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HHD 2 > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

What are corticosteroids?

A

They are any steroid hormones (excluding sex hormone) which are produced by the cortex of the adrenal gland or any synthetic equivalent

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2
Q

What are the zones of the adrenal cortex

A

Zona glomerulosa (outer)
Zona fasciculate (middle)
Zona reticularis (inner)

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3
Q

What hormones reproduced in the zona glomerulosa ?

A

mineralcorticoids such as aldosterone

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4
Q

What is the function of aldosterone?

A

Regulates water and electrolyte balance

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5
Q

What hormones are produced in the zona fasciculate?

A

Glucocorticoids
Cortisol and hydrocortisone

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6
Q

What are the functions of glucocorticoids?

A

carbohydrate, protein and lipid metabolism
Suppression of inflammation and immune response
Mediator of the stress response

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7
Q

What hormone is produced by the zona reticularis?

A

Androgens
Dehydroepiandrosterone

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8
Q

What is the function of dehydroepiandrosterone?

A

Stimulates and maintains mascularisation

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9
Q

What types of cells are found in the medulla of adrenal glands?

A

Chromaffin cells

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10
Q

What hormones are produced by chromaffin cells?

A

Catecholamines
E.g. adrenaline, noradrenaline

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11
Q

What is the function of cathecolamines?

A

Neurohormones; stimulates sympathetic CNS
Flight or fight respones

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12
Q

Cathecholamines have an _______ side chain

A

amine

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13
Q

What is the difference between mineral & glucocorticoids and catecolamines?

A

Mineralcorticoids and glucocorticoid are able to pass through the cell and bind to intracellular receptors whilst catecholamines behave like peptide hormones and are unable to do so

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14
Q

How are glucocorticoids regulated?

A

HPA axis
Hypothalamic- pituitary- adrenal axis

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15
Q

Response to stress involves the HPA axis. Give examples of “stress”

A

Acute illness
Injury
Pain
Anxiety
Infection
Blood loss
Surgery
Hypoglycaemia

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16
Q

Briefly outline the HPA axis

A

Hypothalamus released CRH (corticotrophic releasing hormone
CRH stimulates the anterior pituitary gland to release ACTH (adrenocorticotropic hormone)
ACTH stimulates the adrenal cortex to synthesise and secrete cortisol (zona fasciculate)

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17
Q

ACTH stimulation has a modest effect on __________.

A

Mineralcorticoid (aldosterone) release

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18
Q

Excess cortisol acts as a _____________ to inhibit ________ and ______ hormones.

A

Negative feedback loop
CRH and ACTH

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19
Q

___________ is produced by the posterior pituitary gland. What is its function in the stress response?

A

Vasopressin (Antidiuretic hormone)
It functions to stimulate the production of ACTH in the anterior pituitary gland

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20
Q

Circadian rhythm in glucocorticoid secretion is at its highest in the _________.

A

morning

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21
Q

Circadian rhythm in glucocorticoid secretion is at its lowest in the _________.

A

evening

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22
Q

HPA has a modest effect on the production of which corticosteroid hormone?

A

Aldosterone

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23
Q

HPA is also referred to as the …

A

stress response axis

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24
Q

What stimulates the release of aldosterone?

A

HPA axis (moderate release)
Angiotensin II

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25
Q

What system regulates the release of aldosterone?

A

Renin-angiotensin- aldosterone- system (RAAS)

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26
Q

Briefly describe how the RAAS system regulates aldosterone production

A

Renin is released from the kidney into the blood and converts angiotensinogen into angiotensin-I
Angiotensin converting enzyme (ACE) from the vascular endothelium cleaves angiotensin-I into angiotensin-II
Angiotensin II acts on adrenal cortex (Zona glomerulosa) to release aldosterone

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27
Q

In what way is angiotensin II able to increase blood pressure?

