Block 1 Flashcards
flat cells in the stratum corneum, which have lost nuclei, and lamellated lipids
corneocytes
corium
dermis
where the epidermal appendages, including nails, hair and glands, originate.
dermis
Three important aspects in skin history to seek out
- symptoms attributed to the skin lesion
- chronology of appearance, change, and disappearance of the lesions
- conditions of exposure, injury, or medication that may have induced or altered the disease
In the physical exam of the skin, three categories of observation should be made in sequence:
- anatomic distribution of the lesion 2. configuration of groups of lesions 3. the morphology of the individual lesions
Cardinal Features of skin lesions
Type Shape
Major Characteristics of skin lesions
Color Surface Consistency
First manifestations of the development of the disease
Primary Skin Eruptions
Develop from primary eruptions through transformation, inflammation, regression or healing
Secondary Skin Eruptions
Macule Patch Plaque Papule Nodule Vesicle Bullae Pustule Wheal
Primary Eruptions
Scale Crust Erosion Abrasion Crack Ulcer Scar Atrophy Lichenification
Secondary Eruptions
transitory or persistent change in skin coloration with no change in surface structure or consistency.
Macule
flat lesion greater than 1 cm in diameter
Patch
slightly raised lesion greater than 1 cm in diameter
Plaque
Solid elevations on the skin, up to 1 cm in size
Papule
solid elevations larger than one centimeter
Nodule
transient edema in the corium of light hue and lasting for only a few hours
Wheal
single chambered or multi chambered cavity filled with fluid up to 1 cm in size
Vesicle
fluid filled cavity greater than one centimeter in size
Bullae
eruption which contains a pus-filled cavity visible to the naked eye
Pustule
chronic rubbing leads to thickening of the skin with accentuation of the skin creases
Lichenification
independently scaling particles of corneal cells associated in groups
Scale
deposits which consist of dehydrated secretion, blood or necrotic tissue
Crust
sharply delimited, reddened weeping area from which serous secretion and punctiform hemorrhages are discharged
Excoriations
sharply delimited, reddened area due to a surface loss of epidermal tissue, which does not open a capillary. Heals without scarring
Erosion
fissural tear in the skin, occasionally bleeds
Crack
defect of a previously damaged skin extending to the epidermis or deeper, with poor tendency to heal and healing with scar formation
Ulcer
inferior replacement of a loss of substance with connective tissue
Scar
thinning and transparency of the epidermis or dermis or both
Atrophy
diascopy
press a transparent, firm object such as a glass slide against a lesion
If the lesion blanches or loses its erythematous color, this suggests that the erythema is due to ?
capillary dilation
If the lesion does not blanch or lose its red color, this suggests that the erythema is due to ?
extravasation of blood (this can result from vasculitis or destruction of the vessel wall).
the hard keratin cover of the dorsal portion of the distal phalanx
nail plate
The nail plate is generated by the ________ at the proximal portion of the nail bed
nail matrix
As the nail grows, the distal part of the matrix produces the deeper or superficial layers of the nail plate?
deeper while the proximal portion makes the superficial layers.
The nail is bound proximally by the ?and distally by the distal nail fold (defined by the separation created by the anterior ligament between the distal nail bed and the nail plate;
eponychium (the skin just proximal to the cuticle)
The nail is bound laterally by the?
nail folds
The nail is bound distally by the?
distal nail fold (defined by the separation created by the anterior ligament between the distal nail bed and the nail plate;
3 different layers of the nail:
The nail plate (the nail). The nail bed (ventral matrix, sterile matrix). The eponychium (cuticle).
This is the keratinized structure, which grows throughout life
nail plate (the nail)
This is the vascular bed that is responsible for nail growth and support. It lies protected between the lunula (the “half moon” seen through the nail) and the hyponychium (the posterior part of the nail bed epithelium)
nail bed (ventral matrix, sterile matrix)
The epidermal layer between the proximal nail fold and the dorsal aspect of the nail plate.
eponychium (cuticle).
Fingernails grow ?
2 -3 mm a month or 0.1 – 0.15 mm a day
Toenails grow ?
1 mm a month
Growth rate
(about 6 months from cuticle to free edge)
Loss of normal Lovibond angle Increase in nail fold density Pulmonary and CVs diseases GI Hyperthyroidism <1%
Clubbing
Spoon shaped concave nails, normal in children resolves with aging
Koilonychia
Cause of Koilonychia?
Fe deficiency, diabetes mellitus, protein def, exposure to petroleum based solvents, SLE and Raynaud’s disease
Transverse depression across the nail plate
Beau’s lines
Occurs when growth at the nail root (matrix) is interrupted by trauma OR any severe acute illness e.g. heart attack, measles, pneumonia, or fever.
