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Y2 Endocrinology > Steroid hormone and Water Balance > Flashcards

Steroid hormone and Water Balance Flashcards

1
Q

Non classical action of Aldosterone

A

Vasoconstriction of vascular smooth muscle and endothelial cells

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2
Q

What is C27 Sterol

A

Cholesterol

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3
Q

C 18 steroid

A

Oestradiol

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4
Q

C21 SEX steroid

A

Progesterone

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5
Q

Functional group of Cortisol

A

OH

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6
Q

Difference between testosterone and oestradiol

A

C19 v C18- CH3 removed

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7
Q

First step of steroid synthesis

A

C27 to C21 (SCC, CYP 11A1)

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8
Q

First product in steroid synthesis

A

Pregnenolone

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9
Q

Where does 11B-HSD-1 work and which direction

HSD-2?

A

In liver, bi direction

In kidney, to cortisone only

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10
Q

Which vertebral level are the adrenals located around

A

T12

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11
Q

What adrenal androgens does Zona Reticularis produce

A

DHEA and androstenedione

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12
Q

What provides all the oestrogens in women post menopause

A

DHEA

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13
Q

What is pregnenolone concerted to and through what enzyme

A

Progesterone, 3B-HSD

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14
Q

What is the role of 17a hydroxylase

A

Converted progesterone and pregnenolone to 17OH..

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15
Q

What is the role of 17-20 lysase

A

17-OH pregnenolone to DHEA
17-OH progesterone to Androstenedione in ZR

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16
Q

Role of 21-hydroxylase

A

Converts progesterone or 17-OH progesterone into deoxycorticosterone or 11- Deoxycortisol

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17
Q

Role of Aldo-synthase

A

Concerts DOC all the way to aldosterone

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18
Q

What converts 11-deoxycortisol to its product

A

11B-hydroxylase, cortisol

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19
Q

What converts Androstenedione to what and where

A

17B HSD, in peripheral tissues

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20
Q

What five hormones get secreted more as plasma glucose level falls

A

Glucagon
Growth Hormone
Adrenaline and Na
Cortisol

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21
Q

Which nuclei in the hypothalamus secrete CRH

A

PVN

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22
Q

What factors stimulate release of CRH

A

5HT
ACh
Encephalin
AVP

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23
Q

What factors inhibit release of CRH

A

A adrenergic agonists
GABA and Endorphins
DA
CORTISOL negative feedbak

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24
Q

How is AP hormone production stimulated by CRH

A

CRH binds to GPCR (cAMP and adenyl cyclase) and stimulates production of POMC which is cleaved into ACTH and other peptides

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25
Q

Process of production of Cortisol when ACTH binds to ACTH receptor

A

cAMP, Adenyl cyclase– cholesterol estet hydrolase increases so more cholesterol is free and transported into mitochondria, where sTAR protein bring cholesterol in and then SCC converts it into pregnenolone and eventually cortisol

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26
Q

effect of cortisol on acid secretion and what happens in excess

A

stimulates acid secretion, gastric ulcers in excess

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27
Q

effect of cortisol on appetite

A

increases appetite

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28
Q

effect of cortisol on sexual characteristics

A

can increase adrenal androgens and cause hirsutism, acne, altered hair pattern, menstrual disturbance

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29
Q

What causes Endometriosis? (Genetic Basis)

A

Alteration of DNA methylation that causes ERB overexpression and reduced PR expression

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30
Q

What receptor signaling is involved in breast cancers

A

ERa and PR B

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31
Q

Role of testosterone in male reproductive functions

A

Spermatogenesis, prostate secretions

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32
Q

when should the hpg axis be tested and how

A

during puberty in patients with concerns about puberty delay or teticular function, give GnRH and see how much Gns are produced

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33
Q

Role of testosterone in foetal life

A

for virilisation of genitatlia, esp external genitalia and some internal accessory structuree

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34
Q

What does testosterone get converted to in male foetuses and by what

A

5a reductase converts it to dihydrotestosterone

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35
Q

What cells produce AMH in males

A

sertoli cells

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36
Q

normal age of puberty in males and females

A

8-13 and 9-14

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37
Q

TDS vs DSD- which is environmental

A

TDS- testicular dysgenesis syndrome
Disorders of Sex Development is genetic

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38
Q

one disorder part of DSD and not TDS

A

Ambiguous genitalia

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39
Q

Genes involved in DSD

A

SRY and Sox 9

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40
Q

which chromosome should be sequenced for PAIS

A

X chromosome

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41
Q

what hormones to measure for puberty test, how to measure max production of hormones

A

Gns and Test
Do GnRH stimulation test to see if puberty had begun

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42
Q

Kalmann’s vs Kleinfelter’s

A

Kallman’s- Hypog Hypog, may have anosmia. Kleinfelter’s- 47XXY- HYPERhypog- genetic cause of testicular dysfunction

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43
Q

Inducing puberty vs fertility

A

Testosterone vs Gn

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44
Q

Tumour markers for testicular cancer

A

hCG, AFP, LDH

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45
Q

When does the gonadotropin regulated growth phase start

A

preantral follicle

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46
Q

what cells produce inhibin and AMH

A

Inhibin- granulosa and theca
AMH- granulosa of largerr follicles

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47
Q

what stimulates LH binding sites on outer layers of granulosa cells

A

FSH and estradiol

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48
Q

What is the effect of Gn and steroid hormones on AMH

A

No effect, hence AMH is reliable reflection of growing follicles

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49
Q

what cells proliferate in endometrium in secretory stage and what chemicals/ hormones are there are an abundance of

A

NK cells, prolactin, growth factors, IGFBP1, IL-15

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50
Q

How many days ddoes it take for CL to regress

A

7-8 days after high progesterone - degenerates after 14 days

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51
Q

what cells contract as a result of oxytocin

A

myoepithelial cells

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52
Q

4 causes of high LH

A

Premature ovarian failure
PCOS!!
Asherman’s syndrome
Gonadotroph tumour

53
Q

3 causes of high Test

A

PCOS
Congenital adrenal Hyperplasia
Androgen secreting tumour

54
Q

3 causes of low E2

A

Hypog Hypog
premature ovarian failure
Hyperprolactinaemia

55
Q

What is Turner’s Syndrome

A

A cause of Premature ovarian failure- no eggs even before puberty

56
Q

History for Asherman’s Syndrome

A

Previous termination of pregnancy, miscarraige

57
Q

Is SHBG high or low in PCOS

A

low

58
Q

What conditions likely to have oligomenorrhea

A

PCOS, CAH, hyperprolactinaemia

59
Q

problems with pcos and why

A

may have TIID as androgens are associated with insulin resistance and endometrial hyperplasia

60
Q

treatment for hyperprolactinaemia

A

DA agonist like bromocriptine or surgery

61
Q

treatment for pcos if pregnancy wanted and how

A

clomefine citrate- estrogen antagonist
5 days from 3-7 or fsh injections
need to give progesterone and take it away 4 times a year for woman to have period

62
Q

how does congenital adrenal hyperplasia raise test levels

A

21 hydroxylase has problem so cant make cortisol and substrates used to make testosterone instead

63
Q

treatment of cah

A

glucorticoid replacement

64
Q

what does progesterone do for ovarian cancers

A

antagonises estrogen action by repressing estrogen induced gen expression and enhances apoptosis of epithelial and cancer cells

65
Q

What does E2 induce in breast cancers

A

Rapid ERa signalling which faciliatates cell migratory functions and metastasis- drives excessive cell proliferation

66
Q

How does tamoxifen affect endometrial cancers

A

Partial estrogen agonist which stimulates endometrial growth`

67
Q

How does adipose tissue affect endometrial growth

A

Leads to excess estrogen

68
Q

How does anovulation affect endometrial growth

A

Reduced progesterone production, endometrial growth and hyperplasia

69
Q

What mechanism does aldosterone use to increase ECF

A

Genomic mechanism

70
Q

What is the action of aldosterone in the kidney
Which part of nephron

A

DCT and collecting ducts of nephron
Increases synthesis of ENaC to increase sodium retention and Na takes water with it
H2O reabsorbed via aquaporin channels
Increased exchange of Na+ with K + and H+

71
Q

What pathological effects of aldosterone are there

A

causes vascular smooth muscle hyperplasia and can cause left ventricular hypertrophy and cardiac fibrosis

72
Q

name a mineralocorticoid antagonist

A

spironolactone

73
Q

What is MAP

A

COx TPR

74
Q

CO =

A

HR x SV

75
Q

What has a permissive effect on vascular tone

A

Cortisol

76
Q

What is an inhibitor of RAS (that is not Na+?)

A

ANP

77
Q

How does cortisol affect BP (3 ways)

A

1) Inhibits production of NO (and citrulline) from Arginine by eNOS
2) Potentiate catecholamine action
3) Inappropriately activates kidney MR

78
Q

What is the most common cause of Addison’s disease

A

Autoimmune- antibodies to steroid 21-hydroxylase- may be a consequence of adrenocortical damage

79
Q

Three other main causes of Addison’s

A

TB, Bilateral adrenalectomy, congenital problems like hypoplasia, CAH, androgens (17-OHP, androstenedione, testosterone), urinary steroids`

80
Q

what are the common symptoms of addison’s disease

A

chronic unexplained weight loss, lethargy, weakness, and possibly hypotension

81
Q

Spot symptom for addison’s and why

A

pigmentation in skin creases due to ACTH binding to MSH-1 receptors

82
Q

diagnostic test for Addison’s

A

9am cortisol wil be low
short synACTHen- measure cortisol at 0 min, and at 30 min after injecting SynACTHen, negligible cortisol in Addison’s
Basal pre-synACTHen ACTH will be high in primary adrenal failure but low in Secondary

83
Q

Treatment for Addison’s

A

Hydrocortisone and fludrocortisone for chronic

84
Q

What are the three main causes of primary hyperaldosteronism

A

Conn’s Syndrome, Bilateral Adrenal Hyperplasia and Glucocorticoid-remediable Aldosteronism

85
Q

what are two causes of secondary hyperaldosteronism

A

Renal artery stenosis and Renin-secreting JG cell tumour.

86
Q

What is the main similarity between both causes of secondary hyperaldosteronism

A

BOTH HIGH RENIN

87
Q

How does plasma ACTH level differentiate Cushing’s syndrome vs Disease

A

Cushing’s disease will have HIGH ACTH but Syndrome may have high or low- low if adrenal but high if ectopic production of ACTH

88
Q

What are some symptoms of cushing’s related to blood sugar

A

Glycosuria and hyperglycaemia

89
Q

How to exclude Cushing’s syndrome with a test

A

Dexamethasone suppression test(1mg taken orally at 11pm), plasma cortisol measured at 0am, if plasma cortisol< 40mol/L can exclude
In Cushing’s syndrome cortisol remains high since cortisol secretion no longer under the control of ACTH

24 hr urine cortisol - exclude if <259nmol/day

90
Q

Treatment of non-iatrogenic cushing’s

A

Metyrapone +/- Ketoconazole (11B- Hydroxylase blocker) to pre operatively supress symptoms of cortisol excess by reducing cortisol levels
Dexamethasone pre or post operatively to shrink tumours
Surgery

91
Q

Glucocorticoid Hyperactivity causes- is the genetic cause dom or recessive

A

Autosomal recessive- loss in function mutation in 11B-HSD2- results in decreased conversion of cortisol to cortisone
Carbenoxolone, glycyrrhizic acid and inhibitors of kidney 11B-HSD2 like liquorice

92
Q

Treatment for genetic glucocorticoid hyperactivity

A

MR antagonist again, low Na+, high K+ supplements

93
Q

What is a pheochromocytoma and what does it cause

A

Catecholamine-secreting tumour of the adrenal medulla (chromaffin cell tumour)- releases adrenaline

may have hypertension and diabetes mellitus

94
Q

How does SNS increase blood glucose

A

Increased glucagon secretion and reduced insulin secretion, increased breakdown of glycogen and lipid breakdown

95
Q

Diagnosis and treatment of pheochromocytoma

A

24 hour urinary metanephrines and cathecolamines
a-blockers, B-blockers and surgical

96
Q

Where is the thirst centre located

A

hypothalamus

97
Q

what is normal urine volume

A

0.6 to 1.5-2 l for 0.9-2 l of input

98
Q

What is an excessive urine volume

A

> 2ml/kg/hr (>3.36l/24 hr for 70kg person)
2l when plasma conc of sodium > 145 mmol/l or persistently thirsty

99
Q

How to investigate polyuria

A

1) check urine volume
2) Check glucose, ca2+ (osmotic diuresis) and urea and creatinine ( renal function)
3) Check if urine is normally concentrated (>600 mosmol/kg)
4) Water deprivation test

100
Q

How does water deprivation test work
differentiating between CDI and NDI

A

up to 8 hrs- to test for DI and distinguish between CDI and NDI (
Check weitght, urine sample( osmolality and volume) and BP every hour , and blood tests (Na+ and plasma osmolality +/-AVP)
Stop if Urine osmolality> 600
Give DDVAP (2 microgram IM ) only when water is depleted (plasma osmolality > 296-300) or Na+ > 145
If urine concentrated on vasopressin, is CDI , otherwise NDI

101
Q

What does it mean if urine osmolality < 600 even when water is depleted

A

DI

102
Q

What is the use of hypertonic saline test

A

Copeptin or AVP levels should rise normally at higher blood salt conc. If not, is DI

103
Q

What are some non- genetic causes of CDI

A

Abnormality in hypothal or pp
Includes:
Neurosurgery
HI
Idiopathic
Diseases eg. tumours and sarcoidosis
Hemorrhage- Sheehan’s syndrome (postpartum) or aneurysm

104
Q

Genetic causes of CDI

A

DIDMOAD
Isolated- AVP gene ( autosomal dominant)

105
Q

NDI acquired causes

A

Hypercalcaemia and hypokalemia, urinary tract obstructive , psychogenic polydipsia, lithium and demeclocylcine

106
Q

Inherited causes of NDI

A

V2R X-linked, AQP2 gened, Ch12- A, recessive or A.dom)

107
Q

Treatment for CDI

A

DDAVP( spray/ tablets, injection rately given) and replacement of other hypothalamo-pituitary deficiencies

108
Q

Treatment for NDI

A

Treat deficiencies (hypokalemia etc.) or remove treatment (democycline)
Thiazide/ amiloride diuretics to lower urine volumes
Indomethacin to limit renal prostaglandins
Lower salt diet and lower protein diet to limit urinary osmotic load
May try drugs with SIADH tendency like chlorpropamide to increase renal receptors and response to ADH for partial DI

109
Q

How to compare SIADH with Non SIADH retained water excess

A

urine osmolality more than 2 X plasma osmolality
Urine osmolality more than 500 mmol/l
when plasma osmolality<280/ Na+ <135 (often means excess ADH)

110
Q

3 causes of Non SIADH retainwed water excess

A

low GFR,ACTH/GC deficiency and severe hypothyroidism

111
Q

Causes of SIADH

A

Intrathoracic diseases

Intracranial lesions, neoplasmas esp mediastinal/ lungs
drugs like antipsychotics (phenothiazines),

sedative (morphine, barbarituates)

5 c’s -chlorpropamide, clofibrate,
chlorpromazine,carbamazepine, chlorothiazide

Nicotine, pain, nausea, hypoglycaemia

112
Q

Treatment for SIADH

A

Fluid restriction to 1l/day then 0.8l/day if needed, then increase solute intake via salt supplements(hypetonic saline for urgent ot moderate hyponatramia)
Normalise chronic hyponatremia slowly ( Na conc. less than 10nmol/day)
May use democylcine that can cause partial NDI

113
Q

What is the dual action of cortisol

A

Anabolic in liver to promote gluconeogenesis but catabolic in peripheral muscle to promote protein and lipid breakdown

114
Q

Which chromosome is involved in Glucocrticoid Remediated Aldosteronism

A

Chromosome 8

115
Q

Treatment for renal artery stenosis

A

MR blockers, balloon angioplasty +/- stents, statins, anti-platelet agents

116
Q

renin and aldosterone in cushings

A

Low for both

117
Q

Symptoms of pheochromocytoma

A

Palpitations, headache, episodic sweating, anxiety, hypertension, diabetes

118
Q

Two causes of polyuria

A

BOTH DIABETES

119
Q

Does Osmotic Diuresis cause hypo or hypernatremia

A

Hyponatremia

120
Q

One lung related cause of dehydration

A

CF

121
Q

What is involved in the decidualization of the endometrium

A

Increasing progesterone (and estradiol)

122
Q

How to analyse semen

A

WIthin 60 mins of ejaculation, 2 samples 4-12 weeks apart

123
Q

Most common genetic cause of infertility

A

Kleinfelter’s

124
Q

What Y chromosome deletions may be involved in infertility

A

AZF A,B, C

125
Q

How can CF affect fertility

A

Thickened secretions or Congenital Bilateral Absence of Vas Deferens

126
Q

Effect of ANP on RAAS

A

High ANP inhibits

127
Q

Rate limiting step of steroid synthesis

A

sTAR protein- uptake of cholesterol

128
Q

how does prolactin affects FSH/LH levels

A

negative feedback

Y2 Endocrinology (4 decks)

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