Basic Course in Aesthetic Dermatology & Skincare

1. Basic Course in Aesthetic Dermatology & Skincare

DAY 1:            01st July 2025 (Tuesday) Skin Development Anatomy & Physiology, Clinical Dermatology & Laser Machine Orientation
09:15 – 09:30	Collection of Lecture Course Notes
09:30 – 11:30	Introduction to conclusion of Skin Development Anatomy & Physiology, Introduction to conclusion of Chemical Peeling
11:30 – 11:45	Morning Tea Break
11:45 – 01:30	Clinical Dermatology (Fungal Infection, Viral Infection, Cutaneous/Bacterial Infection), Layer of Skin & Cells of Skin, Fundamental lessions of Skin
01:30 – 02.00	Multiple Choice Question Quiz on Skin Development Anatomy & Physiology & Chemical Peeling
02:00 – 02:30	Lunch Break
03:00 – 17:30	Laser Machine Orientation (Alma Harmony XL PRO, Soprano Titanium LHR, Fractional CO2)
DAY 2:          2nd July 2025 (Wednesday) PRP (Platilet Rich Plasma), Microneedling
09:15 – 09:30	Collection of Lecture Course Notes
09:30 – 11:30	Introduction to conclusion of PRP (Platilet Rich Plasma) & Microneedling
11:30 – 11:45	Morning Tea Break
11:45 – 01:30	Injection Techniques with PRP GUN, Post-Treatment Care & Follow-Up
01:30 – 02.00	Multiple Choice Question Quiz on PRP, Micro Needling, PRP Safety, Risks, and Complications, Post-Treatment Care & Follow-Up
02:00 – 02:30	Lunch Break
03:00 – 17:30	Live Demonstrations and Hands-On Training Workshops in PRP & Microneedling
	& Introduction and Orientation to Dramaturgical Instruments

Course Duration        : 2  Days

Course Target            : Aesthetic Dermatology & Skincare

Faculty                         : Dr. Refazul Alam (refat) , Dr. Jinat Salsabil Khan , Dr. Nizhum Ahmed

Open to All  MBBS Students undergoing Internship , MBBS & BDS.

CPD certificate in Aesthetic Dermatology & Skincare will be awarded.

Fundamental Course in Aesthetic Dermatology & Skincare

Day 01

• Skin Development Anatomy & Physiology
• Chemical Peel

 

Part 1: Embryological Development of Skin        

Origin of Skin                                                                         

• The skin develops from two embryonic layers:
  • Ectoderm: Forms the epidermis, hair, nails, sebaceous and sweat glands.
  • Mesoderm: Forms the dermis and subcutaneous tissue.

Timeline of Skin Development

• 4th Week: Surface ectoderm forms a single layer of squamous epithelial cells.
• 7th Week: Periderm forms; basal layer develops.
• 11th Week: Hair follicles begin to form.
• 13th–20th Week: Stratification into epidermal layers, development of dermal papillae.
• By 21st Week: Skin has all adult-like layers; melanocytes are active.

Key Components Originating in Embryogenesis

• Melanocytes: Neural crest origin.
• Langerhans cells: Bone marrow origin, migrate to epidermis.
• Merkel cells: Possibly neuroectodermal.

Gross Anatomy of the Skin

Layers of the Skin

• Epidermis: Stratified squamous epithelium; avascular.
• Dermis: Connective tissue; contains blood vessels and nerves.
• Hypodermis (Subcutaneous tissue): Fat and connective tissue.

Epidermal Layers (from deep to superficial)

1. Stratum Basale
2. Stratum spinosum
3. Stratum granulosum
4. Stratum lucidum (only in thick skin)
5. Stratum corneum

Dermis Components

• Papillary layer: Loose connective tissue; capillaries and sensory neurons.
• Reticular layer: Dense irregular connective tissue; supports skin elasticity.

Skin Appendages

• Hair follicles, Sebaceous glands, sweat glands, Nails

Histology of the Skin

Epidermis

• Keratinocytes: Main cells; produce keratin.
• Melanocytes: Produce melanin; located in stratum basale.
• Langerhans cells: Antigen-presenting; found in stratum spinosum.
• Merkel cells: Touch receptors in stratum basale.

Dermis

• Contains fibroblasts, mast cells, macrophages.
• Rich in collagen and elastin fibers.
• Contains blood vessels, lymphatics, sensory receptors.

Hypodermis

• Adipocytes, connective tissue, larger blood vessels and nerves.

