Minarcik robbins 2013_ch24-endocrine
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This document provides an overview of the endocrine system and various endocrine disorders. It begins with the major endocrine glands - pituitary, thyroid, parathyroid, pancreas, adrenals - and their functions. It then discusses various pathological conditions that can affect each gland, including tumors, inflammation, and functional abnormalities. Specific disorders covered in more detail include Graves' disease, Cushing's syndrome, diabetes mellitus types 1 and 2, and multiple endocrine neoplasia syndromes. The document emphasizes the clinical manifestations and pathogenesis of different endocrine diseases.
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Minarcik robbins 2013_ch24-endocrine
- 1. ENDOCRINE
- 2. CLASSICAL ALGORHYTHM • PITUITARY – ANTERIOR – POSTERIOR • • • • THYROID PARATHYROID PANCREAS (endo.) ADRENAL – CORTEX – MEDULLA • DEGENERATION (aka, “involution”) • INFLAMMATION • NEOPLASM – BENIGN – MALIGNANT
- 3. BETTER ALGORHYTHM • PITUITARY – ANTERIOR – POSTERIOR • • • • • NON-NEOPLASTIC – HYPER-function – HYPO-function THYROID • NEOPLASTIC PARATHYROID – FUNCTIONAL PANCREAS (endo.) – NON-FUNCTIONAL ADRENAL – CORTEX – MEDULLA – Functional endocrine malignancies are RARE. Why?**********
- 4. FEEDBACK SYSTEMS • CORTEX, SUBCORTEX? • HYPOTHALAMUS • ANTERIOR PITUITARY • ENDOCRINE GLAND • END ORGAN • HYPOTHALAMUS
- 7. HORMONES • POLYPEPTIDE (2nd MESSENGER) • STEROID (DIRECT on NUCLEUS)
- 10. ANTERIOR PITUITARY • ACIDOPHILS (growth) –GROWTH HORMONE –PROLACTIN • BASOPHILS (trophs) –TSH –ACTH –LH, FSH
- 12. POSTERIOR PITUITARY • OXYTOCIN (contracts uterine smooth muscle) • VASOPRESSIN (ADH) (vasoconstriction, gluconeogenesis, platelet aggregation, release of Factor-VIII and vWb factor, concentrates urine, main effects on kidney and brain)
- 13. PITUITARY PATHOLOGY • CLINICAL FEATURES, mimic the endocrine effects, visual effects, or mass effects) • FUNCTIONING ADENOMAS • HYPO-PITUITARISM • POSTERIOR PITUITARY SYNDROMES • HYPOTHALAMIC (SUPRASELLAR) TUMORS
- 14. CLINICAL FEATURES • HYPER: growth(a), lactation(a), thyroid(b), adrenal cortex(b) • HYPO: growth, thyroid, adrenal cortex • MASS EFFECT: visual fields, brain
- 24. HYPO-pituitarism • • • • • • Pituitary tumors, functional or not. NON-pituitary tumors, primary or metastatic Pituitary surgery, of course Radiation, of course “Apoplexy”, i.e., sudden hemorrhage Sheehan’s syndrome (Post-partum ischemic necrosis) • Cysts (Rathke’s cleft) • Empty sella syndrome, (is NOT a disease) • Genetic defects (pit-1 gene mutations)
- 25. POSTERIOR pituitary • DIABETES INSIPIDUS • SIADH (Syndrome of Inappropriate AndiDiuretic Hormone)
- 26. DIABETES INSIPIDUS • ADH deficiency • Head trauma, tumors, inflam. hypothal/pit • Hyperdiureses with LOW sp.gr.
