6 - hyperaldosteronism Flashcards
when should you get your blood tested for aldosterone and renin
if your doctor detects an electrolyte imbalance or you develop symptoms of hyperaldosteronism such as high blood pressure and muscle weakness
what is aldosterone
a hormone that regulates sodium and water retention by the kidney and the removal of potassium
important role in controlling blood pressure
where/how is aldosterone produced
in the adrenal glands - located at the top of each kidney
production is stimulated by a complex process including hormones renin and angiotensin II
Renin - stimulates production of angiotensin II in the bloodstream
Angiotensin II then regulates the release of aldosterone
when renin increases
aldosterone increases
where is renin prodced
in the kidney
what would indicate secondary hyperaldosteronism in the sample
an increase in both renin and aldosterone
what would indicate primary hyperaldosteronism in the sample
High levels of serum and urine aldosterone, along with a low plasma renin
primary hyperaldosteronism - Conn’s syndrome
caused by the overproduction of aldosterone in the adrenal glands
(usually by a benign tumour of one of the glands)
high aldosterone level increases reabsorption of sodium/water and loss of potassium by the kidneys
results high blood pressure/hypertension
muscle weakness can occur if potassium levels are very low.
secondary hyperaldosteronism
more common
occurs as a result of anything causing decreased blood flow/pressure to kidneys or lowers blood Na conc
e.g. narrowing of blood vessels
stimulates renin/aldosterone production which increases blood pressure
renary artery stenosis
narrowing of arteries that carry blood to one or both of the kidneys
can cause hypertension
hypoaldosteronism
lack of aldosterone
occurs as part of adrenal insufficiency
causes dehydration, low bp, low Na and high potassium blood concs.
noradrenaline preferentially binds to which receptors on blood vessles
a1 adrenoreceptors
sympathetic control
NA binds to a1 receptors on blood vessels
what effect does this have
smooth muscle contraction
vasoconstriction
ACh binds to m3 receptor on blood vessels
what effect does this have
coupled to formation of nitric oxide
vasodilation
effect of vasoconstriction on blood vessels
increases vascular resistnance
increases distal blood flow
increases blood pressure
where are baroreceptors found
in arch of aorta and carotid sinus
effects of low bp on baroreceptors
baroreceptors are stretched less
send fewer nerve impulses to CV centre in medulla oblongata
triggers sympathetic response
what is secreted in sympathetic response to low BP
adrenaline and noradrenaline secretion
effect of Adrenaline and NA on blood pressure
increased stroke volume and increased heart rate therefore increased cardiac output
constriction of blood vessels
increased blood pressure
what are the effects of NA and A binding to B1 adrenoreceptor
increased chronotrophy/heart rate
increased ionotrophy/contractilitiy
increased lusitrophy/relaxation
where are B1 receptors found
heart
beta blockers
beta-adrenergic blocking agents
block effects of Adrenaline
reduce blood pressure
treat angina or hypertension
where are B2 receptors found
lungs
which nerves involved in parasympathetic control of heart rate
cholinergic nerves
derived from vagus nerve
release ACh
what type of receptors does ACh bind to at SAN and AVN on the heart
parasympathetic signalling
muscarinic (m2)
leads to G alpha i signalling
effects of ACh binding to M3 receptor on heart
parasympathetic BP control
causes decreased/negative chronotropy/heart rate
decreased BP
importance of counter-current system in LoH
H2O removed to concentrate filtrate
role of kidney
maintain homeostasis and control blood pressure
define GFR
glomerular filtrate rate
volume of fluid filtered from the renal glomerular capillaries into the bowmans capsule per unit time
equation to calculate gfr
gfr = urine conc. x urine flow / plasma conc
what does gfr depend on
difference between lumen size afferent and efferent arterioles (their resistance)
gfr is used to measure
kidney function
how do you test the gfr of someone
inject inulin into plasma
measure rate of excretion
why is inulin used to measure gfr
inulin is neither reabsorbed into the blood or secreted after filtration
rate of excretion is directly proportional to rate of filtration
gfr decreases with
dehydration low blood pressure increased age chronic kidney disease use of sedation
gfr increases with
increased dietary protein
overhydration
what is ADH
peptide hormone
where is ADH made and seceted
made in hypothalamus
secreted by posterior pituitary
function of ADH
regulate osmolality and blood pressure
where are the 2 ADH receptors found
V1 - vascular smooth muscle
V2 - principle cells of renal collecting duct
effect when ADH binds to V1
G alpha q signalling on blood vessels stimulation of phospholipase C constricts arterioles increases blood pressure
effect when ADH binds to V2 receptors
translocation of AQP2 into membrane of collecting duct epithelial cells
G alpha s signalling
increases water back into blood
angiotensin II effect on ADH
stimulates ADH release
what do ANP and BNP stand for
atrial natruiretic peptide
brain natuiretic peptide
(where they are produced)
overall role of ANP
reduce arterial pressure by decreasing blood volume and systemic vascular resistance
ANP/BNP produced in response to…
angiontensin II
stretching caused by increase in ventricular blood volume
effect of ANP on blood vessels
dilates veins - reduces venous pressure and cardiac output
dilate arteries - decreases vascular resistnace and arterial pressure
effect of ANP on kidneys (gfr)
increases gfr because there is more blood plasma in filtrate
what secretes renin
kidneys
pericytes cells
main role of renin
hydrolyse angiotensinogen to angiotensin I
