Year 2 > DERM > Flashcards

DERM Flashcards

(113 cards)

Study These Flashcards
1
Q

Functions of the skin

A 
1. Barrie rot infection 
2> thermoregulation 
3. Protection against trauma
4. Protection against UV
5. Vit D syntehsis
6. Regulate H20 loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pH of the skin

A

5.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is the skin pH 5.5

A

Allows proteases on the skin to do desquamination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the stratum corneum

A

Made of corner-desmosomes and desmosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are cornel-desmosomes

A

Adhesion molecules that keep corneocytes together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the layers of the skin

A
  1. Stratum lucidium
  2. Granulosum
  3. Spinous
  4. Basale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What nerve endings are found in the dermis

A

Meissner’s corpuscules - light touch

2. Pacinian corpuscle (vibration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Role of keratinocytes

A

Produce keratin as a protective barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Role of Langerhans cells

A

Present antigens and activate T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Role of merkel cells

A

Specialised nerve endings for sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Common causes of itch with rash

A
  1. URTICARIA (hives)
  2. ATOPIC ECZMA
  3. Psoriasis
  4. Scabies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Common causes of itch with no rash

A
  1. Renal failure
  2. Jaundice
  3. Iron deficiency
  4. Lymphoma (hodgkin’s)
  5. Polycythaemia
  6. Pregnancy
  7. Drugs
  8. Diabetes
  9. Cholestasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is acne

A

Expansion and blockage of hair follicle and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most common variant of acne

A

Acne Vulgaris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathophysiology of acne

A
  1. Hypercornfiictaion causes narrowing of hair follicle
  2. Increased sebum production
  3. Sebum is trapped which narrows follicle further
  4. Sebum stagnates at pit of follicle where there is no oxygen
  5. Anaerobic conditions allow propionibacterium acne to multiply
  6. P. acne breaks down triglycerides in sebum into free fatty acids = irritation, inflammation and attraction of neutrophils
  7. Pus formation as attract neutrophils come into the area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Whitehead vs blackhead

A

White - closed comedones

Black - open comedones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical presentation of acne

A
  1. Whiteheads
  2. Blackheads
  3. Skin coloured papule (red spots)
  4. Inflammatory lesions when closed wall of comedones rupture
  5. Pustules (yellow spots)
  6. Nodules (large red bumps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diagnosis of acne

A
  1. Skin swabs for culture

2. Hormonal test in females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Treatment of acne

A
  1. BENZOYL PEROXIDE
  2. CLINDAMYCIN GEL
  3. TAZAROTENE GEL (topical retinoid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does Benzoyl peroxide work

A

Increases skin turnover
Clears pores and reduces bacterial count
Causes dryness due to kertaolytic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do topical retinoids work

A

Inhibit formation and reduce number of micromedones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Severe acne treatment

A
  1. ORAL DOXYCYCLINE
  2. ORAL MINOCYCLINE

HORMONE TREATMENT with ORAL CO-CYPRINDIOL (anti-androgen suppresses sebum productioN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is eczema/dermatitis

A

Breakdown of skin due to thinning of stratum corneum - increased risk of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is endogenous eczema

