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PANCE Blueprint Endocrinology Study Practice Solutions
1. What are the clinical features of adrenal insufficiency?: Nausea, vomiting, weakness, fatigue,
lethargy, weight loss, anorexia, and hyperpigmentation
2. 3 types of adrenal insufficiency?: 1. Primary (problem w/ adrenal gland itself)
2. Secondary (steroid withdrawal or pituitary issue)
3. Tertiary (hypothalamus)
3. What is acute and chronic adrenocortical insufficiency?: ÏAcute adrenocortical insufl- ciency (adrenal
crisis) is an emergency caused by insuflcient cortisol ÏChronic adrenocortical insuflciency or primary adrenal insuflciency (Addison disease) is caused by dysfunction or absence of the adrenal cortices
4. What is secondary adrenal insufficiency?: Secondary adrenal insuflciency is adrenal hypofunc- tion due to a
deficient secretion of ACTH by the pituitary gland which may be isolated or occur in conjunction with other pituitary hormone deficiencies. ACTH and cortisol levels both are low.
5. What are causes of secondary adrenal insufficiency?: ÏIatrogenic (adrenal suppression from prolonged
steroid use) ÏPituitary or hypothalamic adenoma ÏLong-term glucocorticoid therapy ÏSheehan syndrome (severe low blood pressure during or after childbirth) ÏTraumatic brain injury
2 / 45 ÏSubarachnoid hemorrhage
6. What is the cause of tertiary adrenal insufficiency?: Tertiary adrenal insuflciency refers to impaired
hypothalamic release of corticotropin-releasing hormone (CRH) with resulting decreased production of ACTH by the pituitary. The most common causes of tertiary adrenal insuflciency, also suppress corticotropin (ACTH) secretion: ÏAbrupt cessation of high-dose glucocorticoid therapy ÏCorrection (cure) of hypercortisolism (Cushing's syndrome)
7. What are the etiologies of primary adrenal insufficiency?: Most commonly from autoim- mune
destruction of the adrenal cortex. Plasma ACTH is high and serum cortisol levels are low. ÏAutoimmune destruction (most common as Addison disease) ÏTuberculosis (leading cause where TB is prevalent) ÏAdrenal hemorrhage (i.e., sepsis, anticoagulation therapy, antiphospholipid antibody syndrome) ÏCongenital
8. Primary? Secondary? Tertiary?: Primary = adrenal (ACTH high and cortisol low) Secondary =
pituitary (ACTH low and cortisol low) Tertiary = hypothalamic (ACTH and cortisol low with exaggerated and prolonged ACTH response with administration of CRH - corticotropin releasing hormone test)
9. Evaluation of patients with possible adrenal insufficiency?: For most patients measur- ing 8 AM serum
cortisol and plasma ACTH, and a high-dose 250 mcg ACTH stimulation test
10. Test to differentiate between secondary and tertiary adrenal insufficiency?-
: CRH Stimulation Test: the ditterentiation between secondary and tertiary adrenal insuflciency can be made by the administration of corticotropin-releasing hormone (CRH) ÏSecondary (pituitary) - low ACTH and low cortisol - there is little or no ACTH response in patients with secondary (pituitary-related)
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ses increased
se-
timulate
ÏInjury to both adrenals (e.g., trauma, hemorrhage, anticoagulant therapy, thrombosis, infection, or metastatic carci- noma) ÏAdministration of etomidate (rapid anesthesia induction or intubation).
17. In which forms of adrenal insufficiency is mineralocorticoid (aldosterone) se- cretion
intact?: Secondary and tertiary. The adrenal cortex maintains responsiveness to the renin-angiotensin system
18. Which form of adrenal insufficiency is associated with hyperpigmentation?-
: Primary adrenocortical insuflciency (Addison's disease)
19. What is the mechanism of hyperpigmentation?: Hypocortisolemia cau cretion
of ACTH and other proopiomelanocortin -derived peptides such as MSH. These peptides s production, resulting in hyperpigmentation.
