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Disease, diagnostics and therapeutics > Endocrine disorders > Flashcards

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
Q

cortisol deficiency in

A

primary hyperaldosteronism

26
Q

secondary hyperaldosteronism

A

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
Q

symptoms of hyperaldosteronism

A

high PB, low (k+), tiredness, headache, muscle weakenss

28
Q

hypoaldosteronism

A

an endocrinological disorder characterised y decreases levels of the hormone aldosterone

29
Q

hyporeniemic hypoaldosteronism

A

when there si a decreased production of renin

30
Q

primary hypoaldosteronism

A
  • primary adrenal insufficiency
  • congenital adrenal hyperplasia
  • aldosterone synthase defence
31
Q

secondary hypoaldosteronism

A
  • seocndary adrenal insufficiency

- disease of the pituitary or hypothalamus

32
Q

Psuedohyperaldosteronism

A

a medical condition which mimics hyperaldosteronsim, producing high B associated with low plasma renin activity and metabolic alkalosis associate with hypokalemia

33
Q

unlike hyperaldosteronism, Psuedohyperaldosteronism…

A

involves normal to low levels of aldosterone (hypoaldosteronism)

34
Q

what does psuedohyperaldosteronism cause

A

SAME

-syndrome of Apparent Mineralocorticoid Excess

35
Q

what can cause psuedohyperaldosteronism

A

Liquorice

36
Q

how do liquorice cause Psuedohyperaldosteronism

A
  • 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
Q

what does 11-B-HSD2 do

A

converts cortisol to cortisone- which cannot cause a cellular epsonse

38
Q

receptor for both aldosterone and cortisol

A

mineralocorticoid

39
Q

both aldosterone and cortisol

A

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
Q

cortisol basically acts as

A

aldosterone

41
Q

hypothalamic disease by result due to

A

malnutrition, genetic disorders, radiation, surgery, lesion, tumour or the physical injury to the hypothalamus

42
Q

the hypothalamus is the control centre for

A

several endocrine functions

43
Q

the hypothalamus releases

A

ADH, gondatropin releasing hormone, GHRH, oxytocin

- many of these hormones impact hypothalamus

44
Q

therefore if the hypothalamus is not working correctly

A

neither will the pituitary which controls the adrenal glands, ovaries/testes and thyroid glands

45
Q

tertiary endocrine disorder

A

HYPOTHALAMUS

46
Q

secondary endocrine disorder

A

PITUITARY

47
Q

primary endocrine disorder

A

PERIPHERAL ENDOCRINE DISORDER

Disease, diagnostics and therapeutics (53 decks)

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