W3P2 Flashcards
What are the five layers of the epidermis?
Stratum Basale/germinativum Stratum spinosum Stratum granulosua (Stratum lucidum) Stratum Corneum
What are the two layers of the Dermis?
Papillary layer
Reticular layer
Difference between Primary vs Secondary lesions
Primary lesions: directly associated with the disease process
Secondary lesions: modification of a primary skin lesion
i.e. blister = primary, a burst bleeding blister = secondary?
Non-palpable (flat) lesions of <0.5 cm in diameter
Macule
Non-palpable lesions of >0.5 cm in diameter
Patch
raised lesions, usually different color than surrounding skin, but can be the same <0.5cm
Papule
Raised lesions, usually a different colour than surrounding skin, but can be the same >0.5
Plaque
Raised, solid, but also has depth, <0.5
Nodule
Raised, solid, but also has depth >0.5cm
Tumor
Vesicle
Raised, fluid-filled <0.5cm
raised, fluid filled, >0.5cm
Bulla
Raised, fluid filled, with pus
Pustule
Can be any size or shape
Lasts LESS than 24 hours*
Edema and erythema
Usually seen in urticaria
Wheal
Raised lesion
Fluid/substance-filled cavity
Encapsulated
Lined with TRUE epithelium
true epi = has ALL three layers
Cysts
What are some examples of secondary lesions
Erosion (epidermis) Ulcer (into dermis -scar forming) Fissure: deep, all three layers Atrophy Excoriation Crust Scale Lichenification Scar Keloid
Surface change
Desquamation
Flakes arising from the stratum corneum
Scale
= secondary lesion
What is Tinea Pedis
Athelet’s foot
Scale (secondary lesion)
Surface change
Hardened deposit from serum, blood, or pus
- what is an example of this morphology
Crust
- Impetigo
secondary lesion
A lack of substance
A wasting of tissue (or failure to form)
Affected skin is clinically thinner or depressed compared to surrounding skin
Atrophy
- secondary lesion
A lack of substance
Moist circumscribed depression
Due to loss of all or part of the epidermis
Erosion
- secondary lesion
A lack of substance
Circumscribed depression due to loss of ENTIRE epidermis and all or part of the dermis
Ulcer
i. e. diabetic ulcer
- secondary lesions
What does “skin” include when you’re doing a physical examination?
skin, Hair, nails and oral mucosa
What are some features you’d use to describe skin lesions?
Primary + secondary lesion morphology (you are experts by now!)
Size
Distribution: where on the body
Grouping: single, several discrete but nearby each other, confluent
Color: red, dark brown, etc. May have more than one color. If so, how are the colors distributed within the lesion?
Shape: Round, oval, polygonal, annular, serpiginous,
Topography: Flat-topped, dome-shaped, etc
Palpation: consistency, tenderness, temperature, mobility
annular
type of shape: ring shaped
Serpiginous
(of a skin lesion or ulcerated region) having a wavy margin:
What are some descriptive terms for topography
flat topped (lichenoid)
dome shaped
filiform
pedunculated: thinner at the base
smooth
verrucous
umbilicated; depression in the middle
What are some special studies for skin
KOH: to confirm superficial fungal infections
Cytology: to look at discrete cells under microscope
Culture: if you suspect infectious etiology (viral, bacterial, fun)
Patch testing -> if you suspect allergic contact dermatitis
Imaging
What are the two basic systems to come up with a diagnosis for a lesion
Morphological
Pathogenesis
Nail Plate
Keratinized structure that continues to grow throughout life
Lateral nail folds
cutaneous folds providing lateral borders to the nail
Proximal nail fold
cutaneous fold providing the visible proximal border of the nail
Cuticle
aka eponychium
extends from the proximal nail fold and adheres to nail plate
Nail matrix
this is the nail root
nail factory, beneath the proximal nail fold
Lunula
half moon:
the convex margin of the matrix seen through the nail
Nail bed
the bed upon which the nail rests, extending from the lunula to the hyponychium
Hyponychium
Cutaneous margin underlying free nail
Onychomadesis
complete separation of the nail plate form the bed
caused by full but temporary arrest of growth of nail matrix
normal nail will start to grow again
Etiology of Onychomadesis
- which quite a common cause?
Trauma: manicure, onychotillomania (picking or pulling of the nails)
dermatologic diseases: eczema, erythroderma
sever systemic conditions
High fever
Viral illness
viral illness being quite a common cause of onychomadesis*
Onychomadesis Mangement
This is bengin and self limiting = it will grow back on its own
so just give reassurance.
Presentation: Holes in finger nails
What is the diagnosis?
What can it be associated with?
