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Pharmacology (Winter) > Adrenal Physiology & Pharmacology > Flashcards

Adrenal Physiology & Pharmacology Flashcards

1
Q

What are the adrenal hormones?

A
  • Mineralocorticoids (aldosterone) –> Zona Glomerulosa
  • Glucocorticoids (cortisol) –> Zona Fasciculata
  • Sex hormones –> Zona Reticularis
  • Epinephrine –> Adrenal Medulla
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2
Q

What is apart of the Hypothalamus-Pituitary-Adrenal Axis?

A

Hypothalamus:
1. Corticotropin-releasing hormone (CRH)

Pituitary:
2. Adrenocorticotropic hormone corticotropin (ACTH)

Adrenal:
3. Cortisol

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3
Q

What are the adrenocorticosteroid receptors?

A
  • Glucocorticoid r –> associated proteins
  • Mineralocorticoid r
  • GPCR –> 2nd messenger cascades
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4
Q

What is the role of the hypothalamus in stress response (SHORT TERM)?

A
  1. Increased HR
  2. Increased BP
  3. Liver converts glycogen to glucose & releases glucose to blood
  4. Dilation of bronchioles
  5. Changes in BF patterns leading to increased alertness & decreased digestive & kidney activity
  6. Increased metabolic rate
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5
Q

What is the role of the hypothalamus in stress response (LONG TERM)?

A

Mineralocorticoids:
1. Retention of sodium & water by kidneys

  1. Increased BV & BP

Glucocorticoids:
1. Proteins & fat converted to glucose or broken down for energy

  1. Increased blood sugar
  2. Suppression of immune system
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6
Q

What is cortisol’s rhythm?

A

a dinurnal rhythm - tapers out & is lower at bedtime & then elevates in morning when you wake up

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7
Q

What is Cortisol?

A

a Glucocorticoid

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8
Q

What are the functions of Cortisol (a Glucocorticoid)?

A
  1. Modulates carbohydrate metabolism
  2. Increased resistance to stress
  3. Alters blood cell levels in plasma
  4. Anti-inflammatory & immunosuppressive actions
  5. Affects other body-wide systems
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9
Q

How do Glucocorticoids enhance metabolism?

A

Favour gluconeogenesis
- increase AA uptake by the liver & kidneys
- more gluconeogenic enzymes

Stimulate protein catabolism & lipolysis

Glucocorticoid insufficiency may result in HYPOglycemia (particularly during stressful periods of fasting)

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10
Q

How do Glucocorticoids increase resistance to stress?

A

Provides body w/ energy to combat stress caused by fright, trauma, disease, etc.

Cause a modest rise in BP by enhancing the vasoconstrictor action of adrenergic stimuli on vessels

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11
Q

How do Glucocorticoids alter blood cell levels in plasma?

A

Decreases eosinophils, basophils, monocytes, & lymphocytes by redistributing them from the circulation to lymphoid tissue
- imp. in tx of leukemia

Increases blood levels of hemoglobin, erythrocytes, platelets

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12
Q

How do Glucocorticoids have an anti-inflammatory & immunosuppressive action?

A

*Most imp. therapeutic property of glucocorticoids

Decrease peripheral immune cells and inflammatory cytokines
* Less cytokines means decreased T-cell activation, less inflammatory cell migration, etc.

Indirect inhibition of phospholipase A2 and arachidonic acid synthesis which is needed for prostaglandin production

COX-2 synthesis is reduced

Interference with mast cell histamine release

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13
Q

What are ex’s of INCREASED transcriptional changes by glucocorticoids?

A
  • β2 adrenoreceptors
  • Anti-inflammatory cytokines (IL-10, IL-12, etc.)
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14
Q

What are ex’s of DECREASED transcriptional changes by glucocorticoids?

A
  • Proinflammatory cytokines (TNFα, IL-1, etc.) and chemokines * Inflammatory enzymes (COX-2)
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15
Q

What other system effects do Glucocorticoids have?

A

Adequate cortisol levels are needed for glomerular filtration

High levels of glucocorticoids stimulate gastric acid and pepsin production (ulcers)

Effect CNS and mental status (insomnia= short term, depression = long term)

Cortisol inhibits bone formation

Production of fetal lung surfactant
(helps maturation)

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16
Q

What are Corticosteroid pharmacokinetics?

A
  • Transcortin (plasma protein) binds about 90% of circulating cortisol
  • Hepatic metabolism
  • Renal excretion
  • T1/2 = 60-90 mins
  • Cortisol levels increased by:
  • stress
  • hypothyroidism
  • liver disease
17
Q

What is Aldosterone (a Mineralocorticoid)?

A

modulation of water balance, promotion of Na+/ K+ transport

18
Q

What are Aldosterone (a Mineralocorticoid) functions?

A
  1. promotes Na+ uptake in kidney tubular epithelial cells
  2. decreases reabsorption of K+ and causes H+ loss in urine
  3. control of water reabsorption
  4. increases blood volume and pressure
  5. secreted only during periods of stress
19
Q

What are adrenal hormones (glucocorticoids) indicated for therapeutically?

A
  • replacement therapy for adrenal insufficiency (ADDISON’S DISEASE or hypothalamic/pituitary problems)
  • arthritis
  • skin conditions
  • allergies
  • asthma
  • renal disease
  • autoimmune disease (ex: Lupus)
  • ulcerative colitis & Crohn’s Disease
  • organ transplants
  • anaemias, thrombocytopenias
  • shock (ex: septic shock)
  • cerebral edema & increased intracranial pressure
  • FETAL LUNG MATURATION (<34 WEEKS GESTATION)
20
Q

What are some diff routes of therapeutic glucocorticoids?

A
  • oral
  • intralesional
  • opthalmic
  • intravenous
  • intramuscular, inhaled, topical intranasal
  • topical
21
Q

What do Corticosteroid therapies vary in?

A

Vary in their anti-inflammatory potency, their duration of action, and the degree to which they cause sodium retention

22
Q

What is Addison’s Disease?

A

↓ secretion of glucocorticoids and sometimes aldosterone

23
Q

What are Addison’s Disease sx’s?

A
  • fatigue
  • syncope
  • G.I. upset
  • CNS effects
  • joint/muscle pain
  • hyperpigmentation(↑ACTH)
24
Q

What does Severe adrenal insufficiency (Addison’s crisis) result in?

A
  • hyponatremia
  • hyperkalemia
  • hypercalcemia
  • convulsions
  • fever
  • death
25
Q

What is the corticosteroid therapy for Addison’s Disease?

A
  • Give hydrocortisone
  • Mimic diurnal rhythm of cortisol- 2/3 in morning, 1/3 in afternoon
  • Also fludrocortisone to raise mineralocorticoid activity to normal levels
26
Q

What is the corticosteroid therapy for Fetal Lung Maturation?

A
  • Betamethasone or dexamethasone given IM to mother in 2 doses- 48 and 24 hours prior to birth
  • Increases lung surfactant production and maturation in the fetus
27
Q

What is the short-term use of exogenous glucocorticoids?

A

1) Therapeutic concentrations must exceed endogenous levels (>10 mg).

2) Single dose of glucocorticosteroid is virtually without harmful effects.

3) A few days of usage is unlikely to produce harmful effects except at extreme doses.

28
Q

What is the long-term use of exogenous glucocorticoids?

A

5) Prolongation of treatment increases the incidence of disabling or life threatening effects.

6) Corticosteroids are neither specific or curative treatment
* pathological processes continue
* clinical manifestations suppressed
* primarily useful where host response causes disease manifestations

7) Abrupt cessation of prolonged high dose treatment may induce adrenal insufficiency serious enough to be life threatening.

29
Q

What is the tx for Secondary Adrenal Insufficiency - HPA Axis Suppression?

A

Hydrocortisone replacement therapy
*Fludrocortisone is typ. NOT needed for tx of secondary adrenal insufficieny

30
Q

What are the adverse effects of glucocorticoids?

A
  • Hyperglycemia
  • Electrolyte imbalance
  • Suppression of growth, amenorrhea
  • Peptic ulcers
  • Suppression of pituitary-adrenal function (1-2 yr
    recovery → supplemental corticosteroids)

*Decrease resistance to infections (systemic & local)

*CNS effects

  • Redistribution of fat (long term therapy)
  • “moonface & buffalo hump”
  • central obesity
  • Muscle weakness and atrophy
  • Osteoporosis/osteonecrosis
  • Poor wound healing
  • Acne, hirsutism, skin thinning, hypertension
  • Cataracts
31
Q

What causes Cushing’s Syndrome?

A

Hyperadrenocorticism (produce too much Aldosterone naturally)

32
Q

What are the adverse effects of corticosteroids - Cushing’s Syndrome?

A

Cataracts

Ulcers

Skin: striae, thinning, bruising

Hypertension/ hirsutism/ hyperglycemia

Infections

Necrosis, osteonecrosis

Glycosuria

Osteoporosis, obesity

Immunosuppression

Diabetes

“CUSHINGOID”

33
Q

What are the Adrenocorticoid Antagonists?

A

Mifepristone

Spironolactone

34
Q

Mifepristone:

A

Glucocorticoid receptor antagonist

  • At HIGHER concentrations, blocks cortisol binding site on GR
  • Reduces excess cortisol effects in Cushing’s
  • At LOWER concentrations, acts as progesterone receptor antagonist
  • Inhibits prostaglandin dehydrogenase → ↑ uterine contraction
  • Used for abortion
35
Q

Spironolactone:

A

Mineralocorticoid receptor antagonist

  • Primarily used as an anti-hypertensive
  • Also treats hyperaldosteronism
  • Can cause hyperkalemia
36
Q

What are the three most important things we discussed today?

A

1) Glucocorticoids have very diverse effects on most systems of the body, but therapeutically the most important are: anti- inflammatory and immunosuppressive effects.

2) Prolonged use of systemic glucocorticoids cause adrenal atrophy and require tapered dosing of supplemental corticosteroids.

3) High levels of cortisol cause many adverse effects (CUSHINGOID)

37
Q

What are the Therapeutic Effects of Glucocortioids?

A
  • Pain relief (secondary)
  • Anti-allergy
  • Immunosuppression
  • Anti-inflammatory
  • DECREASE BV permeability
38
Q

What are the Side Effects of Glucocorticoids?

A
  • Infections
  • Myopathies
  • Osteoporosis, Aseptic necrosis of femur
  • Skin thinning
  • Hyperglycemia, weight gain, fluid retension, cushingoid appearance
  • HPA insufficiency, neuropsychiatric disorders
  • Cataracts, glaucoma
  • Hypertension

Pharmacology (Winter) (23 decks)

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