Skin Flashcards
(255 cards)
1
Q
skin conditions where Topical Coritcosteroids commonly used to treat?
A
Atopic Eczema, Psoriasis, Contact Dermititis
2
Q
Main anti-inflammatory mechanism of TCS?
A
TCS STIMULATE lipocortin-1, which INHIBITS phospholipase A2. (Enzyme which releases arachidonic acid) hence REDUCING Prostaglandins
3
Q
How do TCS affect gene expression?
A
UPREGULATE (increase activity) anti-inflammatory genes + DOWNREGULATE pro-inflammatory genes
4
Q
Anti-proliferative effect of TCS?
A
REDUCE keratinocyte proliferation (rapid growth of skin cells) + collagen synthesis, leading to thinner skin. (Good for Psoriasis)
5
Q
How do TCS exert immunosuppressive effects?
A
INHIBIT immune cell function, REDUCING inflammation in skin diseases e.g. psoriasis.
6
Q
Examples of TCS drugs by potency? (mild to potent)
A
Mild inflammation : Mild: Hydrocortisone 0.1–2.5%
Moderate inflammation : Betamethasone valerate 0.025%
Potent inflammation : Betamethasone valerate 0.1%
7
Q
Common side effects of TCS ?
A
Skin atrophy (thinning skin)
8
Q
What causes TCS-induced skin atrophy?
A
Inhibition of keratinocyte and collagen production, leading to epidermal thinning
9
Q
systemic side effects of TCS?
A
HPa axis supression, Cushings syndrome,
10
Q
Why shouldn’t TCS be used in bacterial skin infections?
A
MASKS infection signs, delaying proper diagnosis and treatment.
11
Q
Roles of skin ?
A
Barrier (mechanical, microbial, UV)
✅ Temperature regulation
✅ Sensory detection
✅ Vitamin D synthesis
✅ Water retention/excretion
12
Q
What is a prodrug?
A
An inactive compound that is converted into an active drug inside the body.
13
Q
Why are prodrugs used?
A
To improve solubility, taste, stability, reduce toxicity, target delivery, and control duration.
14
Q
What are carrier prodrugs?
A
Drug + carrier compound that is metabolised off after absorption.
15
Q
What are bioprecursor prodrugs?
A
Drugs activated by enzymatic or chemical transformation (e.g., levodopa → dopamine).
16
Q
What are photoactivated prodrugs used for?
A
Photodynamic therapy — light-activated drugs that kill target cells (e.g., cancer).
17
Q
What is ProTide technology?
A
A method to deliver nucleoside monophosphate prodrugs into cells effectively.
18
Q
Where is ProTide used?
A
Antiviral (e.g., remdesivir), anticancer, Parkinson’s treatments.
19
Q
What is the common structure of steroids?
A
A tetracyclic (4-ring) backbone found in all steroids.
20
Q
What are glucocorticoids?
A
Steroid hormones that regulate metabolism and reduce inflammation (e.g., cortisol).
21
Q
What are mineralocorticoids?
A
Steroids that regulate salt and water balance (e.g., aldosterone).
22
Q
What conditions are linked to glucocorticoid imbalance?
A
Excess = Cushing’s; deficiency = Addison’s.
23
Q
What condition is caused by mineralocorticoid excess?
A
Conn’s syndrome.
24
Q
What does the 9α-fluoro modification do?
A
Increases both glucocorticoid and mineralocorticoid activity.
25
What does a ∆¹ double bond do in steroids?
Increases glucocorticoid potency without affecting mineralocorticoid action.
26
What is the effect of 6α-methyl or fluoro groups?
Block metabolism, extending half-life.
27
What does a 16-methyl or hydroxyl group do?
Reduces mineralocorticoid activity.
28
What is the main barrier to drug delivery through the skin?
The stratum corneum.
29
Why must drugs have intermediate Log P for topical delivery?
To ensure they are neither too hydrophilic nor too lipophilic, allowing them to permeate the skin.
30
What drug properties favor skin permeation?
Low molecular weight (<500 Da), intermediate Log P, and unionized form if weak acid/base.
31
What structure within the stratum corneum presents a barrier to drug molecules?
Ceramide-rich lipid lamellae with alternating hydrophilic and hydrophobic regions.
32
Why is drug delivery via sweat ducts and hair follicles limited?
Most drug permeation occurs through the stratum corneum, not appendages like sweat ducts or follicles.
33
What are examples of drug targets at the skin surface?
