Snw's Internal Medicine- Endocrinology Review (Usmle Step 3)

Front 1

Pseudohyponatremia

Back 1

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

someone with DKA with high glucose will have low Na

Front 2

Insulin and lipase

Back 2

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

Front 3

Glucagon and epinephrine

Back 3

stimulate gluconeogenesis in liver

w/o insulin, glucagon and epinephrine are increased

Front 4

Fluid management in DKA

Back 4

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

Front 5

Long term tx for DM1

Back 5

long acting basal insulin administered once a day

ultra short acting insulin prior to meals

Front 6

Target glucose for DM1

Back 6

fasting and pre-meal target of 80-130

postprandial levels <180

HgA1c <7%

Front 7

Hyperosmolar hyperglycemic non-acidodic syndrome

Back 7

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

Front 8

Secondary causes of DM

Back 8

Cushing's syndrome

exogenous steroid administration

meds (thiazides, phenytoin, pentamidine)

CF

chronic pancreatitis

Front 9

Prevention of microvascular vs macrovascular complications of DM2

Back 9

Microvascular:

glucose control --> low HgA1c

Macrovascular:

BP and cholesterol control NOT glucose control

Ppx with anti-plt agents

Front 10

Metformin vs sulfonylureas

Back 10

metformin reduces gluconeogenesis so DOES NOT affect insulin levels

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

Front 11

Testing for DM2

Back 11

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)

Front 12

Hypercalcemia DDx

Back 12

primary hyperparathyroidism (most common)

malignancy (older pts)

sarcoidosis

familial hypocalciuric hypercalcemia

hyperthyroidism

meds (eg thiazides,lithium)

immobile pts

Front 13

Primary hyperthyroidism

Back 13

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

Front 14

Acute management of hypercalcemia

Back 14

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

Front 15

DDx for hypothyroid

Back 15

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)

Front 16

Hypothyroid TSH levels

Back 16

TSH --> normal means no thyroid dz

high in primary hypothyroid

low in secondary hypothyroid

Free T4 --> metabolically active T4

low in primary & secondary hypothyroid

Front 17

Classic signs of hypothyroid

Back 17

diastolic HTN

delayed relaxation phase of DTR

pseudodementia in elderly

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

tx with thyroxine

Front 18

Thyroxine and CAD

Back 18

do angioplasty or CABG PRIOR to treating with thyroxine

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

Front 19

DDx for hyperthyroid

Back 19

Grave's dz

toxic multinodular/nodular goiter

subacute thyroiditis

factitious hyperthyroid

Front 20

Toxic multinodular/nodular goiter

Back 20

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

Front 21

Subacute thyroiditis

Back 21

DO NOT have exothalmos & usually present with subtle Sxs

painful thyroid enlargement

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

Front 22

Hyperthyroid TSH levels

Back 22

Primary hyperthyroid:

TSH is low

free T4 is high

Front 23

Radioactive iodine uptake scan

Back 23

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

Front 24

Tx of Grave's dz

Back 24

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

Front 25

Grave's dz Ab

Back 25

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

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

Front 26

Cushing syndrome w/u

Back 26

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

Front 27

Reasons for increased cortisol

Back 27

pituatary lesion

small cell lung cancer

adrenal adenoma (only type where ACTH will be suppressed)

Front 28

Cushing's syndrome Sxs

Back 28

truncal obesity

moon facies

dorsocervical fat pad

skin changes such as striae, acne, and bruising

osteopenia

neuropsychiatric Sxs

menstrual irregularities

impotence

new onset DM

Front 29

Cushing's syndrome and electrolytes

Back 29

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

Front 30

Cortisol effect on metabolism

Back 30

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

Front 31

High dose dexamethasone suppression

Back 31

can suppress Cushing's syndrome due to pituitary adenoma

Front 32

HTN with orthostasis

Back 32

indicates there is volume depletion even in the presence of HTN

think about pheochromocytoma

Front 33

Causes of secondary HTN

Back 33

pheochromocytoma

primary aldosteronism

Cushings syndrome

renal artery stenosis

Front 34

HTN in pheochromocytoma

Back 34

phenoxybenzamine (a-blocker) is a good choice

DO NOT USE B-BLOCKER

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

Front 35

Pheochromocytoma w/u

Back 35

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

Front 36

Classic presentation for pheochromocytoma

Back 36

headache

sweating

palpitations/tachycardia

anxiety attacks

HTN

Front 37

MEN types

Back 37

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

Front 38

Goal of DM care

Back 38

HbA1c <6.5-7%

fasting glucose <126

Front 39

DM drug management

Back 39

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

Front 40

Metformin and renal failure

Back 40

avoid bc can lead to lactic acidosis

Front 41

Glitazones

Back 41

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

Front 42

Earliest sign of diabetic nephropathy

Back 42

microalbuminuria (most sensitive test)

should be done at least once/yr

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

Front 43

Ddx for galactorrhea

Back 43

prolactinoma

hypothyroid (high levels of TSH activates prolactin)

pregnancy

medications (eg haloperidol)

inhibition of dopamine leads to increase in prolactin

Front 44

w/u prolactinoma

Back 44

prolactin level

TSH

pregnancy test

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

Front 45

Tx of prolactinoma

Back 45

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

monitor prolactin levels

Front 46

Adrenal insufficiency

Back 46

leads to hyponatremia & hyperkalemia (no aldosterone)

hypotension

weakness

orthostasis

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

can also cause eosinophilia

Front 47

w/u for adrenal insufficiency

Back 47

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

Front 48

Tx of adrenal insufficiency

Back 48

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

Front 49

Secondary adrenal insufficiency

Back 49

occurs with Sheehan's syndrome, hemochromatosis, pituitary apoplexy

LH, FSH, GH, TSH are low

NO HYPERPIGMENTATION

hypotension and hyperkalemia is uncommon

tx with hydrocortisone

Front 50

Pituitary apoplexy

Back 50

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

Front 51

Presentation of pituitary apoplexy

Back 51

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

Front 52

Tx of pituitary apoplexy

Back 52

initiate hormone replacement with hydrocortisone and levothyroxine

IV fluids to stabilize BP

neurosurg consultation

Front 53

Pituitary apoplexy and emergent hormonal effects

Back 53

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