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Clinical Lab > Endocrinology: HPT Axis & Adrenal > Flashcards

Endocrinology: HPT Axis & Adrenal Flashcards

1
Q

Endocrine vs. Exocrine vs. Paracrine

A

Endocrine: glads secrete hormones into blood stream to act at a distant tissue site

Exocrine: glands secrete non-hormones (ie. enzyme) into ductal system for delivery to distant or adjacent site

Paracrine: cells secrete hormone that acts directly on other nearby cells (ie. testosterone)

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2
Q

Types of hormones

A
  1. Protein/polypeptide = water soluble, no carrier protein, mainly interact with membrane receptors (don’t enter cells)
  2. Steroid = cholesterol based, lipid soluble, bound to transport protein, interact w/ nuclear receptors inside of cell
  3. Aromatic AA Derivatives = derived from tyrosine, T3/T4 & Catecholamines
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3
Q

Endocrine (HPT) Axis concept

A
  • Hypothalamus “releasing hormones” stimulate pituitary secretion of “trophic hormones”
    –> trophic=stimulate production of another
    hormone
  • Trophic hormone stimulates release of primary hormone, which then binds to specific receptor at target tissue
  • Main control mechanism is negative feedback
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4
Q

Levels of Endocrine Disease

A

1’ = End Organ Hormone
- All hormones in axis (primary, secondary, tertiary) increased in hyperfunction or decreased in hypofunction
2’ = Pituitary Trophic Hormone
- Hypofx: Primary increases, Secondary & Tertiary decreased
- Hyperfx: Primary decreased, Secondary & Tertiary increased
3’ = Hypothalamic Releasing Factor
- Hypofx: Primary & Secondary increased, Tertiary decreased
- Hyperfx: Primary & Secondary decreased, Tertiary increased

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5
Q

Posterior Pituitary: Nature & Hormones

A

“Neurohypophysis” - Neural nature

  • Hypothalamic neurons extend into gland and secrete hormones there
  • AVP (ADH) and Oxytocin are produced in the hypothalamus and stored in the P.Pit.
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6
Q

Anterior Pituitary: Nature & Hormones

A

“Adenohypophysis” - Gland nature
- Hypothalamus secretes releasing factors into circulation which directly feeds A.Pit.
Hormones produced:
- hGH & Prolactin –> Direct effector
- ACTH, FSH, LH, TSH –> Trophic

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7
Q

Growth Hormone (hGH)

A
  • Secreted by somatotrophic cells (1/3 wt of AP)
  • Stimulated by GHRH, inhibited by Somatostatin
  • Secreted in pulsatile fashion (avg interval 2-3 hrs) –> diurnal variation: highest during sleep, spikes after meals/exercise, can be undetectable between pulses
  • Anabolic (protein/bone/glucose genesis) & Catabolic (lipolysis) functions
  • Formation of IGFs –> synthesized in liver, IGF-1 measured by immunoassay rather than GH due to pulsatile secretion
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8
Q

Insulin-Like Growth Factor (IGF-1)

A
  • Synthesized in liver in response to GH
  • Unlike other protein hormones, IGF1 is bound to a carrier protein (IGF-BP3)
  • Levels are directly related to GH concentration, and is more commonly measured to asses GH disorders due to higher stability
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9
Q

GH Hypersecretion

A

Gigantism = GH excess during growth phase
Acromegaly = GH excess after growth phase
—> Both commonly result from pituitary tumor

Tested for by Oral GTT (should suppress GH to

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10
Q

GH Hyposecretion

A

Pituitary Dwarfism = very small with proportional sizing, may result from tumors interfering GH secretion or genetic defect in GHRH/gene/receptor/IGF1

Adult Deficiency = vague symptoms (mental issues, osteoporosis, high chol)

Tested for w/ Insulin Tolerance or Arginine (should induce GH elevation, so looking for low levels)

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11
Q

Prolactin

A
  • Primarily influence on lactation and suppressed release of GnRH (no LH/FSH after birth)
  • Pulsatile secretion (similar to GH), not stimulated by a releasing hormone –> pregnancy/suckling (stimulated by TRH in pathological situations)
  • Under constant inhibition by dopamine –>only non-peptide RH, loss of inhibition leads to uncontrolled secretion (drugs)
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12
Q

