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186 Cards in this Set
- Front
- Back
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Adrenal Gland Drainage.
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Left adrenal → left adrenal vein → left renal vein → IVC.
Right adrenal → right adrenal vein → IVC. |
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Pheo vs. Neuroblastoma
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Pheochromocytoma causes episodic hypertension; neuroblastoma does not.
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Pituitary Acidophils.
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GH and prolactin.
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Pituitary Basophils.
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FSH, LH, ACTH, TSH.
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Topography: Islet Cells.
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α cells are peripheral, β cells are central, and δ and randomly interspersed.
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Location: GLUT-1
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RBCs, brain.
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Location: GLUT-2
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β islet cells, liver, kidney, small intestine.
*bidirectional glucose transport* |
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Location: GLUT-4
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Adipose tissue and skeletal muscle.
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Anabolic Effects of Insulin.
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1. ↑ glucose transport
2. ↑ glycogen synthesis and storage 3. ↑ triglyceride synthesis and storage 4. ↑ Na+ retention (kidneys) 5. ↑ protein synthesis (muscles) 6. ↑ cellular uptake of K+ |
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Steps: Insulin Release
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GLUT-2-dep. glucose uptake → glucose metabolism → ↑ [ATP]/[ADP] → inhibition of ATP-sensitive K+ channel → depolarization → Ca2+ influx → insulin exocytosis.
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Non-Insulin-Dependent Tissues
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"BRICK L"
Brain RBCs Intestines Cornea Kidney Liver |
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TRH Potentiates Release of...
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TSH and Prolactin.
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CRH Potentiates Release of...
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ACTH.
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GHRH Potentiates Release of...
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GH.
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GnRH Potentiates Release of...
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LH and FSH.
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Dopamine Inhibits the Release of... (Pituitary)
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Prolactin.
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Somatostatin Inhibits the Release of... (Pituitary)
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GH and TSH.
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Prolactin Inhibits the Release of... (Pituitary)
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GnRH.
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Overview: 17α-Hydroxylase Deficiency.
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Congenital Adrenal Hyperplasia.
↓ sex hormones, ↓ cortisol, ↑ mineralocorticoids. Sx = hypertension, hypokalemia. Males born externally female with no internal reproductive structures. Females phenotypically normal, but lacking 2° sexual characteristics (“sexual infantilism”). |
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Overview: 21-Hydroxylase Deficiency.
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Congenital Adrenal Hyperplasia.
Most common form. ↓ cortisol (increased ACTH), ↓ mineralocorticoids, ↑ sex hormones. Sx = masculinization, female pseudohermaphroditism, hypotension, hyperkalemia, ↑ plasma renin activity, and volume depletion. Salt wasting can lead to hypovolemic shock in the newborn. |
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Overview: 11β-Hydroxylase Deficiency.
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Congenital adrenal hyperplasia.
↓ cortisol, ↓ aldosterone and corticosterone, ↑ sex hormones. Sx = masculinization, HYPERtension (like aldosterone, 11-deoxycorticosterone is a mineralocorticoid and is secreted in excess). |
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Functions: Cortisol.
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Cortisol is BBIIG:
1. Maintains Blood pressure (by upregulating α1 receptors on arterioles) 2. ↓ Bone formation 3. Anti-Inflammatory 4. ↓ Immune function 5. ↑ Gluconeogenesis, lipolysis, proteolysis |
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Function: Parathyroid Hormone.
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1. ↑ bone resorption of calcium and phosphate
2. ↑ kidney reabsorption of calcium in distal convoluted tubule 3. ↓ kidney reabsorption of phosphate 4. ↑ 1,25-(OH)2 vitamin D (calcitriol) production by stimulating kidney 1α-hydroxylase |
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Regulation: Parathyroid Hormone.
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↓ free serum Ca2+ ↑ PTH secretion.
free serum Mg2+ ↓ PTH secretion. |
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Parathyroid Hormone and Bone.
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PTH promotes bone resorption.
PTH stimulates both osteoclasts (indirectly) and osteoblasts (directly). |
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Function: Vitamin D.
