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Dermatology SB > Pharmacology > Flashcards

Pharmacology Flashcards

(76 cards)

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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
why are topically applied drugs generally poorly absorbed
only a small fraction partitions into the stratum corneum
26
how can partitioning be improved
hydration of the skin by occlusion (i.e. cling film) | inclusion of excipients
27
what can affect absorption of topically applied drugs
nature of the skin | drug/pharmaceutical preparation
28
what about the nature of the skin affects absorption
site of application (thickness of stratum corneum) hydration of skin integrity of the epidermis (trauma, inflammation)
29
what about the drug/pharmaceutical preparation affects absorption
drug concentration drug salt vehicle
30
what receptors does glucocorticoids signal via
``` nuclear receptors class 1 GRalpha ```
31
what type of molecules are glucocorticoids
lipophilic
32
what happens when glucocorticoids bind with GRalpha
they release inhibitory heat shock proteins
33
what happens to the activated receptor in glucocorticoids reaction
- 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
what are advantages of subcutaneous route of injection
- 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
what are disadvantages of subcutaneous route of injection
injection volume limited
36
advantages of skin application for drugs for systemic effect
- simple and non-sterile - steady state plasma concentration - avoids first pass metabolism - can be terminated rapidly
37
what drugs are suitable for TDD
- low molecular weight - lipophilic - potent - brief half-life
38
advantages of TDD
- steady state drug delivery - decreased dosing frequency - avoidance of first pass metabolism - user friendly - painless
39
disadvantages of TDD
- allergies - cost - few drugs suitable
40
examples of drugs that use TDD
nicotine, GTN
41
what are the types of drug eruptions
immunologically-mediated reactions ("allergic" - Type I, II, III, IV) not immunologically-mediated reactions
42
which is dose dependant and which is not
immunologically-mediated reactions; not dose dependant | not immunologically-mediated reactions; dose dependant
43
who to consider for drug eruptions
Any patient who is taking medication and develops a symmetric skin eruption of sudden appearance.
44
risk factors for development of drug eruptions
``` 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
what is the most common drug eruption
Exanthematous | - widespread symmetrically distrubyted rash; maculapapula
46
what is spared usually in an exanthematous drug eruption
mucous membrane
47
what is common in an exanthematous drug eruption
pruritus/itch | mild fever
48
what are indicators of a severe reaction
``` 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
common drugs associated with exanthematous reactions
``` NSAID Penicillins Erythromycin Streptomycin Allopurinol ```
50
what are the 2 modes of action of a urticarial drug reaction
- 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
what drugs can cause acne
glucocorticoids androgens lithium
52
what drugs can cause AGEP (Acute generalised exanthematous pustulosis)
antibiotics CCB antimalarials
53
what can ACE inhibitors, penicillin and furosemide cause
Drug-induced bullous pemphigold
54
what are the signs of a fixed drug eruption
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
drugs associated with fixed drug eruptions
NSAIDS Paracetamol Doxycycline Carbamazepine
56
what is SCAR
Severe Cutaneous Adverse Reactions | Combine cutaneous and systemic symptoms
57
what are included in SCARs
Stevens-Johnson syndrome (SJS) Toxic epidermal necrolysis (TEN) Drug reaction with eosinophilia and systemic symptoms (DRESS) Acute generalised exanthematous pustulosis (AGEP)
58
what are acute phototoxic drug reactions
skin toxicity systemic tocisity photodegradation
59
what are chronic phototoxic drug reactions
pigmentation photoagin photocarcinogenesisi
60
what is phytotoxic cutaneous drug reactions
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
signs of phototoxicity
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
management of drug eruptions
stop the drug topical steroids antihistamines
63
topical treatments advantages
direct application | reduced systemic effects
64
topical treatments disadvantages
time consuming correct dosage can be difficult messy to use
65
mode of action of corticosteroids
Vasoconstrictive Anti-inflammatory Antiproliferative
66
what do topical steroids do
reduce inflammation | cause immunosuppression
67
side effects of topical steroids
``` thinning of the skin purpura stretch marks steroid rosacca fixed telangectasia perioral dermatitis ```
68
topical antibiotics used in Acne
clindamycin erythromycin tetracycline
69
topical antibiotics used in Rosacea
Metronidazole
70
topical antibiotics used in impetigo
mupirocin | fusidic acid
71
when are keratolytics (e.g. salicyclin acid) used
soften keratin - viral warts - Hyperkeratotic eczema & psoriasis - Corns and calluses - To remove keratin plaques in scalp
72
possible psoriasis treatment
``` Emollients and choice of: Coal tar Vitamin D analogue Keratolytic Topical steroid Dithranol ```
73
side effect of dithranol
can stain and/or burn skin
74
when is Imiquimod used
genital warts | superficial BCC
75
when are calicneurin inhibitors used
atopic eczema
76
examples and mode of action of calicneurin inhibitors
Tacrolimus, pimecrolimus | Suppress lymphocyte activation

Dermatology SB (11 decks)

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