ENDOCRINE Flashcards
(446 cards)
1
Q
What is the function of endocrine glands?
A
Produce hormones that act on target cells to maintain homeostasis
2
Q
What are the endocrine glands?
A
Adrenal, Thyroid, Pituitary, Parathyroid, Pancreas, and reproductive glands
3
Q
What controls neuroendocrine glands?
A
Controlled by hypothalamus and pituitary. Utilizes signals to know when to make/release hormone
4
Q
Which glands are considered neuroendocrine?
A
Pituitary, thyroid, adrenal cortex, and reproductive glands
5
Q
What does an endocrine gland do?
A
Gland produces the hormone
6
Q
What are examples of glands that produce hormones?
A
Parathyroid and pancreas
7
Q
What happens when there is overproduction of hormones?
A
Hyperthyroidism
8
Q
What happens when there is underproduction of hormones?
A
Hypothyroidism
9
Q
What is inappropriate release of hormones?
A
SIADH
10
Q
What is a loss of response in hormone regulation?
A
DM Type II
11
Q
What is a loss of negative feedback in hormone regulation?
A
Tertiary adrenal insufficiency
12
Q
What is endogenous hormone production?
A
Prolactinoma
13
Q
What is exogenous hormone production?
A
HRT or insulin
14
Q
What do ‘Hypo-‘ and ‘Hyper-‘ refer to?
A
Refers to level of hormone
15
Q
What is the difference between primary and secondary issues?
A
Primary refers to the endocrine gland; Secondary refers to somewhere besides the gland, generally the pituitary
16
Q
What does tertiary refer to in hormone issues?
A
Originating from the hypothalamus
17
Q
What is an exception in hormone levels?
A
Hyperparathyroidism
18
Q
Endocrine gland hierarchy
A
19
Q
Endocrine Gland Response- Negative feedback loop
A
20
Q
What is Primary Adrenal Insufficiency?
A
Adrenal gland is not working correctly (Addison’s disease).
21
Q
What is Secondary Adrenal Insufficiency?
A
Pituitary is not releasing enough ACTH.
22
Q
What is Tertiary Adrenal Insufficiency?
A
Hypothalamus is not producing corticotropin releasing hormone adequately.
23
Q
What are easy ways to measure adrenal function diagnostically?
A
Target organ output, Endocrine gland hormone, Pituitary gland hormone.
24
Q
What are hard ways to measure adrenal function diagnostically?
A
Hypothalamus factors.
25
Hypofunction-decreased target organ output
26
Hyperfunction-increased target organ action
27
Why must diagnostics be interpreted in the context of the patient?
Diagnostics must be interpreted in the context of the patient to ensure accurate assessment of their condition.
28
What does it mean if a lab result is in the normal range?
Just because a lab is in the normal range doesn’t mean that is the correct response.
## Footnote
Example: A patient with very low muscle mass and liver disease should have low BUN and creatinine. Normal levels in this patient likely mean AKI.
29
What is the expected PTH level in a patient with hypercalcemia?
A patient with hypercalcemia should have a low PTH. Normal levels of PTH in a patient with hypercalcemia are consistent with hyperparathyroidism.
## Footnote
Example: Normal PTH levels in hypercalcemia indicate a potential disorder.
30
What is the order of lab testing?
Lab testing has an order: First test - there is an imbalance. High or low? Second test - determine primary vs secondary. Third test and beyond - evaluate cause for disorder.
31
What hormones are produced in the adrenal cortex?
Adrenal hormones produced in the cortex include Aldosterone, Cortisol, and precursors to sex hormones.
32
What hormones are produced in the adrenal medulla?
Adrenal hormones produced in the medulla include Epinephrine (Epi) and Norepinephrine (Norepi).
33
What is the function of Aldosterone?
Aldosterone (mineralocorticoid) acts on nephrons to raise blood volume, raise blood pressure, and regulate levels of Na, K, and H in the blood.
34
What are the functions of Cortisol?
Cortisol (glucocorticoid) manages the body’s use of carbs, fats, and protein, keeps inflammation down, regulates blood pressure, increases blood sugar, controls sleep/wake cycle, and boosts energy to handle stress.
35
How is cortisol primarily found in the blood?
Cortisol is mostly bound in blood, with about 5% free/unbound.
36
What happens to excess free cortisol?
Excess free cortisol is excreted by the kidneys.
37
What are androgens responsible for?
Androgens are responsible for secondary sex characteristics and are precursors to testosterone and estrogen.
38
Where do most sex hormones come from?
Most sex hormones come from the testes or ovaries.
39
Hypercortisolism is aka Cushing’s Syndrome Endogenous
1. Primary hypercortisolism***-adrenal tumor***
2. Secondary hypercortisolism-pituitary tumor **(Cushing’s disease*)**
- Can also see with ectopic ACTH producing tumor- like a small cell lung cancer
3. Tertiary hypercortisolism-hypothalamic dysfunction
40
What is hypercortisolism also known as?
Cushing’s Syndrome
41
What are the forms of exogenous corticosteroids?
Oral, injected, inhaled, and topical
42
Who are patients that may experience hypercortisolism?
Patients waiting for transplants
43
Why is the history of hypercortisolism important?
Due to vague presentation, diagnosis is generally delayed up to 5 years
44
What should be reviewed in patients with suspected hypercortisolism?
Medications for history of prolonged steroid use
45
What routine lab findings may indicate hypercortisolism?
Hypokalemia +/- hypernatremia (in primary disease), Hyperglycemia
46
What is the first step in the workup for hypercortisolism?
Verify hypercortisolism
47
What is the initial test to assess cortisol level?
1. 24 hr urine for free cortisol
2. Midnight serum or salivary total cortisol level
3. Low dose dexamethasone suppression test
48
What should the cortisol level be in a low dose dexamethasone suppression test?
Should be high without doubt (generally 3x upper limits of normal)
49
Why is timing important in measuring cortisol levels?
Cortisol levels vary throughout the day
50
When is peak cortisol usually observed?
Peak cortisol is usually first in the morning and gets lower throughout the day, especially at night.
51
What is the test of choice for diagnosing hypercortisolism?
24 hr urine free cortisol.
52
What are the limitations of the 24 hr urine free cortisol test?
Less accurate in patients with significant CKD and less accurate if > 3L urine is collected.
53
What is the midnight cortisol level?
Can be serum or salivary; serum usually collected in hospital, salivary usually performed as outpatient.
54
What is the expected lowest cortisol level time?
Lowest level should be around midnight, assuming a normal circadian rhythm.
55
What are the limitations of the midnight cortisol level test?
May need to test at least two samples on different days; not as accurate in patients with disrupted sleep schedules.
56
What is the Low Dose Dexamethasone Suppression Procedure?
Cortisol level drawn at 8 AM on Day #1, dexamethasone 1 mg administered at 11 PM on Day #1, cortisol level drawn again at 8 AM on Day #2.
57
What is the expected result for normal patients in the Low Dose Dexamethasone Suppression?
Normal patients will have lower cortisol on Day #2.
58
What will patients with hypercortisolism show on Day #2 in the Low Dose Dexamethasone Suppression?
**Patients with hypercortisolism will have the same or higher cortisol level on Day #2.**
59
What are the limitations of the Low Dose Dexamethasone Suppression?
Oral contraceptives and pregnancy may interfere with results.
60
Determining primary vs secondary hypercortisolism
Measure serum ACTH x2 to verify
61
What is the most common cause of Primary Hypercortisolism?
Most often caused by adrenal tumor
62
What are the types of adrenal tumors associated with Primary Hypercortisolism?
Adrenal adenoma - benign
Adrenal carcinoma - malignant
63
What imaging study should be obtained to assess for adrenal tumors?
CT Abdomen w/ Contrast
64
What should be done if an adrenal mass is present?