A

Angiotensin II binds to its receptor and has an effect on nitric oxide (vasodilator) synthesis; this increases vasoconstriction
Angiotensin II stimulated the release of ACTH from the adrenal cortex

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28
Q

Where are glucocorticoid receptors found?

A

They are found in most cell types

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29
Q

How is cortisol found in the blood?

A

Cortisol is found bound to corticosteroid binding globulin (CBG)
Some cortisol is also found bound to albumin

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30
Q

Whilst bound to CBG or albumin, steroids are biologically active. True or false

A

False
They are biologically inactive

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31
Q

Steroids enter cells as _________ molecules

A

free

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32
Q

Intracellular steroid receptors are bound to what proteins?

A

stabilising proteins e.g. Heat shock proteins (Hsp)
Others (X)?

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33
Q

What happens when steroids initially bind to their intracellular receptors ?

A

Stabilising proteins are released

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34
Q

The steroid-receptor complex enters the nucleus in the form of a ________.

A

dimer

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35
Q

What component on the gene do glucocorticoid-receptor complex bind to?

A

GRE
Glucocorticoid response elements

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36
Q

What is the function of GRE stimulation and inhibition?

A

regulate gene transcription (activation or inhibition) thus potentially yielding protein production

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37
Q

What the onset of steroid hormones? Why is this?

A

hours to days
due to longer duration of exprssion

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38
Q

Class I Nuclear receptors are characterised by the formation of _________.

A

homodimers

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39
Q

Class II nuclear receptors are characterised by the formation of _________ with __________ receptors

A

heterodimers
Retinoid X receptors (RXR)

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40
Q

Give examples of tissues which contain mineralcorticoid nuclear receptors

A

Kidney
Sweat ands salivary glands
Epithelia of colon and bladder

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41
Q

The MOA of mineralcorticoids is similar to that of glucocorticoids. In what way does it differ?

A

-the steroid receptor complex binds to the MRE (mineralcorticoid receptor complex)
-this increases the number of Na+/K+ pumps expressed on the distal tubule

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42
Q

What is the effect of increased expression of Na+/K+ pumps in the distal tubules?

A

Increased Na+ reabsorption into vasculature (increase in serum Na+)
This therefore leads to passive H2O reabsorption
This increases water retention in the serum

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43
Q

What is the physiological effect of aldosterone?

A

maintain adequate fluid volume and electrolyte balance for normal cardiac output and arterial BP

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44
Q

What is the MOA of aldosterone ?

A

Increase Na+/K+ pump expression in distal tubules
Increase Na+ reabsorption and passive reabsorption of water
Increase efflux of H+ and K+ ions, causing increased K+ excretion from kidneys

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45
Q

Mineralcorticoid sensitive organs produce which enzyme to prevent them from responding to cortisol? Briefly explain why this is necessary?

A

11beta hydroxysteroid dehydrogenase type 2 (11B HSD)
This is because cortisol and aldosterone are equiactive Mineralcorticoid receptors- cortisol can activate MRs; this can leads to some adverse effects

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46
Q

What is the function of 11beta hydroxysteroid dehydrogenase type 2 (11B HSD) ?

A

Convert cortisol to inactive cortisone

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47
Q

In liquorice toxicity ________ found in liquorice roots inhibits 11B HSD activity. What is the effect of this.

A

Glycyrrhizin
Cortisol build up in mineralcorticoid sensitive tissues such as the kidney
This can lead to:
-hypokalemia (low serum K+)
-hypernatremia (high serum Na+)
-water retention

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48
Q

What symptoms can be expected in >40 years olds with a history of heard disease/ HBD who experience liquorice toxicity?

A

Oedema
High blood pressure
Muscle cramping or weakness
Abnormal heart rhythm and heart failure

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49
Q

What are the inflammatory actions of glucocorticoids?