Skin Physiology

Barrier Function

• Prevents water loss and entry of pathogens.
• Stratum corneum critical for barrier integrity.

Thermoregulation

• Sweat glands and blood vessels regulate body temperature.
• Vasodilation and vasoconstriction help dissipate or conserve heat.

Sensory Function

• Receptors for touch, pain, temperature, pressure.
• Types: Merkel cells, Meissner corpuscles, Pacinian corpuscles, free nerve endings.

Immunologic Function

• Langerhans cells initiate immune response.
• Skin-associated lymphoid tissue (SALT) plays a defensive role.

Endocrine Function

• Skin synthesizes vitamin D from cholesterol under UV light.
• Contains hormone receptors (e.g., for cortisol, estrogen).

Clinical Correlation

Common Disorders Related to Skin Development and Function

• Ichthyosis: Disorders of keratinization.
• Albinism: Lack of melanin production.
• Vitiligo: Loss of melanocytes.
• Psoriasis: Rapid turnover of keratinocytes.
• Eczema/Dermatitis: Barrier dysfunction.

Diagnostic Tools

• Skin biopsy
• Wood’s lamp examination
• Patch testing

Clinical Dermatology (Fungal Infection, Viral Infection, Cutaneous/Bacterial Infection), Layer of Skin & Cells of Skin, Fundamental lessions of Skin

1. Fungal Infections of the Skin

• Overview: Fungal skin infections (dermatophytoses or “tinea”) are caused by keratinophilic fungi (dermatophytes) and yeasts. Dermatophytes (genera Trichophyton, Microsporum, Epidermophyton) invade the stratum corneum of skin, hair, or nails. They are classified by site: e.g. tinea pedis (athlete’s foot), tinea corporis (body), tinea cruris (groin), tinea capitis (scalp), tinea unguium (onychomycosis), etc. Yeasts like Candida cause intertrigo and thrush; Malassezia causes pityriasis (tinea) versicolor.
• Etiology/Transmission: Dermatophytes require keratin for growth and are transmitted by direct contact (anthropophilic species person‑to‑person), by animals (zoophilic), or from soil (geophilic). Indirect spread via fomites (clothing, hairbrushes) is common. Candida overgrowth occurs in moist, occluded sites (diaper rash, mouth).
• Clinical Presentation: Classic tinea corporis is an annular, scaly, pruritic plaque with an advancing border and central clearing. Tinea pedis shows interdigital maceration or sole scaling; tinea cruris causes itchy red patches in the groin. Tinea capitis causes scaly scalp patches and broken hairs. Onychomycosis leads to thickened, discolored nails. Candidal intertrigo is red and macerated with satellite pustules. Pityriasis versicolor (Malassezia) causes hypopigmented or hyperpigmented scaly macules on the trunk.
• Diagnosis: Scrapings of skin, hair, or nail are examined microscopically (KOH prep) for septate hyphae and spores. Wood’s lamp (UV light) may highlight certain species (e.g. Microsporum canis hairs fluoresce). Fungal culture on Sabouraud’s agar confirms species (takes weeks). Skin biopsy with PAS stain can identify fungi in unusual cases. A single negative KOH/culture does not rule out infection if clinical suspicion is high.
• Treatment: Most localized dermatophytoses are treated with topical antifungals. Allylamines (terbinafine) are fungicidal and achieve higher cure rates than azoles. Terbinafine cream for 1–2 weeks or clotrimazole/ketoconazole twice daily is common for tinea corporis/cruris. Oral therapy is indicated for scalp (tinea capitis), nails, and extensive or refractory disease. Griseofulvin (6–8 weeks) remains first-line for tinea capitis. Terbinafine or itraconazole pulses (with drug holidays) are used for onychomycosis; note nail lacquer (ciclopirox) has low cure rates. For cutaneous candidiasis, topical nystatin or azoles are used; oral fluconazole for refractory thrush. General measures: keep skin dry, avoid sharing towels, treat athlete’s foot to prevent recurrence.

