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PMCOL 200 Final > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

What are the two parts of the Adrenal Gland

A

Medulla

Cortext

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2
Q

What is the adrenal gland

A

Apex of kidney

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3
Q

What does the medulla produce

A

Adrenaline

Catecholamine / amino acid hormone

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4
Q

What does the cortex produce

A

Steroid hormones

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5
Q

Layers of the Cortex

A

Zona Glomerulosa
Zona Fasciculata
Zona Reticularis

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6
Q

Mineralocorticoids
- Function
- Example
- Produced Where

A

Mediate Salt balance
Ex. Aldosterone

Produced by Zona Glomerulosa

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7
Q

Glucocorticoids
- Function
- Example
- Produced Where

A

Metabolic (how body uses sugars) and immune effects
Ex. Cortisol

Zona Fasciculata

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8
Q

Androgens
- Function
- Example
- Produced Where

A

Precursors for strong androgens
Responsible for sex hormones like
Testosterone and
Estrogens
Ex. DHEA

Zona Retucularis

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9
Q

What does HPA Axis control

A

Cortisol release from Zona Fasciculata

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10
Q

Describe main pathway of HPA Axis

A

Hypothalamus controls synthesis of Corticotropin Releasing Factors (CRF/CRH), hormones which controls ACTH production by the anterior pituitary

ACTH (Anterior Pituitary) stimulates steroid production, cortisol in synthesized in the adrenal cortex

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11
Q

Describe Negative Feedback in the HPA Axis

A

Cortisol has a negative feedback on
CRH production (Hypothalamus)
ACTH (Anterior Pituitary)

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12
Q

Why is cortisol important

A

Suppresses stress response and acts on glucocorticoid tissues, catabolism, and immuno surpression

Lack of cortisol can causes hyperproduction of certain products

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13
Q

What is Aldosterone

A

Mineralocorticoid Response

Targets kidneys promoting Na+/Water reabsorption and K+ excretion

Increases blood volume and pressure

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14
Q

Describe the generalized mechanism of steroid hormone action

A

Steroid hormone diffuses into plasma membrane

Cytoplasmic unliganded receptor forms a complex with Hsp90

Hormone binds to cytoplasmic receptor, dissociates from Hsp
Forms a Steroid-receptor dimer (activated state)

Dimerized receptors interact with DNA and influence transcription of target genes: Glucocorticoid receptors

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15
Q

Define spectrum in the context of steroids

A

Drugs can be designed to have different affinities for Glucocorticoid receptors or Mineralocorticoids receptors

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16
Q

What are glucocorticoid target tissues

A

Adipose (body fat), muscle, liver

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17
Q

What kind of steroid do glucocorticoid target tissues express

A

11beta-hydroxysteroid dehydrogenase, type 1

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18
Q

What does 11beta-hydroxysteroid dehydrogenase, type 1 do?

A

Activates Cortisol

Converts cortisone to Cortisol (Type 1)
Ketone to Alcohol group

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19
Q

What causes corticosteroid specificity

A

Affinity of compound/receptor and metabolism in target tissues

20
Q

Prednisone

A

Prodrug

Orally taken and metabolized to prednisolone in the liver and in important glucocorticoid target tissues

21
Q

Prednisolone

A

Strong topical effect (applied on skin)

Active form of prednisone

22
Q

What does cortisol activate

A

Glucocorticoid receptors
Mineralocorticoid receptors

23
Q

What weak effect does cortisol have

A

Weak mineralocorticoid effects in vivo

24
Q

What does 11beta-hydroxysteroid dehydrogenase, type 2 do?

