Endocrine Knowledge

Front 1

Hyperthyroid Medications and Side Effects

Back 1

Methimazole/PPU: Methimazole is first line except in 1st trimester of pregnancy (Can cause aplasia cutis)

Both can cause Agranulocytosis and Liver Failure

Front 2

Labs for hypoglycemia

Back 2

C-peptide, ProInsulin, BMP, Sulfonlyurea/Meglitanide screen

**If patient already received glucagon or D50, C-peptide and ProInsulin are useless because insulin secretion is stiulated by glucagon or D50

Front 3

C-Peptide

Back 3

Liberated when Pro-Insulin is split into Insulin

Will be elevated in insulinoma, sulfonylurea use

Decreased with exogenous insulin, Type 1 DM

Front 4

Causes of Hypoglycemia

Back 4

Munchhausing, Fulminant Liver Failure, Renal Failure, Sepsis, CHF, Adrenal Insuff, Gastric Bypass

Front 5

Dumping Syndrome

Back 5

Occurs after gastric bypass when there is decreased transit time for food to be absorbed, but insulin still produced so you can get hypoglycemia

Early Dumping: Diarrhea

Late Dumping: Hypoglycemia (2-3 hours)

Tmnt: Dietary modification, limit carbs. If unsuccessful can use octreotide

Front 6

Whipple's Triad

Back 6

Hypoglycemic symptoms with documented low blood sugar and improvement in symptoms with glucose

Front 7

Causes of elevated Prolactin

Back 7

Dopamine Blockers (Antipsychotics)

Reglan

SSRI

Anti-Seizure Meds (Except Keppra)

Hypothyroidism

Renal Disease/Cirrhosis

Chest wall stimulation

Front 8

Stress Dose Steroids

Back 8

Hydrocortisone 100mg x 1

50mg q6 hours

Front 9

Sella Turcica

Back 9

Sits in sphenoid bone, below optic chiasm and above cavernous sinus

Front 10

Hyperaldosterone work up

Back 10

First need to check blood work. (Patient cannot be on Aldactone for at least 6 weeks. ACE/ARBs are ok because if renin levels are low on ACE/ARB can still diagnose)

Screen with plasma aldosterone/renin ratio. Levels > 20 are suggestive of Hyperaldosterone.

Also screen with serum aldosterone levels and renin levels. Ald. levels should be > 15 and renin levels should be undetectable (Or Low).

If positive, confirmatory tests are saline infusion, oral saline load, captopril load that all test for aldosterone suppresion.

Once diagnosed patients should have adrenal CT. If nodule is <10 hounsfield units and washout is < 50 (Indicating nodule is holding on to contrast) it's likely active.

If < 40 and there is strong evidence of one sided lesion, can go directly to surgery. If > 40 or there are bilateral nodules will need adrenal vein sampling first to figure out where the aldosterone is coming from

Front 11

Treatment of Hyperaldosterone

Back 11

1) Surgery

2) Spironolactone or Eplerenone

Front 12

HbA1c correlation with glucose

Back 12

HbA1c x 30 - 60

Front 13

PTH Dependent causes of Hypercalcemia

Back 13

Primary HyperParathyroidism

Familial Hypocalcuric hypercalcemia

malignancy of parathyroid gland (Will see an extremely elevated PTH level)

Front 14

PTH Independent causes of hypercalcemia

Back 14

PTHrP/malignancy (Any Squamous cell, renal cell)

***Non HODGKIn LYMPHOMA

Sarcoidosis

Multiple Myeloma

Pagets

Immobilization

Hyperthyroidism (Increased bone turnover)

Vitamin D toxicity

Thiazides

Front 15

Familial Hypocalcuric Hypercalcemia

Back 15

Autosomal dominant disorder (Inactivating mutation) affecting Calcium Sensing Receptors which lead to inappropriately normal or elevated levels of PTH. Completely benign and no treatment needed, but have to destinguish it from Primary Hyperparathyroidism if PTH is mid ot upper normal or mildly elevated by 24 hour Urinary Calcium collection.

If urinary calcium is elevated, it's most likely PHPT.

If urinary calcium is normal it's either Primary Hyperparathyroidism w/Vitamin D deficiency or FHH. Can replete Vitamin D and then check again (Vitamin D deficiency stimulates urinary reabsorption of Calcium)

If urinary Calcium is low it's PHPT w/Vit D deficiency vs FHH. Check Vitamin D level, if normal it's FHH. If low replete and recheck levels.

Front 16

Tertiary Hyperparathyroidism

Back 16

Occurs after longstanding secondary hyperparathyroidism where parathyroid gland undergoes hyperplasia, and autonomous secretion of PTH occurs which leads to hypercalcemia.

Usually seen in patients who were ESRD and received a transplant

Front 17

secondary hyperparathyroidism

Back 17

any condition assocaited with Low vitamin D levels (Kidney Disease, Vitamin D deficiency, malabsorption)

Front 18

synthesis of thyroid hormone

Back 18

Iodide enters the follicular cells with NIS (Na-Iodide symporter). Thyroid peroxidase then oxidises iodide and adds it to thyroglobulin. A coupling reaction then creates T4 or T3 (Depending on number of iodine molecules)

T4 is produced more than T3 and T3 is more potent than T4.

Deiodinase is involved in peripheral conversion of T4 to T3.