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Block 7 - Endocrine, Nutrition, Reproductive Health > Learning Topics - 7.03 > Flashcards

Learning Topics - 7.03 Flashcards

1
Q

Corticosteroids

A

Glucocorticoids

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2
Q

What is the cellular mechanism of glucocorticoid action?

A

They bind to intracellular steroid receptors in the cytoplasm. The complex moves to the nucleus where it binds to nucleotide sequences on target genes. Initiates or depresses the transcription of mRNA

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3
Q

There are 4 mechanisms by which Gglucocorticoids have an anti-inflammatory effect. What are they?

A

Transactivation

Transrepression (includes post genomic effects and deacetylation of histones)

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4
Q

Transactivation

A

Binding of complex results in synthesis of anti-inflammatory proteins

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5
Q

Transrepression

A

Complex binds to transcription factors (which activate the production of mRNA for synthesis of pro-inflammatory cytokines). Binding causes suppression of same mRNA production. (? revise Paul Seale lecture from RA week)

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6
Q

Structure of steroids

A

Three 6-membered rings fused to one 5-membered ring

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7
Q

Name the 5 steroid groups

A 
Glucocorticoids
Mineralocorticoids
Androgens
Oestrogens
Progestogens
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8
Q

What hormones are synthesised in the adrenal cortex?

A

Aldosterone, cortisol, adrenal androgens

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9
Q

What is synthesised in the gonads?

A

Oestradiol, progesterone, testosterone

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10
Q

What is oestradiol?

A

One of the three oestrogens. The other two are oestrol and oestrone.

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11
Q

Zones of the adrenal cortex

A

Zona fasciculata
Zona reticulata
Zona glomerulosa

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12
Q

What is synthesised in the placenta?

A

Oestradiol and progesterone

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13
Q

Hormone synthesised in the zona glomerulosa

A

Aldosterone

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14
Q

Hormone synthesised in the zona reticulata

A

Androgens

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15
Q

Hormone synthesised in the zona fasciculata

A

Cortisol

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16
Q

Testosterone production is stimulated by the secretion of which hormone?

A

LH (under the influence of GnRH)

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17
Q

Cells that synthesise testosterone

A

Leydig cells

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18
Q

Follicular cells

A

Major site of oestrogen production in non-pregnant, pre-menopausal women

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19
Q

Oestradiol production is stimulated by …

A

FSH (under the influence of GnRH)

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20
Q

Progesterone is synthesised by …

A

The corpus luteum after ovulation (stimulated by LH)

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21
Q

Hormones that the placenta secretes during pregnancy

A

Oestradiol and progesterone (under the control of placental HCG - Human Chorionic Gonadotrophin)

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22
Q

Aldosterone synthesis depends on…

A

release of renin from JGA to activate RAAS

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23
Q

Cortisol and adrenal androgen synthesis depends on

A

ACTH (which activates a G protein)

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24
Q

Mineralocorticoid receptors are found where?

A

Kidneys

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25
Q

CBG

A

Corticosteroid binding globulin (glucocorticoids circulate in the blood bound to this)

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26
Q

Glucocorticoids can bind to mineralocorticoid receptors. Why don’t they normally?

A

An enzyme in the kidney (11-beta-hydroxy steroid dehydrogense) converts cortisol to cortisone (inactive)

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27
Q

What effect does cortisol have on glucose?

A

It increases glucose in the bloodstream to allow increased availability to tissues (e.g. heart and brain) in times of stress

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28
Q

Muscle wasting

A

myopathy

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29
Q

Normally, protein breakdown due to cortisol is offset by …

A

continued protein synthesis

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30
Q

Myopathy occurs in Cushings because ….

A

Continued elevation of cortisol means excessive proteolysis

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31
Q

Gluconeogenesis

A

Occurs in the liver, when lactate and amino acids from muscle is converted to glucose

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32
Q

Glucose produced in the presence of cortisol is stored as …

A

glycogen

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33
Q

Primary adrenal insufficiency

A

Both adrenal glands damaged, destroyed or absent

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34
Q

Secondary adrenal insufficiency

A

ACTH (pituitary) is deficient or absent

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35
Q

Tertiary adrenal insufficiency

A

CRH (hypothalamus) is deficient or absent

36
Q

Adrenal insufficiency can be permanent or temporary. Give examples

A

Permanent - destructive lesion

Temporary - exogenous steroid suppression

37
Q

Most common cause of adrenal insufficiency

A

Suppression by exogenous steroid i.e. when a treatment steroid is stopped suddenly.

