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Block F: Defence > W3P2 > Flashcards

W3P2 Flashcards

1
Q

What are the five layers of the epidermis?

A 
Stratum Basale/germinativum 
Stratum spinosum 
Stratum granulosua
(Stratum lucidum)
Stratum Corneum
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2
Q

What are the two layers of the Dermis?

A

Papillary layer

Reticular layer

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3
Q

Difference between Primary vs Secondary lesions

A

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?

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4
Q

Non-palpable (flat) lesions of <0.5 cm in diameter

A

Macule

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5
Q

Non-palpable lesions of >0.5 cm in diameter

A

Patch

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6
Q

raised lesions, usually different color than surrounding skin, but can be the same <0.5cm

A

Papule

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7
Q

Raised lesions, usually a different colour than surrounding skin, but can be the same >0.5

A

Plaque

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8
Q

Raised, solid, but also has depth, <0.5

A

Nodule

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9
Q

Raised, solid, but also has depth >0.5cm

A

Tumor

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10
Q

Vesicle

A

Raised, fluid-filled <0.5cm

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11
Q

raised, fluid filled, >0.5cm

A

Bulla

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12
Q

Raised, fluid filled, with pus

A

Pustule

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13
Q

Can be any size or shape
Lasts LESS than 24 hours*
Edema and erythema
Usually seen in urticaria

A

Wheal

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14
Q

Raised lesion
Fluid/substance-filled cavity
Encapsulated
Lined with TRUE epithelium

A

true epi = has ALL three layers

Cysts

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15
Q

What are some examples of secondary lesions

A 
Erosion (epidermis)
Ulcer (into dermis -scar forming) 
Fissure: deep, all three layers
Atrophy
Excoriation
Crust
Scale
Lichenification
Scar
Keloid
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16
Q

Surface change
Desquamation
Flakes arising from the stratum corneum

A

Scale

= secondary lesion

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17
Q

What is Tinea Pedis

A

Athelet’s foot

Scale (secondary lesion)

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18
Q

Surface change
Hardened deposit from serum, blood, or pus

  • what is an example of this morphology
A

Crust

  • Impetigo

secondary lesion

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19
Q

A lack of substance
A wasting of tissue (or failure to form)
Affected skin is clinically thinner or depressed compared to surrounding skin

A

Atrophy

  • secondary lesion
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20
Q

A lack of substance
Moist circumscribed depression
Due to loss of all or part of the epidermis

A

Erosion

  • secondary lesion
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21
Q

A lack of substance

Circumscribed depression due to loss of ENTIRE epidermis and all or part of the dermis

A

Ulcer

i. e. diabetic ulcer
- secondary lesions

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22
Q

What does “skin” include when you’re doing a physical examination?

A

skin, Hair, nails and oral mucosa

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23
Q

What are some features you’d use to describe skin lesions?

A

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

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24
Q

annular

A

type of shape: ring shaped

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25
Q

Serpiginous

A

(of a skin lesion or ulcerated region) having a wavy margin:

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26
Q

What are some descriptive terms for topography

A

flat topped (lichenoid)
dome shaped
filiform
pedunculated: thinner at the base

smooth
verrucous
umbilicated; depression in the middle

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27
Q

What are some special studies for skin

A

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

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28
Q

What are the two basic systems to come up with a diagnosis for a lesion

A

Morphological

Pathogenesis

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29
Q

Nail Plate

A

Keratinized structure that continues to grow throughout life

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30
Q

Lateral nail folds

A

cutaneous folds providing lateral borders to the nail

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31
Q

Proximal nail fold

A

cutaneous fold providing the visible proximal border of the nail

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32
Q

Cuticle

A

aka eponychium

extends from the proximal nail fold and adheres to nail plate

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33
Q

Nail matrix

A

this is the nail root

nail factory, beneath the proximal nail fold

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34
Q

Lunula

A

half moon:

the convex margin of the matrix seen through the nail

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35
Q

Nail bed

A

the bed upon which the nail rests, extending from the lunula to the hyponychium

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36
Q

Hyponychium

A

Cutaneous margin underlying free nail

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37
Q

Onychomadesis

A

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

38
Q

Etiology of Onychomadesis

  • which quite a common cause?
A

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*

39
Q

Onychomadesis Mangement

A

This is bengin and self limiting = it will grow back on its own

so just give reassurance.

40
Q

Presentation: Holes in finger nails

What is the diagnosis?
What can it be associated with?