20. What are some additional clinical features in acute adrenal crisis?: Fever, abdom- inal
pain, orthostatic hypotension, hypovolemia, hypotension, shock, confusion, and coma
21. What form of adrenal insufficiency is associated with an elevated ACTH?: Pri- mary
22. What forms of adrenal insufficiency are associated with a low ACTH?: Secondary and
tertiary
23. What is the treatment for primary adrenal insufficiency?: Replacement therapy with a
combination of glucocorticoids and mineralocorticoids. Hydrocortisone is the glucocorticoid of choice. Mineralocor- ticoid replacement (fludrocortisone) and increased dietary salt intake. Adjustments in dosage are made according to the clinical response. A proper dose usually results in a normal WBC count ditterential
24. How should patients adjust their medications for when under stress (ill-
ness/surgery)?: Increase glucocorticoid dose 2- to 3-fold during periods of minor illness; intravenous high-dose glucocorticoids during severe illness or major surgery
25. Cushing's is all about an increase in what?: Cortisol (glucocorticoid)
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26. Cushing's syndrome vs. Cushing's disease?: ÏCushing's Syndrome: symptoms from chronic ‘
cortisol levels and doesn't specify cause or source of excess ÏCushing's Disease is Cushing's syndrome that results from excess pituitary production of adrenocorticotropic hormone (ACTH), generally secondary to a pituitary adenoma. Cushing disease accounts for about 40% of Cushing syndrome cases
27. Describe exogenous vs. endogenous Cushing's?: Cushing syndrome can happen because of
exogenous cortisol meaning that it comes from "outside" usually in the form of medications, or because of endogenous cortisol - meaning that the excess cortisol is made by the body.
28. Is the majority of Cushing's syndrome exogenous or endogenous cause?: The majority of
cases of Cushing syndrome occur in individuals using exogenous steroid medications over a long period of time - often to treat autoimmune and inflammatory disorders, like asthma or rheumatoid arthritis. Because the molecular structure of exogenous steroid medications is so similar to cortisol they mimic its actions on various tissues. Exogenous steroid medications can also cause negative feedback on the hypothalamus and the pituitary gland. This causes a decrease in CRH and ACTH, which in turn, shuts down endogenous cortisol production from the zona fasciculata.
29. What is the most common cause of endogenous Cushing's?: The most common reason for
increased levels of endogenous cortisol is excess ACTH caused by a pituitary adenoma, which is a benign tumor of the pituitary gland - and this is called Cushing disease
30. Describe adrenocorticotropic hormone (ACTH)-dependent or ACTH-indepen- dent
Cushing's syndrome?: Hyperfunction of the adrenal cortex can be adrenocorticotropic hormone (ACTH)-dependent or ACTH- independent ACTH-dependent hyperfunction may result from ÏHypersecretion of ACTH by the pituitary gland (Cushing disease) ÏSecretion of ACTH by a nonpituitary tumor, such as small cell carcinoma of the lung or a carcinoid tumor (ectopic ACTH syndrome) ÏAdministration of exogenous ACTH
7 / 45 in the evening, when we're preparing for sleep
37. The body uses negative feedback, which means that high levels of cortisol tell the
hypothalamus and pituitary gland to (decrease or increase) their secre- tion of CRH and ACTH?: The body uses negative feedback, which means that high levels of cortisol tell the hypothalamus and pituitary gland to decrease their secretion of CRH (hypothalamus) and ACTH (pituitary)
38. How does excess cortisol affect glucose and insulin levels in the blood?: Excess cortisol
leads to elevated blood glucose levels, and that leads to high insulin levels
39. What is symptom of Cushing's is related to elevated insulin levels?: Insulin, among its many
actions, targets adipocytes or fat cells in the center of the body - around the waist and buttocks. In those cells, the insulin activates lipoprotein lipase, which is an enzyme that helps those adipocytes accumulate more fat molecules. The result is central obesity (a core symptom of Cushing's syndrome)
40. How does excess cortisol affect muscle, bone and skin?: Excess cortisol leads to severe muscle,
bone and skin breakdown which are the major protein stores of the body
41. Why does excess cortisol cause hypertension?: High cortisol levels cause hypertension for two
reasons. First, it amplifies the ettect of catecholamines on blood vessels. Second, cortisol starts cross-reacting with mineralocorticoid receptors, which normally only binds a related steroid hormone (mineralocorticoids are secreted from the zona glomerulosa layer of the adrenal cortex). Because the cortisol is structurally similar to mineralocorticoid it can bind to that receptor and it can trigger the mineralocorticoid ettect - which is mainly to increase blood pressure by retaining fluid through sodium reabsorption and potassium excretion
42. Most common initial diagnosis of Cushing syndrome?: Diagnosis of Cushing syndrome is initially
based on measuring the free, or unbound cortisol in a 24-hour urine sample, in order to assess the total amount of cortisol excreted in the urine over a 24-hour period. Alternatively, blood or saliva tests late at night can help check if there's a normal daily rise and fall of cortisol levels.