UV radiation (sunscreens), insect bites (repellents like DEET).
34
What conditions are treated by targeting the stratum corneum?
Bacterial and fungal infections, parasitic infestations.
35
Which skin layer contains keratinocytes, T-cells, and melanocytes?
The viable epidermis.
36
Which conditions are treated by targeting keratinocytes?
Psoriasis, atopic dermatitis, skin cancer.
37
Which dosage form is greasy and occlusive?
Ointments.
38
Which topical dosage form is typically aqueous and thickened?
Gels.
39
Which topical dosage forms are best for short-term use on large areas?
Sprays and dusting powders.
40
What is occlusivity in topical drug delivery?
The ability of a formulation to retain moisture and enhance skin hydration.
41
How does occlusion enhance drug delivery?
Hydrates stratum corneum, disrupting lipids and enhancing drug diffusion.
42
What in vivo method uses adhesive tape to sample skin layers?
Tape stripping.
43
What is microdialysis used for in drug delivery evaluation?
To sample drug concentration in the dermis using a perfusate system.
44
What tool is commonly used for in vitro skin permeation studies?
Franz diffusion cells.
45
What is the preferred animal model for skin permeation studies?
Porcine ear skin.
46
Why are synthetic membranes like Strat-M used?
They provide a reproducible alternative to human or animal skin in permeation studies.
47
Why are in vivo methods less favored for topical evaluation?
They are invasive and not ideal for evaluating drug levels within skin layers.
48
What is eczema?
A chronic inflammatory skin condition characterized by dry, itchy, and inflamed skin. Can be atopic or contact type.
49
What is the difference between eczema and dermatitis?
Eczema is typically endogenous (e.g., atopic), while dermatitis refers to reactive changes (e.g., contact dermatitis).
50
What are common eczema triggers?
Soaps, detergents, animal hair, dust mites, pollen, infection, stress, clothing, temperature changes.
51
How is the severity of eczema classified?
Clear, mild, moderate, severe, and infected based on dryness, itching, excoriation, and infection signs.
52
What is the first-line treatment for mild eczema?
Frequent emollient use + mild potency corticosteroids like hydrocortisone 1%.
53
What antibiotics are used for infected eczema?
Flucloxacillin (1st line), clarithromycin (if penicillin-allergic), fusidic acid (topical for localized infections).
54
What is eczema herpeticum?
A herpes simplex virus infection in eczema-affected skin. It's a medical emergency requiring urgent referral.
55
How should emollients be applied?
Liberally and frequently, at least QDS. Apply in the direction of hair growth, ideally 15–30 minutes before steroids.
56
What are the 4 potencies of topical corticosteroids?
Mild, Moderate, Potent, and Very Potent.
57
What are adverse effects of topical corticosteroids?
Skin thinning, striae, infection worsening, acne, allergic dermatitis, depigmentation, excess hair.
58
What is the finger-tip unit (FTU)?
A method to measure topical application: 1 FTU = ~500 mg, covers an area twice the size of a flat hand.
59
What is psoriasis?
A systemic immune-mediated skin disease causing red, scaly plaques due to hyperproliferation and abnormal differentiation of skin cells.
60
What are common psoriasis triggers?
Strep infections, NSAIDs, UV light, trauma, stress, alcohol, obesity, smoking.
61
What are types of psoriasis?
Chronic plaque, guttate, scalp, pustular, flexural, erythrodermic, nail psoriasis, psoriatic arthritis.
62
What is the PASI score?
Psoriasis Area and Severity Index – assesses severity based on lesion characteristics and body surface area.
63
What are first-line topical treatments for psoriasis?
Emollients, corticosteroids, vitamin D analogues, salicylic acid, coal tar.
64
What is the role of vitamin D analogues in psoriasis?
They reduce abnormal keratinocyte proliferation and promote normal skin growth.
65
How is dithranol used in psoriasis?
Applied once daily, starting at 0.1% and increasing weekly. Wash off after 30–60 mins. Stop if irritation occurs.
66
When is phototherapy used for psoriasis?
When topical therapy fails or for widespread disease. Types include UVB alone or PUVA.
67
What are examples of systemic psoriasis treatments?
Methotrexate, ciclosporin, acitretin, biologics (e.g., etanercept, adalimumab).
68
What is the most common cause of folliculitis?
Staphylococcus aureus.
69
What are the symptoms of folliculitis?