2. Viral Infections of the Skin

• Herpes Simplex (HSV): HSV‑1 typically causes orolabial lesions and HSV‑2 genital lesions, but either type can infect any mucocutaneous site. Primary infection may produce systemic symptoms; recurrences present as groups of small (2–3 mm) clear vesicles on an erythematous base, often preceded by tingling or burning. Lesions crust over in ~1 week. Immunosuppressed patients risk severe eczema herpeticum or disseminated disease. Diagnosis is clinical; Tzanck smear shows multinucleated giant cells. First-line therapy is a nucleoside analogue: oral acyclovir/valacyclovir or famciclovir, which shortens outbreak duration. Topical antivirals have limited benefit. Daily suppressive therapy may be used in frequent recurrences.
• Varicella-Zoster Virus: Primary VZV infection causes chickenpox: a generalized itchy vesicular rash in successive crops, often with fever. Reactivation of latent VZV in a dorsal root ganglion causes herpes zoster (shingles): a dermatomal, unilateral vesicular rash on an erythematous base, typically very painful. Common sites are thoracic and ophthalmic dermatomes. Early antiviral therapy (acyclovir/valacyclovir) within 72 hours reduces acute symptoms and postherpetic neuralgia risk. Other measures: analgesics, calamine or cool compresses on blisters. Post-herpetic neuralgia (pain persisting >1 month) is managed with gabapentin or TCA. Zoster vaccine in older adults reduces incidence and severity of shingles. Note: VZV is contagious; isolate lesions until crusted.
• Human Papillomavirus (HPV) – Warts: HPV causes epidermal hyperproliferation. Common warts (verruca vulgaris) are rough, hyperkeratotic papules on hands/feet; plantar warts have tender black dots (thrombosed capillaries)​ dermnetnz.org. Flat warts (verruca plana) are smooth papules on face/legs; filiform warts are threadlike on face. Mucosal/cutaneous anogenital warts (HPV 6,11) present as flesh‑colored papules or plaques. Diagnosis is clinical; biopsy if uncertain. Many warts spontaneously regress. Treatment options include repeated destruction of lesions (e.g. topical salicylic acid, cryotherapy with liquid nitrogen, electrocautery, or lasers). Immune therapies (imiquimod cream) are used for recalcitrant warts. For extensive or periungual warts, cryotherapy or bleomycin injections may be used. Genital warts require STD-focused care.
• Other Viral Exanthems: (Briefly) Molluscum contagiosum (poxvirus) causes umbilicated dome-shaped papules. Hand-foot-and-mouth disease (coxsackievirus) causes vesicular lesions on hands, feet, mouth. These are usually self-limited.

3. Cutaneous Bacterial Infections

• Impetigo: Superficial epidermal infection by Staphylococcus aureus or Streptococcus pyogenes. Nonbullous impetigo (contagiosa) presents as clustered vesicles or pustules that rupture into honey‑colored crusts, often on the face or extremities​aafp.org. Bullous impetigo (exfoliative toxin) causes larger flaccid bullae, usually from S. aureus, affecting flexural areas​aafp.org. Systemic symptoms are uncommon. Complication: post-streptococcal glomerulonephritis (rare)​aafp.org. Treatment: topical antibiotics (mupirocin or retapamulin ointment) for limited disease. Extensive or bullous cases require oral anti‑staphylococcal antibiotics (e.g. dicloxacillin, cephalexin)​aafp.org; in areas with MRSA, use clindamycin or TMP-SMX. Lesions typically heal in 2–3 weeks without scarring​aafp.org.
• Folliculitis: Infection/inflammation of hair follicles, usually S. aureus. Presents as pustules or erythematous papules centered on hairs (e.g. “razor bumps,” beard areas). Pseudomonal “hot tub folliculitis” causes pruritic papulopustules after warm pools. Treatment: antiseptic washes or topical antibiotics (clindamycin or mupirocin ointment). Deep or extensive cases may need oral dicloxacillin or cephalexin. Recurrent folliculitis warrants nasal decolonization or culture to guide therapy.
• Cellulitis: Acute spreading infection of the dermis and subcutaneous tissue. Commonly due to Group A Streptococcus or S. aureus. Presents with diffuse, tender erythema, warmth, swelling, and ill-defined borders; often on the leg. Systemic symptoms (fever, chills) are common. Lymphangitic streaking and regional lymphadenopathy may occur. (Erysipelas is a more superficial form with raised, sharply demarcated edges, often caused by Strep on the face or legs.) Treatment: empirical systemic antibiotics. For nonpurulent cellulitis (no abscess), oral dicloxacillin or cephalexin is first-line​emedicine.medscape.com; penicillin or amoxicillin can cover pure strep. In penicillin-allergic patients, use clindamycin or a macrolide​emedicine.medscape.com. If MRSA is suspected (abscess nearby, MRSA risk factors), add TMP-SMX or doxycycline. Hospitalize for IV antibiotics (cefazolin, nafcillin) if severe or immunocompromised. Key Point: Abscesses require drainage; cellulitis without abscess relies on antibiotics​emedicine.medscape.com.