A

Inactivates Cortisol

Converts Cortisol to Cortisone
Alcohol to Ketone group

25
Q

What is Pseudohyperaldosteronism

A

Excess cortisol can have an effect on aldosterone target tissues (kindeys), increasing blood pressure through water/Na+ reabsorption

Licorice contains an inhibitor of 11beta-hydroxysteroid dehydrogenase, type 2. Preventing inactivation of cortisol

26
Q

How does Pseudohyperaldosteronism occur

A

Licorice contains an inhibitor of 11beta-hydroxysteroid dehydrogenase, type 2. Preventing inactivation of cortisol

27
Q

What is Apparent Minceralocorticoid Exess

A

Looks like an excess of mineralocorticoid but isn’t

Caused by mutations to 11beta hydroxysteroid dehydrogenase, type 2 gene
Inhibits conversion of cortisol to cortisone
Cortisol then acts act aldosterone tissue

28
Q

Glucocorticoid effect on Carbohydrate Metabolism

A

Increases circulating glucose

29
Q

Effect of Glucocorticoid on Fat/Lipid Balance

A

Catabolic breakdown of fat
Loss of muscle and bone mass in limbs
Fat accumulation in viscera and trunk
(Skinny Fat)

30
Q

Describe pathway of glucocorticoid effects (Initial)

A

Food is consumed, calories are transferred to selected sites (Adipose Tissues)

Adipose Tissues: Triglycerides are broken down by lipolytic hormones into free fatty acids
(Short term loss of fat)
(High insulin from desensitization to glucose spike)

31
Q

Describe pathway of glucocorticoid effects (Liver)

A

Glucose inhibits insulin production in muscles

Muscle proteins are broken down to form amino acids which are carried to the liver to be used as glucose precursors

Glucose is formed and is used to inhibit insulin in adipose tissue

32
Q

Cyclooxygenase-2 function and role

A

COX-2 is an inflammatory mediator

Arachidonic acid conversion to different prostanoids depending on cell type (Prostaglandins and Thromboxane)

33
Q

Glucocorticoids relationship with COX-2

A

Glucocorticoids suppress transcription of the COX-2 gene

34
Q

What are the effects of inhibiting COX-2

A

Affects all downstream products like

PGI2,TXA2
PGF2, PGD2, PGE2

35
Q

What is Annexin A1

A

Lipocortin/Annexin with very powerful and broad anti-inflammatory effects

Effects are very early in inflammatory response

36
Q

What are the two effects of Annexin A1

A
  1. Directly effecting Leukocytes and inhibiting their ability to infiltrate tissue
  2. Suppressing phospholipase A2 activity, prevents formation of arachidonic acid, thus, preventing all downstream prostanoids
37
Q

What is Addison’s Disease
Symptoms

A

Insufficient glucocorticoid production (and often mineralocorticoids)

Lack of glucose causes fatigue, salt + sugar balance issues, skin discolouration

38
Q

How is Addison’s Disease treated

A

Hydrocortisone
Glucocorticoid / Mineralocorticoid
supplements can treat hormone deficiency

39
Q

What is Cushing’s Syndrome
Symptoms

A

Excessive cortisol from adrenal overactivity

Round face and fat deposition in trunk
Muscle loss and osteoporosis (Protein and bone catabolism)
Resembles side effects of therapeutic doses of GCs

40
Q

What causes Cushing’s Syndrome

A

Adrenal Tumours (Produces cortisol)
Pituitary Tumours (Produces ACTH, stimulates adrenal cortex)
Drug-Induced (High dose GC)
Ectopic Tumour (Produces ACTH, stimulate adrenal cortex)

41
Q

How is Cushing’s Syndrome treated

A

Resection of adrenal / pituitary tumours

Adjustment of doses of cortisol

42
Q

Side Effects of Synthetic Glucocorticoids

A

Metabolic: Glucose produces high blood sugar - Hyperglycemia

Immunosuppressive

Catabolic: Osteoporosis, muscle wasting

Anti-Inflammatory: Affects cell division, slow wound healing, ulcerations

Hypertension caused by non-specific MC effects of GCs

Psychosis: Especially in elderly

43
Q

Why should Glucocorticoid treatments not be stopped abruptly

A

GC acts as cortisol and negatively inhibits ACTH and CRH production. Body grows dependent on GC and can’t make its own cortisol

Body needs time to synthesize its own cortisol

44
Q

Effects of abruptly stopping GC treatment

A

Addisonian Crisis:
Hypoglycemia (Low Glucose)
Hyponatremia (Low Sodium)
Hyperkalemia (High Potassium)

45
Q

What is Tapering Treatment

A

Slowly reducing a treatment to prevent an abrupt stop
Used in stopping long term glucocorticoid
treatments

PMCOL 200 Final (5 decks)

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