Endocrinology Flash Cards

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Title: Endocrinology
Description: Endo
Number of Cards: 179
Save Count: 0
Author: kishan.parikh
Created: 2011-12-17
Tags: endo
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    • Question
    • Answer
    • Side 3
    • What is the serum osm formula?
    • Osm = 2*Na + Glucose/18 + BUN/2.8
    • What increases prolactin levels?
    • The following increase PRL levels: Dopaminergic inhibition (pregnancy, estrogen, reglan, compazine, amitriptyline), prolactinomas, hypothyroidism (modest increase)
    • Initial workup for pituitary tumor?
    • MRI, PRL, IGF-1, 24-hr urine free cortisol/overnight dex supp/ACTH stim, TSH and FT4, alpha subunit, FSH, LH
    • What is the most common cause of pituitary macroadenoma?
    • Gonadotroph vs Prolactinoma
    • What is the most common functional pituitary tumor?
    • Prolactinoma
    • Manifestation of PRL-oma?
    • decreased GnRH causing decreased LH and FSH, so ED in men and amenorrhea in women. levels correlate with tumor size (if >1cm macroadenoma, level is > 100). visual symptoms often are late.
    • Management of prolactionoma?
    • If micro (<1 cm) -- observation alone; If macro, use D agonists (cabergoline and bromocriptine). Cabergoline at high doses (i.e. Parkinson treatment) causes increased cardiac valvulopathy. Transsphenoidal surgery +/- XRT, but often recurs.
    • How do you manage prolactionoma during pregnancy?
    • Stop drugs but 1/3 of macroadenomas will enlarge during pregnancy, can restart bromocriptine (or cabergoline) if needed
    • What suppresses growth hormone?

      What stimulates GH?
    • Hyperglycemia, somatostatin, chronic corticosteroid use.

      Hypoglycemia and estrogens, via IGF-1 produced by liver
    • How to measure GH?
    • After stimulation testing bc it is released in a pulsatile fashion. Can give glucose load and expect GH suppression.
    • How does GH excess manifest? Associated with anything?
    • Before epiphyseal growth plates of long bones fuse: gigantism. After fusion, acromegaly (growth of soft tissue).

      Increased mortality with it when untreated (especially all types of heart dz, colon ca, DM 2)
    • How to manage somatrotroph adenoma?
    • Treat all patients even if asymptomatic. Start with transsphenoidal surgery and octreotide, +/- dopa agonists or GH receptor antagonist (pegvisomant)
    • How does gonadotroph adenoma present?

      How to manage it?
    • Presents variably, can have mass effect, can have gonadotroph sxs.

      Manage w/transsphenoidal surgery if symptomatic. Observe otherwise.
    • How can severe primary hypothyroidism cause increased prolactin levels?
    • Increased TRH suppresses dopamine which increases PRL.
    • How does posterior pituitary metastasis present? What are common primaries?
    • Presents as diabetes insipidus. Breast and lung cancer mets are most common.
    • What to suspect in patient who presents with variable onset of severe h/a, nausea/vomiting, meningismus, vertigo, visual defects, fluctuating consciousness?
    • Pituitary apoplexy (hemorrhagic infarct of pituitary mass). often superimposed on chronic sxs of hormone problems. most dangerous is adrenal insufficiency.
    • How to treat pituitary apoplexy?
    • C/s neurosurgery to decide re: steroids vs surgery
    • What is Sheehan syndrome?
    • Postpartum infarct of anterior pituitary +/- posterior (causing DI)
    • What is the etiology of neurogenic diabetes inspidius? Nephrogenic DI?
    • 50% genetic, 50% acquired (Sheehan syndrome or any CNS injury); for nephrogenic DI, x-linked or drugs (especially lithium)
    • How does DI manifest in someone who is on water restriction (symptoms, labs, vol status)?
    • Very dilute urine, polyuria and hypernatremia. xs thirst but euovolemic unless they can't access water.
    • How do you diagnose the cause of DI? How does primary polydipsia show up?
    • Water-depreviation test with hourly ADH, urine and plasma osm's. for central DI, see how plasma osm's affect ADH level. for nephrogenic DI, see how ADH affects urine osm's. Primary polydipsia looks like partial nephrogenic DI (some response of urine osm's to increasing ADH)
    • How do you treat neurogenic DI? Nephrogenic DI?
    • DDAVP (aka desmopressin) subc or intranasally (if mild can do PO). Nephrogenic DI treated with low-sodium diet, HCTZ +/- amiloride.
    • What are several causes of siADH?
    • CNS injury, pulm disease, drugs, ectopic pdn (esp SCLC), idiopathic
    • How do you treat chronic hypoNA 2/2 siADH? Anything to watch out for w/ treatment?
    • Besides fluid restriction, you can use demeclocycline (watch out for photosensitivity and nephrotoxicity), flourinef
    • What is the normal thyroid axis?
    • TRH stimulates TSH which makes T4 (thyroxine). Active hormone (T3) mostly made in peripheral tissue from T4. Most T4 and T3 is bound, rest is free and active.
    • High TSH and normal FT4?

