familial, children, malignant, extra-adrenal, bilateral)
    •  
    • Familial syndromes with pheochromocytoma
      • MEN IIa, IIb
      • Von Hippel-Lindau (renal cell carcinoma, cerebellar hemangioblastoma)
      • NF1 (neurofibromas, café-au-lait spots, schwannoma, meningioma, glioma)
      • Sturge-Weber (cavernous hemangioma of 5 th nerve distribution)
    • Sturge-Weber syndrome. Hemangiomatous malformation of the face over the maxillary branch of trigeminal nerve. Hemangiomas may also occur in the oral mucosa.
    • Diabetes Mellitus
      • = hyperglycemia, with secondary damage to:
        • Kidneys  ESRD
        • Eyes  blindness
        • Nerves  peripheral sensory and autonomous neuropathy
        • Blood vessels  extremities amputation
      • 7% of US population
    • Blood glucose
      • Normal: 70-110 mg/dL
      • Diabetes (one of the 3):
        • random: ≥ 200 mg/dL
          • 110-200 mg/dL has impaired glucose tolerance
        • Fasting glucose ≥126 mg/dL
          • 110-126 mg/dL has impaired glucose tolerance
        • OGTT ≥ 200 mg/dL
          • 140-200 mg/dL has impaired glucose tolerance
    • Diabetes Mellitus
      • Type 1: absolute deficiency of insulin secretion
        • Autoimmune destruction of β cells
        • Starts in childhood
        • Depend on exogenous insulin for survival
      • Type 2: relative deficiency of insulin
        • Peripheral resistance to insulin
        • Inadequate β cells function
    • Effects of insulin
      • anabolic effect
      • increased synthesis and decreased degradation of:
        • Glycogen
        • Lipid
        • Protein
    • Acute complications of diabetes
      • Diabetic ketoacidosis
        • Marked hyperglycemia (>500 mg/dL)
        • Dehydration
        • Metabolic ketoacidosis (nausea, vomiting, respiratory difficulties)
      • Hyperosmolar nonketotic coma
      • Hypoglycemia!
    • Long-term complications of diabetes
      • After 15-20 years; responsible for morbidity and mortality
      • Vascular: accelerated atherosclerosis with MI, PVD, renal atherosclerosis
      • Ocular: retinopathy, cataract, glaucoma
      • Kidney: glomerular, vascular, pyelonephritis
      • Neuropathy
      • Increased sensibility to infectious
      • Poor wound healing
    •  
    •  
    • Diabetic nephropathy. Nodular glomerulosclerosis (Kimmelstiel-Wilson lesion). Eventually this will lead to ischemia  scarring of the glomerulus. Diabetic nephropathy. Renal arteriolosclerosis.
    •  
    •  
    •  
    • Oral Complications of Diabetes
      • Lowered resistance to infections with increased fungal infections (Candidiasis)
      • Xerostomia (Dry mouth)
      • Poor or delayed wound healing
      • Increased incidence of periodontal disease with periodontal abscesses
    • Multiple Endocrine Neoplasia Syndromes
      • Autosomal dominant inherited
      • Hyperplasia/adenoma/carcinoma of multiple endocrine organs
      • Younger age than sporadic tumors
      • Multifocal in a given endocrine organ
      • More aggressive, recur more frequently that sporadic tumors
    • Multiple Endocrine Neoplasia Type 1 (MEN-1)
      • Due to inactivation of MEN1 gene on 11q13
      • Involves (“3P”):
        • Parathyroid: parathyroid hyperplasia  primary hyperparathyroidism
        • Pancreas: functional endocrine tumors (leading cause of death in MEN-1)
          • Insulinoma  hypoglicemia
          • Gastrinoma  Zollinger-Ellison syndrome
        • Pituitary: prolactinoma
    • Multiple Endocrine Neoplasia Type 2 (MEN-2)
      • 2 distinct group of disorders
      • Mutations of RET protooncogene (10q11.2)
      • MEN-2A
        • Medullary thyroid carcinoma
          • Develops in ALL cases
          • In the first 2 decades, multifocal
        • Pheochromocytoma
        • Parathyroid hyperplasia  primary hyperparathyroidism
    • Multiple Endocrine Neoplasia Type 2 (MEN-2)
      • MEN-2B
        • Medullary thyroid carcinoma
        • Pheochromocytoma
        • Do NOT develop parathyroid hyperplasia
        • Develop extraendocrine manifestations
          • Ganglioneuromas on mucosal surfaces (lips, tongue, GI tract)
          • Marfanoid habitus
      • Family members with germ-line RET mutations: prophylactic thyroidectomy
    • Medullary Thyroid Carcinoma
    •