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53 Cards in this Set

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Pseudohyponatremia

for every 100mg/dL glucose is above 100 --> reduces serum Na by 1.6




someone with DKA with high glucose will have low Na

Insulin and lipase

insulin normally inhibits lipase




lipase releases fatty acids that are converted to acetyl CoA, which are converted to ketone bodies in the liver




dont usually see DKA in DM2 bc you have insulin production but there is insulin resistance

Glucagon and epinephrine

stimulate gluconeogenesis in liver




w/o insulin, glucagon and epinephrine are increased

Fluid management in DKA

give insulin bolus then start with NS + insulin drip




once glucose becomes <250, continue insulin drip but switch to D5 1/2 NS




cont insulin drip until anion gap becomes normal then give subq insulin & continue to maintain on subq insulin

Long term tx for DM1

long acting basal insulin administered once a day




ultra short acting insulin prior to meals

Target glucose for DM1

fasting and pre-meal target of 80-130




postprandial levels <180




HgA1c <7%

Hyperosmolar hyperglycemic non-acidodic syndrome

occurs in DM2




new onset may be presentation of acute coronary syndrome w/no chest pain bc of autonomic neuropathy




all pts with HHNS should get an EKG




tx with fluids, insulin

Secondary causes of DM

Cushing's syndrome




exogenous steroid administration




meds (thiazides, phenytoin, pentamidine)




CF




chronic pancreatitis

Prevention of microvascular vs macrovascular complications of DM2

Microvascular:


glucose control --> low HgA1c




Macrovascular:


BP and cholesterol control NOT glucose control


Ppx with anti-plt agents

Metformin vs sulfonylureas

metformin reduces gluconeogenesis so DOES NOT affect insulin levels




sulfonylureas increase insulin production so can lead to hypoglycemia and weight gain

Testing for DM2

all DM2 pts should be on statin with annual lipid profile




urine should be checked for microalbumin annually --> with microalbumin, should start ACEI or ARB




annual dilated eye and foot exam




annual influenza vaccine




one-time pneumococcal vaccine (only if 1st dose was given <65 yo & >5 yrs ago)

Hypercalcemia DDx

primary hyperparathyroidism (most common)




malignancy (older pts)




sarcoidosis




familial hypocalciuric hypercalcemia




hyperthyroidism




meds (eg thiazides,lithium)




immobile pts

Primary hyperthyroidism

find an elevated PTH




tx with parathyroidectomy in young & pts with Sxs (eg kidney stones)




main concern is progressive bone loss, increased risk of fractures, & recurrent kidney stones

Acute management of hypercalcemia

when Ca >12 manage acutely




when Ca >15-16 is an emergency




replace with NS to restore the GFR and promote Ca excretion (3-6L/day)




after fluids, give furosemide (increases Ca excretion)




if fluids dont work or with CNS involvement, give calcitonin and bisphosphonates (eg pamidronate or zoledronic acid)




dialysis can be used if hypercalcemia is life threatening

DDx for hypothyroid

Hashimoto's dz (most common) --> can be assoc with other autoimmune dz (eg pernicious anemia, vitiligo, DM, adrenal insuff)


assoc with anti-microsomal Abs




secondary hypothyroid --> hypopituitarism




iatrogenic cause (radioactive iodine, postablative surg)




iodine deficiency




medications (eg lithium, acetylsalicylic acid)

Hypothyroid TSH levels

TSH --> normal means no thyroid dz


high in primary hypothyroid


low in secondary hypothyroid




Free T4 --> metabolically active T4


low in primary & secondary hypothyroid

Classic signs of hypothyroid

diastolic HTN




delayed relaxation phase of DTR




pseudodementia in elderly




weight gain, cold intolerance, feeling tired, dry skin, puffy face




tx with thyroxine

Thyroxine and CAD

do angioplasty or CABG PRIOR to treating with thyroxine




thyroxine can cause anginal pain so bc difficult to distinguish btwn CAD and thyroxine tx

DDx for hyperthyroid

Grave's dz




toxic multinodular/nodular goiter




subacute thyroiditis




factitious hyperthyroid

Toxic multinodular/nodular goiter

hyperthyroid state that normally p/w cardiac manifestations as opposed to Graves

Subacute thyroiditis

DO NOT have exothalmos & usually present with subtle Sxs




painful thyroid enlargement




normal course is hyperthyroid --> hypothyroid --> euthyroid

Hyperthyroid TSH levels

Primary hyperthyroid:


TSH is low


free T4 is high

Radioactive iodine uptake scan

if TSH levels are c/w with primary hyperthyroid, next step is 24 hr radioactive iodine uptake scan




allows for assessment of metabolic activity of thyroid gland




graves dz: diffusely high




nodular goiter: regionally high




thyroiditis: low




factitious hyperthyroid: normal - low

Tx of Grave's dz

b-blocker




anti-thyroid drugs (eg propylthiouracil or methimazole)




once euthyroid --> radioactive iodine ablation that can lead to hypothyroid




do surgery instead of radio-ablation when:


pregnancy


children


obstruction of tracheal compression

Grave's dz Ab

Thyroid-stimulating immunoglobulins (TSI) --> anti-TSH receptor antibodies




bc metabolically more active, may hear a bruit bc of increased vascular supply

Cushing syndrome w/u

24hr free cortisol excretion (gold standard) --> cumbersome so may not be done




o/n 1mg dexamethasone suppression test & check cortisol in AM (good NPV) but if positive then have to do 24hr free cortisol




midnight salivary cortisol measurement (bc this is when cortisol is lowest)




after confirmation of Cushings syndrome:


plasma ACTH


MRI pituitary gland

Reasons for increased cortisol

pituatary lesion




small cell lung cancer




adrenal adenoma (only type where ACTH will be suppressed)

