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Condition in which both cortisol and ACTH are elevated

Secondary Cushing's [due to pituitary adenoma]

Conditions that cause hyperadrenocorticism with decreased ACTH

Primary Cushing [due to adrenal hyperplasia] and Tertiary Cushing [neoplasia, eg small cell]

The most common Cushing etiology. What are the culprits? What's the effect on ACTH?

-Iatrogenic Cushing's
-Chronic steroid use, asthma meds, prednisone.
-All decrease ACTH by negative feedback.

Dexamethasone suppression test results in healthy patients.

Decreased cortisol after low [or high] dose.

Dexamethasone suppression test results in ACTH-producing pituitary adenoma [secondary Cushing}

Cortisol does not decrease after low dose, does decrease after high dose

Dexamethasone suppression test results in adrenal cortex adenoma [primary Cushing] and ACTH-releasing tumor [tertiary Cushing]

Cortisol does not decrease after low dose or high dose

Most common single gene defect, pattern of inheritance, and hallmarks.

-Neurofibromatosis-1 (Von Recklinghausen syndrome)
-Autosomal dominant
-Neural fibromas, Cafe au lait spots, Axillary/inguinal freckles, Optic nerve glioma, Lisch nodules [on iris]

Cushing's findings

HTN, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia, skin changes, osteoporosis, amenorrhea and immune suppression

Primary hyperaldosteronism hallmark characteristics

-Aldosterone secreting tumor [glomerulosa region],
-HTN, hypokalemia, metabolic alkalosis [swap H+ to replace K+], and low plasma renin

Low blood volume or BP [e.g., CHF, cirrhosis, dehydration, renal artery stenosis, renal failure]. Results in overactive RAAS & high plasma renin

Secondary hyperaldosteronism etiology and results

Primary hyperaldosteronism treatment

Spironolactone [aldosterone antagonist diuretic] or amiloride [K-sparing diuretic]

Primary adrenal insufficiency name.
Hallmark findings

-Addison's, resulting in [hypocortiolism and] hypoaldosteronism.
-[Cortisol and] aldosterone low. Hypoglycemia, hypotension, hyperkalemia and bronzing.

Secondary adrenal insufficiency cause & findings

-Insufficient ACTH from anterior pituitary.
-Mimics Addisons' but no bronzing and no hyperkalemia.

Addison's mnemonic

Adrenal Atrophy and Absence of hormone production; involves All three cortices

Waterhouse-Friderichsen syndrome findings and etiology

Acute adrenocortical insufficiency due to adrenal hemorrhage. Associated with meningococcal septicemia

Sheehan's syndrome findings and etiology

Postpartum hypopituitarism. Enlargement of anterior pitutary during pregnancy without corresponding increase in blood supply leads to infarction of the pituitary gland following severe bleeding during delivery.

Sheehan's syndrome hallmark symptoms [post- partum hypopituitarism]

Amenorrhea, poor lactation, loss of pubic and axillary hair, fatigue

Most common tumor of the adrenal medulla in adults. From what tissue is it derived?

-Pheochromocytoma
-Derived from chromaffin cells that arise from neural crest.

Pheochromocytoma rule

10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids, 10% familial

Pheochromocytoma tumor products

Epinephrine, Norepinephrine and Dopamine; can cause episodic hypertension, flushing, palpitations

Pheochromocytoma diagnostic labs

24-hr urinary VMA (vanillylmandelic acid) and plasma catecholamines.

Pheochromocytoma associations

NF, MEN types 2A and 2B

Pheochromocytoma treatment

Alpha blockers, especially phenoxybenzamine [nonselective, irreversible alpha blocker] "Pheo-Knocks-Ben's Amine"

The two episodic hyperadrenergic disorders and their symptoms

Carcinoid tumors & pheochromocytoma. Hypertension [blood Pressure], Pain, Perspiration, Palpitations, Pallor

Most common tumor of adrenal medulla in kids. Where else may it occur? What lab helps to diagnose?

-Neuroblastoma
-Anywhere along the Sympathetic chain.
-24-hr HVA in urine.

MEN 1 [Multiple Endocrine Neoplasia 1] = Werner's syndrome mnemonic and tumor sites

PPP
Pancreas tumors [Z-E syndrome, insulinomas]; Pituitary tumors [prolactin or GH]; Parathyroid tumors [hypercalcemia]

MEN 1 (Multiple Endocrine Neoplasia) tumor sites & presentation

Pituitary [prolactinoma], parathyroid [secretes PTH] & pancreas [gastrinoma or insulinoma].

MEN2A (Multiple Endocrine Neoplasia 2A) (Sipple's syndrome) mnemonic and tumor sites

PPM
Pheochromocytoma, Parathyroid tumor, and Medullary thyroid carcinoma [secretes calcitonin]

MEN 2B mnemonic and tumor sites

MMP
Medullary thyroid carcinoma [secretes calcitonin], Marfanoid appearance, Pheochromocytoma. May also have oral/intestinal ganglioneuromas.

