Pathology Final - Endocrine

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  1. Anterior pituitary HYPERfunction
    • Most cases caused by adenoma in the anterior lobe
    • Produces excess of a single hormone usually
    • Peak ages 20s—60s
    • Prolactinoma - Most common type, causes amenorrhea, infertility, loss of libido, galactorrhea
    • Somatotroph (growth hormone) - If occuring before puberty= gigantism; If occurring after puberty= acromegaly
    • Corticotroph adenoma - Increased ACTH production—can cause Cushings disease
  2. Anterior pituitary HYPOfunction
    • Most often due to a non-secretory adenoma or less commonly ischemic necrosis of the pituitary
    • Sheehan’s syndrome—postpartum ischemic necrosis
    • Empty sella syndrome—herniation of CSF into the sella turcica compressing the pituitary
  3. Posterior Pituitary ADH Hypersecretion
    • (inappropriate ADH secretion) due to ADH producing tumor such as oat cell lung carcinoma
    • Results in water retention and inability to dilute urine
    • Hyponatremia excess secretion of sodium leading to low levels of sodium in the blood
  4. Posterior Pituitary ADH Hyposecretion
    • Promotes resorption of free water
    • Due to post pituitary destruction—neoplasm, trauma, inflammation
    • Can cause diabetes insipidus characterized by excess urination, dilute urine, and extreme thirst
  5. Hyperthyroidism (thyrotoxicosis)
    • Most common cause= Graves disease
    • Increased circulating T3 and T4, increased I-131 uptake, decreased TSH
    • Clinical manifestations - sweating, warm skin, heat intolerance, tachycardia, muscle weakness, exopthalmos, diarrhea, weight loss
    • Thyroid storm—abrupt onset hyperthyroidism
    • Graves disease: Affects 1-2 % of US women; Thyrotoxicosis, exopthalmos, pretibial myxedema; Autoimmune process—autoantibodies to TSH receptor, microsomes, thyroglobulin, and thyroid hormones
  6. Hypothyroidism
    • Decreased T3 and T4, increased TSH
    • Hypothyroidism is manifest as myxedema in adults and cretinism in children (in children usually due to iodine deficiency)
    • Clinical manifestations: Lethargy, mental slowness, rough skin, cardiac enlargement, obesity, cold intolerance, constipation
    • Causes: radiation, surgery, Hashimoto’s
    • Hashimoto’s thyroiditis: Autoimmune disorder; Massive infiltrates of lymphocytes with germinal centers; Hurthle cells prominent (epithelial cells with eosinophilic granular cytoplasm); Gland enlarges but is hypofunctional; Increased risk of lymphoma; Females 12:1; Can have intermittent periods of hyperthyroidism (thyrotoxicosis)
  7. Subacute granulomatous thyroiditis (deQuervain's)
    • Acute onset, often preceded by URI
    • Granulomatous inflammation
    • Self limiting
    • Transient thyrotoxicosis
  8. Reidels thyroiditis
    Fibrous replacement of thyroid, rare, unknown origin
  9. Hyperparathyroidism
    • Most often due to a parathyroid adenoma
    • Also can be caused by gland hyperplasia, or PTH secreting malignant tumor
    • Symptoms: Stones, Moans, bones, groans
    • Increased serum calcium, increased alkaline phosphatase; decreased phosphorus
    • Excessive bone resorption, seizures, pancreatitis, osteoporosis, kidney stones, peptic ulcers
    • Renal failure= most common cause of secondary hyperparathyroidism
  10. Hypoparathyroidism
    • Caused mainly by surgical misadventure
    • Chvostek’s and Troussau’s sign
    • Neuromuscular irritability, carpopedal spasms, occasional seizures
  11. Adrenal cortex HYPERfunction
    • Cushings syndrome: Most frequent cause=exogenous steroids; Other causes; pituitary adenoma, oat cell carcinoma; Clinical: Buffalo hump, moon face, truncal weight gain, muscle wasting, abdominal striae, hypertension, mental disturbances, hirsutism
    • Hyperaldosteronism: Conn’s syndrome (primary hyperaldosteronism) - Usually from adrenal adenoma, hypertension, sodium/water retention, Decreased potassium; decreased renin. Secondary aldosteronism - Due to renal ischemia; increased rennin
    • Adrenal virulism: Virulism in females; precocious puberty in males; Caused by enzyme defects—hydroxylase deficiency or caused by adrenal cortex tumor
  12. Adrenal Cortex HYPOfunction
    • Addison’s disease: Hypotension, increased skin pigmentation, increased potassium, weight loss, somnolence, personality changes; Most often caused by idiopathic adrenal atrophy; Can also be caused by tuberculosis or metastatic tumors
    • Waterhouse-Friedrichsen syndrome: Castastrophic adrenal insufficiency caused by hemorrhagic necrosis of adrenal cortex; Often associated with DIC; Characteristically due to meningoccal meningitis
  13. Pheochromocytomas
    • Adrenal tumor
    • Clinical: tachycardia, headache, sweating, tremors, elevated VMA
    • Important cause of surgically correctable paroxysmal hypertension
    • Rule of tens =10% bilateral, 10% children, 10% malignant
    • Can occur as part of MEN syndrome
  14. Neuroblastoma
    • Adrenal cortex tumor
    • Highly malignant tumor of early childhood (0-3 years of age)
    • Catacholamine producing tumor presenting as an abdominal mass
    • Produces hypertension
    • Characterized by one or more of the following: Amplification of N-myc oncogene, Deletion short arm chromosome 1, Loss of alleles chromosome 14
  15. Multiple endocrine neoplasia syndromes
    • Autosomal dominant syndromes in which more than one endeocrine organ is hyperfunctional
    • MEN I (Wermer)
    • MEN II (Sipple)
  16. MEN I (Wermer)
    • Hyperplasias or tumors of pituitary, parathyroid, or pancreatic islands (3Ps)
    • Hyperparthyroidism is most common manifestation
    • Mutations of MEN I gene
  17. MEN II (Sipple)
    • Pheochromocytoma, medullary carcinoma of the thyroid, and hyperplasia or tumor of parathyroid producing hyperparathyroidism
    • Mutations of ret oncogene
    • Pheochromcytomas, medullary carcinoma of thyroid, and multiple mucosal neuromas
    • Does NOT cause hyperparathyroidism
    • Linked to different mutations of ret oncogene
  19. Acute leukemias
    • most often in children with a second peak over 60 (AML)
    • Death with 6-12 months if no intervention
  20. Acute lymphoblastic leukemia (ALL)
    • Most common malignancy of children
    • Predominance of lymphoblasts in blood and marrow
    • Most responsive to therapy
  21. Acute myeloblastic leukemia (AML)
    • Predominance of myeloblasts
    • Most often in adults >60
    • Responds more poorly to therapy than ALL
  22. Chronic leukemias
    Proliferation of cells more mature than in acute leukemias; longer less devastating course than acute leukemias; generally less responsive to therapy than acute leukemias
  23. Chronic lymphoblastic leukemia (CLL)
    • Usually a B-cell proliferation
    • Lymphadenopathy and spleenomegaly frequently
    • Complications: Warm antibody autoimmune hemolytic anemia and hypogammaglobulinemia; increased susceptibility to infections
    • Avg survival 3-76 years after diagnosis
  24. Chronic myelogenous leukemia (CML)
    • Part of the myeloproliferative syndrome
    • Philadelphia chromosome (translocation 9-22)
    • Marked leukocytosis
    • Prominent spleenomegaly
    • Peak incidence ages 35-50
  25. Hairy cell leukemia
    • Middle age men/ pancytopenia and splenomegaly/hepatomegaly, lymphadenopathy
    • Dramatic response to therapeutic medications
    • Positive staining of cells for tartrate resistant acid phosphatase (TRAP)
  26. Multiple myeloma
    • Malignant monoclonal plasma cell proliferation affecting older (>50) individuals
    • Punched out (lytic) radioluciencies in bone
    • Demineralization of bone (osteopenia)
    • Severe bone pain and spontaneous fractures M protein spike (usually IgG or IgA (either kappa or lambda light chain))
    • Urine contains Bence Jones protein
    • Increased susceptibility to infection
    • Hypercalcemia due to bone destruction
    • Renal insufficiency with azotemia
    • Amyloidosis
    • Plasma cell disorder
  27. Hodgkin lymphoma
    • Malignant lymphoid proliferation with features resembling an inflammatory disorder such as fever, pruritis, leukocytosis
    • Bimodal occurrence: 2 age peaks: 25 and 55
    • Typically follow along lymph node chain
    • Characterized by Reed Sternberg cells ( binucleate large cells with owl-eye appearance)
    • Prognosis related to number of lymphocytes ( the more the better) and the number of Reed-Sternberg cells (RS cells) ( the less RS cells the better)
  28. What are the 4 major types of Hodgkin lymphoma?
    • Lymphocyte predominant---best prognosis
    • Lymphocyte depleted--worst prognosis
    • Mixed cellularity--most often in older individuals
    • Nodular sclerosing--most frequently occurring form (65%) of Hodgkin’s -Most frequent in women; Characterized by fibrous bands and lacunar cells ( a variant of RS cells), relatively good prognosis.
  29. Non-Hodgkin lymphoma
    • Involve lymph nodes and other lymphoid areas/ extra nodal spread
    • Can be either a malignant B or T cell proliferation
    • Follicular lymphoma is most common type
    • Follicular pattern has better prognosis than diffuse
    • Well differentiated lymphomas have a slow course but are less responsive to therapy; high grade lesions include Burkitts and aremore responsive to chemotherapy, but tend to relapse
    • Working formulation or the REAL classification systems
  30. Burkitts lymphoma
    • Aggressive B cell lymphoma
    • Linked to EBV (Epstein Barr) infection
    • Associated with cytogenic change-- translocation (8, 14)
    • African form often involves the mandible or maxilla Micro: "starry sky" appearance
  31. Mycosis fungoides
    Low grade T-cell lymphoma involving the skin
  32. Sezary syndrome
    T-cell proliferation similar to mycosis fungoides but also has malignant T cells in the peripheral blood
Card Set
Pathology Final - Endocrine
Pathology final
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