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332 Cards in this Set

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