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43. Another option for the initial diagnosis of Cushing syndrome?: Another option is also the
dexamethasone suppression test, which is when a person is given a low dose of dexamethasone, which is an exogenous steroid that suppresses ACTH production in the pituitary gland. Normally that should cause a decrease in serum cortisol levels, but if Cushing syndrome is caused by endogenous cortisol production, then the serum cortisol levels should remain unchanged. If that test is positive, the next step is to determine the exact cause of endogenous cortisol production, and ACTH plasma levels can be checked.
44. How do cortisol levels which increase in times of stress affect gluconeo- genesis?: In
times of stress, the body needs to have plenty of energy substrates around, so cortisol increases gluconeogenesis, which is the synthesis of new glucose molecules, proteolysis, which is the breakdown of protein and lipolysis, which is the breakdown of fat.
45. What is a feature of Cushing syndrome due to cortisol-mediated break down of
muscle to produce amino acids for gluconeogenesis.: Muscle weakness is a feature of Cushing syndrome due to cortisol-mediated break down of muscle to produce amino acids for gluconeogenesis.
46. What are the clinical manifestations of Cushing syndrome?: Central obesity, moon facies,
dewlap (under chin), dorsocervical and supraclavicular fat pad thickening Thin extremities with muscle wasting and proximal muscle weakness Thin skin, facial plethora, violaceous striae, easy bruising, slow wound healing Hyperglycemia and glucose intolerance Psychological problems (irritability, depression, psychosis, mania, anxiety, and insomnia) Osteoporosis (vertebral compression fractures, aseptic necrosis, hypercalciuria, and renal calcu Immune suppression, cutaneous fungal infections, lymphopenia, decreased eosinophils Hyperpigmentation, lymphopenia, decreased eosinophils (if ACTH- dependent Cushing syndrome)
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54. What is the usual presentation of ectopic ACTH production?: Rather than the typical
Cushingoid habitus, ectopic ACTH production tends to present with rapidly progressive hypokalemia, metabolic alkalosis, hyperpigmentation, hypertension, edema, and weakness.
55. Does Cushing disease present with hypokalemia or hyperkalemia?: Cushing's causes
increased levels of cortisol. Cortisol, at high levels, acts like a mineralocorticoid (aldosterone), stimulating absorption of sodium and excretion of potassium at the collecting tubules. Hence, any disorder involving an excess of mineralocorticoids will cause hypokalemia.
56. Does primary adrenocortical insufficiency from a pituitary tumor present with
hypokalemia or hyperkalemia?: Primary adrenocortical insuflciency (Addison's disease) results in ‘ACTH (from pituitary hypersecretion) + “Cortisol (failure of the adrenal cortex) + “mineralocorticoid (aldosterone). Aldosterone normally causes absorption of sodium and excretion of potassium at the collecting tubules. Hence, any disorder involving a decrease in mineralocorticoids will cause hyperkalemia.