Beau’s lines
These lines emerge from under the nail folds weeks later, and allow us to estimate when the patient was sick.
Beau’s lines
Probable underlying disease when Beau’s lines are present?
Severe infection, MI, hypotension, shock, hypocalcemia, surgery
Punctate depressions in the nail plate caused by defective layering of the nail plate
Nail Pitting
Usually associated with psoriasis, affecting 10 to 50 % of patients
Nail Pitting
Causes of Nail Pitting?
Also caused by systemic diseases, including Reiter’s syndrome and other CTDs, sarcoidosis, pemphigus, alopecia areata, lichen planus and incontinentia pigmenti. Any localized dermatitis (atopic or chemical dermatitis) that disrupts orderly growth in proximal nail fold also can cause pitting.
Presence of longitudinal striations or ridges, can be due to advanced age or: Rheumatoid arthritis; Peripheral vascular disease; Lichen planus; and Darier’s disease (striations are red/white
Onychorrhexis
Central ridging in Onychorrhexis can be due to ?
protein, folic or Fe deficiency
Median Nail Dystrophy
Central Nail Canal
Causes of Central Nail Canal?
Severe arterial disease (Heller’s fir tree deformity) – peripheral vascular artery disease Severe malnutrition and repetitive trauma
Longitudinal hemorrhagic streaks involving the nail bed.
Splinter hemorrhage
Causes of Splinter hemorrhage?
Trauma (most common), Derm disease (psoriasis), Idiopathic, and Systemic disease (subacute bacterial endocarditis )
If multiple nails are involved simultaneously in splinter hemorrhage and they occur near the lunula think of?
systemic disease.
If one or a few nails are involved in splinter hemorrhage and they occur near the end of the nail plate think of ?
trauma
Red lunula
Cardiovascular disease, collagen vascular disease or hematologic malignancy
Pale blue lunula suggests ?
diabetes mellitus
Proximal portion is white (edema and anemia) and distal portion is red, pink or brown
Lindsay’s half & half nails
Lindsay’s half & half nails could be a sign of?
Renal or liver disease
Clinical: Proximal white nail with narrow distal pink or brown band (0.5 to 3mm)
Terry’s nails
The nail looks opaque and white, but the nail tip has a dark pink to brown band.
Terry’s nails
Causes of Terry’s nails
cirrhosis, CHF, DM, cancer, hyperthyroidism, malnutrition, ageing
Confined to the nail bed. Will disappear when distal digit is squeezed.
Muehrcke’s Lines
Clinical: Double white transverse lines affecting numerous nails.
Muehrcke’s Lines
Causes of Muehrcke’s Lines ?
Chemotherapy and Hypoalbuminemia secondary to nephrotic syndrome, liver disease, or glomerulonephritis.
Transverse type of true leukonychia caused by systemic disease.
Mee’s lines
Clinical: Single or multiple transverse lines that involve multiple nails.
Mee’s lines
The pigment is in the nail plate.
Mee’s lines
Causes of Mee’s lines
Arsenic poisoning, Hodgkin’s disease, CHF, leprosy, malaria, chemotherapy, carbon monoxide poisoning, other systemic insults
Red brown discoloration of the nail bed
oil spot sign, salmon patch
Very common in Psoriasis
oil spot sign, salmon patch
Distal separation of nail plate from nail bed
Onycholysis
Causes of Onycholysis
Thyrotoxicosis, psoriasis, trauma, contact dermatitis, tetracycline, eczema, fungal or bacterial infections
Longitudinal Pigmented Bands (LPB)
Melanonychia
Pigmented band appearing in the distal matrix and extending to the tip of the nail.
