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Lecture 24

Pathology 3500 Lecture Notes - Lecture 24: Pituitary Adenoma, Basal Metabolic Rate, HyperfunctionPremium

7 pages90 viewsSpring 2018

Department
Pathology
Course Code
Pathology 3500
Professor
Jessica Shepherd
Lecture
24

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Lecture 009: Endocrine Disease II
Posterior Pituitary Hyper/Hypofunction
Too much ACTH release
Cancer cells (adenomas) produce this hormone
Cushing’s Syndrome
Hypertension
Too little ACTH release
Lead to diabetes
Addison disease
Summary
Anterior Pituitary
Hyperfunction: adenomas (PRL, GH)
Micro or macroadenomas, may be clinically silent or null cell adenoma
Hypofunction most common cause tumors
Chemical, ablation (surgery or radiation), trauma, other lesion
(inflammation, metastases)
Posterior Pituitary
Hypertension - syndrome of inappropriate ADH (SIADH) secretion
Thyroid Function
Produces 3 hormones under TSH stimulation
Thyroid follicular cells, produces 2 hormones from precursor thyroglobulin
T4 (thyroxine/tetraiodothyronine)
T3 (triiodothyronine)
C cells involved in calcium homeostasis
Calcitonin
T3 and T4 enter circulation
Mostly bound to transport proteins
Concentration of free (i.e. unbound) T3 and T4 is tightly regulated
Secreted T3 and T4 inhibit release of TRH and TSH from the hypothalamus and
pituitary
Free T4 (prohormone) is largely converted to T3 (active hormone) via deiodinase
Thyroid hormone receptor complex binds thyroid hormone response elements (TREs) to
target gene
Serve to increase basal metabolic rate
Increase lipid and carb metabolism
Promote protein synthesis
Hypothalamic Pituitary Thyroid Axis
Negative feedback
Active hormone
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Thyroid
Follicles lined by thyroglobulin
Need iodine
Hyperthyroidism
Thyrotoxicosis
Excess of thyroid hormone
Hypermetabolic state caused by increased T3 and T4 in circulation
Clinical manifestation
Constitution symptoms
Heat intolerance, sweating , weight loss, despite increased appetite
Hypermotility of the GI tract
malalborsptiona and diarrhea
Cardiac effect
Palpitation, increased RT (tachycardia)
Neuromuscular effect
Tremor, muscle weakness
Ocular effects
Upper lid reaction
Causes of hyperthyroidism
Primary causes
Graves disease
Autoimmune condition
Hyperfunction multinodular goitre
Hyperfunctioning thyroid adenoma
Iodine excess (complex pathogenesis)
Secondary causes
Pituitary adenoma (TSH)
Lab diagnosis of hyperthyroidism
TSH levels are decreased and free T4 (and T3) levels are increased
Increased TSH is suggested of a adenoma producing extra TSH
Except for pituitary adenoma that secrete TSH
Radioactive iodine scans may be useful in determining etiology
Hypothyroidism
Decreased circulation T3 and T4
Abnormality interfering with production of thyroid hormones
Cretinism
Infancy developmental abnormalities of skeletal and CNS
Resulting in mental retardation, short stature
Myxedema
Rare cases of long-standing, undiagnosed hypanthodium
Potentially life threatening complication
Severe cold intolerance, obesity, mental sluggishness, and lethargy
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