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Corticosteroids 1/2 > Corticosteroids 1&2 > Flashcards

Corticosteroids 1&2 Flashcards

1
Q

Drug List

A

Hydrocortisone
Prednisone
Methylprednisone
Triamcinolone
Dexamethasone
Metyrapone
Ketoconazole (anti fungal)
Fludrocortisone
Spironolactone

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2
Q

Short to medium acting glucocorticoids

A

Hydrocortisone
prednisone
methylprednisone
(HPM)

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3
Q

Intermediate acting glucocorticoids

A

Triamcinolone

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4
Q

Long acting glucocorticoids

A

Dexamethasone

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5
Q

Glucocorticoid INHIBITOR/ANTAGONIST

A

Metyrapone
Ketoconazole (antifungal)

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6
Q

Minerlocorticoid Agonist

A

Fludrocortisone

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7
Q

Mineralocorticoid Antagonist

A

Spironolactone

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8
Q

Regulation of Adrenocortical Secretion (Understand Physiological mechanism)

A

1) Adrenocortical steroid secretion controller = pituitary release of corticotropin (ACTH)

2) ACTH prod. stimulated by corticotropin releasing hormone (CRH), a peptide synth. in hypothalamus.

3) Blood CRH and ACTH conc. release in circadian like manner between 4-8 am

4)ACTH binds on MC2R receptor in adrenal cortex for secretion of glucocorticoids, mineralocorticoids and androgen precursors

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9
Q

Adrenocorticoid Secretion (part 2)

A

Physical, emotional or other stress… leads to release of CRH through “portal system” stimulating release of ACTH

ACTH important for Glucocorticoid Biosynthesis

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9
Q

Zona Glomerulosa produces what

A

Mineralocorticoid pathway: Aldosterone

  • Inside Zona Glomerulosa, cholesterol is metabolized by mitochondria to pregnenolone ultimately leading to formation of Aldosterone
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10
Q

Zona Fasiculata

A

Glucocorticoid release -> cortisol

Metabolization of pregnenolone to glucocorticoid

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11
Q

Biosynthesis of Cortisol pathway
(Must Know)

A

1) ACTH interacts with MCR2 in adrenal cortex
2) Cholesterol is metabolized in mitochondria to form pregnenolone
(RATE LIMITING STEP!)
which will then eventually be converted to cortisol

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12
Q

Diurnal Rhythm of ACTH & Cortisol
(must know)

A

When ACTH is released it is present in Picograms (1 Billionth of Mg) and stimulates release of Cortisol in ug
(microgram x1000 = 1mg)

4-8am release circadian

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13
Q

skip

A

skip

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14
Q

Mechanims of action of
glucocorticoids/ cortisol

(understand)

A

1) Cortisol enters plasma membrane (its lipid soluble)
2) will bind to glucocorticoid receptor and move into nuclear membrane
3) it will again bind to GRE glucocorticoid receptor element
4) 2 things can happen: it will either stimulate anti-inflammatory proteins or inhibit protein synth

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15
Q

Glucocorticoid Intermediary Metabolism: Cortisol
(understand, will not be asked directly)

A
  • Long term corticosteroid administration will lead to break down of:
    Muscle
    Skin/Connective tissue
    Adipose tissue
  • This will cause release of Amino acids and stimulating Gluconeogenesis
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16
Q

Physiological Effects of Aldosterone
(Must Know)

A

Aldosterone is a mineralocorticoid which will promote reabsorption of Na+ in renal distal tubules but cause excretion of K+ and H+ ions

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17
Q

Blood and Cardio Effects of mineralocorticoids and Gluccorticoids
(understand for context)

A
  • Mineralcorticoids help maintain plasma blood volume due to Na+ retention
  • Glucocorticoids increase plasma hemoglobin, erythrocytes, polymorph (neutrophils) and elevate white blood cell count
  • -However decrease number of circulating eosinophils, basophils monocytes, lymphocytes
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18
Q

Patients who receive Glucocorticoids long term (must know)

A

will be at chronic risk of infections due to suppression of immune system(eosinophils,basophils…)

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19
Q

Immune system Glucocorticoid

A

1) Glucocorticoid inhibit prostaglandin and leukotriene by inducing lipocortin which inhibits phospholipase A

2) surpress inflammatory cytokine and chemokines

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20
Q

Cortico Steroids role in CNS

A

1) Corticosteroids readily diffuse through BBB entering the brain and can influence : mood, sleep patterns, EEG activity

2) Corticosteroids administered in adrenal insufficiency scenarios; Adrenal insufficiency associated with changes in mood (depression irritability)

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21
Q

** Must Know
(Allergic disorders, Nonendocrine)

**Inhaled steroids can be used as first line therapy for mild to moderate asthma;

Steroids are also used for anaphylactic reactions as adjuncts to epinephrine and cardio support

Name the possible treatments(PMTDone)

A

(glucocorticoids)
1) Prednisone
2) methylprednisolone
3) triamcinolone
4) dexamethasone

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22
Q

*** Must Know
(Nonendocrine)

-In a case where a patient has Vasogenic/cerebral edema caused by brain tumors, what is the mechanism as to why edema from brain abscesses respond well to glucocorticoids.

-Also what drug is used in treatment of Vasogenic Brain Edema. ***(Must Know)

A

1) Treatment of Vasogenic brain edema includes the use of glucocorticoid Prednisone

2) Just know that Prednisone works because small size and lipid solubility allow steroid hormones to easily cross the BBB **

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23
Q

*****Must Know
(Meningitis, Nonendocrine)

Approximately 15,000 infants and children develop meningitis each year.
A) Why is it that Glucocorticoids are used in therapy of acute nonturberculous bacterial meningitis?

B) That bacteria responsible contain LPS membrane which lyses after antibiotic treatment triggering what?

C) What is the drug used in treatment of this and why

A

A) Antiinflammitory effects of glucocorticoids reduce brain edema, reduction of TNF-a, interleukins, and prostaglandins

B) LPS lysing leads to cytokine release=inflammation

C) Dexamethasone decrease inflammation of meninges and its ability to diffuse through BBB

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24
Q

*****Must Know
(Collagen Disorder, Nonendocrine)

A) Systemic Lupus erythematosus is a collection of autoimmune diseases which attacks healthy tissues.

B) Polymyalgia Rheumatic is characterized as a inflammatory condition affecting neck shoulders arms… incases of people 60 years or older high dose of corticosteroid therapy works well

What are the treatments included for both of these disorders(PMTD.one)

A

1) Prednisone
2) Methylprednisolone
3) Triamcinolone
4) Dexamethasone

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25
Q

*** Must Know
(Hematological disorders; Nonendocrine)

A) Autoimmune hemolytic anemia (AIHA) occurs when antibodies attack persons own RBC. IgG is binding to RBC (type 2 drug allergy )

B) idiopathic thrombocytopenic purpura is an autoimmune disease where IgG binds to platelets

(PTDone)

A

Both respond to Glucocorticoids ultimately resulting in an increased platelet life span

Treatment includes:
1) Prednisone
2) triamcinolone
3) dexamethasone

26
Q

(Hepatic disease Nonendocrine)

What is the treatment of Subacute Hepatic Necrosis and Autoimmune Chronic Hepatitis. There are two drugs used, what is the purpose of one the second.
(PA)

A

Prednisolone is used together with Azathioprine because it allows for a reduced dosage of the Prednisolone

(prednisolone controls hepatic inflammation)

27
Q

(renal disease Nonendocrine)
In patients less than 16 years old Idiopathic Nephrotic Syndrome is treated how?(CH3)

(nephrotic syndrome collection of symptoms such as protein in urine, low blood albumin, foamy piss)

A

Treatment: Methylprednisolone

Most kids are ok after 4-8 weeks

28
Q

***Must Know
(respiratory disorder Nonendocrine)

A) Sarcoidosis is a disease involving abnormal collections of inflammatory cells that form lumps known as granulomata. (neonates) (one drug)

B) Respiratory Distress Syndrome in premature infants caused by developmental insufficiency of pulmonary surfactant production and structural immaturity in the lungs. (two)

A

A) Use Prednisone

B) Betamethasone or Dexamethasone

29
Q

Adverse Effects of Glucocorticoids

A

Adverse effects correlate with: dose, frequency and rout of admin, duration of therapy, age and underlying risk factors

Adverse effects can range from not serious to displeasing and even life threatening such as Cushingoid

30
Q

***Must Know
Adverse Effects on GI and Stomach of Glucocorticoids

A

1) Glucocorticoids can lead to ulcers in patients being treated for Rheumatoid Arthritis

2) They can cause a decrease in mucous production in GI which is protective and increase acid secretion via pepsinogen

3) Synergism with NSAIDS can lead to increased GI events

4) Glucocorticoids can mask symptoms and pain of peptic ulcers

31
Q

***Adverse effects of Glucocroticoids
Edema in patents with heart or kidney disease

A

Glucocorticoids can cause fluid retention in patients with heart or kidney diseases and it is best to restrict patients intake of dietary sodium

32
Q

***Carbohydrate and Lipid metabolism Adverse effects of Glucocorticoids

1) Glucocorticoids treatment can result in hyperglycemia due to: (2 things)

2) Glucocorticoids increase risk of atherosclerotic vascular disease mediated by elevated lipoprotein levels

A

1A) Enhanced gluconeogenesis
1B) decreased cellular sensitivity to insulin

2) due to frequently elevated Serum Triglyceride conc.

33
Q

Adverse Effects Glucocorticoids:
1) Hypokalemia and 2)Hypophasphatemia

A

1A) Hypokalemia incidence is related to mineralocorticoid activity of a specific glucocorticoids and can result in effects such as: Asthenia, paralysis, arrhythmias
1B) Avoid Hypokalemia by: restrict Na+ intake, consume K+ rich foods, use mineralcorticoid that has Minal activity

2A) Hypophasphatemia will rarely occur due to administration of corticosteroids but could result in muscle weakness, cardiac dysfunction, hemolysis

34
Q

Adverse Effects corticosteroids: Osteonecrosis

A

1) Osteonecrosis commonly associated with
A) prolonged cortico treatment
B) high dose of glucocorticoids

Patient will have joint pain and stiffness after prolonged uses of corticosteroids and the common site affected is femoral head

35
Q

Adverse Effects Glucocorticoids: Nitrogen Balance

A

1) Negative nitrogen balance is caused from excessive breakdown of proteins/ muscle by glucocorticoids
2) Tell patient to stop being such a pussy and eat more meat

36
Q

*** (Must Know)
Adverse Effects corticosteroids: CNS Edema

A

Corticosteroids used in high doses can cause behavioral and personality changes as well as development of euphoria.

Other CNS Signs include: insomnia , appetite changes, nervousness, psychotic episodes

NOTE: Something will be asked about mechanism and how it passes through BBB will be mentioned or asked

37
Q

Adverse Effects corticosteroids: Children and Growth

A

1) Long term glucocorticod use can suppress growth in children and should be stopped
2) Single doses taken @ 7-8am minimizes growth suppression and is preferred over multiple daily doses
3) alternate day admin

38
Q

*** Must Know
Adverse Effects Glucocorticoids: Myopathy

A

1) corticosteroid use causes protein catabolism, myopathy; loss of muscle mass, however it is reversible by reducing dose

2) Myopathy is associated with specifically Triamcinolone (9a- fluorinated steroid)

39
Q

*** Must Know
Adverse Effects Glucocorticoids: Skin and Soft tissue
Cushings Syndrome

A

1) Skin thinning and purapura
2) Increased freq. of Non-melanoma skin cancer in patients taking oral glucocorticoids

3)*** Cushingoid syndrome from prolong glucocorticoid use such as cortisol:
Features: truncal obesity, buffalo humping patients neck, Abdominal striae, moon face, weight gain, bruising

40
Q

**Must know
Adverse Ocular Effects of Glucocorticoids

A

1) Ocular admin of glucocorticoids may elevate intraocular pressure

2)** use can enhance secondary ocular infections by fungi and viruses because they suppress immune system

41
Q

Must know **
Adverse effects glucocorticoids: Infections

A

1) Prolonged use of of glucocorticoids decreases resistance to infection and inhibit mechanisms involved in inflammation

2) patients more susceptible to bacterial, viral, fungal and parasitic infections. Switch to alternate day therapy= less infections

3) *** Reactivation of latent turburculosis

42
Q

***** A patient has been receiving long term treatment of prednisone. During a medical screening it was found that the patient has developed latent turburculosis. Why?

A

Prednisone a glucocorticoid has adverse effects of suppressing the immune system and long term administration can lead to activation of latent turburculosis

43
Q

*** Must know
Adverse Effects Glucocorticoids:
Pregnancy and Lactation

A) Certain drugs have shown to be metabolized and cross through placenta and also diffuse into boob milk

B) what are some of the symptoms/ pathologies associated
(CPPD)

A

A) Drugs which perfuse through placenta:
1) Cortisol,
2) prednisolone,
3) prednisone,
4)dexamethasone

B)
1) High doses of glucocorticoids used during pregnancy can result in fetal adrenal hypoplasia and infants should be monitored for hypoadrenalism
2) Offspring have higher risk of developing cleft palate

43
Q

** must know
Adverse Effects Glucocorticoids: HPA

A

1) exogenous admin of glucocorticoids results in suppression of hypothalamic-pituitary-adrenal axis through negative feedback causing adrenal suppression

44
Q

**Hypoadrenalism (also cleft palate) in infants can be caused by the uptake of corticosteroids through the placenta prior to birth. What characteristics of the drugs are responsible for these effects and what are some examples of the drugs.

A

A) Prednisolone, prednisone, dexamethasone….

B) glucocorticoids have the ability to diffuse through membranes off the BBB and Placenta due to their lipid solubility.

Note: But also idk if this matters but in placenta a lot of shit can diffused through it but the BBB is different bc it has tight junctions

45
Q

Gluco/cortico affects on ACTH/CRH Secretion

A

1) Drug administration of these steroids alter the HPA axis in a negative feedback loop

2) Cortisol at high conc. inhibits the release of ACTH and CRH
The corticosteroids in this lecture are just derivatives of cortisol. Cortisol itself is endogenous in the body but can also be administered exogenously.

3) A patient who has an adrenal gland issue could have excessively high levels of cortisol which would inhibit or cause low levels of ACTH production

46
Q

Aldosterone biosynthesis (mineralocorticoid)

A
  • Aldosterone production occurs in the Zona Glomerulosa, the upper most portion of the adnrela cortex.

1) Cholesterol converted to Pregnenolone in the mitochondria
2) Pregnonolone -> aldosterone via mineralocorticoid pathway
(all you need to know)

47
Q

Aldosterone Physio/pharmacolgical effects
***must knwo

A

1) *Aldosterone -> reabsorption of Na+ from the distal convoluted tubule from the cortical collecting tubes

2) **Gain of Na+ is coupled with excretion/loss of K+ and H+

3)Activates pathway by binding the cytoplasmic mineralocorticoid receptor; ALDO-R

4) **increases expression of Na+/K+ atlases and epithelial Na+ channel

5) **Excessive levels can lead to:
-hypokalemia
- metabolic alkalosis
- increase in plasma vol -> and hypertension

48
Q

Fludrocortisone

A

1) potent steroid w/both glucocorticoids/mineralocorti activity
2) Most widely used mineralocorticoid
3) Use: treat adrenocrticoid insufficiency
(specifically associated with mineralocorticoid insufficiency)

49
Q

Cushing’s syndrome (2 dependent, 1 independent
**Know

A

1) ACTH DEPENDENT: (68% of Cushing. patients)
a) Aka known as hypercortisolism/hyperadrenocorticism (super high cortisol)
b)Cortisol hypersecretion which is ACTH dependent which occurs due to *Pituitary Adenoma
c) Issue: Pituitary does not respond to neg. feedback of high cortisol

2) ACTH DEPENDENT: (12%)
a) hyper secretion of cortisol in *Ectopic ACTH syndrome (12% Cushing patients)
b) patients present with bilateral *Adrenal Hyperplasia due to ACTH secreting tumors
(tumors can be all over body lungs, thyroid, boob, ball sack etc..)

3) ACTH Indépendant: (18%)
a) Cortisol hyper secretion caused by patients with:
- benign adrenal adenomas
-adrenocortical carcinomas

Clinical features: Chronic presence of excessive glucocorticoids in patients with hypertcortisolism

50
Q

1) Normal Pituitary
2) How does Cushing’s effect pituitary
3)What metabolite is seen in the urine
*** Know

A

1) Normal
a) Stim. of Pituitary releases ACTH -> ACTH stimulates adrenals
b) Cortisol levels rise and a rise in 17 OHCS in urine

2) Cushings effect
a) High levels of ACTH dues to adenoma or ectopic tumor
b) excessive cortisol on pituitary results in cushings symptoms
c) 17 OHCS levels are elevated in urine

51
Q

Treatment of Hypercortisolism (2drugs, +synergism )
** KNOw

A

1) Metyrapone
a) inhibits enzyme which converts 11-deoxycortisol to cortisol
b) Metyrapone administation inhibits both cortisol and aldosterone

2) Ketoconazale (anti-fungal) **
a) Inhibits all steroid biosynthesis by block cholesterol conversion to pregnenolone
**(rate limiting step)
b) most effective inhibiter of Cushing’s

3) Synergism of both:
a) Ketoconazole isn the first drug used bc it acts quickly to inhibit cortisol
b) Metyrapone is added if administration of Keotconzale is not suffient to control secretion of cortisol

52
Q

***** Q: A patient is given Ketoconazole to treat Cushing’s disease:
1) How does administration of drug help in treatment of the disease.
2) Where is the drug acting at.
3) How does Ketoconazole differ from Metyrapone

A

1) Ketoconzaole inhibits the production of aldosterone but more importantly cortisol

2) Keto works by inhibiting metabolism of cholesterol to pregnenolone which is the RATE Limiting step

3)
a) Since Ketoconzole inhibits Steroid biosynthesis (Rate limit step) it can affect other steroid pathways such as Testosterone and Estradiol production
b) Metyrapone acts much more specifically on P450 enzymes responsible for aldosterone, and 11-deoxycortisol enzyme responsible for cortisol

53
Q

(he didn’t stress as much on this or give a question/scenario but it seems important)
Conns’ Syndrome or HYPER_aldosteronism
1) Effect of Conn’s
2) In most cases it is caused by
3) treatment

A

1) Conn’s results in increased plasma aldosterone which results in:
decreased plasma renin act, metabolic alkalosis, hypertension

2) Most primary hyperaldosteronism cases caused by
a) adrenal adenomas
b) bilateral glomerulosa hyperplasia

3) Treatment:
a) Administration of Spironolactone to normalize k+ prior to surgery
- also low na+ diet
b) Surgery
c) Post-op Gluc/mineralocorticoid replacement therapy (significant increase in survival)

54
Q

Know*** Hyposecretion of Adrenocortical Hormones
1) Hypoadrenalism effects and cause
2) Addison’s disease/ Primary adrenocortical insufficiency
3) Secondary Adrenocortical insufficiency

A

1) Hypoadrenalism
a) Defects in HPA axis = decrease in corticosteroid release
b) Deficiency of Adrenal Function:
- destruction of adrenal glands
- inadequate secretion og ACTH or CRH
- congenital defects in steroidogenesis

55
Q

Know*** Hyposecretion of Adrenocortical Hormones
(hypoadrenalism cont.)
1) Addison’s disease/ Primary adrenocortical insufficiency
2) Secondary Adrenocortical insufficiency

A

1) Primary adrenocortical insufficiency. AKA Addisons disease
a) usually autoimmune disease characterized by antibodies against adrenal antigens
b) President JFK had Addisions

2) secondary adrenocortical insufficiency
a) ACTH deficiency caused by surgical ablation of pituitary, pituitary disease, or pituitary suppression from prolonged glucocorticoid use

56
Q

Primary Adrenocorticol insufficiency
(not asked directly but understand mechanism to answer related questions on exam)
1) can be checked in the morning bc
2) What is Cosyntropin + utilization

A

1) Pimrary insufficiency can be suspected if ACTH levels in morning elevated by cortisol concentration are low
2) Cosyntropin is synthetic ACTH used to test adrenal function.
a) After single admin of IV Cosynotropin, cortisol and aldosterone should peak after 30-60 min. If not= adnreal insufficiency
b) However if cortisol conc. increase after prolong stim of Coynotropin = adrenal tissue is fine and insufficiency may be caused by pituitary/ hypothalamic issue
c) if cortisol doesn’t change after prolonged admin then adrenal tissue is probably damaged or not present

57
Q

*** Know Cosyntropin test
1) Used to distinguish what
2) rise in cortisol and 17OHCS means what (2)

A

1) Coyntropin/ synthetic ACTH is used to distinguish pituitary vs. Adrenal dysfunction when cortisol is low

2) Cortisol and 17OHCS changes :
A) NO change in both cortisol or 17 OHCS = Addisons due to Adrenal Failure

B) Slow rise in both cortisol and 17OHCS = Pituitary failure

58
Q

Replacement Therapy for Adnreocortical Insufficiency
*** Know
1) Two steroids used in initial treatment

2) Addition of Mineralocorticoid in treatment

3) What are the alternative steroids but lack mineralocorticoid activity and therefore require Concomitant use of this drug

A

1) Hydrocortisone/ cortisone are preferred initial treatment bc they have strong glucocorticoid act with moderate mineralocorticoid properties

2) Fludrocortisone added when a potent mineralocort. is needed but only after the dose of hydrocortisone reduced

3) Prednisone/prednisolone can be used but lack mineralocorticoid activity so Fludrocortison is added to treatment

59
Q

Hydrocortisone (synthetic cortisol)

1) steroid activity
2) Uses

A

1) potent mineralocorticoid activity
2) Adrneocortical insufficiency, anti-inflammatory, but can also be immunosurpressvie

60
Q

Prednisone (synth. Glucocorticoid)
1) activation
2) uses
3) half life

A

1) hepatic metabolism activation to prednisolone with slight but significant mineralocorticoid activity
2) Cheap, reliable uses for allergic states, autoimmune, endocrine disorders, rheumatic disorders…
3) Short half life of 60 min

61
Q

Triamcinolone (synth. Glucocorticoid)
1) metabolism
2) activity
3) half life
4) uses

A

1) Hepatic metabolism and excretion from urine and poopy
2) no mineralocorticoid act
3) 200 min half life
4) Intralesoinal, Allergic states, ophthalmic, asthma, ….. whole lot go look at it im not typing that much shit (page 83 ch 25-26)

62
Q

Cosyntropin (synth. ACTH)
1) Stimulation + Secretions
2) Toxicity
3) uses

A

1) Stim. adrenal cortex to secrete glucocorticoids - cortisol levels peak after injection
2) Toxicity/advers reaction rare but could by:
Bradycardia, Rash, redness @ Injection site
3) Diagnostic uses for primary adrenal, and secondary adnrenal (pituitary) adrenocortical insufficiency

Corticosteroids 1/2 (1 decks)

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