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Gastrointestinal pathophysiology > Corticoid therapy > Flashcards

Corticoid therapy Flashcards

1
Q

What is a hormone?

A

A chemical substance produced in the body that controls and regulates the activity of certain cells or organs

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2
Q

What is a steroid?

A

Any of a large group of fat-soluble organic compounds, as the sterols, bile acids, and sex hormones, most of which have specific physiological action

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3
Q

What is a mineralocorticoid?

A

A corticosteroid which is involved with maintaining the salt balance in the body, such as aldosterone

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4
Q

What is a glucocorticoid?

A

Any of a group of corticosteroids (e.g. hydrocortisone) which are involved in the metabolism of carbohydrates, proteins, and fats, and have anti-inflammatory activity

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5
Q

What are catecholamines?

A

Any of a class of aromatic amines which includes a number of neurotransmitters such as adrenaline and dopamine

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6
Q

Why does the zona reticularis have a brown-ish colour?

A

Due to the presence of lipofuscin in this region

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7
Q

Function of mineralocorticoids

A

Help maintain Na+, K+ and Cl- ion concentrations in the body
- They do this by affecting the fluid volume in the extracellular and intravascular compartments, so they play a key role in blood pressure and normal cardiac output

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8
Q

What can happen without sufficient supply of the mineralocorticoids?

A

Induction of shock due to diminished cardiac output

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9
Q

Which organ do mineralocorticoids target?

A

The kidney

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10
Q

How are mineralocorticoids produced?

A

These are the steps of transformation (1 is transformed into 2 and then 3 etc)

  1. Start point is cholesterol (lipid based molecule)
  2. Pregnenolone
  3. Progesterone
  4. 11-deoxycorticosterone
  5. Corticosterone
  6. Aldosterone
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11
Q

What are glucocorticoids?

A
  • They increase gluconeogenesis
  • They induce glycogen synthase activity & blood glucose levels
  • Act as anti-inflammatory and immunosuppressant agents in times of stress
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12
Q

What is the principal glucocorticoid?

A

Cortisol

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13
Q

What are the effects of cortisol?

A
  1. Increases the catabolism of protein in bone, skin, muscle and connective tissue
  2. Decreases cellular utilisation of glucose
  3. Increases output of glucose from the liver
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14
Q

Which organ do glucocorticoids specifically target?

A

None

- They target the whole body! Unlike mineralocorticoids which target the kidney

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15
Q

How are glucocorticoids produced?

A

These are the steps of transformation (1 is transformed into 2 and then 3 etc)

  1. Cholesterol
  2. Pregnenolone
  3. 17-a-hydroxypregnenolone
  4. 17-a-hydroxyprogesterone
  5. 11-deoxycortisol
  6. Hydrocortisone
    - Each change is associated with the side chains not the carbon backbone
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16
Q

What are androgens?

A

Hormones which influence the growth and development of the male

17
Q

What is the predominant male androgen?

A

Testosterone

18
Q

How are androgens produced?

A

These are the steps of transformation (1 is transformed into 2 and then 3 etc)

  1. Cholesterol
  2. Pregnenolone
  3. 17-a-hydroxypregnenolone
  4. Dehydroepandrosterone
  5. Androstenedione
  6. Testosterone
  7. Oestradiol
    - Changes to the side chains rather than the backbone, this is mediated by enzymes
19
Q

What is the name of the enzyme which converts cholesterol to pregnenolone? (Key step to each pathway we have discussed)

A

Cholesterol desmolase

20
Q

Why is the enzyme 21-hydroxylase important?

A
  • Its role is to convert progesterone into deoxycorticosterone (mineralocorticoid pathway) and progesterone into 11-deoxycortisol (glucocorticoid pathway)
  • It is important because it is linked to congenital adrenal hyperplasia, which is a condition present at birth, effect of this is reduction in mineralocorticoids and glucocorticoids which have multiple effects. At the same time, due to the availability of metabolites to enter the androgen pathway, there is an increase in androgen levels which leads to physical changes and early puberty etc…
21
Q

What are the two types of congenital adrenal hyperplasia?

A
  1. MOST COMMON = Salt wasting. This is due to decrease in aldosterone levels
  2. Simple virilisation = where aldosterone levels are normal but decrease in glucocorticoid and increases in androgen levels
22
Q

How is glucocorticoid production controlled?

A
  1. Hypothalamus detects low glucocorticoid level
  2. Causes synthesis and release of CRH to act on the anterior pituitary where it causes release of ACTH
  3. ACTH acts on the adrenal cortex to cause release of glucocorticoids/cortisol
  4. Increased glucocorticoid level will be recognised by the hypothalamus and causes a negative feedback loop, whereby release of CRH is now reduced
  5. The cortisol will have metabolic/anti-inflammatory/immunosuppressive effects
23
Q

Mechanism of glucocorticoids

A
  • They are able to pass through the lipid bilayer
  • So they bind to their receptor in the cytoplasm
  • Now bound, this complex translocates to the nucleus and binds to GRE on DNA and alter gene expression
  • They will transactivate anti-inflammatory genes and transrepress pro-inflammatory genes
24
Q

Clinical use of glucocorticoids - physiological doses vs pharmacological doses (what do we use them for in each setting)

A

Physiological doses: SMALL REPLACEMENT DOSE

  • Replacement therapy in adrenal failure: Addison’s disease
  • Anti-inflammatory: asthma, arthritis, skin, shock

Pharmacological doses: SUPER PHYSIOLOGICAL DOSE

  • Rheumatoid arthritis (dexamethasone)
  • Organ transplantation (prednisolone)
  • Cancer treatment
  • End of life care
25
Q

What is the effect of synthetic steroids? (Adverse effects of glucocorticoid therapy)

A
  • N.B revisit the HPA axis (hypothalamus –> ant. pituitary –> adrenal cortex –> glucocorticoid release –> neg feedback loop)
  • Synthetic steroids will feedback onto the HPA axis, and so will reduce the natural steroid production by reducing CRH level

^ Means that there will be multiple outcomes/adverse effects of glucocorticoid therapy:

  1. Suppression of endogenous glucocorticoids
    - The adrenal gland may undergo atrophy as it is no longer producing the amount of corticosteroid it once used to, due to the external addition of steroids to the patient which induces the neg feedback loop.
    - This means that if the patient needs to produce steroids (once they stop taking glucocorticoids), they may not be able to do so effectively
  2. Suppression of response to infection
    - Can get local immunosuppression associated with inhaled steroids (oral thrush)
    - Also associated with formation of dysphonia
  3. If taken systemically, this can lead to significant side-effects such as Cushing’s syndrome
26
Q

Additional unwanted side-effects of Cushing’s syndrome (in addition to the normal side effects)

A
  1. Hypertension
  2. LV hypertrophy (cardiac remodelling)
  3. Cardiac arrhythmias
  4. Vascular atherosclerosis (due to glucose tolerance)
  5. Thrombosis diathesis
27
Q

How to prevent adrenal insufficiency?

A

Replacement hydrocortisone therapy which is reduced overtime

28
Q

What are the symptoms of secondary adrenal insufficiency? (as a consequence of long term oral steroid treatment which is not reduced over time before stopping)

A

Fatigue
Nausea
Muscle weakness
Weight loss

29
Q

How does Ang II influence mineralocorticoid production?

A
  1. Elevates cholesterol desmolase activity to drive conversion of cholesterol into pregnenolone
  2. Elevates the enzyme which converts corticosterone into aldosterone
30
Q

Mechanism of mineralocorticoids/aldosterone

A
  1. Binds to mineralocorticoid receptor inside the cell
  2. Receptor moves to the nucleus to drive gene expression
  3. Cell produces new SODIUM channels
  4. Channels are transported to the surface to increase sodium uptake and therefore water will follow
  • Spironolactone inhibits the mineralocorticoid receptor
  • Amiloride inhibits the sodium channels
31
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism AKA mineralocorticoid excess

32
Q

What is Conn’s syndrome caused by?

A
  • Caused by a benign tumour on the adrenal gland (adenoma)
  • Less commonly caused by adrenal cancer or hyperplasia
    The adrenal gland making too much aldosterone which leads to hypertension and low blood K+ levels

Gastrointestinal pathophysiology (22 decks)

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