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Skin ISU Flashcards

1
Q

what are some of the benefits of produgs

A

increased solubility in lipid or water
improved taste
improved stability
reduced toxicity
modify time of duration of action
deliver drug to specific site

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2
Q

differences between bio precursor and carrier prodrugs

A

bio contain the embryo of the active species within their structure and require metabolic modification through a step or series of steps to become active e.g. oxidation or reduction via enzymes.

carrier is a combination of active drug and carrier species which are linked by a functional group which can easily be metabolised such as ester or amide.

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3
Q

how is the protide approach used in nucleoside analogues?

A
  • Add a phosphate or phosphonate group to the NA prodrug
  • this eliminates the slow rate limiting step in vivo
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4
Q

how do photoactivated prodrugs work

A

-they are activated by certain wavelengths of light (visible or UV) to an excited state in order for them to react with a substrate. Generally results in destruction of target cell
- molecule can decay with phosphorescence or fluorescence

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5
Q

important points about the structure of steroids

A
  • all share common tetracyclic structure but have different functional groups and substituents.
  • have a chair conformation where stereochemistry of the three 6 membered rings are all identical in all steroids
    -only one stereoisomer occurs naturally for any particular steroid.
    -double bonds are identified using delta symbol and carbon number.
    -they are hydrophobic in nature
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6
Q

what is the main glucocorticoids and what are they used for

A

corticosterone, cortisone, cortisol
carb,fat,protein metabolism
mainly in liver, muscles and brain cells
excess= Cushing’s syndrome
deficit = Addison’s disease

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7
Q

what is the main mineralocorticoid and what it is used for

A

Aldosterone
regulates electrolyte balance (sodium ion retention in kidney cells)
Excess = Conn’s disease

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8
Q

what do all adrenocorticoids have in their structure

A

pregnane skeleton (2C side chain at C17)

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9
Q

what structural features of cortisol are important for its activity

A

essentially all of them, the removal of groups reduces/eliminates activity

However additional groups can enhance the activity which allows for one of the original functional groups to be removed

for example adding 9alpha-fluoro substituent gives fludrocortisone which has 10 times activity, but also 300-600 increased mineralocorticoid activity

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10
Q

where is the origin of cortisol

A

released from adrenal cortex above the kidneys

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11
Q

what are some clinical uses for topical corticosteroids (TCS)

A

-atopic eczema
-contact dermatitis
-Psoriasis

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12
Q

MOA of TCS for anti-proliferative effect

A
  • Increased Lipocortin 1 reduces keratinocytes proliferation and collagen synthesis in epidermis + dermis.
  • stops migration of T cells, dendritic cells and macrophages to epidermis
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13
Q

MOA of TCS for anti-inflammatory effects

A

-TCS synthesise lipocortin 1
-this inhibits phospholipase A enzyme (which converts phospholipids to arachidonic acid) –> decreases production of prostaglandins and leukotrienes.
-TCS directly inhibit COX-2 enzymes which inhibits production of prostaglandins
-resulting in reduced inflammation.

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14
Q

MOA of TCS for immunosuppressive effect

A
  • inhibit humoral factors involved in the inflammatory response as well as suppression of maturation, differentiation, and proliferation of all immune cells
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15
Q

MOA of TCS for vasoconstrictive effect

A

unknown
-thought to be related to inhibiting vasodilators, histamine,bradykinins)
- vasoconstriction of the blood vessels in the upper dermis decreases inflammatory mediators to the region.

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16
Q

cutaneous adverse effects of TCS

A
  • atrophy - epidermal thinning (reversible with cessation of TCS)
    -Striae - appear as scars and permanent
    -rosacea due to topical fluorinated steroids
    -less common are hypertrichosis (excessive hair growth) and purpura (delayed wound healing)
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17
Q

systemic adverse effects of TCS

A

-HPA axis suppression
-Cushing’s syndrome
-Hypertension
-Hyperglycaemia
-Glaucoma

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18
Q

contraindications related to TCS

A
  • bacterial infections as they mask infection
  • delaying diagnosis and treatment
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19
Q

why are anabolic steroids not topical corticosteroids?

A

-manufactured from male hormone testosterone
-usually abused and taken without medical advice to increase muscle mass and improve athletic performance

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20
Q

Define Eczema and it’s causes and symptoms

A
  • Chronic inflammation of the skin (atopic increased immune response to an allergen or trigger.
  • Causes: genetic link with patients if FHx of atopic disease. Mutation of Filaggrin gene in 50% of cases
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21
Q

Discuss management and treatment options for Eczema

A
  • self care: use of emollients, avoid exacerbating triggers
  • mild: emollients + mild potency topical corticosteroid in red areas (hydrocortisone 1%)
  • moderate: Betamethasone val 0.025% or clobetasone 0.05%, dressings, non-sedative antihistamine for itching
  • severe: very potent TCS betamethasone val 0.1%. Moderate potency for delicate skin areas max 5 days use. Not used in children under 12mo.
    -For infected eczema 1st line is Flucloxacillin
    -Clarithromycin if penicillin allergy.

-emollients used at least 4 times a day and applied 15-30 mins before TCS

-Weekend regiment for TCS is apply on consecutive days, nothing in the week or twice weekly apply on 2 days per week.

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22
Q

Define Psoriasis and it’s causes and symptoms

A

systemic immune-mediated inflammatory skin disease. Well-defined plaques caused by hyperproliferation and abnormal differentiation of immune cells.

-triggered by step infection, drugs, hormonal changes, HIV, smoking, alcohol, obesity

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23
Q

Discuss management and treatment options in Psoriasis

A
  • Emollients
  • vit D preparations e.g. Calcipotriol, Calcitriol, Tacalcitol (not to be used on face and avoid sunlight + contraindicated with calcium disorders, kidney +liver disease and hypersensitivity)
    -corticosteroids
    -salicylic acid
    -coal tar

-Calcipotriol OD/BD max 100g per week, 60mL scalp solution
-if used in combination with Betamethasone OD for 4 weeks (1-4g OD) DONT EXCEED 30% BODY SURFACE

-Calcitriol Apply BD, max 30g/day

-Tacalcitol OD, max 10g/10mL day

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24
Q

define cellulitis and its causes and symptoms

A

acute bacterial infection of dermis
pain, warmth, swelling, redness of infected area, fever, nausea.

