Flashcards in Thyroid Gland disorders Deck (58):
1
where is thyroid gland located
lies adjacent to trachea and immediately below larynx
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hyperthyroidism is essentially
hyperactive thyroid gland
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thyroid gland produces what hormones
T3 & T4 (thyroxine) called thyroid hormone together
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essentially T3 & T4
increase metabloic rate
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thyroid hormone is secreted in response to _______
thyroid stimulating hormone from anterior pituitary
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Goiter is enlargement of
thyroid
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causes of goiter could be from
hyper function or hypo function
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endemic goiter
-iodine deficiency
-decrease in T3 & T4
-compensatory increase in TSH
-hyperplasia & hypertrophy causin goiter
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Toxic goiter
-due to hypersecretion
-Nodular gland (associated with hypothyroidism)
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Hyperthyroidism is due to
autoimmunity
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85% of all hyperthyroidism is ____
Graves disease (so name is used interchangeably)
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Graves disease is usually found in
young women (20-40yrs)
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3 hallmark features of graves disease
-hyperthyroidism
-goiter
-expothalmos (protruding eyeballs)
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Patho of graves disease
-antibodies target TSH receptors on target cell (abnormal thyroid stimulation)
-TSAbs(TS immunoglobulins) mimic TSh & bind to TSH receptors
-Increase in TH secretion
-increase in TH inhibits TSH secretion
-Causes decrease in TSH secretion
-TSabs avoid enzyme degradation (active longer, thyroid doesn't inhibit, enzymes dont break it down)
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Thyrotoxicosis
-"thyroid storm"
-Syndrome of hyperthyroidism (IN UNDIAGONSED & UNTREATED CASES)
-precipitated by stress (emotional & physiologic) (eg. resp infection, DKA, thyroidectomy)
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Mnfts of thyrotoxicosis
- excessive fever, severe cardiovascular & CNS problems
-Increase metabolism (alt pathways, protein & lipid catabolism) --- metabolizes all carbohydrates then moves to proteins & lipids (causes wt loss)
-General increase in metabolism-- increase in metabolic heat ---compensatory heat loss mechanisms--flushed skin & perspiration (if exercising heat already maxed of compensatory mechanisms)
-Intolerance to an increase in temp
-CV: angina, tachycardia, CHF (increase demand for energy, oxygen, waste removal & glucose --- Increase Heart rate & Cardiac output)
-CNS: delirium, agitation, irritability, insomnia (hot & miserable cannot sleep)
-increase mortality rate
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Treatment of hyperthyroidism
producing hormone in excess want to suppress hormones:
1 of 3 options:
-antithyriod drugs (eg. tapazole decreses TH syntehsis): (have an increase in T3 and T4, have a drug that inhibits synthesis of, resolves problem does not irradiate cause which is autoimmunity)
-radioidine therapy:
(gets in thyroid & binds to thyroid omitting radiation which destroys local cells that secrete hormone)
-surgery: (difficult because dont know how much to remove)
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Hypothyroidism
-primary (thyroid)
-secondary (pituitary)
-tertiary (hypothalamus)
-95% is primary - thyriod
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Etiology of hypothyroidism
-autoimmunity
-radiation & surgery for hyperfunction
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Hashimotos thyroditis is the most common
-hyposecretion state
-90% in middle age women (45yrs)
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Hashimotos thyroiditis patho
-autoimmune destruction of gland
-infiltration of lymphocytes
-anti thyroid Abs block TSH binding (even competition for receptors)
-(deficiency of T3 & T4, will not produce thyroid hormone)
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mnfts of hashimotos thyroiditis
-decreased body temp
-decrease in cardiac output (d/t less ATP)
-decrease in CNS function (d/t less ATP)
-weak muscle contraction (d/t less ATP)
-increase body weight (cells not able to utilize ingested nutrients)
-Hypometabolic state & myxedema
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Treatment of hypothyroidism
Replacement therapy (T4 daily)
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Adrenal glands
- 2 glands one in association with each kidney
-2 parts to gland cortex and medulla
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Cortex secretes what 3 kinds of hormones
Cortex: (under pituitary control) (most endocrine disorders related to cortex) glucocorticoids (cheif CORTISOL), mineralocorticoids (cheif ALDOSTERONE),
androgens (cheif testosterone & dihydrotesterone (DHT)
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Medulla
influenced by SNS
-secrese epinephrine & norepinephrine
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ACTH is
Adrenocorticotropic hormone produced by anterior pituitary,
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ACTH is
Adrenocorticotropic hormone produced by anterior pituitary, targets adrenal glands, adrenal cortex, ACTH facilitates the release of cortisol from adrenal cortex (regulates levels of steroid hormone cortisol)
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Hyperfunction of Adrenal glands Etiology & Patho
-cortical tumor or hyperplasia ---increase in cortisol (acts negatively & suppresses ACTH), Low levels of ACTH
-Tumor or hyperplasia of anterior pituitary causes an increase in ACTH
-ectopic ACTH tumor (eg. in the lungs)
