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332 Cards in this Set
- Front
- Back
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-What is Addison's disease? -What is the most common cause? -What hormones are missing?
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-Primary adrenal insufficiency -Autoimmune adrenalitis - -Cortisol and aldosterone
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4 groups of functions of cortisol
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Hemodynamic
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ACTH stimulation when enzymatic defect results in:
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build-up of steroid hormone precursors at step before enzymatic defect
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Acromegaly is also known as __
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somatotroph adenoma
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Acute hypocalcemia treatment
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IV calcium
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Addison's disease: Hormone profile
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High ACTH
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Adrenal Insufficiency: symptoms and signs
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weakness and fatigue
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Adrenal carcinoma: how aggressive?
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aggressive
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Adrenal carcinoma: how common?
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rare
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Adrenal carcinoma: symptoms?
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-sometimes (hormonal hypersecretion)
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Adrenalcortical tumorigenetic mechanisms?
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ras: protooncogene
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Causes of endogenous Cushing's
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Problems of -Pituitary -Adrenal -Ectopic
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Congenital Adrenal Hyperplasia: Mechanism
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Synthetic defects --> Reduced cortisol synthesis --> Less negative feedback --> More ACTH
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Corticotroph adenoma is also known as ____
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Cushing's disease
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Cortisol: Immune system effects
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-Puts neutrophils in the blood and keeps them there -Moves peripheral lymphocytes
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Cortisol: Metabolic effects
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Sugar production: Stimulates gluconeogenesis production and suppresses insulin secretion
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Cortisol: Water regulation effects
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-Keeps water out of cells and promotes it's excretion (suppresses ADH/increases GFR)
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Cortisol: hemodynamic functions
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Maintains cardiac output by -maintaining vascular tone and endothelial integrity -potentiating vasocontriction by catecholamines
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Cortrosyn Stimulation Test: Process
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Cortrosyn is given ------> cortisol levels are drawn over 0
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Cushing's Syndrome: ACTH dependent causes
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Pituitary Cushing's Disease
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Cushing's Syndrome: ACTH independent causes
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Unilateral adrenal adenoma/carcinoma
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Cushing's Syndrome: Treatment
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Surgical removal of adenoma
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Cushing's disease is also known as _____
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Corticotroph adenoma
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Does cortisol have a short/long/both negative feedback loop
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both
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How is the glucocorticoid dose adjusted when someone with adrenal insufficiency is ill?
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It is raised to match what adrenals would normally do.
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How much cortisol is produced daily
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and around what times?
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Indication for surgical removal of adrenal mass
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-4-5 cm or more -Functional
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Lack in aldosterone synthesis in congenital adrenal hyperplasia produces:
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salt-wasting
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Most adrenal tumors are what?
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Benign adrenal adenomas
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Most common form of congenital adrenal hyperplasia ___ results in ____
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21-OHlase deficiency results in excess 17-OHprogesterone
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Most common form of Cushing's syndrome
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Exogenous glucocorticoid therapy
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Most common test for adrenal insufficiency
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Cortrosyn stimulation test
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PAC/PRA: Diagnostic value
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>20: suggestive of disorder >100 & elevated aldosterone levels: aldosterone producing adenoma
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Pheochromocytoma: What does it do?
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Hypersecretes catecholamines
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Pheochromocytoma: symptoms?
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5Ps: Pressure
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Pheochromocytoma: what is it?
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Adrenal medullary tumor
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Pheochromocytoma: Vignette
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Adult: Single intra-adrenal benign mass which does not recur after resection
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Pheochromocytoma: Found in which syndromes
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MEN2A and MEN2B; Neurofibromatosis; Von Hippel Lindau syndrome
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Pheochromocytoma: workup?
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-Biochemical dx -Imaging -Pre-operative bp meds -Surgery
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Primary hyperaldosteronism: Treatment
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APA
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Primary hyperaldosteronism: Workup
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PAC/PRA ---> verification that high volume does not suppress plasma aldosterone ---> imaging (adrenal villous sampling)
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Primary hyperaldosteronism: highly impacted population
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Htn patients
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Primary hyperaldosteronism: most common causes
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Unilateral APA (aldosterone producing adenoma) & IHA (Idiopathic hyperaldosteronism [bilateral hyperplasia])
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Primary hyperaldosteronism: symptoms
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hypertension
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Somatotroph adenoma is also known as ____
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acromegaly
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Specific testing of hypothalamus and pituitary part of axes
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-Insulin tolerance -Metyrapone
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Symptoms of bad Cushing's
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-Devastating catabolism -Severe complications -Medical -Psychological
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Treatment of adrenal insufficiency
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Glucocorticoid replacement
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Two types of pituitary testing
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Basal and dynamic
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What are some rare causes of Addison's?