Caused by microorganisms entering skin e.g. strep pyogenes

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25
management and treatment of cellulitis
-urgent hosp admission if class III or IV suspected or really young or frail or orbital cellulitis - First line Flucloxacillin - pen allergy Clarithromycin -Metronidazole if anaerobe cause, avoid alcohol
26
define acne and its causes and symptoms
chronic inflammatory skin condition, blocked inflamed pilosebaceous unit. Affects face back chest. -non inflam comedones (whiteheads and blackheads) -can develop to papules, nodules and cysts. -excess sebum produced + follicular plugs. -Causes are genetics + diet
27
define Rosacea and its causes and symptoms
-chronic inflammatory skin condition which affects the centrofacial region -symptoms include facial flushing, erythema, papules ,pustules -genetic link, immune system dysregulation and dysregulation in inflammatory response
28
Management and treatment options for acne
6-8 weeks before any improvement Mild - benzoyl peroxide + clindamycin(topical) Moderate - topical adapalene (retinoids) + benzoyl peroxide, PLUS oral lymecycline/doxycycline OD Severe - Combination Azelaic acid BD PLUS oral lymecycline/doxycycline OD oral antibiotics used if topical fail Tetracyclines can't be used in pregnancy so use Erythromycin LFT needed before treatment for oral antibiotics review treatment @6 weeks then every 12 weeks - oral contraceptives (combined) used in acne with patients who have PCOS (use if first line not successful)
29
discuss management and treatment of Rosacea
30
what are the layers of the skin from outside to inside?
stratum corneum, viable epidermis, dermis, subcutaneous fat
31
what is the difference between topical and transdermal drug delivery?
topical - we want the drug to act within the stratum corneum or epidermis locally. transdermal - we want the drug to enter the bloodstream after permeating the skin and act more systemically
32
what is a ceramide - rich lipid region?
within stratum corneum, mortar regions have them in which there are varying areas of hydrophilic and hydrophobic regions. Presents a barrier to permeating drug molecules.
33
what could provide greater occlusivity to keep give greater topical absorption of the drug?
hydrophobic polymer patches ointment if oil-based w/o cream
34
how do we measure topical drug delivery?
in vitro (lab) in vivo (on animals)
35
how does microdialysis work in vivo
insertion of dialysis tubing into the dermis perfusate pump through tubing drug molecules enter perfusate analysis
36
how does tape stripping work in vivo
apply cream or ointment to skin layers of skin are removed using adhesive tape take the tape and remove drug using solvent and quantified tape strips can also be examined under a microscope
37
how does a skin biopsy work in vivo
could be of any layer of skin potentially painful due to network of nerves punch biopsy to quantify drug conc in each layer
38
how does patch testing work in vivo
measure redness within the skin based on physiological response e.g. vasodilation
39
what method of in vitro is used for evaluation of topical and transdermal drugs?
"Franz-type" diffusion cells quantifying what has permeated through the skin into the receptor compartment co-solvent can be used to improve "sink conditions" done at body temp
40
how do we chose skin membranes for "franz-type" diffusion
use human skin: full thickness, heat-separated epidermal membranes or just stratum corneum from surgery donor or donor shortly after death Use of animal skin - permeation characteristics differ synthetic membranes e.g. Strat-M
41
why is the transdermal route desirable?
-avoid first pass metabolism - controlled rate of delivery -avoid GI problems (pH, absorption, irritancy) - can be administered by the patient and favoured by patients -reduced dosage frequency --> better compliance -rapid identification of drug in emergencies -less painful than depot injections
42
limitations and challenges of TD delivery?
- skin is effective barrier -skin can metabolise drugs with bacterial enzymes - can cause irritant -small volume of distribution required, lag-time, tolerance induced by constant plasma levels e.g. nitrates. -more expensive to manufacture
43
what is the lag-time on a permeation profile graph
the start of steady-state delivery where the x-axis is intercepted
44
what is Fick's first law of diffusion?
passive diffusion of a permeant drug across skin at steady state J= Kp * C0 flux = permeability coefficient (cm /s) * permeant conc in the donor phase
45
what are the three ways in which transdermal delivery can be enhanced?
formulation manipulation (occlusive formulation or employing co-solvent) + supersaturation increasing drug conc skin modification - penetration enhancers (disrupt lipid arrangement, interact with intracellular proteins, or increase partitioning within stratum corneum) physical methods
46
what are the 4 common elements to all transdermal therapeutic systems
- drug -adhesive -backing layer -liner
47
what must be required from the adhesive in TTS
non-toxic compatible with drug and excipients allow bathing keeps patch in place for duration of treatment
48
what is required from the backing layer in TTS
- strong + multidirectional stretch - clear or opaque - may be occlusive -not interact with drugs or excipients
49
what is required from a liner in TTS
- removed easily -polymeric - compatible with formulation -usually occlusive
50
what is a drug-in-adhesive patch?
drug is contained in adhesive layer when liner is removed
51
what is a drug-in-matrix patch?
drug is incorporated in separate matrix loading dose may be included in adhesive layer
52
what is a rate-limiting membrane patch?
controls release of drug from liquid membrane is usually polymeric
53
how does electroporation work?
