Derma - urticaria, bacterial skin infxns Flashcards
Urticaria/angioedema
Edema extends to deep dermis and /or subcutaneous and submucosal layers
Angioedema
Urticaria/angioedema
Circumscribed, raised, erythematous, evanescent areas involving the superficial dermis
Urticaria
Pathogenesis of urticaria and angioedema
Mast cells, basophils, eosinophils releases histamine and cytokines
Results to vascular permeability
Then extravasation of fluids and proteins
Causing edema
Acute urticaria recurs for how many days
<30d
Chronic urticaria recurs for how many days
> 30d
Wheals of acute urticaria.
Large wheals, associated with angioedema
Wheals of chronic urticaria.
Small and large wheals
Acute/chronic urticaria
IgE-dependent (with atopic background)
Acute urticaria.
Acute/chronic urticaria
Due to anti-FcR autoantibodies
Chronic urticaria
Acute/chronic urticaria
Related to alimentary agents, parasites and penicillins
ACute urticaria
Acute/chronic urticaria
Intolerance to salicylates and benzoates
Chronic urticaria
Chronic urticaria cannot tolerate
Salicylates and benzoates
Acute/chronic urticaria
Complement mediated in serum sickness-like reaction (whole blood, ig, penicillin)
Acute urticaria
Chronic urticaria common in children/adult, M/F
Adult, F
Acute/chronic urticaria
May persist for 10yrs
Chronic urticaria
Acute/chronic urticaria
Rarely persists for >24hrs
Acute urticaria
Localized urticarias
Solar
Pressure
Vibration
Cold urticaria
Immunologic urticarias
IgE-mediated urticaria
Complement-mediated urticaria
Immunologic contact urticaria
Autoimmune urticaria
Immunologic urticaria due to type 1 HPS with atopic background. Common Ag are food, drug and helminths
IgE mediated urticaria
IgE mediated urticaria HPS type
Type 1 HPS
Acute immunologic urticarias
IgE mediated
Complement mediated
Immunologic contact
Immunologic urticaria which releases anaphylotoxin causing mast cells degradation. Common in serum sickness, ig and admin of whole blood
Complement mediated urticaria
Chronic immunologic urticaria
Autoimmune urticaria
Immunologic urticaria common in children with atopic dermatitis sensitized to environmental allergens and individuals sensitized to latex rubber gloves. Accompanied by anaphylaxis.
Immunologic contact urticaria
Autoimmune urticaria is positive in what test
Autologous serum skin test
The remission of disease activity of autoimmune urticaria is due to
Plasmapheresis
IVIg
Cyclosporin
Physical urticaria with positive linear lesion after storming or scratching skin
Dermographism
Demographics fades in …
30min
Physical urticari confined to sites exposed to cold
Cold urticaria
Diagnosis of cold urticaria
Ice cube test
How to do ice cube test
Application of ice for 10min
Wheal appears within 5min
Diagnostic test for solar urticaria
Test with UVB, UVA and visible light
How to test solar urticaria
260-690nm uv expo for 30-120s
Wheal appears within 30min
Wheezing for <1hr is seen in what Physical urticaria
Solar urticaria
Mediator of solar urticaria
Histamine
Wheezing physical urticaria
Solar
Cholinergic urticaria
Physical urticaria which appears with exercise and sweating
Cholinergic urticaria
Physical urticaria in which the intracutaneous of ACH and mecholyl will produce micropapular whealing
Cholinergic urticaria
Very rare phys urticaria with water of any temperature
Aquagenic urticaria
Aquagenic urticaria lesion is same with
Cholinergic urticaria
Sites of predilection of pressure urticaria
Soles
Palms
Waist
Applications of p perpendicular to skin in pressure urticaria will produce WHEAL after..
1-4hrs
Pressure urticaria is delayed for (time)
30min-12hrs
Physical urticaria which is painful and interferes with quality of life. No lab abnormalities. Associated with fever
Pressure angioedema
Familial, autosomal dominant physical urticaria
Vibratory angioedema
Distinct angioedema syndrome
Hereditary angioedema HAE
Angioedema-urticaria-eosinophilia syndrome AUES
Major mediator of chronic idiopathic urticaria
Histamine.