A

Inhibition of genes regulating expression of inducible COX-2 and NOS and most inflammatory cytokines (decreased production and action of interleukins, granulocyte macrophage CSF, TNFa, INFy)
Upregulation of the expression of annexin A1
Acute inflammation (influx and activity of leucocytes)
Chronic inflammation (decreased activity of mononuclear cells, decreased angiogenesis, decreased fibrosis)

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50
Q

What is the function of annexin A1?

A

directly inhibits PLA2 (phospholipase 2) and COX-2)
PLA2 metabolised the production of AA
this overall lead to decreased prostaglaindin and leukotriene synthesis

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51
Q

An inhibition of genes regulating expression of inducible COX2 and NOS leads to …

A

decreases prostanoids
decreased vasodilation
decreased vascular permeability

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52
Q

What immunosuppressive actions are caused by glucocorticoids?

A

decreased T lymphocyte activation and proliferation
decreased action of cytokine secreting T lypmphocytes
decreased production of plasma cells and antibodies
decreased phagocytosis of antigens by macrophages

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53
Q

Prostanoids are a __________ of eicosanoids

A

subclass

54
Q

What are the adverse effects of glucocorticoids?

A
  • increased infections due to depressed host immune system (oral candiasis whilst on inhaled corticosteroids)
    -decrease protective aspects of inflammation- impaired wound healing, peptic ulcers (loss of protective prostanoid effect) - prostanoids protect the GI mucosa
55
Q

What does adrenocorticoid insufficiency refer to ?

A

this is when adrenal glands produce insufficient corticosteroid hormones

56
Q

What are the 3 types of adrenocorticoid insufficiency?

A

Primary
Secondary
Tertiary

57
Q

What is the cause of primary adrenocorticoid insuffiency?

A

Impairment of adrenal glands

58
Q

What percentage of cortisol is bound to CBG?

A

77%

59
Q

80% of primary adrenocorticoid insufficiency is caused by …

A

Autoimmune disease Addisons disease
Addisons disease is also known as adrenal insufficiency where not enough cortisol and aldosterone are produced

60
Q

Give examples of associated health condition which can develop as a result of addisons disease

A

diabetes
Underactive thyroid

61
Q

List other causes of primary adrenocorticoid insufficiency

A

congenital adrenal hyperplasia
adenoma

62
Q

What is hyperplasia

A

increase in the number of cells in an organ/ tissue

63
Q

Secondary adrenocortical insufficiency is due to an impairment in _____________.

A

the pituitary gland

64
Q

Give an example of a condition that can lead to secondary adrenocortical insufficiency

A

Pituitary adenoma
which supresses production of ACTH

65
Q

Tertiary adrenocortical insufficiency is due to _________.

A

hypothalamic disease

66
Q

Give examples of hypothalamic disease which lead to tertiary adrenocortical insufficiency

A

brain tumours
sudden withdrawal from long-term exogenous steroid use
lead to decrease in release of CRH

67
Q

Left untreated, adrenocortical insufficiency can lead to …

A

Adrenal crisis (medical emergency)
symptoms appear quickly and severely

68
Q

List some signs and symptoms of an adrenal crisis

A

-fever
-syncope
-convulsions (fast, rhythmic uncontrolled movements)
-hypoglycaemia
-hyponatremia (high Na+)
-severe vomiting and diarrhoea

69
Q

What is the treatment for adrenocortical insufficiency?

A

Daily hydrocortisone (replace cortisol)
Daily fludrocortisone (replace aldosterone)

70
Q

Glucocorticoids affect carbohydrate, protein and lipid metabolism. State specifically what these metabolic effects are.

A

Increased liver glucose synthesis from amino acids and fatty acids (gluconeogenesis). The enzymes involves in protein break down are upregulated to provide amino acids and lipolysis is activated.

Reduce glucose uptake and utilisation by peripheral tissues.