38
Q

What can cause secondary/tertiary adrenal insufficiency?

A

Tumour, radiotherapy to H-P area

39
Q

In which condition are patients pigmented?

A

Primary adrenal insufficiency

40
Q

In which condition are patients pale?

A

Secondary/tertiary adrenal insufficiency

41
Q

Tests to conduct for diagnosis of adrenal insufficiency

A

Synacthen stimulation –> synthetic ACTH administered IM, cortisol levels measured before, 30 min and 60 min after (will not rise if abnormal).

42
Q

Name another test to conduct for diagnosis of secondary adrenal insufficiency

A

Insulin-induced hypoglycaemia (but risky)

43
Q

Steroid myopathy

A

Myopathy associated with above physiological levels of corticosteroid hormones

44
Q

What is the first symptom of steroid myopathy?

A

Diffuse myalgia

45
Q

What are the other symptoms of steroid myopathy?

A

Weakness in proximal muscles (initially legs), neck flexor muscles. Difficulty getting out of chairs, walking up hills and stairs, brushing hair (all signs of proximal muscle weakness).
Last is muscle wasting.

46
Q

What corticosteroid dosage is required to produce a myopathy?

A

30mg prednisone (???? This is from the learning topics)

47
Q

Which oral corticosteroid is steroid myopathy most commonly associated with?

A

Dexamethasone

48
Q

How is diagnosis of steroid myopathy made?

A

Excluding other causes of proximal muscle weakness (can be difficult sometimes)

49
Q

Creatinine kinase

A

An enzyme that breaks down ATP to ADP. Elevation indicates damage to muscle.

50
Q

Creatinine kinase levels in steroid myopathy

A

Remain normal (why?)

51
Q

How, histologically, could you exclude other causes of steroid myopathy?

A

Atrophy of type IIB fibres (though it is not diagnostic) on muscle histology

52
Q

Once steroids are reduced/discontinued, normal muscle power returns in …

A

1-4 months

53
Q

Acute quadriplegic myopathy

A

Severe weakness of limbs involving proximal AND distal muscles, AND weakness of respiratory muscles. May also be elevation of CK.

54
Q

Acute quadriplegic myopathy can occur in what kinds of patients?

A

Patients with severe asthma who require ventilation and high dose corticosteroids.

54
Q

Corticosteroids can affect respiratory muscles. How?

A

Reduction in inspiratory muscle endurance and strength –> reduction in strength of hip flexor muscles and loss of type IIB fibres in diaphragm

55
Q

What are the two main causes of glucocorticoid excess?

A 
Endogenous causes
Exogenous causes (iatrogenic pharmacotherpay)
55
Q

What are the endogenous causes of glucocorticoid excess?

A

Adrenal carcinoma, adrenal adenoma (i.e. one that secretes), ectopic ACTH (e.g. by non-pituitary tumour?), ectopic CRH (?), Cushing’s disease

56
Q

What is the most common cause of glucocorticoid excess?

A

Exogenous steroid use, usually when prescribed for high dose immunosuppression (e.g. RA) rather than HRT (e.g. Addison’s)

57
Q

What levels of prednisone will cause a Cushingoid appearance?

A

> 7.5mg/day

58
Q

When would glucocorticoids be given intravenously?

A

Acute Addison’s, or acute immunosuppression. Short term use only.

59
Q

What is the most common route of administration of glucocorticoids?

A

Oral

60
Q

Does inhaled or topical use of glucocorticoids cause side effects?

A

Not usually, as the systemic effect is minimised

61
Q

What are the two effects that glucocorticoids have on the body?

A 
Metabolic changes (blood sugar, bone metabolism, etc)
Tissue changes (as a result of the metabolic changes)
62
Q

Which occurs first, tissue changes or metabolic changes?

A

Metabolic changes.

Tissue changes also take longer to regress.

63
Q

How do glucocorticoids affect CHO metabolism?

A

Glucocorticoids cause insulin resistance.

