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BLOCK B - RESPIRATION > Pharmacology - Corticosteroids > Flashcards

Pharmacology - Corticosteroids Flashcards

1
Q

Why can’t we abruptly stop administering corticosteroid drugs to a patient?

A
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2
Q

Endocrine glands function

A

Making and secreting hormones

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3
Q

What are hormones?

A

Chemical messengers made in one organ (cell) that travel via the bloodstream to affect the activity of other organs (cells).

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4
Q

Name the main components of the endocrine system

A
  • pineal gland
  • hypothalamus
  • pituitary gland
  • thyroid gland
  • thymus
  • pancreas
  • adrenal glands
  • testes/ovaries
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5
Q

Many but not all endocrine glands are controlled by the brain. Describe this process

A

Hypothalamus - portal vein - pituitary (Add!!!)

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6
Q

Describe the pituitary (hypophyseal) portal system

A

Anterior pituitary (adenhypophysis)
Posterior pituitary (neurohypophysis) - brain matter

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7
Q

What happens at the median eminance

A

Peptides are released on the primary capillary plexus and travels to the anterior pituitary gland

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8
Q

What are hypothalamic pituitary (HPA) target organ axes?

A

Hypothalamus releases peptides that stimulate the anterior pituitary, which itself releases peptides that stimulates endocrine glands to produce steroid or steroid-like hormones, whoch will feed back on the pituitary and hypothalamus.

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9
Q

WHat is the paraventricular nucleus?

A

?? makes and secretes a hormone called CRH (corticotropin releasing hormone)

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10
Q

What does CRH do?

A

CRH stimulates the corticotrope cell, which will start producing ACTH

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11
Q

What does ACTH do?

A

?

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12
Q

Descrie the two types ofregulation in the HPA axis?

A
  • can be regulated by circadian rhythm
  • can be regulated by stress ( psychological, physical, emotional, cold exposure, hypoglycemia, pain)
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13
Q

Describe circadian regulation of the HPA axis

A

Morning:
Afternoon:

As you decrease glucose levels s you go through the day…???

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14
Q

How are hormones released?
a) continuously
b) in pulses

A

b) in pulses

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15
Q

ACTH is a type of…

A

glucocorticoid

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16
Q

What is CRH? Where is it expressed? How is it produced?

A

Corticotropin-releasing hormone
- Expressed in paraventricular nucleus (PVN) of the hypothalamus
- CRH gene encodes 196 amino acid pre-pro-CRH
- C-terminal 41 amino acids encode CRH
- CRH neurons in PVN project to median eminance
- stimulates synthesis/secretion of ACTH by pituitary corticotrope cells

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17
Q

What type of cell releases ACTH?

A

Pituitary corticotrope cells

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18
Q

Where is CRH released?

A

From the paraventricular nucleus (PVN)

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19
Q

What is ACTH? Where and how is it produced?

A

Adrenocorticotropic hormone
- corticotropin
- produced in pituitary corticotropes
- produced as a 39. a.a. peptide derived from the pro-opiomelanocortin (POMC) precursosr (cleaved by prohormone convertase 1)

20
Q

After ACTH enters systemic circulation, where does it bind?

A

??? receptor on the adrenal gland

21
Q

Describe the outside and inside of the adrenal gland

A

Cortex: outside layer
Medulla: inside layer (where epinephrine is released)

22
Q

Name the three types of adrenocortical steroids (corticosteroids)

A
  • mineralocorticoids (e.g. aldosterone)
  • glucocorticoids (e.g. cortisol, corticosterone)
  • androgens (e.g. DHEA)
23
Q

Describe mineralocorticoids

A
24
Q

Describe glucocorticoids

A
25
Q

Describe androgens

A
26
Q

All steroids are derived from a precursor molecule called…

A

cholesterol (different enzymes and pathways will convert it into various end products (classes of steroids), like aldosterone, testosterone, estradiol)

27
Q

Describe the mechanisms of ACTH stimulated cortisol synthesis. What is the rate limiting step?

A

Rate limiting step: movement of steroids from outside to the inside of mitochondria

  1. Cholesterol enters the mitochondria
  2. Cholesterol is converted to pregnenolone
    3…..
28
Q

What are the functions of glucocorticoids ?

A

Pleiotropic effects
- inhibit CRH and POMC/ACTH synthesis and secretion (negative feedback)
- Maintain blood glucose (esp. in a fasted state)
- Mobilize amino acids from extrahepatic sources
- Stimulate lypolysis in adipose tissue (increased FA and glycerol release)
- Catabolic and anti-anabolic effects in bone
- Inhibit immune function
- Inhibit inflammation

29
Q

What are the therapeutic effects of glucocoricoids (administered as drugs). What are the side effects?

A
30
Q

Describe glucocorticoid receptors

A
  • Part of the nuclear receptor superfamily
  • Two types: Mineralocorticoid receptor (MR) and Glucocorticoid receptor
  • …
31
Q

Describe the basic structure of nuclear receptors

A
32
Q

Where are hydrophobic molecules buried?

A
33
Q

Describe glucocorticoid action

A

Hydrophobic molecules cross the membrane… dimerization of receptors
Dimers move to the nucleus and interact with the DNA via their DNA-binding domain to alter transcription

34
Q

What are the primary uses of glucocorticoid analogues (clinically)?

A
  • To treat adrenal insufficiency (e.g. Addison’s disease)
  • Anti-inflammation (e.g. asthma, COPD)
  • Immunosuppression
  • Adjuvant to chemotherapy
  • Lung development
35
Q

Describe the differences between primary, secondary and tertiary insufficiency

A

Primary: adrenal disorder

Secondary: pituitary disorder

Tertiary: hypothalamic disorder

36
Q

What is Addison’s disease?

A
  • Primary adrenal insufficiency
  • Relatively rare (prevalence 40-6 per 1,000,000)
37
Q

What are the symptoms of Addison’s disease?

A
  • muscular weakness
  • low blood pressure
  • depression
  • weight loss
  • hyperpigmentation
  • hypoglycemia
38
Q

What is the etiology of Addison’s disease? How is it treated

A

autoimmune (autoimmune system is attacking an enzyme involved in the production ogf?)

Treatment:

39
Q

Describe some anti-inflammatory uses of glucocrticoids?

A
  • rheumatoid arthritis
  • …
40
Q

Because of the brad distribution of the glucocrticoid receptors, the ….?? (anti-inflammatory actions of corticosteroids in asthma)

Why are these drugs so potent at anti0inflammation

A
41
Q

Corticosteroids can increase beta-2 receptors which…

A
42
Q

What are the toxic (side) effects of glucocorticoids?

A
  • impacted glucose utilization
  • induction of siabetic state
  • redistribution of fat
  • osteoporosis
  • impaired wound healing
  • adrenal insufficiency
  • iatrogenoc Cushing’s syndrome
43
Q

What is Addison’s crisis?

A
44
Q

What is iatrogenic Cushing’s syndrome?

A
45
Q

What are symptoms of Cushing’s syndrome?

A
  • thin arms and legs
  • increased fat in face, trunk, across shoulder b;lades, base of the neck
  • moon face (swollen face)
  • thinning and reddening of skin
46
Q

What are the causes of Cushing’s syndrome?

A
  • Prolonged exposure to GCs (e.g. during treatment of asthma, arthritis, lupus…)
  • Pituitary adenomas (Cushing’s disease)
  • Ectopic ACTH syndrome
  • Adrenal adenomas (or carcinomas)

BLOCK B - RESPIRATION (31 decks)

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