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1. ↑ absorption of dietary calcium
2. ↑ absorption of dietary phosphate 3. ↑ bone resorption of Ca2+ and (PO4)3– |
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Regulation: Vitamin D.
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↑ PTH causes ↑ 1,25-(OH)2 vitamin D production.
↓ [Ca2+] causes ↑ 1,25-(OH)2 vitamin D production. ↓ phosphate causes ↑ 1,25-(OH)2 vitamin D production. |
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Function: Calcitonin.
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↓ bone resorption of calcium.
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Regulation: Calcitonin.
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↑ serum Ca2+ causes calcitonin secretion.
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Why Do Steroid Hormones Have Delayed Onsets of Action?
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Because they exert their effects at the level of gene transcription.
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Key Steroid Hormones.
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"PET CAT":
Progesterone Estrogen Testosterone Cortisol Aldosterone T3/T4 |
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Function: T3/T4
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1. Bone growth (synergism with GH)
2. CNS maturation 3. ↑ β1 receptors in heart = ↑ CO, HR, SV, contractility 4. ↑ basal metabolic rate via ↑ Na+/K+-ATPase activity = ↑ O2 consumption, RR, body temperature 5. ↑ glycogenolysis, gluconeogenesis, lipolysis 4 B's: Brain maturation Bone growth Beta-adrenergic effects ↑ BMR |
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Causes: Endogenous Cushing's
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1. Cushing’s disease (70%)—due to ACTH secretion from pituitary adenoma; ↑ ACTH
2. Ectopic ACTH (15%)—from nonpituitary tissue making ACTH (e.g., small cell lung cancer, bronchial carcinoids); ↑ ACTH 3. Adrenal (15%)—adenoma, carcinoma, nodular adrenal hyperplasia; ↓ ACTH |
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Findings: Cushing's Syndrome
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hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia, skin changes, osteoporosis, amenorrhea, and immune suppression
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Differential: Dexamethasone Suppression Test.
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Healthy: ↓ cortisol after low dose.
ACTH-producing pituitary tumor: ↑ cortisol after low dose; ↓ cortisol after high dose. Ectopic ACTH-producing tumor: ↑ cortisol after low dose; ↑ cortisol after high dose. Cortisol-producing tumor: ↑ cortisol after low and high dose. |
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#1 Cause of Cushing's Syndrome.
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Exogenous (iatrogenic) steroids—#1 cause; ↓ ACTH.
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Overview: Conn’s Syndrome.
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AKA Primary hyperaldosteronism.
Caused by an aldosterone-secreting tumor, resulting in hypertension, hypokalemia, metabolic alkalosis, and low plasma renin. May be bilateral or unilateral. |
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Overview: Secondary Hyperaldosteronism.
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Kidney perception of low intravascular volume results in an overactive renin-angiotensin system. Due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome. Associated with high plasma renin.
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Treatment: Hyperaldosteronism.
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Spironolactone: K+-sparing aldosterone antagonist.
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Overview: Addison's Disease.
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Chronic adrenal insufficiency due to adrenal atrophy or destruction by disease (e.g., autoimmune, TB, metastasis).
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Sx: Addison's Disease.
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1° deficiency of aldosterone and cortisol, causing hypotension (hyponatremic volume contraction) and skin hyperpigmentation (due to MSH, a by-product of ↑ ACTH production from POMC).
Characterized by Adrenal Atrophy and Absence of hormone production; involves All 3 cortical divisions. |
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1° versus 2° Adrenal Insufficiency.
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1°: Globally impaired adrenal function. Hypotension and skin hyperpigmentation.
2°: ↓ pituitary ACTH production; no skin hyperpigmentation and no hyperkalemia. |
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Overview: Waterhouse-Friderichsen syndrome.
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Acute adrenocortical insufficiency due to adrenal hemorrhage associated with Neisseria meningitidis septicemia, DIC, and endotoxic shock.
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Pheochromocytoma: "Rule of 10s"
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"Rule of 10s"
10% malignant 10% bilateral 10% extra-adrenal 10% calcify 10% kids 10% familial |
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Overview: Pheochromocytoma
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Most tumors secrete epinephrine, NE, and dopamine and can cause episodic hypertension. Urinary metanephrines and plasma catecholamines are elevated.