57. What 2 screening tests are used to confirm hypercortisolism?: Low-dose dexam- ethasone
suppression test (administered at 11 PM, with an 8 AM serum cortisol the next day) and 24-hour urinary free cortisol test
58. What is the radiographic test of choice for identifying suspected pituitary
adenomas?: MRI of the sella turcica, with and without gadolinium (though up to 50% of adenomas may not be seen)
59. What is the treatment for Cushing disease?: TSS (transsphenoidal surgery)
60. What is the treatment for Cushing syndrome secondary to adrenal adeno- mas and
carcinomas?: Surgical resection of the tumor. Adrenal carcinomas may also require mitotane therapy, although this is controversial. Adrenal enzyme inhibitors can be used to control refractory Cushing syndrome.
61. Normal glucose until 2-8 am when it rises causing high AM blood sugars. Results
from decreased insulin sensitivity and a nightly surge of counterregu- latory hormones during nighttime fasting: Dawn phenomenon - In contrast to Chronic Somogyi rebound, the dawn phenomenon is not associated with nocturnal hypoglycemia
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62. How is dawn phenomenon diagnosed?: By checking 3 am Blood Sugar
63. What is the treatment of dawn phenomenon?: Treat with bedtime injection of long-acting Insulin (NPH)
dose to blunt morning hyperglycemia, avoiding carbohydrate snacks late at night
64. Nocturnal hypoglycemia followed by rebound hyperglycemia: Somogyi ettect - If the blood
sugar level drops too low in the early morning hours, hormones (such as growth hormone, cortisol, and catecholamines) are released. These help reverse the low blood sugar level but may lead to blood sugar levels that are higher than normal in the morning. An example of the Somogyi ettect is a person who takes insulin doesn't eat a regular bedtime snack, and the person's blood sugar level drops during the night. The person's body responds to low blood sugar by releasing hormones that raise the blood sugar level. This may cause a high blood sugar level in the early morning.
65. Treatment of Somogyi effect?: Treat with decreased nighttime NPH dose or give bedtime snack
66. Diagnosis of Somogyi effect?: Check 3 am blood sugar
ÏIf the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi ettect ÏIf the blood sugar level is normal or high at 2 a.m. to 3 a.m., it's likely the dawn phenomenon
67. What term is used to describe progressive rise in glucose from bed to
morning: Insulin waning
68. Treatment of Insulin waning: Treat with change of insulin dose to bedtime
69. Fruity breath, weight loss, rapid respirations, hypotension: Diabetic Ketoacidosis (DKA)
70. Treatment of DKA: Diabetic ketoacidosis (DKA) should always be handled in a hospitalized setting, usually an intensive
care unit, and often with an endocrinologist's consultation, if appropriate. ÏTREAT WITH FLUIDS! Patients with DKA are always dehydrated and need large-volume IV fluid resuscitation, usually isotonic fluids such as normal saline. If the corrected serum sodium level is high, this can be reduced to half-normal saline. Insulin should always be
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75. Preprandial glucose goal: Preprandial glucose 80-110 (60-90 if pregnant)
76. Postprandial blood glucose goal: Postprandial blood glucose goal is < 140
77. Blood pressure goal: ACC/AHA blood pressure targets - the target for patients with comorbidities is < 130/
JNC 8 treatment targets: Reduce BP to < 140/90 mm Hg for everyone < 60 including those with a kidney disorder or diabetes
78. Diabetic statin guidelines: Recommend statins in persons with diabetes mellitus who are 40 to 75 years of
age with LDL-C levels of 70 to 189 mg per dL but without clinical ASCVD
79. This medicine decreases hepatic glucose production and peripheral glucose
utilization, decreases intestinal glucose absorption: Metformin
80. This medicine stimulates pancreatic beta cell insulin release (insulin secret- agogue
- non glucose-dependent): Sulfonylureas (glyburide and glipizide)
81. This medicine increases insulin sensitivity in peripheral receptor site adipose and
muscle and has no effect on pancreatic beta cells: Thiazolidinediones (Pioglitazone - Actos and Rosiglitazone - Avandia)
82. This medicine delays intestinal glucose absorption: α-Glucosidase inhibitors (Acarbose precose
and Miglitol glyset)
83. This medicine stimulates pancreatic beta cell insulin release: Meglitinides (Repaglin- ide
prandin and Nateglinide)
84. This medicine lowers blood sugar by mimicking incretin - causes insulin secretion
resulting in decreased glucagon and delayed gastric emptying: GLP-1 Agonists (Exenatide Byetta)
85. Dipetpidylpetase inhibition - inhibits degradation of GLP-1 so more circulat- ing GLP-
14 / 45 1: DDP-4 Inhibitors (Sitagliptin Januvia)