Eicosanoids and neuropeptides
Urticaria due to mast cells releasing agents and pseudo allergens and chronic idiopathic urticaria
Urticaria due to mast cells releasing agents and pseudo allergens and chronic idiopathic urticaria AGENTS
FAARS Food preservatives Ace inhibitors Additive azo dyes Radio contrast media Salicylate
Due to direct effects of exogenous urticants penetrating into skin and blood vessels
Non immune contact urticaria
Urticaria associated with vascular/connective tissue autoimmune disease
SLE
Sjögren’s syndrome
Urticaria vasculitis lesion persists for
> 12-24hrs
Urticaria associated w vascular or connective tissue autoimmune disease has SLOW/RAPID changes in size and config
Slow
Urticaria associated w vascular or connective tissue autoimmune disease may or may not have residual pigmentation due to
Hemosiderin
Urticaria often with hypocomplementemia and renal disease
Urticaria associated w vascular or connective tissue autoimmune disease
HAE is autosomal dominant/recessive
Dominant
T or F: Uritacaria usually occurs in HAE
Does not usually occur
Lab abnormalities in HAE
Decreased C1-esterase inhibitor
Low C4
May follow trauma (phys/emotional)
AE of face and ext, laryngeal edema, acute abd pain (presents as surgical emergency)
With bradykinin formation
Can be life threatening
HAE
Treatment for HAE
Danazol (long term)
Whole fresh plasma
With severe AE with pruritic urticaria of face, neck, trunk and ext
AUES
AUES lasts for how many days
7-10d
Lab abnormalities of AUES
Leukocytosis
Eosinophilia
HAE/AUES:
No family history
Fever
Marked increase in wt
AUES
Treatment for AUES
Prednisone
HAE/AUES: good prognosis
AUES
Lab in urticarial vasculitis
Increased ESR
Hypocomplementemia
Flushing. Burning. Wheezing.
Cholinergic urticaria
Fever.
Serum sickness
AUES
Hoarseness. Stridor. Dyspnea.
AE
Arthralgia.
Serum sickness
Urticarial vasculitis
Abdominal colicky pain.
HAE
Medications.
Penicillin
Aspirin
NSAIDs
Ace inhibitors
Treatment when severe urticaria is associated with anxiety and depression
Doxepin
Treatment for urticaria with AE
Prednisone
Treatment for AUES
Prednisone
Treatment for acute attack of HAE
Whole fresh plasma or
C1-esterase inhibitor
H2 antihistamine
Cimetidine
Famotidine
Ranitidine
3rd gen H1 antihistamine
Piperadine - desloratadine, fexofenadine
Piperazine - levocetirizine
2nd gen H1 antihistamine
Piperadine - loratadine, terfenadine
Piperazine - cetirizine
1st gen H1 antihistamine
Alkylamine - chlorpheniramine maleate, dimethindene maleate
Aminoalkyl ether (ethinolamine)- clemastine fumarate, diphenhydramine
Ethylenediamine- antazoline
Phenothiazine- mequitazine, phomethazine
Piperidine- azatadine maleate, cyproheptadine
Piperazine- hydroxyzine
Age of onset: eryhtrasma
Adult
Age of onset: impetigo and ecthyma
Primary - children
Secondary- any age
Bullous- children/young adult
Age of onset: abscess, furuncle, carbuncle
Children up to young adult (boys)
Age of onset: erysipelas and cellulitis
Any age
Age of onset: staph-scalded-skin syndrome (Ritter’s dse)
Neonate up to <5y/o
Commonly called as Ritter’s disease
Staph-scalded-skin syndrome
Etiology: eryhtrasma
C. Minutissimum
Etiology: impetigo and ecthyma
Staph aureus-most common
GAS
Etiology: abscess, furuncle, carbuncle
MSSA, MRSA
Etiology: erysipelas and cellulitis
Adult- S.aureus, GAS
Children- HiB, S.aureus, GAS
Etiology: Ritter’s disease
S.aureus grp2
Site of predilection: eryhtrasma
Toe web spaces >groin folds > axilla Interiginous areas (intra gluteal, infra mammary)
Site of predilection: abscess, furuncle, carbuncle
Hair follicles
Break of integrity of skin
Macules, sharply marginated, red-brown, scaling at sites not continuously occluded.