71
Q

What is the effect of cortisol of plasma glucose? What is the mechanism for this

A

Increases plasma glucose levels
Reducing glucose uptake and utilisation by peripheral tissues by:
-antagonising the effect of insulin on peripheral tissues
-stimulating the translocation of glucose transporters from the plasma membrane into the cell

72
Q

Cortisol reduces glucose uptake and utilisation in peripheral tissues. What is the purpose of this?

A

to increase the availability of blood glucose to the brain

73
Q

What are the adverse metabolic effects of glucocorticoids?

A

-due to increased glucose synthesis- hyperglycaemia, worsening diabetes
-protein break down affects multiple tissues including skin and muscle; decreased muscle mass, thinning of the skin (fragile and easy to bruise)
-due to increase free fatty acids, there is a further insulin increase in insulin resistance and a dramatic redistribution of fat

74
Q

What are the adverse metabolic effects of glucocorticoids?

A

-due to increased glucose synthesis- hyperglycaemia, worsening diabetes
-protein break down affects multiple tissues including skin and muscle; decreased muscle mass, thinning of the skin (fragile and easy to bruise)
-due to increase free fatty acids, there is a further insulin increase in insulin resistance and a dramatic redistribution of fat

75
Q

The redistribution of body fat as a result of glucocorticoids presents as …

A
  • buffalo hump (increased fat in the back of the neck)
  • moon face (increased facial fat)
  • loss of fat in body extremeties
76
Q

Glucocorticoids have other adverse systemic effects outside of those associated with metabolism. Briefly state them

A

Diverse neurological effects and behavioural changes
Skeletal effect

77
Q

What is the MOA of diverse neurological effects and behaviour changes that can stem from glucocorticoids?

A

MOA is unclear

78
Q

Give examples of diverse neurological effects and behavioural changes associated with glucocorticoids

A

Insomnia and agitation
Psychological: mild (euphoria, anxiety); pronounced, (manic- depression)

79
Q

What the MOA of skeletal changes associated with glucocorticoids?

A

Decreased Ca2+ absorption into GI tract
Increased Ca2+ excretion into the kidneys
Reduce osteoblast function (deposition of bone matrix affected)
Increased osteoclast activity

80
Q

Skeletal changes observed as a result of glucocorticoid use can lead to the development of _________.

A

osteoporosis

81
Q

What is the function of 11beta hydroxysteroid dehydrogenase (11B HSD)?

A

convert cortisol to cortisone (inactive)

82
Q

In higher, non physiological concentrations, glucocorticoids have some mineralcorticoid actions. True or false

A

True
Cortisol and aldosterone are equiactive on mineralcorticoid receptors

83
Q

What is the MOA of cortisol on mineralcorticoid receptors ?

A

-swamping protective action of 11BHSD and act on mineral corticoid receptors
-increases Na+ and water reabsorption in distal tubules
- increase K+ and H+ efflux from the tubules, this increases K+ excretion

84
Q

What are the adverse effects of glucocorticoid action on mineralcorticoid receptors?

A

Hypertension
Oedema

85
Q

What is Cushings syndrome?

A

a collection of symptoms caused by high levels of glucocorticoid signalling

caused by high levels of cortisol/glucocorticoid drugs in the body

86
Q

List some symptoms of cushings syndrome

A

Euphoria (depression or psychotic symptoms and emotional lability)
Buffalo hump
Hypertension
Thinning skin
Thin arms and legs (muscle wasting)
Benign intracranial hypertension
Cataracts (increased glucose to brain??? cranial glucose availability?)
Moon face with red (plethoric) cheeks
increased abdominal fat
Avascular necrosis of femoral head
Easy bruising
poor wound healing

Also:
osteoporosis
tendency to hyperglycaemia
negative nitrogen balance
increased appetite
increased susceptibility to infection (immunosuppressive action; anti-inflammatory action)
obesity

87
Q

Excessive exposure to glucocorticoids can lead to _____________.

