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Kumar and clark endocrine > - > Flashcards

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1
Q

what is polyuria

A

pee more than usual

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2
Q

what happens to blood pressure in adrenal insufficiency

A

decreases

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3
Q

conductor of the endocrine orchestra

A

pituitary

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4
Q

structures of hormones

A

polypeptide, glycoprotein, steroid or amine

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5
Q

what causes release of hormones

A

intracellular calcium

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6
Q

hypothalamic releasing hormones are released into the

A

pituitary portal system

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7
Q

only unbound/bound hormone is biologically active

A

unbound

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8
Q

cell surface receptors contain – secretions

A

hydrophobic

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9
Q

most peptide hormones activate via

A

G protein coupled receptors

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10
Q

steroid and thyroid hormones act via

A

nuclear receptors

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11
Q

TRH and TSH increases release of

A

T3 and T4

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12
Q

Role of TSH

A

stimulates increased iodine uptake by the thyroid

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13
Q

t3 and t4 bind to what kind of receptors

A

nuclear

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14
Q

secondary gland failure is due to

A

pituitary disease

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15
Q

in secondary gland failure, the pituitary hormone is not

A

suppressed so negative feedback not really working in pituitary disease

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16
Q

hormones are measured by

A

biochemical assays in lab

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17
Q

not possible to measure

A

hypothalamic hormones

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18
Q

circulating levels of most hormones are

A

very low

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19
Q

how do immunoassays work

A

highly specific antibodies bind to hormone and this interaction is measured

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20
Q

immunoassays definitely have their

A

limitations

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21
Q

in women who are pregnant or on the pill can give false impression of

A
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22
Q

in women who are pregnant or on the pill can give false impression of

A

hypercortisolaemia due to high oestrogen levels

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23
Q

in people with diabetes mellitus may give impression of

A

androgen deficiency due to Low testosterone levels

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23
Q

in people with diabetes mellitus may give impression of

A

androgen deficiency due to Low testosterone levels

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24
Q

thyroid hormones show what kind of secretion

A

continuous with very little variation

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25
Q

GH, Lh and FSH show

A

pulsatile secretion

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26
Q

cortisol levels vary greatly with highest levels being in the morning and lowest

A

overnight

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27
Q

stress increases

A

acth and cortisol, GH, prolactin, adrenaline and noradrenaline

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28
Q

secretion of – and – is increased during sleep

A

GH and prolactin

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29
Q

what 2 hormones decreases after digestion of food

A

testosterone and GH

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30
Q

testosterone should be. measured

A

before 11am in the fasting state

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31
Q

cortisol should be checked

A

between 8 and 10 am to exclude hypoadrenalism and and at midnight to exclude cushings

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32
Q

what hormones vary with menstrual cycle

A

Lh/FSH, oestrogen and progesterone

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33
Q

renin and aldosterone vary with

A

sodium , age and posture

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34
Q

dexamethasone decreases

A

cortisol

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35
Q

dopamine restricts production of

A

prolactin

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36
Q

ADH and oxytocin are secreted in hypothalamus but are stored in

A

posterior pituitary

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37
Q

oxytocin produces

A

milk ejection and uterine myometrial contraction

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38
Q

most common cause of pituitary disease

A

pituitary tumours

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39
Q

most common presentation of prolactinoma

A

galactorrhea(milky nipple discharge), amenorrhoea (lack of period), erectile dysfunction, hypogonadism(sex glands produced little if any sex hormones)

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40
Q

central obesity associated with

A

cushings disease

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41
Q

nelsons syndrome occurs

A

post adrenalectomy

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42
Q

excess acth secretion occurs in

A

cushings disease and nelsons syndrome

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43
Q

acidophil

A

acromegaly

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44
Q

basophil

A

Cushings disease and nelson syndrome

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45
Q

usual treatment of choice for pituitary tumour

A

surgery via transphenoidal route and large tumours through trans cranial route usually transfrontal

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46
Q

what drugs can cause shrinkage of particular tumour types

A

somatostatin analogue eg octreotide and or dopamine agonists eg cabergoline particularly in prolactinomas

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47
Q

replacement therapy for adrenal

A

hydrocortisone

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48
Q

replacement for deficiency in gonadal in male and what for female

A

male - testosterone and female - oestrogen/ progestogen

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49
Q

replacement for fertility

A

HCG plus FSH

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50
Q

if thirsty given

A

desmopressin

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51
Q

if breasr deficiency eg prolactin inhibition give

A

dopamine agonist eg cabergoline

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52
Q

reduction of excess hormone for acromegaly treatment drug

A

somatostatin analogue

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53
Q

dopamine agonists for

A

prolactinomas

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54
Q

most common mass lesion of pituitary

A

pituitary adenomas

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55
Q

another pituitary mass lesion

A

craniopharyngioma

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56
Q

arises from rathkes pouch

A

craniopharyngioma and is a cystic tumour

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57
Q

often from tumour growth where there is multiple deficeiceis in these hormones what hormones first affected