Post-inflammatory Hyperpigmentation
Associated with dermatophytoses and candidiasis
Eryhtrasma
Woods lamp of erythrasma
Coral-red fluorescence
Heavy growth of corynebacterium
Erythrasma
T or F: eryhtrasma may relapse if predisposing causes are not corrected
True
Prophylaxis for erythrasma
Benzoyl peroxide
Medicated powders
Topical antiseptics- isopropyl, ethanol
Topical therapy for erythrasma
Benzoyl peroxide
Eythromycin, clindamycin
Mupirocin
Antifungals
Nonspecific inflammation of opposed skin and between redundant skin.
Common among obese.
Intertriginous infection and intertrigo
Management for intertrigo
Wt reduction
Moist dressing/ castellani’s paint
Zinc oxide ointment- reduce friction
Pimecrolimus, tacrolimus
Etiology of pyoderma
Coagulase neg staph
S.aureus, GAS
Portal of entry of primary impetigo
Minor breaks in skin
Portal of entry of secondary impetigo
Traumatic breaks
Duration of lesion of impetigo
Days to wks
Duration of lesion of ecthyma
Wks to mos
Impetigo/ecthyma: variable pruritus (associated w/ AD)
Impetigo
Impetigo/ecthyma:
pain and tenderness (indurated)
Induration with thick adherent crust
Ecthyma
Site of predilection of ecthyma
Distal ext
T or F: mimoetigo is associated with lymphangitis or LA
True
Bullous/nonbollous;
Golden yellow crusts
Nonbullous
Bullous/nonbollous; clear yellow, brown crusts with shallow moist erosion
Bullous
Bullous/nonbollous; with normal appearing skin
Bullous
Bullous/nonbollous; scattered discrete with satellite lesions by auto inoculation
Nonbollous
Distribution of nonbollous
More in intertriginous areas
What happens to an untreated impetigo
leads to ecthyma resulting to healing with scar
T or F: with MRSA infection, impetigo and ecthyma is associated with high morbidity and mortality
True
Topical treatment for impetigo and ecthyma
Mupirocin 3x/d for 7-10d
Systemic treatment for impetigo and ecthyma
Pen G or V
Cephalosporin, vancomycin etc
Prevention of impetigo and ecthyma
Daily bath
Benzoyl peroxide
Check family member
Ethanol or isopropyl for hands
It occurs as a foreign body response to splinter, ruptured inclusion cyst and injection sites
Sterile abscess
Represents as a continuum of severity of staph aureus infection
Folliculitis
Carbuncle
Furuncles
site of predilection of abscess, furuncle, carbuncle
Hair follicle
Break on intergrity of skin
Synonym for abscess, carbuncle, furuncle
Boil
Acute /chronic localized infection with collection of pus and tissue destruction. Arise from dermis, subQ fat and ms or deeper
Abscess
SOP of abscess
Any cutaneous sites, sites of trauma
Acute, deep seated from staph folliculitis. Firm tende nodule with central necrotic plug with central pustule with or without surrounding cellulitis.
Furuncle
SOP of furuncle
Any hair-bearing region
Deeper infection with interconnecting abscess with similar evolution to furuncle.
Multiple adjacent coalescing furuncle.
Carbuncle
SOP of. Carbuncle
Several contiguous hair follicle.
Possible HEMATOGENOUS seeding of abscess, furuncle and carbuncle
Heart valves Joints Spine Long bones Viscera
Abscess/carbuncle/furuncle: accompanied with fever and malaise
Carbuncle
Management for abscess furuncle carbuncle
I and D plus systemic antimicrobial
Adjunctive therapy for absces, Furuncle, carbuncle
Application of heat (promotes localization or consolidation and aids early spontaneous drainage)
Aka soft tissue infection
Cellulitides
An acute, diffus, spreading, edematous, suppurative inflammation of dermis and subQ tissues.
