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Endocrinology > Adrenal/steroids > Flashcards

Adrenal/steroids Flashcards

1
Q

When does physiological cortisol peak?

A

6-9am

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2
Q

Which factors have a positive feedback on cortisol production?

A

stress, Adr/NA, ghrelin

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3
Q

Which drugs have a negative feedback on cortisol production?

A

opioids

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4
Q

Which autoantibodies exist in >90% of addison’s patients?

A

21-hydroxylase

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5
Q

Which complications of addison’s disease should you be wary of?

A

Other autoimmune conditions, e.g. vitligo, coeliac disease, adrenal crisis

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6
Q

What are triggers for adrenal crisis?

A

acute stress, infection, haemorrhage

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7
Q

How to clinically distinguish primary adrenal insufficiency from secondary and tertiary? (signs)

A

no hyperpigmentation and no dehydration in 2+3

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8
Q

What would be the initial management plan for someone with suspected hypoadrenalism?

A

IV fluids, IV hydrocortisone, DVT prophylaxis, antiemetic

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9
Q

What are the causes of hypoadrenalism?

A
  1. Infections (TB, meningococcal)
  2. Drugs
  3. Metastatic destruction of adrenal glands
  4. Congenital adrenal hyperplasia
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10
Q

What is the protocol for short synacthen test?

A
  1. Ensure no glucocorticoid therapy given that morning
  2. Early morning ACTH and cortisol levels taken
  3. Dose of synthetic ACTH 250 micrograms
  4. Blood taken 30 min post ACTH
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11
Q

Which condition that arises in pregnancy can result in adrenal insufficiency?

A

Sheehan syndrome. life-threatening amount of blood in childbirth or who have severe low blood pressure during or after childbirth, which can deprive the body of oxygen. This lack of oxygen that causes damage to the pituitary gland

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12
Q

Which drug prescription can induce adrenal insufficiency?

A

steroids

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13
Q

In secondary and tertiary adrenal insufficiency, are mineralcorticoids still produced?

A

yes

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14
Q

Which is the most common cause of adrenal insufficiency in children?

A

congenital adrenal hyperplasia

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15
Q

What happens to the levels of Na and K in adrenal insuffiency?

A

Decreased Na and incr K

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16
Q

Why does bronzing occur in primary adrenal insufficiency?

A

ACTH stimulates melanocytes

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17
Q

Name two symptoms of adrenal insuffiency

A

muscle cramps, N/V

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18
Q

What is the treatment for adrenal insufficiency?

A

hydrocortisone and fludrocortisone

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19
Q

Is fluodrocortisone necessary in secondary and tertiary adrenal insufficiency?

A

unnecessary

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20
Q

If a patient with addison’s disease is sick, how should this affect their routine medications?

A

double dosage of corticoseroids but maintain the fludrocortisone dose

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21
Q

Two catabolic effects of cushing’s syndrome

A

 Proximal myopathy
 Striae
 Bruising
 Osteoporosis

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22
Q

Two glucocorticoid effects of cushing’s

A

DM

obesity

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23
Q

Two mineralcorticoid effects of cushing’s?

A

HTN

hypokalaemia

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24
Q

Describe three features of the appearance of someone with cushing’s

A 
  Moon face 
  Acne and hirsutism 
  Interscapular and supraclavicular fat pads 
  Centripetal obesity 
  Striae 
  Thin limbs 
  Bruising 
  Thin skin
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25
Q

How is cushing’s syndrome categorised/divided?

A

ACTH independent

ACTH dependent

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26
Q

Two differentials for ACTH independent cushing’s?

A

 Iatrogenic steroids: commonest cause
 Adrenal adenoma / Ca: carcinoma often → virilisation
 Adrenal nodular hyperplasia

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27
Q

Two differentials for ACTH dependent cushing’s?

A

cushing’s disease

ectopic-ACTH

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28
Q

An example of ectopic-ACTH cause?

A

SCLC

Carcinoid tumour

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29
Q

Two investigations for cushing’s syndrome?

A

24hr urinary free cortisol
Late night serum or salivary cortisol
Dexamethasone suppression test
ACTH

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30
Q

Which condition would show cortisol suppression in dexamethasone suppression test?

A

cushing’s disease only

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31
Q

Explain the dexamethasone suppression test

A

low dose test- confirms cushing’s syndrome
high dose test
-low cortisol= cushing’s disease
- high cortisol- high ACTH= ectopic ACTH, low ACTH= adrenal cushings, iatrogenic

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32
Q

What is cushing’s disease?

A

pituitary adenoma producing excess ACTH

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33
Q

What is conn’s syndrome?

A

adrenocorticol adenoma

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34
Q

Two causes of primary hyperaldosteronism?

A

bilateral adrenal hyperplasia

adrenocortical adenoma= conn’ syndrome

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35
Q

Which biochemical abnormality is present in hyperaldosteronism?

A

hypokalaemia

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36
Q

Two causes of secondary hyperaldosteronism?

A 
diuretics
nephrotic syndrome
hepatic failure
CCF
RAS abnormalities
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37
Q

Brief pathophysiology of hyperaldosteronism?

A

increases renin concentration due to reduced renal perfusion

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38
Q

How can you distinguish between primary and secondary hyperaldosteronism?

A

aldosterone: renin ratio
Raised in primary
Normal in secondary

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39
Q

Two symptoms of hyperaldosteornism?

A

HTN

weakness, hypotonia, cramps- hypokalaemia

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40
Q

What are the effects of aldosterone?

A

increases expression in Na/K ATPase and eNaC following steroid receptor activation which results in the transcription of these channels in the distal convoluted tubule (and collecting duct)

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41
Q

Patient has very high aldosterone but low renin. What might be the diagnosis?

A

primary aldosteronism

42
Q

What is the most common cause of secondary hypertension?

A

primary aldosteronism

43
Q

Which test is employed to test aldosterone levels/function?

A

saline suppression test, if aldosterone levels are still high then very suspiscous of primary aldosteronism as aldosterone levels should be reduced

44
Q

Three causes of primary adrenal insufficiency?

A

 Autoimmune destruction: 80% in the UK
 TB: commonest worldwide
 Metastasis: lung, breast, kidneys
 Congenital: CAH

45
Q

Three symptoms of primary adrenal insufficiency?

A

 Wt. loss + anorexia
 n/v, abdo pain, diarrhoea/constipation
 Lethargy, depression
 Hyperpigmentation: buccal mucosa, palmar creases
 Postural hypotension → dizziness, faints
 Hypoglycaemia
 Vitiligo
 Addisonian crisis

46
Q

Two abnormal findings in blood tests of primary adrenal insufficiency

A

hypoglycaemia
hyponatraemia, hyperkalaemia
hypocalcaemia

47
Q

Which autoantibody is present in primary adrenal?

A

21-hydroxylase

48
Q

Which is the main diagnostic test for addison’s?

A

short synACTHen test

49
Q

Treatment for addison’s?

A

hydrocortisone

fludrocortisone

50
Q

Name two pieces of advice to offer adrenal insufficiency patient

A

don’t stop steroids suddenly
increase dosage of steroids during injury, illness
wear a medic-alert bracelet/have emergency info on phone

51
Q

Two causes of secondary adrenal insufficiency?

A

chronic steroid use
Sheehan’s
Pituitary microadenoma

52
Q

What is Sheehan’s syndrome?

A

Excessive blood loss during or after delivery of a baby may affect the function of the pituitary gland, leading to a form of maternal hypopituitarism

53
Q

How to distinguish between primary and secondary adrenal insufficiency?

A

Normal mineralcorticoid in secondary

No pigmentation in secondary

54
Q

Two clinical features of addisonian crisis?

A

shock- tachy, oliguria, confused, postural drop

hypoglycaemia

55
Q

State one hereditary association of phaechromocytomas?

A

MEN2a and 2b

56
Q

Three seminal features of phaechromocytoma presentation?

A

episodic headache, sweating, tachycardia

57
Q

Two investigations for phaechromytoma?

A

Abdo CT and plasma + urine metadrenaline

58
Q

Prior to adrenlectomy for phaeochomocytoma, what must be given pre-op?

A

alpha blocker first, then beta blocker pre-op

59
Q

Emergency presentation of phaechromocytoma?

A

hypertensive crisis

60
Q

Three causes of hypopituitarism?

A

Tumour, inflammation, infection, ischaemia, trauma of hypothalamus, pituitary stalk, or pituitary gland

61
Q

Two common causes of panhypopituitarism?

A

surgery
tumour
irradiation

62
Q

Name three hormone deficiencies that arise in hypopituitarism?

A

GH
LH/FSH
TSH
ACTH

63
Q

Three causes of hyperprolactinaemia?

A 
lactation
pregnancy
prolactinoma
pituitary adenoma
antiemetics: metoclopramide
antipscyhotics: haloperidol
(physiological, pituitary, pharmacological)
64
Q

Three symptoms of hyperprolactinaemia?

A

 Amenorrhoea
 Infertility
 Galactorrhoea
 ↓ libido

65
Q

Patient is exhibiting symptoms of hyperprolactinaemia. The result of their basal prolactin test is 5907. What is the diagnosis?

A

prolactinoma >5000

66
Q

Three investigations for hyperprolactinaemia?

A

Pregnancy test
TFTs
Serum prolactin
MRI

67
Q

What is the treatment for hyperprolactinaemia?

A

DA agonist- cabergoline or bromocriptine

68
Q

What is the number one cause of acromegaly?

A

pituitary adenoma

69
Q

Three symptoms of acromegaly?

A 
  Acroparaesthesia 
  Amenorrhoea, ↓libido 
  Headache 
  Snoring 
  Sweating 
  Arthralgia, back ache 
  Carpal tunnel (50%)
70
Q

Four signs of acromegaly?

A

Hands- thenar wasting, increased skin fold thickness

Face- goitre, widely spaced teeth, wide nose, big ears, prominent supraorbital ridges

71
Q

Two complications of acromegaly?

A 
Impaired glucose tolerance
DM
HTN
Cardiomyopathy
Increased risk of IHD and stroke
72
Q

Why does hyperglycaemia arise in acromegaly?

A

GH fails to suppress glucose in acromegaly

73
Q

Two blood results of acromegaly?

A

Incr IGF1, incr glucose, ca, and PO4

74
Q

Two features of clinical presentation of PCOS

A

symptoms of anovulation- amenorrhoea, oligomenorrhoea, irregular cycles

hyperandrogenism- hirsutism, acne, alopecia.

75
Q

Which hormones are raised in PCOS?

A

testosterone and LH

76
Q

Which endocrine disorder does PCOS increase the risk of?

A

type 2 diabetes

77
Q

What are the three components of POS pathophysiology?

A

gonadotrophins, androgens, insulin resistance

78
Q

Which androgens are raised in PCOS?

A

testosterone, androstenedione, DHEAs

79
Q

What is the major source of androstenedione in women?

80
Q

What about DHEA-S?

A

adrenal gland

81
Q

Which hormone will be able to tell you whether the abnormal androgen production is in the ovary or adrenal?

A

DHEA-S as 95% of this is produced by the adrenal, while testosterone androstenedione are produced in the adrenal gland AND ovary in equal-ish amounts

82
Q

Testosterone is only biologically active when free. If there is increased production in PCOS, is there increased binding globulins?

A

reduced binding globulin, therefore more free androgens, leading to symptoms of PCOS

83
Q

What is the main binding globulin for androgens?

84
Q

Which diabetes treatment can be used to treat PCOS?

A

metformin, improves insulin sensitivity and therefore leads to a decrease in LH levels, increases in SHBG, and decreased free androgens

85
Q

What is the most effective treatment for PCOS symptoms?

A

calorie restriction

86
Q

Which form of testosterone is biologically active?

A

free testosterone

87
Q

Which enzyme converts testosterone to oestrogen?

88
Q

How does hypogonadism present in male child/young adult?

A

slow growth in teens, no growth spurt, small testes and phallus, lack of secondary development

89
Q

How does hypogonadism present in adults?

A

depression/low mood, poor libido, erectile problems, poor muscle, sparse body hair, gynoid weight gain

90
Q

What is gynoid weight gain?

A

weight around the chest, hips, and thighs

91
Q

Once a history suggests hypogonadism, which tests should be done?

A
  1. Testosterone- free, early, SHBG 2. FSH and LH. 3. Semen analysis
92
Q

Why would you want to measure LH and FSH in hypogonadism?

A

to rule out pituitary involvement

93
Q

In general, what are the two sources of causes for hypogonadism?

A
  1. Hypothalamic-pituitary 2. Testicular problem
94
Q

If you suspect hypogonadotrophic hypogonadism as there is low testosterone and low FSH+LH, which further tests should you do and why?

A

prolactin, cortisol, TSH…to ensure the whole pituitary is working

95
Q

Three causes of hypogonadotrophic hypogonadism?

A
  1. pituitary tumour 2. Genetic syndromes 3. Surgery 4. Head injury 5. Cerebellar ataxia 6. Kallmann’s syndrome
96
Q

15 y/o male with poor sense of smell, poor hearing, and impaired growth, what is the likely diagnosis?

A

Kallmann’s syndrome

97
Q

What would the levels of testosterone, LH/FSH, and prolactin be in primary gonadal disease?

A

low test, normal/high FSH/LH, normal prolactin

98
Q

Three differentials for primary gonadal disease?

A

1 Kleinefelter’s
2 trauma/chemo/radiotherapy can lead to seminiferous tubule and leydig cell failure
3 cryptorchodism

99
Q

What is the most common genetic cause of male hypogonadism?

A

Klinefelter’s syndrome

100
Q

How does Klinefelter’s present clinically?

A

wide clinical variation in phenotype due to hormonal respone to LH surges. In general, delayed puberty, suboptimal genital development, reduced secondary male sexual characteristics, behavioural difficulties

101
Q

Two treatments for hypogonadism in males?

A

androgen replacement therapy, fertility treatment

Endocrinology (9 decks)

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