Prolactin Hypersecretion

A
  • Prolactinoma (prl secreting pituitary tumor) –> levels >150-200 ng/ml, proportional to tumor size, HOOK EFFECT**, more obvious in female (effects noticeable)
  • Pituitary stalk damage: dopamine decrease (also certain drugs)
  • Hypothyroidism (1’ or 2’): high TRH
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13
Q

Prolactin testing

A
  • Usually sandwich immunoassay (method dependent reference ranges)
  • Subject to hook effect!! Need a dilution protocol
  • Macroprolactin = IgG bound prolactin (inactive), most common cause of mild hyperprolactinemia
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14
Q

Panhypopituitarism

A

Ineffictiveness of all pituitary function

  • pituitary, parapituitary, hypothalamic tumors
  • trauma to pituitary stalk, radiation, surgery
  • Sheehan’s Syndrome: postpartum infarction
  • Loss of tropic hormones more critical/obvious than direct effector hormones, replacement is used to treat
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15
Q

Thyroid physiology

A
  • Straddles trachea with 4 Parathyroids (2 on each lobe)
  • Thyroid cells arranged as follicles, colloid primarily thyroglobulin
  • Colloid actively takes up iodine –> iodinates tyrosine residues in Tg (plus coupling of residues) –> release of T3 & T4
  • Parafollicular cells release Calcitonin
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16
Q

Thyroid hormone synthesis

A
  1. In presence of inorganic iodide, TPO (thyroid peroxidase) facilitates iodination of tyrosine residues on Tg molecules
  2. Iodinated Tg couples with other iodinated Tg molecules
  3. Coupled Tg is then turned into T4 by Thyroglobulin Protease
17
Q

Thyroid Hormones

A
  • T4 is primary secreted hormone, T3 also secreted in smaller amounts but most is formed via T4 deiodination in peripheral tissues (liver)
  • Transported bound to proteins (Thyroxine-binding globulin, albumin)
  • Only free hormones are biologically active (free T4 measured, total T3 measured) with T3 accounting for most thyroid hormone activity in peripheral tissues
  • Exert primarily intracellular actions by nuclear uptake and mRNA transcription –> increase metabolism, cardiac/CNS/GI activity, **fetal and neonate CNS development
18
Q

Hyperthyroidism

A
  • Increased appetite with weight loss, heat intolerance, upper CV/CNS effects
  • Graves Disease: autoimmune stimulatory Ab to TSH receptor, may have bug eyes (exopthalmos), Ab can cross placenta so seen in neonates (POSITIVE TSI LEVELS)
  • Thyroid nodules: single or multi, benign
  • Thyroiditis: normal hormone production, but leakage from glands
  • Increase in iodine ingestion (meds)
  • Choriocarcinoma: hCG cross-rxn with TSH

10x more common in females

19
Q

Hypothyroidism

A
  • Cold intolerance, weight gain with lethargy, myxedema (puffiness), downer CV/CNS effects
  • Hashimoto’s thyroiditis: Ab and cell-mediated, commonly anti-TPO/TG, most common in developed countries (POS ANTI-TPO)
  • Iodine deficiency: most common worldwide
  • Congenital
  • Thyroid hormone resistance
  • 2’/3’: Pituitary (TSH) or hypothalamic (TRH) failure, very rare
20
Q

Stages of Primary Hypothyroidism

A 
SUB-CLINICAL: lab evidence w/o symptoms
    --> high TSH, normal T4, normal T3
EARLY:
    --> high TSH, low T4, normal T3
MATURE:
    --> high TSH, low T4, low T3
21
Q

Thyroid cancer

A
  • Medullary carcinoma: parafollicular cells, use calcitonin as a tumor marker to monitor once dx is made
  • Epithelial cancers: follicular or papillary, monitor using thyroglobulin assay once dx is made (sandwich assay but has anti-TG interference, LC-MS/MS available w/o interference)

