Endocrinology Flashcards
where does the thyroid originate?
what is it derived from
pharynx floor
endoderm
remnant of thyroglossal duct
foramen cecum
ectopic thyroid tissue
tongue
what are the parafollicular cells of the thyroid derived from?
neural crest cells
zona glomerulosa
zona fasciculate
zona reticularis
medulla
aldosterone
cortisol
sex hormones
catecholamines
posterior pituitary
ADH, oxytocin
pituitary derivatives
anterior - oral ectoderm
posterior - neuroectoderm
alpha subunit in anterior pituitary
subunit common to TSH, LH, FSH, hCG
beta subunit in anterior pituitary
determines hormone specificity
POMC –>
ACTH + MSH
acidophilic anterior pituitary release
GH, PRL
islets of langerhans cells and function
a - glucagon
b - insulin
d - somatostatin
where is insulin precursor synthesised?
RER
preproinsulin
high insulin low C-peptide
exogenous insulin
effects of insulin
triglyceride synthesis (+decrease lipolysis)
Na retention
protein synthesis
increase K+ and a.a. uptake
GLUT 1 2 3 4 5
RBC, brain, cornea, placenta
b islet cells, liver, kidney, small intestine
brain, placenta
adipose, striated muscle - insulin dependent
fructose - spermatocytes, GI tract - insulin dependent
better to injest glucose
bigger insulin release because GLP-1 is released after meals
glucagon inhibition
insulin, hyperglycaemia, somatostatin
somatostatin affect on pituitary
decreases GH and TSH
TRH effect on pituitary
TSH and prolactin stimulation
Dopamine effect on the pituitary
decreases prolactin and TSH
CRH effect on pituitary
increases ACTH, MSH, B-endorphin
how does prolactin inhibit itself?
increases dopamine
prolactinoma Rx
dopamine agonist - bromocriptine
prolactin stimulation
dopamine antagonists - antipsychotics
estrogens
GH stimulates
IGF-1
when does GH stimulation increase?
exercise, deep sleep, puberty, hypoglycaemia
Rx xs GH secretion
somatostatin analogs - octreotide
what is GH stimulated by?
ghrelin
V1 and V2 receptors
1 - serum osm
2 - bp
nephrogenic DI mutation
V2 receptor
Rx central DI
desmopressin acetate (ADH analog)
17-a hydroxylase
pregnenolone/progesterone –>17-hydroxy version
17-a-hydroxylase defeciency
more aldosterione, decreased others
raised bp, low K+
decerased androstenedione
17a-hydroxylase deficiency
ambiguous genitalia, undescended testes
female version
17a-hydroxylase deficiency
lacks secondary sexual development
21-hydroxylase deficiency
decreased Aldosterone and cortisone, increased sex hormones
high renin and 17-hydroxy-progesterone
21-hydroxylase deficiency
salt wasting, precocious puberty
21-hydroxylase deficiency
11-B hydroxylase deficiency
increased aldosterone, cortisol
increased sex hormones, bp
decreased renin
what causes striae
fibroblast activity increase
cortisol decrease in immune response
inhibits leukotrienes and prostaglandins inhibits WBC adhesion --> neutrophilia blocks histamine release form mast cells reduces eosinophils blocks IL-2 production
raised pH and calcium
higher affinity to albumin –> hypocalcemia
vitamin D2
D3
2 - plants, fungi, yeast
3 - sunlight, fish, plants
vitamin D on PTH
increases PTH
PTH effects
increases Ca reabsorption
increases vitamin D3 production
PO4 from bone, PO4 lost in kidney
How does PTH affect bone?
increases RANK-L
raised PO4 on PTH
increases PTH
Mg effect on PTH
low - raises PTH
very low - decreases PTH
Calcitonin action
decreases Ca
opposes PTH
T3 function
brain maturation, bone growth, B adrenergic, Basal metabolic rate increase
changes is TBG leevls
decreased in hepatic failure, steroid use
increased in pregnancy or OCP use (E increases TBG)
Grave’s disease
thyroid stimulating immunoglobulin