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Pharmacology > Exam3Lec7Adrenocortocosteroids > Flashcards

Exam3Lec7Adrenocortocosteroids Flashcards

1
Q

Glucocorticords:
Mineralocorticoids:
Anti-glucocorticoids:

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

What was the effects of giving Dezamethasone to Covid 19 patients

A

effective: ventilator (severe covid)
not effective: no O2 is received (mild COVID)

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3
Q

What was the Conclusion about given corticosteroids with brain trauma patients?

A

DO NOT GIVE GLUCOCORTICOID

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4
Q

What are risk factors for cortiosteroid usage? 4

A
  • increase septsis
  • Increase chance in blood clots
  • Increase in fractures
  • new onset diabetes
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5
Q

how is the adrenal gland broken up? What do they secrete?

A

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

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6
Q

How is the cortex divided and what do they secrete?

A
  • Outer zona glomerulosa → aldosterone which regulates Na+ (H2O) kidney reabsorption
    * Aldosterone 1* regulated by Renin-Angiotensin System -> MINERALCORTICOIDS
  • Middle zona fasciculata → cortisol which involved w/ metabolism & resistance to stress -> GLUCOCORTIOCIDS
  • Inner zona reticularis → dehydroepiandrosterone (DHEA)-> ANDROGENS
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7
Q

With the top-down mechanism, what What is the highest level hormone?
Where is is released from?
What controls its secretion?

A

A
CRH (Corticotropin-releasing hormone)
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 pituirary
* 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 horomone 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

CRH (hypothal)–> ACTH (ant pit)–> cortisol(F)–> androgens (R)

does not control outer layer so no aldosterone acitvated

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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 ant pit and decreases CRH and ACTH?

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)

hormone binds to IC receptor–> dimerize–>translocaet–> DNA expression

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15
Q

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

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

limited=less SE bc not going all over body

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16
Q

Principal human glucocorticoid =

A

Cortisol

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17
Q

How does 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, stress

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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? (5)

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
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20
Q

How does glucocorticoids promote intermediary metabolism?

A
  • ↑ AA uptake by liver & kidney
  • Promotes gluconeogenesis thru ↑ activity 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 does glucocorticoids affect Lipolysis?

A

Promote ↑ hormone-sensitive lipases (Lipolysis).
* Growth hormone (GH) and adrenaline induce lipolysis. Glucocorticoid augment these effect 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)

incr cubcutaneous
decr visceral

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22
Q

How might we get hypoglycemia with glucocorticoids?

A

During stress or fasting → if Glucocorticoid insufficiency → then hypoglycemia

no hormone to break it down

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23
Q

How does glucocortcoids 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?
How?

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 concetrations 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 ENGERY
  • But because they ↓ monocytes & lymphocytes, ↓ ability to fight infections, but useful in tx of leukemia

immune sytem decr, can’t fight infec, anti-infam
decr prostagandins

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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

decr prostaglandins

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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 does 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 of glucocorticoids ?

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 that affects both anti inflammatory and salt retaining effect?

A

Fludrocortisone

45
Q

Semisynthetic glucocorticoids?

A

– Vary in anti-inflammatory potency
– Vary in Na+ retention
– Vary in 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 in 1,2,3 adrenal insuffiency?

A

1: adrenal galnd
2: pit
3: hypothalam

48
Q

What disease is 1* adrenal insufficiency?

A

Addision 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 pituitary (2*)
  • Deficit in CRH production from 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 characterisitcs

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 is an issue with gluco.

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 SE of gluco?

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 appetite of steriods?

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 (26 decks)

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