–> Destroy thyroid gland (ablation) and monitor hormones to make sure no recurrence of tissue

22
Q

Thyroid testing

A
  • TSH: Primary test in thyroid evaluation, immunoassay, measures hypothalamic response –> increase w/ normal T4 suggests sub-clinical hypothyroidism
  • T4/T3: Free T4 strongly recommended, done by competitive immunoassay (sm molecules), must displace bound fractions, T4 in mcg/dL T3 in ng/mL
  • T3 uptake: obsolete, replaced by fT4
23
Q

Free T4 testing

A

Direct dialysis - dialyze sample and measure T4 in dialysate w/ sensitive immunoassay

Equilibrium dialysis - reference method, I-125 T4 added to sample and dialyzed, “% radioactivity added x total T4 = fT4”

Two step fT4 estimate - best estimate, labeled T4 bind to unoccupied Ab sites, unbound is separated out and bound T4 is measured

One step fT4 estimate - T4 analog that binds to Ab, competitive immunoassay, works well in most cases (if >AMR, dilution isn’t an option)

24
Q

Thyroid Autoantibodies

A
  • Anti-TG: automated immunoassay
  • Anti-TPO: automated immunoassay, elevated in Hashimoto’s dz, 10% asymptomatic patients
  • Thyroid stimulating Ig (TSI): Ab to TSH receptor that stimulates when bound
  • Thyrotropin binding inhibitory Ig (TBII): inhibits TSH receptor response
25
Q

Non-thyroidal illness

A
  • Thyroid hormone results may be abnormal in sick patients w/o thyroid disease –> “Euthyroid sick”
  • Typically see decrease in total/free T3, low tT4 with normal fT4, mild TSH fluctuations (starts low and raises during recovery)

**Thyroid testing should not be done if patient has acute illness

26
Q

Adrenal physiology and steroid types

A
  • 90% of organ is cortex: yellowish tissue, three zones (glomerulosa, fasciculta, reticularis), produces steroid hormones
  • 10% of organ is medulla: grayish tissue, produces catecholamines
  • Three types of adrenal steroids hormones: Glucocorticoids, Mineralocorticoids, and Adrenal Androgens
27
Q

Adrenal steroid biochemistry

A
  • Glands have distinct pathways for hormone development, but are all derived from the transformation of Cholesterol to Pregnenolone (rate-limiting step for all paths)
  • Aldosterone has its own pathway: stems from Pregnenolone -> Progesterone
  • Cholesterol transformation stimulated by ACTH (trophic hormone produced by ant. pit.)
  • Transported bound to protein (albumin, CBG) with free fraction biologically active –> lab measures total hormones not free
  • Catabolism happens in the liver, renal excretion
28
Q

Glucocorticoid function and regulation

A
  • Cortisol main glucocorticoid
  • Raises blood glucose and encourages breakdown of fat/protein, suppresses immune system response (anti-inflammatory), and controls blood pressure (increases GFR, effects similar to mineralocorticoids)
  • CRH (hypothal) –> ACTH (a.pit.) –> stimulates cholesterol to pregnenolone transformation (in ZF/ZR)
  • CRH release in response to stress and hypoglycemia, controlled by sleep-wake cycle (diurnal, circadian rhythm)
  • Cortisol has negative feedback on CRH & ACTH release
29
Q

Mineralocorticoid function and regulation

A
  • Aldosterone main mineralocorticoid
  • Increases sodium reabsorption by DCT and collecting duct (K-exchange) in order to maintain blood volume
  • Controlled by Renin-Angiotensin-Aldosterone system (RAAS) –> angiotensin ll stimulates cholesterol to preg transfomation (ZG)
  • Regulated largely by K levels –> stimulated by hyperkalemia, inhibited by hypokalemia
30
Q

Adrenal Androgens

A

DHEA: similar to testosterone, but weaker. Produced in ZR.