- 27. Inappropriate ADH • ADH EXCESS (SIADH) –Hyponatremia (hypervolemia), cerebral edema, neurologic symptoms –Neoplasms, esp. Small Cell CA. –NON-neoplastic lung diseases –Posterior pituitary injury
- 29. 15-25 grams
- 31. HYPER-THYROIDISM • • • • • • • aka, thyrotoxicosis Diffuse (Graves disease) Nodular Adenoma Carcinoma Neonatal Secondary to TSH pituitary adenoma
- 32. HYPER-THYROIDISM • • • • • • • • HYPERMETABOLISM Tachycardia, palpitations Increased T3, T4 Goiter Exophthalmos Tremor GI hypermotility Thyroid “storm”, life threatening
- 34. HYPO-THYROIDISM • • • • • • • 1° Developmental 1° Surgery, I-131, external radiation 1° Auto-immune (i.e., Hashimoto’s) 1° Iodine deficiency 1° Li+, iodides, p-aminosalicylates 2° (pituitary) 3° (hypothalamic, rare)
- 35. HYPO-THYROIDISM • Cretinism – Severe retardation – CNS/Musc-skel – Short stature – Protruding tongue – Umbilical hernia – Maternal iodine defic. • Myxedema (coma) – Sluggishness – Cool skin, ↑cholesterol
- 36. THYROIDITIS • Hashimoto (Auto-Immune) (Lymphoid follicles with germinal centers), MOST COMMON cause of acquired hypothyroidism in USA • Subacute Granulomatous (DeQuervain) • Subacute Lymphocytic (just like Hashimoto’s but NO fibrosis and no germinal centers), often post-partum
- 40. GRAVES DISEASE (aka, diffuse toxic goiter) • HYPERTHYROIDISM • EXOPHTHALMOS • PRE-TIBIAL MYXEDEMA • Autoimmune, auto-antibodies to TSH receptors, thereby stimulating them
- 42. SCALLOPING
- 44. GRAVES DISEASE (aka, diffuse toxic goiter) PLUMMER DISEASE (aka, nodular toxic goiter) HARDER TO TREAT Surg PTU (Propyl Thio Uracil) I-131
- 45. GOITERS (aka, thyromegaly, diffuse or nodular) • IODINE deficiency • Increased TSH • Goitrogens, e.g., cabbage, Brussels sprouts, cauliflower, turnips, cassava) • Associated with HYPO thyroidism eventually, NOT hyperthyroidism
- 47. G O I T E R
- 48. Thyroid Neoplasms • “Nodules” vs. true neoplasms • Adenomas vs. Carcinomas
- 49. “NODULES” • • • • • Solitary vs. Multiple Younger vs. Older Male vs. Female Hx. neck radiation vs. NO Rx. “Cold” vs. HOT (really NOTcold)
- 51. NEOPLASMS • ADENOMAS – FOLLICULAR – HÜRTHLE (oxyphilic) • CARCINOMAS –FOLLICULAR –PAPILLARY – MEDULLARY (AMYLOID) – ANAPLASTIC (worst)
- 54. HÜRTHLE CELL ADENOMA, note “atypia”
- 59. ORPHAN ANNIE CELLS in PAPILLARY CARCINOMA
- 60. MEDULLARY CARCINOMA of the thyroid with “HYALINIZATION”, i.e.,
- 61. HYALINIZATION showing APPLE GREEN birefringence in CONGO RED stain, i.e., AMYLOID
- 62. BIOLOGIC BEHAVIOR • Papillary CA lymph nodes • Follicular CA blood vessels, bone
- 63. 35-50 mg
- 64. PTH • HYPOCALCEMIA is MAIN STIMULUS (9-10.5 mg/dl) • ANTAGONIZES CALCITONIN
- 65. PARATHYROID DISORDERS • HYPER– PRIMARY (usually adenomas) – SECONDARY (LOW CA++ of Renal Failure) • HYPO-: Surgical, congenital, familial, idiopathic • PSEUDO-HYPO– (end organ resistance)
- 66. HYPER-PARATHYROIDISM • • • • • • Bone pain, fractures Nephrolithiasis Constipation, ulcers, gallstones Depression, lethargy short QT interval and a widened T wave Weakness, fatigue • Calcifications, esp. VALVES
- 67. HYPO-PARATHYROIDISM • Neuromuscular irritability • Mental status change • Parkinsonism like effects • Lens calcification* (paradox) • Widened QT interval • Defective, carious, teeth
- 68. ADRENAL CORTEX • Glomerulosa (Salt), mineralocorticoids – ALDOSTERONE • Fasciculata (Sugar), glucocorticoids – CORTISOL • Reticularis (Sex), gonadocorticoids – ANDROGENS, ESTROGENS
- 70. 4 g.