Red, pus-filled pimples around hair follicles, itching and tenderness.
70
What is the difference between a furuncle and a carbuncle?
A furuncle is a deep folliculitis; a carbuncle is a cluster of connected furuncles with deeper inflammation.
71
What bacteria commonly causes erysipelas?
Streptococcus pyogenes.
72
What are signs of erysipelas?
Well-defined, shiny red rash with sharp borders, often on the face or legs, with fever and chills.
73
What is the main difference in appearance between cellulitis and erysipelas?
Cellulitis has less defined borders and involves deeper tissue compared to erysipelas.
74
What bacteria are commonly involved in cellulitis?
Streptococcus pyogenes and Staphylococcus aureus, including MRSA.
75
What characterizes necrotizing fasciitis?
Rapidly spreading infection with severe pain, swelling, blistering, and tissue necrosis.
76
What is first-line treatment for mild cellulitis?
Oral flucloxacillin.
77
What antibiotics are used for severe MRSA infections?
IV vancomycin, teicoplanin, or linezolid.
78
What virus causes common warts and verrucae?
Cutaneous HPV types like HPV-1 and HPV-2.
79
How are cutaneous warts treated?
Topical salicylic acid, cryotherapy, or ablative therapy.
80
What causes cold sores?
Herpes simplex virus type 1 (HSV-1).
81
What is the treatment for cold sores?
Topical acyclovir 5% cream if applied within 24h of symptoms.
82
What is shingles and what virus causes it?
Shingles is the reactivation of varicella zoster virus (VZV), which initially causes chickenpox.
83
What are first-line treatments for superficial dermatomycoses?
Topical imidazole creams like miconazole or clotrimazole.
84
What are symptoms of athlete’s foot?
Itching, scaling, and redness on the feet, especially between toes.
85
What is the mechanism of action of imidazole antifungals?
They inhibit ergosterol synthesis in fungal cell membranes.
86
When should patients with fungal infections be referred?
If there is scalp involvement, severe onychomycosis, or treatment failure.
87
What causes genital warts?
Low-risk mucosal HPV types, such as HPV-6 and HPV-11.
88
89
What are the key symptoms of cellulitis?
Pain, warmth, swelling, redness, possible blisters, fever, malaise.
90
What are the most common causes of cellulitis?
Streptococcus pyogenes, Staphylococcus aureus, Pseudomonas aeruginosa.
91
What are risk factors for cellulitis?
Lymphoedema, venous insufficiency, obesity, diabetes, pregnancy, skin trauma, alcohol misuse.
92
What is the Eron classification for cellulitis?
Class I-IV based on systemic involvement and comorbidity severity.
93
What is first-line treatment for cellulitis?
Flucloxacillin; Clarithromycin if penicillin allergic.
94
What is acne?
A chronic inflammatory condition affecting pilosebaceous units, with comedones, papules, pustules, nodules, and cysts.
95
What bacteria is associated with acne?
Propionibacterium acnes.
96
What are key factors contributing to acne?
Genetics, high GI diet, excess sebum, abnormal keratinization, bacterial colonization.
97
What are the types of acne based on severity?
Mild, moderate, severe, conglobate, and fulminans.
98
How long does it take to see improvement with acne treatment?
6–8 weeks.
99
What is the mechanism of benzoyl peroxide?
Antibacterial and keratolytic action.
100
What are side effects of topical retinoids?
Dryness, irritation, increased UV sensitivity.
101
When is oral isotretinoin used?
For severe, nodulocystic acne unresponsive to other treatments.
102
What is a major caution for isotretinoin?
Teratogenicity; pregnancy prevention required.
103
What are side effects of isotretinoin?
Dry lips, dermatitis, psychological effects, hepatotoxicity, hyperlipidemia.
104
What is rosacea?
Chronic inflammatory skin condition with flushing, erythema, papules, pustules, and telangiectasia.
105
What are common triggers for rosacea?
UV exposure, heat/cold, spicy food, alcohol, stress.
106
What is the first-line treatment for mild rosacea?
Topical brimonidine, ivermectin, metronidazole, or azelaic acid.
107
What is ocular rosacea?
Rosacea affecting the eyes, causing dryness, irritation, and telangiectasia on eyelids.
108
What are severe treatment options for rosacea?
Topical ivermectin + oral doxycycline MR 40 mg for 8-12 weeks.
109
What is acne vulgaris?