Form of inheritance of MEN syndromes

Autosomal Dominant

Hypothyroidism findings

Cold intolerance, hypoactivity, weight gain, fatigue, decreased appetite, constipation, weakness, decreased reflexes, dry cool skin, corase brittle hair

Primary hypothyroidism labs

Elevated TSH, decreased total T4, decreased free T4, decreased T3 uptake

Hyperthyroidism signs & symptoms

Heat intolerance, hyperactivity, weight loss, palpitations, arrhythmias, diarrhea, exophthalmos, warm moist skin, fine hair

Primary hyperthyroidism name and labs

-Graves, thyroid adenoma
-Decreased TSH, increased total T4, & free T4, increased T3 uptake

Grave's disease etiology and hallmark characteristics.

-Autoimmune hyperthyroidism with thyroid-stimulating TSH receptor antibodies.
-Exophthalmia, pretibial myxedema, diffuse goiter. Often presents during stress.

Hashimoto's thyroiditis hallmark charateristics

-Autoimmune hypothyroidism. Moderately enlarged, nontender thyroid produces anti-thyroglobulin antibodies.

Subacute thyroiditis [de Quervain's] symptoms & diagnosis

Self-limited hypothyroidism often following a flulike illness. Elevated ESR, jaw pain, tender thyroid. Granulomatous inflammation.

Riedel's thyroiditis

Thyroid replaced by fibrous tissue. Presents with fixed, hard, painless goiter.

Stress-induced thyrotoxicosis with high fever, cardiovascular and nervous system dysfunction. Possible death by arrhythmia.

Thyroid storm & Grave's disease

Cause: Iodine deprivation followed by iodine restoration. Causes release of T3 and T4. Non malignant.

Toxic multinodular goiter causes & appearance

Jod-Basedow phenomenon description

Thyrotoxicosis in iodine deficiency goiter treated with iodine

Papillary thyroid carcinoma frequency, prognosis, and presentation

-Most common thyroid cancer [>80%]
-Good prognosis.
-Ground glass nuclei, "Orphan Annie eyes"[Daddy Warbucks=Papa-larry] and psamomma [Papa & Momma] bodies, nuclear grooves, increased risk with childhood irradiation.

Follicular carcinoma frequency, prognosis and presentation

Second most common thyroid cancer. [~9-15%]
-Good prognosis.
-Uniform follicles form asymptomatic nodule. Mets to bone and lung occur in 15% . Do CXR, bone scan.

Medullary carcinoma frequency, prognosis and presentation

-Rare [2%]
-Thyroid cancer of parafollicular "C" cells. [Produces calcitonin]. Lump at base of neck that may cause hoarseness or dysphagia.
-25% of cases are associated with MEN types 2A and 2B.

The most rare of thyroid carcinomas and the population affected, prognosis.

-Undifferentiated/anaplastic thyroid cancer
-Older patients, very poor prognosis.

Cretinism etiology

Due to severe fetal hypothyroidism. May be due to endemic lack of iodine, defect in T4 formation, or development failure in thyroid formation.

Cretinism signs & symptoms

MR, pot-bellied, hypotonic with protruding umbilicus and tongue

Acromegaly etiology, signs & symptoms

-Excess GH in adults
-Large tongue with deep furrows, deep voice, large hands and feet, coarse facial features, impaired glucose tolerance [insulin resistance]

Acromegaly diagnostic tests

-Increased serum IGF-1
-Failure to suppress serum GH following oral glucose tolerance test

Acromegaly treatment

Pituitary adenoma resection followed by octreotide treatment

1. Parathyroid adenoma increases PTH
2. Hypercalcemia, hypercalciuria (renal stones), hypophosphatemia. Classic presentation includes weakness and constipation with "stones, bones, and groans"

Primary hyper-parathyroidism cause & signs & symptoms

Cystic bone spaces filled with brown fibrous tissue, found in primary hyperparathyroidism

Osteitis fibrosa cystica (von Recklinghausen's syndrome)

1. Hypocalcemia from decreased Ca absorption in chronic renal failure --> stimulus of parathyroids --> hyperphosphatemia. Ends in osteodystrophy
2. Squamous cell lung cancer [paraneoplastic secretion of PTH]

Secondary hyperparathyroidism symptoms & causes

Bone lesions due to secondary hyperparathyroidism in end-stage renal disease. Hyperphosphatemia and hypocalcemia.

Renal osteodystrophy

Causes: Surgical excision, autoimmune destruction, or DiGeorge syndrome. Effects: Hypocalcemia, tetany.

Hypoparathyroidism causes & effects

Found in hypoparathyroidism. "Tetany-on-demand." Tap CN-7 [facial nerve] --> contraction of facial muscles.

Chvostek's sign from hypocalcemia

Found in hypoparathyroidism. Occlusion of brachial artery with BP cuff --> carpal spasm

Trousseau's sign-- hypocalcemia

AD kidney unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature

Pseudo-hypoparathyroidism

Ca2+ ingestion, Parathyroid tumor, Hyperparathyroidism, Squamous cell lung cancer, Thiazide diuretics, Lithium use, Paget's, Addison's, Z-E, Excess vit D.

All are causes of hypercalcemia--"bones, groans, stones"

Prolactinoma. Dopamine agonists [bromocriptine & cabergoline] cause shrinkage. Tumor may impinge on optic chiasm --> temporal hemianopia

Common pituitary adenoma & its treatment

Amenorrhea, galactorrhea, low libido, infertility

Cushing's sexual findings

Polydipsia, polyphagia, weight loss, DKA (type I), hyperosmolar coma (type 2), unopposed secretion of GH and epi (exacerbating hyperglycemia)

Acute manifestations of DM

Small vessel diease (diffuse thickening of BM) --> retinopathy, glaucoma, nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to HTN, Kimmelsteil-Wilson nodules). Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease and gangrene, cerebrovascular disease.

Chronic manifestations of DM due to nonenzymatic glycosylation

Neuropathy [motor, sensory and autonomic dysfunction]; and cataracts [sorbitol accumulation]

Chronic manifestations of DM due to osmotic damage

Fasting serum glucose, glucose tolerance test, HbA1c (measures long term diabetic control)

DM tests

Juvenile onset, due to viral or immune destruction of beta cells. Always require insulin. Genetic predisposition. Ketoacidosis is common. Polyuria, polydipsia, weight loss.

Type I DM

Adult onset. Increased resistance to insulin. Insulin is sometimes neccessary in tx. Age is >40y at onset. Strong polygenic genetic predisposition. No association with HLA. Mild to moderate glucose intolderance. Ketoacidosis is rare. Beta cell numbers in islets are variable, serum insulin levels are variable. poly sx & weight loss occur sometimes.

Type II DM

One of most important complications of Type I DM. Usually due to increased insulin requirements from increased stress (eg infection). Excess fat breakdown and increased ketogenesis from increased FFAs which are then made into ketone bodies.

DKA

Kussmaul respirations (rapid/deep breathing), N/V, abd pain, psychosis, dehydration, fruity breath

DKA signs and sx

Hyperglycemia, acidosis, decreased HCO3- (anion gap), increased blood ketone levels, leukocytosis, hyperkalemia but depleted intracellular K due to transcellular shift.

DKA (diabetic ketoacidosis) labs

Complications: Life-threatening mucormycosis, cerebral edema, cardiac arrhythmias, heart failure

DKA complications

Monitor/adjust fluids, insulin, K+ [to replace intracellular stores]; glucose if neccessary to prevent hypoglycemia

DKA treatment

Intense thirst and polyuria together with an inability to concentrate urine owing to lack of ADH (central) or to a lack of renal response (nephrogenic)

Diabetes insipidus

Poserior pituitary tumor, trauma, surgery, & histiocytosis X

Causes of central diabetes insipidus

Hereditary or secondary to hypercalcemia, lithium, demeclocycline [ADH antagonist]

Causes of nephrogenic diabetes insipidus

H2O deprivation test - urine osmolality unaffected [remains very low]. Response to desmopressin distinguishes central type [responds] from nephrogenic type [no response].

Diabetes insipidus diagnosis

Urine specific gravity < 1.006; serum osmolality >290 mOsm/L

Diabetes insipidus findings

ALL: Adequate fluid intake. Central: intranasal desmopressin (ADH analog). Nephrogenic: diuretics (Hydrochlorothiazide or amiloride)

Diabetes insipidus treatment

Excessive water retention, hyponatremia[Na is diluted by reabsorbed H2O], urine osmolarity > serum osmolarity

SIADH signs & symptoms

Complication : Extreme hyponatremia [central pontine myelinolysis]. Can lead to seizures [correct slowly!]

Most dangerous SIADH complication

Water restriction, then Demeclocycline [a tetracycline derivative!]; add furosemide in severe cases. Never correct Na faster than 10 mEq in 24 hr!

SIADH treatment

Ectopic ADH [small cell lung cancer], CNS disorders/head trauma; pulmonary disease [pneumonia, TB]; or drugs [cyclophosphamide]

SIADH causes

Tumors of neuroendocrine cells in gut and in lungs . Secrete high levels of 5-HT (serotonin). Paroxysmal flushing, wheezing asthma, diarrhea & RCHF

Carcinoid syndrome causes, signs & symptoms

5-HT (serotonin) undergoes first-pass metabolism in liver

Reason why carcinoid syndrome is not seen in primary GI tumors

Diarrhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.

Carcinoid syndrome signs & symptoms

Octreotide

Carcinoid syndrome treatment

Gastrin-secreting tumor of pancreas. Causes recurrent ulcers. May be associated with MEN type I

Zollinger-Ellison syndrome

Parathyroid [hypercalcemia], pituitary medulla [calcitonin], pancreas [gastrinoma--> ulcers-Zollinger Ellison]

MEN-1 tumor sites

The two types of diabetes insipidus

Central and Nephrogenic

Deficient production of ADH

Central diabetes insipidus cause

Renal ADH receptor defect

Nephrogenic diabetes insipidus cause

Cardiac Abnormality [especially Fallot's Tetralogy]
Abnormal facies
Thymic aplasia [T-cell deficiency]
Cleft palate
Hypocalcemia [Parathyroid aplasia]
22-- chromosome

DiGeorge syndrome

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