4. Layers of the Skin and Clinical Relevance

• Epidermis: The outermost layer, made of stratified squamous keratinocytes. It has five strata (basale, spinosum, granulosum, lucidum, corneum), though lucidum is only in thick skin (palms/soles). Keratinocytes produce keratin and form a waterproof barrier. Melanocytes in the basal layer produce melanin pigment (defects cause albinism or vitiligo). Langerhans cells (in stratum spinosum) act as antigen-presenting immune cells. Merkel cells (in basale) are mechanoreceptors for touch. The epidermis provides the primary barrier against infection and UV. Clinically, diseases like psoriasis (epidermal hyperproliferation) and contact dermatitis involve the epidermis. Sunburn injures the epidermis (1st-degree burn), while deeper burns damage more layers.
• Dermis: Beneath the epidermis, composed of connective tissue (collagen and elastic fibers). It has two layers: the superficial papillary dermis and deeper reticular dermis. It contains blood vessels (nourishing the epidermis), nerves (pain, temperature, touch receptors), hair follicles, sweat and sebaceous glands. Fibroblasts in the dermis produce collagen (wound healing). The dermis provides strength and elasticity. Clinically, inflammation (e.g. urticaria) affects the papillary dermis, while deep blisters in bullous pemphigoid are subepidermal (involving the dermis).
• Hypodermis (Subcutaneous Tissue): The deepest layer, primarily adipose tissue with septa of connective tissue. It insulates the body, absorbs shock, and anchors the skin to underlying fascia/muscle. Injection of subcutaneous fat (“lipodystrophy”) or panniculitis (inflammation of fat) involve this layer. Clinically, cellulite (inflamed fat) or abscesses can form here.

5. Cells of the Skin – Structure, Function, Pathology

• Keratinocytes: Constitute ~90% of epidermal cells. They produce keratin and lipids, forming the physical barrier. Keratinocytes also secrete cytokines and growth factors (e.g. in wound repair). Dysregulated keratinocytes cause diseases like psoriasis (hyperplasia) or squamous cell carcinoma (malignant transformation).
• Melanocytes: Located in the basal layer, these neural-crest–derived cells produce melanin in melanosomes and transfer it to keratinocytes to protect DNA from UV. Mutations in melanin synthesis cause albinism; autoimmune destruction leads to vitiligo. Melanocyte proliferation causes melanoma.
• Langerhans cells: Specialized dendritic immune cells in the epidermis (mostly stratum spinosum). They capture and present antigens to T-cells, initiating immune responses (e.g. in contact dermatitis)​pmc.ncbi.nlm.nih.gov. Human immunodeficiency virus (HIV) and other agents can infect Langerhans cells.
• Merkel cells: Mechanoreceptor cells in the basal epidermis associated with nerve endings. They mediate light touch sensation. Merkel cell carcinoma is a rare, aggressive skin cancer.
• Dermal Cells: Fibroblasts produce extracellular matrix (collagen, elastin); mast cells release histamine in allergic reactions (urticaria); macrophages and lymphocytes in the dermis mediate inflammation (e.g. in lupus or dermatomyositis skin lesions). Subcutaneous adipocytes store fat; panniculitis affects these cells.

6. Fundamental Skin Lesions – Classification and Examples

• Macule: A flat, circumscribed change in skin color < 1 cm (e.g. freckle, lentigo).
• Patch: A flat lesion > 1 cm (e.g. café-au-lait spot, vitiligo area).
• Papule: A solid, raised lesion < 1 cm (e.g. molluscum contagiosum papule, insect bite, verruca).
• Plaque: A plateau-like lesion > 1 cm, often formed by a confluence of papules (e.g. psoriasis, lichen planus).
• Nodule: A deeper, round lesion > 1 cm that extends into the dermis or subcutis (e.g. lipoma, rheumatoid nodule).
• Vesicle: A small fluid-filled blister < 1 cm (e.g. herpes simplex, varicella).
• Bulla: A larger blister > 1 cm (e.g. bullous pemphigoid, second-degree burn blister).
• Pustule: A superficial papule filled with purulent fluid (e.g. acne pustule, chickenpox pustule).
• Wheal (Urticaria): A transient, raised, erythematous (often pruritic) plaque with edema (e.g. hives from allergy).
• Scale: Excess dead epidermal cells, seen as flaking (e.g. in tinea, psoriasis).
• Crust: Dried serum, blood, or pus on the skin surface (e.g. impetigo honey-colored crust).
• Erosion: Partial loss of epidermis; moist and heals without scarring (e.g. ruptured herpes vesicle).
• Ulcer: Full-thickness loss of epidermis and part of dermis; heals with scar (e.g. pressure ulcer, chancre).
• Fissure: A linear crack in skin (e.g. athlete’s foot fissure).
• Atrophy: Thinning of epidermis or dermis (e.g. steroid atrophy of skin).
• Scar: Fibrous tissue replacing normal skin after injury.

