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Pharmacology CP > Pharmacology of Steroids > Flashcards

Pharmacology of Steroids Flashcards

1
Q

What are the two types of steroids?

A
  • Non-hormonal

- Hormonal steroids

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2
Q

What are non-hormonal steroids?

A
  • Cholesterol: important in atherogenesis (CV disease)
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3
Q

What are corticosteroids?

A
  • Steroid hormones from adrenal cortex
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4
Q

What are the two types of corticosteroids?

A
  • Glucocorticoids

- Mineralocorticoids

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5
Q

What is the function of glucocorticoids?

A
  • Metabolic and anti-inflammatory functions like asthma

- E.g. cortisol

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6
Q

What is the function of mineralocorticoids?

A
  • Renal regulation of electrolytes and ater

- E.g Aldosterone

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7
Q

What are the endocrine glands?

A
  • Pituitary glands
  • Thyroid gland
  • Thymus
  • Adrenal glans
  • Pancreas
  • Ovary
  • Testis
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8
Q

What is the function of the pituitary gland?

A
  • Regulation of vital body functions, e.g. temperature
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9
Q

What is the function of thyroid gland?

A
  • Produces thyroid hormones that regulate body’s metabolism
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10
Q

What is the function of thymus?

A
  • Development of T-lymphocytes
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11
Q

What is the function of adrenal gland?

A
  • On top of kidneys

- Produce adrenaline

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12
Q

What is the function of pancreas?

A
  • Insulin secretion

- Maintenance of blood sugar

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13
Q

What are the 4 zones of hormone synthesis in the adrenal glands and what do they synthesise?

A
  • Zona glomerulosa- mineralcoricoids
  • Zona fasciculata- glucocorticoids
  • Zona reticularis- androgens
  • Adrenal medulla- catecholamines (Adrenaline not steroids)
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14
Q

What is cholesterol?

A
  • Precursor of all glucocorticoids, mineralocorticoids and sex hormones
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15
Q

What is the function of cholesterol?

A
  • Vital physiological role in regulating fluidity and function of phospholipid bilayer membranes in all cells
  • Makes membrane less deformable and less water-permeable
  • Means no cell wall is necessary in animals
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16
Q

How is cholesterol derived?

A
  • From diet

- Or synthesised in hepatocytes by hydroxy-methyl-glutaryl (HMG) CoA reductase

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17
Q

How is cholesterol transported between liver and tissues?

A
  • Lipoproteins
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18
Q

What are lipoproteins?

A
  • Not cells
  • Inside- triglycerides (fatty inside)
  • Single phospholipid as the inside is lipid-friendly
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19
Q

What is the name for lipoproteins without lipids?

A
  • Apolipoprotein
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20
Q

What are LDLs?

A
  • Low density lipoproteins
21
Q

What is the danger in excess LDL?

A
  • Excess LDL deposits cholesterol in fatty plaques (Atheroma) leading to CAD
  • Clogging underneath blood vessels
22
Q

How can you prevent the build up of plaques in vessels?

A
  • Statins

- Drugs that inhibit enzyme making cholesterol

23
Q

What are the effects of corticosteroids?

A
  • Survival hormones

- Prepares body for starvation/dehydration

24
Q

How do corticosteroids prepare the body for starvation?

A
  • Mobilising energy storage (first glucose, then fat, then protein)
  • Glycogen, fat stores, protein from bones/muscles
  • Inflammatory response is also suppressed
25
Q

How do corticosteroids conserve water?

A
  • Reduce urine production
  • Retain sodium = retain water
  • Mineralocorticoid action
26
Q

What are the main actions of glucocorticosteroids?

A
  • Metabolic- mobilising nutrients (Catabolism)- although this is unwanted
  • Anti-inflammatory
27
Q

Give examples of synthetic GCS drugs

A
  • Developed to supplement endogenous cortisol in combatting chronic inflammatory disease
  • Prenisolone and dexamethasone for systemic GCS, like arthritis
  • Betamethasone- topical GCS, e.g. eczema
  • Fluticasone- inhaled GCS, e.g. asthma
28
Q

What is the HPA axis?

A

Stress shock –> hypothalamus –> anterior pituitary –> ACTH (through blood) –> adrenal cortex –>

29
Q

What is ACTH?

A

adrenocorticotrophic hormone

30
Q

What are the catabolic effects of the HPA axis?

A
  • Preparation for a period of stavation
  • Hyperglycaemia
  • Mobilisation of lipids
  • Breakdown of proteins
31
Q

What are the anti-inflammatory effects?

A
  • Decreased leucocyte activity

- Decreased inflammatory mediators

32
Q

Describe negative feedback in the HPA axis

A
  • Increased cortisol leads to ACTH –> hypothalamus to reduce
  • Increased cortisol–> x pituitary gland –> x hypothalamus
33
Q

Describe the use of synthetic drugs in the HPA axis

A
  • Exogenous GCS- mimic cortisol
  • Anti-inflammatory mediators
  • Feedback pituitary/hypothalamus
  • Atrophy of hypothalamus
  • Drugs cannot be stopped abruptly if taken for a long period of time
  • Long periods of dosage required
  • Slow withdrawal required to allow HPA axis to recover
  • Reduce systemic metabolic effect
34
Q

Outline the mechanisms of action for GCS

A
  • Binds to cytoplasmic receptors and modulates transcription of hundreds of inflammatory genes
  • GCS blocks transcription of pro-inflammatory genes and induces anti-inflammatory genes
35
Q

How does GCS block the transcription of pro-inflammatory genes?

A
  • Cycloxygenase-2 (source of prostaglandin)
  • Adhesion molecules (ICAM)
  • Complement components, immunoglobulins (IgG, IgE)
  • Cytokines (TNF-α, GM-CSF, interleukins)
36
Q

How does GCS induce anti-inflammatory genes?

A
  • Ribonucleases (break down inflammatory mRNAs)

- Interleukin-10, annexin-1

37
Q

What are the consequences of GCS mechanism of action?

A
  • Effects are slow in onset
  • ->Reducing oedema- 2-6 hours
  • ->Suppressing cytokines 6-18 hours
  • -> Inhibiting leukocytes
  • Effects are slow in offset- might take days
  • More broad spectrum
38
Q

What are some clinical uses for glucocorticoid drugs?

A
  • Anti-inflammatory/ immunosuppressant therapy

- Asthma, allergy, rheumatoid arthritis, inflammatory bowel disease, after organ transplant, cerebral oedema

39
Q

What are the consequences of overuse of synthetic glucocorticoid?

A
  • Excessive production of cortisol
  • Cushing’s disease
  • Inhibited by metrapone
40
Q

What are the signs of Cushing’s disease?

A
  • Euphoria
  • ‘Buffalo’ hump
  • Hypertension
  • Thinning of skin
  • Thin arms and legs
    Cataracts
  • Moon face with red (plethoric) cheeks
  • Increased abdominal fat
  • Easy bruising
  • Poor wound healing
41
Q

How do exogenous GCS suppress HPA axis?

A
  • CNS stress, shock and pain
  • Hypothalamus
  • Corticotrophin releasing factor
  • Anterior pituitary
  • ACTH to adrenal glands
  • Release of cortisol to reduce hypothalamus function
42
Q

What type of therapy reduces hypothalamus function?

A
  • Prednisolone therapy
43
Q

What is the main endogenous mineralocorticoid?

A
  • Aldosterone
44
Q

Where is aldosterone released from and what triggers it?

A
  • Release from zone glomerulosa

- Triggered by low plasma sodium and indirectly by renin-angiotensin system

45
Q

Where do mineralocorticoids act?

A
  • Mineralocorticoid receptor
  • Present mainly in cytoplasm of kidney tubule epithelial cells
  • Fluid can go to bladder or reabsorption
46
Q

What does aldosterone detect and do?

A
  • Detects low volume
  • Increases gene transcription of epithelial Na+ channels (ENac)
  • Increases Na+ an water reabsorption across luminal membrane into blood
  • K+ and H+ secreted in urine
47
Q

Give an example of an MR agonist and its use

A
  • Fludrocortisone

- Used as replacement therapy in adrenal insufficiency (Addison’s disease)

48
Q

Give an example of a competitive MR antagonist

A
  • Spironolactone
  • Diuretic and K+ sparing actions
  • Used with other diuretics to reduce blood volume (e.g. in hypertension) while preventing hypokalaemia
  • Used in hyperaldosternoism (Conn’s syndrome)

Pharmacology CP (11 decks)

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