Endocrine

Question 1

Causes of elevated CK

Answer 1

Hypothyroidism
Polymyositis, Dermatomyositis
Muscular dystrophies
Statins

Question 2

What type of insulin given to those with DKA?

Answer 2

Regular insulin.

Question 3

What mediates insulin resistance in overweight/obese individuals?

Answer 3

Serum FFA and TAG

FFA increase resistance by serine phosphorylation of insulin receptor and decrease insulin secretion.

Question 4

Treatment of congenital adrenal hyperplasia.

Answer 4

Exogenous corticosteroids to suppress ACTH.

Question 5

Central (complete vs. partial) vs. Peripheral DI

Answer 5

Central: > 10% rise in urine osmolality after vasopressin
Complete: > 50%

Question 6

What is used to treat graves opthalmopathy and how?

Answer 6

Glucorticoids (PTU and methimazole do NOT help)

Opthalmopathy develops bc of edema and infiltration of lymphocytes -> stimulate retroorbital fibroblasts to secrete cytokines and produce glycosaminoglycans -> inflam and accum of glycosaminoglycans -> proptosis.

Question 7

How to prevent absorption of radioactive iodide isotopes?

Answer 7

Administer Potassium Iodide - competitive inhibitor of the Na-iodide symporter.

Question 8

What glucose transporter is responsive to insulin and where is it located?

Answer 8

GLUT4 - on skeletal muscle and adipocytes

Question 9

How do glucocorticoids affect the liver vs. muscle/adipose tissue?

Answer 9

Liver - increase gluconeogenesis and glycogenesis.

Muscle/Adipose - antagonize insulin effects - proteolysis and lipolysis. to provide substrates for making glucose.

Question 10

Central DI - caused by damage to what?

Answer 10

Paraventricular and Supraoptic nuclei of the Hypothalamus

(Post pituitary injuries don’t result in permanent central DI since the hypothalamic neurons will hypertrophy to compensate)

Question 11

What causes the increased risk of gallstones in pregnant women or those on OCPs?

Answer 11

1. Estrogen induced cholesterol hypersecretion - increases HMG CoA reductase
2. Progesterone induced gallbladder hypomotility

Question 12

MOA of acarbose

Answer 12

alpha-glucosidase inhibitors - decrease activity of dissacharidases on intestinal brush border.

Question 13

What hormones are Gs?

Answer 13

Glucagon
TSH
PTH

cAMP -> protein kinase a.

Question 14

What paraneoplastic syndrome is associated with neuroblastoma?

Answer 14

Opsoclonus-Myoclonus.

Question 15

TNFalpha facilitates insulin resistance thru what mechanism?

Answer 15

Phosphorylation of serine residues.

This inhibits IRS-1 (insulin receptor substrate) tyrosine phosphorylation by insulin.

Question 16

Histology of Hashimoto’s thyroiditis?

Answer 16

Mononuclear parenchymal infiltration with well-developed germinal center

“looks like a lymph node”

Question 17

Electrolyte abnormalities in primary adrenal insufficiency?

Answer 17

HypoNa
HyperK
HyperCl
Non anion gap metabolic acidosis

(think like the aldo antagonist diuretics)

Question 18

In a patient on chronic glucocorticoids presenting with adrenal crisis s/p surgery, what are pt’s levels of CRH, ACTH, and cortisol?

Answer 18

Decreased CRH, ACTH, and cortisol!

Question 19

Thyroid hormone receptor is located where?

Answer 19

Nucleus!

Question 20

What should diabetics be advised to do to protect against peripheral neuropathy?

Answer 20

DAILY foot inspection
(changing socks, snug shoes, testing water first, etc)

YEARLY neurologic evaluation by physician.

Question 21

How are the following altered in DKA? 
Na
K 
pH
urine HCO3 
urine H2PO4

Answer 21

Hyponatremic:

• osmotic activity of glucose -> Na drops 1.6 mEq/L for every 100 mg/dL rise in glucose
• hyperglycemia induced osmotic diuresis -> Na and free water losses

HyperK:

• K/H exchanger
• but total body K loss

Metabolic Acidosis: Dec. pH

Urine:
Decreased HCO3 = reabsorbed

Increased H2PO4, NH4+: increased secretion of acid buffers (due to H+ secretion from the kidneys)

Hyperglycemia, Hypovolemic

Hyperammonemia: due to muscle degradation.

