Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 Pharmaco > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

What are the 2 types of corticosteroids?

A
  1. Glucocorticoids (cortisol)
  2. Mineralocorticoids (aldosterone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name all the commonly used corticosteroids.

A
  1. Cortisol (prodrug: cortisone)
  2. Prednisolone (prodrug: prednisone)
  3. Methylprednisolone
  4. Triamcinolone
  5. Dexamethasone
  6. Betamethasone

(In order of increasing DOA, GC action & decreasing MC n dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List the metabolic effects of Cortisol.

A
  1. Increases glucose in circulation: via gluconeogenesis & decreased peripheral glucose uptake
  2. Increased glycogen deposition
  3. increased NET fat deposition: via increased lipolysis & increased lipogenesis
    => results in buffalo hump, lipid redistribution
  4. Mineralocorticoid activity (water retention)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List the catabolic effects of Cortisol.

A
  1. Negative Nitrogen & Calcium balance
    - increases nitrogen excretion in urine, from protein breakdown (lose muscle mass)
    - reduces calcium reabsorption & increases calcium excretion (leads to osteoporosis)
  2. Breaks down protein in lymphoid, muscle, skin, bone & connective tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Feedback inhibition of Hydrocortisone/Cortisol:

A
  • increased cortisol => decreases ACTH secretion
  • cuz ACTH triggers adrenal gland to produce cortisol mah
  • reduce endogenous cortisol pdn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Structure of the steroid receptor:

A
  • nuclear receptor that also functions like a transcription factor
  1. Nuclear receptor
  2. Gene-active receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Mechanism of action of Steroids:

A
  1. Highly lipophilic, cross cell membrane => bind to intracellular nuclear receptor
  2. Receptor forms homodimer & enters nucleus => regulate gene expression => regulate protein level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the ‘forms’ of Steroid receptors?

A

Nuclear receptor (gene-active receptor)
- GRα-form: active form of glucocorticoid receptor
- GRβ-form: dominant -ve form => inhibits signalling of alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the pro-drug of Cortisol?

A

Cortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the pro-drug of Prednisolone?

A

Prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name the 2 corticosteroid pro-drugs.

A

Prednisone & Cortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Side effects of Corticosteroids on the Musculoskeletal system.

A
  1. Osteoporosis (trabecular bone)
    - due negative calcium balance
    - decreased Ca reabsorption & increased Ca excretion
  2. Aseptic necrosis of femoral head
    - rarely happens but still documented
    - bilateral, occurs on both sides of femoral head
  3. Myopathy (dexamethasone/triamcinolone)
    - muscle weakness, dysfunction of muscle fiber
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Side effects of Corticosteroids on the Immune system.

A

Opportunistic infections (we often prescribe steroids post-op to suppress immune system, good to prescribe antibiotics tgt to prevent infection)
Can be:
Bacterial (TB), Viral (Herpes & CMV), Fungal (candidal, asperigilles & crytococcal), Parasitic (toxoplasmosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Side effects of Corticosteroids on the GIT system.

A

Peptic ulcers, GI bleeding (esp when combined w NSAIDs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the withdrawal phenomena w corticosteroids?

A

Cuz adrenal cortex has been suppressed from producing endogenous cortisol due to negative feedback

Thus,
no abrupt withdrawal of steroids!, otherwise: lethargy, headache, fever, joint pain, HPA insufficiency (hypothalamic-pituitary-adrenal axis)
must taper dose gradually

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Side effects of Corticosteroids on the Nervous system.

A
  • usually occurs in medical settings at higher doses
  • euphoria, depression, psychosis
17
Q

Side effects of Corticosteroids on the Endocrine-Metabolic system.

A
  1. Hyperglycemia (more glucose in circulation)
  2. Moon face, ‘buffalo hump’ & truncal obesity (increased fat deposition & redistribution)
  3. Muscle wasting (-ve nitrogen + protein breakdown)
  4. Growth retardation (pediatric patients)
  5. Acne, hirsutism (abnormal hair growth) & menstrual disturbances (cuz steroid is a male hormone)
  6. Delayed wound healing (suppressed immune system)
  7. Skin thinning (protein breakdown)
  8. Na/fluid retention, oedema, hypertension, chronic heart failure (mineralcorticoid effects)
18
Q

Anti-inflammatory actions of corticosteroids:

A

First line immunosuppressant in solid organ and hematopoietic stem cell transplantation.