86. At what serum creatinine level should Metformin be stopped: Cr > 1.
87. 3 or more of the following: Abdominal obesity - Increased triglycerides -
Decreased HDL - HTN - Hyperglycemia?: Metabolic Syndrome
88. Define metabolic syndrome: Metabolic Syndrome: 3 or more of the following: Abdominal obesity - Increased
triglycerides - Decreased HDL - HTN - Hyperglycemia
89. What are increased levels of beta-hydroxybutyrate diagnostic of?: Diabetic Ke-
toacidosis (DKA)
90. Which DM medication is contraindicated in NYHA class III or IV heart failure?-
: Pioglitazone
91. Pancreatitis is a side effect of what class of oral DM medication?: DDP-4 Inhibitors
- The drugs Januvia and Byetta were found to be linked with a doubled risk of pancreatitis
92. List two long acting insulins: Insulin glargine - Insulin detemir
93. List three rapid acting insulins: Insulin glulisine - Insulin lispro - Insulin aspart
94. What class of oral diabetic medication should not be given to patients with G6PD?:
Sulfonylureas
95. Nausea and diarrhea are common side effects of which oral diabetic med-
ication?: Metformin
96. List the risk factors for gestational diabetes.: Obesity - Maternal age - Family HX DM - Prior
macrosomal birth
97. What are the two recommended treatment options for gestational dia-
16 / 45 four:: Fasting BG > 126 mg/dl - HbA1C > 6.5% - BG > 200 @ 2 hours on GTT - Random BG > 200 plus signs and symptoms
109. What is the definition of hypogonadism?: Decreased testicular or ovarian functional activity
110. What are the causes of hypogonadism in adults?: Causes of Hypogonadism in Adults:
Hypogonadism in Men: Androgen Decline in the Aging Male and Testicular Failure Hypogonadism in Women: Menopause and Premature Ovarian Failure
111. Clinical features of male hypogonadism (adults/adolescents)?: Clinical features of male
hypogonadism include: ÏDiflculty gaining muscle mass ÏLack of beard ÏFailure of voice to deepen ÏFatigue ÏHot flashes ÏGynecomastia ÏSmall testes
112. What are the two main types of male hypogonadism?: 1. Disease of the testes (primary
hypogonadism)
- Disease of the hypothalamus or pituitary (secondary hypogonadism)
113. Lab findings if primary vs. secondary hypogonadism in males?: Primary: LH/FSH high, T
low Secondary: everything is low
114. What meds affect testosterone production?: High-dose steroids and opioids
115. Two most common situations of abnormal testosterone binding to sex hormone
17 / 45 binding globulin (SHBG)?: 1. Obesity (decreases SHBG concentrations)
- Male aging (increases SHBG)
116. Gynecomastia + small firm testes + behavioral/learning issues suggest what
diagnosis?: Klinefelter
117. Anosmia (loss of smell) + hypogonadism?: Think Kallmann syndrome
118. Peripheral vision issues + hypogonadism?: Pituitary mass
119. What are other causes of hypogonadism?: Chemo and radiation, excessive etOH, bilateral torsion,
trauma, mumps orchitis
120. Testosterone therapy should be given to who?: Only to a man who is hypogonadal, as
evidenced by clinical symptoms and signs consistent with androgen deficiency and a distinctly subnormal serum testosterone concentration
121. When are testosterone levels measured?: 8-10 AM
122. Preferred testosterone regimen?: Gel (AndroGel, Testim, and Fortesta)
123. Contraindications to testosterone therapy?: Contraindications to testosterone therapy in- clude:
ÏProstate cancer ÏBreast cancer ÏErythrocytosis (Hct >50%) ÏSleep apnea severe/untreated ÏUncontrolled heart failure
