Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

53 Cards in this Set

  • Front
  • Back


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)


chronic pancreatitis

Prevention of microvascular vs macrovascular complications of DM2


glucose control --> low HgA1c


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)


familial hypocalciuric hypercalcemia


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


anti-thyroid drugs (eg propylthiouracil or methimazole)

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

do surgery instead of radio-ablation when:



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


neuropsychiatric Sxs

menstrual irregularities


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


primary aldosteronism

Cushings syndrome

renal artery stenosis

HTN in pheochromocytoma

phenoxybenzamine (a-blocker) is a good choice


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




anxiety attacks


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


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


hypothyroid (high levels of TSH activates prolactin)


medications (eg haloperidol)

inhibition of dopamine leads to increase in prolactin

w/u prolactinoma

prolactin level


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)




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


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