Chemical Peeling

1. Introduction to Chemical Peels

• Definition: Chemical peeling involves the application of a chemical solution to the skin to remove its outer layers, promoting exfoliation and regeneration of a smoother, clearer skin surface.
• Purpose: Treatment of pigmentary disorders, acne, scars, and signs of aging.
• Historical Background: Used since ancient Egypt (Cleopatra’s milk baths – lactic acid). Modern dermatologic peels started in the 19th century.

2. Skin Anatomy & Physiology Relevant to Peels

• Target Area: Epidermis and/or dermis (depending on peel depth)
• Physiological Response:
  • Controlled chemical injury → exfoliation and wound healing response
  • Stimulates collagen and elastin synthesis
  • Regeneration of healthier epithelium

3. Classification of Peels

By Depth of Penetration:

Type	Skin Layer Affected	Examples
Superficial	Epidermis	Glycolic acid (20-40%), salicylic acid (20-30%), lactic acid, mandelic acid
Medium-depth	Papillary dermis	TCA (35%), Jessner’s solution
Deep	Reticular dermis	Phenol, high-concentration TCA

4. Common Chemical Agents

Agent	Type	Indications
Glycolic Acid (AHA)	Superficial	Acne, melasma, fine wrinkles
Salicylic Acid (BHA)	Superficial	Acne, oily skin, comedones
Lactic Acid	Superficial	Pigmentation, dry skin
Mandelic Acid	Superficial	Sensitive skin, rosacea
TCA (10-35%)	Medium-depth	Acne scars, wrinkles, pigmentation
Jessner’s Solution	Medium-depth	Photoaging, melasma
Phenol Peel	Deep	Deep wrinkles, actinic damage

5. Indications

• Acne and post-acne pigmentation
• Melasma and hyperpigmentation
• Fine lines and wrinkles
• Actinic keratoses
• Enlarged pores
• Skin rejuvenation (texture, tone)

6. Contraindications

• Active infections (e.g., herpes, bacterial)
• Open wounds or dermatitis
• Recent isotretinoin use (<6 months)
• Keloidal tendency
• Fitzpatrick skin types IV-VI (for deeper peels, due to PIH risk)
• Poor wound healing (e.g., in diabetes)

7. Patient Selection & Assessment

• History: Skin type, prior treatments, allergies, medical history
• Examination: Skin tone, texture, lesions, scarring
• Fitzpatrick Skin Type: Important for peel selection and PIH risk
• Consent: Discuss downtime, outcomes, and risks

8. Procedure Steps

Pre-Peel Preparation:

• Priming with retinoids, hydroquinone, or glycolic acid (2–4 weeks prior)
• Discontinue exfoliants 3–5 days before
• Antiviral prophylaxis in patients with HSV history

Peel Application:

1. Cleanse and degrease skin with alcohol/acetone.
2. Apply peel uniformly with brush, gauze, or cotton-tipped applicator.
3. Observe endpoints:
   • Erythema
   • Frosting (for TCA)
4. Neutralize (if required; some peels are self-neutralizing).
5. Apply soothing agent or sunscreen.