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Infections
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Pheochromocytoma: Tests
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24-hour urine collection and plasma catecholamines and metanephrines
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What does PAC/PRA stand for?
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Plasma aldosterone concentration to plasma renin activity
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What is APS?
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Autoimmune Polyendocrine Syndrome
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What is the autoantigen in APS 2?
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21-hydroxylase
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What is the autoantigen in APS-1?
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P450-SSC
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What is the hormone profile for secondary adrenal insufficiency? What is the most common cause?
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Low ACTH & Low cortisol caused by long-term glucocorticoid therapy leading to atrophy.
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Workup for adrenal hypersecretion if:
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Incidental adrenal mass
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Workup for primary hyperaldosteronism
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Determination that aldosterone overproduction -Independent of renin secretion -Cannot be suppressed Distinguish between adenoma AND bilateral hyperplasia
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use of ACTH level
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Distinguish between primary and secondary adrenal insufficiency
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Acute hypocalcemia treatment
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IV calcium
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Cause of FHH
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Mutation in the calcium sensor
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Causes of hypocalcemia
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-PTH deficiency or resistance -Vitamin D deficiency or resistance -Complexation of Calcium
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Chvostek's sign / Weiss' sign
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Indicates: Hypocalcemia and respiratory alkalosis (hyperventilation) How done: Tap facial nerve at angle of jaw Result: Ipsilateral facial twitch. Sensitive
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Common inpatient cause of hyperparathyroidism
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Malignancy
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Common outpatient cause of hyperparathyroidism
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Single monoclonal PT adenoma ==> PHP (primary hyperparathyroidism)
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Distribution of extracellular calcium (bound/free ratio)
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1:1
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FHH resembles what?
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PHP (Primary Hyperparathyroidism)
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Hypercalcemia: Lab Dx Algorithm
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High Ca and PTH: PHP High Ca and Low PTH: further biochemical workup
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Hypercalcemia: Symptoms
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Stones
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Hypercalcemias effects
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-Kidney (Nephrolithiasis) -Bones (Osteoporosis) -System (Malaise
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Malignancy associated hypercalcemia: humoral factors
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PTHrP
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Most common hypocalcemia etiology
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Total thyroidectomy or pt-ectomy
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PTH functions
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Stimulates -Vitamin D activation -Calcium from bone to serum -Kidney: -Ca reabsorption -Phosphorus excretion (Phosphate trashing hormone)
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Acute hypocalcemia: signs and symptoms
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-Trousseau's sign (bp cuff) -Chvostek's sign (facial nerve tap) -Acroparesthesias
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Symptoms of Parathyroid adenoma
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Most patients are asymptomatic
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Trousseau's sign
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Indicates: Hypocalcemia How done: Inflate blood pressure cuff over systolic for three minutes Result: Carpal-pedal spasm
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Vitamin D and PTH relationship
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PTH activates 25-OH-D into 1
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Vitamin D function
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Promotes calcium absorption from small intestine
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Hypercalcemia: Treatment
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-Increase urinary calcium excretion (volume restoration then loop diuretic) -Inhibit bone resorption (bisphosphonates) -Decrease intestinal absorption (glucocorticoids
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Chronic hypocalcemia: Major sign
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QT interval prolongation
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Phosphorus levels in hypocalcemia
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Low levels: Vit. D abnormality. High levels: Hypoparathyroidism
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25-OH-Vitamin D levels in hypoparathyroidism
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Low: Inadequate intake or skin production
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1
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25-OH-Vitamin D levels in hypoparathyroidism
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Anabolic effects of insulin (bolus insulin) in adipose tissue
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Increases glucose transport (GLUT-4) and activity of Lipoprotein Lipase --> uptake of FFA and glycerol
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Anabolic effects of insulin (bolus insulin) in the liver
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Stimulates glycolysis
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Anabolic effects of insulin (bolus insulin) in the muscle
