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Bio 252- atherosclerosis > Thyroid Gland disorders > Flashcards

Thyroid Gland disorders Flashcards

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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

A
  • 2 glands one in association with each kidney

- 2 parts to gland cortex and medulla

25
Q

Cortex secretes what 3 kinds of hormones

A

Cortex: (under pituitary control) (most endocrine disorders related to cortex) glucocorticoids (cheif CORTISOL), mineralocorticoids (cheif ALDOSTERONE),
androgens (cheif testosterone & dihydrotesterone (DHT)

26
Q

Medulla

A

influenced by SNS

-secrese epinephrine & norepinephrine

27
Q

ACTH is

A

Adrenocorticotropic hormone produced by anterior pituitary,

28
Q

ACTH is

A

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
Q

Hyperfunction of Adrenal glands Etiology & Patho

A
  • 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
Q

Cushings syndrome is _____function of the ________

A

hyperfunction of the adrenal cortex

31
Q

Cushings syndrome

A
  • glucocorticoid (CORTISOL) hypersecretion causing increase hormone action
  • protein catabolism (weak muscle)
  • gluconeogenisis (elevates glucose in circulation from proteins & lipids)
  • Alt glucose metabolism
32
Q

Mnfts of cushings syndrome

A

-rounded “moon face”
-“buffalo hump” - fat pad on neck & shoulders
Affecting just women:
-androgen hypersecretion: causes facial hair, receding hairline

33
Q

Diagnosing cushings syndrome

A
  • 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
Q

Treatment of cushings syndrome

A
  • excise tumor
  • irradiate pituitary (radiation)
  • drugs for ectopic tumor
  • adrenalectomy
35
Q

Conn syndrome is ______ function of _______

A

hyperfunction of adrenal cortex

36
Q

Conn syndrome

A
  • excess production of aldosterone (mineralocorticoids)
  • primary hyperaldosterionism
  • rare, increased incidence in women (unkown why) (30-50yrs)
37
Q

Conn syndrome Etiology

A
  • mostly cortical adenoma (benign, glandular epithelial tumor)
  • idiopathic hyperplasia of cortex
  • renin secreting tumor (kidney) – RAAS – then causes increase in aldosterone
38
Q

Mnfs of Conn syndrome

A
  • 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
Q

Treatment of Conn syndrome

A
  • unilateral adenectomy for adenmoa

- aldosterone recepetor antagonist (blocks receptor drug)

40
Q

Hypoaldosteronism also known as

A

addisons diseas

41
Q

Hypoaldosteronism _addisons disease

A
  • primary cortical deficiency
  • all 3 groups of hormones affected: Corticosteriods, mineralocorticoids, androgens
  • uncommon
42
Q

Hypoaldosteronism _addisons disease etiology

A
  • autoimmunity
  • non-functioanl tumor, infection (may affect cortex directly)
  • high doses of steroids (glucocorticoids) suppress ACTH
43
Q

Cortex has enormous functional reserve therefore

A

lots of damage before deficiency becomes evident

44
Q

almost ___ percent of destruction of cortex before mnfts become evident

A

90%

45
Q

Mnfts of Hypoaldosteronism _addisons disease

A
  • 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
Q

Treatment of Hypoaldosteronism _addisons disease

A 
acute addisonian crisis: 
-IV fluids 
-IV glucocorticiods 
Chronic: 
-glucocorticoids
-mineralocorticoids
47
Q

most pituitary disorders are of the

A

anterior pituitary, posterior pituitary less common

48
Q

what is myxedema

A
  • 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
Q

hyperfunction of the anterior pituitary are caused by

A

adenomas of the secretory cells

50
Q

what does ADH do?

A

retains water

51
Q

what does aldosterone do?

A

retains sodium

52
Q

hyperfunction of anterior pituitary

A
  • 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
Q

what are trophic hormones

A

trophic hormones act on another endocrine gland

54
Q

what are non-trophic hormones

A

those that act directly on targeted tissues or cells, and not on other endocrine gland to stimulate release of other hormones.

55
Q

syndrome of inappropriate ADH (SIADH)

A
  • 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
Q

SIADH causes dilutional hyponatremia for 2 reasons:

A
  • water retention is so high dilutional concentration of sodium
  • hormone responsible for sodium re absorption (aldosterone) being suppressed
57
Q

Treatment of SIADH

A
  • restrict fluids if mild
  • diuretics
  • ADH antagonists (anit-diuretic)
  • aquaretic (diuretic with electrolyte sparing properties) V2 receptor blocker
58
Q

why is renin & aldosterone secretion suppressed during SIADH

A

stimulation of renin is from decreased perfusion to kdenys, this trigger for renin secretion is absent (impaired Na+ reabsorption because aldosterone being suppressed)

Bio 252- atherosclerosis (37 decks)

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