Cushing's syndrome Sxs

truncal obesity


moon facies


dorsocervical fat pad


skin changes such as striae, acne, and bruising


osteopenia


neuropsychiatric Sxs


menstrual irregularities


impotence


new onset DM

Cushing's syndrome and electrolytes

increased mineralocorticoid activity leads to increased secretion of K+ and H+ so leads to metabolic alkalosis with hypokalemia




can also increase BP




mimics aldosteronism but aldosterone is NOT increased

Cortisol effect on metabolism

increases hepatic gluconeogenesis --> hyperglycemia --> increases insulin secretion --> insulin increases storage of fat leading to weight gain & obesity

High dose dexamethasone suppression

can suppress Cushing's syndrome due to pituitary adenoma

HTN with orthostasis

indicates there is volume depletion even in the presence of HTN




think about pheochromocytoma

Causes of secondary HTN

pheochromocytoma




primary aldosteronism




Cushings syndrome




renal artery stenosis

HTN in pheochromocytoma

phenoxybenzamine (a-blocker) is a good choice




DO NOT USE B-BLOCKER


contraindicated bc alpha receptors are uninhibited that could actually rise BP further

Pheochromocytoma w/u

24 hr urine for catecholamines/vanillylmandelic acid (gold standard)




plasma free metanephrines




if positive, then do CT to localize the lesion (90% in adrenal)




if not in abdomen & to check for metastasis --> MIBG scan to identify extra-adrenal tumor




tx with surgical removal

Classic presentation for pheochromocytoma

headache


sweating


palpitations/tachycardia


anxiety attacks


HTN

MEN types

MEN type 1- pituitary adenoma, parathyroid, pancreatic (PitParPan) --> MEN1




MEN type 2a- parathyroid, medullary thyroid, pheochromocytoma (PheoMedPar) --> RET




MEN type 2b- neuroma, medullary thyroid, pheochromocytoma (NeuMedPheo) --> RET

Goal of DM care

HbA1c <6.5-7%




fasting glucose <126

DM drug management

metformin --> metformin + sulfonylurea (eg glipazide, glyburide) --> metformin + sulfonylurea + glitazone --> metformin + sulfonylurea + glitazone + insulin

Metformin and renal failure

avoid bc can lead to lactic acidosis

Glitazones

eg pioglitazone




assoc with cardiac events so avoid in cardiac pts and renal pts




lower glucose by sensitizing cells to insulin




not very effective as single agent so almost always use in combination




can cause edema and weight gain




lower triglycerides but increase LDL and HDL

Earliest sign of diabetic nephropathy

microalbuminuria (most sensitive test)




should be done at least once/yr




microalbuminuria >30mg/d should be started on ACEI --> slows diabetic nephropathy

Ddx for galactorrhea

prolactinoma




hypothyroid (high levels of TSH activates prolactin)




pregnancy




medications (eg haloperidol)




inhibition of dopamine leads to increase in prolactin

w/u prolactinoma

prolactin level




TSH




pregnancy test




if prolactin level is elevated and others are normal --> MRI to localize tumor

Tx of prolactinoma

dopamine agonists (eg cabergoline or bromocriptine but cabergoline is preferred)




monitor prolactin levels

Adrenal insufficiency

leads to hyponatremia & hyperkalemia (no aldosterone)




hypotension




weakness




orthostasis




hyperpigmentation (bc ACTH is secreted along with melanocyte stimulating hormone)




can also cause eosinophilia

w/u for adrenal insufficiency

cosyntropin/ACTH stimulation test (gold standard that tests for increase in cortisol level after stimulation) --> reduced in both primary and secondary adrenal insuff (but secondary insuff do not have hyperpigmentation bc ACTH is low)




HIV test




TB testing (esp if there is scarring in adrenals)




CT w/contrast of adrenals

Tx of adrenal insufficiency

hydrocortisone and fludrocortisone (if mineralocorticoids/aldosterone are missing) for life

Secondary adrenal insufficiency

occurs with Sheehan's syndrome, hemochromatosis, pituitary apoplexy




LH, FSH, GH, TSH are low




NO HYPERPIGMENTATION




hypotension and hyperkalemia is uncommon




tx with hydrocortisone

Pituitary apoplexy

Endocrine emergency




bleeding into or impaired blood supply of the pituitary




normally will have hx of pituitary adenoma




emergent CT w/o contrast to distinguish btwn subarachnoid bleed




best imaging is MRI but initial imaging is CT

Presentation of pituitary apoplexy

most common initial sx is a sudden headache



assoc with blurry vision



oculomotor nerve (CNIII) is predominantly affected leading to ptosis



some also have neck stiffness & photophobia w/o fever

Tx of pituitary apoplexy

initiate hormone replacement with hydrocortisone and levothyroxine




IV fluids to stabilize BP




neurosurg consultation

Pituitary apoplexy and emergent hormonal effects

decreased ACTH --> lowers cortisol --> adrenal crisis (addison's crisis) --> hypotension and hypoglycemia --> can be life threating




lack of cortisol is most important effect so must replace with hydrocortisone




hyponatremia can also be very severe bc of inappropriate ADH --> restrict fluid intake