Nail pitting:
Punctate depressions on nail plate common can be associated with: - psoriasis, - atopic dermatitis - alopecia areata or - trauma
Management of Nail pitting
Bengin, so no worries
Acute Paronychia
- common cause?
very Painful, erythmatous, indurated swelling of nail fold(s) with purulent drainage developing over a few hours
- usually caused by staphylococcus aureus
Chronic Paronychia
inflammation affecting nail matrix = dystrophic nails
Not uncommon in thumb suckers
Non purulent, glistening erythema around nail fold with nail dystrophy (yellowish, crumbling)
Major causes: Candida and irritation caused by saliva
Herpetic Whitelow
cloudy vesicles: confluent or separate on erythematous base
white sudden swelling. recurrent.
no purelence
Infection cased by HSV (herpes) 1 or 2 infection of the fingertip and perionychium
Can be confused with acute bacterial paronychia
There is pain, edema and erythema
Melanonychia
brown line/band on nail
Tan brown or black pigmented band along the length of nail
DDX of solitary melanonychia:
- Nail matrix nevus
- Nail matrix lentigo
- Subungual melanoma
based on retracting the nail fold
Racial Melanonychia
now you have dark lines/bands affecting several nails
more common in darker skin phototypes
it is a varient of NORMAL
77% of african-american young adults and almost 100% of those >50 years
management: reassurance
onychomycosis
thick yellow toe nails
fungal infection of the nail unit
you have to look for the source; look between toes, groin etc
i.e. look for tinea pedis in patient and their family
Distal subungual onychomycosis
Invasion of nail bed and inferior portion of nail plate
onycholysis
subungual hyperkeratosis
yellow/brown discoloration
White superficial onychomycosis
Superficial infection of nail plate
well demarcated whitish, opaque, friable plaques on dorsal nail plate
How do you diagnose onychomyosis
KOH preparation and fungal culture
Periodic acid-schiff (PAS) stain
Recommended to do diagnostic tests prior to initiating treatment
because there could be an alternative causes of nail changes
hair root
part below the surface of the scalp
Hair shaft
part above the surface of the scalp
Hair follicle
each hair grown from a hair follicle, a tiny, sac-like hole in the skin
Hair bulb
A club-shaped structure forming the lower par of the hair root
matrix cells in hair bulb proliferate and differentiate to make the hair shaft
Hair growth phases
- Anagen
- Catagen
- Telogen
Anagen
first hair growth phase
matrix cells grow, divide and become keratinized to form the growing hair
Lasts 2-6 year- longest period
makes up 85-90% of terminal scalp hair
Catagen
Matrix proliferating cells abruptly cease proliferating so that hair bulb involutes and regresses
lasts 2-3 weeks - shortest
less than 1% of terminal scalp hair
this is a transitional phase
Telogen
phase 3 of hair growth
club-shaped proximal end of hair sheds from the follicle
lasts- 3 months
10-15% of terminal scalp hair
Alopecia
refers to hair loss generally, depends on category by:
Localized vs diffuse
cicatricial vs non cicatricial (scarring)
if there is scarring you cannot regrow hair
Non cicatricial alopecia
you see that the follicles are still open. no scaring
the hair will grow back
Cicatricial alopecia
Lack of follicular ostia
Shiny atrophic skin
this is the scarring type, won’t grow back
Alopecia Areata
what is its natural course
non scarring, recurrent, non scaly type of hair loss
one or more alopetic patches: localized
it can affect the scalp but also the eye lashes, eye brows, beard area etc
natural course:
unpredictable
spontaneous regrowth in 50-80% of cases
single episode vs multiple recurrences
Tinea Capitis
circular patches of alopecia with marked scaling and broken hairs, also itchy
infection of the scalp with a dermatophyte fungus
most common in preschool and school-age children
more common in black children
Tinea Capitis: Kerion
-what might it be misdiagnosed for?
A boggy inflammatory mass surrounded by follicular pustules
May be accompanied by fever and local lymphadenopathy
May be misdiagnosed as: impetigo, cellulitis, or an abscess
What is the most common cause of tinea capitis in Canada and US
Trichophyton tonsurans
spread:
from one person to another as it naturally infects humans (anthropophilic)
remains viable on combs, hairbrushes and other fomites for long periods of time
How do you diagnose Tinea Capitis?
Similar to any other form of tinea
Scraping of fungal area
KOH, to highlight fungus
Culture
What is the treatment for Tinea Capitis?
