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Endocrinology Flashcards

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1
Q

Cushing’s syndrome is driven by:

A

Cortisol Excess

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2
Q

The two ACTH dependent causes of Cushing’s syndrome are? How does it work?

A
  1. Lung tumor (small cell) secreting ACTH
  2. Tumor on anterior pituitary secreting ACTH (Cushing’s disease)
    - ACTH triggers release of cortisol- High ACTH present
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3
Q

The two ACTH independent causes of Cushing’s syndrome are? How does it work?

A
  1. Exogenous steroid intake
  2. Primary tumor of adrenal gland producing cortisol
    - Excess cortisol suppresses ACTH- low ACTH present
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4
Q

Excess cortisol causes:

A

Blood pressure, sugars (excess–> HTN, diabetes, obesity)
- Moon facies, truncal obesity, purple striae (also easy bruising), buffalo hump

  • bone loss
  • hirsutism
  • painless muscle weakness with normal ESR/CK (catabolic effect of cortisol on muscle)

-

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5
Q

Diagnostic Workup for Cushing’s syndrome
(Low THen High)

A

Low Then High:

  1. Low dose dexamethasone suppression test (also with 24 hr urine cortisol or late night salivary cortisol)
  2. ACTH (low= tumor, high= ACTH dependent)
  3. High dose dexamethasone suppression test if ACTH high
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6
Q

How do you interpret a low dose dexamethasone test to indicate Cushing’s syndrome?

A

Positive test is failure to suppress cortisol

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7
Q

What does a low ACTH mean after a positive low dose dexamethasone test?

A

If you have excluded exogenous medications, then it indicates an adrenal tumor making excess cortisol –> CT/MRI then resect

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8
Q

How do you interpret a high dose dexamethasone test to distinguish between ACTH dependent causes of Cushing’s syndrome?

A
  1. Suppression= Cushing’s disease (tumor of anterior pituitary)–> resect
  2. Fail to suppress= ectopic tumor–> Pan Scan to find where it is
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9
Q

Addison’s disease is driven by?
What are the two most common etiologies?

A

Primary cortisol deficiency via destruction of adrenal gland
- Autoimmune, TB (developing world)

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10
Q

What are the two etiologies of cortisol deficiency?

A
  1. Pituitary gland (only deficiency of cortisol)
  2. Adrenal gland (deficiency of cortisol AND aldosterone)
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11
Q

Acute Addison’s disease i.e. hemorrhage: the loss of cortisol and aldosterone cause?

A

Cortisol is necessary for blood vessels to work; aldosterone is required to retain sodium/fluid–> no volume, no tone; Hypotension, nausea, vomiting, coma

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12
Q

Chronic Addison’s disease i.e. infiltrative disease, autoimmune, metastatic malignancy

A
  • Orthostatic hypotension
  • No cortisol is being made but ACTH still being made–> no feedback to suppress ACTH production; byproduct–> hyperpigmentation
  • Low sodium, high K due to lack of aldosterone
  • Loss of mineralcorticoids, glucocorticoids, and androgens: **(salt craving, weight loss), (fatigue/anorexia, psychiatric manifestatinos (depression irritability)), (low libido, reduced pubic hair)
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13
Q

Diagnostic workup for Addison’s disease

  • 2 diagnostic tests
  • Imaging
  • Treatment
A
  1. Early am cortisol: low cortisol indicates addison’s (normal= not addison’s)
  2. Cosyntropin stim test (giving ACTH)
    - If cortisol rises- problem is with anterior pituitary (get MRI); will just need to replace cortisol
    - If cortisol does not change- problem with adrenal gland (CT or MRI) - must replace cortisol and give fludrocortisone
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14
Q

Conn’s syndrome causes:

A

Excess aldosterone (primary hyperaldosteronism)

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15
Q

Which axis is affected by primary hyperaldosteronism?

A

Renin-angiotensin-aldosterone system

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16
Q

What are the two etiologies of hyperaldosteronism?

A
  1. Primary tumor of adrenal gland
  2. Renovascular HTN
    - FMD - women
    - atherosclerosis- men
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17
Q

Diagnostic workup of Conn’s Syndrome
- Treatment

A

Aldo:Renin ratio
- Aldo/Renin not elevated (licorice, CAH)
- Aldo/Renin both elevated (ratio less than 10)– renovascular HTN–> stent for FMD, handle BP for AS
- Aldo much higher than Renin (ratio greater than 30)–> Conn’s
Confirmatory Test= Salt suppression (failure to suppress aldo= conn’s)
**get adrenal vein sampling (renin high on affected side)

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18
Q

Pheochromocytoma secretes?

