Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Clin Med I > Skin conditions I and II > Flashcards

Skin conditions I and II Flashcards

(115 cards)

Start Studying
1
Q

how do cellulitis, erysipelas and abscesses normally present?

A
  • erythema
  • edema
  • warmth
  • d/t breach in skin barrier -> bacterial entry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

where/who is erysipelas normally found

A
  • upper dermis and superficial lymphatics

- kids and older adults

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

where/who is cellulitis normally found

A
  • deeper dermis and subcutaneous fat

- middle aged and older adults

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

where are abscesses normally found

A

upper and deeper dermis

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

risk factors for cellulitis/ erysipelas

A
  • skin barrier disruption
  • preexisting skin conditions
  • skin inflammation i.e. d/t radiation
  • edema - lymphatic or venous insufficiency
  • obesity
  • immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

most common cause of erysipelas

A
  • beta hemolytic strep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

most common cause of cellulutis

A
  • beta hemolytic strep

- staph aureus (including MRSA)

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

most common cause of skin abscess

A
  • staph aureus (including MRSA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

clinical manifestations of cellulitis

A
  • erythema, warmth, edema
  • unilateral almost always
  • common in lower extremities
  • +/- purulence
  • slower onset
  • localized sx develop over days
  • less distinct boarders
  • +/- drainage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

clinical manifestations of erysipelas

A
  • erythema, warmth, edema
  • unilateral almost always
  • common in lower extremities
  • nonpurulent
  • acute onset sx
  • clear demarcation- butterfly involvement on face
  • systemic manifestations- fever/ chills
  • raised above level of surrounding skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does induration mean

A

hard surrounding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does fluctuant mean

A

soft and moveable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is a skin abscess

A
  • collection of pus

- in dermis or subcutaneous space

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

clinical presentation of skin abscess

A
  • painful
  • fluctuant
  • erythematous nodule
  • +/- cellulitis
  • surroudning induration
  • regional adenopathy
  • systemic sx rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

furuncle

A

infection of hair follicle -> abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

carbuncle

A

infection of multiple hair follicles -> abscess

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

what are common areas for skin abscesses to develop?

A
  • neck
  • face
  • axillae
  • buttocks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is LRINEC score?

A
  • lab risk indicator for necrotizing fasciitis

- distinguish NF from other soft tissue infections like cellulitis

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

when would you use the LRINEC score

A
  • concerning hx and exam
  • pain out of proportion to exam
  • rapidly progressive cellulitis
  • score >6 means NF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

complications of cellulitis

A
  • NF
  • bacteremia and sepsis
  • osteomyelitis
  • septic joint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

conditions that may be hard to distinguish from cellulitis

A
  • gout
  • DVT
  • venus stasis dermatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

management of cellulitis/ abscess/ erysipelas

A
  • depends on severity
  • should see improvement in 24- 48 hours
  • tx duration of 7-10 days, up to 14
  • if no improvement consider underlying abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