Melanonychia
Be suspicious if: Develops in a single digit in adult life especially in 6th decade or later Develops abruptly in previously normal nail Becomes suddenly darker or wider
Melanonychia
the number of hairs on the head
120,000–150,000
number of hairs/cm2
250
the total surface area of a head of hair 20 cm long
6 m2
rate of growth of hair
1 cm/month
strands of hair we naturally lose each day
100 – 120
weight a single hair can withstand
100 gms
not greasy or dry, not permed or colored, holds style well, looks healthy
Normal
limp, looks flat lacks volume, soon gets greasy after shampoo
Fine/Greasy hair
looks dull, feels dry and rough, tangles easily, treated chemically, dry and frizzy, may have split ends
Dry
Alternating light and dark bands The light bands are areas on the shaft with vacuoles May be autosomal dominant
Pili annulati
Beaded appearance due to periodic narrowing of the hair shaft Autosomal dominant Fragile hair and dystrophic alopecia
Monilethrix
Bamboo hair
Trichorrhexis invaginata
Netherton’s syndrome, autosomal recessive
Trichorrhexis invaginata
Regularly spaced nodules along the shaft caused by intermittent fractures with invagination of the distal hair into the proximal portion
Trichorrhexis invaginata
Hair is twisted along the long axis Maybe congenital or acquired
Pili torti
Results from a disturbance of the follicle from a scarring inflammatory process, mechanical stress or cicatricial alopecia
Pili torti
Brittle hair shaft with breaks at varying lengths
Pili torti
Present in Menke’s, Bjornstad, Crandall syndromes
Pili torti
Abnormal fragility
Trichorrhexis nodosa
Congenital – Menke’s syndrome, Trichodystrophy, arginosuccinic aciduria
Trichorrhexis nodosa
May be accompanied by mental retardation, motor defect, ichthyosis, seizure disorders, growth abnormalities
Trichorrhexis nodosa
Acquired – excessive hair styling
Trichorrhexis nodosa
Split ends
Trichoptilosis
Most common complaint about hair
Hair loss
Most common hair problems
Telogen effluvium Male Pattern Baldness Female Pattern Baldness Trichotillomania Alopecia areata
Skilled interviewing techniques
The skin accounts for how many percent of the adult body weight?
6% (Dr. Montero)
16% (Bates)
Thin avascular keratinized, epithelium
Epidermis
Outer Layer of epidermis
stratum corneum (dead keratinized cells)
Inner Layer of the epidermis
stratum basale
(malphigian layer);site
where melanin and keratin are formed
Stratum spinosum
Migration from inner to outer layer is about?
1 month
dense layer of interconnecting collagen and
elastic fibers containing sebaceous and sweat
gland, hair follicles, and terminals of the
cutaneous nerves.
dermis
consists of spongy connective tissue with
energy-storing adipocytes (fat cells).
SUBCUTANEOUS TISSUE
Melanocytes are freely distributed along?
cytoplasm
protects DNA mutation caused by ultraviolet rays
melanin
brown pigment
Eumelanin
black pigment
Pheomelanin
ORIGINAL LESION
Exact site
Duration
Appearance
Distribution
Progression
SYMPTOMS
Pruritus
Pain
Burning
SETTING AND TIMING OF ATTACKS
Occupation
Topical agents
Drug history
Season of year
Environment
Distribution of Lesions:
Acne Vulgaris
face, chest, back
Distribution of Lesions:
Atopic Dermatitis
Body folds
Distribution of Lesions:
Photosensitive Eruptions
sun exposed area
Distribution of Lesions:
Pityriasis Rosea
90% sun covered area
Distribution of Lesions:
Psoriais
Predisposed to trauma
Distribution of Lesions:
Seborrheic dermatitis
Sebaceous in origin
These lesions are small
and itchy at first.
It can be due to
cutaneous larva
migrants of dog
or cat hookworm
Serpiginous
lesions
•Surface Features
- Normal or smooth
- Scaly
- Keratinous
- Crust
- Warty, papillomatous
- Umbilicated
- Lichenified
Shape of Lesions
Round
Oval
Irregular
Pedunculated
Yellow
Cholesterol deposits
Solar elastosis
Carotenemia
Xanthomas
→ Xanthalesma
→ Eruptive
Xanthogranulomas
Adnexal tumors and hyperplasias with
sebaceous differentiation
Necrobiosis lipoidica
Capillaries [Yellow-Brown Background]
Drugs/Deposits
→ Tophi
→ Quinacrine
Red
Vasodilation
Gray
Post inflammatory hyperpigmentation [Dermal]
→ Erythema dyschromicum perstans
Drugs/Deposits
→ Argyria
→ Chrysiasis
→ Mercury deposits
→ Combined melanocytic nevus
→ Traumatic tattoos
Green
Pseudomonas infection
→ Characterized with a “fruity smell”
Tattoo
Chloroma
Green hair due to copper deposits
Blue
Ceruloderma
Dermal melanocytosis
→ Mongolian spot
→ Nevus of Ota
Dermal melanocytomas
→ Blue nevi
Cyanosis
Ecchymoses
Venous congestion
→ Venous malformations
Drugs/Deposits
→ Minocycline
→ Traumatic tattoos
Brown
Pigmented lesion
→ Lentigines
→ Seborrheic keratosis
→ Junctional, compound and congenital
melanocytic nevi
→ Café-au-lait spot
→ Dermatofibromas
→ Melanoma
→ Pigmented actinic keratosis, Bowen’s disease
Post inflammatory hyperpigmentation
[Epidermal]
Melasma
Phytophotodermititis
Drug-induced hyperpigmentation
→ Cyclophosphamide
Metabolic
→ Addison’s disease