Question 22

Which antidiabetic drug increases GLUT4 transport to adipocytes?

Answer 22

Glitazones

activate PPARalpha -> increase transcription of insulin responsive genes -> GLUT4 translocation to cell membrane (adipocytes, skeletal muscle)

Question 23

Mech of acarbose

Answer 23

alpha-glucosidase inhibitor - inhibit intestinal brush border alpha-glucosidases - dec. postprandial hyperglycemia.

Tox: GI disturbance, hepatotoxic (miglitol)

Question 24

What are the GLP-1 analogs and DPP-4 inhibitors? Mech?

Answer 24

GLP1: exenatide, liraglutide
DPP-4 inhibitor: -gliptin (inhibit degradation of GLP1)

Mech: increase insulin, decrease glucagon release (in response to glucose, like physiologic), delay gastric emptying

Tox: (X) No hypoglycemia or weight gain (nl physiology)

• n/v
• pancreatitis
• mild urinary or resp infections

Question 25

During fasting, normoglycemic with higher than normal baseline insulin levels = what?

Answer 25

Insulin Resistance - DM II READ THE FUCKING GRAPHS.

Question 26

Labs in PCOS

Answer 26

High LH, LH/FSH ratio | Low to nl FSH - bc FSH is dec. compared to LH, can't aromatize the testos to estrogen.

Question 27

HOW DOES HYPOTHALAMUS REGULATE PROLACTIN?!

Answer 27

Dopamine INHIBITS Prolactin. Hypothalamic destruction => Hyperprolactin!

Question 28

What is the presentation of Type I DM?

Answer 28

Subacute with polyuria, polydipsia, polyphagia with weight loss and fatigue. Young adult, sometimes recent viral infection will be in picture.

Question 29

Histology of medullary thyroid cancer?

Answer 29

Polygonal or spindle shaped cells with extracellular amyloid deposits (stain with congo red)

Question 30

Glucagonoma

Answer 30

1. Diabetes 2. GI sx 3. Necrolytic Migratory Erythema: erythematous papules and plaques that coalesce, leaving bronze-colored central indurated area with peripheral blistering/scarring.

Question 31

Hyperthyroidism - what lab needs to be checked before treating?

Answer 31

PTU and Methimazole can cause agranulocytosis!!

Question 32

Papillary Thyroid Carcinoma - Histo findings

Answer 32

Orphan Annie nuclei (Large cells with finely dispersed chromatin) Psammoma Bodies Inclusion bodies and nuclear grooves

Question 33

Medullary Carcinoma Histo

Answer 33

Sheets of cells with amyloid stroma.

Question 34

Metyrapone test

Answer 34

Blocks 11b-hydroxylase (increases 11 deoxycorticosterone but this doesn't feedback negatively) -> dec cortisol -> increased ACTH -> increased 11 deoxycorticosterone, 17-OHS (its metabolite) if you have normal HPA axis.

Question 35

Pituitary Apoplexy - presentation, tx.

Answer 35

Intrapituitary hemorrhage, most often in an underlying pituitary adenoma. EMERGENCY. Sx: Chronic sx of pituitary adenoma (h/a, decreased libido) Acute severe headache, bitemporal hemianopsia Signs of meningeal irritation may be seen Will eventually develop cardio collapse due to ACTH deficiency and glucocorticoid deficiency. Tx: Glucocorticoids - prevent cardio collapse Surgery to decompress. Note: May have similarities to subarachnoid, but the hx of pit adenoma sx and acute cardiovascular collapse favor pit hemorrhage.

Question 36

Polyuria and Polydipsia - what 3 things should you immediately think of?

Answer 36

1. DM 2. DI 3. Psychogenic Polydipsia.

Question 37

Pathophysiology of Graves Proptosis/Opthalmopathy

Answer 37

Lymphocytes infiltrate orbital tissue -> secrete cytokines that activate fibroblasts -> secrete increasing amounts of glycosaminoglycans/hyaluronic acid -> draws water into orbit resulting in extraocular muscle edema. Can result in sensations of grittiness, tearing since the lids don't cover the eyes fully. Note: neutrophil infiltration would be in like orbital cellulitis.