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Stimulates glucose uptake (GLUT-4) and glycogen synthesis and amino acid uptake and protein synthesis
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Anti-catabolic effects of insulin (basal insullin) in adipose tissue
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Inhibits intracellular lipolysis
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Anti-catabolic effects of insulin (basal insullin) in the liver
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Inhibits gluconeo/glycogen breakdown and promotes triglyceride synthesis
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Anti-catabolic effects of insulin (basal insullin) in the muscle
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Inhibits gluconeo and glycogen breakdown
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CHRONIC Complications of Diabetes due to: Macrovascular problems
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-CAD -Stroke -Peripheral vascular disease
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CHRONIC Complications of Diabetes due to: Microvascular problems
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-Retinopathy -Nephropathy -Peripheral and Autonomic neuropathies
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Characterization of diabetes
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Metabolic disorders Problem: abnormal fuel metabolism Result: hyperglycemia and dyslipidemia
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DKA: Treatment
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Fluid resuscitation - Bolus of insulin -insulin infusion until DKA resolves -Give potassium
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DKA: signs
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5 -deyhydration -tachycardia -hypotension -fruity breath -diffuse abdominal tenderness
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DKA: Symptoms
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6 -polyuria -polydipsia -fatigue -nausea -vomiting -abdominal pain
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DKA: cause
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Lack of insulin
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Diabetes dx criteria (glucose
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other)
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Diabetes: Blood pressure recommendation
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<130/80
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Diabetes: HDL recommendation
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>40 mg/dl
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Diabetes: LDL recommendation
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<100 mg/dl
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Diabetes: TG recommendation
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<150 mg/dl
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Diabetic retinopathy: treatment
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None
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Drugs that induce type 2 diabetes
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Glucocorticoids
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Genes implicated in DM-1
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HLA DQ and DR
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Genes implicated in type 2 diabetes
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MODY 2: Glucokinase defects MODY 1 & MODY 3-6: Beta cell transcription factors
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Gestation diabetes cause
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Insulin resistant state of pregnancy
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Gestation diabetes risks
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-Fetal macrosomia (high birth weight) -Cesarean section higher rate -High risk for type 2 diabetes in future
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HHNS: Acidemia?
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No
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HHNS: Treatment
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Fluid replacement
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HHNS: What does it stand for?
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Hyperglycemia
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HbA1c goal for diabetics
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Less than 6.5-7% per day
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How do you test for an insulinoma?
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High insulin (and corresponding C-peptide) levels
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How many hours of fasting are required to deplete glycogen stores?
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42
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Infections associated with diabetes
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Congenital Rubella (type 1); Coxsackievirus B
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Infections that happen more frequently in DM patients
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UTIs
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Insulinoma: treatment
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Surgery
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Major autoantigens in diabetes
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GAD-65
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Mechanisms for obesity management drugs
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-Suppression of appetite -Limiting absorption of fat in small intestines -Increase in energy expenditure (future drugs)
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Metabolic syndrome characteristics
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CHAOS -Coronary artery disease -Htn -Adult onset diabetes (dyslipidemia and insulin resistance) -Obesity (central) -Stroke (CVD and death)
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Metabolic Syndrome: Abdominal Obesity requirement
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Waist circumference: >102 cm in men; > 88 cm in women
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Metabolic Syndrome: High fasting glucose
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Over 110 mg/dL
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Metabolic Syndrome: Hypertriglyceridemia (how much?)
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>= 150 mg/dL
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Metabolic Syndrome: Low HDL (How low?)
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Men: <40 mg/dL Women: <50 mg/dL
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Most important tests when someone seems to be hypoglycemic?