Referral to surgery for removal
65
What should be done if an adrenal mass is not obvious?
Refer to endocrinology
66
What does a normal/high ACTH level indicate?
Could indicate Secondary, Tertiary, or Ectopic causes
67
What is the next step if ACTH is normal/high?
High dose dexamethasone suppression test to determine secondary vs ectopic
68
What does the High Dose Dexamethasone Suppression test assess?
Should suppress cortisol levels in secondary hypercortisolism
69
What is the procedure for the High Dose Dexamethasone Suppression test?
Cortisol level drawn at about 8 am on Day 1
Dexamethasone 2 mg administered q6 hours for 48 hours
Cortisol level drawn again at ~8 AM on Day #3
70
What is expected in patients with secondary hypercortisolism after the suppression test?
A fall in AM cortisol by > 50%
71
What will occur in ectopic ACTH production during the suppression test?
Will not experience a significant drop
72
What is the most common cause of Secondary Hypercortisolism?
Most commonly from pituitary adenoma - known as Cushing’s disease
73
What imaging study is needed to confirm Secondary Hypercortisolism?
Need MRI pituitary to confirm
74
What additional workup may be needed for adrenal issues?
CT Chest/Abdomen/Pelvis and/or PET scan
CRH Stimulation Test
Petrosal sinus sampling
75
Hypercortisolism Causes
76
Hypercortisolism workup
1. Cortisol
2. ACTH
77
What are the two varieties of hypocortisolism?
Acquired and Congenital
78
What is the primary type of acquired hypocortisolism?
Aka Adrenal Insufficiency
79
What is the most common cause of primary hypocortisolism?
Autoimmune
80
What are other causes of primary hypocortisolism?
Infections, tumor, medications, hemorrhage
81
What is secondary hypocortisolism usually associated with?
Multiple endocrine issues due to hypopituitarism
82
What is tertiary hypocortisolism often related to?
Extended courses of exogenous steroids
83
What is congenital hypocortisolism?
Congenital adrenal hyperplasia
84
What is the initial test to verify hypocortisolism?
Assess cortisol level
85
When should cortisol levels be measured?
Early AM serum or salivary cortisol
86
Why is timing important in cortisol level measurement?
Cortisol levels vary throughout the day
87
What should the 8 AM cortisol level be in normal individuals?
At its highest
88
What should be expected in patients with adrenal insufficiency regarding 8 AM cortisol?
Expect a low 8 AM cortisol
89
When is ACTH level generally measured?
In the AM
90
What does an elevated ACTH level likely represent?
Primary hypocortisolism/adrenal insufficiency
91
What does a low ACTH level likely represent?
Secondary or tertiary hypocortisolism/adrenal insufficiency
92
What is the Cosyntropin Stimulation Test?
Serial cortisol levels drawn after synthetic ACTH (cosyntropin) given IV
93
When are cortisol levels drawn during the Cosyntropin Stimulation Test?
1st level at injection, subsequent levels at 30 and 60 minutes after injection
94
What does insufficient elevation of cortisol after injection likely represent?
Primary disorder
95
What does a sufficient increase in cortisol after injection likely represent?
Secondary/tertiary disorder
96
What imaging should be done if hypocortisolism is primary?
CT abdomen with contrast adrenal protocol
97
What should be checked if hypocortisolism is primary?
Aldosterone level
98
What imaging should be done if hypocortisolism is secondary?
MRI pituitary protocol
99
Hypocortisolism and Hypoaldosteronism
Hyperpigmentation due to ACTH stimulation of melanocytes
Decreased libido, pubic, and axillary hair in biological females due to decreased adrenal androgens
100
Primary vs Secondary Hypocortisolism
101
Movement of hormones
102
Hypocortisolism
103
What is Congenital Adrenal Hyperplasia?
It is an inborn error of metabolism involving adrenal hormone biosynthesis.
104
What is the most common deficiency in Congenital Adrenal Hyperplasia?
**The most common deficiency is the 21-hydroxylase enzyme.**
105
What does the deficiency of 21-hydroxylase enzyme lead to?
**It leads to increased 17-hydroxyprogesterone.**
106
What is the consequence of increased 17-hydroxyprogesterone?
It leads to hyperplasia of the adrenal glands.
107
How is Congenital Adrenal Hyperplasia tested?
Through newborn screening for elevated 17-hydroxyprogesterone level.
108
What is hypoaldosteronism?
It is a condition where there is low aldosterone levels.
109
When is isolated hypoaldosteronism generally not an adrenal issue?
When it is due to decreased renin levels.
110
What are some causes of isolated hypoaldosteronism?
Kidney disease, medications (ACE/ARB/DRI, NSAIDs, heparin).
111
If isolated hypoaldosteronism is an adrenal issue, what is it classified as?
It is classified as primary adrenal insufficiency.
112
Workup for Hypoaldosteronism
1. First, check aldosterone levels
Aldosterone level should be low in hypoaldosteronism
2. Second, check renin levels to determine primary vs other etiology
3. check for other causes.
In primary hypoaldosteronism, cause is likely autoimmune
Check anti-21-hydroxylase antibodies
Imaging of adrenal glands
113
What is Hyperaldosteronism?
Usually, a primary issue due to adrenal tumor/hyperplasia
Most common symptom is refractory/difficult to treat HTN
114
Workup for Hyperaldosteronism
1. First, check aldosterone level
Should be high in hyperaldosteronism
2. Second, check renin levels to determine if primary vs other etiology
3. Last, check for other causes
- In primary hyperaldosteronism, causeis likely tumor
- Check CT Adrenal
115
Common lab findings for Hyperaldosteronism
Hypokalemia, Hypernatremia, Metabolic alkalosis
116
What does the thyroid produce?
The thyroid makes and stores T3 & T4.
117
When are T3 & T4 released into the bloodstream?
They are released when signaled by TSH.
118
Which is more prevalent in serum, T4 or T3?
T4 > T3 in serum.
119
What is TSH mostly bound to?
Transport proteins.
120
What percentage of TSH is free or unbound?
< 1% free or unbound.
121
Name some transport proteins for TSH.
Thyroxine binding globulin (TBG), Albumin, etc.
122
What is the significance of free forms of TSH?
Free forms of TSH are biologically active as T4 is converted to T3 in tissues.
123
Which thyroid hormone is more significant physiologically?
T3 is more significant physiologically.
124
What thyroid labs are commonly used?
TSH, Total T4 and Free T4, Total T3 and Free T3, T3 Uptake and Free Thyroxine Index (FTI).
125
What are autoimmune antibodies in serology?
Autoimmune antibodies related to thyroid function.
126
What are the indications for TSH testing?
Initial screening test of thyroid function, Monitor response to treatment.
127
What does a high TSH indicate?
Thyroid gland is NOT producing enough T3 or T4, or inappropriate release of TSH or TRH.
128
What does a low TSH indicate?
Thyroid gland is making TOO much T3 or T4, or insufficient production of TSH or TRH.
129
What should be considered with TSH levels?
TSH increases with age, can be altered by illness, affected by pregnancy, and high doses of biotin can interfere.
130
What are the two ways to assess Free Thyroxine?
Free T4 direct measurement and Free Thyroxine Index.
131
What does Free T4 measure?
Unbound T4 in serum.
132
What is the normal percentage of Free T4?
Normally, free T4 is < 0.03% of T4 released by thyroid.
133
What is the Free Thyroxine Index (FT4)?
FTI = T3 Uptake (%) x Total T4.
134
What does Total T4 measure?
Measures bound and free thyroxine levels.
135
What can affect the reliability of Total T4?
Conditions that affect thyroid binding proteins.
136
What are reasons for increased Total T4?
Pregnancy, OCPs, hormone replacement therapies, some cancers.