124. How often should hematocrit be measured in people on testosterone ther- apy?: After
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3. Ovarian and ovulatory dysfunction
4. Anatomic issues
133. Prolactin inhibits what?: GnRH
134. What are the CNS causes of SIADH?: Skull fracture, subdural hematoma, subarachnoid hemor- rhage, acute
encephalitis, TB meningitis, Guillain-Barré syndrome
135. What are the symptoms and signs of SIADH?: Confusion, seizures, and coma attributable to brain
edema secondary to osmotic water shifts
136. What are the laboratory findings for SIADH?: Decreased Na+ (<130 mEq/L), decreased plasma
osmolarity (<270 mOsm/kg), and hypertonic urine
137. What is a complication of correcting serum Na+ too quickly?: Central pontine
myelinolysis
138. What are the MEN syndromes?: Familial syndromes associated with multiple endocrine tumors
139. What is the inheritance pattern for MEN syndromes?: Autosomal dominant
140. Parathyroid tumors, pituitary adenomas, and pancreatic endocrine tumors are all
associated with?: Parathyroid tumors, pituitary adenomas, and pancreatic endocrine tumors are all associated with multiple endocrine neoplasia 1 syndrome. Remember 3 P's for MEN 1: Pituitary, Parathyroid, Pancreatic.
141. What is MEN 2A associated with?: MEN 2A is associated with parathyroid hyperplasia, medullary thyroid
carcinoma, and pheochromocytoma. Remember MEN 2A = 2 P's: Parathyroids and Pheochromocytoma.
142. What is MEN 2B associated with?: MEN 2B is associated with medullary thyroid carcinoma,
pheochromocytoma, and mucosal neuromas. MEN 2B = 1 P: Pheochromocytoma
143. How should patients with pheochromocytoma be treated?: Patients with pheochro-
20 / 45 mocytoma should be treated first with a(n) alpha-blocker and then a beta-blocker prior to surgery
144. How is the recurrence of medullary thyroid carcinoma monitored?: Recurrence of medullary
thyroid carcinoma is monitored for with calcitonin, CEA, and provocative calcitonin testing
145. What is believed to explain the pathogenesis of multiple endocrine neopla- sia type
2?: A point mutation in the RET oncogene is believed to explain the pathogenesis of multiple endocrine neoplasia type 2
146. What is associated with marfanoid habitus and mutation in RET gene?: MEN 2B is
associated with marfanoid habitus and mutation in RET gene
147. What do medullary carcinomas of the thyroid, which are seen in multiple endocrine
neoplasia 2A and 2B, secrete?: Medullary carcinomas of the thyroid, which are seen in multiple endocrine neoplasia 2A and 2B, secrete calcitonin
148. Which MEN is associated with multiple neuromas on the lips and mouth?
MEN 2B is associated with multiple neuromas on the lips and mouth
149. What biochemical testing may be recommended to monitor for recurrent or
metastatic pheochromocytomas and paragangliomas?: Lifelong annual biochemical testing for plasma and urine levels of metanephrines may be recommended to monitor for recurrent or metastatic pheochromocytomas and paragangliomas.
150. Mucosal neuromas, medullary carcinoma of the thyroid, pheochromocy- toma, and
marfanoid body habitus are all associated with which multiple endocrine neoplasia type?: Mucosal neuromas, medullary carcinoma of the thyroid, pheochromocytoma, and marfanoid body habitus are all associated with multiple endocrine neoplasia 2B.
151. Name the FIVE main types of thyroid carcinoma and their relative percent- ages: The
FIVE main types of thyroid carcinoma and their relative percentages:
1. Papillary carcinoma: 80% (Popular Papillary)