- 73. HYPERADRENALISM • HYPERALDOSTERONISM (g) • CUSHING SYNDROME (CORTISOL) (f) (most common of the three) • ADRENOGENITAL (VIRILIZING) SYNDROME (r)
- 74. CUSHING SYNDROME • • • • • • • • CENTRAL OBESITY MOON FACIES WEAKNESS HIRSUTISM HYPERTENSION DIABETES OSTEOPOROSIS STRIAE
- 76. CUSHING SYNDROME • • • • • PITUITARY ACTH INCREASE TUMOR ACTH INCREASE HYPERPLASIA OF CORTEX ADENOMA OF CORTEX CARCINOMA OF CORTEX • EXOGENOUS STEROIDS (90%)
- 77. PRIMARY HYPERALDOSTERONISM (Conn’s Syndrome) • Na+ RETENTION • K+ EXCRETION • HYPERTENSION
- 78. PRIMARY HYPERALDOSTERONISM • CORTICAL NEOPLASM • CORTICAL HYPERPLASIA • FAMILIAL (rare)
- 79. SECONDARY HYPERALDOSTERONISM • DECREASED RENAL PERFUSION • EDEMA (HEART, LIVER, KIDNEY) • PREGNANCY
- 80. ADRENOGENITAL SYNDROME • • • • VIRILIZATION/feminization CORTICAL NEOPLASM CORTICAL HYPERPLASIA 21-Hydroxylase Deficiency, with buildup of 17-hydroxy progesterone
- 82. ADRENAL INSUFFICIENCY • PRIMARY ACUTE (ADRENAL CRISIS) • PRIMARY CHRONIC (autoimmune ADDISON DISEASE) • SECONDARY (PITUITARY)
- 83. PRIMARY ACUTE • RAPID WITHDRAWAL OF STEROIDS • MASSIVE ADRENAL HEMORRHAGE (WATERHOUSE-FRIDERICHSEN, if it follows infection [meningo, staph, H. flu] and shock) – Newborns with DIFFICULT DELIVERY – ANTICOAGULANT RX – POSTSURGICAL DIC PATIENTS
- 84. PRIMARY CHRONIC • Most of Addison disease is auto- immune adrenalitis [ACAs]) • INFECTIONS (fungal diseases, histo-) • METASTASES (adrenals are an amazingly preferred site for early lung carcinoma metastases) • GENETIC DISORDERS
- 85. NEOPLASMS • ADENOMAS of ADRENAL CORTEX • CARCINOMAS of ADRENAL CORTEX
- 90. ADRENAL MEDULLA • PHEOCHROMOCYTOMAS, aka, primary tumors of the adrenal medulla – 10% arise in an MEN setting – 10% are EXTRA-adrenal – 10% are bilateral – 10% are malignant – 10% are in childhood – You can only call them malignant if they metastasize, but this is no bad thing, because they are all removed anyway
- 91. PHEO
- 93. TWO crucially important points specific for endocrine tumors: • 1. FUNCTIONING carcinomas are very RARE in ANY endocrine gland. Why? (KEY principle of endocrine oncology) • 2. Benign adenomas may have extremely bizarre nuclei, but are most usually BENIGN!!!
- 94. MEN-1, aka, Wermer Syndrome (3 P’s) • HYPERPARATHYROIDISM, chiefly hyperplasia • Pancreatic endocrine tumors • Pituitary adenoma, usually prolactinoma
- 95. MEN-2 • MEN-2A (SIPPLE): Pheo, Medullary CA., Parathyroid hyperplasia • MEN-2B: NO hyperparathyroidism, but neuromas present • Familial Medullary Thyroid CA
- 100. Exocrine Endocrine Islets Alpha Cells Beta Cells Delta Cells (somatostatin, suppress insulin and glucagon) Pancreatic Polypeptide (PP) cells Epsilon Cells make gherlin, which causes hunger
- 101. DIABETES MELLITUS • 16 Million in the USA • 1 Million/yr • 50K people die of it per year in the USA
- 102. How to Diagnose Dm: • • • • • Glucose >200 Or……………. Fasting glucose >126 trice Or……………. Post-prandial glucose > 200, 2 hrs AFTER standard OGTT (Oral Glucose Tolerance Test)
- 103. * MODY might be regarded as the third type TWO* Types of DM •1 • Genetic • Autoimmune • Childhood (juvenile) onset • Antibodies to beta cells, insulitis • Beta cell depletion • NON-OBESE patients •2 • Genetic, but diff. from Type 1 • NOT autoimmune • Adult, or maturity onset, e.g., 40’s, 50’s • Insulin may be low, BUT, peripheral resistance to insulin is the main factor • OBESE patients
- 104. Dm •POLY•POLY•POLY-
- 105. • FAT INSULIN –IN-creased glucose uptake – IN-creased lipogenesis – DE-creased lipolysis • MUSCLE – IN-creased glucose uptake – IN-creased glycogen synthesis – IN-creased protein synthesis • LIVER – DE-creased gluconeogenesis – IN-creased glycogen synthesis – IN-creased lipogenesis
- 106. PATHOGENESIS •1 • T-Lymphocytes reacting against poorly defined beta cell antigens • Inflammatory inflitrate, chronic, i.e., “INSULITIS” •2 • • • • Diet Life Style Obesity INSULIN RESISTANCE • Beta cells UN-able to adapt to the “long term demands of insulin resistance”
- 107. MODY (Maturity Onset Diabetes of the Young) • • • • Multiple types 2-5% of diabetics Primary beta cell defects Multiple genetic mechanisms, especially GLUCOKINASE mutations
- 108. PANCREAS in Dm
- 109. PANCREAS in Dm
- 110. COMPLICATIONS • MACRO-VASCULAR disease, i.e., ASCVD • MICRO-VASCULAR disease, kidneys, retina, nerves • IMMUNE related problems, INFECTIONS, e.g., TB, pneumonia, pyelonephritis, candida, etc.