A

GH and gonadatrophins

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58
Q

last affected

A

tsh and acth

59
Q

hypoadrenalism causes

A

mild hypotension, hyponatraemia and cardiovascular collapse during severe intercurrent stressful illness

60
Q

– leads to loss of libido (sex drive), sexual hair, amenorrhoea dn erectile dysfunction and eventually osteoporosis

A

hypogonadism

61
Q

pallor with hairlessness

A

panhypopituitarism

62
Q

loss of smell

A

kallmanns syndrome

63
Q

3 zones of the adrenal cortex

A

zona glomerulosa, fasciculata and reticularis

64
Q

zona glomerulsoa secretes

A

aldosterone

65
Q

inner medulla synthesises, stores and secretes

A

catecholamines

66
Q

zona fasciculata and reticularis produce

A

glucocorticoids, cortisol, sex steroids and androgen

67
Q

catecholamines such as

A

adrenaline and noradrenaline

68
Q

main role of mineralocorticoids

A

on extracellular balance of sodium and potassium in kidney

69
Q

glucocorticoids main effects on

A

carbohydrate metabolism

70
Q

what contains melanocytes stimulating hormone

A

ACTH

71
Q

circulatimg acth stimulates – in the adrenal

A

cortisol

72
Q

crH - acth - —–

A

cortisol

73
Q

following adrenalectomy or other adrenal damage eg Addisons disease, cortisol secretion is absent or reduced and acth levels will

A

rise

74
Q

— secretion is mainly controlled by the renin angiotensin system

A

mineralcorticodi

75
Q

– increases in response to stress

A

cortisol

76
Q

administration of dexamethasone does what to CRH and ACTH levels and thus cortisol

A

decreases them

77
Q

dexamethasone test for

A

cushings syndrome

78
Q

for stimulation tests what is given

A

synthetic ACTH to stimulate adrenal cortisol production

79
Q

cushings syndrome most often iatrogenic Fromm administering what

A

steroids

80
Q

Cushings disease is caused by excess secretion of ACTH from a

A

pituitary adenoma

81
Q

cushings syndrome divided into 2 categories

A
  1. increased circulating ACTH from the pituitary known as cushings disease (65%) or ectopic non pituitary tumour acth producing tumour from elsewhere in the body (10%)
  2. excess of cortisol secretion by an adrenal tumour(25%)
82
Q

pigmentation in cushings only occurs

A

with acth dependent causes most frequently in ectopic acth syndrome

83
Q

– is common in all causes of cushings syndrome

A

hypertension

84
Q

what is common with ectopic acth secretion in cushings

A

hypokalaemia and impaired glucose tolerance and pigmentation

85
Q

signs more specific to Cushings

A

plethora (moon face), thin skin, bruising, proximal myopathy

86
Q

confirm diagnosis for cushings with

A

48hr low dose dexamethasone test

87
Q

why is overnight dexamethasone test used as more of an initial screening test in cushings

A

as has a higher false positive rate and takes less time.

88
Q

tests for cushings

A

48hr low dose dexamethasone test
24hr urinary free cortisol measurements
circadian rhythm

89
Q

classic ectopic acth syndrome of cushings is

A

pigmentation ,weight loss, hypokalaemia, diabetes and plasma acth levels above 200ng/L

90
Q

in cushings severe hirsutism suggests

A

adrenal tumour

91
Q

for a dexamethasone test, failure of significant plasma cortisol suppression suggests an

A

ectopic source of acth ( or an adrenal tumour)

92
Q

exaggerated ACTH and cortisol response to CRH suggests

A

pituitary dependent cushings disease

93
Q

untreated cushings syndrome can cause death from

A

venous thromboembolism, hypertension, MI, infection and heart failure

94
Q

drugs to control cortisol hypersecretion prior to surgery

A

usual drug is metyrapone but ketocanazole can also be given

95
Q

treatment of choice for cushings disease

A

transphenoidal removal of the tumour

96
Q

what is mainly used after failed pituitary surgery in

A

external pituitary irradiation

97
Q

what is last resort in treatment of cushings disease

A

bilateral adrenalectomy

98
Q

cushions due to adrenal adenomas should be

A

resected laparoscopically

99
Q

if source of acth is not clear in cushings , cortisol hyperesecretion should eb controlled with medical therapy until diagnosis eg

A

metyrapone or ketoconazole

100
Q

what occurs after 20% of cases after bilateral adrenalectomy for cushings disease