-creates transitory pores in cell membranes by applying a high voltage electrical current for short periods of time -acts on stratum corneum to create pores of <10nm -charged permeants move during voltage pulse + molecular diffusion occurs in pulse and afterwards. -enhances delivery of high MW drugs -challenges include pain or skin irritation.
54
how does sonophoresis work?
- uses ultrasound to modify stratum corneum arrangement -low freq used (20kHz-16MHz) - mechanism relies on thermal effects + cavitation in stratum corneum -uses coupling medium to transfer energy from probe to the skin
55
what is microneedling and what types of microneedles are there?
- 25 -2000 micrometres needles used - puncture the stratum corneum, but doesn't trigger nerves in dermis (painless) -allows entry for delivery of drugs types of microneedles: solid: puncture then apply TTD coated: coating of drug is on the needles when punctured Hollow: Attached to a reservoir Dissolving: needles stay stuck in the skin and slowly dissolve over time with the drug Hydrogel: designed to swell after being placed on skin
56
how does iontophoresis work?
Use of low electrical current to drive drugs across stratum corneum. cationic drug at the anode, anionic buffer ions at cathode electroosmosis occurs systemically so uncharged molecules can be "dragged" through stratum corneum. Trans appendageal routes e.g. sweat ducts are important for permeation also cationic (pos drugs) drugs are more efficient in iontophoresis
57
what is reverse iontophoresis and how could it be used?
extracting drug molecules through the stratum corneum using charge. Useful for needle-free blood monitoring potential used for charged and uncharged glucose molecules
58
What are Psoralen compounds and how do they react with UV radiation for PUVA therapy?
-found naturally -similar structure to coumarin (lactone) -used for vitilligo, psoriasis, cutaneous T-cell lymphoma. -intercalates into DNA + activated by exposure to UV radiation -known as PUVA therapy to create photoadduct (usually thiamine) -monoadduct can be excited by another photon so it can bond again and crosslink within the DNA -capable of releasing singlet oxygen + have been shown to block ion channels
59
give an example of a psoralen drug
Methoxasalen, Khellin, Photofrin
60
how can you eliminate the activity of deoxysteroids such as cortisol?
removal of 21-OH group
61
how can you further activate deoxysteroids such as cortisol?
add substituents at C6 +C9 esterification of the 17-OH (+ introduce halogen at C-21)
62
how is activity dropped in ketosteroids and brought back
- dropped by loss of 11-OH group with keto group -restored by halogen at C-9 and C-21
63
how are wounds to the skin classified
Grade I - only epidermis Grade II - epidermis and dermis Grade III + IV - exposed to tendons, muscle and bone
64
what are the four physiological stages of wound healing?
Haemostasis phase Inflammation phase Proliferation/Granulation Remodelling phase
65
how does the haemostasis phase work?
vasoconstriction - release of endothelins + prostaglandins primary haemostasis - platelet plug formation (release of ADP, serotonin + thromboxane A2) secondary haemostasis - coagulation cascade --> thrombus formation (soluble prothrombin to insoluble thrombin)
66
How does the inflammation phase work in wound healing? (4-6 days)
aim to minimize infection, activate keratinocyte regeneration + promote new vessel formation Early phase - chemokines --> activate neutrophils, toxic proteolytic granules kill microbes and phagocytosis Late phase - Macrophages replace neutrophils + cause neutrophil clearance
67
what happens in the proliferation phase of wound healing? (day 4 to 21)
formation of granulation tissue, angiogenseis, wound contraction, epidermal resurfacing Granulation - fibroblasts migrate + synthesise ECM Angiogenesis - mediated by macrophages + formation of new blood vessels+ endothelial cells are activate to proliferate toward hypoxia and differentiate into capillaries Wound contraction - myofibroblasts contract reducing the size of the wound Re-epithelialisation - Keratinocytes at the wound edge are activated to: lose cell adhesions to migrate over the wound bed, divide and undergo keratinisation to reform the epidermal layer in the gap
68
What happens in the remodelling phase of wound healing? (21 st day to 2 years)
further wound contraction + scar maturity Macrophages break down the excess ECM and engulf ECM tissue --> tissue reshape Collagen III of granulation tissue is replaced with stronger collagen I
69
what factors influence choice of wound dressing?
type of wound wound characteristics treatment goals anatomical location patient related factors
70
what UV radiation penetrates the skin
UVA - longer wavelengths goes 20% deep into the dermis UVB- shorter wavelength 10% in dermis
71
what effect does UVA have on the skin
skin ageing DNA damage - cancer
72
what effect does UVB have on the skin
tanning + skin cancer inflammation + sunburn
73
how does vitamin D3 biosynthesis work
UVB photons absorbed by 7 -dehydrocholesterol which is photochemically converted into PRE-vitamin D3--> thermal isomerisation to form vitamin D3--> bloodstream in the liver: inactive vit D3 is converted to 1,25 dihydoxyvitamin D3 (active) by two hydroxylations in the liver and kidneys
74
how does vit D3 effect the skin
keratinocytes respond at vitamin D receptors (deficiency is associated with psoriasis and atopic dermatitis)
75
how does phototherapy work
controlled amin of UV radiation to treat psoriasis and chronic eczema 2-3 times per week for 6-10 weeks uses narrowband UVB or PUVA (with psoralins) mechanism: anti inflammatory effect (reduces cytokine production and keratinocyte proliferation) keratinocyte regulation: (increased keratinocyte apoptosis) immunosuppression effect: decreased infiltration of T cells) Antipruritic effect
76
what are the main cells effected within skin cancer
squamous basal melanocytes
77
how does DNA damage occur from UVB radiation
incorrect base pairing which causes mutations or breaks in key genes such as oncogenes
78

PMP202 (5 decks)

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