- 111. COMPLICATIONS • ADVANCED GLYCATION – collagen, laminin, polypeptides, GBM (glomerular basement membrane), Hgb1c • ACTIVATION of PROTEIN KINASE C, VEGF, endothelin-1, increased ECM, decreased fibrinolysis, inflam. cytokines • INTRACELLULAR HYPERGLYCEMIA
- 112. COMPLICATIONS MORPHOLOGY • (MACRO-vascular) Atherosclerosis • MICRO-vascular –*Retinopathy –*Nephropathy- glomerular, vascular, KW –*Neuropathy (most common cause of neuropathy) • Infections
- 113. ATHEROSCLEROSIS
- 114. ATHEROSCLEROSIS
- 115. RETINOPATHY in Dm Shows microaneurysms, areas of hemorrhage, cotton wool spots, hard exudates, venous beading, neovascularization, retinal detachment, vitreous detachment, pre retinal hemorrhage
- 121. INFECTIONS in Dm • SKIN • TUBERCULOSIS • PNEUMONIA • PYELONEPHRITIS • CANDIDA
- 122. NEOPLASMS of the Endocrine Pancreas • Islet cell tumors – Beta cells INSULINOMAS (NOT rare) – Alpha cells GLUCAGONOMAS (rare) – Delta cells SOMATOSTATINOMAS (rare) – GASTRINOMAS, producing ZOLLINGER-ELLISON SYNDROME, consisting of increased acid and ulcers
Editor's Notes
- Classical endocrine glands and classical disease categories
- Classical endocrine glands and BETTER (i.e., more appropriate) disease categories. ********** One of the most KEY concepts in all of pathology!
- Positive and negative feedback systems are the principles of of the endocrine system and there effects upon each other and target organs. The concept of the so called pituitary as being the MASTER gland, has long been abandoned!
- Generally, “releasing” hormones are between the hypothalamus and adenohypophysis, and “stimulating” hormones are between the pituitary and other major endocrine glands. Build up of a hormone to tell the hypothalamus and pituitary to DECREASE production is called NEGATIVE FEEDBACK. Build up of a hormone to tell a gland to INCREASE production is called POSITIVE FEEDBACK. It is important to understand the difference between POSITIVE and NEGATIVE feedback. Feedback systems are the basis of endocrinology. “Minarcik your course SUCKS” is called NEGATIVE feedback. “Minarcik your course ROCKS” is called POSITIVE feedback.
- Anterior pituitary lobe = adenohypophysis = Rathke’s pouch = pars distalis. Hormones released here are also made here. Anterior lobe is WiFi. Posterior pituitary lobe = neurohypophysis = infundibulum = pars nervosa. Hormones released here are made in the hypothalamus. Posterior lobe is Hard-Wired.
- Overall cellular mechanisms of action of the two major classes of hormones, polypeptide and steroid. Second Messenger: 1) -glycerol 2) c-amp, c-gmp 3) NO, CO
- All three lobes of the pituitary: Anterior, intermediate, and posterior lobes. Note that the pituitary also has a “portal” circulation, i.e., arterycapillariesveinscapillaries, rather than just acv. Why? Ans: to create a “secondary” circulation between the pituitary and the hypothalamis releasing factors!