what stimulates renin secretion
decrease in arteriole pressure (detected by baroreceptors)
sympathetic NS activity (B1 receptors)
decreased Na+ conc. in distal tubule
2 renin secretory pathways
constitutive - secretion of precursor renin
regulated - secretion of mature renin
effect of increase in intracellular Ca2+ on renin secretion
increase Ca2+ inhibits renin secretion
effects of cAMP on renin release
cAMP stimulates renin release
effect of ANP/BNP on renin release
decrease
where is angiotensinogen produced
liver
what converts Ang I to Ang II
ACE
angiotensin converting enzyme
effects of Ang I and Ang II
increased Na+/H+ exchange in PCT leads to increased H2O reabsorption
aldosterone/ADH release
too much angiotensin
high blood pressure
too little angiotensin
low blood pressure
loss of Na+
increased urine output
potassium retention
what secretes aldosterone
adrenal cortex
role of aldosterone
water and sodium retention
potassium removal
effects in distal tubules of nephron
receptors affected by aldosterone
mineralocorticoid receptors of distal tubule and collecting duct
what is aldosterone
mineralocorticoid hormone synthesised from cholesterol
what is pseudohyperaldosteronism
responses as if there was over-production of aldosterone
high cortisol
what causes pseudohyperaldosteronism
intoxification
e..g glycyrrhizin
liquorice
concentrations of aldosterone/renin/cortisol in pseudohyperaldosteronism
aldosterone - low/normal
renin - low
cortisol - normal/high
primary hyperaldosteronism
conn’s syndrome
over-production of aldosterone from adrenal cortex
cause of primary hyperaldosteronism
adrenal gland pathology
e.g. adenoma
concentrations of aldosterone/renin/cortisol in primary hyperaldosteronism
aldosterone - high
renin - low
cortisol - normal
concentrations of aldosterone/renin/cortisol in secondary hyperaldosteronism
aldosterone - high
renin - high
cortisol - normal
secondary hyperaldosteronism
decrease in blood flow to the kidney
decrease in blood pressure
decrease in blood Na+
what is 11-B-HSD2
enzyme
degrades cortisol to cortisone
what is cortisol
glucocorticoid
where is 11-B-HSD2 expressed
mineralocorticoid target tissues (where aldosterone binds)
what happens when aldosterone binds to mineralocorticoid receptoss
transcribes proteins for Na+ reabsorption
cortisol binds to the same receptors as…
aldosterone
if circulating cortisol levels are high
it must be degraded to prevent over-stimulation of receptors
over-stimulation of mineralocorticoid receptors causes…
hypokalemia
increased blood pressure
metabolic alkilosis
dipstick testing
strips on dipstick have different chemicals on them
the strips change colour when they react to the different chemicals in urine
causes of uti
gram -ve bacteria from colon
e.g. e coli
risk factors of uti
unprotected sex
poor hygiene
why are uti’s more common in women
shorter urethra
easier for bacteria
biomarkers for uti
white blood cells and nitrites in urine
urine may appear cloudy or red
function of posterior pituitary
secrete hormones into bloodstream after hormone stimuation from hypothalamus
hormones released by hypothalamus that cause release from anterior pituitary gland
TRH
GnRH
CRH
GHRH
TRH
thryotropin releasing hormone
causes thryotropin stimulating hormone to be released from anterior pituitary
what effect does GnRH have on anterior pituitatry
causes release of LH and FSH
hormones released by posterior pituitarty
ADH
oxytocin
release of ADH from posterior pituitary stimulates…
G alpha q signalling
vasoconstriction
increased Blood pressure
what is CRH
corticotropin-releasing hormone
causes anterior pituitatry to stimulate adrenal glands and produce corticosteroids
e.g. 11-B-HSD2
metabolic and immune regulation
hormones released by hypothalamus to anterior pituitarty are transported by
blood vessels
hormones released by hypothalamus to posterior pituitary are transported by
neurones
cells of hypothalamus detect
molecular and electrical stimul through surrounding capillaries
electrolyte-water balance of the body
plasma osmolality
normal range of plasma osmolality
275-299
increase in serum osmolality causes
increase in ADH secretion
how do you estimate plasma osmolaliy
plasma Na+ conc
plasma glucose conc
blood urea nitrogen (BUN)
is osmolality independent of temp and pressure
yes
effect of dehydration on osmolality of bloo
blood osmolality increases with dehydration
anabolism
building of molecules
requires energy
catabolism
breaking down of larger molecules into smalelr ones
release energy
what stimulates release of growth hormone (GH)
GHRH
what inhibits growth hormone
somatostatin
what happens when TSH is released from anterior pituitary gland
stimulates release of T3 and T4 hormones into the blood
cause increase in metabolism
more actions of T3 and T4
increased cardiovascular output - more myosin - more contraction
increased growth
increased metabolism - increased glucose absorption
increases GH production
increases basal metabolic rate - increased O2 consumption
thyroid gland negative feedback
regulates its own release
T3 and T4 signal negatively to hypothalamus and anterior pituitary to prevent over relase
where is the thyroid gland
between larynx and trachea
neck
function of thyroid gland
secretes hormones for development and metabolism
is T4 stable or active
stable and inactive
T3 is the active form
hyper-thyroidism
over-reactive thyroid gland
too much T3 and T4 produced, low TSH
hypo-thyroidism
under-reactive thyroid gland
not enough T3/T4 produced
high TSH
characteristics of hyper-thyroidism
increased metabolism/ catabolism
weight loss
rapid heart rate
characteristics of hypo-thyroidisms
decreased catabolism cells slow down increased weight gain bradycardia low blood pressure
calcitonin hormone
produced by thyroid gland
regulates Ca2+ and phosphate in blood
promotes formation of bone
