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Endocrine Pathology Crines… Molecular Signaling Endocrine Pathology Endocrine Pathology Endocrine Pathology Crines… Molecular signaling Autocrine Paracrine Endocrine Endocrine Pathology Endocrine Pathology Cell signaling system Too much hormone activity Surface receptors Too little hormone activity cAMP and tyrosine kinase system Autoimmune destruction Cytoplasmic receptors Inflammatory destruction Penetrate cell membrane Tumor or vascular destruction Gene activation -> transcription -> translation Space occupying lesions (tumors) Intranuclear receptors Malignant Gene activation -> transcription -> translation Benign 1 Endocrine Pathology Endocrine Pathology All parts of the endocrine system interconnect. All parts of the endocrine system interconnect Pituitary Pathology Too much Too little Especially space occupying lesions The Basics Pituitary Vascular Signaling proteins Anterior are release in hypothalmus. Comes from GI Travel by blood to Controlled by hypothalmus anterior pituitary Cause release of Posterior many activating Hormones orginate hormones further up. System of amplification 2 Pituitary Control Space Occupying Lesions Tumors Embryonic rests Squeeze gland out of existence. Generalized failure Visual field changes Visual Fields Loss of temporal fields. Nasal retina Damage to decusating optic nerve fibers 3 Acromegaly Pituitary Adenomas Rare Growth hormone excess after closing Make nothing or of epiphyses. Prolactin Periosteal bone ACTH, GH,TSH are very rare growth. More often end up with pituitary Diabetes failure. Prognathism Squeeze the daylights out of the gland. Hypopituitarism Craniopharyngioma Destruction of gland. Ischemia ‘Benign’ adenoma destroying gland Craniopharyngioma Rathke’s pouch remenant Benign cyst, but really in the wrong place. Ischemic Destruction Sheehan’s Syndrome Sheehan’s syndrome Post delivery problem No lactation In time general failure of ‘downstream’ systems Thyroid Adrenal cortex Ovulation 4 Posterior Pituitary Loss of ADH Diabetes insipidis Dose not make concentrated urine Large volumes of dilute urine Head injuries Tumors of periventricular area Control of Thyroid Hormone Thyroid Disease Hypothalmus Pituitary Thyroid Tissue level Establishes metabolic rate for the whole organism Laboratory Measurement Be sure the values fit the clinical story. Repeat if necessary. TSH T4 Total Free FTI Approximates Free T4 T3RU Binding sites T3 RIA Anti-thyroid antibodies 5 Total T4 is of little value Available binding sites Most T4 is protein bound Be sure the values fit the clinical story. Circulating storage Repeat if necessary. 99% bound TSH T4 1% free and available for Total metabolism Free FTI Free T4, this is it Approximates Free T4 Computed, no label Change in protein changes T3RU (resin uptake) total, but not free Measures binding sites T3 RIA Pregnancy, total is up Free T3 Liver disease, total is down Anti-thyroid antibodies They are euthyroid T3RU tried to take binding sites into account Attempted Fix was the T 7 Here serum protein T 7 or FTI (free thyroxin index) content changed Total T4 X T3RU = T 7 Changed number of T4 FTI closely followed free T4 binding sites Today we measure Free T4 Total T4 changed to Not always where we start make up for extra sites Free T4 did not All are euthyroid See the problem? Hyperthyroidism Clinical findings Heat intolerance Tremor Tachycardia Hyperactive Increased body metabolism and temperature Ocular changes Main causes Graves Disease Toxic goiter Toxic adenoma 6 Hyperophthalmia Grave’s disease Antibody stimulates TSH receptors in extraocular muscles. Increased tissue in orbit causes eye to protrude. Won’t go down Dry conjunctiva and increased risk of eye infections. Hyperthyroidism People Share Clinically hyperthyroid Low TSH High or above normal T4 No thyroid enlargement No tenderness No masses Struma Ovari Hypothyroidism Genetics Gland destruction Inflammatory Surgical removal Radiation treatment for hyperthyroidism Iodine deficiency Can’t make T4 Hypothalmic and/or pituitary failure 7 Hypothyroidism Cretinism Genetics: Cretinism Cannot make T4 Growth retarded Severe mental retardation Must recognize early Hypothyroidism Hypothyroidism Clinical Cold intolerance Bradycardia Heart failure High lipids Lethargic Photophobia Myxedema Skin and hair changes Tumor(ous) Enlargement Excess growth True neoplasm Benign Malignant Cell type Activity and TSH response? 