- The differentiation between acidophils and basophils is usually not too difficult unless the stain is really lousy. Chromophobes are uncommon, and have minimal cytoplasm and no granules. Chromophobe cytoplasm stains close to basophil cytoplasm in color, but is less granular and has is a minimal cytoplasm. Can you find a few chromophobes here?
- Hormones from basophils go to other endocrine glands, thyroid, adrenal cortex, ovary, testis. Cells from acidophils do NOT. Acidophils make GROWTH related hormones. Basophils make hormones which STIMULATE OTHER endocrine glands. Chromophobes make NOTHING.
- The posterior pituitary (aka, pars nervosa or neurohypophysis) looks like typical brain tissue. Why? Ans: It IS typical brain tissue. The pituicytes are glial cells. Herring bodies are massively dilated terminal axons from the hypothalamus, which RELEASE the hypothalamic made hormoines.
- The posterior pituitary does not make these hormones, it just releases them. The hypothalamus actually makes the hormones and transfers it down the stalk to the neurohypophysis.
- Note the extreme proximity of the pituitary stalk (infundibulum) to the optic chiasm
- Galactorrhea in a young woman (non pregnant of course) is often the expression of an acidophil tumor of the adenohypophysis. Lets say galactorrhea in a non pregnant woman is an acidophilic adenoma of the anterior pituitary until proven otherwise How many lobes do you think this woman has in her breast? Ans: (Count the white dots).
- Recognize this famous pituitary giant? What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)
- What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)
- What kind of cells of the pituitary might be proliferating here? (acidophil or basophil) Which layer of the adrenal cortex (G,F,R), do you think is primarily involved?
- Normal pituitary. With Turkish saddle, i.e., sella turcica.
- Find the pituitary adenoma.
- What part of the optic nerves/chiasm/tracts would have to be injured to produce this?
- Usually the bitemporal hemianopsia is NOT perfectly symmetrical. Why? Because pituitary tumors are under no law to grow perfectly midline.
- The usual differential of hypopituitarism, hopefully, all logical. ESS is: Primary ESS happens when a small anatomical defect above the pituitary gland increases pressure in the sella turcica and causes the gland to flatten out along the interior walls of the sella turcica cavity. Primary ESS is associated with obesity and hypertension in women. The disorder can be a sign of idiopathic intracranial hypertension. Secondary ESS is the result of the pituitary gland regressing within the cavity after an injury, surgery, or radiation therapy. Individuals with secondary ESS due to destruction of the pituitary gland have symptoms that reflect the loss of pituitary functions, such as amenorrhea, infertility, fatigue, and intolerance to stress and infection.
- Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane.
- (SIADH) is characterized by excessive release of ADH, or vasopressin, from the posterior pituitary gland or another source.
- Recall the basic thyroid blood supply, from subclavian artery (inferior posterior) and carotid (superior anterior)
- The normal weight of the thyroid, in grams, is also the same as its 24 hour radioactive iodine uptake percentage. Why? Ans: Because it take up 1% per gram. Is the presence of a “nodularity” of the thyroid very very very common? YES
- Find the colloid, follicular cells, and para-follicular cells (also known as C cells or light cells)
- If there was such a thing as a hypothalamic adenoma producing excessive TRF (thyroid releasing factor), would this be tertiary hyperthyroidism? Ans: Yes. Is there such a thing? NO Would an adenoma or a carcinoma more likely produce hyperthyroidism? Ans: Adenoma Why?
- Thyrotoxic crisis (or thyroid storm) is a rare but severe complication of hyperthyroidism, which may occur when a thyrotoxic patient becomes very sick or physically stressed. Its symptoms can include: an increase in body temperature to over 40 degrees Celsius (104 degrees Fahrenheit), tachycardia, arrhythmia, vomiting, diarrhea, dehydration, coma, and death.
- Exophthalmos can be measured precisely to follow the course of hyperthyroidism treatment, with calipers.
- Reidel’s struma = fibrosis from ANY cause.
- The diagnosis of Hashimoto thyroiditis requires not only lymphoid follicles in the thyroid, but SECONDARY (i.e., germinal centers) follicles should be present. If the thyroid gland looks like a lymph node, the diagnosis is Hashimoto thyroiditis, Hashimoto = auto-immune
- Is this “granulomatous” thyroiditis? Answer: Of course it is!
- NO scalloping
- Scalloping
- Podiatric case of the week. Myxedema is autoimmune edema.