31
Q

Adrenal Function Tests

A
  • Serum Cortisol
  • Serum Aldosterone
  • ACTH (stabilized by EDTA)
      • all of above by competitive immunoassay or LC-MS/MS
  • Anti-adrenal Antibody: done by ELISA or IFA, present in Addison’s Dz
  • Urinary free cortisol: 24hr urine, requires solvent extraction/evaporation to remove polar cross-reacting metabolites –> preferred marker but pre-analytical issues (24hr urine)
  • Salivary cortisol: collected by patient at home
32
Q

Hypoadrenalism

A
  • Hyperpigmentation, develops slowly, symptoms vague and non-specific, low Na and high K, hypoglycemia
  • Primary Dz: low cortisol, high ACTH, w/ anti-adrenal antibodies (Addison’s dz)
  • Secondary Dz: low cortisol, low ACTH due to pituitary dz or tumor, no primary symptoms or electrolyte disturbance (RAAS), panhypopituitarism
  • Tertiary Dz: low CRH, very rare, commonly caused by exogenous steroids

Testing: ACTH stimulation –> draw baseline cortisol/ACTH and inject w/ synthetic sub, take cortisol at 30&60 min –> should increase, if subnormal suggests insufficiency

Treatment: Gluco/Mineralocorticoid replacement –> Prednisone, Florinef

33
Q

Addison’s Disease

A
  • Primary adrenal insufficiency –> not responding to ACTH stimulation
  • 70% of cases are autoimmune
  • Can also be a result of granulomatous dz (TB), infiltrative dz (neoplasia), infarction, adrenoleukodystrophy (degeneration of adrenals), congenital adrenal hyperplasia
  • Addisonian Crisis: life threatening, develops with added stressors
34
Q

Hyperadrenalism

A
  • Hypertension, central obesity, carb intolerance, abdominal striae –> stemming from excess cortisol
  • 68% Cushing’s disease: commonly due to pituitary hypersecretion of ACTH
  • Adrenal adenoma or carcinoma, ectopic ACTH secretion (non-endocrine tumor), iatrogenic causes
  • Pseudohyperadrenalism –> increase in serum cortisol due to high CBG (estrogens), urine cortisol will be normal
35
Q

Hyperadrenalism testing

A
  • Urinary free cortisol: 24 hr urine, 90% accuracy with proper collection, preferred test
  • Salivary cortisol: elevation indicates loss of diurnal variation (serum cort has poor sensitivity)
  • Dexamethasone Suppression: administer dexamethasone which should exhibit negative feedback, if cortisol still elevated = hypercortisolism
  • ACTH test run to differentiate adrenal tumor –> low = primary adrenal tumor, high = pit or ectopic origin

also: RAAS testing in cases of hypertension, 17-hydroxyprogesteron or DHEA test in cases of virilization

36
Q

Adrenal steroid biochemistry

A
  • 21-Hydroxylase Deficiency : defect in CYP21 in aldosterone & cortisol pathways, accumulation of weak androgens (dehydroepi/andostrenedione)
  • 11-B-Hydroxylase Deficiency : defect inCYP11 in aldosterone & cortisol pathways (one step farther than CYP21), accumulation of mid-products deoxy/corticosterone

Hyperaldrenalism:
Cushings Dz: high ACTH/Cortisol
Ectopic ACTH Syndrome: very high ACTH, high Cortisol
Adrenal Tumor: low ACTH, high Cortisol

37
Q

Adrenal Medulla

A
  • Synthesized and secretes catecholamines (epi, norepi, dopamine)
  • Stimulate aderenergic receptors (alpha = vasoconstriction etc, beta = vasodilation etc)
  • Catecholamines released in response to hypotension, hypoxia, exertion, cold, pain, fear –> epi & norepi converted to Vanillylmandelic Acid (VMA)
38
Q

Adrenal medullary disorders & testing

A
  • Pheochromocytoma: rare & benign tumor of medullary chromaffin cells
  • May occur in multiple endocrine neoplasia (MEN): genetic mutations determine type 2a or 2b
  • Hypertension in main symptom due to increase in catecholamines

Testing: Plasma metanephrines (midproduct between epi -> VMA), Urinary catecholamines or metanephrines (ratio to cr), Chromogranin A (tumor marker protein, not specific)

Clinical Lab (5 decks)

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