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
Q

what type of receptors does ACh bind to at SAN and AVN on the heart
parasympathetic signalling

A

muscarinic (m2)

leads to G alpha i signalling

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26
Q

effects of ACh binding to M3 receptor on heart

A

parasympathetic BP control
causes decreased/negative chronotropy/heart rate
decreased BP

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27
Q

importance of counter-current system in LoH

A

H2O removed to concentrate filtrate

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28
Q

role of kidney

A

maintain homeostasis and control blood pressure

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29
Q

define GFR

A

glomerular filtrate rate

volume of fluid filtered from the renal glomerular capillaries into the bowmans capsule per unit time

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30
Q

equation to calculate gfr

A

gfr = urine conc. x urine flow / plasma conc

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31
Q

what does gfr depend on

A

difference between lumen size afferent and efferent arterioles (their resistance)

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32
Q

gfr is used to measure

A

kidney function

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33
Q

how do you test the gfr of someone

A

inject inulin into plasma

measure rate of excretion

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34
Q

why is inulin used to measure gfr

A

inulin is neither reabsorbed into the blood or secreted after filtration
rate of excretion is directly proportional to rate of filtration

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35
Q

gfr decreases with

A
dehydration
low blood pressure 
increased age
chronic kidney disease 
use of sedation
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36
Q

gfr increases with

A

increased dietary protein

overhydration

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37
Q

what is ADH

A

peptide hormone

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38
Q

where is ADH made and seceted

A

made in hypothalamus

secreted by posterior pituitary

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39
Q

function of ADH

A

regulate osmolality and blood pressure

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40
Q

where are the 2 ADH receptors found

A

V1 - vascular smooth muscle

V2 - principle cells of renal collecting duct

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41
Q

effect when ADH binds to V1

A
G alpha q signalling
on blood vessels 
stimulation of phospholipase C
constricts arterioles
increases blood pressure
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42
Q

effect when ADH binds to V2 receptors

A

translocation of AQP2 into membrane of collecting duct epithelial cells
G alpha s signalling
increases water back into blood

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43
Q

angiotensin II effect on ADH

A

stimulates ADH release

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44
Q

what do ANP and BNP stand for

A

atrial natruiretic peptide
brain natuiretic peptide

(where they are produced)

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45
Q

overall role of ANP

A

reduce arterial pressure by decreasing blood volume and systemic vascular resistance

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46
Q

ANP/BNP produced in response to…

A

angiontensin II

stretching caused by increase in ventricular blood volume

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47
Q

effect of ANP on blood vessels

A

dilates veins - reduces venous pressure and cardiac output

dilate arteries - decreases vascular resistnace and arterial pressure

48
Q

effect of ANP on kidneys (gfr)

A

increases gfr because there is more blood plasma in filtrate

49
Q

what secretes renin

A

kidneys

pericytes cells

50
Q

main role of renin

A

hydrolyse angiotensinogen to angiotensin I

51
Q

what stimulates renin secretion

A

decrease in arteriole pressure (detected by baroreceptors)
sympathetic NS activity (B1 receptors)
decreased Na+ conc. in distal tubule

52
Q

2 renin secretory pathways

A

constitutive - secretion of precursor renin

regulated - secretion of mature renin

53
Q

effect of increase in intracellular Ca2+ on renin secretion

A

increase Ca2+ inhibits renin secretion

54
Q

effects of cAMP on renin release

A

cAMP stimulates renin release

55
Q

effect of ANP/BNP on renin release

A

decrease

56
Q

where is angiotensinogen produced

A

liver

57
Q

what converts Ang I to Ang II

A

ACE

angiotensin converting enzyme

58
Q

effects of Ang I and Ang II

A

increased Na+/H+ exchange in PCT leads to increased H2O reabsorption

aldosterone/ADH release

59
Q

too much angiotensin

A

high blood pressure

60
Q

too little angiotensin

A

low blood pressure
loss of Na+
increased urine output
potassium retention

61
Q

what secretes aldosterone

A

adrenal cortex

62
Q

role of aldosterone

A

water and sodium retention
potassium removal

effects in distal tubules of nephron

63
Q

receptors affected by aldosterone

A

mineralocorticoid receptors of distal tubule and collecting duct

64
Q

what is aldosterone

A

mineralocorticoid hormone synthesised from cholesterol

65
Q

what is pseudohyperaldosteronism

A

responses as if there was over-production of aldosterone

high cortisol

66
Q

what causes pseudohyperaldosteronism

A

intoxification
e..g glycyrrhizin
liquorice

67
Q

concentrations of aldosterone/renin/cortisol in pseudohyperaldosteronism

A

aldosterone - low/normal
renin - low
cortisol - normal/high

68
Q

primary hyperaldosteronism

A

conn’s syndrome

over-production of aldosterone from adrenal cortex

69
Q

cause of primary hyperaldosteronism

A

adrenal gland pathology

e.g. adenoma

70
Q

concentrations of aldosterone/renin/cortisol in primary hyperaldosteronism

A

aldosterone - high
renin - low
cortisol - normal

71
Q

concentrations of aldosterone/renin/cortisol in secondary hyperaldosteronism

A

aldosterone - high
renin - high
cortisol - normal

72
Q

secondary hyperaldosteronism

A

decrease in blood flow to the kidney
decrease in blood pressure
decrease in blood Na+

73
Q

what is 11-B-HSD2

A

enzyme

degrades cortisol to cortisone

74
Q

what is cortisol

A

glucocorticoid

75
Q

where is 11-B-HSD2 expressed

A

mineralocorticoid target tissues (where aldosterone binds)

76
Q

what happens when aldosterone binds to mineralocorticoid receptoss

A

transcribes proteins for Na+ reabsorption

77
Q

cortisol binds to the same receptors as…

A

aldosterone

78
Q

if circulating cortisol levels are high

A

it must be degraded to prevent over-stimulation of receptors

79
Q

over-stimulation of mineralocorticoid receptors causes…

A

hypokalemia
increased blood pressure
metabolic alkilosis

80
Q

dipstick testing

A

strips on dipstick have different chemicals on them

the strips change colour when they react to the different chemicals in urine

81
Q

causes of uti

A

gram -ve bacteria from colon

e.g. e coli

82
Q

risk factors of uti

A

unprotected sex

poor hygiene

83
Q

why are uti’s more common in women

A

shorter urethra

easier for bacteria

84
Q

biomarkers for uti

A

white blood cells and nitrites in urine

urine may appear cloudy or red

85
Q

function of posterior pituitary

A

secrete hormones into bloodstream after hormone stimuation from hypothalamus

86
Q

hormones released by hypothalamus that cause release from anterior pituitary gland

A

TRH
GnRH
CRH
GHRH

87
Q

TRH

A

thryotropin releasing hormone

causes thryotropin stimulating hormone to be released from anterior pituitary

88
Q

what effect does GnRH have on anterior pituitatry

A

causes release of LH and FSH

89
Q

hormones released by posterior pituitarty

A

ADH

oxytocin

90
Q

release of ADH from posterior pituitary stimulates…

A

G alpha q signalling
vasoconstriction
increased Blood pressure

91
Q

what is CRH

A

corticotropin-releasing hormone
causes anterior pituitatry to stimulate adrenal glands and produce corticosteroids
e.g. 11-B-HSD2
metabolic and immune regulation

92
Q

hormones released by hypothalamus to anterior pituitarty are transported by

A

blood vessels

93
Q

hormones released by hypothalamus to posterior pituitary are transported by

A

neurones

94
Q

cells of hypothalamus detect

A

molecular and electrical stimul through surrounding capillaries

95
Q

electrolyte-water balance of the body

A

plasma osmolality

96
Q

normal range of plasma osmolality

A

275-299

97
Q

increase in serum osmolality causes

A

increase in ADH secretion

98
Q

how do you estimate plasma osmolaliy

A

plasma Na+ conc
plasma glucose conc
blood urea nitrogen (BUN)

99
Q

is osmolality independent of temp and pressure

A

yes

100
Q

effect of dehydration on osmolality of bloo

A

blood osmolality increases with dehydration

101
Q

anabolism

A

building of molecules

requires energy

102
Q

catabolism

A

breaking down of larger molecules into smalelr ones

release energy

103
Q

what stimulates release of growth hormone (GH)

A

GHRH

104
Q

what inhibits growth hormone

A

somatostatin

105
Q

what happens when TSH is released from anterior pituitary gland

A

stimulates release of T3 and T4 hormones into the blood

cause increase in metabolism

106
Q

more actions of T3 and T4

A

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
Q

thyroid gland negative feedback

A

regulates its own release

T3 and T4 signal negatively to hypothalamus and anterior pituitary to prevent over relase

108
Q

where is the thyroid gland

A

between larynx and trachea

neck

109
Q

function of thyroid gland

A

secretes hormones for development and metabolism

110
Q

is T4 stable or active

A

stable and inactive

T3 is the active form

111
Q

hyper-thyroidism

A

over-reactive thyroid gland

too much T3 and T4 produced, low TSH

112
Q

hypo-thyroidism

A

under-reactive thyroid gland
not enough T3/T4 produced
high TSH

113
Q

characteristics of hyper-thyroidism

A

increased metabolism/ catabolism
weight loss
rapid heart rate

114
Q

characteristics of hypo-thyroidisms

A
decreased catabolism 
cells slow down
increased weight gain
bradycardia
low blood pressure
115
Q

calcitonin hormone

A

produced by thyroid gland
regulates Ca2+ and phosphate in blood
promotes formation of bone