Bio 252- atherosclerosis > Thyroid Gland disorders > Flashcards

Thyroid Gland disorders Flashcards

(58 cards)

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1
Q

where is thyroid gland located

A

lies adjacent to trachea and immediately below larynx

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2
Q

hyperthyroidism is essentially

A

hyperactive thyroid gland

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3
Q

thyroid gland produces what hormones

A

T3 & T4 (thyroxine) called thyroid hormone together

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4
Q

essentially T3 & T4

A

increase metabloic rate

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5
Q

thyroid hormone is secreted in response to _______

A

thyroid stimulating hormone from anterior pituitary

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6
Q

Goiter is enlargement of

A

thyroid

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7
Q

causes of goiter could be from

A

hyper function or hypo function

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8
Q

endemic goiter

A
  • iodine deficiency
  • decrease in T3 & T4
  • compensatory increase in TSH
  • hyperplasia & hypertrophy causin goiter
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9
Q

Toxic goiter

A
  • due to hypersecretion

- Nodular gland (associated with hypothyroidism)

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10
Q

Hyperthyroidism is due to

A

autoimmunity

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11
Q

85% of all hyperthyroidism is ____

A

Graves disease (so name is used interchangeably)

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12
Q

Graves disease is usually found in

A

young women (20-40yrs)

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13
Q

3 hallmark features of graves disease

A
  • hyperthyroidism
  • goiter
  • expothalmos (protruding eyeballs)
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14
Q

Patho of graves disease

A
  • 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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15
Q

Thyrotoxicosis

A
  • “thyroid storm”
  • Syndrome of hyperthyroidism (IN UNDIAGONSED & UNTREATED CASES)
  • precipitated by stress (emotional & physiologic) (eg. resp infection, DKA, thyroidectomy)
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16
Q

Mnfts of thyrotoxicosis

A
  • 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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17
Q

Treatment of hyperthyroidism

A

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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18
Q

Hypothyroidism

A
  • primary (thyroid)
  • secondary (pituitary)
  • tertiary (hypothalamus)
  • 95% is primary - thyriod
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19
Q

Etiology of hypothyroidism

A
  • autoimmunity

- radiation & surgery for hyperfunction

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20
Q

Hashimotos thyroditis is the most common

A
  • hyposecretion state

- 90% in middle age women (45yrs)

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21
Q

Hashimotos thyroiditis patho

A
  • 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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22
Q

mnfts of hashimotos thyroiditis

A
  • 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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23
Q

Treatment of hypothyroidism

A

Replacement therapy (T4 daily)

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24
Q

Adrenal glands

Study These Flashcards
A
  • 2 glands one in association with each kidney

- 2 parts to gland cortex and medulla

25
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)
26
Medulla
influenced by SNS | -secrese epinephrine & norepinephrine
27
ACTH is
Adrenocorticotropic hormone produced by anterior pituitary,
28
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)
29
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)
30
Cushings syndrome is _____function of the ________
hyperfunction of the adrenal cortex
31
Cushings syndrome
- glucocorticoid (CORTISOL) hypersecretion causing increase hormone action - protein catabolism (weak muscle) - gluconeogenisis (elevates glucose in circulation from proteins & lipids) - Alt glucose metabolism
32
Mnfts of cushings syndrome
-rounded "moon face" -"buffalo hump" - fat pad on neck & shoulders Affecting just women: -androgen hypersecretion: causes facial hair, receding hairline
33
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
34
Treatment of cushings syndrome
- excise tumor - irradiate pituitary (radiation) - drugs for ectopic tumor - adrenalectomy
35
Conn syndrome is ______ function of _______
hyperfunction of adrenal cortex
36
Conn syndrome
- excess production of aldosterone (mineralocorticoids) - primary hyperaldosterionism - rare, increased incidence in women (unkown why) (30-50yrs)
37
Conn syndrome Etiology
- mostly cortical adenoma (benign, glandular epithelial tumor) - idiopathic hyperplasia of cortex - renin secreting tumor (kidney) -- RAAS -- then causes increase in aldosterone
38
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)
39
Treatment of Conn syndrome
- unilateral adenectomy for adenmoa | - aldosterone recepetor antagonist (blocks receptor drug)
40
Hypoaldosteronism also known as
addisons diseas
41
Hypoaldosteronism _addisons disease
- primary cortical deficiency - all 3 groups of hormones affected: Corticosteriods, mineralocorticoids, androgens - uncommon
42
Hypoaldosteronism _addisons disease etiology
- autoimmunity - non-functioanl tumor, infection (may affect cortex directly) - high doses of steroids (glucocorticoids) suppress ACTH
43
Cortex has enormous functional reserve therefore
lots of damage before deficiency becomes evident
44
almost ___ percent of destruction of cortex before mnfts become evident
90%
45
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
46
Treatment of Hypoaldosteronism _addisons disease
``` acute addisonian crisis: -IV fluids -IV glucocorticiods Chronic: -glucocorticoids -mineralocorticoids ```
47
most pituitary disorders are of the
anterior pituitary, posterior pituitary less common
48
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)
49
hyperfunction of the anterior pituitary are caused by
adenomas of the secretory cells
50
what does ADH do?
retains water
51
what does aldosterone do?
retains sodium
52
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
53
what are trophic hormones
trophic hormones act on another endocrine gland
54
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.
55
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
56
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
57
Treatment of SIADH
- restrict fluids if mild - diuretics - ADH antagonists (anit-diuretic) - aquaretic (diuretic with electrolyte sparing properties) V2 receptor blocker
58
why is renin & aldosterone secretion suppressed during SIADH
stimulation of renin is from decreased perfusion to kdenys, this trigger for renin secretion is absent (impaired Na+ reabsorption because aldosterone being suppressed)
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