A chronic condition of the pilosebaceous unit affecting face, chest, and back, triggered by androgens, C. acnes, and genetics.
110
What hormonal mechanism contributes to acne?
Increased 5α-reductase converts testosterone to DHT, which stimulates sebaceous gland activity and keratinocyte hyperproliferation.
111
What forms the initial lesion in acne?
Microcomedone due to clogged hair follicles with keratin and sebum.
112
What bacteria contributes to inflammation in acne?
Cutibacterium acnes.
113
What are the clinical goals of acne treatment?
Reduce lesions, control inflammation, inhibit C. acnes, reduce sebum, and prevent scarring.
114
What is the mechanism of benzoyl peroxide?
Releases free radicals and benzoic acid to kill C. acnes and reduce inflammation.
115
How do topical retinoids work?
Bind retinoic acid receptors to modulate gene expression, normalize keratinisation, and reduce inflammation.
116
Why is oral isotretinoin effective in severe acne?
It reduces sebum production, inflammation, and normalizes keratinisation.
117
What is the mechanism of antibiotics in acne?
Inhibit bacterial protein synthesis, exerting a bacteriostatic effect against C. acnes.
118
How does azelaic acid help in acne?
Inhibits 5α-reductase, reduces C. acnes, and has mild anti-inflammatory effects.
119
What are key signs of plaque psoriasis?
Well-demarcated, silvery scaly plaques on elbows, knees, and scalp.
120
What cytokines are involved in psoriasis?
TNF-α, IL-17, and IL-23.
121
What triggers psoriasis?
Stress, infection, trauma, certain drugs, alcohol, and smoking.
122
What is the pathogenesis of psoriasis?
T-cell activation releases cytokines, causing keratinocyte hyperproliferation and inflammation.
123
How do vitamin D analogues treat psoriasis?
They bind intracellular receptors to reduce keratinocyte proliferation and inflammation.
124
What does coal tar do in psoriasis?
Inhibits DNA synthesis, reduces mitotic activity, and acts anti-inflammatory and anti-pruritic.
125
What is the mechanism of dithranol in psoriasis?
Generates free radicals in keratinocytes to reduce mitotic activity.
126
How does methotrexate help in psoriasis?
Inhibits DHFR, reducing DNA synthesis and suppressing T-cell activation.
127
What are biologics in psoriasis?
Engineered proteins that block inflammatory cytokines like TNF-α and IL-17.
128
What is a risk of vitamin D analogues?
Hypercalcaemia and irritation; avoid in severe liver/kidney disease and calcium metabolism disorders.
129
What is the aim of transdermal drug delivery (TDD)?
To deliver drugs through the stratum corneum and viable epidermis into systemic circulation.
130
What are the benefits of transdermal drug delivery?
Avoids first-pass metabolism, offers controlled drug release, improves compliance, avoids GI issues, and allows self-administration.
131
What are the challenges of TDD?
Skin barrier, enzymatic metabolism in skin, unsuitable for irritant drugs, pharmacokinetic limitations, and cost of formulations.
132
What are ideal properties for transdermal drugs?
MW < 500 Da, Log P 1–3.5, neutral at skin pH, high potency, water solubility > 100 µg/mL, non-irritant, high diffusivity.
133
What drugs are commonly administered via TDD?
Hyoscine, nicotine, fentanyl, buprenorphine, glyceryl trinitrate, estradiol, rivastigmine, levonorgestrel.
134
What is the permeability coefficient (Kp)?
A measure of how easily a drug diffuses through the skin; units are cm/s.
135
What is 'flux' in TDD?
The rate of drug delivery per unit area (mg/cm²/h), calculated using J = Kp × C₀.
136
What does Fick’s first law of diffusion describe?
Passive diffusion of a drug across the skin at steady state: J = Kp × C₀.
137
What methods are used to evaluate TDD?
In vivo methods (e.g., blood sampling) and in vitro models like Franz-type diffusion cells.
138
Why are Franz diffusion cells used?
To measure drug permeation and calculate flux through a skin or synthetic membrane.
139
How is lag time represented in a permeation profile?
The initial delay before steady-state flux is achieved on the cumulative permeation graph.
140
What are key limitations of drugs for TDD?
Drugs must have low dose requirements, be potent, non-irritant, and skin permeable.
141
What is the purpose of using mathematical models in TDD?
To predict permeability coefficients (Kp) and assess drug suitability for transdermal delivery.