A

Hypersensitivity caused (food allergies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is exogenous eczema
Contact dermatitis due to chemicals, sweat and abrasives
26
Pathophysiology of eczema
1. Damaged filaggrin | 2. CD4 lymphocytic activation = inflammation
27
Role of filaggrin
Skin barrier protein
28
Clinical presentation of eczema
1. face and flexure surfaces of limbs 2. Itchy, erythematous and scaly patches 3. Dryness of skin 4. Very acute lesions RECURRENT STAPHYLOCOCCUS AUREUS INFECTIONS
29
Diagnosis of eczema
1. Atopic dermatitis: High serum IgE Itchy skin for 6 months ``` PULS: History of involvement of skin creases Asthma or hay fever Dry skin history Childhood ```
30
Treatment of eczema
1. Eductaion 2. Avoid allergens 3. Keep nails short 4. E45 CREAM 5. Topical corticosteroids 6. Second line: Topical calcineurin inhibitors
31
How does E45 work (EMOLLIENT THERAPY)
1. Traps moisture in skin to increase hydration and acts as barrier to water loss Natural moisturising factor in corneocytes is depleted in eczema
32
How often is E45 applied
Every 4hours / 3 - 4 times a day
33
What topical corticosteroids are given as first line treatment for eczema
1. CLOBETASOL PROPIONATE 2. FLUCINONIDE 3. CLOBETASOL BUTYRATE 4. HYDROCORTISONE used for inflamed skin
34
What topical calcineurin inhibitors are given
PIMECROLIMUS or TACROLIMUS ointment
35
How do topical calcineurin inhibitors work
1. Inhibit IL 2 which reduces inflammation and do not cause skin atrophy
36
3rd line treatment for eczema
1. CICLOSPORIN 2. AZOTHIOPRINE 3. ORAL PREDNISOLONE 4. FLUCLOXACILLIN 5. PHOTOTHERAPY with UV A 6. CHLORPHENAMINE
37
What is psoriasis
Hyper proliferation of keratinocytes + inflammatory cell infiltration
38
What aged people are effected by psoriasis
ADULTS
39
What environmental triggers cause psoriasis
1. Infection by group A strep 2. Lithium 3. UV 4. Alcohol 5. Stress
40
Pathophysiology of psoriasis
1. T cell activation = up regulation of INF gamma, IL1,2,8 | 2. Increased uncontrolled proliferation of keratinocytes
41
Clinical presentation of psoriasis
1. Pitting and onycholysis (separation of finger nail from nail bed)
42
Clinical presentation of chronic plaque psoriasis
1. Disc shaped salmon-pink-silvery plaques on exterior surfaces of elbows and knees 2. Plaques on hair margin 3. Thickened epidermis 4. New plaques at skin trauma sites
43
How is chronic plaque psoriasis treated
1. E45 2. CALCIPQOTRIOL CREAM (topical vit D analogues) 3. HYDROCORTISONE CREAM (topical corticosteroids) 4. TAZAROTENE GEL (topical retinoid) 5. UV B 6. COAL TAR 7. DITHRANOL CREAM (anti-mitotic) - ------SEVERE------- 1. UV A 2. DMARD (METHOTREXATE and FOLIC ACID) 3. CICLOSPORIN
44
Clinical presentation of flexural psoriasis
1. Red, glazed non-scaly plaques | 2. Confined to flexures (groin, natal cleft and sub-mammary areas)
45
How is flexural psoriasis treated
1. HYDROCORTSIONE - causes atrophy 2nd line: CALCIPQOTRIOL CREAM (irritating so don't use for face)
46
Clinical presentation of Guttate psoriasis
1. Trunk, upper arms and legs 2. Small circular and oval plaques afterr 2 weeks of strep sore throat 3. CHILDREN
47
treatment of GUTTATE PSORIASIS
1. HYDROCORTISONE or CLOBETASOL UTYRATE 2. UV B 3. Coal tar
48
Clinical presentation of Palmoplantar psoriasis
1. Thickening of palms and soles
49
Treatment of palmoplantar psoriasis
1. Emollients 2. SALICYLIC ACID 3. FLUCINONIDE 4. UV A 5. ORAL ACITRETIN (anti-proliferative) 6. Anti-TNF biologics (IV INFLIXIMAB or IV ADALIMUMAB)
50
Define venous skin ulcers
Loss of skin below knee on leg or foot that takes 2 weeks to heal
51
What causes venous skin ulcers
Sustained venous hypertension in superficial veins
52
What causes sustained venous hypertension
1. Incompetent valves in deep veins 2. Previous DVT 3. Atherosclerosis 4. Vasculitis (RA and SLE)
53
Risk factors for venous skin ulcers
DVT
54
Pathophysiology of venous skin ulcers