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Glucose and simultaneous insulin
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Order of diabetic nephropathy
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Increased GFR (>150 mL/min); Microalbuminuria (30-300 mg/24 hours); Macroalbuminuria ( >300 mg/24 hours)
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Pre-diabetes: definition
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Impaired: -fasting glucose -glucose tolerance
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Pre-diabetes: risk
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Increased risk for CVD and death
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Principal behind dynamic testing for fasting hypoglycemia
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Patient begins to fast ==> glucose level falls --> insulin should shut off --> euglycemia is maintained. If insulin does not shut off --> pathology
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Rare or common: insulinomas
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rare
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Reasons diabetics should exercise
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Exercise improves: -Glucose tolerance -Insulin sensitivity
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Risk factor management for CVD in diabetics
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-Smoking -Htn -Dyslipidemia
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Source of acute complications of diabetes
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severe hyperglycemia
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Source of chronic complications of diabetes
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vascular damage
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Treatment for diabetic neuropathy
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Symptomatic: Tricyclic antidepressants
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Treatment of diabetic nephropathy
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ACEI
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Type 1 DM cause
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Autoimmune destruction of beta islets due to nature and nurture
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Type 2 Diabetes definition
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Insulin resistance and deficiency
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What and where are the principal hypoglycemic sensors?
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Carotid body (hypothalamus)
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What are organ insufficiencies/conditions associated with hypoglycemia and HIGH insulin levels?
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Diabetes
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What are organ insufficiencies/conditions associated with hypoglycemia and LOW insulin levels?
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Adrenal insufficiency
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What happens when the glucose level reaches: <30 mg/dl
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Coma
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What happens when the glucose level reaches: <50 mg/dl
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Weakness
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What happens when the glucose level reaches: <60 mg/dl
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GH
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What happens when the glucose level reaches: <65 mg/dl
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Autnomic system is activated --> increased glucagon
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What happens when the glucose level reaches: <70 mg/dl
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Insulin shuts off --> Sugar production goes up and sugar uptake goes down
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What is Whipple's triad?
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-Signs and symptoms of hypoglycemia -A documented low blood glucose level -Improvement of symptoms and glucose levels by administration of glucose
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When does a prolonged fast lead to hypoglycemia?
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When the liver cannot maintain glucose output.
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Why should one eat when they drink alcohol?
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Alcohol interferes with hepatic gluconeogenesis AND hypoglycemia feels like being drunk
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ACUTE Complications of Diabetes due to: Severe hyperglycemia
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-Diabetic ketoacidosis -Hyperglycemia hyperosmolar nonketotic state
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# of daily insulin shots most type 1 diabetics need
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3-4
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Acute hypocalcemia treatment
|
IV calcium
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Amylin analogue
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Pramlintide
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Approximate % basal insulin for DM1
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50% basal 50% bolus
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Bone resorption blocker example
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bis-phos-pho-nates
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Carbohydrate absorption blockers
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Alpha-glucosidase inhibitors
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Chronic hypocalcemia treatment
|
Oral calcium with active form of vitamin D
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DPP-IV inhibitor
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Sitagliptin
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Day to day glucose goals for diabetics: After meals
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Under 160 mg/dl
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Day to day glucose goals for diabetics: Before meals
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80-120 mg/dl
|
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Evaluation of PHP prior to treatment
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Kidney and bone evaluation
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GLP-1 analogue
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Exenatide
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Insulin resistance improvers
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Bi-guan-ide thia-zoli-dine-di-ones
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Insulin secretagogues
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Sulfonylureas Meglitinides
|
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Mechanisms of DMII drugs:
|
-Insulin secretagogues -Insulin resistance improvement -Carbohydrate absorption restriction -Hormone analogues
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PT adenoma treatment
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PT-ectomy
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Classes of drugs in obesity treatment
|
Amphetamine-like appetite suppresants
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Amphetamine-like appetite suppresants
|
Sibutramine
|
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GI Lipase Inhibitor
|
Orlistat
|
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Cannibinoid Antagonist
|
Rimonabant
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Sibutramine mechanism
|
Inhibits NE
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Sibutramine side effects
|
tachycardia
|
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Phentermine's difference from Sibutramine
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NE re-uptake inhibition mostly
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Orlistat's mechanism
|
GI Lipase inhibitor
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Orlistat side effects
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Diarrhea
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Rimonabant mechanism
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Selective blockade of endocannibinoid CB1 receptor
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Rimonabant side effects
|
Nausea
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Treatment for adrenal adenoma
|
Surgery
|
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Treatment for bilateral adrenal hyperplasia
|
Spironolactone or Eplerenone (aldosterone receptor antagonist)
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Treatment of FHH
|
not surgery
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Treatment of hypothyroidism
|
L-thyroxine replacement
|
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Why are 1st generation sulfonylureas rarely used today?
