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Step 2 > Endocrinology > Flashcards

Endocrinology Flashcards

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

A
24
Q

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

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
Q

Prolactinoma in men vs. women

A

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
Q

Diagnostic workup of prolactinoma
Treatment

A

Check meds (dopamine antagonists i.e. antipsychotics)
TSH (hypothyroidism induces hyperprolactinemia)
Prolactin
- Treat with dopamine agonists: cabergoline, bromocriptine (dopamine inhibits prolactin)

27
Q

Diagnostic workup of Acromegaly
Tx

A

ILGF-1 level
Glucose suppression test (fail to suppress)- get MRI–> resect
Tx: octreotide

28
Q

Sxs acromegaly adults vs. kids

A

Kids: gigantism
Adults: Hands, feet, face, diabetes (GH tells liver to make glucose), diastolic HF

29
Q

Sxs of acute hypopituitarism
(Think lost cortisol, lost T4)
- Etiologies (hemorrhagic)

A
  • Cortisol: hypotensive, tachycardic
  • T4: lethargy, coma, weight loss
    Sheehan’s- pregnancy (large hemorrhage–> coma)
    Apoplexy = tumor
30
Q

Sxs of chronic hypopituitarism (autoimmune, deposition disease (sarcoid, amyloid), mass effect from slow growing tumor)

A
  • less essential hormones will be lost first (i.e FSH, GH)– presentation with low libido, fatigue, menstrual cycle
31
Q

Two etiologies of SIADH (body reabsorbs water inappropriately)

A
  1. Brain lesion secreting ADH
  2. Lung lesion secreting ADH (small cell)
32
Q

What happens to Uosm and Una in SIADH?
What happens to serum osms?
Tx?

A 
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
Q

Diabetes insipidus etiologies + tx (not enough ADH, body does not reabsorb enough water)

A
  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
Q

What happens to Uosm and Una in diabetes insipidus?

A

Uosm decrease (excess water released into urine)

  • polydipsia, polyuria
  • Normal blood glucose, no glucose in urine
35
Q

Water deprivation test for Diabetes insipidus

A
  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
Q

T4 allows the body to:

A

movement, mentation, metabolism

37
Q

Sxs of Hyperthyroidism
(Thyrotoxicosis= too much T4)
Heart
Bowels
Metabolism
reflexes
weight

  • T4, TSH levels
A

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
Q

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

A

-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
Q

Sxs/Tx for Thyroid storm

A

Afib/shock
Burning up- severe fever
Hypotensive
Altered
- IVF blankets for cooling, Beta blocker (propranolol to reduce autonomic sis), PTU/methimazole, steroids

40
Q

Tx
Graves
- everything else

A

Grave’s responds to medical therapy or surgery b/c radioactive iodine ablation makes exopthalmos worse
- all others will require radioactive iodine ablation

41
Q

Sxs Hypothyroidism (increased TSH, low T4)
Heart
Bowels
Metabolism
reflexes
weight

Menses/libido

Muscles

A

Bradycardia
Constipation
Cold intolerance
Diminished DTR
weight gain
- tx: give levothyroxine

  • menstrual irregularities
  • painful muscle weakness
42
Q

Grave’s Antibodies
Hashimoto’s Antibodies

A
  • Thyroid stimulating antibodies
  • Thyroid peroxidase antibodies (TPO)
43
Q

Risk factors for malignant thyroid nodules
Patient factors
Nodule factors
US
Biopsy- shows cancer–> resect

A
  • 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
Q

Diagnostic workup of thyroid nodule
**hot= not malignancy
**cold= risk for malignancy

A
  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
Q

Thyroid cancers
Papillary
Follicular
Medullary
Anaplastic

A
  • 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
Q

Men 1 (MEN gene)

A

Pituitary
Parathyroid (hypercalcemia)
Pancreas (zollinger ellison- ulcers, insulinoma-hypoglycemia- with c-peptide)

47
Q

Men 2a (ret oncogene)

A

Pheo, medullary thyroid cancer, parathyroid

48
Q

Men 2b (ret oncogene)

A

Pheo, medullary thyroid cancer, neuronal tumors

49
Q

Primary vs. Secondary vs. Tertiary Hyperparathyroidism

A

Table of levels

50
Q

Symptoms of Addison’s disease

Mineralcorticoids

Glucocorticoids

Androgens

A

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
Q

How does chronic vitamin D deficiency lead to osteomalacia (and secondary hyperparathyroidism)?

Lab findings in osteomalacia?

A

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
Q

Low specific gravity of urine (<1.006), polyuria (urine outpt>3L over 24 hrs) in setting of normal serum sodium and fluid intake (2L)

A

Diabetes insipidus

53
Q

When does hyperprolactinemia require tx?

A
  • 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
Q

1st line interventions following first gout attack

A
  • Alcohol cessation and weight loss
55
Q

Milk Alkali syndrome (hypercalcemia 2/2 intake i.e. patient taking calcium carbonate for osteoporosis)

A
  • Nausea, vomiting, constipation, polyuria, polydipsia

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