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88 Cards in this Set

  • Front
  • Back
Functions of the skin
Immunologic barrier
Temperature regulation
Protection from radiation
Nerve sensation
Injury repair
Appearance
Layers of skin
Epidermis
Dermis
Subcutis
What are the layers of skin
What are the layers of skin
Epidermis and Dermis
Epidermis and Dermis
Layers of the skin
Layers of the skin
4 major layers of epidermis
4 major layers of epidermis
Stratum Corneum

Stratum granulosum (granualar cell layer)

Stratum Spinosum (spiny layer)

Stratum basale (basal cell layer)
Stratum Corneum

Stratum granulosum (granualar cell layer)

Stratum Spinosum (spiny layer)

Stratum basale (basal cell layer)
Three main types of cells that make up the epidermis
Keratinocytes
Melanocytes
Langerhans Cells
Two layer of dermis
Two layer of dermis
Papillary dermis 
Reticular dermis
Papillary dermis
Reticular dermis
Structures in the dermis
blood vessels
lymphatic vessels
nerves
pilosebaceous units
apocrine glands
eccrine glands
Cells of the dermis
Fibroblasts
-- synthesize collagen

Mast cells
-- immune response; release histamine
Collagen synthesis
Collagen synthesis
Vessicles and bulla both contain clear fluid.

Vessicle < 1cm
Bulla > 1 cm
Vessicles and bulla both contain clear fluid.

Vessicle < 1cm
Bulla > 1 cm
Secondary lacerations
Secondary lacerations
Herpes Simplex
Herpes simplex viruses 1 and 2
Painful, grouped vesicles on an erythematous base
-- may appear pustular (white to yellow)
-- may see just erosions

Pain and recurrence suggests HSV
HSV Pathogenesis: Course of infection
Primary infections (once in a lifetime!)
Virus transmission to mucosa or abraded epithelium
Robust lytic replication that is limited to inoculation site
Which cell types support HSV replication
Many
Which cell types support HSV latency
Neurons
In what situations will HSV disseminate systemically
In cases such as severely immunocompromised host. May disseminate systematically and seed to several organs (adrenal glands, liver, CNS)
What does herpes simplex virus infect?
Sensory neurons innervating the site of inoculation - retrograde transport to the sensory ganglia where the virus establishes latency
Sites of herpes simplex latency : HSV-1
Trigeminal ganglia
Sites of herpes simplex latency : HSV-2
Sacral ganglia
Stimuli that trigger herpes simplex
Stress
Physical trauma
these trigger viral reactivation leading to a switch from latent to lytic life cycle
Reinfection of an individual with HSV
Reinfection of a seropositive indiv with a different strain of HSV is possible, but uncommon - exogenous reinfection
Diagnosis of Herpes SImplex
- Tzanck Smear (low sensitivity and specificity)

- Molecular test (direct fluorescent antigen, polymerase chain reaction ) - rapid <24 hours & high sensitivity and specificity
Positive Tzanck Smear

Merged with other cells. They are fusigenic. Becomes a large gigantic multinucleated cell.
Positive Tzanck Smear

Merged with other cells. They are fusigenic. Becomes a large gigantic multinucleated cell.
HSV Treatment
No treatment needed for most infections
-- treatment started within first 24 hours can shorten duration or decrease severity
Treatment that is needed for certain infections:
Severe gingivostomatitis
Extensive cutaneous disease
Ocular involvement
Pregnant patient
Immunocompromised patient
Acyclovir Mechanism
Acyclovir Mechanism
Acyclovir
Valacyclovir is the prodrug of acyclovir

Ganciclovir, valganciclovir, and famciclovir have similar MOA
Adverse effects of acyclovir
Oral
-- nausea, vomiting, diarrhea
-- headache

IV
-- phlebitis at injection site
-- Nephrotoxicity (crystal formation)
Herpes Zoster
- Caused by an eruption of latent varicella zoster virus (VZV)

