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Dermatology SB > Pharmacology > Flashcards

Pharmacology Flashcards

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Dermatology Board Prep flashcards
1
Q

what is the most important barrier for drug penetrations

A

stratum corneum

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2
Q

what does the SC consist of

A

corneocytes (hardened, dead keratinocytes)

surrounded by intercellular lipids

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3
Q

what are corneocytes embedded in

A

matrix of filaggrin surrounded by a cornified cell envelope that is highly cross linked

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4
Q

what are adjacent corneocytes held together by

A

corneodesmosomes

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5
Q

what is contained in the intercellular lipids

A

ceramides
cholesterol
free fatty acids

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6
Q

the intercellular lipids are highly hydrophilic - true or false

A

false

highly hydrophobic

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7
Q

what can the intercellular lipid act as

A

reservoir for lipid-soluble drugs i.e. topical corticosteroids
allows it to be released over a long period of time

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8
Q

what is the problem with drugs penetrating SC

A

only allows diffusion of small, hydrophobic drugs

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9
Q

what are vehicles of topical drugs

A 
ointments
creams
gels
lotions 
pastes powders
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10
Q

Conventional transdermal drug delivery is a passive process, driven by diffusion - true or false

A

true

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11
Q

what does Fick’s law described

A

rate of absorption

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12
Q

what is Fick’s law

A

J = KpCv

where J = flux
Kp = permeability coefficient
Cv = concentration of drug in the vehicle

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13
Q

what can Kp be substituted with

A

Km - the partition coefficient
D - diffusion coefficient
L - length of diffusion pathway

J = (DKm/L)Cv

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14
Q

what factors are highly dependent on the vehicle

A

Cv - concentration of drug in vehicle

Km - partition coefficient

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15
Q

what does Cv also represent

A

solubility of the drug in vehicle

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16
Q

what is an important factor in the rate and extent of absorption in vehicles

A

Maximizing the movement/partitioning of the drug from vehicle to the SC (Km) – the drug must ‘escape’ from the vehicle

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17
Q

what is Km described as

A

the equilibrium solubility of the drug in the SC relative to its solubility in the vehicle
Km = Csc/Cv

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18
Q

a lipophilic drug in lipophilic base diffuses poorly - true or false

A

false

it diffuses well

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19
Q

a lipophilic drug in hydrophilic base diffuses poorly - true or false

A

false

it diffuses very well

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20
Q

a hydrophilic drug in lipophilic base diffuses poorly - true or false

A

true

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21
Q

a hydrophilic drug in hydrophilic base diffuses poorly - true or false

A

true

it barely diffuses at all

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22
Q

what provides the driving force of drug transfer in topically applied drugs

A

soluble fraction

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23
Q

what do excipients do in a vehicle

A

enhance solubility and absorption

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24
Q

how can the duration of effectiveness in a transdermal patch be increased and provide a constant rate of delivery

A

excess, non dissolved drug

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25
Q

why are topically applied drugs generally poorly absorbed

A

only a small fraction partitions into the stratum corneum

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26
Q

how can partitioning be improved

A

hydration of the skin by occlusion (i.e. cling film)

inclusion of excipients

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27
Q

what can affect absorption of topically applied drugs

A

nature of the skin

drug/pharmaceutical preparation

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28
Q

what about the nature of the skin affects absorption

A

site of application (thickness of stratum corneum)
hydration of skin
integrity of the epidermis (trauma, inflammation)

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29
Q

what about the drug/pharmaceutical preparation affects absorption

A

drug concentration
drug salt
vehicle

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30
Q

what receptors does glucocorticoids signal via

A 
nuclear receptors class 1
GRalpha
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31
Q

what type of molecules are glucocorticoids

A

lipophilic

32
Q

what happens when glucocorticoids bind with GRalpha

A

they release inhibitory heat shock proteins

33
Q

what happens to the activated receptor in glucocorticoids reaction

A
  • translocates to the nucleus aided by importing
  • receptor monomers assemble into homodimers and bind to glucocorticoid response elements (GRE)
  • transcription of specific genes is either ‘switched-on’ (transactivated) or ‘switched off’ (transrepressed) to alter mRNA levels and the rate of synthesis of mediator proteins
34
Q

what are advantages of subcutaneous route of injection

A
  • absorption slow due to poor vascular supply
  • route of administration for many protein drugs
    suitable for oil-based drugs
  • can introduce depot of drug under skin that is slowly released
  • simple and painless
35
Q

what are disadvantages of subcutaneous route of injection

A

injection volume limited

36
Q

advantages of skin application for drugs for systemic effect

A
  • simple and non-sterile
  • steady state plasma concentration
  • avoids first pass metabolism
  • can be terminated rapidly
37
Q

what drugs are suitable for TDD

A
  • low molecular weight
  • lipophilic
  • potent
  • brief half-life
38
Q

advantages of TDD

A
  • steady state drug delivery
  • decreased dosing frequency
  • avoidance of first pass metabolism
  • user friendly
  • painless
39
Q

disadvantages of TDD

A
  • allergies
  • cost
  • few drugs suitable
40
Q

examples of drugs that use TDD

A

nicotine, GTN

41
Q

what are the types of drug eruptions

A

immunologically-mediated reactions (“allergic” - Type I, II, III, IV)
not immunologically-mediated reactions

42
Q

which is dose dependant and which is not

A

immunologically-mediated reactions; not dose dependant

not immunologically-mediated reactions; dose dependant

43
Q

who to consider for drug eruptions

A

Any patient who is taking medication and develops a symmetric skin eruption of sudden appearance.