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Tx: Pheochromocytoma
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Treatment: α-antagonists, especially phenoxybenzamine, a nonselective, irreversible α-blocker.
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Sx: Pheochromocytoma.
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Episodic hyperadrenergic symptoms (5 P’s):
Pressure (elevated blood pressure) Pain (headache) Perspiration Palpitations (tachycardia) Pallor |
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Overview: Neuroblastoma
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The most common tumor of the adrenal medulla in children. Can occur anywhere
along the sympathetic chain. HVA (a breakdown product of dopamine) in urine. Less likely than pheochromocytoma to develop hypertension. N-myc oncogene. |
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Sx: Hypothyroidism.
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Cold intolerance (↓ heat production)
Weight gain, ↓ appetite Hypoactivity, lethargy, fatigue, weakness Constipation ↓ reflexes Myxedema (facial/periorbital) Dry, cool skin; coarse, brittle hair |
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Labs: Hypothyroidism.
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↑ TSH
↓ total T4 ↓ free T4 ↓ T3 uptake |
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Sx: Hyperthyroidism.
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Heat intolerance (↑ heat production)
Weight loss, ↑ appetite Hyperactivity Diarrhea ↑ reflexes Chest pain, palpitations, arrhythmias Warm, moist skin; fine hair |
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Labs: Hyperthyroidism.
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↓ TSH (if 1°)
↑ total T4 ↑ free T4 ↑ T3 uptake |
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Overview: Hashimoto’s Thyroiditis.
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The most common cause of hypothyroidism; an autoimmune disorder (can have thyrotoxicosis during follicular rupture).Slow course; moderately enlarged, nontender thyroid.
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Antibodies: Hashimoto’s Thyroiditis.
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Antimicrosomal and antithyroglobulin antibodies.
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Overview: Cretinism.
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Due to severe fetal hypothyroidism. Endemic cretinism occurs wherever endemic goiter is prevalent (lack of dietary iodine); sporadic cretinism is caused by defect in T4 formation or developmental failure in thyroid formation.
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Findings: Cretinism.
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Findings: pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue.
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Overview: Subacute (de Quervain’s) Thyroiditis.
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Self-limited hypothyroidism often following a flulike illness. Elevated ESR, jaw pain, early inflammation, and very tender thyroid gland.
Lymphocytic subacute thyroiditis is painless. |
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Overview: Riedel’s Thyroiditis.
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Thyroid replaced by fibrous tissue (hypothyroid). Presents with fixed, hard (rock-like), and painless
goiter. |
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Overview: Graves' Disease.
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An autoimmune hyperthyroidism with thyroid-stimulating/TSH receptor antibodies.
Graves’ is a type II hypersensitivity. |
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Sx: Graves' Disease.
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Ophthalmopathy (proptosis, EOM swelling), pretibial myxedema, diffuse goiter. Often presents during stress (e.g., childbirth)
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Overview: Toxic Multinodular Goiter.
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Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation inTSH receptor. ↑ release of T3 and T4. Nodules are not malignant.
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"Jod-Basedow Phenomenon"
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Thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.
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Overview: Papillary Thyroid Carcinoma.
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Most common, excellent prognosis, “ground-glass” nuclei
(Orphan Annie), psammoma bodies, nuclear grooves. ↑ risk with childhood irradiation. |
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Overview: Follicular Thyroid Carcinoma.
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Good prognosis, uniform follicles.
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Overview: Medullary Thyroid Carcinoma.
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From parafollicular “C cells”; produces calcitonin, sheets of cells in amyloid stroma. Associated with MEN types 2A and 2B.
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Overview: Undifferentiated Thyroid Carcinoma.
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Older patients; very poor prognosis.
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Overview: Thyroid Lymphoma.
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Associated with Hashimoto’s thyroiditis.
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Overview: Pituitary Adenomas.