142
What equation is used to predict permeability coefficient Kp?
log Kp = 0.71 log P – 0.0061 MW – 2.74 (Potts & Guy model).
143
What does QSAR stand for?
Quantitative Structure-Activity Relationship.
144
What are three categories of TDD enhancement techniques?
Formulation manipulation, skin modification, and physical methods.
145
What is supersaturation in TDD formulations?
A formulation state where drug concentration exceeds saturation, increasing thermodynamic activity for enhanced permeation.
146
How do penetration enhancers work?
By disrupting lipid layers, interacting with proteins, or increasing drug partitioning into the skin.
147
Name three ideal properties of a penetration enhancer.
Non-toxic, non-irritant, reversible action, compatible with drugs and excipients.
148
What is the mechanism of ethanol as a penetration enhancer?
Disrupts lipid order and increases drug partitioning into skin.
149
What is the role of the adhesive in a TTS (transdermal patch)?
To affix the patch to the skin and potentially contain the drug and excipients.
150
What are the four key components of a transdermal patch?
Drug, adhesive, backing layer, and liner.
151
What is a drug-in-adhesive patch?
A patch where the drug is incorporated within the adhesive layer.
152
What is a drug-in-matrix patch?
A patch where the drug is in a separate matrix layer that may or may not be in direct contact with the skin.
153
What is a rate-limiting membrane patch?
A patch with a membrane that controls the release rate of the drug from a reservoir.
154
Why are pressure-sensitive adhesives (PSAs) used in TDD?
They adhere based on applied pressure and are compatible with drug formulations.
155
What is the function of the liner in a patch?
Protects the formulation before use and is removed prior to application.
156
What types of materials are used for patch backing layers?
Polyethylene, polyester, or PVC depending on occlusivity needs.
157
Why might gels be used for transdermal delivery instead of patches?
They allow dose variation by adjusting the application area on the skin.
158
What is the main benefit of using a rate-limiting membrane in TTS?
It provides controlled drug release from the patch reservoir.
159
160
What is electroporation in transdermal drug delivery?
A technique using high-voltage pulses to create temporary pores in the stratum corneum for enhanced drug diffusion.
161
How does electroporation enhance drug delivery?
By electrophoresis during pulse and prolonged molecular diffusion through created pores.
162
What are drawbacks of electroporation?
Pain, skin irritation, and potential lasting changes to the stratum corneum.
163
What is sonophoresis?
Ultrasound-based method to disrupt SC lipids via thermal effects and cavitation, enhancing drug permeation.
164
What are two key mechanisms in sonophoresis?
Thermal effect (increased temperature) and cavitation (bubble formation).
165
What are microneedles?
Micron-sized needles that create microchannels in the SC to facilitate drug delivery.
166
List four types of microneedles.
Solid, coated, hollow, and dissolving microneedles.
167
What are hydrogel microneedles?
Microneedles that swell upon insertion, aiding delivery of hydrophilic and large molecules.
168
What are challenges with microneedle use?
Manufacturing cost, long-term safety, tip retention, and microbial contamination risks.
169
What is iontophoresis?
Use of low electric current to drive charged and neutral drugs across the skin.
170
How does iontophoresis work for neutral drugs?
Electroosmosis creates convective flow that drags neutral molecules across skin.
171
Why is iontophoresis more efficient for cationic drugs?
Because skin is negatively charged at pH 7, facilitating cation movement.
172
What limits current strength in iontophoresis?
Skin tolerance, typically up to 0.5 mA/cm².
173
What is reverse iontophoresis?
Extraction of molecules from the body through the skin using electrical current.
174
What was the GlucoWatch G2 Biographer?
A device for glucose monitoring via reverse iontophoresis; withdrawn due to accuracy and irritation issues.
175
What is the FreeStyle Libre system?
A subcutaneous glucose monitoring device, not truly transdermal.
176
What is a major advantage of physical enhancement methods?
They enable transdermal delivery of hydrophilic and macromolecular drugs.
177
What is psoralen and where is it found?
A photoactivated compound found in figs, celery, parsley, and citrus fruits.
178
What is the mechanism of action of psoralen in PUVA therapy?
Psoralen intercalates DNA and forms covalent crosslinks with thymine upon UVA exposure, inhibiting cell multiplication.
179
What is methoxsalen used for?
To treat vitiligo and psoriasis via PUVA therapy.
180
What are side effects of psoralen drugs?
Nausea, skin blistering, immune dysfunction, and risk of skin cancer.
