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PHAR 253 - Therapeutics (2) > Corticosteroids / Endocrine Physiology > Flashcards

Corticosteroids / Endocrine Physiology Flashcards

1
Q

Main hormone secreted by Zona Glomerulosa?

A

Aldosterone

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2
Q

Main hormone secreted by Zona Fasciculata?

A

Cortisol

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3
Q

Main hormone secreted by Zona Reticularis?

A

Testosterone

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4
Q

Primary functions of Cortisol?

A

-Mediate stress response

-Regulate carb / lipid / protein metabolism

-Regulate inflammatory & immune responses

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5
Q

What bodily responses are generated due to Cortisol release?

A

-Increase HR & BP

-Liver conversion of Glycogen to Glucose

-Bronchiolar Dilation

-Reduced digestion & urine production

-Metabolic Rate goes up

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6
Q

Long term stress responses of the body… What are they?

A

Mineralocorticoids: Retain Na+ & H2O, increased BV & BP

Glucocorticoids: Protein / fat conversion to glucose, immunosuppression

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7
Q

Explain the HPA Axis.

A

1) Stressors (ie. Low Blood Sugars or BP, Fever, Injuries) trigger Hypothalamic release of CRH.

2) CRH targets Pituitary (along with Vasopressin & Cytokines) & ACTH is released.

3) ACTH targets Adrenal Gland, Cortisol is released.

4) Persistent Cortisol negatively feeds back on the loop, suppressing further CRH & ACTH release / production.

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8
Q

The two primary functions of Glucocorticoids?

A

-Inflammatory Suppression

-Suppressed Immune Response

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9
Q

How do Glucocorticoids suppress inflammation?

A

-Reduce Cytokine release

-Reduced vasoactive substance release

-Inhibit leukocyte / macrophagic migration & adhesion to capillary surfaces

-Interfere with phagocytosis

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10
Q

How do Glucocorticoids suppress Immune Responses?

A

-Alter gene / cell function

-Affect WBC function

-Inhibit T cell activation

-Inhibit Interleukins, Cytokines, Gamma Interferon, TNF-alpha synthesis

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11
Q

How might Corticosteroids be of use to somebody with Plaque Psoriasis?

A

-Reduce epidermal cell turnover & inhibit cellular DNA synthesis

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12
Q

How do Corticosteroids infer anti-tumor effects?

A

-Inhibit cellular glucose transport

-Induce cell death to immature lymphocytes

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13
Q

Major issue with Ophthalmic / Otic Corticosteroid formulations?

A

-How to properly administer the drug

Punctal Pinch being done? Getting any drug in the eye / ear? Closing eye after drug admin?

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14
Q

Indications for Nasal Corticosteroids?

A

-Rhinitis
-Nasal Polyps
-Sinusitis

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15
Q

Issue with Nasal Corticosteroids?

A

Delivery Techniques (same as Drops)

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16
Q

Pros & Cons of Metered Dose Inhalers?

A

Pros: Portable

Cons: Inhalation Technique, # of Doses Left Not Displayed

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17
Q

Pros & Cons of Diskus Inhalers?

A

Pros: Portable & Display Remaining Doses

Cons: Powder Deposition, Age Restrictions (young kids lower lung capacity)

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18
Q

Generic name of the Nebular product used as a Corticosteroid?

A

Budesonide (brand name is Pulmicort)

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19
Q

Pros & Cons of Nebulizers?

A

Pros: Good lung delivery for those who cannot generate sufficient respiratory flow rate. Also easy to use the mask on young kids.

Cons: Time Consuming, $$$, Not Portable, False Security.

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20
Q

Rank the following Corticosteroid Creams by potency (from least to greatest):

-Betamethasone Dipropionate

-Betamethasone Valerate

-Hydrocortisone

-Clobetasol Propionate

A

Hydrocortisone (7)

Betamethasone Valerate (5)

Betamethasone Dipropionate (3)

Clobetasol Propionate (1)

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21
Q

Rank the following Corticosteroid Ointments by potency (from least to greatest):

-Betamethasone Dipropionate

-Hydrocortisone

-Clobetasol Propionate

-Betamethasone Valerate

A

Hydrocortisone (7)

Betamethasone Valerate (5 @ 0.05%; 3 @ 0.1%)

Betamethasone Dipropionate (2)

Clobetasol Propionate (1)

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22
Q

Rank the following Corticosteroid Lotions by potency (least to greatest):

-Betamethasone Valerate

-Clobetasol Propionate

-Betamethasone Dipropionate

A

Betamethasone Valerate (5 to 6 depending upon product)

Betamethasone Dipropionate (3 to 5 depending upon product)

Clobetasol Propionate (1)

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23
Q

High potency topical steroid use should be limited to what therapeutic duration?

A

< 2-4wks (followed by usage of less potent agents)

-Should also never be applied more than twice daily.

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24
Q

Maximum topical corticosteroid dose per week (for Ultra Potent Agents)?

A

50g / wk

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25
Q

Factors that affect topical corticosteroid absorption?

A

-Moisture (increases absorption 4-5x)

-Potency

-Dosage Form

-Concentrations

-Formulation

-How You Apply It

-Occlusion (decreases by up to 10x)

-Site of Admin

-Condition of Skin

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26
Q

IM vs. IV vs. Intra-Articular: Rank them by onset of action.

A

1) IV (fastest & best for high dosing)

2) IA (quicker & short duration)

3) IM (slowest & prolonged duration)

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27
Q

How many times per year can Intra-Articular injections be administered?

A

3-4x / yr

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28
Q

T or F: IV Corticosteroid doses are equivalent to Oral Corticosteroid doses?

A

True!

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29
Q

List the generic oral dosage forms of corticosteroids.

A

Betamethasone
Cortisone
Dexamethasone
Hydrocortisone
Methylprednisolone
Prednisone
Triamcinolone

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30
Q

Oral Solution form of Corticosteroids we discussed in class?

A

Prednisolone

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31
Q

What is a physiologically normal amount of Cortisol production per day?

A

10 - 20mg / day

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32
Q

What is the daily Prednisone equivalency that mimics endogenously produced Cortisol amounts?

A

5mg / day

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33
Q

What would be considered a “low or maintenance dose” of Prednisone?

A

5 - 15mg / day

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34
Q

What would be considered a “moderate dose” of Prednisone?

A

0.5mg / kg / day

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35
Q

What would be considered a “high dose” of Prednisone?

A

1 - 3mg / kg / day

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36
Q

What would be considered a “massive dose” of Prednisone?

A

15 - 30mg / kg / day

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37
Q

What are the Short Acting Corticosteroids?

A

Cortisone & HC

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38
Q

What are the Intermediate Acting Corticosteroids?

A

-The “Preds” (Prednisone & Prednisolone)

-Methylprednisolone

-Triamcinolone

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39
Q

What are the Long Acting Corticosteroids?

A

Dexamethasone & Betamethasone

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40
Q

Short Acting Corticosteroids have a half life of how many hours?

A

8 - 12h

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41
Q

Intermediate Acting Corticosteroids have a half life of how many hours?

A

12 - 36h

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42
Q

Long Acting Corticosteroids have a half life of how many hours?

A

36 - 72h

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43
Q

Which Corticosteroids have Na+ Retaining Potencies? What are their relative potencies?

A

Cortisone & HC: 1

The “Preds”: 0.8

Methylprednisolone: 0.5

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44
Q

Anti-Inflammatory Potencies of the Corticosteroids… List them all.

A

Cort: 0.8
HC: 1
Preds: 4
Methylpred: 5
Triam: 5
Dexa: 25
Beta: 25

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45
Q

Cortisone equivalent dose?

A

25mg

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46
Q

HC equivalent dose?

A

20mg

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47
Q

Prednisone / Prednisolone equivalent dose?

A

5mg

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48
Q

Methylprednisolone / Triamcinolone equivalent dose?

A

4mg

49
Q

Dexamethasone / Betamethasone equivalent dose?

A

0.75mg

50
Q

Ophthalmic CS side effects?

A

-Stinging & Redness
-Tearing & Burning
-Secondary Infection
-Cataract Development

51
Q

Inhaled CS side effects?

A

-Thrush
-Hoarseness
-Dry Mouth
-Dysphoria (altered voice)
-Swallowing Difficulties

52
Q

Nasal CS side effects?

A

-Runny Nose
-Bloody Nose
-Burning
-Sneezing

53
Q

How can we minimize Nasal / Inhaled CS side effects?

A

-Rinse Mouth (ICS)

-Point Device away from Septum (NCS)

54
Q

Topical CS side effects?

A

-Burning
-Irritation
-Skin Atrophy
-Tachyphylaxis (effects wear off with LTU)
-Telangiectasia (spider veins)

55
Q

Systemic side effects attributed to Oral CS?

A

-Hypertension
-Skin Thinning
-Muscle Wasting
-Moon Face
-Cataracts
-Abdominal Fat
-Bruise Easy / Slowed Wound Healing

56
Q

Psychological side effects of Systemic CS?

A

-Euphoric
-Insomnia / Restlessness
-Memory Impairment

57
Q

Long term psychological side effects of Systemic Corticosteroids?

A

-Depression
-Mania
-Psychosis

58
Q

What do we recommend long term corticosteroid users do (regarding exams)?

A

Routine Eye Exams (as Cataract damage is irreversible)

59
Q

CS’s can cause GI upset & dyspepsia… It also can increase one’s risk of developing Peptic Ulcer Disease if taken concurrently with what medications?

A

NSAIDs

60
Q

Blood Glucose increases due to CS usage typically take place above what Prednisone dose? How long after d/c do effects persist?

A

> 15mg / day

-Effects can persist for months after.

61
Q

T or F: Na+ / H2O retention doesn’t normally resolve itself upon CS d/c.

A

False… Normally does resolve itself.

62
Q

T or F: High Dose CS therapies can increase appetite.

A

True.

63
Q

Suggest mechanisms of action in which CS’s suppress childhood growth.

A

-Suppress Osteoblastic activity.

-Suppress Growth Hormone secretion.

-Inhibition of Insulin Receptors.

64
Q

What CS formulation do we see the most pronounced effects on childhood growth?

A

Oral CS Therapies

65
Q

T or F: Short term CS use in kids for acute reasons will permanently affect growth.

A

False… Can maybe stunt growth, but more so for chronic use & d/c of the medication sees a catch-up growth period.

66
Q

When are Cortisol levels highest during the day?

A

AM (7 - 8 in the morning)

67
Q

Why must we taper CS’s gradually (rather than a complete stop)?

A

-Continual Corticosteroid use completely suppresses the HPA… Means that produced levels of CRH & ACTH are basically null & body cannot respond to stressor events.

68
Q

Bodily effects of complete HPA Axis Suppression?

A

-Hypotension / Hypoglycemia

-Flu Like Symptoms (NV / Fatigue / Chills / Fever / Muscle Aches)

-Weight Loss

-Confusion

69
Q

Factors that predict HPA Axis Suppression?

A

-Type of Steroid Used

-Dose Used

-ROA

-Duration

-Admin Time (Hypotensive / Hypoglycemic crashes more likely with PM dosing)

-Intervals of Dosing (more with QID than OD dosing)

70
Q

Length of time that it may take the HPA Axis to restore normal functioning once CS’s are d/c?

A

Weeks to over a year (sometimes even as long as 1 - 3yrs)

71
Q

What is the SST (Short Synacthen Test) used for?

A

-To determine degree of HPA Axis Supression… ACTH given & plasma Cortisol levels measured at 0, 30, 60min intervals in order to determine Cortisolic responsiveness to ACTH release.

72
Q

Describe the trends of Adrenal Insufficiency risk as it pertains to the following dosage forms:

Nasal
Intra-Articular
Oral

A

Nasal: Least risk (around 5%)

Intra-Articular: Somewhat high risk (around 42%)

Oral: Highest risk (around 49%)

73
Q

Low dose, medium dose, high dose: What are the relative risks of suffering from Adrenal Insufficiency while on these CS dosing regimens?

A

Low Dose: Very low risk (around 2%)

Medium Dose: Relatively low risk (around 8-9%)

High Dose: Moderate risk (around 22%)

74
Q

As dosing regimens on CS’s go on for longer periods of time (ie. Beyond a year), how does the relative risk of suffering from Adrenal Insufficiency change?

A

Increases dramatically (less than a month 1.4%; over a year in length risk increases to beyond 27% of suffering from Adrenal Insufficiency)

75
Q

Susceptibility to viral, bacterial, and fungal infections increase when one takes a CS dose of > ____mg / day of Prednisone.

A

Over 10mg / day

-Typically does not occur in doses < 10mg / day.

76
Q

Because of the nature of how CS’s inhibit cell division, what skin-related condition might people see an increased risk of obtaining when taking these medications?

A

Acne

77
Q

Gladys is a middle aged woman (52yrs) with arthritis. She comes to your pharmacy complaining of recent foot fractures. You probe deeper and determine she’s been recently put on corticosteroids about 2 months ago. Explain mechanistically how her steroid therapy may be contributing to her recent run of fractures.

A

-Reduced Ca2+ absorption from the diet and reabsorption from the Kidneys.

-Inhibition of Osteoblast activity (no bone regeneration).

-Length of therapy itself contributing to increased fracture risk ( >2-3 months of therapy greatly increases risk).

-Potential Osteoporosis (30-50% on chronic therapy develop it).

78
Q

Fracture Risk Assessments should be conducted on all adults initiating or continuing GC therapies above a dose of ____ mg / day and beyond a therapy length of > ___ months.

A

> 2.5mg / day ; > 3 months in duration

79
Q

What add-on therapy / therapies are strongly recommended for high risk GIOP adults on Corticosteroids?

A

-Bisphosphonate (to enhance Ca2+ absorption and promote bone health).

-Vitamin D (to enhance Ca2+ absorption from diet).

-Potential Ca2+ supplementation.

80
Q

Why can muscle wasting occur in patients on high dose CS’s?

A

-CS’s have catabolic effects (as well as suppress protein synthesis).

81
Q

Above a Prednisone dose of ___ mg / day is when myopathy becomes more common.

A

> 10mg / day

82
Q

Amongst kids on short term CS therapies (< 14d duration), what was the most common reason for discontinuing the therapy?

A

Vomiting (due to bitter taste)

83
Q

T or F: Short term CS use (< 2 wks) outright eliminates the risk of side effects.

A

False… Risk is quite small of obtaining things such as Sepsis / Venous Thromboembolism / Fracture, but there is still a risk.

84
Q

What is the recommended short term corticosteroid therapy regimen for COVID treatment?

A

Dexamethasone 6mg OD (for up to 10 days duration of therapy)

85
Q

CS treatment in COVID patients saw an increase in ______ _______ and a decrease in ________ in those requiring oxygen.

A

increase in clinical outcomes ; decrease in mortality

86
Q

T or F: CS dosing has set guidelines for all individuals.

A

False… Very patient specific (want to bring inflammation & immunological responses under control via the MED).

87
Q

Order the following dosing regimens by their immunosuppressive potentials:

TID
OD
BID

A

OD < BID < TID

-More frequent the dosing, the more potent immunosuppression is.

88
Q

What is the most typical weight based maintenance dose for those on CS’s?

A

0.5 - 1mg / kg / day

89
Q

Is a taper necessary to conduct with a patient on CS’s for < 2 weeks length?

A

Probably not.

90
Q

Beyond what length of time on CS therapies should we begin to consider taping a patient?

A

> 3wks… Dependent upon cumulative dose, dosing frequency, physiological circumstances, etc.

91
Q

When desiring a CS taper, what is a good rule of thumb to follow?

A

5 - 10% / wk as a desired dose reduction.

92
Q

“Every Other Day” (EOD) dosing is typically done with what class of CS’s?

A

Intermediate Acting CS’s… Long Acting work too long & Short Acting work for too short of a duration.

93
Q

What situations would warrant EOD Corticosteroid dosing?

A

-Chronic Admin

-Kids needing maintenance doses

94
Q

What are the three systems / molecules in charge of regulating Aldosterone secretion?

A

1) RAAS
2) Potassium
3) ACTH

95
Q

What three things stimulate Aldosterone release?

A

1) Drop in BP
2) Salt Depletion
3) CNS Excitation

96
Q

What condition arises due to the actions of Aldosterone (as it pertains to Na+ / K+)?

A

Hypokalemia… Na+ retention is increased, and thus K+ excretion in the Distal Collecting Tubules of the Kidneys increases.

97
Q

What is Cushing’s Syndrome?

A

Persistent exposure (either Exogenous or Endogenous in nature) to excessive Glucocorticoids.

98
Q

T or F: Men are more affected by Cushing’s Syndrome than Women.

A

False… Women > Men (incidence is 5:1 W to M).

99
Q

T or F: Exogenous GC use raises Cushing’s incident rates by a substantial amount (relative to Endogenous overexposure).

A

True.

100
Q

What causes Endogenous overproduction of Cortisol in Cushing’s Syndrome?

A

1) Pituitary Tumors (overproducing ACTH, leading to more Cortisol secretion from Adrenals). Incidence is 80% of Endogenous cases.

2) Tumors on the Adrenal Gland itself (leading to more Cortisol production). Incidence is 20% of Endogenous cases.

101
Q

What are the clinical features of Cushing’s?

A

Face: Moon Face, Facial Plethora, Acne

Abdomen: Weight Gain / Obesity

Systemic: Hypertension, Bruise Easy, Glucose Intolerance, Muscle Weakness, Thinning Skin / Striae, Fatigue

Bones: Osteopenia / Increased Fractures

Miscellaneous: Irregular Periods, Reduced Sex Drive, ED, Depression / Emotional Instability, Reduced Linear Growth (kids)

102
Q

How does the prognosis of Cushing’s change when therapeutic goals are achieved (signs / symptoms resolved)?

A

Untreated: 5yr Survival Rates of 50%

Treated: 20yr Survival Rates of 87%

103
Q

What treatment is sometimes required upon surgical removal of Pituitary Adenomas in Cushing’s patients?

A

Supplemental CS therapies (as Cortisol levels will be dropping too pronouncedly).

104
Q

If surgical removal of Pituitary Adenomas is unsuccessful, what else can we do?

A

1) Repeat surgery

2) Medication Therapies

3) Radiation Therapies

4) Bilateral Adrenalectomy

105
Q

In cases of Drug-Induced Cushing’s Syndrome, what is our treatment option?

A

Taper off of the medication (no shit Sherlock).

106
Q

What pharmacological agents can be used as therapies for treating Cushing’s Syndrome patients?

A

1) Steroidogenesis Inhibitors

-Ketoconazole
-Metyrapone
-Mitotane

2) ACTH Secretion Inhibitors

-Pasireotide

107
Q

What is our DOC for Cushing-oid pharmacotherapies?

A

Ketoconazole (effective drug & lesser adverse effects profile).

108
Q

S/E’s of Ketoconazole?

A

-Stomach Upset
-Boobies (gynecomastia)
-Headaches
-Sedation
-ED (dick don’t work)
-Sex Drive like Adam :(
-Increased LFT needed

109
Q

Other things to look out for with Ketoconazole?

A

LOTS OF DRUG INTERACTIONS!!!

-CYP1A2 Drugs
-CYP2C9 Drugs
-CYP3A4 Drugs

110
Q

What use does Metyrapone have in treating Cushing-oid symptoms?

A

-Often used concurrently with Ketoconazole (to offset individualistic s/e’s).

111
Q

S/E’s of Metyrapone?

A

-Androgenic side effects (ie. Hirsutism, Acne)

-N/V, Abdominal Discomfort

-Dizziness & Headaches

-Allergic Rashes

112
Q

What is Mitotane’s indication in Cushing’s treatment regimens?

A

Inoperable Adrenal Carcinomas

113
Q

Why is Mitotane initiated in hospital?

A

-Because of its Cytotoxic nature (kills both cancerous cells & healthy cells) & s/e profile.

-Substantially drops Cortisol levels (can drop dangerously low & requires quick hospital team response).

114
Q

S/E profile of Mitotane?

A

-NVD (80%)

-Depression

-Lethargic / Somnolence (40-80%)

-Hypercholesterolemia

-Rash

-Hepatotoxicity

115
Q

MOA of Pasireotide?

A

-Binds Somatostatin receptors, which inhibits ACTH secretion from producing Adenomas.

116
Q

Pasireotide s/e’s?

A

-Hepatotoxic

-CV events (Bradycardia / QT Prolongation)

-Hyperglycemia

-Gall Bladder Events

117
Q
A
118
Q
A

PHAR 253 - Therapeutics (2) (8 decks)

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