      Low TSH and normal FT4?
    • sublicinal hypothyroidism.

      euthyroid sick syndrome, subclinical hyperthyroidism, or multinodular goiter w/autonomous pdn
    • In a thyroid uptake scan, what causes increased RAIU?
    • Graves disease, TSH-secreting pituitary tumor, hot nodules, iodine deficiency
    • In a thyroid uptake scan, what causes decreased RAIU?
    • thyroiditis, xs exogenous thryoid supplementation, iodine excess (contrast dye, diet, amio)
    • How does thyroiditis present on labs?
    • High TSH/low FT4 or low TSH/high FT4 depending on where it is in its stage.
    • What is a thyroid scan (scintigraphy)?
    • shows anatomy and hot vs cold spots. still indicated per guidelines.
    • How do you titrate synthroid dose when starting treatment for hypothyroidism? What can overtreatment cause?

      What supplements should patients avoid when taking synthroid?
    • Check in 6-8 weeks after a dose adjustment. If elderly and CAD, start low and slowly titrate up. can cause afib, osteoperosis.

      avoid iron, calcium, aluminum
    • Hypothermia is associated clasically with what thyroid d/o?
    • Myxedema coma (general slowing of all processes including hypoglycemia, BP, HR)
    • How do you treat myxedema coma?
    • 1) Passive rewarming is very important (mortality directly related to degree of hypothermia).
      2) Treat with T3 (rapid onset) and IV T4.
      3) Give stress dose steroids bc adrenal gland does not work in severe hypothyroidism.
      4) Give broad spectrum abx until infection excluded.
    • What is apathetic hyperthyroidism?
    • Depression 2/2 hyperthyroidism in elderly patient, causing failure to thrive
    • Which is safe in pregnancy for Rx of Graves' disease, methimazole or PTU?
    • PTU, can do surgery too (Methimazole is first-line med in non-pregnant patients)
    • How do you treat thyroid storm?
    • 1) IV propanolol or esmolol.
      2) PTU or methimaozle (block new synthesis)
      3) stable iodide (block preformed hormone release)
      4)propanolol, steroids, iodinated contrast (block peripheral conversion of T4 to T3)
      5)abx
      6)most important- large amounts of steroids (pts die from CV collapse 2/2 relative adrenal insufficiency although it is working OK)
    • How is thyroiditis classified?
    • Acute (bacterial infection of gland); subacute (caused by virus resulting in granulomas); chronic (caused by autoimmune aka Hashimoto's or postpartum)
    • How does subacute thyroiditis present?
    • Very tender neck, usually 30-50 year olds, maybe fever
    • What is the natural course of postpartum thyroiditis?
    • They all recover (but you can treat). Will need annual follow-up though for the risk of overt hypothyroidism later.
    • When is RAIU helpful?
    • In hyperthyroidism when distinguishing Graves (high) from thyroiditis (low). Other reasons for RAIU to be high: exogenous T4 ingestion, struma ovarii (thyroid tissue in an ovarian teratoma), idoine excess
    • What are labs like in euthyroid sick syndrome?
    • TSH/FT4 are variable, T3 is low because reverse T3 (rT3) is high.
    • Are most solitary thyroid nodules hot or cold? Potential for malignancy?
    • 95% of solitary nodules are cold, and most of these are benign. All hot nodules are benign. Do not biopsy hot nodule (and it may be indistinguishable from follicular ca)
    • What do you do with cold nodules in multinodular goiter (with both hot and cold nodules)?
    • They have same malignant risk as solitary cold nodules- evaluate them the same way.
    • If palpable thyroid nodule is suspicious by hx or u/s, what is next step?
    • FNA regardless of size or type of nodule
    • If palpable thyroid nodule is not suspicious by u/s, what is next step?
    • Consider TSH - if high think Hashimoto's and measure anti-TPO ab. If low, do thyroid scan to see if hot or cold. If normal --> FNA
    • What do you do with nondiagnostic FNA path result?
    • Repeat FNA
    • What do you do with incidentaloma thyroid nodule?
    • Same workup -- FNA if > 1cm or suspicious (calcifications, etc)
    • How do you treat toxic adenoma?
    • Growing hot nodule that suppresses TSH production. Rx is ablation or surgery (not meds) or ethanol
    • DDx for high RAIU? for low RAIU?
    • Graves and toxic multinodular goiter, sometimes toxic adenoma.