As a result, there is

  • increased hepatic gluconeogenesis
  • decreased muscle glucose uptake
64
Q

What are the effects of insulin resistance on the body?

A

Hyperglycaemia, impaired glucose tolerance, type 2 diabetes development

65
Q

How do glucocorticoids affect protein metabolism?

A

They increase protein catabolism (biggest effect). They also inhibit protein synthesis, inhibit collagen protein synthesis and increase collagen protein catabolism.

66
Q

What are the effects of the increased protein catabolism on the body?

A

Decreased lean body mass, decreased BMR, myopathy

67
Q

What are the effects of glucocorticoids on lipid metabolism?

A

Increase production of LDL, VLDL, triglycerides (?). Increase lipoprotein lipase. (??)

68
Q

How long does it take for type 2 diabetes to manifest in a Cushingoid person?

A

It happens quickly.

69
Q

What is in the buffalo hump?

A

Increased cervical fat. It is soft!

70
Q

What are the effects of glucocorticoids on the skin?

A

Skin is fine because of inhibited collagen production. It will have abdominal striae and facial plethora.

Also will have acanthosis nigricans (hyperpigmentation in the folds of the skin) (relates to insulin resistance)

71
Q

What are the effects of glucocorticoids on the hair?

A

Hypertrichosis (fine downy hair on forehead and cheeks) –> don’t know why

72
Q

Cushing’s disease and Cushing’s syndrome

A

Cushing’s disease is specifically caused by high ACTH. Cushing’s syndrome results in symptoms because of high glucocorticoids, but ACTH may not be high

73
Q

Adrenal carcinoma

A

Aggressive, rapidly growing tumour of the adrenal cortex. Have effects on all three layers (ZG, ZR, ZF) –> therefore additional symptoms include HTN because of mineralocorticoid effect.

74
Q

Why does adrenal carcinoma cause Cushing’s disease?

A

I don’t know. Because ACTH should probably be low.

75
Q

What are the effects of glucocorticoids on bone?

A

Osteoporosis and increased fractures.
Main reason is due to inhibition of osteoblasts and increased osteoclasts. And decreased gut absorption of Ca and Vit D. –> causes scondary hyperparathyroidism.

76
Q

What effects can glucocorticoids have in children?

A

Poor linear growth –> short stature

Because glucocorticoids inhibit secretion of GH (why?)
They also have a direct effect on epiphyseal cartilage

77
Q

What are some other effects that glucocorticoids can have on bone

A

Aseptic necrosis –> primary ischaemic effect causing death of bone. Can result in collapse if bone is a weight-bearing bone e.g. femur

Fractures of tarsal bones, ribs, vertebrae

78
Q

What effect can vertebral fractures have on lung capacity?

A

9% loss for every fracture

79
Q

Glucocorticoids immunosuppress. How?

A

They decrease the inflammatory response.

  • Neutrophilia (why?)
  • decreased eosinophils
  • impaired phagocytosis
80
Q

What are the cardiovascular effects of glucocorticoid use?

A

HTN –> IF there is a mineralocorticoid effect also (i.e. increased ACTH)

Accelerated atheromatosis - because of lipid metabolism changes

81
Q

What are the effects of glucocorticoid use on the respiratory system?

A

Dyspnoea, obstructive sleep apnoea (both because of increased fat)
Osteoporotic rib fractures (compromise respiratory function)
Pneumonia and other opportunistic infections

82
Q

What are the electrolyte effects of excess glucocorticoid use

A

hyperkalaemia (secondary to mineralocorticoid effect)

nocturia (Why?)
polyuria if diabetic (Why?)

83
Q

What is the effect of excess electrolyte on the gonads?

A

Hypogonadism (why?)
impotence, oligomenorrhea, infertility
Reduction in libido

84
Q

What are the psychological effects of excess glucocorticoids?

A

Psychosis (important, steroid excess can be missed if this is a primary presenting symptom), depression, impaired cognition, insomnia, inability to concentrate, fatigue, apathy, irritability,

85
Q

Adrenal androgens are:

A

Androgens produced by the adrenal cortex. Specifically, DHEA. Which is converted to other androgens in the gonads.

Block 7 - Endocrine, Nutrition, Reproductive Health (5 decks)

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