1. Increased pressure causes extravasation of fibrinogen through capillary walls giving his ego perivascular fibrin deposition = poor oxygenation of surrounding skin
55
Clinical presentation of venous skin ulcers
1. Sloping and gradual edges 2. Large, irregular ulcer 3. Minimal pain 4. Oedema of lower leg 5. Venous eczema 6. Brown pigmentation from haemosiderin 7. Varicose veins 8. Pulses present 9. Warm skin
56
Diagnosis of venous skin ulcers
1. Ankle brachial pressure index is normal | 2. Doppler ultraosund
57
Treatment of venous skin ulcers
1. High compression 4 layered bandage 2. Leg elevation to reduce hypertension 3. Antibiotics 4. IBUPROFEN 5. Support stockings for life
58
What are arterial ulcers
Present as punched-out, painful higher up the leg or on the feet
59
Risk factors for arterial ulcers
1. Atherosclerosis 2. Smoking 3. Hypercholesterolaemia 4. Diabetes Mellitus
60
Clinical Presentation of arterial ulcers
1. Punch-out ulcers higher up on the leg or on feet 2. Pain is worse when elevated 3. Leg is cold and pale 4. Ulcer is small and sharply defined with necrotic base 5. Shiny pale skin and loss of hair 6. Absent peripheral pulses 7. Arterial bruits (murmurs caused by turbulent blood flow 8. NO OEDEMA
61
Diagnostics of arterial ulcers
1. Doppler Ultrasound | 2. ABPI
62
Treatment of arterial ulcers
1. Cover and clean ulcer 2. Analgesia (IBUPROFEN) 3. Vascular reconstruction 4. NEVER USE COMPRESSION BANDING
63
What is a neuropathic ulcer
Seen over pressures of the feet which are painful DIABETES and LEPROSY
64
Clinical presentation of neuropathic ulcer
Warm skin and normal peripheral pulses
65
Treatment of neuropathic ulcer
1. Keep ulcer clean and remove pressure or trauma from affected areas 2. Correctly fitting shoes and specialist podiatrist help for diabetics
66
What is a vasculitic ulcer
1. Blood vessels causing endothelial damage
67
How is cutaenosu vasculitis diagnosed
SKINBIOPDY
68
What is Leucocytoclastic vasculitis
1. Appears on the lower legs as symmetrical palpable purport
69
What causes lecuocytoclastic vasculitis
1. Drugs 2. Infection 3. Inflammatory disease 4. Malignant disease
70
Clinical presentation of leucocytoclastic vasculitis
1. Haemorrhagic papules 2. Pustules 3. Nodules 4. Plaques 5. NON BLANCHING PURPURIC LEISIONS 6. Pyrexua and arthralgia
71
Treatment of leucocytoclastic vasculitis
1. Analgesia 2. Support stocking s 3. DAPSONE or PREDNISOLONE
72
What kind of cancer is skin cancer
SQUAMOUS CELL CARCINOMA of the keratinocytes
73
Why is SCC more aggressive than BCC
Metastases to the lymph nodes
74
What is Bowen's disease
SCC confined to the epidermis
75
Risk factors of SCC
1. UV | 2. Chronic inflammation
76
Clinical presentation of SCC
1. Sun-exposed sites 2. Lesions are keratotic that may ulcerate 3. Grow very rapidly 4. Ulcerates lesions on lower lip or ear ar more aggressive 5
77
Treatment of SCC
1. Surgical excision with margin of 5mm | 2. Raiodtherapy
78
Where are Basalc ell carcinomas found
Elderly on head and neck
79
What is a rodent ucler
Ulceration of basal cell carcinoma
80
What is basal cell carcinoma
Tumour of basal keratinocytes
81
Risk factors of BCC
1. UV 2. Skin type I 3. Ageing
82
What is skin Type I
Skin that burns and doesn't tan
83
Clinical presentation of BCC
1. Border of ulcerated lesion raised with pearly appearance 2. Slowly enlarging, shiny nodule on head and neck area which bleeds following minor trauma and does not heal 3. Slowly causes local tissue destruction if not treated
84
How is BCC treated
1. Surgically excised to ensure clear and adequate tumour margins 2. Cryotherapy + Photodynamic therapy 3. Radiotherapy for those who don't tolerate surgery
85
What is malignant melanoma
1. Malignant tumour of melanocytes
86
Age effected by malignant melanoma
Younger patients
87
Risk factors for malignant melanoma
