Endocrine disorders Flashcards
normal level of T3 in the blood
0.8-2 ng/mL
normal level of T4 in the blood
45-120 ng/mL
normal level of TSH in the blood
0.4-4.5MU/L
normal level of try in the blood
5-25 mU/mL
2 main thyroid diseases
Hashimoto’s disease and Graves disease
Hashimotos
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
hormone profile of Hashimoto’s (underachieve)
- low T3/T4
- high TSH
autoimmune nature of Hashimoto’s
- 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
Graves disease
- 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
hormone profile for overactive thyroid
- high T3/T4
- low TSh
overactive thyroidism
metabolic rate increased
- oxygen consumption increase
- heat production increase
- protei synthesis increase
weight loss, heat intolerant,e tenor, tachycardia, muscle weakness, diarrhea
underachieve thyroidism
metabolic rate slowed
- oxygen consumption decreases
- protein synthesis decreases
fatigue, weight gain, cold intolerance, bradycardia, slow reflexes and speech, dry skin
primary endocrine disorder
-dysfucntion originates in the peripheral endocrine gland itself
secondary endocrine
Under/over stimulation by the pituitary
hyper function of the endocrine flanks my result in overstimulation by the pituitary gland, but is most commonly due to
hyperplasia or neoplasia of the gland itself e.g. tumour growth which produces more of the hormone
ectopic hormone production
when cancerous tumours from other tissues can produces hormones
exogenous hormone administration
hormone excess can also be due to exogenous hormone admin- taking extra hormones orally)
antibodies can stimulate
peripheral endocrine glands e.g. hyperthyroidism in graves disease (primary)
enzyme defects
increase stimulation- increase in hormone production
physical disruption of peripheral gland
can also rapidly release stored hormones
hyperaldosteronism
disorder in which the adrenal glands produce too much aldosterone and too much is released into the blood
primary hyperaldosteronism
-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
levels of renin in primary hyperaldosteronism
low e.g. will be providing negative feedback since blood pressure will be increased
example of primary hyperaldosteronism
Cons syndrom and additions
cortisol deficiency in
primary hyperaldosteronism
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
symptoms of hyperaldosteronism
high PB, low (k+), tiredness, headache, muscle weakenss
hypoaldosteronism
an endocrinological disorder characterised y decreases levels of the hormone aldosterone
hyporeniemic hypoaldosteronism
when there si a decreased production of renin
primary hypoaldosteronism
- primary adrenal insufficiency
- congenital adrenal hyperplasia
- aldosterone synthase defence
secondary hypoaldosteronism
- seocndary adrenal insufficiency
- disease of the pituitary or hypothalamus
Psuedohyperaldosteronism
a medical condition which mimics hyperaldosteronsim, producing high B associated with low plasma renin activity and metabolic alkalosis associate with hypokalemia
unlike hyperaldosteronism, Psuedohyperaldosteronism…
involves normal to low levels of aldosterone (hypoaldosteronism)
what does psuedohyperaldosteronism cause
SAME
-syndrome of Apparent Mineralocorticoid Excess
what can cause psuedohyperaldosteronism
Liquorice
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
what does 11-B-HSD2 do
converts cortisol to cortisone- which cannot cause a cellular epsonse
receptor for both aldosterone and cortisol
mineralocorticoid
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
cortisol basically acts as
aldosterone
hypothalamic disease by result due to
malnutrition, genetic disorders, radiation, surgery, lesion, tumour or the physical injury to the hypothalamus
the hypothalamus is the control centre for
several endocrine functions
the hypothalamus releases
ADH, gondatropin releasing hormone, GHRH, oxytocin
- many of these hormones impact hypothalamus
therefore if the hypothalamus is not working correctly
neither will the pituitary which controls the adrenal glands, ovaries/testes and thyroid glands
tertiary endocrine disorder
HYPOTHALAMUS
secondary endocrine disorder
PITUITARY
primary endocrine disorder
PERIPHERAL ENDOCRINE DISORDER
