6 - hyperaldosteronism Flashcards

1
Q

when should you get your blood tested for aldosterone and renin

A

if your doctor detects an electrolyte imbalance or you develop symptoms of hyperaldosteronism such as high blood pressure and muscle weakness

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2
Q

what is aldosterone

A

a hormone that regulates sodium and water retention by the kidney and the removal of potassium

important role in controlling blood pressure

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3
Q

where/how is aldosterone produced

A

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

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4
Q

when renin increases

A

aldosterone increases

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5
Q

where is renin prodced

A

in the kidney

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6
Q

what would indicate secondary hyperaldosteronism in the sample

A

an increase in both renin and aldosterone

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7
Q

what would indicate primary hyperaldosteronism in the sample

A

High levels of serum and urine aldosterone, along with a low plasma renin

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8
Q

primary hyperaldosteronism - Conn’s syndrome

A

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.

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9
Q

secondary hyperaldosteronism

A

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

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10
Q

renary artery stenosis

A

narrowing of arteries that carry blood to one or both of the kidneys
can cause hypertension

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11
Q

hypoaldosteronism

A

lack of aldosterone
occurs as part of adrenal insufficiency
causes dehydration, low bp, low Na and high potassium blood concs.

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12
Q

noradrenaline preferentially binds to which receptors on blood vessles

A

a1 adrenoreceptors

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13
Q

sympathetic control
NA binds to a1 receptors on blood vessels
what effect does this have

A

smooth muscle contraction

vasoconstriction

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14
Q

ACh binds to m3 receptor on blood vessels

what effect does this have

A

coupled to formation of nitric oxide

vasodilation

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15
Q

effect of vasoconstriction on blood vessels

A

increases vascular resistnance
increases distal blood flow
increases blood pressure

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16
Q

where are baroreceptors found

A

in arch of aorta and carotid sinus

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17
Q

effects of low bp on baroreceptors

A

baroreceptors are stretched less
send fewer nerve impulses to CV centre in medulla oblongata
triggers sympathetic response

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18
Q

what is secreted in sympathetic response to low BP

A

adrenaline and noradrenaline secretion

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19
Q

effect of Adrenaline and NA on blood pressure

A

increased stroke volume and increased heart rate therefore increased cardiac output
constriction of blood vessels
increased blood pressure

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20
Q

what are the effects of NA and A binding to B1 adrenoreceptor

A

increased chronotrophy/heart rate
increased ionotrophy/contractilitiy
increased lusitrophy/relaxation

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21
Q

where are B1 receptors found

A

heart

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22
Q

beta blockers

A

beta-adrenergic blocking agents
block effects of Adrenaline
reduce blood pressure
treat angina or hypertension

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23
Q

where are B2 receptors found

A

lungs

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24
Q

which nerves involved in parasympathetic control of heart rate

A

cholinergic nerves
derived from vagus nerve
release ACh

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25
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
26
effects of ACh binding to M3 receptor on heart
parasympathetic BP control causes decreased/negative chronotropy/heart rate decreased BP
27
importance of counter-current system in LoH
H2O removed to concentrate filtrate
28
role of kidney
maintain homeostasis and control blood pressure
29
define GFR
glomerular filtrate rate | volume of fluid filtered from the renal glomerular capillaries into the bowmans capsule per unit time
30
equation to calculate gfr
gfr = urine conc. x urine flow / plasma conc
31
what does gfr depend on
difference between lumen size afferent and efferent arterioles (their resistance)
32
gfr is used to measure
kidney function
33
how do you test the gfr of someone
inject inulin into plasma | measure rate of excretion
34
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
35
gfr decreases with
``` dehydration low blood pressure increased age chronic kidney disease use of sedation ```
36
gfr increases with
increased dietary protein | overhydration
37
what is ADH
peptide hormone
38
where is ADH made and seceted
made in hypothalamus | secreted by posterior pituitary
39
function of ADH
regulate osmolality and blood pressure
40
where are the 2 ADH receptors found
V1 - vascular smooth muscle | V2 - principle cells of renal collecting duct
41
effect when ADH binds to V1
``` G alpha q signalling on blood vessels stimulation of phospholipase C constricts arterioles increases blood pressure ```
42
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
43
angiotensin II effect on ADH
stimulates ADH release
44
what do ANP and BNP stand for
atrial natruiretic peptide brain natuiretic peptide (where they are produced)
45
overall role of ANP
reduce arterial pressure by decreasing blood volume and systemic vascular resistance
46
ANP/BNP produced in response to...
angiontensin II | stretching caused by increase in ventricular blood volume
47
effect of ANP on blood vessels
dilates veins - reduces venous pressure and cardiac output | dilate arteries - decreases vascular resistnace and arterial pressure
48
effect of ANP on kidneys (gfr)
increases gfr because there is more blood plasma in filtrate
49
what secretes renin
kidneys | pericytes cells
50
main role of renin
hydrolyse angiotensinogen to angiotensin I
51
what stimulates renin secretion
decrease in arteriole pressure (detected by baroreceptors) sympathetic NS activity (B1 receptors) decreased Na+ conc. in distal tubule
52
2 renin secretory pathways
constitutive - secretion of precursor renin | regulated - secretion of mature renin
53
effect of increase in intracellular Ca2+ on renin secretion
increase Ca2+ inhibits renin secretion
54
effects of cAMP on renin release
cAMP stimulates renin release
55
effect of ANP/BNP on renin release
decrease
56
where is angiotensinogen produced
liver
57
what converts Ang I to Ang II
ACE | angiotensin converting enzyme
58
effects of Ang I and Ang II
increased Na+/H+ exchange in PCT leads to increased H2O reabsorption aldosterone/ADH release
59
too much angiotensin
high blood pressure
60
too little angiotensin
low blood pressure loss of Na+ increased urine output potassium retention
61
what secretes aldosterone
adrenal cortex
62
role of aldosterone
water and sodium retention potassium removal effects in distal tubules of nephron
63
receptors affected by aldosterone
mineralocorticoid receptors of distal tubule and collecting duct
64
what is aldosterone
mineralocorticoid hormone synthesised from cholesterol
65
what is pseudohyperaldosteronism
responses as if there was over-production of aldosterone | high cortisol
66
what causes pseudohyperaldosteronism
intoxification e..g glycyrrhizin liquorice
67
concentrations of aldosterone/renin/cortisol in pseudohyperaldosteronism
aldosterone - low/normal renin - low cortisol - normal/high
68
primary hyperaldosteronism
conn's syndrome over-production of aldosterone from adrenal cortex
69
cause of primary hyperaldosteronism
adrenal gland pathology | e.g. adenoma
70
concentrations of aldosterone/renin/cortisol in primary hyperaldosteronism
aldosterone - high renin - low cortisol - normal
71
concentrations of aldosterone/renin/cortisol in secondary hyperaldosteronism
aldosterone - high renin - high cortisol - normal
72
secondary hyperaldosteronism
decrease in blood flow to the kidney decrease in blood pressure decrease in blood Na+
73
what is 11-B-HSD2
enzyme | degrades cortisol to cortisone
74
what is cortisol
glucocorticoid
75
where is 11-B-HSD2 expressed
mineralocorticoid target tissues (where aldosterone binds)
76
what happens when aldosterone binds to mineralocorticoid receptoss
transcribes proteins for Na+ reabsorption
77
cortisol binds to the same receptors as...
aldosterone
78
if circulating cortisol levels are high
it must be degraded to prevent over-stimulation of receptors
79
over-stimulation of mineralocorticoid receptors causes...
hypokalemia increased blood pressure metabolic alkilosis
80
dipstick testing
strips on dipstick have different chemicals on them | the strips change colour when they react to the different chemicals in urine
81
causes of uti
gram -ve bacteria from colon | e.g. e coli
82
risk factors of uti
unprotected sex | poor hygiene
83
why are uti's more common in women
shorter urethra | easier for bacteria
84
biomarkers for uti
white blood cells and nitrites in urine | urine may appear cloudy or red
85
function of posterior pituitary
secrete hormones into bloodstream after hormone stimuation from hypothalamus
86
hormones released by hypothalamus that cause release from anterior pituitary gland
TRH GnRH CRH GHRH
87
TRH
thryotropin releasing hormone | causes thryotropin stimulating hormone to be released from anterior pituitary
88
what effect does GnRH have on anterior pituitatry
causes release of LH and FSH
89
hormones released by posterior pituitarty
ADH | oxytocin
90
release of ADH from posterior pituitary stimulates...
G alpha q signalling vasoconstriction increased Blood pressure
91
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
92
hormones released by hypothalamus to anterior pituitarty are transported by
blood vessels
93
hormones released by hypothalamus to posterior pituitary are transported by
neurones
94
cells of hypothalamus detect
molecular and electrical stimul through surrounding capillaries
95
electrolyte-water balance of the body
plasma osmolality
96
normal range of plasma osmolality
275-299
97
increase in serum osmolality causes
increase in ADH secretion
98
how do you estimate plasma osmolaliy
plasma Na+ conc plasma glucose conc blood urea nitrogen (BUN)
99
is osmolality independent of temp and pressure
yes
100
effect of dehydration on osmolality of bloo
blood osmolality increases with dehydration
101
anabolism
building of molecules | requires energy
102
catabolism
breaking down of larger molecules into smalelr ones | release energy
103
what stimulates release of growth hormone (GH)
GHRH
104
what inhibits growth hormone
somatostatin
105
what happens when TSH is released from anterior pituitary gland
stimulates release of T3 and T4 hormones into the blood | cause increase in metabolism
106
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
107
thyroid gland negative feedback
regulates its own release | T3 and T4 signal negatively to hypothalamus and anterior pituitary to prevent over relase
108
where is the thyroid gland
between larynx and trachea | neck
109
function of thyroid gland
secretes hormones for development and metabolism
110
is T4 stable or active
stable and inactive | T3 is the active form
111
hyper-thyroidism
over-reactive thyroid gland | too much T3 and T4 produced, low TSH
112
hypo-thyroidism
under-reactive thyroid gland not enough T3/T4 produced high TSH
113
characteristics of hyper-thyroidism
increased metabolism/ catabolism weight loss rapid heart rate
114
characteristics of hypo-thyroidisms
``` decreased catabolism cells slow down increased weight gain bradycardia low blood pressure ```
115
calcitonin hormone
produced by thyroid gland regulates Ca2+ and phosphate in blood promotes formation of bone