- Decreased Iodine leads to decreased thyroid hormone, which leads to increased TSH which leads to increased growth of follicles. That’s how an iodine deficiency leads to a goiter. The probability of having a goiter is DIRECTLY proportional to how far you live from the ocean.
- Many vegetables are goiterogens, fruits are NOT. Which one is NOT a goiterogen?
- Most goiters worldwide are due to iodine deficiency. Why? Ans: The thyroid enlarges to try to trap more iodine, when serum levels are low. This is a adaptive response.
- The differentiation between a “nodule” and a solitary neoplasm can be quite fuzzy, but it doesn’t matter.
- Every type of thyroid disorder known is more common in females than males? Why? Ans: unknown What is the difference between a cold and a not-cold nodule isotopically?
- Which side is the “cold” nodule on? Might it be palpable. Intellectual dishonesty runs wild. It is amazing how many people claim to palpate a nodule just because they know there is one!
- Did you ever know anybody who died from thyroid cancer? Why not? Thyroid neoplasms, like most endocrine neoplasms have TWO worrisome principles” Benign tumors often have extreme pleomorphism Malignant tumors may have NO pleomorphism For this reason follicular thyroid neoplasms are diagnosed benign or malignant often by its BEHAVIOR (e.g., capsular invasion), rather than by the appearance of the cells. Papillary thyroid neoplasms are EASY to diagnose benign vs. malignant because they are ALL malignant.
- EXTREMELY well encapsulated tumor. Benign.
- EXTREMELY well encapsulated tumor. Benign. Would you like to call this a MICRO-follicular adenoma? YES Would you still call it a benign adenoma if it invaded the capsule? NO
- Note the resemblance of Hürthle cells to oncocytes, oxyphil cells, gastric parietal cells and apocrine cells, i.e., very bright red and abundant cytoplasm. In general however, please remember that “ATYPIA” in benign endocrine neoplasms is VERY COMMON, and, in contrast with other organ systems of the body, ususlly does NOT imply malignancy or PRE-malignancy! Why are Hürthle cells RED? Increased and altered mitochondria
- EXTREMELY NON well encapsulated tumor. Malignant. Thyroid tissue can look perfectly normal, but come out of bone or liver? NOTE the complete lack of pleomorphism. In contrast with marked atypia seen in BENIGN endocrine neoplasms, often NO ATYPIA is seen with malignant endocrine neoplasms, and invasion or metastases is often the only evidence that endocrine tissue is malignant.
- Papillary neoplasms do NOT usually look uniform on cut surface, which many follicular neoplasms do.
- To make things simple, let’s just say you can regard ALL papillary thyroid neoplasms as malignant!
- Note the lack of a pupil in Orphan Annie’s eye, just like the lack of nucleoplasm in the nuclei of cells of papillary carcinoma of the thyroid.
- Orphan Annie cells are papillary carcinoma of the thyroid cells in which considerably cytoplasm has invaginated into the nucleus.
- Is amyloid a type of “Hyaline”? What are some other types? What is hyaline?
- This is just a generality, not a law. Most common thyroid carcinomas occur in younger, and most of them survive it!
- Find the chief cells, find the oxyphil cells, find the fat.
- PTH stimulates osteoclasts to chew up bone and transfer calcium from the bone to the serum “compartments”.
- How are most parathyroid adenomas picked up? Incidental measurements of serum calcium.
- Hyperparathyroidism symptoms are the same as hypercalcemia symptoms, and vice versa. Remember “metastatic” calcification is due to hypercalcemia!
- Hypoparathyroidism symptoms are the same as hypocalcemia symptoms, and vice versa.
- The deeper you go, the sweeter it gets (Madonna)
- Is this a right or a left adrenal gland? Ans: LEFT Why: Right is usually flatter and much less triangular. Think of the liver as squishing it. Notice: Cortex YELLOW, Medulla BROWNISH RED Is this a right or a left adrenal? Ans: LEFT
- Remember: GFR = Salt, Sugar, Sex “The deeper you go, the sweeter it gets”
- Note that the COLOR and CONSISTENCY of the tumor is the same as that of the CORTEX. That is precisely WHY you know this is a tumor of the adrenal cortex.
- Hyper fasciculata hormones, i.e., cortisol
- What kind of cells of the pituitary might be proliferating here? (acidophil or basophil)
- Hyper glomerulosa hormones.
