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Memorize for 2nd Year Exams > Endocrine II > Flashcards

Endocrine II Flashcards

1
Q

What are the two types of DI?

A

Cranial - low ADH

Nephrogenic - not responsive to ADH

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2
Q

Which two drugs can cause DI?

A

Lithium

Demeclocycline

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3
Q

How is DI diagnosed?

A

Fluid depravation for 8h, then ADH
Step 1 - fluid depravation
- If urine osmolality >600 then stop
- If urine osmolality <600 then continue to stage 2
Step 2 - give desmopressin IM
- Cranial DI: urine osmolality increases to >600 after desmopressin
- Nephrogenic DI: no increase in urine osmolality after desmopressin

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4
Q

Treatment of nephrogenic DI?

A

NSAIDs

Thiazides

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5
Q

Treatment of hirsutism?

A

Cyproterone

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6
Q

Definitive test for acromegaly?

A

Oral glucose tolerance test (suppression test)
Rising levels of glucose inhibit GH secretion
In healthy patient, in OGTT, GH levels should be undetectable
In acromegaly, there is failure to suppress GH secretion

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7
Q

Patient >60 with bone pain, hypercalcaemia, increased ALP = ?

A

Multiple myeloma

Osteolytic lesions seen on x-ray

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8
Q

Really long arms + legs + gynaecomastia = ?

A

Klinefelter’s syndrome

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9
Q

List three clinical features of Kartagener’s syndrome

A

Dextrocardia
Abnormal frontal sinus
Primary ciliary dyskinesia

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10
Q

Decreased anti-malarian hormone + increased FSH = ?

A

Reduced ovarian reserve

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11
Q

In hypopituitarism, which hormones area affected in which order?

A 
GH
FSH + LH
PRL 
TSH
ACTH
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12
Q

Describe the treatment for hypopituitarism

A
  1. Hydrocortisone - before any other hormone
  2. Thyroxine if hypothyroid
  3. Men - testosterone replacement
  4. Women (premenopausal) - oestrogen patches or contraceptive pill
  5. Gonadotrophin therapy is needed to induce fertility in both men and women
  6. GH - refer to endocrinologist for insulin tolerance testing
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13
Q

Treatment of chlamydia?

A

Azithromycin

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14
Q

What is Sheehan’s syndrome?

A

Post partum hypopituitarism caused by ischaemic necrosis due to blood loss and hypocolaemic shock during and after childbirth

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15
Q

WHAT DO STEROIDS DO TO BLOOD GLUCOSE LEVELS

A

STEROIDS INCREASE BLOOD GLUCOSE LEVELS

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16
Q

List the four main functions of cortisol

A
  1. Maintain normal plasma glucose levels
  2. Under stress it allows the body to have a fuel source
  3. Increased responsiveness of adrenoreceptors to adrenaline - helps with circulation to prevent patient going into shock
  4. Anti-inflammatory roles at high levels
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17
Q

What effect does cortisol have on metabolism?

A

Increases the amount of raw material that the body can use as energy in times of stress

  • Increases lipolysis
  • Decreases glucose uptake into tissues
  • Increases gluconeogenesis
  • Increases proteolysis
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18
Q

What does uncontrolled secretion of cortisol do to blood glucose?

A

Dramatically increases blood glucose

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19
Q

If cortisol increases blood glucose, what symptoms will this give the patient?

A

Polyuria

Polydipsia

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20
Q

What is the classic triad of symptoms of excess adrenaline?

A

Hypertension
Sweating
Headaches

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21
Q

What is the stimulus for erythropoietin secretion?

A

Hypoxia - causes stem cells in the bone marrow to produce RBCs to increase the oxygen carrying capacity of the blood

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22
Q

What is calcidiol?

A

A prehormone produced in the liver, originating in the skin
In the kidneys is is converted to calcitriol
This is stimulated by PTH

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23
Q

What are the two roles of angiotensin II?

A

Directly vasoconstricts

Indirectly elevates BP by aldosterone

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24
Q

What should you think of cortisol as?

A

A stress hormone

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25
Q

What are the three main clinical uses of corticosteroids?

A
  1. Suppress inflammation e.g. asthma
  2. Suppress immune system e.g. autoimmune conditions - Crohn’s
  3. Replace treatment - for people who don’t produce enough
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26
Q

What are the end product deficiencies in each of these enzymatic deficiencies?

  • 21aOH
  • 11bOH
  • 17aOH
A

21aOH - problem with glucocorticoid and mineralocorticoid -> increased androgen
11bOH - problem with glucocorticoid and mineralocorticoid -> increased androgen
17aOH - problem with glucocorticoid and androgen -> normal aldosterone

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27
Q

What are the clinical features of 11bOH deficiency?

A

Females virilised

Salt wasting rare

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28
Q

What are the clinical features of 17aOH deficiency?