Oral antifungal
Topical therapy reduce infectivity
Trichotillomania
Habitual compulsive plucking of hair
A well define area of hair loss with shortened, broken-off hairs of different lengths
Frontotemporal or parietotemporal
hard to diagnose because pt usually doesn’t admit it
Treatment;
psychiatric eval
worse prognosis with older patients
Androgenetic alopecia
Genetically determined sensitivity of scalp hair follicles to adult levels of androgens
common disorder affecting 50% of men and women older than 40 years
loss of hair in frontotemporal and vertex area
Androgenetic alopecia in men
Starts with bitemporal recession
then diffuse thinning over the vertex of scalp
the bald patch progressively enlarges and eventually join the receding frontal hairline
ultimately just marginal parietal and occipital hair
Androgenetic alopecia in women
Diffuse central thinning of the crown with preservation of the frontal hair line
Pathogenesis of androgenetic alopecia
Testosterone metabolite; DHT plays a dominant role in AGA
DHT production is regulated by 5a reductase
hair follicles have 5a reductase
in AGA: pts have higher levels of 5a reductase AND more androgen receptors
DHT shortens the growth phase of the hair leading to miniaturization of the follicles and production of progressively fewer and finer anagen hairs
Telogen effluvium
looks like a diffuse alopecia
Common condition
Hair follicle gets shifted prematurely to telogen phase by some triggers
starts 2-3 month after trigger**
What are the triggers of Telogen Effluvium
SEND
Stress: any sever systemic disease, surgery, fever, psyhcological stress
Endocrine: hypo/hyperthyroidism, postpartum
Nutritional: iron deficiency
Drug: acitretin, anticoagulant, allopurinol
Natural course of Telogen effluvium
Shedding continues for about 3-4 months AFTER removal of inciting cause
hair density may take 6-12 months to return to baseline
What are Human Leucocyte Antigens
- What are the two classes?
aka: Major Histocompatibility Complex
Series of cell surface receptors falling into 2 main classes MHC class I aka HLA A,B,C MHC class II aka HLA DR,DQ, DP
Which chromosome are HLA expressed on?
Found on the short arm of chromosome 6 these genes are co-dominantly expressed. Thus genes from both chromosomes and transcribed and translated into protein.
HLA polymorphism
- order of most to least?
is referring to all the subtypes (isotypes?)
within MHC1 there are B, A, C in order of most to least
within MHCII there are DR, DP, DQ in order of most to least
likely to match with siblings
MHC I
In humans there are 3 different types of class I proteins A, B, C.
aka HLA
MHC II
MHC class II have restricted tissue distribution, found on antigen presenting cells such as dendritic cells, macrophages, B cells. MHC class II proteins present antigen to CD4+ Tcells.
Aka: HLA
In regards to HLA/MHC: Any given individual can express ___ Class I and ____ Class 2 molecules on the cells surface at minimum
6 class I 8 class 2
So with all the subtypes of HLA, what are the chances of a match?
Based on random mendelian genetics, chances of match would be poor
However, HLA genes are in LINKAGE DISEQUILIBRIUM which means that gene families tend to stick together and are inherited as blocks thus increasing the possibility of matches.
HLA matching is done for BOOOOTH HLA class I and class II antigens
How is Tissue Typing done
- There are two types
This is to find MATCHES for HLA/MHC
Serology
Using antibodies that recognize the different families of HLA patients or donor cells are typed. Antibodies recognize components on the HLA proteins that are unique to the class/family/allele.
e.g. With serologic typing you will receive a report of tissue type: HLA A2/A16, B2/B8, C1/C4 and DR4/6.
Genetic
Gene sequencing is used to better define the allele carried by the patient. This is important because small allelic variations, not detectable by serologic typing can be identified and there is better precision of the HLA match
e.g. HLA DRB-7 (the 7-type allele of DR4).
What is Functional Typing
Occasionally a functional assay, the mixed lymphocyte reaction, can be performed to identify important functional mismatches.
May be done for patients with previous solid organ transplants.
In this test, lymphocytes from the patient are mixed with inactivated cells from the donor and the degree of activation assessed. If there is a significant amount of activation the patient is likely to reject the graft. The opposite can also be done.
What happens with MISmatched transplants
- in what cases is matching REQUIRED?
Depending on the type of transplant and how the donor tissue is treated, mismatches can sometimes be tolerated.
Matching of Class I is essential for kidney grafts and solid organs
Additional matching of Class II is required for bone marrow transplants
Does blood type (ABO) matching matter for HLA transplants?
NO because RBCs are ANUCLEATED!! they don’t have MHC/HLA antigens!! SO IT DON’T MATTER
What is the percentage chance of HLA match if a sister is donating to the brother?
1/4
sex does NOT matter :)
Public Health Message #1: Good Science is NEVER Static
Vaccine ‘experts’ and public health MDs
give advice based on the best science
available in good faith
Either science or the situation (or both)
can change over time
Stay open-minded and try not to indulge
in 20/20 ‘rear-view’ vision
Message #2: it’s all about the math
understanding attack rate: absolute value of vaccinated that are infected is comparable to absolute value of infected who are unvaccinated. HOWEVER relative values show there is a big difference. i.e. 4>2 however 4/100 is not greater than 2/2
One BILLION doses of
vaccine sounds like a lot!
Most vaccines need 2 doses
With 7.8 billion people in the world
Message 3: Takes a long time to make a vaccine
and its VERY expensive, you need support from big companies
PRE-COVID the record was 2.5 yrs to create vaccine for the rotavirus
Vaccines have always been political
who produces them: wealthy countries
thus doesn’t get distributed to third world counteries
massive inequalities ensue