137
What are reasons for decreased Total T4?
Testosterone, high dose steroids, phenytoin, salicylates, cirrhosis, malnutrition, nephrotic syndrome.
138
What is Total T3 primarily used for?
To assess for hyperthyroidism.
139
What is the accuracy of Free T3?
Not as accurate, especially when T3 is low.
140
What is the ratio of thyroid hormones released?
90% T4 + 10% T3.
141
What are the three autoimmune antibodies?
Antithyroglobulin antibodies, Antithyroperoxidase antibodies, Anti-TSH receptor antibodies.
142
What do Antithyroglobulin antibodies target?
Thyroglobulin, indicative of autoimmune disease.
143
What do Antithyroperoxidase antibodies target?
Thyroid peroxidase, indicative of autoimmune disease.
144
What do Anti-TSH receptor antibodies target?
TSH receptor on thyroid cells, primarily found in Graves’ disease.
145
What are the indications for a Thyroid Uptake Scan?
Thyroid nodule or enlarged thyroid on exam, Hyperthyroidism.
146
What is the procedure for a Thyroid Uptake Scan?
Radioactive tracer injected into IV or oral tracer ingested 24 hrs prior.
147
What does a Thyroid Uptake Scan interpretation indicate?
Nodules with increased or decreased uptake are concerning and need biopsy.
148
What are the contraindications for a Thyroid Uptake Scan?
Iodine allergy, Pregnancy/breast feeding.
149
What is this?
150
Indications for Thyroid US
Thyroid nodule on exam or other imaging study
Assessment of goiter
Biopsy guidance
Pre-operative planning for thyroidectomy
151
Hypothyroidism
152
What is the first step in the workup for hypothyroidism?
Check TSH
## Footnote
For hypothyroidism, TSH should be elevated.
153
What is the second step in the workup for hypothyroidism?
Check free T4
## Footnote
For hypothyroidism, free T4 should be low.
154
What additional testing should be considered in hypothyroidism workup?
Consider antibody testing and +/- imaging.
155
What is the most common cause of primary hypothyroidism?
Chronic autoimmune thyroiditis
## Footnote
This is also known as Hashimoto’s thyroiditis.
156
What causes secondary hypothyroidism?
Failure of anterior pituitary to secrete TSH
## Footnote
Most commonly from pituitary adenoma.
157
What causes tertiary hypothyroidism?
Failure of hypothalamus to produce TRH
## Footnote
This condition is very, very rare.
158
What is the first step in the workup for hyperthyroidism?
Check TSH
## Footnote
For hyperthyroidism, TSH should be low.
159
What is the second step in the workup for hyperthyroidism?
Check free T4 and Total T3
## Footnote
For hyperthyroidism, both should be high.
160
What additional testing should be considered in hyperthyroidism workup?
Consider anti-TSH receptor Ab testing and imaging.
161
Hyperthyroidism
162
What is the primary cause of primary hyperthyroidism?
Overproduction of thyroid hormone
163
What are the most common causes of primary hyperthyroidism?
1. Diffuse Toxic Goiter (Graves’ Disease)
2. Toxic Multinodular Goiter (Plummer’s disease)
164
What causes secondary hyperthyroidism?
Overproduction/inappropriate production by anterior pituitary
165
What is the most common cause of secondary hyperthyroidism?
Pituitary adenoma
166
What causes tertiary hyperthyroidism?
Overproduction/inappropriate production of TRH by hypothalamus
167
Can tertiary hyperthyroidism be medication-induced?
Yes, it can be medication-induced.
168
Which medications can induce tertiary hyperthyroidism?
1. Amiodarone
2. Lithium
169
Pituitary gland anatomy review
170
What is SIADH?
Syndrome of inappropriate ADH secretion.
171
What are the types of Diabetes Insipidus?
Central and nephrogenic.
172
What disorders are associated with the anterior pituitary?
Hypogonadism, Gigantism/Acromegaly, Hyperprolactinemia, Hypopituitarism, Multiple pituitary hormone deficiencies, Oxytocin dysfunction.
173
Where is ADH (Vasopressin) made and stored?
Made in the hypothalamus and stored in the posterior pituitary.
174
What stimulates the release of ADH?
Osmoreceptors and baroreceptors of the hypothalamus.
175
What does ADH regulate?
Renal handling of free water and augments permeability of collecting tubules to increase water reabsorption.
176
What stimulates normal ADH release?
Hypovolemia, Thirst, Increased serum osmolality, Angiotensin II.
177
What is SIADH?
Too much ADH present, also known as 'Hyper-ADH-ism.'
178
What is Diabetes Insipidus?
Deficiency or decreased response to ADH, also known as 'Hypo-ADH-ism.'
179
What causes SIADH?
Nervous system disorders, cancers, pulmonary diseases, medications, post-operative pain.
180
What are the symptoms of SIADH?
1. Headaches
2. Nausea/Vomiting
3. Muscle cramps
4. Tremors
5. Cerebral edema (more severe cases og hyponatremia)
* Confusion
* Mood swings
* Hallucinations
* Seizures
* Coma
* Death.
181
What is hyponatremia?
Sodium < 135 mEq/L.
182
What are the classifications of hyponatremia?
Mild (130-134 mEq/L), Moderate (120-129 mEq/L), Severe (< 120 mEq/L).
183
What are the symptoms of hyponatremia?
CNS: headache, agitation, AMS, seizure, coma/death; CV: HTN, tachycardia, edema; GI: N/V; Musculoskeletal: cramps, weakness, gait/movement disturbance.
184
What is involved in the workup for hyponatremia?
CMP, Serum osmolality, Urine sodium, Urine osmolality.
185
What are the lab values for SIADH?
* Serum sodium low (< 135 mEq/L)
* Serum osmolality low (< 280 mOsm/kg)
* Urine sodium high (> 40 mEq/L)
* Urine osmolality high (> 100 mOsm/kg).
186
What additional workup may be needed for SIADH?
Thorough history, review of medications, +/- MRI or CT Brain, +/- CXR or CT lungs.
187
What does Diabetes Insipidus refer to?
It has nothing to do with blood glucose; 'Diabetes' means to pass excessive urine, and 'Insipidus' means tasteless.
188
What are the classical presentations of Diabetes Insipidus?
Polyuria (> 3L/day), polydipsia, hypernatremia.
189
What causes Central Diabetes Insipidus?
Decreased ADH release from the posterior pituitary.
190
What are common causes of Central Diabetes Insipidus?
Damage to hypothalamus or pituitary stalk, genetic, autoimmune, idiopathic.
191
What is Nephrogenic Diabetes Insipidus?
Decreased response of receptors on nephrons to ADH.
192
What causes Nephrogenic Diabetes Insipidus?
Lithium, Hypercalcemia, Kidney disease, Sickle cell disease, Genetic component.
193
Diabetes Insipidus Evaluation
1. Normal/High serum sodium
2. Confirm polyuria by 24 hr urine for volume. Defined based on age and wieght: Adults > 50 mL in 24 hrs
3. Measure urine osmolality.
* low rine osmolality consistent with DI
* High urine osmolality consistent with osmotic diuresis
194
What to do if Diabetes Insipidus (DI) is suspected?
Refer to endocrinology.
195
What test will probably be performed for DI?
Water deprivation test followed by desmopressin challenge.
196
What are the indications for the Water Deprivation Test?
Suspected DI.
197
What is the procedure for the Water Deprivation Test?
1. No fluid for 8-24 hours.
2. Serum sodium, urine sodium, and urine osmolality checked every 2 hours.
3. Monitor until serum sodium is in the 145-150 mEq/L range. May discontinue early if symptoms appear.
198
How to interpret the Water Deprivation Test results?