|
Long half lives and increased risk for hypoglycemia
|
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Name the 1st generation sulfonylureas
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Chlorpropamide
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Name the second and third generation sulfonylureas
|
G--ide: Glybur-ide
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Name the meglitinides
|
glinide: Repa-glinide
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Side effects of sulfonylureas
|
Hypoglycemia
|
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Name the major biguanide
|
Metformin
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Name the thiazolidinediones
|
Glitazones: Rosi-glitazone
|
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Sites and actions of metformin
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Liver: decreases gluconeo. Peripheral tissues: Increases glucose uptake
|
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Side effects of metformin
|
GI cramping diarrhea anorexia metallic taste
|
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Side effects of TZDs (thiazolidinediones)
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Fluid retention
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Sites and action of TZDs
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Muscle and fat: enhances glucose uptake
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Name the alpha-glucosidase inhibitors
|
Acarbose
|
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Sites and action of alpha-glucosidase inhibitors
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Small intestine: delays carb digestion and slows glucose absorption
|
|
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Side effects of alpha-glucosidase inhibitors
|
Flatulence
|
|
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Name the incretin mimetics
|
Exenatide
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Sites and action of incretin mimetics
|
Pancreas
|
|
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Side effects of exenatide
|
Nausea
|
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Name the amylin analogue
|
Pramlintide
|
|
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What are the sites and action of Pramlintide?
|
inhibits glucagon
|
|
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Side effects of Pramlintide
|
Weight loss
|
|
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DPP-IV inhibitors
|
-agliptin: sit-agliptin
|
|
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mechanism of sitagliptin
|
Inhibits DPP-IV
|
|
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Side effects of sitagliptin (so far)
|
URIs
|
|
|
Side effects of meglitinides
|
Hypoglycemia
|
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Class to use for LDL over 130 with moderate TG elevation.
|
Statins
|
|
|
Class to use for high TG
|
high-ish LDL
|
|
|
Class to use for raising HDL
|
Niacin
|
|
|
Thionamides: Mechanism
|
Inhibit TPO --> inhibit thyroid hormone synthesis
|
|
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Thionamides: Drugs
|
Prophylthiouracil (PTU) and Methimazole
|
|
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Thionamides: Side effects
|
agranulocytosis
|
|
|
ACTH (2nd messenger system?)
|
cAMP
|
|
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LH (2nd messenger system?)
|
cAMP
|
|
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FSH (2nd messenger system?)
|
cAMP
|
|
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TSH (2nd messenger system?)
|
cAMP
|
|
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ADH (V2 receptor)
|
cAMP
|
|
|
HCG (2nd messenger system?)
|
cAMP
|
|
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MSH (2nd messenger system?)
|
cAMP
|
|
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CRH (2nd messenger system?)
|
cAMP
|
|
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Calcitonin (2nd messenger system?)
|
cAMP
|
|
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PTH (2nd messenger system?)
|
cAMP
|
|
|
Glucagon (2nd messenger system?)
|
cAMP
|
|
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beta-1 and beta-2 receptors (2nd messenger system?)
|
cAMP
|
|
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GnRH (2nd messenger system?)
|
Phospholipase C (IP3/Ca2+)
|
|
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TRH (2nd messenger system?)
|
Phospholipase C (IP3/Ca2+)
|
|
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GHRH (2nd messenger system?)
|
Phospholipase C (IP3/Ca2+)
|
|
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Angiotensin II (2nd messenger system?)
|
Phospholipase C (IP3/Ca2+)
|
|
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ADH (V1 receptor) (2nd messenger system?)
|
Phospholipase C (IP3/Ca2+)
|
|
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Oxytocin (2nd messenger system?)
|
Phospholipase C (IP3/Ca2+)
|
|
|
alpha-1 receptors (2nd messenger system?)
|
Phospholipase C (IP3/Ca2+)
|
|
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Glucocorticoids (2nd messenger system?)
|
Nuclear Receptors
|
|
|
Estrogen (2nd messenger system?)
|
Nuclear Receptors
|
|
|
Progesterone (2nd messenger system?)
|
Nuclear Receptors
|
|
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Tesosterone (2nd messenger system?)