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Most commonly prolactinoma. Findings: amenorrhea, galactorrhea, low libido,
infertility. Bromocriptine or cabergoline (dopamine agonists) causes shrinkage. Can impinge on optic chiasm → bitemporal hemianopia |
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Factors Affecting [Thyroid Binding Globulin]
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↓ TBG in hepatic failure
↑ TBG estrogen (↑ TBG in pregnancy and OCP use) |
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Overview: Acromegaly.
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Excess GH in adults. Findings: large tongue with deep furrows, deep voice, large hands and feet, coarse facial features, impaired glucose tolerance (insulin resistance).
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Diagnosis: Acromegaly.
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↑ serum IGF-1; failure to suppress serum GH following oral glucose tolerance test.
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Treatment: Acromegaly.
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Pituitary adenoma resection followed by octreotide administration.
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Overview: Diabetes Insipidus.
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Characterized by intense thirst and polyuria together with an inability to concentrate urine owing to lack of ADH (central DI) or to a lack of renal response to ADH ("nephrogenic" DI)
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Dx: Diabetes Insipidus.
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Water deprivation test—urine osmolality doesn’t ↑.
Response to desmopressin distinguishes between central and nephrogenic. |
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Labs: Diabetes Insipidus.
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Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L.
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Tx: Diabetes Insipidus.
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Adequate fluid intake.
Central DI: intranasal desmopression. Nephrogenic DI: diuretics |
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Overview: SIADH
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"Syndrome of inappropriate antidiuretic hormone"
1. Excessive water retention 2. Hyponatremia 3. Urine osmolarity > serum osmolarity |
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Tx: SIADH
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Demeclocycline (induces nephrogenic diabetes insipidus) or H2O restriction.
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Causes: SIADH
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1. Ectopic ADH
2. CNS disorders/head trauma 3. Pulmonary disease 4. Drugs (e.g. cyclophosphamide) |
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Acute Manifestations: Diabetes Mellitus
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Polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), hyperosmolar coma (type 2),
unopposed secretion of GH and epinephrine (exacerbating hyperglycemia). |
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Chronic Manifestations: Diabetes Mellitus
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Microvascular disease: diffuse basement membrane thickening → retinopathy, glaucoma, nephropathy, neuropathy
Macrovascular disease: large-vessel atherosclerosis, CAD, PVD, CVD, etc |
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Testing: Diabetes Mellitus
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Fasting serum glucose, glucose tolerance test, HbA1c
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Genetics: Type I vs. Type II DM
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Type I has a weak, polygenic association, whereas type II has a very strong, polygenic association.
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Glucose Intolerance: Type I vs. Type II DM
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Type I: Severe glucose intolerance
Type II: Mild/moderate glucose intolerance |
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Serum [Insulin]: Type I vs. Type II DM
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Type I: very low/undetectable
Type II: high to depressed |
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Overview: Diabetic Ketoacidosis.
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One of the most important complications of type 1 diabetes. Usually due to ↑ insulin requirements from ↑ stress (e.g., infection). Excess fat breakdown and ↑ ketogenesis from ↑ free fatty acids, which are then made into ketone bodies (β-hydroxybutyrate
> acetoacetate). |
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Sx: Diabetic Ketoacidosis
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Kussmaul respirations (rapid/deep breathing), nausea/vomiting, abdominal pain, psychosis/delirium, dehydration. Fruity breath odor (due to exhaled acetone).
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Labs: Diabetic Ketoacidosis
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Hyperglycemia, ↑ H+, ↓ HCO3
– (anion gap metabolic acidosis), ↑ blood ketone levels, leukocytosis. Hyperkalemia, but depleted intracellular K+ due to transcellular shift from ↓ insulin. |
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Complications: Diabetic Ketoacidosis
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Life-threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmias,
heart failure. |
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Tx: Diabetic Ketoacidosis
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Fluids, insulin, and K+ (to replete intracellular stores); glucose if necessary to prevent
hypoglycemia. |
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Overview: Carcinoid Syndrome.
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Rare syndrome caused by neuroendocrine cell tumors, especially metastatic small bowel tumors, which secrete high levels of 5-HT.
Not seen if tumor is limited to GI tract (5-HT subject to first-pass metabolism). Most common tumor of appendix. |
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Sx: Carcinoid Syndrome.
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Results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.
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Labs: Carcinoid Syndrome.
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↑ 5-HIAA in urine.
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Tx: Carcinoid Syndrome.
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Octreotide.
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Carcinoids: "Rule of 1/3s"
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Rule of 1/3s:
1/3 metastasize 1/3 present with 2nd malignancy 1/3 multiple sites |
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Overview: Zollinger-Ellison Syndrome.
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Gastrin-secreting tumor of pancreas or duodenum. Causes recurrent ulcers. May be associated with MEN type 1.
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Overview: MEN-1
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AKA "Wermer's Syndrome"
Parathyroid tumors Pituitary tumors Pancreatic tumors (Zollinger-Ellison, insulinoma, VIPoma, glucagonoma) Commonly presents with kidney stones and stomach ulcers. |
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Overview: MEN-2A
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AKA "Sipple's Syndrome"
Medullary thyroid carcinoma Pheochromocytoma Parathyroid tumors |
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Overview: MEN-2B
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Medullary thyroid carcinoma
Pheochromocytoma Oral/intestinal ganglioneuromatosis (associated with with marfanoid habitus) |
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Inheritance: MEN Syndromes.
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All MEN syndromes have an autosomal-dominant inheritance pattern.
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MOA: Insulin Agents.
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Liver: ↑ glucose stored as glycogen.
Muscle: ↑ glycogen and protein synthesis, K+ uptake. Fat: aids TG storage. |
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Indication: Insulin Agents.
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Both type I and type II DM.
Also, life-threatening hyperkalemia and stress-induced hyperglycemia. |
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Toxicity: Insulin Agents.
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Hypoglycemia, type II hypersensitivity reaction (very rare).
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MOA: Sulfonylureas
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Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx.
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Indication: Sulfonylureas
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Stimulate release of endogenous insulin in type 2 DM.
Require some islet function, so useless in type 1 DM. |
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Toxicity: Sulfonylureas.
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First-gen: disulfiram-like reaction
Second-gen: hypoglycemia |
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MOA: Biguanides.
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Exact mechanism is unknown. Possibly ↓ gluconeogenesis, ↑ glycolysis, ↓ serum glucose levels. Overall acts as insulin sensitizer.
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Indication: Biguanides.
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Used as oral hypoglycemic.
Can be used in patients without islet function. |
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Toxicity: Biguanides.
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Lactic acidosis.
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MOA: Thiazolidinediones.
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PPAR-γ activation:
↑ insulin sensitivity in peripheral tissue. |
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Indication: Thiazolidinediones.
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Used as monotherapy in type 2 DM or combined with other agents.
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Toxicity: Thiazolidinediones.
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Weight gain, edema, hepatotoxicity, CV toxicity.
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MOA: α-Glucosidase Inhibitors
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Inhibit intestinal brush-border α-glucosidases. Delayed sugar hydrolysis and glucose absorption lead to ↓ postprandial hyperglycemia.
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Indication: α-Glucosidase Inhibitors.
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Used as monotherapy in type 2 DM or combined with other agents.
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Toxicity: α-Glucosidase Inhibitors.
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GI disturbances.
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MOA: Pramlintide.
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Synthetic amylin analogue; ↓ glucagon, induction of gastroparesis.
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Indication: Pramlintide.
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Type 2 DM.
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Toxicity: Pramlintide.
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Hypoglycemia, nausea, diarrhea.
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MOA: Incretins.
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↑ insulin, ↓ glucagon release.
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Clinical Use: Incretins.
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Type 2 DM.
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Toxicity: Incretins.
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Nausea, vomiting, pancreatitis (rare).
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MOA: Orlistat.
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Alters fat metabolism by inhibiting pancreatic lipases.
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Indication: Orlistat.
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Long-term obesity management (in conjunction with modified diet and lifestyle).
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Toxicity: Orlistat.
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Steatorrhea, GI discomfort, reduced absorption of fat-soluble vitamins, headache.