1. If urine osmolality increases to > 800 mOsm/kg, this indicates polydipsia.
2. If urine osmolality stays < 800 mOsm/kg, this is **likely DI** and a **desmopressin challenge is needed.**
199
What are the indications for the Desmopressin Challenge?
To help discern Central DI from Nephrogenic DI.
200
What is the procedure for the Desmopressin Challenge?
1. Urine osmolality is measured for baseline.
2. A dose of desmopressin (DDAVP) is given.
3.** Urine osmolality is then checked every 30 minutes for 2 hours.**
201
How to interpret the results of the Desmopressin Challenge?
1. In **Central DI**, kidneys respond to the challenge and urine osmolality increases to **> 300 mOsm/L. **
2. In **Nephrogenic DI, kidneys do NOT respond** to the challenge and urine osmolality remains **< 300 mOsm/L.**
202
Lab values for DI
203
What is hypogonadism?
Hypogonadism is more common to have issues with deficiencies or decreased response than over secretion.
204
What are the causes of hypogonadism in males?
Causes include congenital conditions (Klinefelter, cryptorchidism) or acquired conditions (radiation, medications, chronic diseases).
205
What are the causes of hypogonadism in females?
Causes include congenital conditions (Turner syndrome, hypopituitarism) or acquired conditions (pituitary apoplexy, chronic illness).
206
Which hormones are involved in hypogonadism?
FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone).
207
What is the role of FSH in males?
FSH is responsible for the induction and maintenance of spermatogenesis.
208
What is the role of FSH in females?
FSH is involved in estrogen production and follicular development.
209
What is the role of LH in males?
LH stimulates the release of testosterone from Leydig cells of the testes.
210
What is the role of LH in females?
LH triggers ovulation and releases progesterone from the corpus luteum.
211
What defines hypogonadism in males?
Testosterone deficiency with associated symptoms and/or deficiency of spermatozoa production.
212
What are indications for testing hypogonadism in males?
Indications include infertility workup and evaluation of hypopituitarism.
213
What is the initial test for hypogonadism in males?
The initial test is serum total testosterone level, drawn between 8AM-10AM and should be fasting.
214
How is hypogonadism confirmed in males?
Decreased testosterone levels on two separate days confirm hypogonadism.
215
What distinguishes primary from secondary hypogonadism in males?
1. Primary hypogonadism shows low testosterone and high FSH and LH
2. Secondary shows low testosterone with low/normal FSH and LH.
216
How is the cause of hypogonadism evaluated in males?
1. Primary hypogonadism requires imaging of the testes
2. Secondary requires MRI of the pituitary.
217
What defines hypogonadism in females?
Decreased function of the ovaries either in estrogen production or ovulation.
218
What are indications for testing hypogonadism in females?
Indications include amenorrhea workup and evaluation of hypopituitarism.
219
What is the initial test for hypogonadism in females?
The initial test is serum estradiol, which should be low in hypogonadism.
220
What distinguishes primary from secondary hypogonadism in females?
1. Primary hypogonadism shows high estradiol
2. Secondary shows low/normal estradiol.
221
How is the cause of hypogonadism evaluated in females?
For secondary hypogonadism, an MRI of the pituitary is obtained.
222
What is the primary function of growth hormone?
The primary function is to induce growth.
223
How does growth hormone impact metabolism?
It upregulates production of insulin-like growth factor-1 (IGF-1), enhancing insulin sensitivity and promoting glucose uptake into cells.
224
What are the effects of hypo-GH-ism in childhood and adulthood?
In childhood, it leads to dwarfism; in adulthood, it causes vague non-pathognomonic signs.
225
What are the effects of hyper-GH-ism in childhood and adulthood?
In childhood, it leads to gigantism; in adulthood, it causes acromegaly.
226
Why are growth hormone levels unreliable for diagnosis?
Growth hormone levels vary greatly throughout the day.
227
Relationship between Somatostatin and GnRH
228
What is the initial test for Growth Hormone Deficiency?
Measure IGF-1.
## Footnote
Low IGF-1 suggests GH deficiency, but normal IGF-1 does not rule it out.
229
What is the second step in the workup for Growth Hormone Deficiency?
Use GH stimulation test.
## Footnote
The gold standard is the Insulin Tolerance Test.
230
What indicates GH deficiency in the GH stimulation test?
GH that does not rise above a cutoff.
231
What is the next step after the GH stimulation test in the workup for Growth Hormone Deficiency?
Imaging of the pituitary.
232
What is the initial test for Gigantism/Acromegaly?
Measure IGF-1.
## Footnote
High IGF-1 is strong evidence for GH excess.
233
What is the second test for Gigantism/Acromegaly?
GH suppression test (Glucose Tolerance Test).
## Footnote
Measure GH level before and after giving 75g oral glucose.
234
What indicates a normal patient in the GH suppression test?
GH level should be suppressed to < 1 ng/mL.
235
What is the third test for Gigantism/Acromegaly?
Image the pituitary.
236
What is the effect of Prolactin deficiency?
Rarely causes issues.
237
What can hypersecretion of Prolactin lead to?
Infertility in females and males by reducing estrogen and testosterone respectively.
238
What are some causes of hypersecretion of Prolactin?
Prolactinoma, Pituitary adenoma, CKD, Hypothyroidism, Medications (metoclopramide, risperidone, haloperidol).
239
What is the initial test for Hyperprolactinemia?
Measure serum prolactin level.
## Footnote
In females, perform a pregnancy test to rule out pregnancy.
240
What is considered strongly suspicious for prolactinoma?
High serum prolactin level (> 200 ng/mL).
241
What is the second test for Hyperprolactinemia?
Rule out other causes of hyperprolactinemia.
## Footnote
Check TSH, pregnancy, renal function, and review medications.
242
What is the third test for Hyperprolactinemia?
MRI pituitary with contrast looking for prolactinoma.
## Footnote
This is the gold standard for diagnosing prolactinoma.
243
What is Hypopituitarism?
Low/decreased pituitary function with more than one pituitary hormone deficient.
244
What are indications for testing for Hypopituitarism?
Any secondary endocrine disorder or multiple symptoms concerning for more than one problem.
245
What is needed for testing Hypopituitarism?
MRI pituitary (if not contraindicated) and consider other hormone testing based on symptoms.
246
Pt is a 52-year-old male Construction Manager who has presented to the family medicine clinic with complaint of persistent headaches, muscle weakness, and episodes of palpitations for the past few months. He notes that despite having taken his blood pressure medication his BP continues to run on higher side.
Medical History: Diagnosed with hypertension 6 years ago
BP 160/100 mmHg
PRA= Plasma Renin Activity
Primary Hyperaldosteronism, Adrenal Tumor, CT Adrenal
247
Pt is a 63-year-old female who presents to the Internal Medicine clinic for her yearly exam. When you ask how she has been doing, she replies, “I’m tired all the time and I don’t know if you saw but my weight went up this year! I’m not eating more than usual and in fact have tried to eat a little healthier!”
Review of Systems
Gen: Progressive fatigue
HEENT: Hair thinning, “fullness” in her neck
Abd: Constipation
Endo: Cold intolerance
Skin: Dry skin
Physical Exam
Vitals: HR 58 bpm BP 124/84 mmHg RR 16 O2 97% RA T 97.9F
Gen: Appears tired, puffy face
Skin: dry, cool, rough to touch
Hair: thinning of scalp hair and outer eyebrows
Neck: Firm, non-tender goiter with no apparent nodules
Labs:
TSH = 12.8 mIU/L (Normal: 0.4-4.0 mIU/L)
Free T4 = 0.6 ng/dL (Normal: 0.8-1.8 ng/dL)
Anti-thyroglobulin Ab +
Anti-thyroperoxidase Ab +
Hashimoto's Thryoiditis
Start Levothyroxine, refer to endocrinology
248
Bonnie now presents to the ED about 1.5 years later during the heart of winter via EMS after family sent out a welfare call and pt was found unresponsive. EMS reports they found the patient in a disheveled apartment with no lights on and it was rather chilly. You call her family who live out of state and they note she had a recent cold. They called to check on her because she had a “rough year.” They note she had been depressed since losing her husband and were unsure if she was taking care of herself.