A

Catecholamine (from medulla of adrenal gland)

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19
Q

Sxs of pheochromocytoma

A

Paroxysmal
Pain (headache)
Pressure (HTN)
Palpitations (tachy)
Perspiration

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20
Q

Diagnostic workup of pheochromocytoma

A

plasma free catecholamines (urgent)
24 hr urine metanephrines (more sensitive)
- find mass w/ CT/MRI- adrenal vein sampling

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21
Q

Tx of pheochromocytoma

A
  1. Give alpha blockade first, then beta blockade then resect
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22
Q

Posterior pituitary secretes:

A

ADH, oxytocin

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23
Q

HPA Axis

24
Q

Hypothalamus secretes:
Anterior pituitary secretes:
Organ:
Hormone:
Activity:

Study These Flashcards
A

CRH, TRH, GHrH, GnRH
ACTH, TSH, GH, FSH/LH
Adrenal, Thyroid, Liver, Repro
Cortisol, T4, ILGF, testosterone/estrogen
stress, metabolic activity, growth, repro

25
Prolactinoma in men vs. women
Women: amennhorrea, galactorrhea- usually present earlier so no field cuts in vision (micro adenoma caught early, does not have mass effect) Men: decreased libido, tumor will grow to macroadenoma-- compresses optic chiasm (bitemporal hemianopsia)
26
Diagnostic workup of prolactinoma Treatment
Check meds (dopamine antagonists i.e. antipsychotics) TSH (hypothyroidism induces hyperprolactinemia) Prolactin - Treat with dopamine agonists: cabergoline, bromocriptine (dopamine inhibits prolactin)
27
Diagnostic workup of Acromegaly Tx
ILGF-1 level Glucose suppression test (fail to suppress)- get MRI--\> resect Tx: octreotide
28
Sxs acromegaly adults vs. kids
Kids: gigantism Adults: Hands, feet, face, diabetes (GH tells liver to make glucose), diastolic HF
29
Sxs of acute hypopituitarism (Think lost cortisol, lost T4) - Etiologies (hemorrhagic)
- Cortisol: hypotensive, tachycardic - T4: lethargy, coma, weight loss Sheehan's- pregnancy (large hemorrhage--\> coma) Apoplexy = tumor
30
Sxs of chronic hypopituitarism (autoimmune, deposition disease (sarcoid, amyloid), mass effect from slow growing tumor)
- less essential hormones will be lost first (i.e FSH, GH)-- presentation with low libido, fatigue, menstrual cycle
31
Two etiologies of SIADH (body reabsorbs water inappropriately)
1. Brain lesion secreting ADH 2. Lung lesion secreting ADH (small cell)
32
What happens to Uosm and Una in SIADH? What happens to serum osms? Tx?
``` Uosm increase (very concentrated because reabsorbing too much water) - To compensate for excess water, body turns off aldosterone (reabsorption of Na) b/c water follows salt and it wants to get rid of the excess water Una increases as well - Serum Na= low --\> hyponatremia Tx= water restriction, reverse underlying disease, demeclocycline if that fails ```
33
Diabetes insipidus etiologies + tx (not enough ADH, body does not reabsorb enough water)
1. Lack of production of ADH in brain--\> central --\> DDAVP (vasopressin) 2. ADH receptors on kidney not working--\> nephrogenic (demeclocycline or lithium toxicity) --\> gentle diuresis, HCTZ, amilioride
34
What happens to Uosm and Una in diabetes insipidus?
Uosm decrease (excess water released into urine) - polydipsia, polyuria - Normal blood glucose, no glucose in urine
35
Water deprivation test for Diabetes insipidus
1. Fluid restriction - if Uosm increase and become less dilute--\> psychogenic polydipsia alone - if Uosm stay dilute --\> DI 2. Give ADH - if Uosm correct (didn't have enough ADH around)--\> central - If Uosm stay low--\> nephrogenic, kidney cannot respond
36
T4 allows the body to:
movement, mentation, metabolism
37
Sxs of Hyperthyroidism (Thyrotoxicosis= too much T4) Heart Bowels Metabolism reflexes weight - T4, TSH levels
Tachycardia, increased sensitivity to catecholamines- heart too fast, increased contractility, increased oxygen demand Diarrhea - bowels too fast Heat intolerant - metabolizing more Increased deep tendon reflexes Weight Loss Afib - Excess FT4, low TSH (due to feedback)
38
Radioactive iodine uptake for causes of Hyperthyroidism: Grave's Thyroiditis (hashimoto's= painless, de quervain= painful (infectious, acute granulomatous) Multinodular goiter/toxic adenoma Factitious Struma Ovarii