A

cushings syndrome

88
Q

Cushings syndrome can be caused by …

A

Disease: ACTH secreting pituitary gland tumour
Prolonged administration of large doses of glucocorticoid drugs (iatrogenic cushings syndrome)

89
Q

What is the treatment for cushings syndrome?

A

Decrease or withdraw use of corticosteroids

90
Q

Withdrawal of corticosteroids must be done _________. Why is this?

A

Gradually
to avoid any unwanted effects
avoid adrenal insufficiency

91
Q

Chronic glucocorticoid therapy can be described as…

A

taking a dose of 30 mg of daily hydrocortisone or equivalent for greater than/equal to 4 weeks
Negative feedback effect on CRH and ACTH
Reduction in release of ACTH
Overtime this can result in the atrophy of cortisol producing cells in the adrenal gland (zona fasciculata)

92
Q

What is the consequence of adrenal atrophy?

A

can reduce normal levels of ACTH stimulated cortisol release
this results in signs and symptoms of adrenal insufficiency

93
Q

How can you avoid adrenal insufficiency following glucocorticoid withdrawal? Why is it important to do it this way?

A

gradual tapering of dosages over a period of weeks to months prior to complete discontinuation
This is recommended to allow time for recovery of the HPA axis

94
Q

What is the treatment suggested for adrenal insufficiency?

A

Hydrocortisone (first line drug to replace cortisol); closest to cortisol
Absorbed quicker than other corticosteroids
adult daily dose of hydrocortisone is usually 15-30mg split into 2-3 doses
the highest dose is administered in the morning and the lowest in the evening to follow cortisol circardian rhythm
this enables a slow recovery to reach full adrenal function (8weeks to >18 months)

95
Q

Adrenal insufficiency can rarely but quickly lead to __________ and _________.

A

Acute adrenal insufficiency
Adrenal crisis (medical emergency)

96
Q

What are the physiological effects of an adrenal crisis?

A

coma or death if left untreated
reduce oxygen supply to brain and can lead to brain damage

97
Q

What are some symptoms of an adrenal crisis?

A

Abdominal pain
pale, cold and clammy skin
confusion
rapid, shallow breathing
dizziness
severe dehydration
fever
severe drowsiness or unconsciousness
headache
severe muscle weakness
hypotension
severe, persistent vomiting and diarrhoea

98
Q

What is the treatment of an adrenal crisis?

A

intravenous fluids
intravenous hydrocortisone

99
Q

Give some examples of conditions treated with corticosteroids

A

Adrenal insufficiecy
cerebral oedema and increased intracranial pressure (brain tumour, meningitis, trauma, cerebrovascular events)- this is because of the anti-inflammatory action of corticosteroids.
Collagen vascular diseases e.g. lupus, polymyositis, temoporar arteritis, mixed connective tissue disease synfrime
Dermatologic conditions-psoriasis, dermatitis
GI diseases- UC, crohns disease, celiac disease (immunosuppressive effect)
Haematologic diseases- malignancies, hemolytic anaemia,
Hepatic diseases- autoimmune hepatitis
MS (immunosuppresive effect)
pulmonary diseases- asthma, chronic bronchitis, aspiration pneumonia
rheumatic diseases and joint ailments- rheumatic arthritis, rheumatic carditis, osteoarthritis
Refractory shock (septic, anaphylactic)
solid tumours (breast)
tissue grafts and organ transplants

100
Q

All natural an synthetic glucocorticoids are well absorbed from the GI tract. True or false

A

true

101
Q

In what manner do glucocorticoids exist in blood plasma?

A

Protein bound
77% protein bound?
To CBG (corticosteroid binding globulin) or albumin

102
Q

How is hydrocortisone metabolised?

A

rapidly degraded in the liver by reduction
Conjugated with glucoronic acid and excreted in the urine

103
Q

What is the plasma half life of hydrocortisone?

A

1.5 hours

104
Q

The time course of the effect of hydrocortisone is not representative of plasma concentration. What doe this mean?

A

A longer duration of action ?

