Lecture 6+7 Flashcards
What regulates aldosterone?
what part of the adrenal again?
regulated by Ag II and K+
zona glomerulosa
what regulates cortisol and androgens?
what parts of the zona?
ACTH
Fasciculata: cortisol
reticularis: androgens
hormones of the medulla? what controls?
releases epinephrine and norepinephrine
under sympathetic control
what is the blood supply of the adrenal gland?
superior, middle, and inferior suprarenal A.
venous: drain to IVC and renal vein
medulla has a dual blood supply
regulation of cortisol?
paraventricular nucleus secrete CRH
corticotropes respond to CRH by releasing ACTH
ACTH will target adrenal cortex
free cortisol will neg feedback on hypothalamus and anterior pituitary
mechanism of CRH
bind to receptor
increase cAMP and calcium
fusion of ACTH vesicles and exocytosis
short term and long term effects of ACTH?
short: increased conversion of cholesterol to pregnenolone
long: increased LDL-R and increased enzymes
effect of Ag II on the cell?
increase DAG and IP3 and PKA activation
increase Ca
stimulation of aldosterone synthesis
release of aldosterone (restore blood volume)
effect of hyperkalemia on the cell? aldosterone?
increased K depolarizes the cell
increased Ca
activation of aldosterone synthesis and release
increase K+ excretion in the urine
Na reabsorption into the blood
Hyperaldosteronism
primary and secondary?
symptoms?
increased secretion of aldosterone from the adrenal cortex
hypertension, deceased K, metabolic alkalosis
primary: Conn’s syndrome
adrenal adenoma
or idiopathic hyperplasia of zona G
increased Aldo, decreased renin
secondary:
increased aldosterone and renin
how to tell between primary and secondary hyperaldosteronism?
primary: renin is low
secondary: renin is high
hypoaldosteronism?
hyperkalemia
metabolic acidosis
hyponatremia
the process of catecholamine release from the adrenal medulla?
- ACh from sympathetic preganglionic neuron stimulated nicotinic receptors
- Na influx in the chromaffin cell
- depolarization of chromaffin cell
- Ca influx
- fusion of vesicles and exocytosis
short term and long term response to stress?
short: sympathoadrenergic system HR and BP increases metabolic rate increase bronchodilation increased blood glucose
long: ACTH-cortisol system (adrenocortical system) protein breakdown fat lipolysis immune suppression increased BP
what hormone is a tripeptide
TRH or thyrotropin releasing hormone
mechanism and target of TRH?
thryotroph’s are the target
bind to receptor
increase IP3 and DAG
increase Ca
release TSH
action of TSH on the thyroid
bind to receptor
increase cAMP and maybe PLC
modulation of many cellular processes
the importance of iodine
the synthesis of thyroid hormones requires Iodine
need at least 150ug per day
pregnant or lactating women need more
what are the steps of thyroid hormone synthesis?
- synthesis and extrusion of TH into the lumen (happens in RER and golgi)
- pull I into the cell with Na
- oxidize I at apical membrane
- organification of I2 to MIT and DIT
- couple MIT and DIT
- endocytosis of TH
- hydrolyze T4 to T3
- deiodination of MIT and DIT (to reuse)
what are some inhibitors of the production of TH?
at the Na-I pump? oxidation step?
high levels of I-, thyrocyanate, and perchlorate inhibit the channel
oxidation and other steps can be inhibited by PTU
what are the whole body effects of TH?
increase basal metabolic rate
promote bone formation
increase O2 consumption
TH effects on the heart?
increase SV and HR, thus CO is increased
what effects TBG levels?
pregnancy and estrogen increase TBG
liver disease will lower TBG levels
hyperthyroidism
possible diseases?
symptoms?
increase levels of TH in the blood
can have thyroid enlargement (graves)
overactive lump (plummer’s disease)
toxic goiter
symptoms: irritability weight loss CHF in older people palpations amenorrhea increased bowel movements (not loose) sweaty
Graves disease
how?
symptoms?
autoimmune
more likely in females
due to antibody that mimics TH
symptoms: thyroid enlargement opthalmopathy pretibial myxedema low levels of TRH and TSH, but high TH
hypothyroidism?
how? primary and secondary causes?
low levels of TH in the blood can be due to: hashimoto's thyroiditis thyroidectomy iodine deficiency
secondary:
insufficient pituitary action
resistance to TH
hypothyroidism in newborns?
how?
symptoms?
may be due to iodine deficiency
placental transfer of TSH antibody
symptoms? respiratory issues jaundice poor feeding reduction in bone development
TH deficiency in children?
growth and mental disability
adults with hypothyroidism? symptoms?
fatigue cold intolerance weight gain menstrual issues constipation dry skin bradycardia puffiness due to GAG accumulation
