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Pharmacology: Exam 3 > Lecture 7: Adrenocortocosteroids > Flashcards

Lecture 7: Adrenocortocosteroids Flashcards

1
Q

List drugs for each class:
Glucocorticoids (3):
Mineralocorticoids (1):
Anti-glucocorticoids (1):

A
  • Glucocorticoids: Prednisone, Triamcinolone, Dexamethasone
  • Mineralocorticoid: Fludrocortisone
  • Anti-glucocorticoids: Ketoconazole
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2
Q

What were the effects of giving Dexamethasone to Covid 19 patients?

A
  • Effective Ventilator: Severe Covid
  • No Effective when no O2 was received: Mild Covid
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3
Q

What was the conclusion about giving corticosteroids to brain trauma patients?

A

DO NOT GIVE GLUCOCORTICOID

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4
Q

What are the risk factors for corticosteroid usage (4)?

A
  • increase sepsis
  • Increase chance of blood clots
  • Increase in features
  • new-onset diabetes
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5
Q

What 2 tissues make up the adrenal gland? What do they secrete?

A

Adrenal gland: cortex & medulla
– Cortex: adrenocorticosteroids & androgens
– Medulla: epinephrine (catecholamines)

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6
Q

What are the 3 zones of the cortex? What hormones does each secrete?

A
  • Outer zona glomerulosa → aldosterone which regulates Na+ (H2O) kidney reabsorption
    Aldosterone regulated by Renin-Angiotensin System → MINERALCORTICOIDS
  • Middle zona fasciculata → cortisol which involved w/ metabolism & resistance to stress → GLUCOCORTICOIDS
  • Inner zona reticularis → dehydroepiandrosterone (DHEA) → ANDROGENS
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7
Q

With the top-down mechanism, what is happening at the highest level?

A

Corticotropin-releasing hormone (CRH)

  • CRH is released from the hypothalamus
  • CRH controls the secretion of ACTH
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8
Q

With the top-down mechanism, what is happening after CRH?

A

Adrenocorticotropic hormone (ACTH, corticotropin)

  • ACTH is secreted from the anterior pituitary
  • Enters the circulation and induces secretion of hormones from the adrenal cortex
  • Stimulates the secretion from the two inner zones (not zona glom)
  • DOES not exert significant control on hormones in the outer zone (Ang II)
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9
Q

Cortisol mediates feedback inhibition of what?

A

ACTH and CRH secretion

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10
Q

Synthetic glucocorticoids are used in the treatment of what?

A

many diseases

  • Asthma, RA, allergies
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11
Q

Explain what is happening with CRH, ACTH and the adrenal cortex

A
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12
Q

Zona glomerulosa is under the control of what?

A

RAAS

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13
Q

What gives neg feedback on hypothalamus and decreases CRH?

A

Cortisol

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14
Q

Explain the mechanism of action of adrenocorticosteroids

A
  • Step 1: Hormones bind to specific intracellular cytoplasmic receptor
  • Step 2: Dimerization of ligand-bound receptor subunits
  • Step 3: Dimerized receptor-hormone complexes translocate to the nucleus
  • Step 4: Complexes attach to gene promoter elements
    – “transcription factor”
    – genes turned on or off (can be modified by co-adaptor proteins)
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15
Q

Adrenocorticosteroid:
1. Fast or slow?
2. Glucocorticoids localized?
3. Mineralocorticoid localized?

A
  1. Takes time to produce an effect
  2. Glucocorticoid receptors are widely distributed
  3. Mineralocorticoid receptor distribution is more limited - kidney, colon, salivary & sweat glands (i.e., excretory organs)-> LESS SE
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16
Q

Principal human glucocorticoid =

A

Cortisol

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17
Q

How do cortisol levels work in our bodies?

A

Diurnal production w/ early morning peak followed by decline & then smaller peak(s) in late afternoon

peak during meals

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18
Q

What can influence cortisol secretions?

A

Meals, Stress, & Cortisol Plasma Concentration

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19
Q

What are the general effects of glucocorticoids? (6)

A
  1. Promote normal intermediary metabolism
  2. Glucocorticoids increase resistance to stress
  3. Alter blood cell concetrations in plasma
  4. Anti-inflammatory action
  5. Endocrine sytem effect
  6. Additional effects
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20
Q

How does glucocorticoids promote intermediary metabolism?

