ENDOCRINOLOGY Flashcards
What enzymes produced by acidophil cells use JAK-STAT signalling
growth hormone
prolactin
other cells using JAK-STAT: EPO, TPO, leptin, IL-2, IL-6, IFN-Y
cause of increased BMR in hyperthyroidism
increased synthesis **Na-K ATPase **
cause of increased SNS activity in hyperthyroidism
increased expression B1 adrenergic receptors
what happens to mensturation, cholesterol and blood glucose levels in hyperthyroidism
oligo = menorrhoea
hypo = cholesterolemia
hyper = glycemia
gluconeogenesis, glycogenolysis increased
glycosaminoglycans are made up of
chondroitin sulfate
hyaluronic acid
exopthalmos and pretibial myxoedema are caused by
fibroblasts express TSH
TSH activation results in glycosaminoglycan (GAGs) buildup –> inflammation, fibrosis, oesema
AB stimulation of fibroblasts
autoantibody IgG stimulates TSH receptor
HSII
Graves disease
increased synthesis/release thyroid hormone
non-tender goiter
raised TSH, T4, T3
ADHD
thyroid hormone resistance
decreased sensitivty peripheral tissues to thyroid h. - receptor defect
receptor defect
graves disease is triggered by -?antibodies binding to -?
thyrotropin receptor antibodies
activating TSH receptor
TSH receptor on other cells - fibroblasts, adipocytes -> exothalmous
thyrotropin also called TSH(thyroid stimulating hormone)
propanolol can be used to treat hyperthyroid B-adrenergic (SNS) symptoms. what is used to treat exopthalmos
glucocorticoids
(it is immune mediated (TSH driven), not treated by BB)
other SNS symptoms can be addressed with BB use
brittle hair/nails, fatigue
low TSH
low T4
menstural cycle not returned
postpartum
secondary hypothyroidism
(Sheehan syndrome)
hypothalamic-pituitary dysfunction
ischaemic necrosis pituitaty gland –> from systemic hypotension during delivery
Hashimoto and postpartum thyroiditis (variant of hashimoto occuring with 1yr pregnancy) = high TSH (primary hypothyroid)
mental retardation
short stature
coarse facial features
enlarged tongue
umbilical hernia
maternal hypothyroidism early pregnancy
cretinism
(neonate hypothyroidism)
affects brain, skeletal development
also occur due to dyshormonogenetic goiter - TPO defect (cant do oxidation, organification, coupling)
most common congenital adrenal hyperpasia
21-hydroxylase deficiency
AR
adrenal hyperplasia
skin hyperpigmentation
3 types
congenital adrenal hyperplasia
ACTH stim –> MSH production –> skin pigmentation
17a
21
11B
(starts with 1) = causes HTN
(ens with 1) = causes virulisation
increased BP
decreased K
low cortisol
decreased sex hormones
17a-hydroxylase deficiency
XX lacks 2’ sexual dev
XY atypical genitalia, undescended testes
decreased BP
increased K
decreased cortisol
increased sex hormones
21-hydroxylase deficiency
salt wasting
increased renin
increased 17-hydroxyprogesterone
XX virilisation
infancy (newborn)
increased BP
decreased K
decreased coristol
increased sex hormones
11B-hydroxylase deficiency
decreased aldosterone
increased 11B-deoxycortisterone
decrease renin
infancy - severe HTN
childhood - precocious puberty
XX virilisation
weakness
fatigue
decreased appetite
constipation
renal calculi
osteitis fibrosis cystica
increased calcum
decreased phosphorous
parathyroid adenoma
part of MEN1 (parathyroid adenoma)
main cause of primary pyperparathyroidism
‘stones, thrones, bones, grones, psychiatric overtones’
functino of chief cells of parathyroid gland
secrete PTH
woman
loss of peripheral vision
amennorhoea
prolactinoma
(pituitary adenoma) m/c
mass effect -> optic chiasm compression -> bitemoral hemianopsia
suppress GnRH -> inhibit FSH, LH -> amenorhhoea
acute viral illness
diffusely tender thyroid
absence of iodine uptake
multinucleated giant cells on FNA
subacute granulomatous thyroiditis
(de quervains)
attenuated vaccine properties
non viable organism
still posses antigens
Leptin inhibits hunger by counteracting the effect of
hypothalamic neuropeptide Y (NPY)
(potent stimulator of hunger)
skin tags
hyperhydrosis
prognathism, brow protrusion
broadening hands, feet
arthritis
carpel tunnel
organomegaly
acromegaly
hyperplasia articular cartilage & synovial hypertrophy
excess GH
increased IGF-1
what can stimulate lactotrophs
TRH
(thyroid regulating hormone)
dopamine inhibits prolactin
hyperosmotic volume contraction is
loss of free water
retention of electrolytes
diabetic insipidus
decreased fluid intake
excessive sweating (sweat is hypotonic)
sweat is
hypotonic
example of isoosmotic volume contraction
gastrointestinal haemorrhage/diarrhoea
isotonic loss ECF
no effect osmolality or ICF
in diabetes insipidus you will see
osmolality
ECF
ICF
osmolality increased
ECF decreased
ICF decreased
hyperosmotic volume contraction
in pheochromocytoma, treatment of ___ is given first before treatment og ___ to prevent
alpha blocker
beta blocker
hypotensive crisis
if BB given first, unopposed vasoconstriction
hypertension
headache
sweating
tachycardia
polycythemia
are symptoms of what tumour
pheochromocytoma
neuroendocrine (adrenal tumour)
tx with a-blocker THEN b-blocker
function of epinephrine in hypoglycaemia
selective ativation of adrenal medullary epinephrine
**
key ligant in glycogenolysis & gluconeogenesis
acts on hepatocytes a and b receptors -> release intreacellular Ca -> activates glycogen phosphorylase
increases gluconeogenesis through fructose bisphosphate 2 activation (b adrenergic)
factors (3) required to increase bone minral density
Wolffs law
stress - weightbearing/strenuous
available calcium, Vit D
oestrogen/testosterone (key regulators)
stress
vitamins
hormones
hihger sex hormone levels puberty –> mineral density increases most
tails of 3rd decade (not reoccur readily)
osteoclast then > osteoblast
what hormones regulate physeal growth, ossification and closure
testosterone and oestrogen
aromitisation of testosterone to oestrogen –> closure of physis in later puberty
effects (2) of cortisol on bone
increased osteoclast activity
decreased bone mineral density
‘glucocorticoid’
osteoporosis is more common women than men because
women start out with lower peak bone mass compared to males
female bone mineral density decreases more rapidly after menopause