  1. decreases T cells, B cells, monocytes, eosinophils & basophils but increases circulating neutrophils
    - immune cells downregulated thru increased apoptosis
    - increases neutrophils in circulation via increased pdn & reduced extravasation
    - reduced extravasation: neutrophils constrained within circulation, cannot reach tissues => reduces excessive tissue damage
  2. Decreases size & lymphoid content of lymph nodes
    - due to catabolic effect (break down) on proteins in lymph nodes
  3. Has more effects on cellular immunity than on humoral immunity
    - aka more effect on t cells than on b cells & pdn of immunoglobulins
  4. Increases macrophage efferocytosis & promotion of resolution of inflammation
    - more cleaning up & eating of dead cells
  5. Decreased type-IV delayed hypersensitivity reaction (e.g. transplantation rejection)
19
Q

How can corticosteroid drugs be administered?

A

Systemic: oral, IV, IM
Local: (decreased systemic adverse effects)
- topical (mouthwash, ointments)
- ophthalmic forms
- inhalation for asthma
- nasal sprays for allergic rhinitis
- intra-articular injection for joint disease
- enemas for ulcerative colitis

20
Q

Clinical uses of corticosteroids:

A
  1. Allergic rxns: asthma, atopic dermatitis, rhinitis
  2. Collagen-vascular disorders:** Lupus erythematosus** (autoimmune, attack of own tissues, widespread inflammation), rheumatoid arthritis
  3. GI diseases: Crohn’s disease, ulcerative colitis (both are types of inflammatory bowel)
  4. Haematologic disorders: leukemia (blood cancer), lymphoma (lymph cancer), Hemolytic anemia, thrombocytopenia
  5. Organ transplants: tranplantation rejection
  6. Dental conditions: gingivitis, oral lichen planus (chronic inflammatory condition that affects mucus membranes in mouth), surgical swelling
  7. Eye diseases: Uveitis, Conjunctivitis
  • most of these diseases involve inflammation, except leukemia & lymphoma (emphasis on these on reduction of blood cells & break down of lymph nodes)
21
Q

Effects of aldosterone. + what happens in excess?

A

Mineralocorticoid. Binds to mineralocorticoid receptor to upregulate Na+/K+ ATPase gene expression at distal renal tubule
- Na+ reabsorption
- K+ & H+ excretion

In excess: hypernatremia, hypokalemia, metabolic alkalosis(due to loss of H+), edema

22
Q

Name the glucocorticoid drugs that do not have water-retention side effects.

A
  1. Methylprednisolone
  2. Triamcinolone
  3. Betamethasone
  4. Dexamethasone
23
Q

Which glucocorticoids still have water-retention side effects?

A

Cortisol/cortisone
Prednisolone/prednisone (less water retention than cortisol)

24
Q

Steroids are not ________, only ________ inflammation.

A

Steroids are not curative, only suppress inflammation.

25
Q

What are the gene targets decreased by steroids?

A
  1. Cytokines: TNF-α, IL-1β,IL-6
  2. Chemokines: RANTES
  3. Inflammatory enzymes: COX-2, 5-LOX, phospholipase A2
  4. Adhesion molecules: ICAM-1, VCAM-1 (prevent cell infiltration into inflammatory sites)
  5. Receptors: IL-2 receptor, T-cell receptor (decreased expression of pro-inflammatory genes)

-> general effect: less inflammation

26
Q

What are the gene targets increased by corticosteroids?

A
  1. Annexin-A1 (phospholipase A2 inhibitor)
  2. β-adrenoreceptor (related to asthma)
  3. IKB-α (inhibitor of NF-KB) (NF-KB: pro-inflammatory TF)
27
Q

Side effects of corticosteroids on the eye.

A
  • cataracts
  • glaucoma

Y2 Pharmaco (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions