Endocrine disorders

Question 1

Diagnosing diabetes

Answer 1

Serum fasting glucose ≥ 126 on 2 occasions
A1c greater than 6.5-7
“impaired glucose tolerance”: fasting glucose 100-126
normal fasting glucose: 60-100
DM1- ketones in blood/urine

Question 2

Managing DM1

Answer 2

Baseline labs: ketones, diagnostic markers, lipid panel, EKG, renal studies, peripheral pulses and neuro, eye/foot exams
Dietary teaching: total carb intake 55-60 percent of diet
Insulin for ketones: 0.5 units/kg/day, 2/3 dose in AM and 1/3 in PM

Question 3

DM2: pathology, s/sx

Answer 3

• circulating insulin exists enough to prevent ketoacidosis but inadequate to meet patient’s insulin needs
• caused by either tissue insensitivity to insulin or insulin secretion defect
• S/sx: insidious onset, recurrent vaginitis, blurred vision, chronic skin infections, 3P’s (lesser extent than DM1)

Question 4

Management of DM2

Answer 4

Obtain baseline: lipid panel, check for ketones, renal studies, EKG, peripheral pulses and neuro, eye/foot exam
Dietary teaching: carbs 55-60 percent of diet
Early oral antidiabetics: first choice is Metformin

Question 5

Syndrome X

Answer 5

obesity, hypertension, abnormal lipids (low HDL, high triglycerides)

Question 6

Metabolic syndrome

Answer 6

Expansion of “Syndrome X”; positive for 3 of the following:

1. Waist circumference ≥ than 40 inches (102cm) in men, and ≥ 35 inches (89cm) in women
2. BP ≥ 130/85
3. triglycerides ≥ 150
4. Fasting blood glucose ≥ 100
5. HDL

Question 7

Sulfonylureas

Answer 7

Stimulate pancreas to release more insulin

glipizide, glimepiride, glyburide

Question 8

Biguanides

Answer 8

Metformin
standard of care for DM2
lactic acidosis is a potential side effect (presents with muscle pain)

Question 9

alpha glucosidase inhibitors

Answer 9

less glucose absorbed by gut

acarbose (precose) and miglitol (glyset)

Question 10

thiazolidinediones, or “glitazones”

Answer 10

rosiglitazone (avandia), pioglitazone (actos)
decrease gluconeogenesis
assoc. with possible HF or MI, therefore not widely used

Question 11

non-sulfonylurea insulin release stimulators

Answer 11

repaglinide (Prandin)

nateglinide (Starlix)

Question 12

Exenatide (Byetta)

Answer 12

injectable that mimics effects of incretins (signals pancreas to increase insulin secretion and stops gluconeogenesis)
may cause significant nausea, vomiting, diarrhea

Question 13

Symlin (pramlintide)

Answer 13

injectable for DM1 and DM2
slows glucose absorption and inhibits action of glucagons
promotes weight loss while decreasing blood glucose levels

Question 14

DD-4 inhibitor

Answer 14

Januvia (sitagliptin)

breaks down incretins (signal pancreas to increase insulin production, stops gluconeogenesis)

Question 15

Somogyi effect

Answer 15

common in Type 1
low sugar at 3am, refractory increase in BG for morning fasting check
tx: lower evening/HS insulin

Question 16

Dawn phenomenon

Answer 16

common in DM2
tissue desensitized to insulin nocturnally
slow increase in BG overnight to cause early AM hypoglycemia

Question 17

Hyperthyroidism

Answer 17

Grave’s disease is most common cause
TSH low, T3 elevated, serum ANA usually elevated without other cause
radioactive iodine uptake scan- high uptake consistent with Graves
MRI of orbits to visualize Grave’s ophthalmopathy
Tx: refer, propranolol for symptom relief, thiourea drugs (methimazole/tapazole, PTU/propylthiouracil), radioactive iodine, surgery
can lead to thyroid crisis

Question 18

Hypothyroidism

Answer 18

Hashimoto’s thyroiditis is most common cause
TSH elevated, T4 low
levothyroxine
can lead to myxedema coma

Question 19

Negative feedback loop for thyroid

Answer 19

Hypothalamus –> TRH –> anterior pituitary –> TSH –> thyroid –> T3 T4 –> Hypothalamus

Question 20

Cushings

Answer 20

too much cortisol (pituitary- ACTH hypersecretion, adrenal tumors, chronic steroids)
S/sx: obesity, moon face, buffalo hump, acne, hirsutism, HYPERTENSION, labile mood, amenorrhea, frequent infections
Lab: HYPERglycemia, HYPERnatremia, HYPOkalemia, elevated plasma cortisol in AM, dexamethasone suppression test to differentiate cause, serum ACTH
Tx: Refer

Question 21

Addison’s

Answer 21

deficient cortisol, androgens, and aldosterone
some causes: autoimmune destruction of adrenal gland, metastatin cancer, pituitary failure (decreased ACTH)
S/sx: hyperpigmentation in buccal mucosa and skin creases, diffuse tanning and freckles, HYPOTENSION, fever and change in LOC in acute cases
Lab: HYPOglycemia, HYPOnatremia, HYPERkalemia, elevated ESR, plasma cortisol

Question 22

DM1: pathology, s/sx

Answer 22

• assoc with HLA (human leukocyte antigens) and islet cell antibodies
• ketones, 3P’s, weight loss
• A1c may be normal on initial diagnosis