Minarcik robbins 2013_ch24-endocrine
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ENDOCRINE
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CLASSICAL ALGORHYTHM• PITUITARY
– ANTERIOR– POSTERIOR
• THYROID• PARATHYROID• PANCREAS (endo.)• ADRENAL
– CORTEX– MEDULLA
• DEGENERATION (aka, “involution”)
• INFLAMMATION
• NEOPLASM– BENIGN
– MALIGNANT
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BETTER ALGORHYTHM• NON-NEOPLASTIC
– HYPER-function– HYPO-function
• NEOPLASTIC– FUNCTIONAL– NON-FUNCTIONAL– Functional endocrine
malignancies are RARE. Why?**********
• PITUITARY– ANTERIOR– POSTERIOR
• THYROID
• PARATHYROID
• PANCREAS (endo.)
• ADRENAL– CORTEX– MEDULLA
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FEEDBACK SYSTEMS• CORTEX, SUBCORTEX?• HYPOTHALAMUS • ANTERIOR PITUITARY • ENDOCRINE GLAND • END ORGAN • HYPOTHALAMUS
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AntPitWiFiPostPitWired
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HORMONES•POLYPEPTIDE (2nd MESSENGER)
•STEROID (DIRECT on NUCLEUS)
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ACIDOPHILS
BASOPHILS
CHROMOPHOBES
AXONS
AXONS and “PITUI-”cytes
A
I P
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ANTERIOR PITUITARY• ACIDOPHILS (growth)
–GROWTH HORMONE
–PROLACTIN
• BASOPHILS (trophs)–TSH
–ACTH
–LH, FSH
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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)
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PITUITARY PATHOLOGY
• CLINICAL FEATURES, mimic the endocrine effects, visual effects, or mass effects)
• FUNCTIONING ADENOMAS
• HYPO-PITUITARISM
• POSTERIOR PITUITARY SYNDROMES
• HYPOTHALAMIC (SUPRASELLAR) TUMORS
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CLINICAL FEATURES• HYPER: growth(a), lactation(a),
thyroid(b), adrenal cortex(b)
• HYPO: growth, thyroid, adrenal cortex
• MASS EFFECT: visual fields, brain
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G
A
L
A
C
T
O
R
R
H
E
A
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GIGANTISM
(excess somatotropin [GH]
BEFORE
epiphyseal
closure)
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ACROMEGALY:
(excess somatotropin
[GH] AFTER epiphyseal closure)
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MOON FACIES
BUFFALO HUMP
STRIAE
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BITEMPORAL
HEMIANOPSIA
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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)
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POSTERIOR pituitary
•DIABETES INSIPIDUS
•SIADH (Syndrome of Inappropriate Andi- Diuretic Hormone)
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DIABETES INSIPIDUS
• ADH deficiency• Head trauma, tumors,
inflam. hypothal/pit• Hyperdiureses with
LOW sp.gr.
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Inappropriate ADH• ADH EXCESS (SIADH)
–Hyponatremia (hypervolemia), cerebral edema, neurologic symptoms
–Neoplasms, esp. Small Cell CA.
–NON-neoplastic lung diseases
–Posterior pituitary injury
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15-25 grams
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HYPER-THYROIDISM• aka, thyrotoxicosis
• Diffuse (Graves disease)
• Nodular
• Adenoma
• Carcinoma
• Neonatal
• Secondary to TSH pituitary adenoma
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HYPER-THYROIDISM• HYPERMETABOLISM
• Tachycardia, palpitations
• Increased T3, T4
• Goiter
• Exophthalmos
• Tremor
• GI hypermotility
• Thyroid “storm”, life threatening
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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)
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HYPO-THYROIDISM• Cretinism
– Severe retardation– CNS/Musc-skel– Short stature– Protruding tongue– Umbilical hernia– Maternal iodine defic.
• Myxedema (coma)– Sluggishness– Cool skin, ↑cholesterol
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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
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GRAVES DISEASE(aka, diffuse toxic goiter)
• HYPERTHYROIDISM
• EXOPHTHALMOS
• PRE-TIBIAL MYXEDEMA
• Autoimmune, auto-antibodies to TSH receptors, thereby stimulating them
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SCALLOPING
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GRAVES DISEASE(aka, diffuse toxic goiter)
PLUMMER DISEASE(aka, nodular toxic goiter)
HARDER TO TREAT
Surg
PTU (Propyl Thio Uracil)
I-131
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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
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GOITER
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Thyroid Neoplasms• “Nodules” vs. true neoplasms
• Adenomas vs. Carcinomas
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“NODULES”• Solitary vs. Multiple
• Younger vs. Older
• Male vs. Female
• Hx. neck radiation vs. NO Rx.
• “Cold” vs. HOT (really NOT-cold)
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NEOPLASMS• ADENOMAS
–FOLLICULAR–HÜRTHLE
(oxyphilic)
• CARCINOMAS
–FOLLICULAR–PAPILLARY– MEDULLARY
(AMYLOID)– ANAPLASTIC
(worst)
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HÜRTHLE CELL ADENOMA, note “atypia”
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ORPHAN ANNIE CELLS in PAPILLARY CARCINOMA
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MEDULLARY CARCINOMA of the thyroid with “HYALINIZATION”, i.e.,
AMYLOID!!!