44
Q

risk factors for development of drug eruptions

A 
Age (younger adults > infants/elderly)
Gender (F>M)
Genetics
Concomitant disease (viral infections i.e. HIV/EBV; and CF)
Immune status 
Chemistry (high molecular weight, NSAIDS)
Route
Dose
Kinetics/half life
45
Q

what is the most common drug eruption

A

Exanthematous

- widespread symmetrically distrubyted rash; maculapapula

46
Q

what is spared usually in an exanthematous drug eruption

A

mucous membrane

47
Q

what is common in an exanthematous drug eruption

A

pruritus/itch

mild fever

48
Q

what are indicators of a severe reaction

A 
Involvement of mucous membrane and face.
Facial oedema & erythema.
Widespread confluent erythema.
Fever (>38.5⁰C).
Blisters, purpura, necrosis.
Lymphadenopathy, arthalgia.
Shortness of breath, wheezing.
49
Q

common drugs associated with exanthematous reactions

A 
NSAID
Penicillins 
Erythromycin
Streptomycin
Allopurinol
50
Q

what are the 2 modes of action of a urticarial drug reaction

A
  • immediate IgE- mediated hypersensitivity reaction (Type I) after rechallenge with drug (β-lactam antibiotics)
    OR
  • Direct release of inflammatory mediators from Mast cells on first exposure (aspirin, opiates, NSAIDs, muscle relaxants, vancomycin)
51
Q

what drugs can cause acne

A

glucocorticoids
androgens
lithium

52
Q

what drugs can cause AGEP (Acute generalised exanthematous pustulosis)

A

antibiotics
CCB
antimalarials

53
Q

what can ACE inhibitors, penicillin and furosemide cause

A

Drug-induced bullous pemphigold

54
Q

what are the signs of a fixed drug eruption

A

Well demarcated round/ovoid plaques.
Red, painful.
Hands, genitalia, lips, occasionally oral mucosa.
Resolves with persistent pigmentation when the drug is stopped.
Can re-occur on the same site on re-exposure to the drug.
Usually mild when restricted to a single lesion.
Can present as eczematous lesions, papules, vesicles or urticaria.

55
Q

drugs associated with fixed drug eruptions

A

NSAIDS
Paracetamol
Doxycycline
Carbamazepine

56
Q

what is SCAR

A

Severe Cutaneous Adverse Reactions

Combine cutaneous and systemic symptoms

57
Q

what are included in SCARs

A

Stevens-Johnson syndrome (SJS)
Toxic epidermal necrolysis (TEN)
Drug reaction with eosinophilia and systemic symptoms (DRESS)
Acute generalised exanthematous pustulosis (AGEP)

58
Q

what are acute phototoxic drug reactions

A

skin toxicity
systemic tocisity
photodegradation

59
Q

what are chronic phototoxic drug reactions

A

pigmentation
photoagin
photocarcinogenesisi

60
Q

what is phytotoxic cutaneous drug reactions

A

Non-immunological mediated skin reaction which will arise in any individual providing there is enough photo-reactive drug and the appropriate wavelength of light.

61
Q

signs of phototoxicity

A

Immediate prickling with delayed erythema and pigmentation
Exaggerated sunburn
Exposed telangiectasia (dilatation of capillaries)
Delayed 3-5 days erythema and pigmentation
Increased skin fragility (skin takes longer to heal)

62
Q

management of drug eruptions

A

stop the drug
topical steroids
antihistamines

63
Q

topical treatments advantages

A

direct application

reduced systemic effects

64
Q

topical treatments disadvantages

A

time consuming
correct dosage can be difficult
messy to use

65
Q

mode of action of corticosteroids

A

Vasoconstrictive
Anti-inflammatory
Antiproliferative

66
Q

what do topical steroids do

A

reduce inflammation

cause immunosuppression

67
Q

side effects of topical steroids

A 
thinning of the skin
purpura
stretch marks
steroid rosacca
fixed telangectasia
perioral dermatitis
68
Q

topical antibiotics used in Acne

A

clindamycin
erythromycin
tetracycline

69
Q

topical antibiotics used in Rosacea

A

Metronidazole

70
Q

topical antibiotics used in impetigo

A

mupirocin

fusidic acid

71
Q

when are keratolytics (e.g. salicyclin acid) used

A

soften keratin

  • viral warts
  • Hyperkeratotic eczema & psoriasis
  • Corns and calluses
  • To remove keratin plaques in scalp
72
Q

possible psoriasis treatment

A 
Emollients and choice of:
 Coal tar 
 Vitamin D analogue
 Keratolytic
 Topical steroid
 Dithranol
73
Q

side effect of dithranol

A

can stain and/or burn skin

74
Q

when is Imiquimod used

A

genital warts

superficial BCC

75
Q

when are calicneurin inhibitors used

A

atopic eczema

76
Q

examples and mode of action of calicneurin inhibitors

A

Tacrolimus, pimecrolimus

Suppress lymphocyte activation

Dermatology SB (11 decks)

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