- Clues to the diagnosis
- Dermatomal (zosteriform) eruption on one side of the body
- Grouped vesicles on an erythematous base
- Most often on trunk but can be anywhere
- Usually preceded by pain or burning
- Generally shingles occurs only once in the immunocompetent , in contrast to herpes simplex virus which frequently recurs.
Which herpes virus is resistant to acyclovir and requires high dose
CMV (lack thymidine kinase)
Varicella Zoster pathogenesis
VZV is an alpha herpes virus and belongs to the same subfamily as HSV
Primary Infection of Varicella Zoster
VZV replicated in the upper respiratory tract, is efficiently aerosolized during coughing and is readily acquired via respiratory route


VZV spreads systematically and replicates throughout the body

Secondary viremia seeds VZV to the skin, where it causes widespread vesicular rash -- chicken pox
Latency of HSV virus
Viral latency is supported by many ganglia as opposed to one of a few for HSV

Virus can reactivate from ANY infected ganglia later in life to cause shingles

Unlike HSV several viral gene products are actively transcribed and translated within latently infected neurons -- how the virus deals with the immune system recognition in vivo is unclear
VZ Vaccine
Live, attenuated virus-oka strain
given to young children
Main mechanism is to decrease the symptoms of primary infection and therefore decrease the efficiency of virus spread

15-20% of vaccinated individuals do get eventually infected with wild type VZV that foes on to establish latency. Symptoms of primary infection are not present and a vaccinated individual does not know that they picked up wt VZV.
Wild type VZV in a vaccinated individual
Wild type VZV can reactivate and cause zoster later in life, in spite of immunization

Oka vaccine strain establishes a lifelong latent infection, reactivation can occur, but is very inefficient in immocompetent indiv; reactivation of vaccine strain , at worst, results in mild symptoms
Oka Vaccine strain can be transmitted to?
Immunocompromised individuals - use caution when vaccinating healthy children with immunocompromised siblings
Usefulness of Oka Vaccine
Elderly patients to prevent zoster. Recent studies show that immunization can limit zoster.
Immunity in aged not as long lasting, booster is recommended in pop > 60
Chicken Pox
VZV primary infection
Diffusely scattered vesicles on an erythematous base
- vesicles arise in crops and are in different stages
- "Dewdrops on a rose petal"

Can be extensive and severe, especially in adult
Impetigo
Bacterial infection caused by gram pos bacteria
-- S. aureus
-- S. pyogenes
--- aka group A beta-hemolytic strep

Majority of lesions are crusted papules (impetigo contagiosa)
S. aureus
Gram pos cocci
Encodes many toxins that are responsible for virulence
Where does S. aureus colonize?
Anterior nares of healthy individuals
How does S. Aureus spread?
Via person to person or person-fomite contact
Can survive on artificial surfaces for a long time

Methicillin-resistant strains are of particular concern
Staphylococcal Scalded Skin Syndrome
Focus of infection secretes toxin into the blood
- Epidermolytic toxin A
- Epidermolytic toxin B

Widespread superficial blisters
- skin peels away in sheets
- Wound cultures from erosions are negative
Who is at risk for Staphylococcal Scalded Skin Sydrome
Kids < 2 years and adults with renal disease

Consult dermatology immediately
Psoriasis
Chronic plaque psoriasis most common variant
Sharply defined plaques with silvery-white scale, often symmetric
-- most common on elbows, knees, scalp, presacrum, hands, and feet

-- genitalia involved in up to 30%

Arthritis in 20-30% of patients
Increased risk of metabolic syndrome and CVD
Several other variants; more than one may coexist simultanceously
Immunology of psoriasis
Considered a prototypic type 1 helper T cell disease
-- increased IL-2, IL-12, IFN-gamma, TNF-alpha
- decreased IL-1, IL-10

Th17 and Th22 cells more recently found to be crucial in pathogenesis
Treatment of Psoraisis
Individualized balancing extent and severity of disease

Topical treatments: topical corticosteroids, topical vit D analogs, tar based therapies, topical retinoid

Phototherapy (PUVA, NBUVB, excimer laser)