181
What is khellin and how is it used?
An orally administered psoralen derivative used with UVA (KUVA therapy) to treat vitiligo and psoriasis.
182
What is Photofrin and how is it activated?
A photoactivated drug mixture used for tumors, activated by red light (590–640 nm) to generate singlet oxygen and radicals.
183
Why is cholesterol important in the body?
It's a cell membrane component, precursor for steroid hormones, vitamin D, and bile acids.
184
How can glucocorticoid activity be retained in deoxysteroids?
By adding substituents at positions 6 & 9 or halogens at C-21 to enhance activity.
185
What causes reduced activity in ketosteroids?
Replacing the 11β-OH with a keto group reduces activity unless in vivo reduction or other substitutions restore it.
186
What is the mechanism of spirothiazolidine derivatives of hydrocortisone?
Undergo ring opening to form imine and thiol, which forms disulfide bonds with tissue and allows slow drug release.
187
Why are spirothiazolidine derivatives effective?
They provide sustained release, higher activity than hydrocortisone, and lower systemic absorption.
188
What are the four phases of wound healing?
Haemostasis, Inflammation, Proliferation, Remodelling.
189
What occurs during the haemostasis phase?
Vasoconstriction, platelet plug formation, coagulation cascade and thrombus formation.
190
What triggers vasoconstriction after injury?
Release of endothelins and prostaglandins by damaged endothelium.
191
What is the role of thrombin in secondary haemostasis?
Converts fibrinogen to fibrin, forming a stable mesh.
192
What are the main goals of the inflammation phase?
Minimize infection, remove debris, promote angiogenesis, and initiate tissue repair.
193
Which cells are involved early and late in inflammation?
Neutrophils early, macrophages later.
194
What are the aims of the proliferation phase?
Granulation tissue formation, angiogenesis, wound contraction, and re-epithelialisation.
195
Which cells produce granulation tissue?
Fibroblasts synthesizing collagen III and proteoglycans.
196
What mediates angiogenesis during wound healing?
Macrophages releasing VEGF and PDGF.
197
What happens during the remodelling phase?
ECM reorganization, collagen III replaced by collagen I, and scar maturation.
198
What is a keloid scar?
A type of abnormal scar due to excessive collagen deposition.
199
What factors can impair wound healing?
Infection, poor oxygenation, foreign bodies, systemic diseases, smoking, age.
200
What is the TIME framework for wound assessment?
Tissue management, Inflammation/infection control, Moisture balance, Edge of wound.
201
What properties make an ideal wound dressing?
Moisture retention, oxygen permeability, thermal insulation, non-adhesive, non-toxic, microbial barrier.
202
What is the difference between primary and secondary dressings?
Primary is applied directly to the wound; secondary covers the primary dressing.
203
What are hydrocolloid dressings used for?
Clean granulating or sloughy/necrotic wounds; they are waterproof and assist autolytic debridement.
204
What type of wounds are alginate dressings best suited for?
Wounds with moderate exudate; they form a gel in presence of moisture.
205
What are hydrogel dressings used for?
To hydrate and soften dry necrotic tissue; provide soothing effect.
206
What is the role of antimicrobial dressings like honey or silver?
Control infection, reduce inflammation, manage odour, and stimulate healing.
207
What is wound debridement?
Removal of necrotic tissue to allow proper wound healing; can be autolytic, surgical, enzymatic, or mechanical.
208
What are the three types of UV radiation?
UVA (320–400 nm), UVB (290–320 nm), and UVC (100–290 nm).
209
Which UV rays penetrate the skin deepest?
UVA rays, reaching the dermis.
210
What is the main biological role of UVB in the skin?
UVB initiates vitamin D3 synthesis and contributes to tanning and sunburn.
211
How does UVB contribute to vitamin D synthesis?
It converts 7-dehydrocholesterol in the skin into pre-vitamin D3, which becomes vitamin D3.
212
What are the effects of vitamin D3 in the skin?
Regulates keratinocyte proliferation and differentiation, maintains skin barrier, and has mild immunosuppressive effects.
213
What is PUVA therapy?
Psoralen plus UVA therapy used for conditions like psoriasis by causing DNA crosslinking and apoptosis.
214
How does Narrowband UVB phototherapy differ from PUVA?
NB-UVB uses 311–312 nm light, is better tolerated, and less carcinogenic.
215
What are the mechanisms of phototherapy in psoriasis?