8 Tumors and Changes in Size Goiter Nodular Uniform increase Scarring Cysts Generally euthyroid May cause airway compression Goiter Mutlinodular Goiter Thyroid Nodules Radioactive iodine injection then scan the gland. ‘Cold Nodule’ ‘Hot Nodule’ 9 Thyroid Adenomas Thyroid Adenoma Benign Benign Solitary Three features Common Encapsulatd Compression of Encapsulated surrounding tissue Generally not Different from the rest hyperactive of the gland Malignancies of Thyroid Origin Arising from follicular cells Papillary Carcinoma Follicular Carcinoma Mixed pattern Interstitial cells (Calcitonin producing cells) Anaplastic, who knows Very aggressive tumor Papillary Carcinoma Papillary groups May have multiple sites Not actively producing T4 Readily treated Spread Nodes Lung Bone Brain 10 Psamommoma Bodies Papillary Carcinoma Orphan Annie Nuclei Needle aspirates Open eyed Little Orphan Annie debuted in the special pink edition nuclei of the New York Daily News on August 5, 1924. Harold Gray injected his own conservative beliefs into indicative of his strip. Little Orphan Annie was highly motivated, fiercely independent, minded her own business, and papillary ca believed in action. In the years that followed, Gray created a family for Annie by introducing "Daddy" Warbucks in 1924 "Daddy" Warbucks and Harold Gray were diagnosed with cancer in 1967, and while "Daddy" beat it, Gray died of cancer on May 9, 1968 after a 44-year career of drawing and writing one of the world's greatest newspaper comic strips, Little Orphan Annie. Follicular Carcinoma Sometime hard to distinguish from adenoma. Capsular invasion Vascular invasion 11 C Cell Carcinoma C Cell Carcinoma Interstitial cells Makes calcitonin Makes amyloid Beta pleated sheet protein Often part of a multiple endocrine neoplasia syndrome Inflammatory Conditions Autoimmune Viral Bacterial Hashimoto’s Thyroiditis Hashimoto’s Thryoiditis Many antibodies T & B cells Active germinal centers Women 5:1 Scarring In time hypothyroid Other autoimmune Arthritis PA Lupus Addison’s 12 Hashimoto’s Thryoiditis Hurthle Cells Reidel’s Struma (Thyroiditis) De Quervain’s Thyroiditis Super scaring Subacute Neck structures Giant cells Airway trapped Granulomas Viral? Destroyed Painful neck parathyroids Parathyroid Come from the pharyngeal pouches Most of us have 4 Make PTH Mobilizes calcium Released by low serum calcium High serum phosphate 13 Forms of Serum Calcium Hyperparathyroidism Primary Parathyroid adenoma 80% Hyperplasia 10-15% Parathyroid ca <5% Hypercalcemia Stones, bones, abdominal groans and psychic moans Bone wasting Generalized Osteoitis fibrosa cystica Parathyroid Adenoma 14 Secondary Hyperparathyroidism Renal failure almost always Phosphates build up in the blood. Cause calcium to drop. PTH is made Phosphate itself can cause release of PTH Glands begin to function autonomously Non PTH Driven Hypercalcemia Osteolytic bone mets Osteoclast activation Multiple myeloma Vitamin D Intoxication Hypoparathyroidism Increased neuromuscular excitability May lead to tetany Irritability and possibly even psychosis Parkinson-like symptoms Cataracts Causes Autoimmune destruction Accidental removal with thyroid Congenital absence 15 Pseudohypoparathyroidism End-organ insensitivity All tissues Skeletal abnormalities Labs Low calcium, High phosphate High PTH Look for low urinary cAMP Pseudopseudohypo…. Physically look like this, but no hormonal abnormality Calcium and PTH together Endocrine Pancreas 16 Diabetes Mellitus Beta Cell Insulin Release Chronic disease Carbohydrates Fats Amino acids Small vessel disease AGE proteins DM 1 DM 2 Monogenic (rare) Insulin Action Diabetes, Many Possibilities Insulin response Absent beta cells End-organ response Diabetes Mellitus Chronic disease Carbohydrates Fats Amino acids Small vessel disease AGE proteins DM 1 DM 2 Monogenic causes 17 Type 2 Diabetes AGE Proteins Structural proteins Obesity Leaky membranes Insulin resistance Crosslinking Liver a special problem LDL entrapment because of gluconeogenesis Signally proteins FFA Smooth muscle cell growth Inflammation Neovascularization Insulin potentiates Increased production Adipokines of extracellular PPAR material. 18 Intracellular High Glucose Sorbitol production Use up the NADPH Cannot regenerate glutathione Oxidative damage Sorbitol is also an osmotic force. Nerve swelling and entrapment Diabetic Neuropathy Diabetic Neuropathy Vascular Sorbitol Sensory DM Nephropathy 19 Osmotic Force and Blood Brain Barrier Dr. Joseph Bell and Sir Arthur Conan Doyle Diagnosis and Follow-up Ketoacidosis Random BS >200 mg% Fasting BS > 126 mg% GTT Monitoring Regular BSs Hbg A1c Urine for microalbuminuria Good ocular exam Pancreatic Islet Cell Tumors Extrapancreatic Gastrinomas Benign or malignant Hormone depends on cell of origin Beta cell, insulin secreting Hypoglycemic episodes Delta cell, Zollinger- Ellison syndrome Gastrin secreting Intractable
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