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Cushings syndrome is _____function of the ________
hyperfunction of the adrenal cortex
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Cushings syndrome
-glucocorticoid (CORTISOL) hypersecretion causing increase hormone action
-protein catabolism (weak muscle)
-gluconeogenisis (elevates glucose in circulation from proteins & lipids)
-Alt glucose metabolism
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Mnfts of cushings syndrome
-rounded "moon face"
-"buffalo hump" - fat pad on neck & shoulders
Affecting just women:
-androgen hypersecretion: causes facial hair, receding hairline
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Diagnosing cushings syndrome
-urinary, serum & salivary cortisol (late night sample, when cortisol supposed to be low, will be high during this time with cushings syndrome)
-Dexamethasone suppression test: elevated cortisol suppresses ACTH, if ACTH is not suppressed may have cushings
-CT & MRI: location of tumor
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Treatment of cushings syndrome
-excise tumor
-irradiate pituitary (radiation)
-drugs for ectopic tumor
-adrenalectomy
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Conn syndrome is ______ function of _______
hyperfunction of adrenal cortex
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Conn syndrome
-excess production of aldosterone (mineralocorticoids)
-primary hyperaldosterionism
-rare, increased incidence in women (unkown why) (30-50yrs)
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Conn syndrome Etiology
-mostly cortical adenoma (benign, glandular epithelial tumor)
-idiopathic hyperplasia of cortex
-renin secreting tumor (kidney) -- RAAS -- then causes increase in aldosterone
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Mnfs of Conn syndrome
-HTN (major problem) aldosterone cause re absorption of sodium, which cause water retention, causing hypervolemia and increasing BP
-Hypokalemia (because aldosterone excretes potassium)
-Alkalosis (because aldosterone also secretes H+ ions -minor function)
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Treatment of Conn syndrome
-unilateral adenectomy for adenmoa
-aldosterone recepetor antagonist (blocks receptor drug)
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Hypoaldosteronism also known as
addisons diseas
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Hypoaldosteronism _addisons disease
-primary cortical deficiency
-all 3 groups of hormones affected: Corticosteriods, mineralocorticoids, androgens
-uncommon
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Hypoaldosteronism _addisons disease etiology
-autoimmunity
-non-functioanl tumor, infection (may affect cortex directly)
-high doses of steroids (glucocorticoids) suppress ACTH
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Cortex has enormous functional reserve therefore
lots of damage before deficiency becomes evident
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almost ___ percent of destruction of cortex before mnfts become evident
90%
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Mnfts of Hypoaldosteronism _addisons disease
-sodium, chloride FLUID loss causing hypovolemia causing decreased cardiac ouput causing hypotension causing weakness & fatigue (result of inadequate perfusion)
-poor stress tolerance (ex. SX infection)
-Wt loss (glucocorticoids)
-Hyperpigmentation (increase in ACTH, breakdown of ACTH formation of MSH -melaoncyte stimulating hormone)
-addisonian crisis = acute insufficient management d/t stress
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Treatment of Hypoaldosteronism _addisons disease
acute addisonian crisis:
-IV fluids
-IV glucocorticiods
Chronic:
-glucocorticoids
-mineralocorticoids
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most pituitary disorders are of the
anterior pituitary, posterior pituitary less common
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what is myxedema
-acquired
-chronic decrease of thyroid hormone secretions in adults (HYPOSECRETION/HYPOTHYROIDISM)
-characterized by non-pitting edema "puffy-face" gel like material
-glycoprotein deposition in dermis (everywhere but most obvious in face)
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hyperfunction of the anterior pituitary are caused by
adenomas of the secretory cells
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what does ADH do?
retains water
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what does aldosterone do?
retains sodium
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hyperfunction of anterior pituitary
-adenomas of secretory cells (trophic & non-trophic hormones) -- growth hormone & procalcitonin are non-trophic
-increaset stimulation & hyperfunction of target gland
ex. ACTH ---- adrenal cortex
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what are trophic hormones
trophic hormones act on another endocrine gland
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what are non-trophic hormones
those that act directly on targeted tissues or cells, and not on other endocrine gland to stimulate release of other hormones.
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syndrome of inappropriate ADH (SIADH)
-increase ADH production from pituitary (ADH hypersecretion) --failure of negative feedback
-ectopic tumor (eg. in Lungs) --ADH like substances
-increase water retention (affects blood volume & electrolytes) --- dilutional hyponatremia
-renin & aldosterone secretion suppressed
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SIADH causes dilutional hyponatremia for 2 reasons:
-water retention is so high dilutional concentration of sodium
-hormone responsible for sodium re absorption (aldosterone) being suppressed
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Treatment of SIADH
-restrict fluids if mild
-diuretics
-ADH antagonists (anit-diuretic)
-aquaretic (diuretic with electrolyte sparing properties) V2 receptor blocker
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