Reduces keratinocyte proliferation, suppresses immune response, and induces apoptosis.
216
What are common side effects of phototherapy?
Skin rash, blistering, nausea (PUVA), and long-term risk of skin ageing and cancer.
217
What are the three main types of skin cancer?
Basal cell carcinoma, squamous cell carcinoma, and melanoma.
218
What are warning signs of melanoma (ABCDE)?
Asymmetry, Border irregularity, Colour variation, Diameter >6 mm, Evolving shape or colour.
219
Which skin cancer type is most aggressive?
Melanoma.
220
What is actinic keratosis?
A precancerous lesion that may progress to squamous cell carcinoma.
221
How can actinic keratosis be treated?
With cryotherapy or surgical removal.
222
Which skin cancer is most common?
Basal cell carcinoma.
223
Which skin cancer is known for metastasis?
Squamous cell carcinoma (less than melanoma) and especially melanoma.
224
What are common risk factors for skin cancer?
Fair skin, UV exposure, sunburns in childhood, artificial tanning, genetics.
225
How does melanin protect against UV damage?
By absorbing UV photons and aiding in DNA repair.
226
What is the recommended SPF and UVA rating for sunscreens?
SPF 30 or higher with a UVA rating of 4 stars or more.
227
How often should sunscreen be reapplied?
Every 2 hours, using 6–8 teaspoons to cover the body.
228
What species of fly is used in maggot therapy?
Green bottle fly (Lucilia sericata).
229
What are medicinal maggots used for?
To debride wounds, remove infection, and promote healing.
230
What type of wounds are treated with maggot therapy?
Infected, necrotic, chronic wounds.
231
What are the three main benefits of maggot therapy?
Debridement, antimicrobial activity, and promotion of healing.
232
What historical uses support modern maggot therapy?
Used by Indigenous Australians, Mayan tribes, and military doctors like Baron Jean Larrey.
233
When was sterile maggot therapy first introduced?
1930s, in over 300 hospitals in the USA and Canada.
234
What compound from maggots shows antibacterial activity?
Seraticin® – a compound <500 Da under investigation.
235
What is the effect of maggot secretions on biofilms?
They destroy preformed biofilms and prevent new ones from forming.
236
How does maggot therapy affect wound oxygen levels?
Increases oxygen pressure around the wound (from 12 mmHg to 54 mmHg in studies).
237
What do maggots promote by attracting fibroblasts?
Formation of new tissue and wound healing.
238
Which amino acids in maggot secretions help new blood vessel formation?
Histidine, Valinol, and 3-guanidinopropionic acid (GPA).
239
What protein in maggot secretions resembles human growth factors?
A protein homologous to TGF-β (Transforming Growth Factor beta).
240
What is a chronic wound?
A wound that has not healed within 6 weeks.
241
List three ideal characteristics of a wound dressing.
Maintains moisture, allows gas exchange, promotes angiogenesis and healing.
242
What are traditional dressing materials still used today?
Absorbent cotton, gauze, lint, non-extensible bandages (though with limited roles).
243
What are the four main wound types classified by appearance?
Pink (epithelialising), Red (granulating), Yellow (sloughy), Black (necrotic).
244
What is the recommended dressing for a pink, low-exudate wound?
Low adherence dressing or vapour-permeable film.
245
Which dressings are used for red, moderate-exudate wounds?
Foam or alginate dressings.
246
Which dressing type forms a gel when in contact with wound exudate?
Alginate dressings.
247
What dressing is best for dry necrotic tissue?
Hydrogel dressings.
248
What are signs of wound infection?
Heat, pain, erythema, swelling, pus, delayed healing, and malodour.
249
What antimicrobial agents are used in infected wound dressings?
Honey, iodine, silver, and polyhexanide.
250
What are low-adherence dressings and when are they used?
Non-absorbent dressings placed directly on low exudate wounds, used with a secondary dressing.
251
What is a vapour-permeable film dressing?
A polyurethane film that allows oxygen and moisture to pass but blocks microbes and water.
252
What material are foam dressings typically made from?
Polyurethane.
253
Which dressing type can deliver local analgesia?
Foam dressings impregnated with ibuprofen (e.g., Biatain® Ibu).
254
What polymers are commonly used in hydrocolloid dressings?
Carboxymethyl cellulose, pectin, and gelatin.
255
What dressing helps manage hypertrophic or keloid scarring?
Soft polymer silicone dressings (e.g., Cica-Care®).
