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Compendium Chemistry > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Total T4 (thyroxine)

A
  • elevated in most hyperthyroid patients and decreased in hypothyroidism
  • <5% of hyperthyroid patients have normal T4 but elevated T3
  • T4 is highly bound, so fluctuations in serum proteins limit the value of total T4 and total T3
    • Bound to prealbumin (transthyretin) and thyroid binding globulin (TBG)
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2
Q

Thyroglobulin increased by ___ and decreased by ___

A
  • Increased by
    • pregnancy
    • oral contraceptives
    • estrogen therapy
    • active hepatitis
    • hypothyroidism
  • Decreased by
    • hypoproteinemic states
    • androgen therapy
    • cortisol
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3
Q
A
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4
Q

T3 resin uptake (T3RU)

A
  • no longer used
  • in hyperthyroidism there is high T3 resin uptake and in hypothyroidism there is low T3 resin uptake
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5
Q

Free T4 and free T3

A

Correlate well with clinical thyroid status

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6
Q

Euthyroid sick syndrome

A
  • Reverse T3 (rT3) is a metabolic product of T4 (most of which is metabolized to T3)
  • rT3 is elevated
  • T3 and T4 are low
  • seen in patients with nonthyroidal systemic illness
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7
Q

Thyroid releasing hormone (TRH)

A
  • TRH stimulation test is used in evaluation of hypothyroidism
  • In primary hypothyroidism there is exaggerated secretion of TSH in response to TRH
  • An inappropriate TSH response to TRH suggests hypopituitarisim
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8
Q

TSH (thyrotropin)

A
  • best first line test for diagnosing hypo and hyperthyroidism
  • TSH elevated in hypothyroidism
  • Not as helpful in hypothalamic or pituitary dysfunction and neonatal screening
    • fT4 indicated in these patients in addition to TSH
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9
Q

Hyperthyroidism

  • diagnosis
  • disease
  • labs
A
  • Diagnosis
    • low TSH
    • high serum FT4
    • when FT4 is normal despite a low TSH, free T3 should be measured to assess for T3 thyrotoxicosis
  • Diseases
    • Graves disease is most common cause
    • toxic multinodular goiter
    • toxic adenoma (Plummer syndrome)
    • transient hyperthyroidism in various kinds of thyroiditis
    • exogenous thyroxine
    • pituitary adenoma
    • thyroid carcinoma
  • Labs
    • thyroid stimulating immunoglobulin in Graves, aka long acting thyroid stimulating antibodies
    • antimicrosomal antibodies (aka, TPO antibodies found in 60% of cases of Graves
    • antithyroglobulin antibodies in 30% of cases of Graves
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10
Q

Hypothyroidism

  • diagnosis
  • causes
A
  • Elevated TSH and low free T4
  • Causes
    • Hashimoto thyroiditis is most common cause
    • Thyroidectomy
    • Lymphocytic and granulomatous thyroiditis (de Quervain)
    • I-131 therapy
    • radiation
    • drugs (iodine, lithium, IL-2, alpha-IFN)
  • Hashimoto characterized by anti tissue peroxidase and antithyroglobulin (>90%) antibodies
    • TSI not identified in Hashimoto
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11
Q

Neonatal hypothyroidism

A
  • Caused by
    • Most often caused by thyroid dysgenesis
    • familial thyroid dyshormonogenesis
    • peripheral hormone resistance (autosomal dominant Refetoff syndrome)
    • hypopituitarism
    • maternal factors (maternal autoantibodies and medications)
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12
Q

Nonthyroidal illness syndrome (euthyroid sick syndrome)

A
  • abnormal thyroid function tests in euthyroid person suffering from a nonthyroidal illness
  • decreased T3 and T4
  • increased rT3
  • normal TSH
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13
Q

Medications that affect thyroid hormones

A
  • Amiodarone causes hypothyroidism in iodine rich parts of the world and hyperthyroidism in iodine poor parts of the world
  • Lithium inhibits release of thyroxine resulting in hypothyroidism
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14
Q

Effect of exogenous estrogen on thyroid hormones

A
  • Increase circulating thyroid binding globulin (TBG)
  • thus total thyroxine (T3 and T4) are elevated
  • Free thyroxine and TSH remain normal
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15
Q

Characteristics of cortisol secretion

A
  • Diurnal variation
    • trough around midnight
    • peak at 8 AM
  • depends on levels of cortisol binding globulin
  • low 8 AM secretion suggests adrenal insufficiency
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16
Q

Cushing syndrome

A
  • Elevated serum cortisol
  • loss of diurnal variation
  • Low dose DST does not suppress cortisol
  • High dose DST should suppress cortisol
17
Q