Post-Peel Care:

• Avoid sun exposure for at least 7 days
• Use gentle cleanser, moisturizer, and broad-spectrum sunscreen
• Avoid makeup for 24–48 hrs
• Expect peeling/flaking for 2–5 days (depending on peel type

9. Complications & Side Effects

• Immediate:
  • Stinging, burning, erythema
• Delayed:
  • Post-inflammatory hyperpigmentation (PIH)
  • Hypopigmentation
  • Scarring (rare)
  • Infection (HSV reactivation)
• Prevention: Appropriate peel choice, priming, sun protection

10. Chemical Peeling in Different Skin Types

• Fitzpatrick I–III: Most peels can be used with caution
• Fitzpatrick IV–VI: Prefer superficial peels (mandelic, salicylic, glycolic <30%)
  • Avoid medium and deep peels due to PIH risk

11. Combination Treatments

• Chemical peel + Microneedling (staggered)
• Peel + Laser (not on same day)
• Peel + Topicals (vitamin C, retinoids, lightening agents)
• Peel + PRP (for acne or rejuvenation protocols)

Fundamental Course in Aesthetic Dermatology & Skincare

Day 02

• PRP (Platilet Rich Plasma)
• Microneedling
• PRP Gun Using Techniques , Application

Theoretical Sheet on PRP (Platilet Rich Plasma)

Platelet-Rich Plasma (PRP)

🔹 1. Introduction to PRP

• PRP is an autologous concentration of platelets in a small volume of plasma.
• Rich in growth factors (PDGF, TGF-β, VEGF, EGF, IGF).
• Used to enhance healing, tissue regeneration, and rejuvenation.

🔹 2. PRP Preparation

2.1 Blood Collection

• 10–30 mL of venous blood is drawn using ACD (anticoagulant citrate dextrose).

2.2 Centrifugation (2-step method)

• Soft spin: Separates RBCs from plasma.
• Hard spin: Separates platelet-poor plasma (PPP) and PRP.

2.3 Yield

• PRP contains 4–5 times the baseline platelet count.

🔹 3. Mechanism of Action

• Platelets release alpha granules → growth factors.
• Stimulates:
  • Fibroblast activity
  • Collagen synthesis
  • Angiogenesis
  • Tissue remodeling

🔹 4. Clinical Applications

• Aesthetics:
  • Skin rejuvenation (“vampire facial”)
  • Fine lines and wrinkles
  • Dark circles under eyes
• Hair Restoration:
  • Androgenic alopecia
  • Telogen effluvium
• Orthopedics, Wound healing, Post-surgical healing

🔹 5. Injection Techniques

• Mesotherapy technique (multiple microinjections)
• Nappage technique
• Direct dermal injection with insulin syringes or mesoguns

🔹 6. Contraindications

• Platelet dysfunction syndromes
• Blood disorders (anemia, thrombocytopenia)
• Active infections at site
• Use of anticoagulants
• Pregnant or breastfeeding

🔹 7. Side Effects

• Mild redness, swelling
• Bruising at injection site
• Temporary tenderness or discomfort

Microneedling (Dermaroller/Dermapen)

🔹 1. Introduction

• Also known as collagen induction therapy.
• Involves creation of controlled micro-injuries in the skin using fine needles.

🔹 2. Mechanism of Action

• Stimulates:
  • Wound healing cascade
  • Neocollagenesis and elastin production
  • Capillary proliferation
• Increases absorption of topical agents.

🔹 3. Equipment

• Dermaroller: Handheld device with needle-covered cylinder.
• Dermapen: Motorized pen-like device with adjustable depth.

Needle Lengths:

Condition	Depth
Fine wrinkles	0.25 – 0.5 mm
Acne scars	1.0 – 2.5 mm
Hair loss	0.5 – 1.5 mm
Drug delivery	0.2 – 0.5 mm

🔹 4. Indications

• Acne scars
• Wrinkles & stretch marks
• Hyperpigmentation
• Hair loss (combined with PRP or minoxidil)
• Enlarged pores, dull skin

🔹 5. Procedure Steps

1. Cleanse skin and apply topical anesthetic
2. Sterile microneedling in multiple directions
3. Apply serum or PRP (optional)
4. Post-procedure soothing cream and sunblock

🔹 6. Post-care Instructions

• Avoid makeup and direct sun for 24–48 hrs
• Use soothing moisturizers and physical sunscreen
• No active products (retinoids, AHA/BHA) for 3–5 days

🔹 7. Side Effects

• Redness, pinpoint bleeding (usually resolves in 24–48 hours)
• Swelling or bruising
• Rare: post-inflammatory hyperpigmentation, infection

🔹 8. Contraindications

• Active acne, eczema, or psoriasis
• Keloidal tendency
• Anticoagulant therapy
• Recent chemical peel or laser treatment

🔹 9. Microneedling + PRP Combination

• Enhances results by synergizing collagen stimulation with growth factors.
• Common for:
  • Facial rejuvenation
  • Hair regrowth
  • Scar treatment

Clinical Tips

• Always obtain informed consent.
• Use sterile techniques.
• Avoid over-treatment; sessions should be spaced 4–6 weeks apart.
• Assess patient expectations realistically.

