Endocrine disorders Flashcards

1
Q

normal level of T3 in the blood

A

0.8-2 ng/mL

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2
Q

normal level of T4 in the blood

A

45-120 ng/mL

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3
Q

normal level of TSH in the blood

A

0.4-4.5MU/L

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4
Q

normal level of try in the blood

A

5-25 mU/mL

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5
Q

2 main thyroid diseases

A

Hashimoto’s disease and Graves disease

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6
Q

Hashimotos

A

underachieve thyroid

  • thyroid being stimulated properly by TSH, however it is unable t produce enough T3/T4 for the body to function properly
  • autoimmune thyroidistis causing iodine deficiency
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7
Q

hormone profile of Hashimoto’s (underachieve)

A
  • low T3/T4

- high TSH

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8
Q

autoimmune nature of Hashimoto’s

A
  • aut-reactive CD3+ T cells recruit B cells and CD8 T cells to the thyroid
  • anti TPO Avs and anti-thyroid cytotoix T lymphocytes result in follicular cell destruction
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9
Q

Graves disease

A
  • over active
  • hyperthyroidism
  • too much T3/T4 is produced. Anti-TSH- R antibodies generated that mimic TSH and stimulate receptor after binding to it
  • more T3/T4 synthesised
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10
Q

hormone profile for overactive thyroid

A
  • high T3/T4

- low TSh

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11
Q

overactive thyroidism

A

metabolic rate increased

  • oxygen consumption increase
  • heat production increase
  • protei synthesis increase

weight loss, heat intolerant,e tenor, tachycardia, muscle weakness, diarrhea

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12
Q

underachieve thyroidism

A

metabolic rate slowed

  • oxygen consumption decreases
  • protein synthesis decreases

fatigue, weight gain, cold intolerance, bradycardia, slow reflexes and speech, dry skin

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13
Q

primary endocrine disorder

A

-dysfucntion originates in the peripheral endocrine gland itself

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14
Q

secondary endocrine

A

Under/over stimulation by the pituitary

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15
Q

hyper function of the endocrine flanks my result in overstimulation by the pituitary gland, but is most commonly due to

A

hyperplasia or neoplasia of the gland itself e.g. tumour growth which produces more of the hormone

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16
Q

ectopic hormone production

A

when cancerous tumours from other tissues can produces hormones

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17
Q

exogenous hormone administration

A

hormone excess can also be due to exogenous hormone admin- taking extra hormones orally)

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18
Q

antibodies can stimulate

A

peripheral endocrine glands e.g. hyperthyroidism in graves disease (primary)

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19
Q

enzyme defects

A

increase stimulation- increase in hormone production

20
Q

physical disruption of peripheral gland

A

can also rapidly release stored hormones

21
Q

hyperaldosteronism

A

disorder in which the adrenal glands produce too much aldosterone and too much is released into the blood

22
Q

primary hyperaldosteronism

A

-due to problem with the adrenal glands which cause them to release too much aldosterone e.g. a non cancerous tumour growing on the gland and releasing aldosteorne

23
Q

levels of renin in primary hyperaldosteronism

A

low e.g. will be providing negative feedback since blood pressure will be increased

24
Q

example of primary hyperaldosteronism

A

Cons syndrom and additions

25
cortisol deficiency in
primary hyperaldosteronism
26
secondary hyperaldosteronism
caused by a problem elsewhere in the body using too much aldosterone to be released e.g. heart (ANP/BNP), kidney (renin) or high BP
27
symptoms of hyperaldosteronism
high PB, low (k+), tiredness, headache, muscle weakenss
28
hypoaldosteronism
an endocrinological disorder characterised y decreases levels of the hormone aldosterone
29
hyporeniemic hypoaldosteronism
when there si a decreased production of renin
30
primary hypoaldosteronism
- primary adrenal insufficiency - congenital adrenal hyperplasia - aldosterone synthase defence
31
secondary hypoaldosteronism
- seocndary adrenal insufficiency | - disease of the pituitary or hypothalamus
32
Psuedohyperaldosteronism
a medical condition which mimics hyperaldosteronsim, producing high B associated with low plasma renin activity and metabolic alkalosis associate with hypokalemia
33
unlike hyperaldosteronism, Psuedohyperaldosteronism...
involves normal to low levels of aldosterone (hypoaldosteronism)
34
what does psuedohyperaldosteronism cause
SAME | -syndrome of Apparent Mineralocorticoid Excess
35
what can cause psuedohyperaldosteronism
Liquorice
36
how do liquorice cause Psuedohyperaldosteronism
- inhibits the enzyme 11B-HSD2 - therefore cortisol is not converted to cortisone - cortisol can bind to the mineralcortiocoid receptor in the nucleus of principle cells - causing excess gene transcription of Na+/K+ pumps - causing excess sodium retention in the body, causing BP to increase
37
what does 11-B-HSD2 do
converts cortisol to cortisone- which cannot cause a cellular epsonse
38
receptor for both aldosterone and cortisol
mineralocorticoid
39
both aldosterone and cortisol
when bound to mineralocorticoid receptors on DNA of principle cells, cause the gene transcription of Na+/K+ pumps- causing sodium retention and less diuresis, increasing BP
40
cortisol basically acts as
aldosterone
41
hypothalamic disease by result due to
malnutrition, genetic disorders, radiation, surgery, lesion, tumour or the physical injury to the hypothalamus
42
the hypothalamus is the control centre for
several endocrine functions
43
the hypothalamus releases
ADH, gondatropin releasing hormone, GHRH, oxytocin | - many of these hormones impact hypothalamus
44
therefore if the hypothalamus is not working correctly
neither will the pituitary which controls the adrenal glands, ovaries/testes and thyroid glands
45
tertiary endocrine disorder
HYPOTHALAMUS
46
secondary endocrine disorder
PITUITARY
47
primary endocrine disorder
PERIPHERAL ENDOCRINE DISORDER