1. UV exposure 2. Red hair 3. High density freckles 4. Skin type I 5. Atypical moles 6. Multiple melanocytic nave 7. Sun sensitivity 8. Immunosuppression 9. Family History 10. Pale Skin
88
Clinical Presentation of Malignant Melanoma
1. Men - Back 2. Women - Lower legs 3. Very dark colour, black 4. ABCDE: A - Asymmetrical shape B - Border irregularity C - Colour Irregularity D - Diameter > 6 E - Elevation/Evolution (change of lesion) 5. Itching 6. Inflammation, crusting or bleeding
89
Types of melanomas
1. Superficial Spreading 2. Lentigo maligna (on face) 3. Acral (restricted to palms and soles
90
Differential diagnosis of melanomas
1. Benign pigmented naevus 2. Seborrhoeic wart 3. Pyogenic granuloma
91
How is Malignant Melanoma treated
1. Surgical excision in early stages | 2. Removal of regional lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy and chemotherapy
92
Metastases of malignant melanoma
1. Lung, Liver, CNS
93
Prognosis of Malignant Melanoma
1. Thin lesions (<1mm) have best prognosis 2. If over 60 then lower 5 year survival 3. Generally there is a female advantage in prognosis 4. Ulceration 5. Poor prognosis if present on trunk vs limbs
94
What is cellulitis
1. Bacterial Infection of the deep sub-cutaneous tissues
95
Where is cellulitis commonly seen
Lower extremities
96
What causes cellulitis
1. STREPTOCOCCUS PYOGENES (Group A beta-haemolytic) | 2. Staph Aureus
97
Risk factors for cellulitis
1. Lymphedema 2. Leg Ulcer 3. Immunosuppression 4. Traumatic wounds 5. Athletes for 6. Leg Oedema 7. Obesity
98
Clinical Presentation of cellulitis
1. Local inflammation (spreads to proximal body) 2. Hot erythema in affected area 3. Poorly demarcated margins, swelling, warmth and tenderness 4. Blister if oedema is present 5. FEVER
99
Diagnosis of cellulitis
1. Clinical 2. Skin Swabs negative 3. Serological testing for streptococcal infection (antistreptolysin O titre)
100
How is cellulitis treated
1. ORAL PHENOXYMETHYLPENICILLIN or ERYTHROMYCIN if allergic to penicillin 2. IV for 3-5 days of antibiotics if infection is widespread 3. PHENOCYMETHYPENICILLIN ORALLY twice a day for prophylaxis
101
What is Necrotising Fasciitis
1. Deep-seated infection of the subcutaneous tissue causing fulminant and spreading destruction of fascia and fat which spares the skin initially
102
What is type I necrotising fasciitis
1. Caused by a mixture of aerobic and anaerobic bacteria following abdo surgery or in diabetics
103
What is type II necrotising fasciitis
1. Caused by group A beta-haemolytic streptococci
104
Risk factors for type II necrotising fasciitis
1. Abdo surgery | 2. Immunosuppression
105
Clinical presentation of type II necrotising fasciitis
1. Severe pain out of proportion to the skin findings at initial site of infection 2. Infection rapidly spreads along tissue planes causing erythema and pain + crepitus 3. Patients with fever, toxicity and pain that is out of proportion to skin findings - necrotising fasciitis should be suspected 4. Multi-organ failure is common and mortality is high
106
Diagnostics of necrotising fasciitis
1. Soft tissue gas seen on X-ray 2. Raised CRP 3. Raised WCC 4
107
Treatment of necrotising fasciitis
1. IV BENZYLPENICILLIN and IV CLINDAMYCIN 2. IV METRONIDAZOLE for widespread IV antibiotics if unknown cause 3. Surgical debridement or amputation
108
Adverse effects of corticosteroids
1. Skin thinning, telangiectasia and contact dermatitis 2. Perioral dermatitis and acne on the face 3. Withdrawal
109
Adverse effects of Emollients
Greasiness of skin and exacerbates acne on face
110
Name two kertolytics
ALLANTOIN and SALICYLIC ACID
111
Role of keratolytics
Softens skin and causes cells of epidermis to shed more rapidly, opening clogged pores
112
Adverse effects of keratolytics
Hypersensitivity and chemical burns | 2. Sun protection needed
113
When should retinoids be avoided
SEVERE TERATOGEN
Year 2
flashcards
Decks in class (155)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions