L3 - Pharmacology of Skin Disorder Treatment Flashcards

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1
Q

Glucocorticoids treat ______ and _____ and modulate ____

A

Dermatitis, psoriasis and inflammation

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2
Q

General mechanism of action of glucocorticoids

A

Must be soluble enough to get into cell, Act on nuclear receptors, alter protein synthesis, inhibit or promote gene synthesis.

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3
Q

Describe the three prong effect of glucocorticoids!

A
  1. Interact with DNA ( glucocorticoid response element), stimulate synthesis of anti inflammatory genes
  2. Interact with DNA GRE to turn off inflammatory genes
  3. Affects gene transcription of other genes e.g pomC and ca2+ levels..
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4
Q

Glucocorticoid anti inflammatory mechanism - hint: purely anti-inflammatory effect.

A

Binds to intracellular steroid receptor
Steroid receptor hormone complex, translocated to nucleus,

Binds to to DNA = produces lipocortin 1 which turns off synthesis if inflammatory mediators

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5
Q

Glucocorticoid reduced inflammatory mechanism - hint: turns off decent branch of immune system.

A

Decreases immune response in skin

Binds to steroid receptor = turns things off
Reduces production of cytokines, chemokines, inflammatory proteins, enzymes and receptors.

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6
Q

Adverse effects: Glucocorticoids

A

Dose dependent, but can worsen infection or suppress HPA axis, stunt growth in children. AVOID ABSORPTION INTO MAIN BS.

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7
Q

Retinoids mechanism in terms of ACNE. Give an example of a retinoid to treat severe ACNE.

A

Vitamin derivative. Regulation of epidermal cell growth, turn it down. Reestablish regulation of sebaceous cell activity.

Acne = dysfunction in Vit A processes

ISOTRETINOIN

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8
Q

Adverse effects: VIT A RETANOIDS

A

dry, flaky skin, reduced activity of sebaceous glands.

Can be teratogenic

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9
Q

Calcipotriol is classified as a ______ treatment for psoriasis. Briefly describe what it does.

Hint: type of medicine

A

Vit D derivtive, retinoid. Primarly reduces TH2 mediated response (WBC activation). Has a +ve effect on differentiation.

Anti proliferation, pro differentiation.

Note: in psoriasis, skin replicates too fast and are pushed to the surface before maturation.

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10
Q

e.g Vit A > Retinal > retanoic acid > Nuclear transcription.

4 consequences of retinoids affecting nuclear transcription?

A
  1. Keratinocyte epithelial differentiation
  2. Reduce size of sebaceous glands
  3. Reduction in sebum
  4. Inhibition of leukocyte migration
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11
Q

Adverse effects: VIT D RETANOIDS

A

Dysfunction of calcium phosphate metabolism, bone disorder

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12
Q

What are the two classes of antibacterials that inhibit/kill protein synthesis?

A

Bacteriostatic: stops division, lets immune system catch up

Bactericidal - KILLS BACTERIA = good for immunocompromised

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13
Q

The three targets for antibacterials.

Briefly describe how each works with an example.

A
  1. Inhibition of cell wall synthesis: peptidoglycan bacteria wall, has sugars and amino acids cross linked mesh structure, B lactation, antibiotics inhibit enzymes involved in cross link mesh = disrupt cell wall = kill bacteria e.g flucloxacillin
  2. Inhibition of protein synthesis, act on bacteria enzyme ribosome 70s, generally bacteriostatic. e.g Doxycycline.
  3. Inhibition of DNA synthisis: Interfere with folic acid process, ANTIFOLATES e.g sulphonamides - cotrimoxazole.
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14
Q

Hown do antibacterials inhibit DNA synthesis?

Relate to folic acid process, referencing PABA and sulphonamides.

A

Cells need folic acid for DNA synthesis.

Mammalian cells get from diet, bacteria make their own.

So inhibit that process within bacteria = no folic acid = can’t replicate.

Sulphonamides are analogues of PABA, with compete with PABA to inhibit folic acid synthesis.

Humans also have dihydrofolate reductase but bacteria version slightly different

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15
Q

In terms of antibacterials:

Trimethoprim often used in combination with ___________ to inhibit dihydrofolate reducatase. Resulting a lesser chance for _________ as not being exposed to too much of the drug.

A

Sulphonamides, resistance

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16
Q
  1. What is mean target for ANTIFUNGALS
  2. Human and fungi versions of these targets?
  3. Briefly describe general mechanism.
A

Steroles

Human = cholesterol
Fungi = ergosterol 

Target sterols in cell membranes, disrupt integrity of fungal cell wall = affects how well fungus attaches to each other and replicate

17
Q

Antifungals

Clotrimazole inhibits and reduces fungi _____.

Adverse effects?

A

reduces fungi ergosterol

Can inhibit CYP3a4, lots of DDI, GI disturbance and hepatotoxicity.

18
Q

Terbinafine is an azalea, which is classed as an anti-______

A

anti fungal

19
Q

Methotrexate is an ___________ medicine used for treatment of psoriasis and dermatitis. Works by altering immune system.

Adverse effects:

A

pancytopenia (low RBC), GI epithelium damage and photosensitivity.

Immune system weak = opportunistic infection.

20
Q

ALCAR > ADENOSINE > STRONG ANTI-INFLAMMATORY EFFECTS

Briefly describe MTX mechanism.

A

MTX inhibits enzyme which results in more ALCAR, decreasing immune response

MTX similar to human version of folic acid, inhibits DNA synthesis. Targets rapidly dividing cells (non-specific)

21
Q

Cytotoxic chemotherapy medication for cancer, 5-FU mechanism?

A

5-FU mimics uricil structure, gets incorporated into DNA, false substrate = cells can’t divide properly.

22
Q

Adverse effects: MTX

A

opportunistic infection, pancytopenia (reduction in blood cells, dec immune system response) GI epithelium damage and photosensitivity

23
Q

Imiquimod ____ -regulates the immune response.

Main treatment for _____ ______

Mechanism of action:

Adverse effects:

A

UPREGULATE

Actinic keratosis

Immune modifier via TLR7 - inc. TH1 pathway

erythema, oedema, scaling and ulceration (increased immune response)