A

Males virilised
Females fail to achieve puberty
Salt wasting not observed

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29
Q

What is significant about hypovolaemia in hyponutraemia?

A

This implies that there is a very big sodium deficit

Must give the patient the sodium which they lack

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30
Q

What does oedema tell you?

A

Water is in the wrong place

You are likely to have too much sodium, in the wrong place

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31
Q

Which genes are associated with

  • Carney complex
  • McCune-Albright
  • Von Hippel-Lindau disease
  • Nerofibromatosis type I
A

Carney complex - PRKAR1A
McCune-Albright - GNAS1
Von Hippel-Lindau disease - VHL
Nerofibromatosis type I - NF1

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32
Q

What are glucose levels in Addison’s?

A

Low - CORTISOL INCREASES GLUCOSE LEVELS

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33
Q

List some causes of primary and secondary adrenal insuffifiency

A 
Primary 
- Addisons
- CAH
- TB, tumor
Secondary
- Exogenous steroid use
- Pituitary/hypothalamic tumours
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34
Q

Diagnosis of secondary adrenal insufficiency?

When might this be negative?

A

Long synacthen test

If acute this may be negative - give steroid anyway

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35
Q

What is biochemistry like in Addison’s?

A

Hyponatraemia
Hyperkalaemia
Hypercalcaemia
Hypoglycaemia

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36
Q

Unexplained abdominal pain + vomiting = ?

A

Addison’s

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37
Q

Which antibodies are positive in autoimmune addisons?

A

21-hydroxylase adrenal autoantibodies

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38
Q

Hypertension + hypokalaemia = ?

A

Primary aldosteronism

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39
Q

High Na
High h20 (hypertension)
Low K
= ?

A

Conn’s syndrome

40
Q

Medical treatment of primary hyperaldosteronism?

A

Spironolactone - aldosterone receptor antagonist

41
Q

How is diagnosis of primary hyperaldosteronism diagnosed?

A

First do aldosterone renin ratio - if >750 then move on to next step
Saline suppression test
Failure of aldosterone to suppress by 50% is diagnostic

42
Q

How is diagnosis of congenital adrenal hyperplasia made?

A

Basal (or stimulated) 17-OH progesterone

43
Q

Biochemistry of SIADH?

A

Increased ADH
Hyponatraemia
Increased urinary sodium

44
Q

What is an important cause of SIADH to keep in mind?

A

SCLC

45
Q

Treatment of SIADH?

A

If symptomatic then fluid restrict to 500-1000 ml in 24h

46
Q

What are the three P’s of MEN1?

A

Parathyroid
Anterior pituitary - prolactinoma, acromegaly, Cushing’s
Enteropancreatic
Other tumours - carcinoids of thymus, lung, stomach, adrenal cortex adenomas

47
Q

Genetics of MEN1?

A

Mutation in MEN gene on chromosome 11
Leads to loss of function of menin
Menin = nuclear tumour suppressor protein

48
Q

How should you screen for MEN1?

A

Serum calcium

49
Q

Three classic tumour types in MEN2A?

A

Medullary thyroid carcinoma
Adrenal medulla - phaeochromocytoma
Parathyroid hyperplasia

50
Q

Three classic tumour types in MEN2B?

A

Medullary thyroid carcinoma
Adrenal medulla - phaeochromocytoma
Mucosal neuromas

51
Q

Genetics of MEN2?

A

Mutation in RET proto-oncogene

52
Q

How should you screen for MEN2?

A

Genetic testing for RET mutation

53
Q

Medical treatment of phaeochromocytoma?

A

Alpha blockade - phenoxybenzamine
THEN
Beta blockade - atenolol
Chemotherapy - radio labelled MIBG

54
Q

List the clinical features of Carney complex

A

ACTH independent Cushing’s
Acromegaly due to GH producing adenoma
Thyroid cancer
Spotty pigmentation of skin

55
Q

Polyostotic fibrous dysplasia + Cafe-au-lait + precocious puberty + autonomous endocrine hyperfunction + scoliosis = ?

A

McCune-Albright syndrome

56
Q

Visceral cysts and benign tumours in multiple organ systems = ?

A

Von Hippel Lindau disease

57
Q

DI + DM + optic atrophy + deafness + neuro problems = ?

A

DIDMOAD or Wolfram syndrome

58
Q

Obese + polydactyly + hypogonadal + visual impairment + hearing impairment + mental retardation = ?

A

Bardet-Biedl syndrome

59
Q

Describe the process of vitamin D metabolism

A

Originates in skin as 7-dehydrocholesterol
UV light acts on this to produce cholecalciferol (vitamin D3)
In the liver this is converted to 25-hydroxyvitamin D3 (calcidiol)
In the kidneys this is converted by 1aOH to 1,25-dxydroxyvitamin D3 (calcitriol)

60
Q

What is calcitriol and what are its functions?