A
  • Promotes ↑ AA uptake by liver & kidney
  • Promotes gluconeogenesis thru ↑ activity of gluconeogenic enzymes in the liver
  • Promotes enzymes that increase protein catabolism (except liver-> anabolism because increasing glucose)
  • Overall Objective: Provide (a) building blocks & (b) energy for glucose synthesis

breaking things down for energy

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21
Q

How do glucocorticoids affect Lipolysis?

A

Promote ↑ hormone-sensitive lipases (Lipolysis)

  • Growth hormone (GH) and adrenaline induce lipolysis. Glucocorticoids augment these effects.
  • Glucocorticoids primarily increase lipolysis in subcutaneous adipose tissue.
  • Glucocorticoids can decrease lipolysis and increase lipogenesis in visceral adipose tissue (abdominal) (more on this later)
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22
Q

How might we get hypoglycemia with glucocorticoids?

A

During stress or fasting → if Glucocorticoid insufficiency → then hypoglycemia

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23
Q

How do glucocorticoids increase resistance to stress?

A

↑ glucose concentrations. Provides the body w/ energy to combat stress

  • trauma, fright, infection, bleeding, disease
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24
Q

How can glucocorticoids affect BP?

A

Can cause a modest ↑ Blood Pressure (BP)

  • Mechanism: Enhances vasoconstrictor actions of catecholamines/vasopressin
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25
Q

What may cause low BP?

A

Adrenal insufficiency

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26
Q

What has been shown favorable for surivival after in hospital cardiac arrest?

A

Vasopressin, sterioids, and epinephrine -> work synergic and increase chance of ROSC

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27
Q

how can glucocorticoids alter blood cell concentration in plasma? ⭐️

A
  • ↑ plasma erythrocytes (increase O2 delivery), platelets (stop bleeding), & neutrophils (but shifts neutrophils away from sites of tissue inflammation)
  • ↓ eosinophils, basophils=> decrease histamine, monocytes, lymphocytes. Also, redistribution from circulation to lymphoid tissue-> TO SAVE ENERGY
  • But because they ↓ monocytes & lymphocytes, ↓ ability to fight infections, but useful in tx of leukemia
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28
Q

What is the anti-inflammatory action of glucocorticoids?

A
  • Very important therapeutic property!
  • Dramatically ↓ inflammatory response & suppress immunity
  • ↓ plasma monocytes & lymphocytes
  • ↑ lipocortin, which ↓ phospholipase A2 (indirect inhibition). Blocks production/release of arachidonic acid. => ↓ PG & LT.
  • Inhibition of NFκB → ↓ IL-6, IL-8, MCP-1, COX-2 (↓ PG)
  • ↓ mast cell degranulation, ↓ histamine → ↓ capillary permeability
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29
Q

What is the endocrine system effects of glucocorticoids?

A
  • ↑ exogenous glucocorticoid levels cause feedback inhibition
  • ↓ ACTH production w/ ↓ endogenous cortisol, can ↓ TSH, and alter GH production (In Vivo Decrease GH and In Vitro Increase GH)
30
Q

Glucocorticoids affect renal blood flow how?

A

Physiological cortisol concentration essential for normal glomerular filtration (↑ renal blood flow)

31
Q

How does glucocorticoids affect gastric acid and pepsin? What is the effect?

A
  • Glucocorticoid high doses, ↑ gastric acid & pepsin production (breaksdown proteins).
  • May exacerbate ulcers
32
Q

How do glucocorticoids affect bone?

A

Glucocorticoid chronic therapy may cause severe bone loss

  • Decreased intestinal Ca2+ absorption
  • Increased renal Ca2+ excretion

LOTS OF Ca LOSS

33
Q

How can glucocorticoids affect muscles

A

myopathy-> weaknesss

becasue breaking down amino acids from muscles

34
Q

How does Glucocorticoids affect CNS?

A
  • initially insomnia & euphoria → depression
  • High doses ↑ intracranial pressure (worse after discontinuation – possible from decreased absorption of CSF)

After you stop taking them=> ICP

35
Q

What is the function of mineralocorticoids

A

Control of plasma H2O volume & concentrations of Na+ & K+

36
Q

What is the main mineralocorticoids?

A

aldosterone

37
Q

What does aldosterone do/cause?

A
  • ↑ reabsorption of Na+, HCO3- & H2O in kidney collecting tubules & ducts
  • ↓ reabsorption of K+ and H+ in urine (i.e., ↑ excretion)
  • Effects mediated by activation of mineralocorticoid receptors
38
Q

What are the consequences and SE?

A
  • Hypertension: Retention of Na+ & H2O, ↑ blood volume → ↑ BP
  • Hypokalemia & Alkalosis-> can alter heart rhythm and pH
39
Q

What is identical to endogenous cortisone?

A

hydrocortisone

40
Q

What gets metabolized by liver enzymes to inactivate ?

A
  • C3 Ketone Group
  • C4-5 Double Bond
41
Q

What is important for glucocorticoid activity? ⭐️

A

C11 hydroxyl group

42
Q

Fill in

A
43
Q

What drugs are selective for anti-inflammatory?

A
  • Triamcinolone
  • betamethasone
  • Dexamethasone
  • Paramethasone
44
Q

What mineralocorticoids affect both anti-inflammatory and salt-retaining mechanisms?

A

Fludrocortisone

45
Q

Semisynthetic glucocorticoids?

A
  • Vary in anti-inflammatory potency
  • Vary in Na+ retention
  • Vary in the duration of action
46
Q

What is the duration of action:

  • Short-acting
  • intermediate-acting
  • long-acting
A
  • Short Acting, 8-12 hrs (Cortisol, Cortisone)
  • Intermediate Acting, 12-36 hrs (Prednisone, Triamcinolone)
  • Long Acting, 36-72 hrs (Betamethasone, Dexamethasone)
47
Q

What is affected by 1°,2°, and 3° adrenal insufficiency?

A
  • 1°: adrenal gland
  • 2°: pituitary gland
  • 3°: hypothalamus
48
Q

What disease is 1° adrenal insufficiency?

A

Addison disease: inadequate secretion of cortisol by adrenal glands

49
Q

Addision disease
1. Symptoms?
2. Cause?
3. Dianostic test?
4. Treatment?
5. Divide dosage?

A
  1. Symptoms: weakness, no energy, low BP
  2. Possible Cause: Autoimmune damage to the adrenal cortex resulting in dysfunction
  3. Diagnostic Test: Negative response to the administration of ACTH (ACTH NEGATIVE)-> if adrenal glands dont make cortisol then the gland is not working-
  4. Treatment: Hydrocortisone (identical to natural cortisol)
  5. Divide Dosage: 2/3 in morning & 1/3 in afternoon. Approximates daily cortisol conc.
50
Q

Besides Hydrocortisone for addison disease, what else you might adminster and why?

A

Administration of Fludrocortisone may also
be necessary to ↑ mineralcorticoid activity to normal

51
Q

What conditions can be for 2° or 3° adrenal insufficiency?

A
  • Deficit in ACTH production from the pituitary (2°)
  • Deficit in CRH production from the hypothalamus (3°)
52
Q

What are the possible causes of 2° or 3° Adrenal Insufficiency

A
  • Adenoma of the Pituitary (2°)
  • Brain Tumor (3°)
  • Acute Brain Injury (2° or 3°)
  • Withdrawal of Synthetic Glucocorticoids (2°or3°)-> because you shut down natural hormones
53
Q

2° or 3° Adrenal Insufficiency:
1. Diagnostic test
2. Treatment
3. Additional characteristics

A
  1. Diagnostic Test: Adrenal cortex responds to ACTH bolus injection by syn & releasing adrenal corticosteroids (ATCH POSITIVE
  2. Treatment: Hydrocortisone
  3. Additional Characteristics: Aldosterone synthesis less impaired than cortisol
54
Q

Cushing syndrome:
1. Condition?
2. Cause?
3. Presentation?

A
  1. Condition: Pathologically increased cortisol
  2. Possible Cause: Pituitary tumor causing excess ACTH (Cushing’s Disease)
  3. Presentation: ↑ cortisol → ↑ weight, ↑ hair, ↑ BP, osteoporosis
55
Q

What is the diagnostic test for cushing syndrome?

A
  • Dexamethasone suppression test
  • If High Dose Dex causes ↓ cortisol release, suggestive of pituitary tumor (Cushing’s Disease)
  • If High Dose Dex has no effect, suggestive of adrenal tumor or ectopic ACTH secreting tumor
56
Q

Chronic high dose glucocorticoids can also cause what?

A

a Cushing-like syndrome

57
Q

What is congenital adrenal hyperplasia

A

Group of diseases that produce a deficiency in the enzymes that synthesize cortisol

58
Q

congenital adrenal hyperplasia:
1. Findings?
2. Symptoms?
3. Treatment?

A
  1. Diagnostic Findings: ↑ ACTH
  2. Virilization of ♀, overproduction of adrenal androgens
  3. Treat with corticosteroids
    • Normalizes androgen concentrations (i.e., ↓ androgen production) by ↓ the release of CRH & ACTH though feedback inhibition
59
Q

How does glucocorticoids relief inflammatory? SE?

A
  • Glucocorticoids ↓ inflammation (redness, swelling, heat, tenderness), e.g., RA, OA, skin
  • Mechanism of Action: ↓ plasma conc. of leukocytes by redistribution, ↓ lymphocytes, ↓ basophils, ↓ eosinophils, ↓ monocytes
  • ↓ ability to respond to mitogens & antigens
  • ↓ PG & LT, important inflammatory effect
  • ↓ histamine release from mast cells & basophils
60
Q

how does glucocorticoids alleviate severe allergies? What drugs? ⭐️

A
  • Glucocorticoids alleviate symptoms of asthma, allergic
    rhinitis, drug allergies, transfusion allergies
  • Beclomethasone, Triamcinolone
  • Inhalation therapy for Asthma, ↓ systemic side effects
61
Q
  • What is common in premature infants?
  • What is the regulator of lung maturation?
A
  • Premature infants → respiratory distress syndrome
  • Fetal cortisol → regulator of lung maturation
62
Q

What is used to help respiratory distress syndrome? ⭐️

A

Intramuscular injection (IM) of Betamethasone or Dexamethasone to the mother 24 hrs before birth (prenatal period)

63
Q

How does sterioids affect immunosuppression?

A

Organ transplants: Prevent/treat rejection

64
Q

What is the metabolism of adrenocortcosteroid

A

Corticosteroids metabolized 1° by liver enzymes

  • Glucuronosyltransferase (UGT)
  • Sulfotransferase (SULT)
  • Hepatic dysfunction with ↑ t1/2
65
Q

What occurs with the Suppression of the hypothalamic-pituitary-adrenal axis (HPA)?

A

Suppression of hypothalamic-pituitary-adrenal axis (HPA)

  • Large doses of glucocorticoids, e.g., > 2 weeks
  • Limit suppression by QOD dosing (every other day). Allows HPA to recover
  • Do not abruptly stop administration of corticosteroids; may cause severe withdrawal symptoms & exacerbate disease processes
  • Slowly taper off the use of synthetics to alleviate HPA suppression & prevent acute adrenal insufficiency syndrome → otherwise can cause death
66
Q

What are the side effects of Glucocorticoids?

A
  • osteoporosis
  • increase appetite
  • cushing like syndrome
  • cataracts
  • Hyperglycemia => new onset diabetes
  • hypokalemia
  • Peptic ulcers
  • Glaucoma
  • Hypertension
  • Edema
  • Euphoria/Depression/Psychosis
  • Impaired wound healing: ↑ infection risk
67
Q

How do you get osteoporsis? treatment?

A
  • ↓ intestinal Ca2+ absorption, ↓ bone formation, ↓ sex hormone syn.
  • Treat these side effects with Ca2+ & Vit D (helps absorption)

side affect of steroids

68
Q

What effect is on the appetite of steroids?

A

increase

  • predinisone-> chemotherapy
69
Q

What are symptoms of cushing like syndrome?

A
  • Redistribution of fat (buffalo hump), Puffy face (moon face), ↑ hair, Acne, Insomnia
70
Q

What is the antiglucocorticoids?

A

Ketoconazole

71
Q

Ketoconazole
1. Therapeutic use?
2. MOA?
3. SE?

A
  • Therapeutic use: Cushing Syndrome (increase cortisol) and Antifungal
  • Mechanism of action: Inhibits cortisol biosynthesis by Inhibiting CYP17A1 & CYP11A1 (at higher doses)
  • Side effects: Hepatoxicity and Heart Function by ↑ QTc prolongation (delayed ventricular repolarization), Tachycardia and Caused by drug inhibition of cytochrome P450 enzymes (CYP)
72
Q

Where does ketoconazole block

A

Pharmacology: Exam 3 (8 decks)

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