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									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                 Syndromes:
    produced by
    adrenal cortex:
       Cortisol                 Cushing Syndrome

       Aldosterone              Hyperaldosteronism
                                  (Conn syndrome)

       Sex hormones             Adrenogenital (or
        (androgens)               virilizing)
                                  syndromes
          Cushing Syndrome
Endogenous
1. Pituitary hypersecretion of ACTH

2. Adrenal hypersecretion of cortisol (adenoma,
   carcinoma, nodular hyperplasia)
3. Ectopic ACTH (small cell lung cancer)

Exogenous
4. Adm. of exogenous glucocorticoids
         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)
 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
       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
    5th 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.
Renal arteriolosclerosis.




Diabetic nephropathy.
Nodular glomerulosclerosis
(Kimmelstiel-Wilson lesion).
Eventually this will lead to
ischemia  scarring of the
glomerulus.
       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

								
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