A

Nail pitting:

Punctate depressions on nail plate 
common
can be associated with:
- psoriasis, 
- atopic dermatitis
- alopecia areata or 
- trauma
41
Q

Management of Nail pitting

A

Bengin, so no worries

42
Q

Acute Paronychia

  • common cause?
A

very Painful, erythmatous, indurated swelling of nail fold(s) with purulent drainage developing over a few hours

  • usually caused by staphylococcus aureus
43
Q

Chronic Paronychia

A

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

44
Q

Herpetic Whitelow

A

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

45
Q

Melanonychia

A

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

46
Q

Racial Melanonychia

A

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

47
Q

onychomycosis

A

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

48
Q

Distal subungual onychomycosis

A

Invasion of nail bed and inferior portion of nail plate
onycholysis
subungual hyperkeratosis
yellow/brown discoloration

49
Q

White superficial onychomycosis

A

Superficial infection of nail plate

well demarcated whitish, opaque, friable plaques on dorsal nail plate

50
Q

How do you diagnose onychomyosis

A

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

51
Q

hair root

A

part below the surface of the scalp

52
Q

Hair shaft

A

part above the surface of the scalp

53
Q

Hair follicle

A

each hair grown from a hair follicle, a tiny, sac-like hole in the skin

54
Q

Hair bulb

A

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

55
Q

Hair growth phases

A
  1. Anagen
  2. Catagen
  3. Telogen
56
Q

Anagen

A

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

57
Q

Catagen

A

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

58
Q

Telogen

A

phase 3 of hair growth

club-shaped proximal end of hair sheds from the follicle
lasts- 3 months
10-15% of terminal scalp hair

59
Q

Alopecia

A

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

60
Q

Non cicatricial alopecia

A

you see that the follicles are still open. no scaring

the hair will grow back

61
Q

Cicatricial alopecia

A

Lack of follicular ostia
Shiny atrophic skin

this is the scarring type, won’t grow back

62
Q

Alopecia Areata

what is its natural course

A

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

63
Q

Tinea Capitis

A

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

64
Q

Tinea Capitis: Kerion

-what might it be misdiagnosed for?

A

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

65
Q

What is the most common cause of tinea capitis in Canada and US

A

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

66
Q

How do you diagnose Tinea Capitis?

A

Similar to any other form of tinea

Scraping of fungal area
KOH, to highlight fungus
Culture

67
Q

What is the treatment for Tinea Capitis?

A

Oral antifungal

Topical therapy reduce infectivity

68
Q

Trichotillomania

A

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

69
Q

Androgenetic alopecia

A

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

70
Q

Androgenetic alopecia in men

A

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

71
Q

Androgenetic alopecia in women

A

Diffuse central thinning of the crown with preservation of the frontal hair line

72
Q

Pathogenesis of androgenetic alopecia

A

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

73
Q

Telogen effluvium

A

looks like a diffuse alopecia
Common condition
Hair follicle gets shifted prematurely to telogen phase by some triggers
starts 2-3 month after trigger**

74
Q

What are the triggers of Telogen Effluvium

A

SEND
Stress: any sever systemic disease, surgery, fever, psyhcological stress
Endocrine: hypo/hyperthyroidism, postpartum
Nutritional: iron deficiency
Drug: acitretin, anticoagulant, allopurinol

75
Q

Natural course of Telogen effluvium

A

Shedding continues for about 3-4 months AFTER removal of inciting cause

hair density may take 6-12 months to return to baseline

76
Q

What are Human Leucocyte Antigens

- What are the two classes?

A

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
77
Q

Which chromosome are HLA expressed on?

A

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.

78
Q

HLA polymorphism

- order of most to least?

A

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

79
Q

MHC I

A

In humans there are 3 different types of class I proteins A, B, C.

aka HLA

80
Q

MHC II

A 
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

81
Q

In regards to HLA/MHC: Any given individual can express ___ Class I and ____ Class 2 molecules on the cells surface at minimum

A 
6 class I
8 class 2
82
Q

So with all the subtypes of HLA, what are the chances of a match?

A

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

83
Q

How is Tissue Typing done

- There are two types

A

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).

84
Q

What is Functional Typing

A

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.

85
Q

What happens with MISmatched transplants

- in what cases is matching REQUIRED?

A

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

86
Q

Does blood type (ABO) matching matter for HLA transplants?

A

NO because RBCs are ANUCLEATED!! they don’t have MHC/HLA antigens!! SO IT DON’T MATTER

87
Q

What is the percentage chance of HLA match if a sister is donating to the brother?

A

1/4

sex does NOT matter :)

88
Q

Public Health Message #1: Good Science is NEVER Static

A

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

89
Q

Message #2: it’s all about the math

A

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

90
Q

Message 3: Takes a long time to make a vaccine

A

and its VERY expensive, you need support from big companies

PRE-COVID the record was 2.5 yrs to create vaccine for the rotavirus

91
Q

Vaccines have always been political

A

who produces them: wealthy countries
thus doesn’t get distributed to third world counteries

massive inequalities ensue

Block F: Defence (9 decks)

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