A

nelson syndrome

101
Q

when is there destruction of the entire adrenal cortex

A

Addisons disease

102
Q

if entire adrenal cortex is destructed then what are reduced

A

glucocorticoid, mineralocorticoid and sex steroid production

103
Q

what generally remains intact in hypothermic pituitary disease

A

mineralocorticoid secretion also sex steroid

104
Q

in Addisons disease, reduced cortisol levels lead through feedback to increased CRH and __ production, the latter being directly responsible for the hyperpigmentation

A

ACTH

105
Q

Addisons disease is usually caused by

A

autoimmune disease

106
Q

most common cause of primary adrenal insufficiency in kids is

A

congenital adrenal hyperplasia

106
Q

most common cause of primary adrenal insufficiency in kids is

A

congenital adrenal hyperplasia

107
Q

what is the predominant sign in Addisons

A

pigmentation (dull, slaty, grey-brown) especially of new scars and palmar creases and postural systolic hypotension

108
Q

if adddisons disease is suspected, investigation is

A

urgent

109
Q

what is given to suspected add-ons disease if hypotensive or seriously ill

A

hydrocortisone and IV saline

110
Q

random cortisol. measurement of below – during the day is highly suggestive of Addisons

A

100nmol/L

111
Q

ACTH stimulation test should be performed in

A

Addisons

112
Q

absent or impaired cortisol response to acth stimulation test confirms presence of hypoadrenalism but does not

A

differentiate Addisons from acth deficiency or iatrogenic suppression by steroid medication

113
Q

what may be normal but classical seen in Addisons

A

hyponatraemia, hyperkalaemia and high urea

114
Q

long term treatment of Addisons is with

A

glucocorticoid and mineralocorticoid replacement

115
Q

is measuring cortisol levels during the day for Addisons while on replacement therapy recommended as an assessment for dose adequacy

A

NO

116
Q

patients should double dose of steroid in Addisons during

A

intercurrent illness

117
Q

long term steroid therapy can lead to

A

acth suppression

118
Q

hydrocortisone needs to be started before

A

t4 replacement

119
Q

in secondary hypoadrenalism, acth levels are

A

low

120
Q

disorder resulting in a defiency of an enzyme in the cortisol synthetic pathway

A

congenital adrenal hyperplasia

121
Q

in CAH, as cortisol secretion is reduced,

A

acth is increased causing adrenal hyperplasia

122
Q

what test for congenital adrenal hyperplasia

A

synacthen test

123
Q

long term steroids (greater than 3 weeks) will often mimic

A

cushings syndrome

124
Q

steroids can affect endocrine system by causing what

A

weight gain and glycosuria(urine contains lots of glucose)/hyperglycaemia/ diabetes

125
Q

what accounts for 5-10% of all hypertension

A

primary hyperaldosteronism

126
Q

what is characterised by excess aldosterone, leading to sodium retention, potassium loss and the combination of hypokalaemia and hypertension

A

primary hyperaldosteronism

127
Q

secondary aldosteronism is when there is

A

excess renin

128
Q

most common cause of primary hyperaldosteronism

A

bilateral adrenal hyperplasia followed by conns syndrome ( adrenal adenomas)

129
Q

usually presentation for primary hyper aldosteronism is simply

A

hypertension

130
Q

screening test for primary hyperaldosteronism

A

plasma aldosterone :renin ratio

131
Q

2 main causes of hyperaldosteronism

A

adrenal adenoma or hyperplasia

132
Q

how to treat an adenoma and hypoerplasia causing primary hyperaldosteronism

A

adenoma - laparoscopically
hyperplasia- aldosterone anatoginst (spironolactone)

133
Q

increase in levels in urine of — is a marker of abnormal hyper secretion of them

A

catecholamines

134
Q

rare tumours of the sympathetic nervous system

A

pheochromocytoma and paraganglioma

135
Q

metabolism of virtually all nucleated cells of many tissues is controlled by the

A

thyroid hormones

136
Q

thyroid gland moves on

A

swallowing

137
Q

embryonically what originates from the base of the tongue and descends into the middle of the neck

A

thyroid gland

138
Q

does thyroid gland have rich blood supply

A

yes

139
Q

thyroid gland consists of

A

follicles

140
Q

colloid is the

A

iodinated glycoprotein thyroglobulin

141
Q

parafollicular cells contain

A

c cells

142
Q

what is a prohorome

A

T4

143
Q

iodine + thyroglobulin =

A

T3 and t4

144
Q

majority of t3 and t4 in plasma is bound to hormone binding proteins

A

true

145
Q

only – hormone is available for action in the target tissues where t3 binds to nuclear receptors

A

free

Kumar and clark endocrine (3 decks)

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