A

Active form of vitamin D - a steroid hormone
Kidneys - increases absorption of Ca2+ and increases absorption of PO43-
Increases bone resorption to increase serum calcium

61
Q

When is calcitonin secreted?

What is it’s function

A

In extremes of hypercalcaemia
Decrease serum calcium
Decrease serum phosphate

62
Q

What does deficiency/excess calcitonin do to bone?

A

Has no effect

63
Q

What are the two causes of hypercalcaemia to remember?

What is PTH like in each?

A

Primary hyperparathyroidism - high PTH

Malignancy - low PTH

64
Q

What are the three types of hyperparathyroidism and what are levels of Ca and PTH like in each?

A

Primary - overactivity of parathyroid - increased PTH and calcium
Secondary - physiological response to low calcium - high PTH, low calcium
Tertiary - parathyroid gland becomes autonomous after many years of secondary - high PTH and high calcium

65
Q

What is the most common cause of hypercalcaemia?

What is the most common cause of this condition?

A

Primary hyperparathyroidism

Parathyroid adenoma

66
Q

What does a diagnosis of primary hyperparathyroidism require a triad of?

A
  1. Raised serum calcium
  2. Raised serum PTH
  3. Increased urine calcium excretion in the absence of diuretics
67
Q

What is hypocalcuric hypercalcaemia?

A

AD mutation in calcium sensing receptor
Mild hypercalcaemia with reduced urine calcium excretion
PTH may be marginally elevated

68
Q

Treatment of acute hypocalcaemia?

A

IV calcium gluconate

69
Q

Biochemistry in hypoparathyroidism?

A

Low PTH
Low Ca
High phosphate

70
Q

What is pseudohypoparathyroidism?

A

Genetic resistance to PTH
High PTH
Low calcium
High phosphate

71
Q

Symptoms of pseudohypoparathyroidism and pseudopseudohypoparathyroism

A

Subcutaneous calcification
Mental retardation
Blunting of 4th metacarpal
Obesity

72
Q

Treatment for Rickets?

A

Adcal D3

73
Q

What is the preferred osteoporosis indicator?

A

QFracture

74
Q

What should you treat osteoporosis with if bisphosphonates are giving GI side effects?

A

Zoledronic acid once yearly IV infusion for 3 years

If renal impairment, use Denosumab

75
Q

Deafness + frontal bossing + bowing of the legs = ?

A

Pagets disease

76
Q

Which cancer is Pagets associated with?

A

Osteosarcoma

77
Q

Two causes of rickets + osteomalacia?

A
  1. Problem with calcium or vitamin D

2. Phosphate deficiency caused by increased renal losses

78
Q

What is the function of leptin?

A

Tells your body how thin you are

79
Q

How does orlistat work?

A

Inhibits lipase to block absorption of dietary fat

80
Q

What are the types of gastric bypass surgery and which are restrictive/absorptive?

A

Banding - restrictive
Sleeve gastrectomy - restrictive
Bypass - restrictive and malabsorptive

81
Q

Why are some genes activated by steroids and some suppressed?

A

In one gene is more numerous, then multiple GRs can bind and expression is induced
If there is only one gene expressed, then binding of the GR will block the gene and so expression is supressed

82
Q

Why do some steroids cause fragile skin?

A

Glucocorticoids act on both GC and MR receptor

Can stop this by using something which saturates the MR receptor e.g. spironolactone cream

83
Q

Treatment of osteogenesis imperfecta?

A

Bisphosphonates

84
Q

What causes gestational diabetes?

A

Progesterone and hPL cause insulin resistance

85
Q

Which diabetic drugs are safe in pregnancy?

A

Metformin

Glibenclamide

86
Q

What must be checked more regularly in diabetic pregnancy?

A

Eye - accelerated pre-existing retinopathy

87
Q

Which blood pressure drugs can be used in pregnancy?

A

Labetalol
Nifedipine
Methyldopa

88
Q

How should you maintain good blood glucose during labour?

A

IV insulin

IV dextrose

89
Q

What should you do post natally for gestational diabetes?

A

Make sure it has gone away - 6 week post natal glucose tolerance test

90
Q

What should you do with hypothyroidism in pregnancy?

A

Increase dose of thyroxine by 25mcg as soon as pregnancy is suspected

91
Q

Which condition can give similar symptoms to hyperemesis in pregnancy?

A

Hyperthyroidism

92
Q

How should you treat hyperthyroidism in pregnancy?

A

Propylthiouracil 1st trimester

Carbimazole 2/3 trimester

93
Q

How does treatment of DKA vary between adults and children?

A

Careful fluid resuscitation - risk of cerebral oedema

Insulin started one hour after IV fluid - fluids are started first

94
Q

Which endocrine disorder are all babies screened for on day 5?

A

Congenital thyroid disease - look at TSH

Called the Guthrie test

95
Q

Which beta blocker is used in thyrotoxicosis?

A

Propranolol (non selective)

Memorize for 2nd Year Exams (13 decks)

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