where does impetigo most commonly occur

A

on face of kids 2-5

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

what is the most common form of impetigo

A
  • non-bullous
  • papules progress to vesicles surrounded by erythema
  • dev into pustules which break down and form golden crust
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
ectyhma impetigo
- ulcerative - extend deep into dermis - "punched out ulcers" with yellow crust
26
possible consequences of impetigo
- post-strep glomerulonephritis | - rheumatic fever
27
sx of post-streph glomerulonephritis
- edema - HTN - hematuria - occurs 1-2 weeks post infection
28
most common cause of impetigo?
- s. aureus
29
most common cause of bullous impetigo?
- s. aureus strain that produces toxin -> cleavage of superficial skin
30
most common cause of ecthyma impetigo?
- strep pyogenes
31
urticaria
- hives, welts, wheels - common - intensely pruritic - usually no identifiable trigger - sometimes accompanied by angioedema - anyone can get it
32
acute urticaria
- less than 6 weeks
33
chronic urticaria
- recurrent | - signs and sx recur most days of week for more than 6 weeks
34
clinical manifestations of urticaria
- circumscribed, raised, erythematous plaque with central palor - round/oval - very itchy - most severe at night - any area of body - transiently appearing - can get angioedema in lips, extremities, genitals
35
pathophys of urticaria
- mediated by mast cells in dermis - release histamine -> itching - release vasodilatory mediators -> swelling
36
dx of urticaria
- mainly clinical exam and history - signs and sx of allergic reaction - any underlying disorders - allergy test
37
management of urticaria
- focused on short term relief - 2/3 spontaneously resolve and are self limited - can use H1 and H2 antihistamines - may use steroids
38
lipomas
- most common benign soft tissue neoplasm - mature fat cells enclosed by fibrous capsule - dx based on history and PE
39
where are lipomas usually found?
- most common in upper extremities and trunk - can be found anywhere - range in size
40
pathophys of lipomas
- >50% develop in subcutaneous tissue | - cause unknown but associated with gene rearrangement of chromosome 12
41
clinical manifestations of lipomas
- superficial - soft - painless - round, oval, multilobulated - pt may confuse them for enlarged lymph nodes
42
management of lipomas
- if stable/asymptomatic then no tx | - can surgically excise
43
epidermal inclusion cyst
- most common cutaneous cyst - skin colored dermal nodules - visible central punctum - usually small in size
44
where are epidermal inclusion cysts usually found
- face - scalp - neck - trunk - can occur anywhere - 2X more common in men
45
what disease is epidermal inclusion cysts associated with?
gardener syndrome- predisposition to colon polyps
46
pathophys of epidermal inclusion cysts
- d/t trauma - implantation and proliferation of epithelial elements into dermis - spontaneous rupture can occur - cheesy material
47
clinical manifestations of epidermal inclusion cysts
- firm - asymptomatic - overlyting a punctum (where hair follicle comes out)
48
management of epidermal inclusion cysts
- asymptomatic- none - excesion of cyst or incision and drainage - intralesional injection with triamcinolone
49
tetanus cause
- clostridium tetani - found in soil - rarely seen in US d/t vaccine - incidence increases after natural disasters
50
pathophys of tetanus
- c. tetani produces matalloprotease tetanospasmin (toxin) - toxin released in brain stem -> blocks neurotransmission that modulates muscle contraction - result- increased muscle tone, painful spasm, widespread autonomic instability
51
what is the incubation period for tetanus?
- 8 days | - further the inoculation site is from CNS the longer the incubation pd
52
clinical manifestations of tetanus
- trismus (lock jaw) - massester muscle reflex . spasm - tonic contractions of skeletal muscles - no impairment in consciousness
53
when does acne typically resolve?
- 3rd decade | - post adolescent usually impacts women
54
pathogenesis of acne
- inflammation of pilosebaceous follicles - follicular hyperkeratinization - increased sebum production - cutibacterium acnes - inflammation
55
sebaceous gland changes in ance
- gland enlarges - sebum production increases during puberty -> medium for c. acne - micromedones = enviornment for bacteria
56
closed comedone
- white head | - accumulation of sebum and keratinous material
57
open comedone
- black head - keratinocytes - oxidized lipids - melanin
58
pathogenesis of inflammatory acne
- follicle ruptures -> proinflammatory lipids and keratin released into surrounding dermis - family history has 3X risk - stress doesnt appear to be associated
59
androgens and acne
- stimulates growth of secretory fn of sebaceous glands - high levels at birth -> acne until about 2 y/o - acne onset correlated to DHEA-s levels - most pts with acne have normal androgen levels*
60
external factors that cause acne
- soaps/ detergents/ astrigents - repetitive mechanical trauma like scrubbing - bra straps, shoulder pads, helmets
61
milk and acne
- milk can exacerbate acne d/t increased levels of IGF
62
insulin resistance and acne
- stimulates androgen production - associated with increased IGF-1 - increased facial sebum production - normal rise in insulin resistance and IGF-1 in puberty
63
BMI and acne
- possible that low BMI reduces risk of acne in males | - increased risk of high BMI and acne only in women
64
ways to classify acne
- comedonal acne- noninflammatory - inflammatory acne- papules, pustules - nodular acne- aka cystic acne
65
dx of acne
- PE - type and location - medication hx - endocrine fn - DHEA-S, total testosterone, free testosterone
66
counseling points for acne tx
- no cure - 4-6 weeks for improvement - may get worse before better
67
Rosacea
- chronic disorder - relapses - primarily in central face - 4 main subtypes - more common in fair skinned and adults (F) >30
68
main subtypes of rosacea
- erythematotelangiectatic - papulopustular - phymatous - ocular
69
pathogenesis of rosacea
- abnormalities in innate immunity - inflammatory reactions to cutaneous microorganisms - UV damage - vascular dysfunction
70
erythematotelangiectatic rosacea
- presistant central erythma - flushing - rough and scaling - enlarged cutaneous BV - skin sensitivity - erythema congestivum
71
erythema congestivum
after exacerbation of facial redness in rosacea, return to baseline is slow
72
papulopustular rosacea
- papules and pustules in central face - can be mistaken for acne - comedones dont occur - inflammation extends beyond follicle
73
phymatous rosacea
- tissue hypertrophy - irregular contours - usually on nose - can occur on chin, cheeks, forehead - most common in men
74
ocular rosacea
- happens in more than 50% of pts - conjunctival hyperemia - blepharitis - keratitis - lid margin teleangiecstasis - abnormal tearing - chalazion - refer to ophthalmologist
75
rosacea exacerbating factors
- extreme temps - sun exposure - hot drinks - spicy food - alcohol - exercise - irritation from topical products - emotions - drugs - skin barrier disruption
76
dx for rosacea
- clinical assessment | - no biopsy or serologic studies
77
management of erythematotelangiectatic rosacea
- first line- behavioral changes/ avoid triggers | - second line- laser and light based therapy
78
psoriasis
- well demarcated plaques with silver scales - associated with many comorbidities - peak age onset: 30-39 and 50-69
79
risk factors for psoriasis
- genetics *
80
exacerbating factors for psoriasis
- smoking - obesity - drugs - infection- post strep flaares and HIV - alcohol - vit D deficiency - stress
81
pathophys of psoriasis
- immune mediated - scaling, induration, erythema hyperproliferation - abnormal differentiation of epidermis - inflammatory cell infiltrates - vascular dilitation
82
categories of psoriasis
- chronic plaque psoriasis - guttate - pustular - erythrodermic - inverse - nail
83
chronic plaque psoriasis
- most common - symmetrical distribution - asymptomatic or pruritis
84
common places for plaque psoriasis
- scalp - extensor elbows, knees - gluteal cleft
85
guttate psoriasis
- multiple small papules and plaques - trunk and proximal extremities common - strong assoc with recent strep infection - child or YA with no hx psoriasis
86
pustular psoriasis
- life threatening - acute onset - wide spread erythema, scaling, and sheets of superficial pustules - maialse, fever, diarrhea, leukocytosis, hypocalcemia
87
causes of pustular psoriasis
- pregnancy - infection - withdrawal from glucocorticoids
88
erythrodermic psoriasis
- uncommon - acute or chronic - generalized erythema and scaling from head to toe - complications d/t loss of adequate barrier
89
inverse psoriasis
- inguinal, perineal, genital, intergluteal, axillary and inframammory areas - sometimes misdx as fungal or bacterial infections
90
nail psoriasis
- more common in pts with psoriatic arthritis | - nail pitting
91
dx of psoriasis
- family hx* - clinical exam - skin biopsy
92
management of psoriasis
- emollients - topical corticosteroids - vit D analogs - Tar- T/gel - topical retinoids - UVB light therapy - photochemothearpy - excimer laser - biologics
93
alopecia
- targets anagen hair follicles -> non-scarring hair loss - usual onset before 30 - men and women equally affected
94
classifications of alopecia
- areata - totalis - universalis
95
alopecia areata
discrete patches
96
alopecia totalis
entire scalp
97
alopecia universalis
entire body
98
pathophys of alopecia
- T cell mediated inflammation disrupts normal hair cycle - no destruction of hair follicle - premature transition of active follicle to inactive - collapse of immune privileged status - inappropriate trigger of immune response vs follicular antigen
99
alopecia risk factors
- genetics - severe stress - drugs and vaccines - infections - vit D def
100
clinical manifestations of alopecia
- smooth, circular, discrete patches of hair loss - dev over 2-3 weeks - pruritis or burning may precede - beard may be first site in men - can spread in bizarre patterns - nail abnormalities possible
101
onychorrhexis
- longitudinal fissuring of nail plate | - can occur in pts with alopecia
102
diseases associated with alopecia
- thyroid disease*** - lupus - vitiligo - atopic dermatitis - allergic rhinitis - psoriasis - down syndrome - polyglandular autoimmune syndrome type I
103
clinical course of alopecia
- 50% with limited patchy hair loss spontaneously recover in 1 yr - some have multiple episodes - 10% progress to totalis or universalis
104
dx of alopecia
- clinical exam - exclamation point hair at margins - skin biopsy only in uncertain cases- show inflammatory infiltrates surrounding follicles aka swarm of bees
105
management of alopecia
- topical or intralesional corticosteroids (caution skin atrophy and hypopigmentation) - topical immunotherapy for severe - rogaine - phototherapy - oral steroids or biologics as last line
106
hidradenitis supprativa
- chronic follicular occlusive skin condition - aka acne inversa - inertriginous area involvement - onset usually puberty to 40, women more than men
107
pathogenesis of HS
- follicular occlusion, follicular rupture and associated immune response - ductal keratinocyte proliferation - ductal plugging then expansion -> rupture - stim immune response leading to sinus tracts
108
risk factors and exacerbating factors of HS
- genetics* - mechanical stress - obesity - smoking - hormones- perimenstrual flares, goes away during pregnancy - bacteria- staph and strep - drugs
109
clinical manifestations of HS
- axilla most common site - inguinal, inner thigh, perianal, inframammary, buttock, scrotum, vulva - primary lesion is solitary, painful, deep seated inflamed nodule - dev sinus tracts with chronic disease - scarring
110
what is the staging system called for HS?
hurley staging
111
Stage I hurley manifestation and management
- abscess formation - topical clindamycin - intralesional corticosteroid - punch debridement - chemical peel
112
stage II hurley manifestation and management
- recurrent abscess - sinus tract formation and scarring - oral tetracyclines for several months - clindamycin or rifampin - oral retinoids - antiadrenergics - punch biopsy of fresh lesions
113
stage III hurley manifestation and management
- diffuse involvement - multiple interconnected sinus tracts - TNF alpha inhibitors - systemic glucocorticoids - cyclosporine - surgery
114
dx of HS
- patient history - clinical exam - skin biopsy not necessary
115
prevention of HS
- avoid skin trauma - stop smoking - weight management - antiseptics - emollients - management of comorbidities

Clin Med I (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions