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PPP 249 SPRING QUARTER 2023 > Glucocorticoids and Mineralocorticoids > Flashcards

Glucocorticoids and Mineralocorticoids Flashcards

1
Q

Where are the following produced?

  1. Mineralocorticoids (Aldosterone)
  2. Glucocorticoids (Cortisol)
  3. Androgens
A
  1. Zona glomerulosa
  2. Zona Fasciculata
  3. Zona reticularis
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2
Q

What are the two main effects of glucocorticoids (cortisol)?

A
  1. Decr inflammation
  2. Incr Glucose
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3
Q

Physiological Effects of glucocorticoids (Cortisol effects)

  1. Increases ____ by ___
  2. _____ of skin, muscle, blood vessels –> ___ –>_____
  3. how do they make fatty acids for cellular fuel?
  4. Has a role in your ___
A
  1. cellular fuel sources, gluconeogenesis
  2. proteolysis , amino acids, gluconeogenesis
  3. lipolysis
  4. appetite
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4
Q

What are the symptoms of deficiency of cortisol (glucocorticoids)?

Name 2

A
  1. tendency for hypoglycemia
  2. weight loss, nausea, anorexia
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5
Q

Sx’s of excess of cortisol (glucocorticoids)?

Name 4 !

A
  1. Insulin resistance and insulinemia ; tendency for hyperglycemia
  2. stria in skin, limb muscle wasting, bruising
  3. central deposition of fat
  4. weight gain
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6
Q

Name the normal organ functions for Cortisol effects (4)

Name (3) things that happen when you’re deficient of cortisol

Name (4) things that happen when you’re in excess of cortisol

A
  1. Maintains Alpha receptor expression
  2. RBC formation
  3. Bone formation and maintenance
  4. Muscle function
  5. hypotension
  6. anemia
  7. weakness
  8. mild hypertension
  9. easy bruising
  10. poor growth or osteoporosis
  11. muscle weakness due to wasting
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7
Q

Name the usual cortisol anti inflam effects (2)

Name 2 symptoms of deficiency

Name 2 symptoms of excess

A
  1. decr production of inflamm mediators (pro inflamm cytokines, PLA2)
  2. decr T cell response
  3. exaggerated immune response
  4. fever
  5. decr immune response
  6. incr susceptibility to infections
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8
Q

How do glucocorticoids incr gene expression?

A

glucocorticoid comes and binds to GR (nuclear receptor) which is in cytosol
GR is bound to HSP, but when cortisol binds the HSP goes away and then the complex goes to nucleus.
It then binds DNA –> dimerizes –> acts as a TF

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9
Q

How do glucocorticoids decr gene expression?

A

Cortisol binds GR. HSP goes away. Goes to nucleus where NFKB (TF for inflammatory cytokine genes) has co-activator bound. Transcription is activated, GR+cortisol competes to push out the coactivator –> Transcription now suppressed

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10
Q

explain the regulation of aldosterone release?

Include AGT, ANG1, ANG 2, and aldosterone in answer. Include neg feedback regulation and how serum K affects aldosterone

A

RAAS system activated by decrease in blood pressure. If BP goes down, increase renin which converts angiotensinogen to ANG1, then ACE converts ANG1 to ANG2 which binds AT1 receptors in adrenal cortex –> ALDOSTERONE!

ANG 2 has neg feedback on renin to decrease it.
High serum K increases aldosterone. Aldosterone works to decr serum K by incr K excretion and incr Na/H2O retention to raise BP

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11
Q

Aldosterone effects :
1. Increases ___ and with ___ present, ___ follows

  1. Increases ____
  2. Symptoms of deficiency? (3)
  3. Symptoms of excess? (3)
A
  1. sodium reabsorption, ADH, water
  2. potassium excretion
  3. hypotension ; compensatory high ADH –> hyponatremia ; hyperkalemia
  4. Hypertension ; compensatory low ADH –> hyPERnatremia ; HYPOkalemia
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12
Q

How does aldosterone ( a mineralocorticoid) act on ENAC, SGK1, and the Na/K ATPase?

A
  1. Increases SGK1 expression (Ub ligase)
  2. Inhibits proteasomal degradation of ENAC which incr Na reabs, and incr K excretion in urine
  3. activates Na/K ATPase –> more K inside cell that can leave through ROMK channel –> excrete more potassium
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13
Q

Overall, the net effect of mineralocorticoids is? (2)

A
  1. INCR na reabsorption
  2. INCR K+ excretion
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14
Q

What’s cortisol’s (glucocorticoid) activity at the MR and GR?

What happens when cortisol acts at both of these receptors?

What ensures that aldosterone can act at MR without cortisol interfering?

A

Cortisol has equal activity at both MR and GR

Aldosterone may not have equal opportunity to act at the MR

B-11-HSD2 (11 beta hydroxysteroid dehydrogenase) makes cortisone (inactive) from cortisol! Cortisol now inactive , cant act on MR

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15
Q

Indications for Corticosteroids : Addison’s (replacement therapy)

What happens in this disease?

A

Primary adrenal insufficiency (damaged adrenal gland)

  • does not make enough cortisol, no negative feedback, so INCR ACTH and CRH
  • Very little mineralocorticoids (Aldosterone), cortisol, AND sex steroids (androgens)
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16
Q

What are the symptoms of addison’s disease? (4)

A
  1. hypoglycemia
  2. postural hypotension
  3. weight loss
  4. weakness
17
Q

Indications for corticosteroids : Congenital Adrenal disorder (replacement therapy)

What is it? what is incr or decr?

A

Several enzyme defects that do not allow you to make cortisol. Consequence –> ACTH and CRH are increased.

As ACTH is up, adrenal gland also grows .

18
Q

What does the dexamethasone test do?

A

It mimics cortisol. Give dexamethasone to see if CRH and ACTH go down (it should).

If CRH and ACTH go down, so should cortisol.
If your cortisol is still elevated, u have an issue with HPA axis

19
Q

Corticosteroids : Adverse effects

Generally develop with?

Even large doses have ?

A

Extended use

minimal AE’s when administered once or twice

20
Q

What are the side effects of corticosteroids in clinical use? (10)

M + I, M, I, F, O, H, N, T, A, T +P+B

A
  1. mood disturbances and insomnia
  2. moon face
  3. incr susceptibiity to infection
  4. fat deposit on face and back of shoulders
  5. osteoporosis
  6. HYPERGLYCEMIA
  7. Na and Fluid retention
  8. Thin extremities
  9. Abdominal fat deposits
  10. thin skin, purple striae, bruises+petechiae
21
Q

For the following corticosteroid ae’s, describe the management techniques?

  1. HPA suppression
  2. weight gain
  3. glucose intolerance
  4. edema/hypertension
  5. hypokalemia
  6. osteoporosis
  7. ulcer/gi bleeding
A
  1. tapering and alternate day therapy
  2. monitor daily caloric intake
  3. diabetic diet
  4. restrict sodium intake
  5. K+ suppls
  6. Calcium/Vit D, Biphosphanates
  7. Avoid nsaids
22
Q

Why must you taper your patient off of corticosteroids instead of just stopping the dosing all together (cold turkey)?

A

Prednisone (corticosteroid) works at receptors in pituitary and hypothalamus. CRH and ACTH BOTH GO DOWN so the adrenal gland shrinks and makes very little endog androgens, cortisol, and aldost.

23
Q

What is another endocrine disorder that is an indication for corticosteroid use?

What are the inflammatory disorders (non endocrine) that are indications for corticosteroid use? (4)

Corticosteroids used as immunosuppressant therapy in which disease states? (3)

A

Diagnosis of cushing’s syndrome (primary hyper cortisolism)

  1. osteoarthritis
  2. ulcerative colitis + Crohn’s
  3. RHINITIS
  4. asthma
  5. Rheumatoid arthritis
  6. Multiple schlerosis
  7. organ transplant
24
Q

CI and precautions for corticosteroid usage?
(8)
S,D,P,O,H,C,P,C

A

Systemic infections (Tb , herpes lesions)
Diabetes mellitus, peptic ulcer, osteoporosis , heart failure + hypertension, cataracts and glaucoma, pregnancy, CNS disorders (psychosis)

25
Q

Corticosteroids interactions with?

  1. Nsaids
  2. Diabetic agents
  3. Drugs affecting potassium levels
  4. anti hypertensive medications
A
  1. Associated with GI irritation and ulcerations
  2. hyperglycemia associated with glucocorticoids requires close monitoring
  3. diuretics + digoxin
  4. Corticosteroids may cause incr in BP due to sodium and water retention
26
Q

Interactions of corticosteroids with CYP inducers like phenytoin and phenobarb?

CYP inhibitors like ritonavir + ketoconazole?

Also has interactions with?

A
  1. enhance clearance of corticosteroids
  2. incr plasma levels of corticosteroids
  3. live vaccines
27
Q

Dosing considerations for corticosteroids?

A

Dose first thing in morning before 9AM bc adrenal glands secrete most of corticosteroids in morning

28
Q
  1. You should only treat your patient with Glucocorticoids in the following? (3)
  2. treat your pt with gluco + mineralocorticoids in the following?
A

Non endocrine disorders such as : Inflammatory disorders + immunological disorders
Endocrine disorders : Diagnosis of cushing’s syndrome

  1. Endocrine disorders that need replacement therapy like the treatment of adrenal insufficiency, and congenital hyperplasia
29
Q

Speak about the glucocorticoid (anti inflamm potency) and mineralocorticoid potency (Na retaining potency) for the following

  1. Hydrocortisone + cortisone
  2. Fludrocortisone
  3. Prednisone + Methylprednisolone
  4. Triamcinolone, betamethasone, dexamethasone
A
  1. weak gluco + weak mineralo
  2. potent gluco + potent mineralo
  3. potent gluco + Weak mineralo
  4. Potent gluco + NO MINERALO
30
Q

Routes of admin :

  1. parenteral used for?
  2. oral used for?
  3. Non systemic like topical/inhaled/intranasal?
A
  1. used for emergencies
  2. chronic therapy
  3. used to minimize systemic effects like inhalation for asthma, topical for inflamm skin disorders
31
Q

For the following state their routes of admin?

  1. hydrocortisone
  2. cortisone
  3. fludrocortisone
  4. prednisone
  5. methylprednisolone
  6. triamcinolone
  7. betamethasone
  8. dexamethasone
A
  1. po, injectable, topical
    2-4 –> oral , po
  2. po + injectable
  3. po, injectable, topical, inhalatioon
  4. po, injection, topical
  5. po, injection, topical
32
Q

For Parenteral glucocorticoids like : hydrocort, methylpred, triam, beta, and dexa, what are they mainly used for?
Agent of choice?

A
  1. mainly used for emergencies (acute adrenal crisis)
  2. hydrocortisone bc has both GC and MC activity
33
Q

Oral Glucocorticoids : Hydrocortisone , prednisone, methylpred, dexameth
–> Used for

  1. ___ insufficiency
  2. __ and __ diseases (Asthma, IBD,RA)
  3. Solid ____ for ___
  4. C___ especially for certain lymphoid malignancies
A
  1. adrenal
  2. inflamm and autoimmune
  3. organ transplantation , immunosuppression
  4. chemotherapy
34
Q

Inhaled Glucocorticoids : triamcinolone
Clinical uses (3)?

Specific AE”s for Triamcinolone?

A
  1. Asthma, inhaled
  2. allergic and non allergic rhinitis (nasal inhalation)
  3. COPD , inhaled

Oropharyngeal candidiasis
throat irritation

35
Q

Topical Glucocorticoids : Hydrocorti, triam, beta, dexa

In general, safest for ___
Clinical use? (2)

A
  1. chronic application
  2. inflamm dermatoses (Eczema and psoriasis)
36
Q

Mineralocorticoid Agonists: FLUDROCORTISONE

  1. clinical use?
  2. MOA?
  3. AE’s? (3)
A
  1. adrenal insufficiency (Addison’s )
  2. V potent Mineralocorticoid ; primary used for its mineralocorticoid effects
  3. salt and fluid retention, hypertension, HF
37
Q

MC Receptor Antagonist : Spironolactone

  1. Clinical uses , (3)?
  2. MOA?
  3. Ae’s (3) ?
A
  1. Primary Hyperaldosteronism
    hypokalemia, HF
  2. Antag at Mineralocorticoid receptor
  3. Hyperkalemia, hyponatremia, Gynecomastia

PPP 249 SPRING QUARTER 2023 (11 decks)

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