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Step 3 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the criteria for making a diagnosis of DM?

A

(i) Fasting BG > 126
(ii) Random BG > 200 with symptoms
(iii) A1C > 6.5%
(iv) Abnormal 2hr glucose tolerance test

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2
Q

If diet, exercise, and metformin fail for treating T2DM what is your next treatment option?

A

Sulfonylurea

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3
Q

What are two scenarios in which metformin is contraindicated?

A

Patient has renal insuffiency (risk of lactic acidosis)

Patient inpatient and receiving contrast agents

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4
Q

What are the adverse effects of sulfonylureas (e.g. glipizide, glyburide)?

A

Weight gain (due to insulin release)
SIADH
Hypooglycemia

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5
Q

Gliptins are what class of agents? How do they work?

A

DPP-IV inhibitors

Promote insulin release and block glucagon release

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6
Q

How do thiazolidinediones work (e.g. rosglitazone and pioglitazone)? In what situations do you want to avoid their use?

A

Increase peripheral insulin sensitivity

Avoid in CHF

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7
Q

Acarbose and miglitol are what type of agents? What side effects do they have and why?

A

Alpha-glucosidase inhibitors which block the absorption of glucose in the GI tract which can lead flatulence and diarrhea

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8
Q

Nateglinide and reapaglinide are what type of medicaiton?

A

Insulin secretagogues. Similar to sulfonylureas by promoting insulin secretion

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9
Q

SGLT inhibitors such as canagliflozin and dapagagliflozin have what side effects?

A

May cause UTIs

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10
Q

What is the best initial test for DKA?

A

Serum bicarbonate

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11
Q

What are lab findings of DKA?

A

AG metabolic acidosis
Hyperkalemia (but systemically deplete of K)
Hyperglycemia
Acetone, acetoacetate, and beta hydroxybutyrate

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12
Q

Acidosis generally leads to what potassium disturbance? Why?

Te reverse is true for alkalosis.

A

Hyperkalemia. Cells begin taking in H+ in exchange for K+

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13
Q

What is the best way to initially manage the patient with DKA (i.e. labs and treatment)?

A

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+

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14
Q

What is goal BP in DM?

A
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15
Q

What is the LDL goal in DM patient? What if they have CAD too?

A

LDL

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16
Q

How do you treat DM proliferative retinopathy?

A

Laser photocoagulation

If fails then VEGF inhibitors like bevacizumab

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17
Q

If patients with microscopic proteinuria and DM what should they be started on?

A

ACEi

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18
Q

In patients with DM neuropathy how should they be treated?

A

Gabapentin or pregabalin

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19
Q

Why does DM lead to gastroparesis?

What agents can be used to help?

A

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)

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20
Q 
What are the radioactive iodine uptake levels in:
Graves disease
Silent thyroiditis
Subacute thyroiditis
Pituitary adenoma
A

Graves: elevated
Silent thyroiditis: low
Subacute thyroiditis: low
Pituitary adenoma: elevated

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21
Q

Tx for subacute thyroiditis

A

Aspirin for pain

22
Q

Tx for Graves disease

A

PTU/Methimazole
Radioactive iodine ablation
Propranolol

23
Q

Separation from the nail from the nail bed may be a sign of what disease?

A

Graves disease, called onycolysis

24
Q

What is silent thyrioditis? What Abs may be present?

A

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

25
Q

Atrophy of the thyroid gland with elevated T4 suggests ….

A

Exogenous thyroid hormone supllementation

26
Q

What are treatments for a thyroid storm?

A

Iodine
PTU/Methimazole
Dexamethasone
Propranolol

27
Q

How should you evaluate a solitary thyroid nodule?

A

Fine Needle Aspiration

28
Q

Most common cause of hypercalcemia in outpatients

A

Primary hyperparathyroidism

29
Q

What are the effects of PTH?

A

Increased calcium release from bone
Increased calcium reabsorption from distal renal tubule
Increased phosphate excretion
Activation of vitamin D

30
Q

What are signs and symptoms of acute, severe hypercalcemia?

A 
Confusion
Kidney stones/renal insufficiency/ATN
Short QT
Constipation
Polyuria/polydipsia
31
Q

What is the treatment protocol for severe hypercalcemia?

A

1) Hydration
2) Bisphosphonates (take a while to work)
3) Furosemide diuretic
4) Calcitonin
5) Steroids if granulomatous disease

32
Q

What ion disturbance may cause hypocalcemia?

A

Hypomagnnesia (Mg needed to release PTH from the gland)

33
Q

What is pseudohyperparathyroidism? How does it present?

A

High PTH but low Ca due to PTH resistance

Short fourth finger, round face, mental retardation

34
Q

What do calcium level perturbations do to QT length?

A

Hypercalcemia shortens QT

Hypocalcemia lengthens QT

35
Q

What is the only cause of Cushing Syndrome which is suppressed by high dose dexamethasone?

A

Pituitary adenoma

36
Q

What acid/base disturbance does excess cortisol lead to?

A

Metabolic alkalosis due to loss of hydrogen ions at late distal/early collecting duct

37
Q

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?

A

1mg overnight dexamethasone suppression testing. If abnormal and there is not suppression of morning release of cortisol then do a 24 hr urine cortisol

38
Q

What metabolic and lab values are seen in patients with Addison’s disease?

A

Mild metabolic acidosis
Hyperkalemia
Hyponatremia

39
Q

Besides a CT scan of the adrenal gland what is the best test for diagnosing Addison’s disease?

A

Cosyntropin stimulation test: artifiical ACTH is given and should elevate cortisol release, if not then suggestive of Addison’s disease

40
Q

Tx of Addison’s disease patients

A

Steroids followed by prednisone once stable

Fludrocortisone

41
Q

What acid base disturbance do patients with hyperaldosteronism have?

A

Metabolic alkalosis

42
Q

How does mgmt of hyperaldosteronism differ if a solitary adenoma is present vs hyperplasia?

A

Solitary adenoma: surgical resection

Hyperplasia: spironolactone

43
Q

What is the most accurate test to find metastatic disease associated with pheochromocytoma?

A

MIBG scan (nuclear scan)

44
Q

What is the tx of pheochromocytoma in the correct order?

A

Phenoxybenzamine first to control BP and then give propranolol afterwards. Next is surgical/laparoscopic resection.

45
Q

All forms of CAH have what changes to steroid levels?

A

Low aldosterone and low cortisol levels

46
Q

The three different kinds of CAH can be differentiated based on presence/absence of HTN and virilization. Explain and distinguish.

A

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

47
Q

Increased 17-hydroxyprogesterone levels are indicative of ….

A

21 hydroxylase deficiency

48
Q

What effect does TRH have on PRL?

A

TRH increases release of PRL

Hypothyroidism then may increase PRL levels

49
Q

What is the best initial test for dx of acromegaly?

A

IGF1 levels

50
Q

If you give glucose to a patient with acromegaly what effect should this have on GH release?

A

There won’t be any suppression of GH release

51
Q

Besides surgical mgmt, what medication may help control acromegaly?

A

Octreotide (SST analog)

Step 3 (19 decks)

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