      thyroiditis and ioidine excess, exogenous drugs
    • What is unique about medullary thyroid cancer?
    • Associated with hyperplasia of parafollicular C cells and also elevated calcitonin. Associated with MEN IIA and IIB (RET oncogene with tyrosine kinase pdn)
    • After thyroid ca initial Rx (surgery, ablation), what next in management?
    • After several days start thyroxine -- most differentiated thyroid ca (like follicular) is responsive to TSH, so keep it suppressed to prevent recurrence
    • What to worry about in a patient with Hashimoto's who develops a fast-growing thyroid mass? If it is this, how do you manage it?
    • Thyroid lymphoma-- responds well to chemo and XRT. Avoid surgery at first because it can spread cancer cells
    • How do you manage nontoxic multinodular goiter?
    • If no sxs, conservative management. If compression or disfiguring can use ablation or surgery
    • What is the anatomy of the adrenal gland?
    • Cortex with 3 zones and the medulla. Cortex: GFR: outer zona glomerulosa (Salt), middle zona fasciulata (Sugar), inner zona reticularis (sex). Also the adrenal medulla has chromaffin cells that make epinephrine (ACTH-independent)
    • What do adrenal androgens do in males vs females?
    • In normal males, adrenal androgens (DHEA and T) are overshadowed by teh effects of testicular androgens. In normal females, they contribute 50% (rest is from ovaries)
    • What is the mode of transmission of congenital adrenal hyperplasia? Definition of CAH? What are most 2/2 to specifically? What is the phenotype?
    • autosomal recessive, decrease in production of cortisol. Most are due to mutation in CYP21A2 -- so 17-OH progresterone accumulates. In females this builds up DHEA and T --> ambiguous genitalia in newborn girls (or virilization in females/preocious puberty in males postnatally)
    • When does CAH present?

      How do you diagnose CAH?
    • can happen in utero, postnatal or late onset (Postpubertal) 2/2 partial CYP21A2 impairment.

      increased early AM 17-OH progesterone (either ACTH stimulated or unstimulated) and increased urinary 17-ketosteroids and blood DHEA
    • What are some late-onset CAH 2/2 to?
    • impairment of CYP11B1 causing buildup of 11-deoxycortisol and potent mineralocorticoid precursors w/mineralocorticoid activity, also shunting to androgen excess.
    • What does a CYP17 (17-alpha hydroxylase) mutation do?
    • Cortisol and androgen deficiency (needed to go into either pathway). Mineralocorticoid excess. Rare.
    • What does a CYP11b1 (11-beta hydroxylase) mutation do?
    • late-onset CAH. elevated 11-deoxycortisol. xs androgen and aldosterone precursors. (needed in both aldosterone and corisol pathways but in aldosterone, there are precursors that are before 11-beta hydroxylase)
    • What does CYP21A2 (21-hydroxylase) mutation do?
    • classical CAH. Androgen xs only. (needed in both aldosterone and cortisol pathways)
    • In elderly what is the most common cause of Cushing's syndrome?
    • Small cell lung cancer ectopic ACTH secreting tumor. (otherwise iatrogenic, pituitary adenoma aka Cushing disease)
    • How do you diagnose true Cushing syndrome?
    • significantly elevated urinary free cortisol or dex suppression test. however urinary free cortisol can be elevated in pseudo-Cushing (depression, obese, alcoholic) -- in this case do low-dose dexamethasone test and it should supress. Next measure ACTH.
    • How will physical exam differ between Cushing disease and other causes of Cushing syndrome?
    • virilization in Cushing disease too
    • Primary adrenal insufficiency is usually 2/2 to what?
    • autoimmune adrenalitis (Addison like in the polyglandular autoimmune diseases) and granulomatous infections, HIV
    • How are manifestations of AI different in primary vs secondary?
    • In secondary AI, the zone glomerulosa is not diseased and responds normally to angiotensin II.
    • What should you suspect and do if there is primary AI and hypothyroidism?
    • Schmidt syndrome. Can also so DM 1. Replace cortisol first before giving thyroid replacement (to prepare for increased metabolic demand with thyroid)
    • What is the RAA axis?
    • Renin converts angiotensinogen to angiotensin I which goes to angiotensin II by ACE (in the lungs) which then stimulates aldosterone release.
    • How do you screen for hyperaldosternoism? What can interfere?
    • PAC:PRA ratio (aldosterone: renin). However ACE's and ARB's interfere with this.

      Primary aldosteronism (hyporenin)- ratio is elevated 2/2 adrenal disease

      Secondary aldosteronism (hyperrenin)- ratio is decreased 2/2 kidneys (tumor or revnovascular dz)
    • What is the next step to confirm dx of primary aldo based on PAC:PRA ratio?
    • give oral sodium load for a few days and then measure the PAC. and then image adrenals to look for hyperplasia vs tumor (Conn syndrome)
    • What is the next step if PAC:PRA ratio is low?
    • Renal angiography
    • What is the most common cause of hypoaldo? How to confirm dx of hypoaldo?
    • Decreased renin production (in juxtoglomerular apparatus) in diabetics with renal failure. Salt restrict and then measure aldo level.
    • What drugs suppress aldosterone?
    • ACE inhibitors, NSAIDs, and chronic heparin use
    • Family history of what is important as risk factor for pheo?
    • Pheo, MEN II, neurofibromatosis, or von Hippel-Lindau disease
    • How to screen for pheo's?
    • Fractionated metanephrines/catecholamines on 24 hour urine (preferred). Or plasma free metanephrines.