Systemic Therapy
- methotrexate
- cyclosporine
- retinoids
- biologic agents
Methotrexate
Synthetic analog of folic acid
Competitively inhibits DHFR
-- necessary for pyrimidine and purine synthesis

Adverse Effects
-- nausea, anorexia, fatigue, alopecia, stomatitis
-- leukopenia, thrombocytopenia
-- hepatotoxicity

Also effective in treating psoriatic arthritis
Leucovorin
Active metabolite of folic acid
Displaces methotrexate from intracellular binding sites and restores the folate required for DNA/RNA synthesis

Used for inadvertent methotrexate overdose or high dose methotrexate rescue
Exanthematous Drug Eruption
Morbilliform drug eruptions
MC type of drug-induced eruption
Mechanism likely immunologic; often thought to be delayed (type IV) hypersensitivity reaction
Occurs 7-14 days after drug started
Low grade fever may be present
Spontaneously resolve in 1-2 weeks
MC caused by aminopenicillins, sulfonamides, cephalosporins, anticonvulsants
Signs of a possible severe cutaneous reaction
Mucous membrane involvement
Temperature above 38.5 C
Blisters
Facial edema and erythema
Lymphadenopathy
Painful skin lesions
Marked peripheral blood eosinophilia
Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis
Onset between 1-3 weeks of drug initiation
Typical lesions are tender dusky red or purpuric macules that progress to flacid bullae and erosions

Often fever, LAD, hepatitis, cytopenias
Where is Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis found
Buccal, ocular, and genital mucosae in > 90%

Respiratory tract involved in 25%
What typically causes Stevens Johnson Syndrome/ Toxic Epidermal Necrolysis?
Allopurinol, anticonvulsants, antibiotics, NSAIDs
Top layer of epidermis slides away from underlying skin
Top layer of epidermis slides away from underlying skin
Hypersensitivity reaction and EBV
Occurs in up to 90% of patients with EBV induced infections mononucleosis treated with amoxicillin or ampicillin
-- less often PCN or cephalosporins

Occurs 7-10 days after starting med
Atopic Dermatitis
Chronic disease with periods of worsening and remission
Atopic Dermatitis : Infantile Stage
More acute; involves face, scalp, extensor surfaces of the extremities, diaper area spared, secondary impetiginization common
Atopic Dermatitis: Childhood Stage
More chronic; involved flexural folds and extremities, more lichenification
Atopic Dermatitis: Adult Stage
Variable course; hand dermatitis common
Immunology of Eczema
Considered a prototypic type 2 helper T cell disease:

-- Increased IL-4, IL-5, IL-13
-- Decreased IL-2, IFN-gamma

Defects in epidermal skin barrier
-- decreased essential fatty acids
-- fillagrin mutations
-- increased susceptibility to allergens
-- increased water loss

Defects in cell mediated immunity
-- increased susceptibility to viral, bacterial, and fungal infections of the skin
Molluscum Contagiosum
Most common in children; increased risk with atopic dermatitis
Appears 7 weeks after exposure to the virus
Firm, small, pink, or flesh colored dome-shaped papules
Spread by contact with infected skin or clothing
Most people have complete clearing in 2-4 months
Lesions persist and are more numerous in those with weakened immune systems
Structure of Molluscum Contagiosum
Very large DSDNA virus - poxvirus family
Virion is ovoid to brick shaped, complex structure

Replictes exclusively in the cytoplasm of infected cell -- a unique feature for a DNA virus

Single life cycle -- lytic replication
Histology of Molluscum Contagiosum
Includes molluscum bodies - large eosinophilic inclusions in the cytoplasm -- viral factories
Includes molluscum bodies - large eosinophilic inclusions in the cytoplasm -- viral factories
central depression - umbilication
central depression - umbilication
Eczema Herpeticum
AKA Kaposi varicelliform eruption
Refers to viral infection of a pre-existing dermatosis
Sudden eruption of painful, edematous, crusted vesicles, pustules, and erosions

May be associated with high temperature, malaise, LAD

Most commonly caused by disseminated HSV infection in patients with atopic dermatitis and referred to as eczema herpeticum

requires IV acyclovir