Initial Vitals: T 91.8F HR 42 bpm BP 80/50 mmHg RR 8 O2 89% RA
Exam:
Neuro-pt is responsive to painful stimuli only and unable to participate in exam, hyporeflexia noted
Skin-cool, dry
HEENT-periorbital puffiness
CV-bradycardia
Resp-CTA but shallow respiratory effort
What complication of Hashomoto's does this patient have?
Myxedema Coma
1. IV levothryoxine (T4) +/- liothyronine (T3)
2. IV hydrocortisone
3. Passive rewarming
4. Correct hyponatremia, hypoglycemia, hypoventilation
249
Pt is a 42-year-old female who presents to your family medicine clinic with complaint of increasing weakness/fatigue. On ROS she lists several vague complaints: back pain, decreased focus, and weight gain. What other ROS questions may indicate an endocrine issue?
What findings are expected on physical exam?
During the rest of your history and physical you find out that she has been having longer irregular periods and sometimes skips months altogether but has taken several pregnancy tests that have all been negative. Her exam is relatively benign except you notice her abdomen is obese with several purple striae that were not mentioned on prior visits. She also seems to have some peripheral muscle wasting and a hump on her back at the base of her neck. BP was mildly elevated at 138/89 but remainder or vitals were within normal limits.
What’s going on and what is the main hormone abnormality associated with this?
1. Oligomenorrhea/amenorrhea, thirst/polyuria, history of unusual infections or poor wound healing
2. moon facies, buffalo hump, central obesity with thin extremities, muscle, purple striae, hirsutism
3. Cushings Disease- Hypercortisolism
4. Workup with 24 hr urine free cortisol, midnight salviary/serum cortisol, low dose dexamethasone test, Serum ACTH, maybe a CT abdominal w/ contrast of adrenals, High dose dexamethasone and MRI pituitary
250
Pt is a 29-year-old male who presents to the Urgent Care with complaint of feeling jittery and racing heart. He reports the symptoms began about 2 months ago and have been progressively worsening. He finally got to where he was so anxious he couldn’t take it anymore.
Past Medical History: previously healthy with no chronic illnesses
Past Surgical History: tonsils and adenoids as a child
Family History: sister (26) has T1DM
Social History: No tobacco, alcohol, or drugs.
Pertinent positives on ROS:
Lost 15 pounds despite increased appetite. Frequent loose stools and difficulty sleeping. Coworkers have asked if he’s on drugs because his eyes are “bulgy.”
Physical Exam:
Vitals: BP 135/72, HR 112 bpm, T 37.8°C (100°F)
General: Thin, anxious-appearing male, sweating and fanning himself
Skin: Warm, moist
Eyes: Bilateral exophthalmos, mild periorbital edema
Neck: Diffuse, non-tender goiter
Cardiac: Tachycardia, irregularly irregular
Graves Disease
1. TSH
2. Free T4
3. Total T3
4. Anti-TSH Receptor Antibody
5. Anti-TSH Receptor Antibody
6. Thyroid Uptake Scan
251
About 6 months later you’re working in the ED and Daniel rolls in via EMS. EMS reports they were called out for chest pain. Daniel appears quite anxious on exam. Triage vitals include a T 103.6F, HR 164 bpm, BP 150/60 mmHg, RR 30 and O2 Sat 95% on 2L.
You ask Daniel what’s going on and his response is, “I just got over a cold about a week ago then started feeling worse. It’s just like when I saw you a few months ago but much worse.” You ask about any recent changes to his treatment for his Graves’ disease. He reports he felt much better so he stopped his meds 2 months ago.
What is your main concern?
Thryoid Storm
252
If this was a secondary hypocortisolism, what would you expect?
AM Cortisol = Low or High
ACTH = Low or High
ACTH Stim Test
Baseline cortisol = Low or High
Cortisol (30 min) = Same or Higher
Cortisol (60 min) = Same or Higher
1. AM cortisol= Low
2. ACTH= Low
3. ACTH Stim Test
* Baseline cortisol= low
* Cortisol (30 mins)= higher
* Cortisol (60 mins) =higher
252
Pt is a 42-year-old female who presents to your clinic in Fairbanks Alaska during the Winter Solstice with her daughter. She is an elementary school teacher and on Winter Break. She has noticed over the past 3 months she has been persistently fatigued and weak feeling. She also reports some unintentional weight loss of about 12 pounds.
On further questioning, she admits to some episodes of dizziness on standing, nausea, and craving of salty foods which is outside of her usual diet of salads and baked chicken.
Medical History: Autoimmune hypothyroidism
Vitals: HR 88 bpm BP 90/60 mmHg T 98.4* RR 18 O2 Sat 98% RA
Exam: Appears tired. You note she is quite tan appearing compared to her daughter and inquire about any recent travel. She notes no recent travel as the school year has been in progress and with the short days she barely sees the sun.
What additioanl studies do we want for the suspectd diagnosis?
Primary Hypocortisolism (likely Addison's disease)
CT abdominal adrenal protocol and aldosterone level
AM Cortisol-low (2 ug/dL)
ACTH-high
ACTH Stim Test-
Cortisol (baseline) = 2.1 ug/dL
Cortisol (30 min) = 2.5 ug/dL
Cortisol (60 min) = 2.7 ug/dL
253
What is the primary function of the parathyroids?
Maintain calcium homeostasis through release of PTH
254
How does PTH function in the skeletal system?
Inhibits osteoblasts and stimulates osteoclasts
255
What is the effect of PTH on osteoblasts?
Inhibits osteoblasts, leading to no bone formation and no use of calcium from blood
256
What is the effect of PTH on osteoclasts?
Stimulates osteoclasts, leading to bone breakdown and release of calcium
257
How does PTH function in the renal system?
Increases reabsorption of calcium from urine and blocks phosphate reabsorption
258
What is an indirect effect of PTH in the renal system?
Inadvertently increases active Vitamin D, which acts on bones similarly to PTH
259
What is the function of PTH in the GI system?
Increased Vitamin D acts to increase calcium and phosphate reabsorption in the small intestine
260
What characterizes primary hyperparathyroidism?
Parathyroid is the problem and makes PTH regardless of Ca2+ levels
261
What is the most common cause of primary hyperparathyroidism?
Most commonly from a single parathyroid adenoma
262
What characterizes secondary hyperparathyroidism?
Parathyroid is normal but makes excess PTH in response to chronic hypocalcemia
263
What is the most common cause of secondary hyperparathyroidism?
Most commonly from chronic kidney disease (CKD)
264
What characterizes tertiary hyperparathyroidism?
Patients who have had longstanding secondary hyperparathyroidism develop primary hyperparathyroidism
265
Labs for Primary hyperparathyroidism
266
Patient: Maria R., 58-year-old female
Chief Complaint: Fatigue, bone pain, and forgetfulness
History of Present Illness:
Progressive fatigue, constipation, and cognitive changes for 3–4 months
Bone and joint aches, especially in the back and hips
Increased thirst and urination
Recent kidney stone (calcium oxalate) 2 months ago
PMH/Medications:
Hypertension, on hydrochlorothiazide
No surgeries
Family history of osteoporosis
Primary hyperparathyroidism
267
What are the general labs for primary hyperparathyroidism?
CBC, CMP, +/- Mg, urinalysis
268
What are the 2 specific tests for primary hyperparathyroidism?
