Flashcards in Endocrinology Deck (51):
What are the criteria for making a diagnosis of DM?
(i) Fasting BG > 126
(ii) Random BG > 200 with symptoms
(iii) A1C > 6.5%
(iv) Abnormal 2hr glucose tolerance test
If diet, exercise, and metformin fail for treating T2DM what is your next treatment option?
What are two scenarios in which metformin is contraindicated?
Patient has renal insuffiency (risk of lactic acidosis)
Patient inpatient and receiving contrast agents
What are the adverse effects of sulfonylureas (e.g. glipizide, glyburide)?
Weight gain (due to insulin release)
Gliptins are what class of agents? How do they work?
Promote insulin release and block glucagon release
How do thiazolidinediones work (e.g. rosglitazone and pioglitazone)? In what situations do you want to avoid their use?
Increase peripheral insulin sensitivity
Avoid in CHF
Acarbose and miglitol are what type of agents? What side effects do they have and why?
Alpha-glucosidase inhibitors which block the absorption of glucose in the GI tract which can lead flatulence and diarrhea
Nateglinide and reapaglinide are what type of medicaiton?
Insulin secretagogues. Similar to sulfonylureas by promoting insulin secretion
SGLT inhibitors such as canagliflozin and dapagagliflozin have what side effects?
May cause UTIs
What is the best initial test for DKA?
What are lab findings of DKA?
AG metabolic acidosis
Hyperkalemia (but systemically deplete of K)
Acetone, acetoacetate, and beta hydroxybutyrate
Acidosis generally leads to what potassium disturbance? Why?
Te reverse is true for alkalosis.
Hyperkalemia. Cells begin taking in H+ in exchange for K+
What is the best way to initially manage the patient with DKA (i.e. labs and treatment)?
Order labs and ABG quickly and start bolus of normal saline. Once confirmed hyperglycemia then start insulin drip. Monitor the K+ and watch to see if it is going down and once so then begin repleting K+
What is goal BP in DM?
What is the LDL goal in DM patient? What if they have CAD too?
How do you treat DM proliferative retinopathy?
If fails then VEGF inhibitors like bevacizumab
If patients with microscopic proteinuria and DM what should they be started on?
In patients with DM neuropathy how should they be treated?
Gabapentin or pregabalin
Why does DM lead to gastroparesis?
What agents can be used to help?
Basically neuropathy of GI tract and impaired stretch receptors which causes impaired motility
Erythromycin promotes release of motilin
Metoclopramide (D2 R antagonist; mixed effect at 5HT R)
What are the radioactive iodine uptake levels in:
Silent thyroiditis: low
Subacute thyroiditis: low
Pituitary adenoma: elevated
Tx for subacute thyroiditis
Aspirin for pain
Tx for Graves disease
Radioactive iodine ablation
Separation from the nail from the nail bed may be a sign of what disease?
Graves disease, called onycolysis
What is silent thyrioditis? What Abs may be present?
Nontender gland with hyerthyroidism (auotimmune process) caused by leaking of thyroid hormone. Radioactive iodine uptake is normal/low. Thyroid peroxidase and antithyroglobulin antibodies may be present
Atrophy of the thyroid gland with elevated T4 suggests ....
Exogenous thyroid hormone supllementation
What are treatments for a thyroid storm?
How should you evaluate a solitary thyroid nodule?
Fine Needle Aspiration
Most common cause of hypercalcemia in outpatients
What are the effects of PTH?
Increased calcium release from bone
Increased calcium reabsorption from distal renal tubule
Increased phosphate excretion
Activation of vitamin D
What are signs and symptoms of acute, severe hypercalcemia?
Kidney stones/renal insufficiency/ATN
What is the treatment protocol for severe hypercalcemia?
2) Bisphosphonates (take a while to work)
3) Furosemide diuretic
5) Steroids if granulomatous disease
What ion disturbance may cause hypocalcemia?
Hypomagnnesia (Mg needed to release PTH from the gland)
What is pseudohyperparathyroidism? How does it present?
High PTH but low Ca due to PTH resistance
Short fourth finger, round face, mental retardation
What do calcium level perturbations do to QT length?
Hypercalcemia shortens QT
Hypocalcemia lengthens QT
What is the only cause of Cushing Syndrome which is suppressed by high dose dexamethasone?
What acid/base disturbance does excess cortisol lead to?
Metabolic alkalosis due to loss of hydrogen ions at late distal/early collecting duct
What is the best initial diagnostic test in a patient with elevated ACTH causing Cushing syndrome? What is the best test to follow-up with?
1mg overnight dexamethasone suppression testing. If abnormal and there is not suppression of morning release of cortisol then do a 24 hr urine cortisol
What metabolic and lab values are seen in patients with Addison's disease?
Mild metabolic acidosis
Besides a CT scan of the adrenal gland what is the best test for diagnosing Addison's disease?
Cosyntropin stimulation test: artifiical ACTH is given and should elevate cortisol release, if not then suggestive of Addison's disease
Tx of Addison's disease patients
Steroids followed by prednisone once stable
What acid base disturbance do patients with hyperaldosteronism have?
How does mgmt of hyperaldosteronism differ if a solitary adenoma is present vs hyperplasia?
Solitary adenoma: surgical resection
What is the most accurate test to find metastatic disease associated with pheochromocytoma?
MIBG scan (nuclear scan)
What is the tx of pheochromocytoma in the correct order?
Phenoxybenzamine first to control BP and then give propranolol afterwards. Next is surgical/laparoscopic resection.
All forms of CAH have what changes to steroid levels?
Low aldosterone and low cortisol levels
The three different kinds of CAH can be differentiated based on presence/absence of HTN and virilization. Explain and distinguish.
21-hydroxylase: Hypotensive and virilization (due to low aldosterone and high T)
17-hydroxylase: HTN and no virilization (low T)
11-hydrooxylase: HTN and virilization
Increased 17-hydroxyprogesterone levels are indicative of ....
21 hydroxylase deficiency
What effect does TRH have on PRL?
TRH increases release of PRL
(Hypothyroidism then may increase PRL levels)
What is the best initial test for dx of acromegaly?
If you give glucose to a patient with acromegaly what effect should this have on GH release?
There won't be any suppression of GH release