Endocrinology Flashcards
Cushing’s syndrome is driven by:
Cortisol Excess
The two ACTH dependent causes of Cushing’s syndrome are? How does it work?
- Lung tumor (small cell) secreting ACTH
- Tumor on anterior pituitary secreting ACTH (Cushing’s disease)
- ACTH triggers release of cortisol- High ACTH present
The two ACTH independent causes of Cushing’s syndrome are? How does it work?
- Exogenous steroid intake
- Primary tumor of adrenal gland producing cortisol
- Excess cortisol suppresses ACTH- low ACTH present
Excess cortisol causes:
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)
-
Diagnostic Workup for Cushing’s syndrome
(Low THen High)
Low Then High:
- Low dose dexamethasone suppression test (also with 24 hr urine cortisol or late night salivary cortisol)
- ACTH (low= tumor, high= ACTH dependent)
- High dose dexamethasone suppression test if ACTH high
How do you interpret a low dose dexamethasone test to indicate Cushing’s syndrome?
Positive test is failure to suppress cortisol
What does a low ACTH mean after a positive low dose dexamethasone test?
If you have excluded exogenous medications, then it indicates an adrenal tumor making excess cortisol –> CT/MRI then resect
How do you interpret a high dose dexamethasone test to distinguish between ACTH dependent causes of Cushing’s syndrome?
- Suppression= Cushing’s disease (tumor of anterior pituitary)–> resect
- Fail to suppress= ectopic tumor–> Pan Scan to find where it is
Addison’s disease is driven by?
What are the two most common etiologies?
Primary cortisol deficiency via destruction of adrenal gland
- Autoimmune, TB (developing world)
What are the two etiologies of cortisol deficiency?
- Pituitary gland (only deficiency of cortisol)
- Adrenal gland (deficiency of cortisol AND aldosterone)
Acute Addison’s disease i.e. hemorrhage: the loss of cortisol and aldosterone cause?
Cortisol is necessary for blood vessels to work; aldosterone is required to retain sodium/fluid–> no volume, no tone; Hypotension, nausea, vomiting, coma
Chronic Addison’s disease i.e. infiltrative disease, autoimmune, metastatic malignancy
- 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)
Diagnostic workup for Addison’s disease
- 2 diagnostic tests
- Imaging
- Treatment
- Early am cortisol: low cortisol indicates addison’s (normal= not addison’s)
- 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
Conn’s syndrome causes:
Excess aldosterone (primary hyperaldosteronism)
Which axis is affected by primary hyperaldosteronism?
Renin-angiotensin-aldosterone system
What are the two etiologies of hyperaldosteronism?
- Primary tumor of adrenal gland
- Renovascular HTN
- FMD - women
- atherosclerosis- men
Diagnostic workup of Conn’s Syndrome
- Treatment
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)
Pheochromocytoma secretes?
Catecholamine (from medulla of adrenal gland)
Sxs of pheochromocytoma
Paroxysmal
Pain (headache)
Pressure (HTN)
Palpitations (tachy)
Perspiration
Diagnostic workup of pheochromocytoma
plasma free catecholamines (urgent)
24 hr urine metanephrines (more sensitive)
- find mass w/ CT/MRI- adrenal vein sampling
Tx of pheochromocytoma
- Give alpha blockade first, then beta blockade then resect
Posterior pituitary secretes:
ADH, oxytocin
HPA Axis
Hypothalamus secretes:
Anterior pituitary secretes:
Organ:
Hormone:
Activity:
CRH, TRH, GHrH, GnRH
ACTH, TSH, GH, FSH/LH
Adrenal, Thyroid, Liver, Repro
Cortisol, T4, ILGF, testosterone/estrogen
stress, metabolic activity, growth, repro
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)
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)
Diagnostic workup of Acromegaly
Tx
ILGF-1 level
Glucose suppression test (fail to suppress)- get MRI–> resect
Tx: octreotide
Sxs acromegaly adults vs. kids
Kids: gigantism
Adults: Hands, feet, face, diabetes (GH tells liver to make glucose), diastolic HF
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
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
Two etiologies of SIADH (body reabsorbs water inappropriately)
- Brain lesion secreting ADH
- Lung lesion secreting ADH (small cell)
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
Diabetes insipidus etiologies + tx (not enough ADH, body does not reabsorb enough water)
- Lack of production of ADH in brain–> central –> DDAVP (vasopressin)
- ADH receptors on kidney not working–> nephrogenic (demeclocycline or lithium toxicity) –> gentle diuresis, HCTZ, amilioride
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
Water deprivation test for Diabetes insipidus
- Fluid restriction
- if Uosm increase and become less dilute–> psychogenic polydipsia alone
- if Uosm stay dilute –> DI - Give ADH
- if Uosm correct (didn’t have enough ADH around)–> central
- If Uosm stay low–> nephrogenic, kidney cannot respond
T4 allows the body to:
movement, mentation, metabolism
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)
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
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
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
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
Grave’s Antibodies
Hashimoto’s Antibodies
- Thyroid stimulating antibodies
- Thyroid peroxidase antibodies (TPO)
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)
Diagnostic workup of thyroid nodule
**hot= not malignancy
**cold= risk for malignancy
- Get TSH - low TSH= low risk for malignancy
- 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
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
Men 1 (MEN gene)
Pituitary
Parathyroid (hypercalcemia)
Pancreas (zollinger ellison- ulcers, insulinoma-hypoglycemia- with c-peptide)
Men 2a (ret oncogene)
Pheo, medullary thyroid cancer, parathyroid
Men 2b (ret oncogene)
Pheo, medullary thyroid cancer, neuronal tumors
Primary vs. Secondary vs. Tertiary Hyperparathyroidism
Table of levels
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)
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
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
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
1st line interventions following first gout attack
- Alcohol cessation and weight loss
Milk Alkali syndrome (hypercalcemia 2/2 intake i.e. patient taking calcium carbonate for osteoporosis)
- Nausea, vomiting, constipation, polyuria, polydipsia