269
Additional labs needed for primary hyperparathyroidism
270
CKD stages and symptoms
271
Labs for secondary hyperparathyroidism
Low calcium
272
Patient: Jamal T., 62-year-old male with CKD stage 4
Chief Complaint: Generalized weakness and muscle cramps
History of Present Illness:
Chronic fatigue and muscle cramps for months
Diffuse bone discomfort
No nephrolithiasis
PMH:
Type 2 Diabetes, Hypertension, CKD stage 4
On phosphate binders, calcitriol
Secondary hyperparathyroidism
273
Workup for Secondary hyperparathyroidism
In the nephrology realm, we get routine labs and additional labs that we know are relevant at the same time.
274
Labs for tertiary hyperparathyroidism
low calcium
275
Patient: Laura M., 55-year-old female with ESRD s/p kidney transplant (9 months ago)
Chief Complaint: Persistent hypercalcemia on labs post-transplant
History of Present Illness:
No current symptoms but persistent elevated calcium on routine labs
History of long-standing secondary hyperparathyroidism pre-transplant
PMH:
ESRD from polycystic kidney disease
Kidney transplant 9 months ago
Previously on dialysis for 6 years
tertiary hyperparathyroidism
276
Workup for tertiary hyperparathyroidism
In the nephrology realm, we get routine labs and additional labs that we know are relevant at the same time.
277
Labs for hypoparathyroidism
278
Patient: Steven B., 46-year-old male
Chief Complaint: Tingling in hands and around mouth
History of Present Illness:
Numbness and tingling in fingertips and perioral area for 2 days
Occasional muscle cramps and recent hand spasms
Symptoms began shortly after thyroid surgery 3 weeks ago
PMH:
Papillary thyroid cancer → Total thyroidectomy 3 weeks ago
Hypertension
hypoparathyroidism
279
Workup for hypoparathyroidism
General labs: CBC, CMP, +/- Mg
280
Parathyroid disorders
281
Calcium Homeostasis
282
Because of 50% of serum calcium being bound to
albumin, in cases of significant hypoalbuminemia you must correct for this:
283
What is this pathology?
parathyroid adenoma
284
What is hypercalcemia?
Hypercalcemia is defined as serum calcium greater than 10.5 mg/dL.
285
What is the normal range for serum calcium?
The normal range for serum calcium is 8.5-10.5 mg/dL.
286
What serum calcium level is highly suspicious for cancer?
A serum calcium level greater than 14 mg/dL is highly suspicious for cancer until proven otherwise and requires urgent evaluation.
287
What are the causes of hypercalcemia?
The causes of hypercalcemia can be remembered by the acronym CHIMPS: Cancer, Hyperthyroid, Iatrogenic, Myeloma, hyperParathyroidism, Sarcoidosis.
288
What are the signs and symptoms of hypercalcemia?
Hypercalcemia is usually asymptomatic but can include neuro symptoms, cardiac issues, musculoskeletal problems, gastrointestinal symptoms, and renal issues.
289
What neuro symptoms can occur with hypercalcemia?
Neuro symptoms may include blurred vision, slowed or absent reflexes, fatigue, anxiety, confusion, and hallucinations.
290
What cardiac symptoms are associated with hypercalcemia?
Cardiac symptoms can include arrhythmias, shortened QT interval, bradycardia, and hypertension.
291
What musculoskeletal symptoms can occur with hypercalcemia?
Musculoskeletal symptoms may include muscle weakness and bone pain or weak bones.
292
What gastrointestinal symptoms can occur with hypercalcemia?
Gastrointestinal symptoms can include anorexia, nausea/vomiting, and constipation.
293
What renal symptoms can occur with hypercalcemia?
Renal symptoms may include kidney stones, polyuria, and polydipsia.
294
What is Parathyroid Hormone Related Peptide (PTHrP)?
PTHrP is released by some cancers and acts as a PTH agonist, but it is not a screening tool for cancer.
295
What are the common cancers associated with PTHrP release?
The most common cancers associated with PTHrP release are breast, lung, renal, and female reproductive cancers.
296
What are the indications for testing PTHrP?
Indications for testing PTHrP include unexplained hypercalcemia.
297
What are the two types of vitamin D levels that can be ordered?
The two types of vitamin D levels are 25-hydroxyvitamin D (25(OH) Vit D) and 1,25-dihydroxyvitamin D (1,25-(OH)2 Vit D).
298
What does 25-hydroxyvitamin D represent?
25-hydroxyvitamin D represents the general vitamin D level that is typically measured.
299
What does 1,25-dihydroxyvitamin D represent?
1,25-dihydroxyvitamin D represents the active form of vitamin D and is not measured as frequently.
300
What other lab tests are relevant for calcium evaluation?
Other relevant lab tests include phosphorus, magnesium, renal function, and a 24-hour urine test for calcium.
301
What is the purpose of a 24-hour urine test for calcium?
A 24-hour urine test for calcium is useful in distinguishing Familial Hypocalciuric Hypercalcemia from Primary Hyperparathyroidism.
302
What is a Parathyroid Scan?
A Parathyroid Scan, also known as a Sestamibi Scan, is a nuclear medicine study.
303
When is a Parathyroid Scan indicated?
A Parathyroid Scan is indicated when there is suspicion of a parathyroid adenoma.
304
What are the indications for testing PTH?
Indications for testing PTH include abnormal calcium or phosphorus levels, signs or symptoms of parathyroid disease, and CKD monitoring.
305
How is phosphorus related to calcium?
Phosphorus is inversely proportional to calcium.
306
How does magnesium affect calcium levels?
Magnesium affects calcium by multiple pathways; hypomagnesemia can cause hypocalcemia, and hypermagnesemia can suppress PTH.
307
What are the effects of chronic kidney disease (CKD) on calcium?
CKD can lead to hypocalcemia due to decreased reabsorption and decreased vitamin D activation, as well as hyperphosphatemia.
308
What are the two types of serum calcium?
The two types of serum calcium are total calcium and ionized calcium.
309
What is calcitonin and where is it produced?
Calcitonin is produced by the thyroid and is released in response to hypercalcemia.
310
How does calcitonin decrease calcium levels?
Calcitonin decreases calcium levels by increasing bone formation and decreasing renal reabsorption.
311
What percentage of the body's calcium is found in the bones?
99% of the body's calcium is found in the bones.
312
What are the signs and symptoms of hypoparathyroidism?
Signs and symptoms of hypoparathyroidism include paresthesias, Chvostek/Trousseau signs, muscle cramps, long QT, and seizures.
313
What are common causes of hypoparathyroidism?
Common causes of hypoparathyroidism include surgical removal of parathyroid glands, autoimmune conditions, genetics, and pseudohypoparathyroidism.
314
Hypercalcemia workup
315
Hypercalcemia summary table
316
Hypocalcemia
Normal range: 8.5-10.5 mg/dL
Hypocalcemia = serum calcium < 8.5 mg/dL
DON’T FORGET TO CORRECT FOR HYPOALBUMINEMIA!
317
Comparison of Thyroid Diseases
318
What is the most likely explanation for the lab findings of a 55-year-old woman with ESRD who underwent a kidney transplant, with calcium at 11.6 mg/dL and PTH at 190 pg/mL?
Tertiary hyperparathyroidism
319
Which test best differentiates familial hypocalciuric hypercalcemia from primary hyperparathyroidism?
24-hour urine calcium
320
A patient presents with elevated PTH and hypercalcemia, and a 24-hour urine calcium level is low. Which diagnosis should be considered?
Familial hypocalciuric hypercalcemia (FHH)
321
What is the most likely diagnosis for a 59-year-old woman with fatigue, bone pain, constipation, and recent nephrolithiasis, with serum calcium at 11.5 mg/dL, PTH at 130 pg/mL, and phosphate at 2.1 mg/dL?
Primary hyperparathyroidism
322
What additional test would best help localize the cause of a patient's primary hyperparathyroidism?
Neck ultrasound
323
What best explains the elevated PTH in a 63-year-old man with CKD presenting with fatigue and muscle cramps, with serum calcium at 8.2 mg/dL, phosphate at 6.0 mg/dL, and PTH at 410 pg/mL?
Chronic kidney disease
324
What are the causes for hypocalcemia?
Parathyroid issue, Acute illness (e.g., Pancreatitis), Medications (e.g., cinacalcet, phenytoin), Low vitamin D, Kidney disease, Low magnesium, High phosphate
325
What are the signs and symptoms of hypocalcemia?
Paresthesias, Chvostek/Trousseau signs, Muscle cramps, Long QT, Seizures
326
What is the initial workup for hypocalcemia?
Calcium is obtained and comes back low. Correct for albumin and if still low will need to repeat to confirm.
327
What tests should be done to identify the cause of hypocalcemia?
Shoot broad: ionized calcium, PTH, phosphate, magnesium, Vitamin D, creatinine
328
What are the two functions of the pancreas?
Exocrine and endocrine functions
329
What does the exocrine function of the pancreas do?
Secretes substances through ducts, including digestive enzymes
330
What does the endocrine function of the pancreas do?
Secretes substances directly into the blood, including insulin and glucagon
331
What hormones are involved in glucose regulation?
Insulin and glucagon
332
What are the glucose diagnostics?
Fasting Plasma Glucose, A1C, Oral Glucose Tolerance Test (OGTT)
333
What is required before a Fasting Plasma Glucose test?
Patient should have nothing to eat or drink (NPO) for at least 8 hours prior to lab collection (water is ok)
334
What are the indications for Fasting Plasma Glucose?
Concern for diabetes mellitus, Monitor treatment for diabetes mellitus
335
What is the procedure for Fasting Plasma Glucose?
Should be performed via intravenous collection; FSBS (finger stick blood sugar) is not as accurate and cannot be used for diagnosis
336
What does A1C measure?
Measure of glycosylated hemoglobin
337
What is the normal range for A1C?
Normal 4-5.6%
338
What are the indications for Oral Glucose Tolerance Test (OGTT)?
Screening and diagnosis of DM, Diagnosis of gestational diabetes, Evaluation of insulin resistance, Evaluation of reactive hypoglycemia
339
What is the procedure for Oral Glucose Tolerance Test (OGTT)?
Fasting blood glucose obtained; Patient drinks a glucose-containing drink (typically 75 g); Serial blood glucose levels obtained at fixed intervals
340
What is considered a normal result for OGTT?
Glucose < 140 mg/dL at 2-hour mark
341
What are the ADA criteria for diagnosing Diabetes Mellitus?
Hgb A1c ≥ 6.5%, Fasting Plasma Glucose (FPG) ≥ 125 mg/dL, 2-hr plasma glucose of ≥ 200 mg/dL, Any random glucose ≥ 200 mg/dL
## Footnote
All should be repeated on a second day to confirm
342
What are the ADA criteria for diagnosing Prediabetes?
Hgb A1c: 5.7-6.4%, Fasting Plasma Glucose (FPG) of 100-124 mg/dL, 2-hr plasma glucose of 140-199 mg/dL
343
DM Summary Table
344
What is Type 1 DM?
Lack of insulin due to destruction of beta cells. Most often autoimmune.
## Footnote
Other abbreviations: T1DM, IDDM*
345
What is Type 2 DM?
Characterized by insulin resistance and complex pathophysiology.
## Footnote
Other abbreviations: T2DM, NIDDM*
346
What is Gestational DM?
Occurs during pregnancy, thought to be caused by hormones released by the placenta leading to insulin resistance.
347
What are other causes of DM?
Pancreatic disease, drug-induced, cystic fibrosis related, or due to other endocrine disorders.
348
How to differentiate between T1DM and T2DM?
By measuring autoantibodies and C peptide levels.
349
What routine monitoring should all DM patients undergo?
A1C every 3 months, lipid panel yearly, and urine microalbumin/creatinine ratio yearly.
350
In which type of DM are autoantibodies more common?
T1DM.
351
What are the autoantibodies associated with T1DM?
Glutamic acid decarboxylase (GAD), Islet cell Ab, Insulin Ab, Insulinoma associated protein 2 Ab (IA-2), Zinc transporter Ab (ZnT8).
352
What does low C-peptide indicate?
It is more consistent with T1DM.
353
What is DKA?
Diabetic Ketoacidosis; milder but serious, more common in T1DM, often a presenting sign of T1DM.
354
What triggers DKA?
Significant insulin deficiency leads to lipolysis, increased gluconeogenesis, and ketogenesis.
355
What is HHS?
Hyperglycemic Hyperosmolar State; more severe and common in T2DM.
356
What triggers HHS?
Increased stress hormones lead to gluconeogenesis, with no lipolysis and minimal ketoacids produced.
357
What are common lab findings for DKA?
Hyperglycemia and ketoacidosis.
358
What does hyperglycemia in DKA lead to?
Elevated serum osmolality, hyponatremia (factitious), glucosuria, and osmotic diuresis.
359
What does ketoacidosis in DKA lead to?
High anion gap metabolic acidosis, low bicarbonate (acidosis), +/- hypokalemia, urine ketones, and serum ketones (beta-hydroxybutyrate).
360
What is euglycemic DKA?
Rare condition where glucose is generally < 200 mg/dL, but acidosis and ketosis are present. More common in T1DM.
361
What are the causes of euglycemic DKA?
Starvation, SGLT2 inhibitors, carbohydrate restriction, heavy alcohol use, liver disease, pregnancy, acute illness.
362
What are common lab findings for HHS?
Severe hyperglycemia (generally > 600 mg/dL but often in 1000s), significantly elevated serum osmolality (> 320 mOsm/kg), hyponatremia (factitious), glucosuria.
363
What is the rule of thumb for correcting serum sodium in severe hyperglycemia?
For every 100 mg/dL over 100 mg/dL in glucose, add 1.6 mg/dL to serum sodium.
364
DKA and HHS lab tables
365
Hypoglycemia summary table
366
What is hypoglycemia?
A condition characterized by abnormally low blood glucose levels.
367
What is the most common cause of hypoglycemia in diabetic patients?
Medication effect.
368
What are the two scenarios when hypoglycemia can happen?
Reactive/postprandial hypoglycemia and fasting hypoglycemia.
369
What are the causes of reactive/postprandial hypoglycemia?
Developing diabetes mellitus and gastrointestinal malfunction.
370
What are the causes of fasting hypoglycemia?
Insulinoma, exogenous/excess insulin administration, autoimmune conditions, cirrhosis, adrenal insufficiency, and sepsis.
371
What is Whipple’s Triad for hypoglycemia?
Symptoms of hypoglycemia, plasma glucose < 55 mg/dL when symptoms occur, and decrease in symptoms with correction of glucose level.
372
What is key in diagnosing hypoglycemia?
History is key!
373
What tests are conducted if no obvious etiology for hypoglycemia is found?
Insulin level, C-peptide, and proinsulin.
374
What are some additional tests for hypoglycemia?
Insulin antibodies, beta-hydroxybutyrate, sulfonylurea levels, workup of adrenal insufficiency, 48- or 72-hour fast, and mixed meal study.
375
What is the purpose of a 48 or 72-hour fast?
Useful in the evaluation of fasting hypoglycemia.
376
What is the purpose of a mixed meal study?
Useful in the evaluation of postprandial hypoglycemia.
377
What types of endocrine cancers are associated with hypoglycemia?