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MOA: Sibutramine
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Sympathomimetic serotonin and norepinephrine reuptake inhibitor.
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Indication: Sibutramine.
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Short-term and long-term obesity management.
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Toxicity: SIbutramine.
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Hypertension and tachycardia.
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MOA: Propylthiouracil
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Thyroperoxidase antagonist: inhibitions iodine organification and coupling.
Also ↓ peripheral conversion of T4 to T3. |
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Indication: Propylthiouracil
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Hyperthyroidism.
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Toxicity: Propylthiouracil
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Skin rash, agranulocytosis (rare), aplastic anemia.
Risk of sudden hepatic failure (rare). |
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MOA: Methimazole.
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Thyroperoxidase antagonist: inhibition of iodine organification and coupling to thyroglobulin.
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Indication: Methimazole.
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Hyperthyroidism.
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Toxicity: Methimazole.
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Skin rash, agranulocytosis (rare), aplastic anemia.
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Toxicity: Levothyroxine.
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Thyrotoxicosis: Tachycardia, heat intolerance, tremors, arrhythmias.
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Indication: Exogenous Growth Hormone.
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GH deficiency, Turner’s syndrome.
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Indication: Exogenous Somatostatin.
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AKA Octreotide.
Acromegaly, carcinoid, gastrinoma, glucagonoma. |
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Indication: Exogenous Oxytocin.
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Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage.
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Indication: Exogenous ADH.
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AKA Desmopressin.
Pituitary (central, not nephrogenic) DI |
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MOA: Demeclocycline
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ADH antagonist (member of the tetracycline family).
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Indication: Demeclocycline.
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SIADH.
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Toxicity: Demeclocycline.
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Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.
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MOA: Exogenous Glucocorticoids.
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↓ the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2.
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Indication: Exogenous Glucocorticoids
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Addison’s disease, inflammation, immune suppression, asthma.
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Toxicity: Exogenous Glucocorticoids
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Iatrogenic Cushing’s syndrome (buffalo hump, moon facies, truncal obesity, muscle
wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes) |
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Overview: Sheehan's Syndrome.
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Postpartum hypopituitarism. Enlargement of anterior pituitary (↑ lactotrophs) during
pregnancy without corresponding ↑ blood supply leads to ↑ risk of infarction of the pituitary gland following severe bleeding and hypoperfusion during delivery. May cause fatigue, anorexia, poor lactation, and loss of pubic and axillary hair. |
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Overview: Primary Hyperparathyroidism.
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Usually an adenoma. Hypercalcemia, hypercalciuria (renal stones), hypophosphatemia, ↑ PTH, ↑ alkaline phosphatase, ↑ cAMP in urine. Often asymptomatic, or may present with weakness and constipation.
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Overview: Secondary Hyperparathyroidism.
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2° hyperplasia due to ↓ gut Ca2+ absorption and ↑ phosphorus, most often in chronic renal disease (causes hypovitaminosis D → ↓ Ca2+ absorption). Hypocalcemia, hyperphosphatemia, ↑ alkaline phosphatase, ↑ PTH.
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Overview: Hypoparathyroidism.
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Due to accidental surgical excision (thyroid surgery), autoimmune destruction, or DiGeorge syndrome.
Findings: hypocalcemia, tetany. |
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Overview: Pseudohypoparathyroidism
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AKA "Albright’s hereditary osteodystrophy"
autosomal-dominant kidney unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature. |
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Pathology Above the Pectinate Line.
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Internal (painless) hemorrhoids and adenocarcinoma.
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Pathology Below the Pectinate Line.
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External (painful) hemorrhoids and squamous cell carcinoma.
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Blood Supply Above Pectinate Line.
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Arterial: Superior rectal artery.
Venous: superior rectal vein →inferior mesenteric vein →portal system. |
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Blood Supply Below Pectinate Line.
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Arterial: inferior rectal artery.
Venous: inferior rectal vein → internal pudendal vein → internal iliac vein → IVC. |
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Innervation: External Hemorrhoids.
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Inferior rectal nerve (from pudendal nerve).
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Hepatic Acinar Zones.
