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Dermatology Block > Pharmacology (General) > Flashcards

Pharmacology (General) Flashcards

1
Q

The stratum corneum
The Bricks are …
The Mortar is….

A

flatted dead cells (corneocytes)

multiple bilayer of lipids in plate like structure

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2
Q

water and lipids dont mix t/f

A

t

lipid r hydrophobic

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3
Q

Two routes of crossing stratum corneum?

A

transcellular

intercullalr

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4
Q

wHAT INFLUENCES DIFFUSION

A

HOW PERMEABLE
CONCENTRATION
HOW MUCH HAS TO CROSS

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5
Q

VEHICLE DOES NOT INFLUENCE RATE AND EXTEN OF ABSORP t/f

what factors affect?

A

f (permiability,concentration, solb)
vehicle dictates permeability and conc (with regards to crossing stratumn corneum)

Drug solubility in vehicle important and is dictated by vehicle

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6
Q

Lipophilic drug in hydrophilic base will diffuse across the stratum corneum …. and diffuse into blood stream …..

A

lots, lots
like attracts like, hydropgilic base will stay on stratum corneum and repel the lipophilic drug into the mortar of the skin

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7
Q

Lipophilic drug in lipophilic base will diffuse across the stratum corneum …. and diffuse into blood stream …..

A

moderately, moderately

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8
Q

hydrophillic drug in hydrophilic base will diffuse across the stratum corneum …. and diffuse into blood stream …..

A

not at all, not at all

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9
Q

hydrophilic drug in Lipophilic base will diffuse across the stratum corneum …. and diffuse into blood stream …..

A

a tiny bit, a tiny bit

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10
Q

When drugs are applied topically only the soluble fraction provides the driving force for absorption
t/f

A

t

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11
Q

Physical and chemical factors that can influence how readily the drug disassociates from the vehicle?

A

Hydratig the skin (prevents water loss)
Choose the right vehicle (ointments over some creams)

Site of application

Integrity of skin (trauma, inflammation)

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12
Q

Decreased partitioning results from a reduction in the barrier function of the stratum corneum
t/f

A

F

increase partitioning

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13
Q

Describe molecular mechanism of glucocorticosteroids

A

1) Glucocorticosteroids diffuse across lipophilic cell membrane
2) Bind to receptor GR2a and activates it
Heats shock proteins disassociate from GR2a receptor
GR”a and glucocorticosteroid translocate to nucleus and form homodimers
3) Bind to glucocorticoid receptor elements on promoter region of DNA
Results in transcription of certain genes switched. Less mediator proteins, less synthesis rate.

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14
Q

Subcutaneous route of administration?

A

Drug delivered by a needle into adipose tissue just beneath epidermis

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15
Q

Advantages of subcutaneous route?

A

Slow absorption due to less circulation in adipose tissue

Can be used to introduce a depot of drug under the skin that is slowly released into circulation

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16
Q

Subcut administration is used for many …. drugs, such as insulin and many …. based drugs such as steroids

A

protein, oil based

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17
Q

Skin is a good route because?

A

Avoids first pass metabolism
Avoids potential toxicity of drugs to organs such as liver
Simple and non sterile (topical application)
Allows for steady state plasma conc to be achieved (slow release)

18
Q

Skin bad route because?

A

Only limited drugs diffuse across epidermis

19
Q

How does TDD work?

A

Drug accumulated in adhesive patch and diffuse across cutaneous barrier

20
Q

TDD can only be used topically t/f

A

F can be used to treat systemic disease

21
Q

TDD is most suitable for drugs that are.. (4)

A

1 low molecular weight
2 moderately lipophilic
3 potent
4 brief half life

22
Q

Chemical enhancers of TD interact with ….. to increase permeability mainly to drugs that can already ……

A

lipid matrix, cross skin reasonably well

23
Q

Chemical enhancers of TDD do not have an issue with irritation/toxicity t/f

A

F they do

24
Q

Chemical enhancers of TDD are highly effective for highly water soluble drugs or macromolecules

A

F

they are NOt HIGHLY effective for highly waater soluble drugs, mostl work for drugs that lipophilic

25
Q

agents for chemical enhancers of TDD include
…… - this creates a ‘pore’ pathway and causes prolonged occlusion
………, such as ehthanol
………, such as sodium dodecyl sulphate

A

water, solvents, surfactants

26
Q

Management of itch?

A

1) Treat CAUSE (ONDANESTRON opiate antagonist - buildup causes itch in liver problems, anti epileptics for certain neurogenic causes of itch)

2) Anti itch ttreatment
- anti histamines
- cooled emollients
- antidepressants
- phototherapy (dampens immune response)

27
Q 
Mild: 
Moderate: 
Potent:
Very potent:
(mometasone, hydrocortisone, clobetasol,modrasone)
A

Mild: Hydrocortisone
Moderate: Modrasone
Potent: Mometasone
Very potent: Clobetasol

28
Q

Side effects of topical corticosteroids?

A
  • Thinning of skin
  • Purpura
  • Stretch marks
  • steroid rosacea
  • fixed telangectasia
  • Perioral dermatitis
  • May mask infections
  • Tachypulaxis: decrease in response to anti-inflammatory effects
  • rebound flare disease (body stops producing own steroids)
29
Q

What is an example of an antipuritic?

A

Menthol lotion

Capaicin - reduces neural transmission from red chilli peppers

30
Q

An example of a keratolytic? Where is it used?

A

Used for viral warts, hyperkeratotic eczema and psoriasis, corns

SALICYLIC ACID

31
Q

Dithranol works how? Used where? Disadvantages?

A

Slows cell replication
Stable chronic plaque psoriasis
Messy and smelly

32
Q

Vitamin D analogue works how? Used where? Pros and cons?

A

Affects rate of cell division
Stable chronic plaque psoriasis
Can be irritant. Clean no smell, easy to apply

33
Q

Coal tar works how? Used where? Disadvantages?

A

antiinflammatory
Stable chronic plaque psoriasis
Messy and smelly

34
Q

Treatment for scalp psoriasis?

A

Greasy ointments to soften scale
Tar shampoo
Steroids in alcohol base or shampoo
Vitamin D analogues

35
Q

Wet wrap therapy?

A 
This is used for
very dry (xerotic) skin
with mosituriser, cooling and soothing. 
prevent scratch
aply paste
time consuming
36
Q

Indications for topical corticosteroids?

A

Eczema

Psoriasis (eg flexures) Beware rebound, triggering pustular psoriasis)

Other non-infective inflammatory dermatoses e.g. lichen planus

Keloid scars (usually intralesional)

37
Q

Tacrolimus and pimecrolimus are examples of?

A

Calicneurin inhibitors

38
Q

Calcineurin inhibiter work how? When and for what? Risks and cons?

A

Suppress lymphocyte activation.
Second line treatment eczema
Risk infection and skin cancer?
burning sensation on application

39
Q

Antiseptics indicated for? Examples?

A

Recurrent infections
Antibiotic resisistance
Wound irrigation
Triclosan, hydrogen peroxide

40
Q

Treatment for shingles?

A

Treat with acyclovir 800mg 5 times daily for 7-10 days
Tramadol for 4 days
Local cooling agents

41
Q

Dermatitis herpetiformis lab confirmation? What condition is associated w dermatitis herpetiformis?

A

IGA anti tissue transglutaminase and FBC

celiac disease

Dermatology Block (8 decks)

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