Urine free cortisol test

A
  • 24 hour urine collection
  • reflects free (unbound) serum cortisol
  • independent of time of day
18
Q

Dexamethasone suppression test

A
  • dexamethasone suppresses ACTH and cortisol in a normal patient
  • abnormal suppression seen in Cushing syndrome, which includes Cushing disease
    • low dose DST given in two forms
      • rapid (overnight) DST
      • standard (2 day) DST
      • normal people have suppression of cortisol
      • abnormal suppression confirms diagnosis of Cushing syndrome or pseudoCushing (severe stress, alcohol abuse, major depression)
    • high dose DST determines if patient has Cushing syndrome or Cushing disease (pituitary adenoma)
      • Suppression implies pituitary adenoma
      • Nonsuppression means
        • ectopic ACTH production by tumor OR
        • primary adrenal hypercortisolism
        • The above two diseases can be distinguished by plasma ACTH measurement
19
Q

Cortisol releasing hormone (CRH) stimulation test

A
  • like high dose DST, is aimed at determining cause of Cushing syndrome
  • exaggerated elevation of ACTH and cortisol suggests Cushing disease (pituitary adenoma)
  • No response seen in adrenal tumor or ectopic ACTH
20
Q

Diagnosis of Cushing syndrome

A
  • Persistent hypercortisolism
  • Screening tests (positive test should be confirmed by repeat test)
    • low dose DST
    • 24 hour urinary free cortisol
    • midnight salivary or serum cortisol
  • Measure ACTH
  • ACTH dependent Cushing is evaluated with bilateral inferior petrosal sinus sampling (BIPSS) OR high dose DST and/or CRH stimulation tests
  • Imaging of pituitary lacks S and S when used in isolation
  • ACTH independent Cushing requires adrenal imaging (also need to exclude surreptitious steroid administration)
21
Q

Etiology of Cushing syndrome

A
  • Iatrogenic Cushing syndrome - administration of steroids for treatment of inflammatory disease - is most common cause
  • noniatrogenic causes
    • pituitary adenoma (Cushing disease) - usually microadenoma of basophilic cells (corticotrophs)
    • adrenal gland abnormality
      • adenoma
      • carcinoma
      • bilateral adrenal hyperplasia
    • ectopic ACTH
      • small cell lung CA
      • lung carcinoid
      • pancreatic endocrine tumors
      • non-small lung CA
      • thymic tumors
      • medullary thyroid carcinoma
      • breast carcinoma
22
Q

Effects of Cushing syndrome

A
  • hyperglycemia
  • hypoK
  • protein catabolism
  • osteoporosis
  • centripetal fat deposition
  • skin thinning with striae
23
Q

Illness that looks like Cushing clinically and chemically, but isn’t

A
  • depression
  • anorexia
  • alcoholism
  • pregnancy
24
Q

Diagnosis of Addison disease

A

Primary adrenal insufficiency

  • low 8 AM serum cortisol and/or blunted increase in cortisol following cosyntropin stimulation
  • ACTH guides further evaluation
    • Elevated ACTH: primary adrenal insufficiency
      • perform autoantibody studies and/or imaging
    • Normal or low ACTH suggest secondary adrenal insufficiency, most likely related to pituitary pathology or exogenous glucocorticoid administration
25
Q

Etiology of Addison disease

A
  • Primary destruction of adrenal gland by granulomatous disease (TB)
  • Autoimmunity
  • Metastatic tumor
  • Amyloid
  • Bilateral hemorrhage (Waterhouse Friderichsen syndrome)
  • Congenital diseases
    • CAH
    • Adrenoleukodystrophy
  • Drugs
    • ketoconazole etomidate
    • mitotane
26
Q

Addisonian crisis and other symptoms

A
  1. AMS
  2. hypotension (including postural)
  3. hypoglycemia
  4. hypoNa
  5. hyperK
  6. metabolic acidosis
  7. fatigue
  8. weight loss
  9. weakness
  10. mood alteration
  11. skin hyperpigmentation
27
Q

Secondary adrenal insufficiency

A
  • exogenous steroids usually that lead to irreversible suppression of endogenous ACTH production
  • not as severe as Addison disease because renin-angiotensin system maintains mineralcorticoid production
  • hyperK is absent and hypoNa is mild
  • hyperpigmentation is not seen
28
Q

Conn syndrome

A

Hyperaldosteronism

  • Usually due to an adrenal adenoma or bilateral adrenal hyperplasia
  • secondary hyperaldosteronism is seenin hyperreninemic states such as renal artery stenosis or renin producing juxtaglomerular cell tumor of the kidney
  • Results in
    • HTN
    • hypoK
    • metabolic alkalosis
  • ratio of plasma aldosterone concentration to plasma renin activity is considered best screening test; must be confirmed by a 24 hour urinary aldosterone level
29
Q

congenital adrenal hyperplasia

A
  • Etiology
    • 21 hydroxylase deficiency is the most common cause
    • 11 hydroxylase deficiency is second most common cause
  • Native Americans and Yupic Eskimos
  • gene for 21 hydroxylase is on 6p21.3 within the HLA complex
  • compensatory increase in ACTH by the pituitary leads to increased production of steroid hormone precursors in the adrenal cortex
  • Resulting adrenal hyperplasia causes
    • salt wasting
    • HTN
    • virilization
  • Increased 17 hydroxyprogesterone
  • Decreased cortisol
  • Increase ACTH
  • Increased androgens
  • Increased 17-ketosteroids
  • Decreased aldosterone
31
Q

Pituitary adenoma

A
  • Hypersecretion of anterior pituitary is almost always caused by a pituitary adenoma
  • Prolactinoma is most common
32
Q

Pituitary hypofunction

A
  • rarely involves a single hormone
  • causes
    • tumors impinging on pituitary gland (nonsecretory pituitary adenoma, craniopharyngioma)
    • infarction (Sheehan syndrome, sickle cell anemia)
    • sarcoidosis
    • histiocytosis X
    • hemochromatosis
    • irradiation
    • autoimmune destruction
33
Q

Hypothalamic disorders and interruption of pituitary stalk

A
  • All anterior pituitary hormones except prolactin are suppressed (i.e., “stalk effect”)
  • Hormones in anterior pituitary:
    • somatotropes (GH)
    • prolactins (PRL)
    • gonadotropes(LH and FSH)
    • corticotropes (ACTH)
    • thyrotropes (TSH)
34
Q

Growth hormone hyposecretion

A
  • dwarfism in children
  • adults are asymptomatic
  • undetectable GH levels occur in healthy subjects and are not diagnostic of hyposecretion
  • provocative testing is required performed by measuring GH in
    • fasting state
    • during sleep
    • following exercise
    • following insulin or arginine administration
35
Q

Growth hormone hypersecretion

A
  • gigantism in children
  • acromegaly in adults
  • IGF-1 consistently elevated in GH hypersecretion
  • normal IGF-1 excludes GH excess
  • markedly elevated GH from a random blood sample or a relatively normal level that fails to suppress with glucose administration can diagnose GH excess
36
Q

Follicle stimulating hormone

A
  • FSH assays can be useful in women < 45 yo presenting with possible early menopause
  • persistently elevated FSH suggests ovarian failure
37
Q

Prolactin

  • regulation
  • causes of hyperPRL
  • findings in hyperPRL
A
  • does not have a dedicated stimulator for its release
  • instead, the hypothalamus produces an inhibitor: dopamine
  • if connection between hypothalamus and pituitary is severed, all anterior pituitary hormones decrease except prolactin, which markedly increases due to lack of inhibition
  • HyperPRL
    • amenorrhea galactorrhea syndrome in women
    • testicular atrophy, impotence, and gynecomastia in men
    • usually 2/2 prolactin secreting pituitary adenoma
    • other causes
      • pregnancy
      • lactation
      • stalk compression
      • macroprolactinemia
      • phenothiazine therapy
38
Q

Diabetes insipidus

A
  • Results from inadequate ADH activity
  • Polyuria and polydipsia with low urine osmolarity and hyperNa
  • Types
    • Central DI
      • inadequate ADH secretion caused by
        • head trauma
        • mass lesions involving pituitary
        • X linked recessive familial form
    • Nephrogenic DI
      • renal tubules unresponsive to ADH
      • Caused by
        1. hyperCa
        2. hypoK
        3. very low protein diet
        4. demeclocycline
        5. lithium
        6. relief of longstanding obstruction
        7. familial
        8. normal aging
  • Confirmed by overnight water deprivation test followed by administration of ADH (vasopressin)
  • in healthy people urine osmolarity progressively increases during water deprivation and administration of exogenous ADH has no additional effect on urine concentration
  • In central DI there is failure to appropriately concentrate urine in response to dehydration and a rise in urine osmolarity in response to administered ADH
  • In nephrogenic DI urine cannot be concentrated in either case (dehydration or with ADH admin)
39
Q

Syndrome of inappropriate ADH (SIADH)

A
  • hypoNa normovolemia
  • urine sodium > 20 mmol/L
  • urine osmolarity > 100 mOsm/kg
  • Caused by
    • tumors
      • small cell carcinoma of the lung
      • pancreatic adenocarcinoma
      • intracranial tumors
    • interstitial lung disease
    • cerebral trauma
    • chlorpropamide

Compendium Chemistry (13 decks)

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