Endocrine

Question 1

Nonclassic Congenital Adrenal Hyperplasia

Answer 1

Decreased 21 Hydroxylase activity. Normal electrolytes, glucocorticoids and mineralocorticoids. Increased Androgens. Increased 17 hydroxyprogesterone.

Presents in teen years Hirsutism, severe acne, oligomenorrhea

DDx: PCOS & exogenous steroids (Both of these will have normal 17 OHP

Question 2

Central Precocious Puberty

Answer 2

Breast development, testicular enlargement, hair growth before the ages of 8/9. Advanced bone age. Central PP will have increased LH. Evaluation should include MRI to rule out pituitary pathology.
Tx; GnRH agonist (Leuprolide)

Question 3

Thyrotoxicosis subtypes

Answer 3

Increased Radio Iodine Uptake: Grave’s, Nodules

Decreased Radio Iodine Uptake: Hashimoto’s (silent), De Quervain’s, Post partum

Question 4

Hashimoto's Thyroiditis
Presentation
Labs
Complications
Tx

Answer 4

Decreased RAIU with increased T4 and decreased TSH. TPO antibodies present.
Can cause miscarriage, even if euthyroid
Usually, self-limiting, if symptomatic beta blockers are the first line.

Question 5

Mullerian agensis vs Androgen Insensitivity

Answer 5

Mullerian Agensis: Phenotypically female, no upper third of the vagina, no uterus, normal pubic and axillary hair

Androgen Insensitivity: Phenotypically female, no upper third of the vagina, no uterus, sparse pubic and axillary hair.

Question 6

Primary Adrenal Insufficiency Presentation

Answer 6

Weakness, weight loss, hyponatremia, hyperkalemia, low-normal cortisol levels

Question 7

Causes of Adrenal insufficiency

Answer 7

Most granulomatous diseases can cause it (TB, Sarcoidosis, Histo)

Question 8

Hyperosmolar hyperglycemic state

Answer 8

Normal anion gap and normal pH but glucose >1000, serum osmolality >320.
Causes an osmotic diuresis, which can leave the patient 8-10L down on fluids.
Tx: Aggressive rehydration with NS, insulin, careful monitoring of K levels.

Question 9

Cushing’s Syndrome Presentation

Answer 9

Obese, striae, proximal muscle weakness, HTN, glucose intolerance, skin hyperpigmentation.

Question 10

Subacute thyroiditis (de Quervain’s)

Answer 10

postviral, fever, hyperthyroid symptoms, enlarged and tender thyroid. Elevated ESR/CRP. Low RAIU

Question 11

Suppurative thyroiditis

Answer 11

tender thyroid without changes in thyroid hormone or tsh

Question 12

5a Reductase Deficiency

Answer 12

XY Genotype, impaired testosterone to DHT, impaired virilization during embryogenesis. Normal Male estrogen and testosterone levels.

Phenotypically female (no breast development), but testes are present. Will virilize during puberty.

Question 13

Causes of SIADH

Answer 13

CNS disturbance, Meds (Carbamazepine, SSRIs, NSAIDs), Lung disease, Small cell lung cancer, pain/nausea

Question 14

SIADH presentation and treatment

Answer 14

mild: nausea, forgetfulness
severe: seizures, coma
with euvolemia

Fluid restriction, salt tablets, hypertonic saline

Question 15

Evaluation of PP

Answer 15

Bone age first

Normal Bone Age: breast development only?: premature thelarche. Pubic hair development only” premature adrenarche.

Advanced Bone Age:

• High LH: Central PP
• Low LH: GnRH Stim test
  
  • High LH: Central PP
  • Low LH: PPP

Question 16

Euthyroid Sick Syndrome

Answer 16

Normal TSH and T4 but decreased T3 in the setting of acute illness. Thought to be due to decreased peripheral conversion of T4 to T3. Labs should be re-evaluated after the acute illness is over. Does not warrant immediate treatment.

Question 17

Causes of congenital hypothyroidism

Answer 17

Thyroid dysgenesis is the most common cause.

Problems with thyroid hormone synthesis are much rarer and all are autosomal recessive disorders.

All conditions should be treated with prompt thyroid hormone replacement to avoid neurologic damage.

Question 18

Cushing’s Evaluation

Answer 18

24hour urinary cortisol, late-night salivary cortisol, low dose dexamethasone suppression test. (2 must be positive) then measure ACTH levels.

Question 19

Primary Adrenal Insufficiency Evaluation

Answer 19

Testing: 8am serum cortisol, ACTH levels/ACTH stimulation test (ACTH analog)

In primary adrenal insufficiency, ACTH stimulation will cause a minimal rise in cortisol due to adrenal atrophy.

Question 20

DKA

Answer 20

Glucose >200
Bicarb <15
pH <7.3
Anion gap >14
Serum/urine ketones

Tx: 10mL/kg isotonic fluids over the first hour. Insulin plus fluids with K+ (will have been depleted).

Question 21

Pathogenesis of metabolic syndrome

Answer 21

Increased insulin resistance

Question 22

Familial Hypocalciuric Hypercalcemia

Answer 22

Insensitive Calcium-sensing receptors. Results in hypercalcemia with normal/high PTH. Decreased urine calcium due to increased reabsorption. (Hyperparathyroidism has normal urine calcium)

Question 23

K+ levels in DKA and HHS

Answer 23

Serum levels elevated but total levels depleted.

Question 24

Hyperparathyroidism

Answer 24

Hypercalcemia, HTN

Possible link to MEN2, consider investigating for pheochromocytoma in those with uncontrolled HTN.

Question 25

Central DI

Answer 25

Decreased ADH from pituitary
Idiopathic, trauma, pituitary surgery, ischemic encephalopathy
High serum Na

Question 26

Increased thyroglobulin levels following thyroidectomy for cancer

Answer 26

reoccurrence of the cancer

Question 27

Kallman Syndrome

Answer 27

Abnormal migration of the olfactory and GnRH releasing neurons.

Anosmia and hypogonadotropic hypogonadism

Question 28

XXX Syndrome

Answer 28

Usually fairly normal, tend to be taller

Question 29

Neonatal thyrotoxicosis

Answer 29

Baby born to mother with Grave’s disease. Anti TSH receptor antibodies can cross the placenta and cause hyperthyroidism
Tx: Short term methimazole and BB. Will resolve over a couple months..

Question 30

MoA for increased T4 2/2 increased estrogen

Answer 30

Increased thyroid binding globulin production