|
Nuclear Receptors
|
|
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Aldosterone (2nd messenger system?)
|
Nuclear Receptors
|
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1
|
25-D (2nd messenger system?)
|
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Thyroid hormones (2nd messenger system?)
|
Nuclear Receptors
|
|
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Insulin (2nd messenger system?)
|
Tyrosine Kinase
|
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IGF-1 (2nd messenger system?)
|
Tyrosine Kinase
|
|
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ANP (2nd messenger system?)
|
cGMP
|
|
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EDRF (2nd messenger system?)
|
cGMP
|
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NO (2nd messenger system?)
|
cGMP
|
|
|
Most common pituitary adenomas
|
-Non-secreting adenomas -Prolactinomas
|
|
|
POMC is the precursor of what hormone?
|
ACTH
|
|
|
Pituitary: Embryologic derivation from
|
Anterior Pituitary: Rathke's pouch Posterior: Part of brain
|
|
|
Secretion from anterior pituitary is dependent on what circulation
|
portal plexus
|
|
|
Transcription factors which have defects in hypopituitarism
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HESX-1: Septo-optic dysplasia
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Wolfram Syndrome: What else is it called? What is it due to? Genetic component? What is the syndrome?
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DIDMOAD
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General pituitary hormone effects from hypothalamus destruction
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elevation of PRL
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TRH (Where from? What kind of hormone? What does it do?)
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Hypothalamus
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CRH (Where from? What kind of hormone? What does it do?)
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Hypothalamus
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GnRH (Where from? What kind of hormone? What does it do?)
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Hypothalamus
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Somatostatin (Where from? What kind of hormone? What does it do?)
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Hypothalamus/delta cell of pancreas
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Dopamine (Where from? What kind of hormone? What does it do?)
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Hypothalamus
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GHRH (Where from? What kind of hormone? What does it do?)
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Hypothalamus
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TSH (Where from? What kind of hormone? What does it do?)
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Anterior Pituitary
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FSH (Where from? What kind of hormone? What does it do?)
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Ant. Pituitary
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LH (Where from? What kind of hormone? What does it do?)
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Ant. Pituitary
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GH (Where from? What kind of hormone? What does it do?)
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Anterior Pituitary
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Prolactin (Where from? What kind of hormone? What does it do?)
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Ant. Pituitary
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ACTH (Where from? What kind of hormone? What does it do?)
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Ant. Pituitary
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MSH (Where from? What kind of hormone? What does it do?)
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Ant. Pituitary
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Oxytocin (Where from? What kind of hormone? What does it do?)
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P. Pituitary
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ADH (Where from? What kind of hormone? What does it do?)
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Posterior pituitary
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T3 and T4 (Where from? What kind of hormone? What does it do?)
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Thyroid
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Calcitonin (Where from? What kind of hormone? What does it do?)
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Thyroid C-cells
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PTH (Where from? What kind of hormone? What does it do?)
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Parathyroid gland
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Cortisol (Where from? What kind of hormone? What does it do?)
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Ad. cortex
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Aldosterone (Where from? What kind of hormone? What does it do?)
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Adrenal cortex
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Dehydroepiandrosterone/androstenedione (Where from? What kind of hormone? What function?)
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Adrenal cortex
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Testosterone (Where from? What kind of hormone? What does it do?)
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Testes
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Estradiol (Where from? What kind of hormone? What does it do?)
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Ovaries/corpus luteum
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Insulin (Where from? What kind of hormone? What does it do (in a nutshell)? Approximate half-life?)
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Beta cells of pancreas
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Glucagon (Where from? What kind of hormone? What does it do?)
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Alpha cells of pancreas
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Progesterone (Where from? What kind of hormone? What does it do?)
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Ovaries/corpus luteum
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Common causes of hyperthyroidism
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-Graves disease -Toxic multinodular goiter -thyroxtoxic phase of subacute thyroiditis -toxic adenoma
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Do androgens lead to increased or decreased TBG?
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decreased
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Does Estrogen lead to increased or decreased TBG?
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increased
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Does acute hepatitis lead to increased or decreased TBG?
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increased
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Does hyperthyroidism lead to increased or decreased TBG?
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decreased
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Does hypothyroidism lead to increased or decreased TBG?
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increased
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Does liver failure lead to increased or decreased TBG?