Injection Techniques with PRP GUN, Post-Treatment Care

I. Injection Techniques with PRP Gun

🔹 1. Introduction to PRP Gun

• A mesotherapy gun (PRP gun) is a motorized injector that delivers multiple small injections of Platelet-Rich Plasma (PRP) into the dermis or subcutaneous layer.
• Benefits:
  • Precise depth control
  • Reduced practitioner fatigue
  • Uniform distribution of PRP
  • Less painful than manual injection

🔹 2. Anatomy Review for Injection

• Face: PRP is injected into mid to deep dermis.
• Scalp: Inject into subdermal layer overlying the galea aponeurotica.
• Neck, hands, under-eye area: Use superficial dermal level.

🔹 3. Injection Techniques

A. Nappage Technique (Multiple Puncture Technique)

• Rapid superficial injections at 1–2 mm depth.
• Ideal for: Facial rejuvenation, neck lines.
• PRP gun setting: Short depth, rapid succession.

B. Point by Point (Papular) Technique

• Small amounts (0.05–0.1 mL) injected 1 cm apart.
• Used for: Scalp PRP, deeper skin rejuvenation.
• PRP gun setting: Medium to deep injection mode.

C. Linear Threading Technique

• PRP is injected while withdrawing the needle in a linear path.
• Good for: Under-eye area, nasolabial folds, stretch marks.

D. Stamping Technique

• Gun remains in position for each drop, especially in sensitive areas.
• Suitable for: Periorbital region, acne scars.

🔹 4. Step-by-Step Procedure with PRP Gun

1. Skin Preparation:
   • Cleanse area thoroughly
   • Apply topical anesthetic (lidocaine) for 30–45 minutes
   • Cleanse again with antiseptic solution
2. Load PRP:
   • Use sterile syringe and connect it to PRP gun
   • Choose appropriate needle length (0.5 mm to 2.5 mm)
3. Set Parameters:
   • Depth (based on area)
   • Speed or frequency (rapid for face, slower for scalp)
4. Inject:
   • Follow chosen technique: nappage, papular, or linear threading
   • Maintain consistent spacing (1 cm)
5. Post-Injection Massage (optional):

		Area		Depth		Needle Length		Remarks
		Scalp		1.5–2.5 mm		30–32 gauge		Subdermal, for hair growth
		Face (cheeks)		1.0–1.5 mm		31 gauge		For skin rejuvenation
		Under-eye area		0.5–1.0 mm		33 gauge		Use stamping, avoid bruising
		Neck & décolleté		0.5–1.0 mm		30–31 gauge		Superficial injections

5.  Gentle massage helps even distribution
6. Especially effective in hair and facial treatments

🔹 5. Recommended Injection Depths

 II. Post-Treatment Care After PRP Therapy

🔹 1. Immediate Post-Treatment Advice

• Avoid touching or washing the area for at least 4–6 hours.
• Do not apply makeup or skin products for 24 hours.
• Avoid sun exposure and heat (sauna, steam) for 48 hours.

🔹 2. Medication & Topicals

• Mild analgesics (paracetamol) if there is discomfort.
• Cold compresses for swelling or redness.
• Avoid NSAIDs (like ibuprofen) for 48 hrs, as they may interfere with PRP activity.

🔹 3. Skincare Instructions

• Use gentle cleanser and moisturizer starting the next day.
• Begin broad-spectrum sunscreen (SPF 50+) after 24 hours.
• Resume active agents (retinol, AHA/BHA, vitamin C) only after 3–5 days.

🔹 4. Activity Restrictions

• No strenuous exercise, swimming, or alcohol for 24–48 hours.
• Avoid facial massage or other aesthetic treatments for 1 week.

🔹 5. Follow-Up & Re-Treatment

• Results start appearing in 2–4 weeks post-procedure.
• For best results:
  • Hair PRP: Every 4 weeks × 3–6 sessions
  • Facial PRP: Every 4–6 weeks × 3 sessions, then maintenance

Key Clinical Tips

• Always test PRP gun settings on gauze or dummy skin before patient use.
• Monitor for signs of infection or hypersensitivity.
• Educate the patient on realistic expectations—results vary by individual.