-Grave's: whole thyroid lights up (antibody receptors are all over thyroid) \*\*exopthalmos, pretibial myxedema, thyroid stimulating antibodies -- medical therapy (PTU, methimazole) - Thyroiditis - transient hyperthyroid state because an insult broke the thyroid and preformed T4 spilled out--\> thyroid either heals or dies (hashimoto's); no new T4 being made so RAIU looks cold - Multinodular goiter- a bunch of small hot spots, one large hot spot - factitious= exogenous T4 ingested- cold thyroid - Struma ovarii= ovarian lesion making T4- cold thyroid
39
Sxs/Tx for Thyroid storm
Afib/shock Burning up- severe fever Hypotensive Altered - IVF blankets for cooling, Beta blocker (propranolol to reduce autonomic sis), PTU/methimazole, steroids
40
Tx Graves - everything else
Grave's responds to medical therapy or surgery b/c radioactive iodine ablation makes exopthalmos worse - all others will require radioactive iodine ablation
41
Sxs Hypothyroidism (increased TSH, low T4) Heart Bowels Metabolism reflexes weight Menses/libido Muscles
Bradycardia Constipation Cold intolerance Diminished DTR weight gain - tx: give levothyroxine - menstrual irregularities - **painful muscle weakness**
42
Grave's Antibodies Hashimoto's Antibodies
- Thyroid stimulating antibodies - Thyroid peroxidase antibodies (TPO)
43
Risk factors for malignant thyroid nodules Patient factors Nodule factors US Biopsy- shows cancer--\> resect
- Radiation of head/neck - Hoarseness (potential invasion of local tissue) - Age (less than 20, greater than 60) - fixed, firm, hard, nontender lymphadenopathy - solid mass, hypoechogenic, \>2cm, micro calcifications, irregular borders -- with these present, get biopsy (FNA)
44
Diagnostic workup of thyroid nodule \*\*hot= not malignancy \*\*cold= risk for malignancy
1. Get TSH - low TSH= low risk for malignancy 2. RAIU scan - hot nodule (hyper functioning)- tx with radioactive iodine ablation - cold nodule (non-functioning)- risk for caner --\> do US then FNA - if TSH was normal or elevated--\> High-risk for cancer- get US - If US shows nodule over 1 cm- do FNA - if US shows less than 1 cm- watch and wait
45
Thyroid cancers Papillary Follicular Medullary Anaplastic
- Papillary (most common)= orphan annie nuclei- resect - Follicular- hematogenous spread--\> radioactive iodine ablation - Medullary- C cells/calcitonin (hypocalcemia)l ret oncogene/pheochromocytoma - Anaplastic- elderly, rapidly invasive
46
Men 1 (MEN gene)
Pituitary Parathyroid (hypercalcemia) Pancreas (zollinger ellison- ulcers, insulinoma-hypoglycemia- with c-peptide)
47
Men 2a (ret oncogene)
Pheo, medullary thyroid cancer, parathyroid
48
Men 2b (ret oncogene)
Pheo, medullary thyroid cancer, neuronal tumors
49
Primary vs. Secondary vs. Tertiary Hyperparathyroidism
Table of levels
50
Symptoms of Addison's disease Mineralcorticoids Glucocorticoids Androgens
Min: Renal salt wasting, hypotension, weight loss, hyponatremia, hyperkalemia (no aldosterone), salt craving Gluc: fatigue, anorexia, hypotension, psychiatric manifestations Androgens: loss of libido, reduced pubic hair (not as pronounced in men b/c testosterone still made in testes)
51
How does chronic vitamin D deficiency lead to osteomalacia (and secondary hyperparathyroidism)? Lab findings in osteomalacia?
Vitamin D deficiency leads to decreased reabsoprtion of calcium/phosphate in the intestines. Low calcium triggers high PTH secretion. Osteomalacia- characterized by bone pain, muscle weakness - reduced mineralization of osteoid at bone-forming sites due to lack of vitamin D/calcium - High alk phos, high PTH, low phos, low to normal calcium
52
Low specific gravity of urine (\<1.006), polyuria (urine outpt\>3L over 24 hrs) in setting of normal serum sodium and fluid intake (2L)
Diabetes insipidus
53
When does hyperprolactinemia require tx?
- premenopausal women with hypogonadal sxs to avoid osteoporosis 2/2 estrogen deficiency - galactorrhea - macroprolactinoma (\>10mm) - risk or presence of neurologic sxs (mass effect) treat with cabergoline/bromocriptine
54
1st line interventions following first gout attack
- Alcohol cessation and weight loss
55
Milk Alkali syndrome (hypercalcemia 2/2 intake i.e. patient taking calcium carbonate for osteoporosis)
- Nausea, vomiting, constipation, polyuria, polydipsia

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