105
Q

What is the biological latency of hydrocortisone?

A

2-8 hours

106
Q

Many glucocorticoids in therapeutic use have different _________ and _________.

A

potency
physiochemical propertis

107
Q

What are the different routes of administration of glucocorticoids?

A

Oral
Inhaled (aerosol)
Intramuscular
Intravenous
Intra-articular (entering joint)
Topically (ointment or spray)

108
Q

What is the benefit of topical administration of glucocorticoids ?

A

Diminishes the likelihood of systemic toxic effects

109
Q

When on prolonged treatment of glucocorticoids, what manner of administration may decrease the suppression of HPA and other unwanted effects?

A

administration on alternative days

110
Q

What is the drug of choice for replacement therapy (cortisol)

A

hydrocortisone

111
Q

Cortisone is a prodrug and therefore remains inactive until converted to __________.

A

hydrocortisone

112
Q

Cortisone is uses primarily as an anti-inflammatory agent due to

A

the mineral corticoid effects
(increased BP, oedema)

113
Q

Deflazacort is a prodrug. How is it activated?

A

converted by plasma esterases into active metabolite

114
Q

Deflazacort has a similar utility to what other glucocorticoid compound?

A

Prednisolone

115
Q

What compound is the drug of choice for anti-inflammatory and immunosuppresive effects?

A

Prednisolone

116
Q

What compound is inactive until converted to prednisolone?

A

Prednisone

117
Q

What is the use of methylprednisolone?

A

immunosuppresive and anti-inflammatory effects

118
Q

What is the drug of choice for ACTH suppression ?

A

dexamethasone

119
Q

Dexamethasone is used as a potent anti-inflammatory and immuno-suppressive agent when …

A

water retention is undesirable (for instance where there is cerebral oedema)
Affinity for mineralcorticoid receptors?
Minimal sodium retention

120
Q

State the use of betamethasone

A

Anti-inflammatory and immunosuppresive agent especially where water retention is undesirable

121
Q

What is the drug of choice for mineralcorticoid effects?

A

Fludrocortisone

122
Q

Topical corticosteroids therapies are in the DPF. What can they be used for?

A

oral ulcerations

123
Q

What is an oral ulcer?

A

small, painful patch/lump inside the mouth

124
Q

Why are glucocorticoids indicated for treatment of oral ulcerations?

A

calm down immune system
help reduce pain and swelling
helping ulcers heal

125
Q

Beclomethasone is delivered by …

A

pressurised inhalation (spray)

126
Q

50ug of beclomethasone is used to treat/manage…

A

oral ulcerations

127
Q

Betamethasone are available as _______. How are they administered and what are they used to treat?

A

soluble tablets (500ug)
they can be dissolved and used as a mouthwash used to treat oral ulcerations

128
Q

Hydrocortisone is available in the DPF as…

A

1% cream
oromucosal tablets

129
Q

How are hydrocortisone oromucosal tablets administered?

A

allowed to dissolve next to the oral ulcer

130
Q

List some dental considerations for patients on long term glucocorticoid therapy

A

decreased resistance to infection
poor wound healing response
source of oral infection (carious teeth, inflammed tissue) should be promptly treated due to immunosuppression
suppressed pituitary adrenal function
schedule appointment in the morning when circulating cortisol concentrations are highest
check medical history and consult GP
a patient with adrenal insufficiency may become hypotensive under the stress of a dental visit

131
Q

How should patients on long term glucocorticoid therapy be managed in the dental practice ?

A

lay patient flat
give oxygen
transfer patient urgently to hospital
BP must be monitored and presence of osteoporosis (jaw bone and loss of tooth support)
avoid analgesics such as NSAIDs; increases risk of GI bleed (loss of prostanoid protection)

132
Q

How many interactions are listed in the BNF for hydrocortisone? Of these, how many are severe?

A

> 150
100

HHD 2 (37 decks)

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