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Human Diseases > 4.2 Adrenal steroids > Flashcards

4.2 Adrenal steroids Flashcards

1
Q

What is the outside and inside of the adrenal gland called?

A

Outisde = adrenal cortex
Inside = adrenal medulla

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2
Q

The adrenal cortex is under the control of what?

A

The anterior pituitary gland

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3
Q

Name the 3 morphologically distinct zones of the adrenal cortex from the most external to most internal.

A
  • Zona Glomerulosa (mineralocorticoids)
  • Zona Fasciculata (glucocorticoids)
  • Zona Reticularis (gondocorticoids)
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4
Q

What causes the cortex to have these 3 distinct zones?

A

Presence of different enzymes.

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5
Q

Name a mineralocorticoid.

A

Aldosterone

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6
Q

Name a glucocorticoid.

A

Cortisol

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7
Q

All of the hormones produced by the adrenal cortex are ……. hormones.

A

Steroid hormones

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8
Q

Synthesis of these steroid hormones are under the control of which family of enzymes?

A

The P450 superfamily of enzymes.
Most diseases caused by a deficiency in steroid hormones are caused by an enzyme deficiency.

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9
Q

What are the 2 effects of enzyme deficiency?

A
  • Steroid hormone deficiency
  • Excess precursor compounds (used in diagnostic testing)
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10
Q

Which enzyme is crucial in the conversion of cholesterol to an adrenal steroid?

A

Cholesterol desmolase

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11
Q

What regulates cholesterol desmolase activity?

A

Cholesterol desmolase activity is tightly regulated by ACTH and angiotensin II.

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12
Q

Are steroid hormones stored in vesicles?

A

No, as they are derived from cholesterol they are highly lipophilic so cannot be stored in vesicles.

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13
Q

Where does adrenal steroid synthesis occur?

A

In the mitochondria, some later steroids form in the endoplasmic reticulum.

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14
Q

Describe the action of adrenal steroid hormones.

A

Work at the level of gene expression.
Typically act through modifying gene transcription.

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15
Q

What effect does it have that adrenal steroids work at the level of gene expression?

A
  • Means that the pharmacodynamic effects are much longer than the pharmacokinetics of the drug
  • Means that there is a latency period between drug administration and seeing physiological effects
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16
Q

Where are adrenal steroids metabolised?

A

In the liver (heaptic metabolism)

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17
Q

What occurs after adrenal steroids are metabolised?

A

They undergo conjugation with glucuronic acid or sulphates and are excreted through urine.

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18
Q

What are the potential targets of pharmacological drugs in steroid action?

A
  • The secretagogue: similar action to the hormone itself. Can create agonists which mimic the action of hormones, or antagonists which can block the effect of hormones.
  • The enzymes required for synthesis of hormones.
  • Deliver the hormone itself.
  • Drugs to target the drug receptor, or a co-factor for the target receptor.
19
Q

Which enzyme controls the conversion of pre-aldosterone to aldosterone?

A

Aldosterone synthase

20
Q

Where does the conversion of pre-aldosterone to aldosterone occur?

A

In the Zona Glomerulosa

21
Q

How are patients with low aldosterone treated?

A
  • Excessive salt and water replacement
  • Delivery of exogenous mineralocorticoids
22
Q

Describe the actions/functions of aldosterone.

A
  • Maintains sodium/potassium balance
  • Regulates ECF volume, in turn regulates BP
  • Minor role in regulating acid/base balance through H+/K+ exchange
  • Some role in repairing tissue damage
23
Q

What are the main secretagogues involved in increasing aldosterone synthase?

A
  • Angiotensin II
  • Extracellular potassium concentration (higher K = higher aldosterone)
  • ACTH
  • Paracrine factors
24
Q

What is familial hyperaldosteronism I?

A

A genetic condition
- Gene mutation causes excess aldosterone
- Leads to hypertension
- Treated with glucocorticoids to suppress ACTH

25
Q

What is familial hyperaldosteronism II?

A

A genetic condition
- Causes pt to have large adrenal glands and high aldosterone secretion
- Treated surgically

26
Q

What are the 2 other causes of hypertension related to aldosterone?

A
  • Adenoma (benign tumour of the adrenal gland)
  • Adrenal cortex carcinoma (rare)
27
Q

Which drugs are used to treat primary and secondary hyperaldosteronism?

A

Aldosterone antagonists aka Diuretics
- Spironolactone
- Eplerenone

These drugs reduce aldosterone concentrations.

28
Q

What is cortisol also known as?

A

Hydrocortisone

29
Q

Describe glucocorticoid biosynthesis.

A
  • Anterior pituitary releases ACTH which influences amount of synthesis of adrenal hormones
  • 11 beta hydroxylase is the important enzyme in the conversion of cholesterol to cortisol
30
Q

What are the effects of excessive ACTH?

A
  • Increased beta MSH
  • Causes excessive pigmentation (dark mucosa)
31
Q

Describe the metabolic actions of glucocorticoids.

A
  • Stimulates gluconeogenesis
  • Mobilises AAs from proteins in liver and muscle
  • Decreases cellular utilisation of glucose
  • Mobilise fatty acids
32
Q

Describe the role of glucocorticoids in stress and inflammation modulation.

A
  • Maintain a low level of anti-inflammatory tone
  • Used at high doses pharmacologically to inhibit a wide range of inflammatory functions through acting on cytoplasmic receptors
33
Q

How are glucocorticoids used clinically?

A
  • Used as an anti-inflammatory to treat asthma, connective tissue disorders, hypersensitivity reactions etc.
  • Used for immunosuppression
  • Used to treat people with Addison’s disease in adrenal failure
  • Oncology: used in combination with cytotoxic drugs to target cancer cells
34
Q

What does excess cortisol lead to?

A

Cushing’s syndrome

35
Q

What are the signs and symptoms of Cushing’s syndrome?

A
  • Hypomania (emotional changes, euphoric)
  • Increased abdominal fat
  • Decreased muscle mass
  • Poor wound healing, bruise easily
  • Hypertension
  • Buffalo hump
  • Round face with red cheeks
  • Bone thinning, increased risk of osteoporosis
36
Q

Name 3 things that can cause Cushing’s syndrome.

A
  • Cushing’s disease: excessive pituitary ACTH
  • Excess cortisol: most common cause, iatrogenic, e.g. excessive exogenous steroids for extended periods of time
  • Ectopic ACTH: extra-adrenal tumours e.g. types of lung cancer
37
Q

Describe the early side effects of glucorticoids.

A
  • Emotional changes
  • Insomnia
  • Increased appetitie/weight gain
38
Q

Describe the medium side effects of glucorticoids.

A
  • Osteonecrosis
  • Infections
  • Delayed wound healing
  • Myopathy
  • Cushingoid features
39
Q

Describe the late side effects of glucorticoids.

A
  • Osteoporosis
  • Cataracts
  • Skin atrophy
  • Atherosclerosis
  • Fatty liver
  • Growth retardation
40
Q

Give examples of common adrenal steroid drugs used therapeutically.

A
  • Prednisolone: glucocorticoid used for its inflammatory effects.
  • Dexamethasone: potent glucocorticoid. Can have more severe side effects than prednisolone so used in select circumstances.
  • Fludrocortisone: some anti-inflammatory effects. Not as effective as aldosterone as a mineralocorticoid.
41
Q

What is adrenal insufficiency/adrenal crisis?

A

A medical emergency causing hypotension, dizziness, abdominal pain, potential loss of consciousness.
Can be fatal.
Management in dental practice:
- Lay patient flat
- Give oxygen 15 litres per min
- Call 999
- 100mg IM hydrocortisone

42
Q

Why may adrenal insufficiency occur?

A

Main cause is glucocorticoid withdrawal.
When people have been on long term corticosteroid therapy e.g. prednisolone and stop their use.
Patient may seem healthy until stress is introduced e.g. surgery or infection.

Can also be caused by pituitary failure or adrenal failure.

43
Q

Describe Addison’s disease.

A
  • Caused by adrenal or pituitary gland damage or autoimmune destruction of adrenal cortex
  • Low coritsol, low androgens, low aldosterone
  • Pigmented mucosal membranes
44
Q

Does Addison’s cause increased or decreased ACTH?

A

Increased

Human Diseases (47 decks)

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