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HYALINIZATION showing APPLE GREEN birefringence in CONGO RED stain, i.e., AMYLOID
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BIOLOGIC BEHAVIOR• Papillary CA lymph nodes
• Follicular CA blood vessels, bone
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35-50 mg
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PTH• HYPOCALCEMIA is MAIN
STIMULUS (9-10.5 mg/dl)
• ANTAGONIZES CALCITONIN
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PARATHYROID DISORDERS
• HYPER-–PRIMARY (usually adenomas)
–SECONDARY (LOW CA++ of Renal Failure)
• HYPO-: Surgical, congenital, familial, idiopathic
• PSEUDO-HYPO-–(end organ resistance)
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HYPER-PARATHYROIDISM• Bone pain, fractures
• Nephrolithiasis
• Constipation, ulcers, gallstones
• Depression, lethargy
• short QT interval and a widened T wave
• Weakness, fatigue
•Calcifications, esp. VALVES
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HYPO-PARATHYROIDISM
• Neuromuscular irritability
• Mental status change
• Parkinsonism like effects
• Lens calcification* (paradox)
• Widened QT interval
• Defective, carious, teeth
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ADRENAL CORTEX• Glomerulosa (Salt), mineralocorticoids
– ALDOSTERONE
• Fasciculata (Sugar), glucocorticoids– CORTISOL
• Reticularis (Sex), gonadocorticoids– ANDROGENS, ESTROGENS
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4 g.
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SALT
SUGAR
SEX
STRESSSTRESS
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HYPERADRENALISM• HYPERALDOSTERONISM (g)• CUSHING SYNDROME
(CORTISOL) (f) (most common of the three)
• ADRENOGENITAL (VIRILIZING) SYNDROME (r)
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CUSHING SYNDROME
• CENTRAL OBESITY• MOON FACIES• WEAKNESS• HIRSUTISM• HYPERTENSION• DIABETES• OSTEOPOROSIS• STRIAE
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MOON FACIES
BUFFALO HUMP
STRIAE
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CUSHING SYNDROME
• PITUITARY ACTH INCREASE• TUMOR ACTH INCREASE• HYPERPLASIA OF CORTEX• ADENOMA OF CORTEX• CARCINOMA OF CORTEX
•EXOGENOUS STEROIDS (90%)
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PRIMARY HYPERALDOSTERONISM
(Conn’s Syndrome)
• Na+ RETENTION• K+ EXCRETION• HYPERTENSION
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PRIMARY HYPERALDOSTERONISM
• CORTICAL NEOPLASM• CORTICAL HYPERPLASIA• FAMILIAL (rare)
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SECONDARY HYPERALDOSTERONISM
• DECREASED RENAL PERFUSION
• EDEMA (HEART, LIVER, KIDNEY)
• PREGNANCY
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ADRENOGENITAL SYNDROME
• VIRILIZATION/feminization• CORTICAL NEOPLASM• CORTICAL HYPERPLASIA• 21-Hydroxylase Deficiency, with
buildup of 17-hydroxy progesterone
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ADRENAL INSUFFICIENCY
• PRIMARY ACUTE (ADRENAL CRISIS)
• PRIMARY CHRONIC (auto-immune ADDISON DISEASE)
• SECONDARY (PITUITARY)
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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
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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
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NEOPLASMS• ADENOMAS of ADRENAL
CORTEX
• CARCINOMAS of ADRENAL CORTEX
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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
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PHEO
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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!!!
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MEN-1, aka, Wermer Syndrome (3 P’s)
• HYPERPARATHYROIDISM, chiefly hyperplasia
•Pancreatic endocrine tumors
•Pituitary adenoma, usually prolactinoma
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MEN-2• MEN-2A (SIPPLE): Pheo,
Medullary CA., Parathyroid hyperplasia
• MEN-2B: NO hyperparathyroidism, but neuromas present
• Familial Medullary Thyroid CA
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PINEAL “GLAND”• PINEALOMAS
–PINEOBLASTOMAS
–PINEOCYTOMAS
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ENDOCRINE
PANCREAS
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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
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DIABETES MELLITUS
• 16 Million in the USA
• 1 Million/yr
• 50K people die of it per year in the USA
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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)
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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
* MODY might be regarded as the third type
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Dm•POLY-
•POLY-
•POLY-
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INSULIN• FAT
–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
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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”
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MODY (Maturity Onset Diabetes of the Young)
• Multiple types
• 2-5% of diabetics
• Primary beta cell defects
• Multiple genetic mechanisms, especially GLUCOKINASE mutations
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PANCREAS in Dm
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PANCREAS in Dm
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COMPLICATIONS• MACRO-VASCULAR disease, i.e.,
ASCVD
• MICRO-VASCULAR disease, kidneys, retina, nerves
• IMMUNE related problems, INFECTIONS, e.g., TB, pneumonia, pyelonephritis, candida, etc.
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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
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COMPLICATIONSMORPHOLOGY
• (MACRO-vascular) Atherosclerosis• MICRO-vascular
–*Retinopathy
–*Nephropathy- glomerular, vascular, KW
–*Neuropathy (most common cause of neuropathy)
• Infections
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ATHEROSCLEROSIS
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ATHEROSCLEROSIS
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RETINOPATHY in DmShows microaneurysms,
areas of hemorrhage,
cotton wool spots, hard exudates, venous beading, neovascularization, retinal detachment, vitreous detachment, pre retinal hemorrhage
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NEPHROPATHYKimmelstiel-Wilson (KW) Kidneys
IS…………
“Nodular” glomerulosclerosis
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NEPHROPATHYNEPHROSCLEROSIS
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NEPHROPATHYGBM thickening
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NEPHROPATHYDiffuse
Mesangial
Sclerosis
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INFECTIONS in Dm• SKIN
• TUBERCULOSIS
• PNEUMONIA
• PYELONEPHRITIS
• CANDIDA
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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