Adrenal, thyroid, pituitary, parathyroid, pancreatic, and multiple endocrine neoplasia (MEN).
378
What are the types of adrenal cortex tumors?
Benign adenoma (functioning and non-functioning), malignant adrenocortical carcinoma, and metastases.
379
How are adrenal cortex tumors often found?
Incidentally, termed incidentaloma.
380
What is the CT adrenal protocol for imaging adrenal cortex tumors?
Initial imaging does NOT use contrast and assesses for functionality.
381
What factors matter in adrenal cortex tumor imaging?
Size (> 4 cm more likely malignant) and Hounsfield units (>10 more likely malignant).
382
What is done if CT is not appropriate for adrenal cortex tumor imaging?
MRI is used.
383
What labs are used for adrenal insufficiency?
AM cortisol and cosyntropin stimulation test.
384
What labs are used for Cushing syndrome?
24-hour urine free cortisol, dexamethasone suppression test, and fasting glucose.
385
What should be checked if a patient is hypertensive with low potassium?
Aldosterone and renin levels.
386
What are the indications for testing for pheochromocytoma?
Classic triad (headache, sweating, tachycardia) +/- hypertension, onset of hypertension at a young age (< 20 years old)/resistant hypertension, familial syndrome associated with pheo (MEN2, neurofibromatosis 1, or von Hippel-Lindau), and family history of pheochromocytoma.
387
What is this pathology?
Adrenal cortex tumors
388
What is this pathology?
Pheochromocytoma
389
Pheochromocytoma Imaging
CT or MRI abd/pelvis
Can have extra-adrenal tumor
390
Pheochromocytoma Labs
24 hr urine fractionated metanephrines and catecholamines (Test of Choice)
+/- plasma fractionated metanephrines and catecholamines
391
What is this pathology?
Pheochromocytoma
392
Thyroid Cancers
Papillary carcinoma, Follicular carcinoma, Anaplastic carcinoma, Oncocytic carcinoma
High grade, poorly differentiated carcinoma, Medullary thyroid cancer
393
This patient most likely has
Thyroid Cancers
394
What is this pathology?
Thyroid Cancer
395
What are the thyroid cancer markers?
None
## Footnote
Exception: CEA (carcinoembryonic antigen) in medullary cancer
396
What imaging is used for thyroid cancer?
Ultrasound (US)
397
What labs are used for thyroid cancer?
TSH, free T4 (total T3), thyroglobulin level
## Footnote
Used for treatment monitoring and monitoring for recurrence.
398
What is used to monitor recurrence of medullary cancer?
Calcitonin
399
What is the definitive diagnosis method for thyroid cancer?
Biopsy/Fine Needle Aspiration (FNA)
400
What are the primary pituitary tumors?
Adenoma (most common), carcinoma, craniopharyngioma, meningioma
401
What metastatic tumors can affect the pituitary?
Lung and breast tumors
402
What imaging is used for pituitary tumors?
MRI brain with/without pituitary protocol
403
What labs are checked for hypersecretion in pituitary tumors?
IGF-1, 24 hr urine free cortisol, ACTH, prolactin, free T4, LH/FSH
404
What labs are checked for hyposecretion in pituitary tumors?
IGF-1, AM cortisol, free T4, AM testosterone (males), LH/FSH/estradiol (females if amenorrhea)
405
What is the definitive diagnosis method for pituitary tumors?
Resection and pathology
406
What is this pathology?
Normal Pituitary MRI
407
What is this pathology?
Pituitary adenoma
408
What is the most common type of parathyroid tumor?
Adenoma
409
What is a rare type of parathyroid tumor?
Carcinoma
410
What imaging method is used for diagnosing parathyroid tumors?
Nuclear med scan (Sestamibi)
411
What are the diagnostics for parathyroid tumors?
Ionized calcium + PTH
Definitive diagnosis: resection/path
412
What are the two types of pancreatic tumors?
Exocrine and Endocrine
413
What is the most common malignant exocrine pancreatic tumor?
Ductal adenocarcinoma (85-95%)
414
What is a type of endocrine pancreatic tumor?
Pancreatic neuroendocrine tumor
415
What are some metastases that can go to the pancreas?
Renal cell carcinoma and Melanoma
416
What is a diagnostic marker for pancreatic cancer?
CA 19-9
417
What imaging diagnostics are used for pancreatic cancers?
Ultrasound / EUS, CT, MRI / MRCP, ERCP
418
What lab diagnostics are used for pancreatic cancers?
Liver function tests, Lipase/amylase, Gastrin, Fasting glucose
419
What is the definitive diagnosis for pancreatic cancers?
Biopsy, resection, and pathology
420
What are Multiple Endocrine Neoplasia (MEN)?
Genetic disorders that cause tumors to form in endocrine glands
421
What are the types of Multiple Endocrine Neoplasia?
MEN Type 1, MEN Type 2a, MEN Type 2b
422
What gene mutation is associated with MEN Type 1?
MEN1 gene mutation on Chromosome 11
423
What types of tumors are associated with MEN Type 1?
Parathyroid adenoma, Pancreatic endocrine tumor, Pituitary adenoma - Prolactinoma
424
What is involved in the diagnosis of MEN Type 1?
Workup of individual diseases, Genetic testing
425
What gene mutation is associated with MEN Type 2a?
RET gene mutation on Chromosome 10
426
What types of tumors are associated with MEN Type 2a?
Medullary thyroid cancer, Pheochromocytoma, Parathyroid hyperplasia
427
What is involved in the diagnosis of MEN Type 2a?
Workup of individual diseases, Genetic testing
428
What gene mutation is associated with MEN Type 2b?
RET gene mutation on Chromosome 10
429
What types of tumors are associated with MEN Type 2b?
Medullary thyroid cancer, Pheochromocytoma, Mucosal neuromas
430
What is involved in the diagnosis of MEN Type 2b?
Workup of individual diseases, Genetic testing
431
Cancer Summary Tables
432
Hypercortisolism
433
Hypocortisolism
434
Hypothyroidism
435
Hyperthyroidism
436
Hypoaldosterone and Hyperaldosterone
437
DM
HgbA1c- ≥ 6.5%
Fasting Plasma Glucose- ≥ 126 mg/dL
Oral Glucose Tolerance Test- 2 hr plasma glucose ≥ 200 mg/dL
438
Prediabetes
HgbA1c- 5.7-6.4%
Fasting Plasma Glucose- 100-124 mg/dL
Oral Glucose Tolerance Test- 2 hr plasma glucose of 140-199 mg/dL
439
Compare the DKA and HHS
440
SIADH
Typical presenting symptom is hyponatremia
Labs: serum and urine sodium and osmolality
Add’l eval: +/- MRI brain and CXR/CT chest
441
Diabetes Insipidus
Typical presenting symptom is polyuria/polydipsia
Labs: 24 hr urine volume, urine osmolality
Add’l eval: water deprivation and desmopressin challenge (should be able to explain these)
442
A 58-year-old woman presents with fatigue and bone pain. Labs show:
Serum calcium: 11.2 mg/dL PTH: Elevated Phosphate: Low
What is the most likely diagnosis?
Primary Hyperparathyroidism
443
A patient has the following labs:
Morning cortisol: 3 µg/dL ACTH: Elevated Electrolytes: Na+ 129, K+ 5.6
What is the most likely diagnosis?
Primary adrenal insufficiency
444
A 34-year-old woman complains of weight loss, palpitations, and tremors.
Labs: TSH: <0.01 Free T4: High
What is the most likely diagnosis?
Graves’ disease (Hyperthyroidism)
445
A post-thyroidectomy patient presents with tingling and muscle cramps.
Labs: Calcium: 7.2 mg/dL Phosphate: High PTH: Low
What is the most likely diagnosis?
Post-surgical hypoparathyroidism