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Zone I: "periportal"; immune dense → most susceptible to viral hepatitis
Zone II: "intermediate zone" Zone III: "pericentral"; contains P450 enzymes; most susceptible to ischemia, toxic injury, and alcoholic hepatitis |
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Overview: Hepatic Sinusoids.
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Fenestrated endothelium. No
basement membrane. Allow macromolecules of plasma full access to basal surface of hepatocytes through perisinusoidal space (space of Disse). |
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Structures: Femoral Region.
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NAVEL:
(Femoral) Nerve (Femoral) Artery (Femoral) Vein Empty Space (Femoral) Lymphatics |
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Contents: Femoral Triangle.
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Contains femoral nerve, artery, and vein.
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Contents: Femoral Sheath.
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Contains femoral vein, artery, and canal (deep inguinal lymph nodes) but NOT femoral nerve.
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Most common tumor of the adrenal medulla in adults.
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Pheochromocytoma
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Most common tumor of the adrenal medulla in children.
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Neuroblastoma
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From which embryonic layer is the adrenal cortex derived?
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Mesoderm
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From which embryonic layer is the adrenal medulla derived?
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Neural crest (ectoderm)
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Hormones from the anterior pituitary.
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FSH, LH, ACTH, TSH, prolactin, GH, melanotropin
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Hormones from the posterior pituitary.
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Vasopressin and oxytocin
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From which embryonic layer is the anterior pituitary derived?
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Oral ectoderm (Rathke's pouch)
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From which embryonic layer is the posterior pituitary derived?
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Neuroectoderm.
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Which pituitary hormones share a common α subunit?
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Subunit common to TSH, LH, FSH, and hCG.
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Which subunit of pituitary hormones determines specificity?
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β subunit
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What is the most common cause of congenital adrenal hyperplasia?
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21-Hydroxylase Deficiency
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Hormone Abnormalities: 17α-Hydroxylase Deficiency
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↓ sex hormones, ↓ cortisol, ↑ mineralocorticoids
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Hormone Abnormalities: 21-Hydroxylase Deficiency
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↓ cortisol (increased ACTH), ↓ mineralocorticoids, ↑ sex hormone
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Hormone Abnormalities: 11β-hydroxylase Deficiency
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↓ cortisol (increased ACTH), ↓ mineralocorticoids, ↑ sex hormones.
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Symptoms: 17α-Hydroxylase Deficiency
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HTP, hypokalemia.
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Symptoms: 21-Hydroxylase Deficiency
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Masculinization, female pseudohermaphroditism, hypotension, hyperkalemia, ↑ plasma renin activity, and volume depletion.
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Symptoms: 11β-hydroxylase Deficiency
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Masculinization, hypertension
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What do all congenital adrenal hyperplasia syndromes have in common?
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All have low cortisol and high ACTH (hence the adrenal hyperplasia)
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Common causes of hypomagnesemia.
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Common causes of ↓ Mg2+ include diarrhea, aminoglycosides, diuretics, and alcohol abuse.
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How do PTH and Vitamin D differe with respect to handling of Ca2+ and phosphate?
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PTH ↑ calcium reabsorption and ↓ phosphate reabsorption, while vitamin D ↑ absorption of both calcium and phosphate.
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How do steroid hormones circulate?
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Due to their lipophilicity, all steroid hormones circulate bound to steroid-binding globulins.
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What would you expect to find in a man with elevated levels of sex hormone-binding globulin?
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Low free testosterone ---> gynecomastia
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What would you expect to find in a woman with low levels of sex hormone-binding globulin?
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Elevated free testoterone ---> hirsutism.
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Is more T3 or more T4 produced?
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The thyroid gland primarily produces T4, which has low biologic activity; T4 is then converted to active T3 within peripheral tissues
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What disease state features low levels of steroid-binding globulins?
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Hepatic failure: the liver makes 'em, so they'll be low with a broken liver ---> elevated free hormone levels.
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Which adrenal layers does Addison's affect?
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All three layers are affected, and the adrenal cortex is globally small.
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Genetic lesion in neuroblastoma.
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N-myc oncogene mutation.
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