- Once again, the amazing reninangiotensinaldosterone axis
- Congenital adrenal hyperplasia is generally synonymous with adrenogenital syndrome.
- Note that the COLOR and CONSISTENCY of the tumor is the same as that of the CORTEX. What is the normal thickness of a bright yellow adrenal cortex? Ans: about 1 mm
- Most incidental cortical adenomas seen COMMONLY at autopsy are NON-functional)
- Note that the COLOR and CONSISTENCY of the tumor is the same as that of the CORTEX. That is precisely WHY you know this is a tumor of the adrenal cortex.
- Adenoma
- Adenoma
- Carcinoma of the adrenal cortex. Why doesn’t it look too yellow?
- Note that the COLOR and CONSISTENCY of the tumor is the same as that of the MEDULLA.
- Neuroblastoma. Find the rosettes!
- MEN-1 is the three “P”s
- Madullary thyroid carcinoma is present in ALL three types of MEN-2
- Younger looking cells “BLASTomas” are primarilly in kids, more mature looking cells CYT-omas are in adults. BOTH are quite rare.
- 4 hormones of the islets: glucagon, insulin, somatostatin. and pancreatic polypeptide from alpha, beta, delta, and PP cells, respectively. Can you tell from routine H&E microscopy which cell is which? Answer: NO. Why not? Can immunoperoxidase help? Somatostatin is classified as an inhibitory hormone, also made in the stomach and intestine, and has a variety of inhibitory effects on other hormones. The function of PP is to self regulate the pancreas secretion activities (endocrine and exocrine), it also has effects on hepatic glycogen levels and gastrointestinal secretions.
- Can you prove to me that Dm is NOT the same disease as atherosclerosis?
- These are the criteria for the diagnosis of diabetes, but, the borderline values can be thought of as PRE-diabetes, often.
- Even though there are TWO types of diabetes the complications from both are identical, although, of course, the effects of type-1 may have been present longer in a persons life.
- Fill in the blanks, or better yet, get a tattoo!
- Insulin puts glucose into cells!
- Glucokinase is an enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate, and has a massive influence on how glucose is handled in the body.
- Like just about ANY auto-immune disorder we see inflammatory changes against tissue with NO known external pathogen, in this case LYMPHOCYTES (T-Cells) attacking islets. Could this be called an isletitis or islitis? YES
- Hyalinization in the Islets of Langerhans is a common finding in type 2 diabetes. Often, the “hyaline” is amyloid. I hope nobody asks me if this hyalinization is a CAUSE or EFFECT of diabetes. Anyway, the answer is : BOTH
- A multiplicity of functions have been ascribed to Protein Kinase C. Recurring themes are that PKC is involved in receptor desensitization, in modulating membrane structure events, in regulating transcription, in mediating immune responses, in regulating cell growth, and in learning and memory. These functions are achieved by PKC mediated phosphorylation of other proteins
- * Remember the three classic areas of microvascular disease!
- In pathology, you almost assume if you get an amputation specimen, it is from a diabetic.
- NORMAL fundoscopic appearance on the LEFT. Microaneurysms, hemorrhage, cotton wool spots in the AB-normal retina on the RIGHT. Cotton wool spots are an abnormal finding on fundoscopic exam of the retina of the eye. They appear as puffy white patches on the retina. They are caused by damage to nerve fibers. The nerve fibers are damaged by swelling in the surface layer of the retina. The cause of this swelling is due to the reduced axonal transport (and hence backlog of intracellular products) within the nerves because of the ischemia.
- In “nodular” glomerulosclerosis, aka, K-W kidneys, “nodules” of PAS positive matrix trapping mesangial cells, are found at the periphery of glomeruli. Also remember that diabetes has pathologic effects on GMB and other large and small vessels of the kidney as well.
- If a pathologist tells you this gross appearance is diagnostic of diabetes, he probably already knew that patient had diabetes (i.e., intellectual DIS-honesty). What it is in HONESTY is a lot of cortical scarring! NOW you know why, the autopsy report often mentions that “the capsule strips with ease”, in normal kidneys!
- Diffuse mesangial sclerosis. Note the “sclerotic” part, or fibrosis, is stained blue by the trichrome stain.
- Like any other neoplasm of the endocrine system, islet cells tumors can produce whatever normal islet cells produce, the one exception being GASTRIN. If islet cells are more numerous in the tail of the pancreas, then where would you think an islet cell tumor would most likely arise from?