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decreased
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Hashimoto's hypothyroiditis: Which gender is it more common in? Men
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women
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Hashimoto's thyroiditis: What kind of antibodies are visible?
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anti-thyroglobulin and anti-TPO
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Hashinmoto's thyroiditis: Strong familial component?
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Yes
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How common is hypothyroidism?
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very common
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How does the thyroid receptor work in the nucleus?
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Binds to DNA and activates or represses transcription (depending on whether or not T3 is boud.)
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How is serum thyroglobulin used?
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It is leaked when there is a high amount of thyroid being produced. So it's a tumor marker for thyroid cancer
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Hypothyroidism: Cardiovascular
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Bradycardia
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Hypothyroidism: Ear
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Nose
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Graves Disease: AKA
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Diffuse Toxic Goiter
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Toxic MNG: Findings
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Level of circulating thyroid hormones mild compared to Graves. Symptoms similar to Graves (CV and muscular) but less evident
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Toxic MNG: Labs
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TSH suppressed. T4 and T3 upper range of normal/marginally elevated. I-123/T99m hot and cold nodules
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Subacute thyroiditis: etiology
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Hyperthyroid phase only. Destruction of thyroid gland in the setting of autoimmune illness --> release of thyroid hormone
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Subacute thyroiditis: Dx
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Very low I-123 uptake
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Subacute thyroiditis: Treatment
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Supportive
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Toxic Adenoma: etiology
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single hyperfunctioning follicular thyroid adenoma
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Hyperthyroidism: Signs and symptoms (except ocular)
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Weight loss
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Hyperthyroidism: Therapy
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Beta blockers (adrenergic symptoms)
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Hypothyroidism: GI
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Reduced appetite and intestinal peristalsis
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Hypothyroidism: Hematologic
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mild normochromic normocytic anemia
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Hypothyroidism: Nervous system
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Cretinism if during birth
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Hypothyroidism: Neuromuscular
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Stiffness
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Hypothyroidism: Ocular findings
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Baggy swelling of upper and lower eyelids
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Hypothyroidism: Pulmonary
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Dyspnea
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Hypothyroidism: Skeleton
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Lack of growth (due to synergistic effects of T4 and growth hormone)
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Hypothyroidism: Skin findings
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Dry rough
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Hypothyroidism: Which drugs cause it?
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Lithium
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Method of differentiating between common causes of hyperthyroidism
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Radioactive iodine uptake( Graves: high
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Most common causes of hypOthyroidism
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Thyroiditis -Hashimoto's -Subacute
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Most important thyroid function test
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TSH
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Small changes on (T4
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TSH) produce big changes on (T4
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Subacute thyroiditis: What's important?
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Starts with a hyperthyroid phase and then moves to hypothyroid phase
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T or F: Mild hypothyroidism during pregnancy does not affect fetal development
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False. Adverse effects on development.
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T4
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normal value
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Three types of hyperthyroidism
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Primary Secondary Exogenous
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Thyroid: Resistance - Where does it come from
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Mutation in Thyroid nuclear receptor gene
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Type of imaging to assess thyroid function
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Nuclear imaging
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Type of imaging to assess thyroid structure
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Ultrasound
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What does it mean for a nodule in the thyroid gland to be to be "cold"?
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There is no activity in the nodule but there is activity in the surrounding tissue.
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What does it mean for a nodule in the thyroid gland to be to be "hot"?
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There is no activity in surrounding tissue
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What does it mean for a nodule in the thyroid gland to be to be "warm"?
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It has as much activity as surrounding tissue.
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What does total T4 measure?
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free and bound T4
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What is myxedema coma?
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End stage of severe long-standing hypothyroidism. Weakness
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Myxedema treatment
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supportive therapy (IV
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Hyperthyroidism: Common causes
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Graves' disease
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Graves disease: Familial component?
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Yes
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Graves' Disease: Basic defect
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HLA-related organ specific defect
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Graves disease: Signs and symptoms
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High circulating thyroid
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Graves opthalmopathy: signs and symptoms
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periorbital edema
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Hyperthyroidism: Ocular symptoms
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Lid retraction
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Graves disease: Labs and tests.
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High T4 and T3
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Graves Disease: Antibody to what?
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TSH receptor
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