Often with malaise, fever and Chills
Soft tissue infection a
History of human bite
Erysipelas and cellulitis
Spread on infection in soft tissue infection is due to
Hyaluronidase - polysaccharide ground subs
Fibrinolysin - fibrin barriers
Lecithinase - cell mem
Soft tissue infection is more on a reaction to..
Cytokine and bacterial superantigens
SOP of erysipelas in adult
Low leg
SOP of erysipelas in young male
Arm
SOP of erysipelas in female
Post mastectomy
SOP of erysipelas ff rhinitis and conjunctivitis
Face
SOP of erysipelas in operative wound site
Trunks
SOP of erysipelas in children
Head and neck - HiB
Ext - staph aureus, GASP
Unlike other types of cellulitis, that which is cause by ___ usually ff a primat enteritis with bacteremia and dissemination
V. Vulnificus
Management for erysipelas and cellulitis: primary with pneumococcus
Benzoyl peroxide plus immunize those at risk
Management for erysipelas and cellulitis: primary with HiB
Benzoyl peroxide plus chemo prophylaxis for household contacts of <4y/o
Management for erysipelas and cellulitis: primary with vibrio
Benzoyl peroxide plus avoid eating uncooked seafood
Antimicrobial treatment for erysipelas and cellulitis
S. Aureus and beta lactam antibiotics
Staph aureus phage grp 2 in Ritter’s dse produces what toxin
Exfoliating toxin A and B
Site of ET production
Purulent conjunctivitis Otitis media Omphilitis Occult nasopharyngeal Bullous impetigo
Pathogenesis of Ritter’s disease.
Colonize. ET production. Transport by blood to skin. _________ = __________
Acantholysis and intraepidermal cleavage within stratum granulosus = local Bullous imopetigo or mild scarlatiniform rash
Ritter’s disease spont heals in
5-7d
Macular scarlatiniform rash or diffuse ill defined erythema.
Fine stippled sandpaper apparance.
SSS syndrome or Ritter’s disease
Ritter’s disease spreads within
24-48hr
(+) nikolsky sign
Ritter’s dse
Ddx for Ritter’s disease
TEN
TSs
Kawasaki syndrome
T or F: In Ritter’s disease, staph aureus is seen at site of infection, NOT from sites of sloughing skin or bullae
True
T or F: In Ritter’s disease, gram(+) cocci only at colonized site
True
Ritter’s disease spont heals with adeq antibiotic treatment in
3-5d
T or f: Ritter’s disease lesion produces scarring
False
Psedudomonas aeroginosa prefers dry/moist environment
Moist environment
Pseudomonas aeroginosa colonized what part of the body
Skin External ear URT Large bowel (In those who are compromised )
Entry sites of pseudomonas infection
Breaks in MC barrier
Aspiration
Decubitus or skin ulcers
Thermal burns
3 stages of infection of pseudomonas
Bacterial attachemt and colonization
Local invasion and damage of tissue
Disseminated systemic disease
T or F: psedomonas infection may stop at any stage
True
Clinical syndrome of pseudomonas infection
Nail colonization Folliculitis Toe web infection 1and2 pyoderma Ext. otitis
Nail colonization of pseudomonas infection is seen undersurface of oncholytic nails. What is the discoloration
Green
Hot tub folliculitis of pseudomonas infection infects multiple hair follicle. Is it self limited?
True
Color of exudate and odor ofPyoderma of pseudomonas infection
Blue green exudates and fruity odor
Is external otitis in pseudomonas infection self limited?
True
Invasive infection of pseudomonas
Ecthyma gangrenosum
Erythematous macule which leads to hemarhagic bluish infarction to black in central necrosis with erythematous halo
Ecthyma gangrenosum
SOP of ecthyma gangrenosum
Axilla
Groin
Perianal
Everywhere