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186 Cards in this Set
- Front
- Back
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What are the functions of the skin?
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- Immunologic barrier
- Temperature regulation - Protection from radiation - Nerve sensation - Injury repair - Appearance |
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What are the layers of the skin?
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- Epidermis
- Dermis - Subcutis |
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What are layers A and B?
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- A = Epidermis
- B = Dermis |
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What is the top, middle and, lower layer?
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What are the the four major layers of the epidermis?
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What is layer A?
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A = Stratum Corneum
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What is layer B?
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B = Stratum Granulosum
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What is layer C?
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C = Stratum Spinosum
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What is layer D?
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D = Stratum Basale
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What are the three main types of cells in the epidermis?
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- Keratinocytes
- Maloncytes (basal layer) - Langerhans cells |
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What are the two layers of the dermis?
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What structures are found in the dermis?
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- Blood vessels
- Lymphatic vessels - Nerves - Pilosebaceous units - Apocrine glands - Eccrine glands |
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What types of cells are found in the dermis? Functions?
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- Fibroblasts: synthesize collagen
- Mast cells: immune response, release histamine |
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How is collagen synthesized?
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Inside fibroblasts:
1. Synthesis (RER) 2. Hydroxylation (RER) 3. Glycosylation (RER) 4. Exocytosis Outside fibroblasts: 5. Proteolytic processing 6. Cross-linking |
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Case 1:
- 18 yo HS senior presents w/ 1 day of painful blisters around her mouth - She had an eruption like this about a year ago in same location - No PMH, allergies, or family hx - Meds: ibuprofen as needed How would you describe the skin exam? |
Clusters of vesicles on erythematous base on R lower lip
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What are these types of lesions?
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- Left: vesicles (<1 cm)
- Right: bulla (>1 cm) |
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What kind of lesion is this?
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Vesicle (<1 cm)
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What kind of lesion is this?
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Bulla (>1 cm)
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What are the terms for the secondary lesions that are a result of a primary lesion changing (eg, vesicle or bulla ruptures)?
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Erosions (only in epidermis) and Ulcers (extended into dermis)
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What kind of lesion is this?
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Erosion
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What kind of lesion is this?
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Ulcer
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What kind of lesion is this?
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Crust
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Cassie’s exam shows grouped vesicles on an erythematous base on her right chin and lip, and a pustular vesicle on his left lip. What is the most likely diagnosis?
a) Allergic contact dermatitis to poison ivy b) Bullous impetigo c) Chicken pox d) Herpes simplex e) Shingles |
Herpes Simplex
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What are the types of Herpes Simplex? What are the characteristics of these lesions?
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Herpes Simplex 1 and 2
- Painful, grouped vesicles on an erythematous base - May appear pustular (white to yellow) - May just see erosions (if vesicles have already burst) - Pain and recurrence suggests HSV |
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What kind of lesion is this?
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Herpes Simplex (clustered vesicles on erythematous base)
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What kind of lesion is this?
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Intraoral Herpes Simplex - usually won't see vesicles on mucosa, rather just see erosions
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What does HSV infection?
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Virus is transmitted to mucosa or abraded epithelium
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Where does lytic replication of HSV occur?
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- Robust lytic replication is limited to site of inoculation
- Many cell types can support lytic HSV replication - Only neurons are suitable for HSV latency |
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Where does HSV infect?
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- Primarily stays in mucosa, epithelium, and neurons
- In immunocompromised hosts, HSV may disseminate systemically and seed to several organs (adrenal glands, liver, CNS) - Virus infects sensory neurons innervating the site of innoculation |
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What happens to HSV that has gotten into sensory neurons?
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Retrograde transport to the sensory ganglia where the virus establishes latency
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What are the sites of latency of HSV?
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- HSV-1 is latent in trigeminal ganglia
- HSV-2 is latent in sacral ganglia |
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What can trigger viral reactivation from latent to lytic life cycle of HSV?
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Poorly understood stimuli (stress, physical trauma)
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Where are mature HSV virions produced?
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Around the site of inoculation
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How can reinfection with HSV occur?
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- Reinfection of epithelial cells as mature virions are produced around the site of inoculation
- Reinfection with a different strain of HSV is possible, but uncommon (exogenous reinfection) |
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How do you diagnose HSV infection?
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- Tzanck smear (in-office and rapid, but low specificity and sensitivity)
- Molecular test = Direct Fluorescent Antigen, PCR (rapid <24 hours, high sensitivity and specificity) |
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Which diagnostic test for HSV is highly sensitive and specific?
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Molecular test: Direct Fluorescent Antigen or PCR
- Rapid <24 hrs |
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What is this an image of?
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Positive Tzanck smear (multinucleated giant cells)
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Should HSV infections be treated?
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- No treatment is needed for most infections
- Treatment started within first 24 hours can shorten duration or decrease severity - Treatment is needed for certain infections |
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Under what circumstances is treatment for HSV necessary?
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- Severe gingivostomatitis
- Extensive cutaneous disease - Ocular involvement - Pregnant patient - Immunocompromised patient |
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Which of the following medications would be used to treat HSV?
a) Azithromycin b) Acyclovir c) Zidovudine d) Oseltamivir e) Ribavirin |
Acyclovir
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What is the mechanism of Acyclovir for treatment of HSV?
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1. Acyclovir + ATP is activated/phosphorylated by HSV Thymidine Kinase to Acyclovir Phosphate
2. Human enzymes convert to Acyclovir Triphosphate 3. HSV DNA polymerase incorporates Acyclovir Triphosphate into viral DNA 4. Viral DNA synthesis is inhibited |
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What other drugs have similar mechanisms of action as Acyclovir?
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Other drugs that end with "-cyclovir":
- Valacyclovir (prodrug of Acyclovir) - Ganciclovir - Valganciclovir - Famciclovir |
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What are the adverse effects of Acyclovir (and -cyclovir derivatives) when administered orally?
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- Nausea, vomiting, diarrhea
- Headache |
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What are the adverse effects of Acyclovir (and -cyclovir derivatives) when administered by IV?
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- Phlebitis at injection site (inflammation of veins where injected)
- Nephrotoxicity (crystal formation) |
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Which herpes virus is resistant to acyclovir and requires higher dose to be effective?
a) VZV b) HSV1 c) HSV2 d) CMV e) EBV |
CMV
CMV does not have thymidine kinase, so theoretically you can overcome that by giving very high dose acyclovir; but realistically you would give a different type of medication Acyclovir has weak activity against EBV |
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What is the mechanism of action of foscarnet?
a) Blocks viral penetration b) Inhibits IMP dehydrogenase c) Inhibits DNA polymerase d) Inhibits RNA polymerase e) Blocks viral particle assembly |
Inhibits DNA Polymerase
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Case 2:
- 58 yo man presents with 4 days of blisters on L chest How would you describe the skin exam? |
Grouped vesicles on erythematous base in dermatomal distribution
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Mr. Berman’s exam shows grouped vesicles only on his left upper chest. How would you describe this eruption?
a) Acral b) Arcuate c) Dermatomal d) Intertriginous e) Linear |
Dermatomal
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What additional symptom is most likely to be associated with these blisters?
a) Pain b) Itch c) Fever d) Fatigue e) Vomiting |
Pain
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Mr. Berman has a dermatomal grouping of vesicles on an erythematous base, on his trunk. What is the most likely diagnosis?
a) Allergic contact dermatitis to poison ivy b) Bullous fixed drug eruption c) Dyshidrotic eczema d) Herpes simplex type 2 e) Shingles |
Shingles
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What is the cause of Herpes Zoster (Shingles)?
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Eruption of latent varicella zoster virus (VZV)
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What are the clues for diagnosis of Herpes Zoster (Shingles)?
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- Dermatomal (zosteriform) eruption on one side of the body
- Grouped vesicles on erythematous base - Most often on trunk, but can be anywhere - Usually preceded by pain or burning - Generally shingles occur only one in the immunocompetent, in contrast to HSV which frequently recurs |
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What is the most likely cause of this rash?
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Herpes Zoster
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What is the most likely cause of this rash?
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Herpes Zoster
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What type of virus is the VZV virus?
a) Single-stranded RNA b) Double-stranded RNA c) Single-stranded DNA d) Double-stranded DNA |
Double-stranded DNA
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What type of virus is Varciella Zoster?
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Alphaherpesvirus
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How is VZV spread?
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- Primary infection: efficiently aerosolized during coughing and readily acquired via respiratory route
- Latency/reactivated infection: only spread via direct contact |
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Where does VZV replicate in a primary infection?
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- Replicates in upper respiratory tract
- Spreads systemically and replicates throughout the body - Secondary viremia seeds VZV to the skin, where it causes widespread vesicular rash = Chicken Pox |
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Is VZV latent in one or many ganglia?
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Latency is within many ganglia and can reactivate from any infected ganglia later in life to cause shingles
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What happens when VZV is reactivated?
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Unlike HSV, several viral gene products are actively transcribed and translated within latently infected neurons
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Which herpes viruses have vaccines? What kind of vaccine?
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Varicella Zoster Virus (live attenuated virus-Oka strain)
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What is the mechanism of the Varicella Zoster vaccine?
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- Decreases symptoms of primary infection and, therefore, decrease the efficiency of virus spread
- Does not protect against infection with wild-type VZV, just decreases the chance of getting it, provided the majority of the population is vaccinated |
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How often do vaccinated individuals get infected with wild-type VZV?
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- Up to 15-20% of vaccinated individuals get infected with wt VZV that goes on to establish latency
- Because symptoms of primary infection are not present, a vaccinated individual does not know that they picked up wt VZV |
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Can patients immunized against Varicella Zoster get shingles?
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Yes, if they are of the 15-20% of vaccinated patients that get infected with wt VZV
- It can reactivate and cause Zoster/shingles later in life, in spite of immunization |
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Can patients get reactivation of the Oka vaccine strain (in the Varicella Zoster vaccine)?
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- Oka vaccine strain does establish a lifelong latent infection, so reactivation can occur, but is very inefficient in immunocompetent individuals
- Reactivation of vaccine strain, at worst, results in mild symptoms |
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What are the concerns for a patient getting the Oka vaccine strain (Varicella Zoster vaccine) if they are around immunocompromised patients?
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Oka vaccine strain can be transmitted to immunocompromised individuals - caution when vaccinating healthy children with immunocompromised siblings
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When should elderly patients get the Varicella Zoster vaccine? Why?
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- Recommended in patients >60 years of age, regardless of zoster occurrence
- Used to prevent Zoster/Shingles as it can limit Zoster - Immunity in aged is not as long-lasting, so booster is recommended in >60 years |
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What is the presentation of Chicken Pox?
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Diffusely scattered vesicles on an erythematous base
- Vesicles arise in crops and are in different stages (compared to smallpox which are all in the same stage) - Looks like "dewdrops on a rose petal" - Can be extensive and severe, especially in adults |
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What does this image show?
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Small vesicles on red background = Dewdrops on a Rose Petal
- Sign of chicken pox |
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Case 3:
- 6 yo girl w/ a week of blisters on her arms How would you describe these lesions? |
Multiple bullae and crusted erosions
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Case 3:
- 6 yo girl w/ a week of blisters on her arms Jessica is afebrile and her exam shows multiple bullae and crusted erosions on the bilateral arms. Which test would you order? a) Bacterial culture b) Biopsy for direct immunofluorescence test c) Direct fluorescence antibody (DFA) test d) Potassium hydroxide (KOH) exam e) Tzanck prep |
Bacterial culture
Looking for infection (specific bacteria) Biopsy for direct immunofluorescence would be good if you suspected an auto-immune blistering disorder (unlikely in a young patient) |
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Case 3:
- 6 yo girl w/ a week of blisters on her arms What organism is most likely to grow on bacterial culture? a) Staphylococcus epidermidis b) Staphylococcus aureus c) Streptococcus pyogenes d) Streptococcus pneumoniae e) Escherichia coli |
Staphylococcus aureus
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What are the most common causes of Impetigo?
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Bacterial infection caused by G+ bacteria
- Staphylococcus aureus - Streptococcus pyogenes (aka group A β-hemolytic strep) |
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What is the appearance of Impetigo?
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Majority of lesions are crusted papules (impetigo contagiosa)
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What is the description of this rash? What is it?
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Crusted lesions (where it has ruptured) and pustules (cloudy pustules)
- Honey colored crust is characteristic of impetigo - Caused by bacterial infection |
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What is the description of this rash? What is it?
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Crusted lesions (where it has ruptured) and pustules (cloudy pustules)
- Honey colored crust is characteristic of impetigo - Caused by bacterial infection |
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What is the description of this rash? What is it?
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Crusted lesions (where it has ruptured) and pustules (cloudy pustules)
- Honey colored crust is characteristic of impetigo - Caused by bacterial infection |
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Which Gram smear shows S. aureus?
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D
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What toxin does S. aureus produce that causes the blisters?
a) Toxic shock syndrome toxin b) Epidermolytic toxin A c) α toxin d) Enterotoxin e) Protein A |
Epidermolytic Toxin A
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What kind of bacteria is Staphylococcus aureus?
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G+ cocci (in clusters)
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Where does S. aureus colonize healthy individuals? How does it spread?
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- Colonizes anterior nares of healthy individuals
- Spreads via person-person or person-fomite contact (can survive on artificial surfaces for a long time) |
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What is the cause of Staphylococcal Scalded Skin Syndrome?
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Staphylococcus aureus infection secretes toxin into blood:
- Epidermolytic toxin A - Epidermolytic toxin B |
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What is the presentation of Staphylococcal Scalded Skin Syndrome?
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Widespread superficial blisters
- Skin peels away in sheets - Wound cultures from erosions are negative |
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Who is most at risk for getting Staphylococcal Scalded Skin Syndrome?
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- Kids < 2 years
- Adults with renal disease |
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What does this infant have?
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Staphylococcal Scalded Skin Syndrome
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What does this infant have?
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Staphylococcal Scalded Skin Syndrome
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What is the mechanism of action of acyclovir?
a) Blocks viral penetration b) Inhibits IMP dehydrogenase c) Inhibits DNA polymerase d) Inhibits RNA polymerase e) Blocks viral particle assembly |
Inhibits DNA polymerase
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How is the varicella-zoster virus transmitted, most commonly?
a) Direct contact b) Respiratory secretions c) Fecal-oral d) Vector-borne |
Respiratory secretions
(direct contact is also possible, but less common) |
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What toxin does S. aureus produce that causes the blisters?
a) Toxic shock syndrome toxin b) Exfoliative toxin A c) α toxin d) Enterotoxin e) Protein A |
Exfoliative Toxin A
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Case 4:
- 32 yo Caucasian female w/ 3-year history of scaly lesions on elbows and knees - In past month, similar lesions on torso, lesions are mildly pruritic - Maternal grandmother has similar lesions How would you describe these lesions? |
Multiple large erythematous plaques with overlying scales
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What is the term for the lesion on the left? Right?
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- Left: Papule (raised lesion <1 cm)
- Right: Plaque (raised lesion >1 cm) |
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What kind of lesion is this?
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Papule (raised lesion <1 cm)
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What kind of lesion is this?
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Plaque (raised lesion >1 cm)
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What kind of secondary change is this?
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Scale
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What kind of secondary change is this?
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Fissure (linear erosion in plaques)
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Case 4:
- 32 yo Caucasian female w/ 3-year history of scaly lesions on elbows and knees - In past month, similar lesions on torso, lesions are mildly pruritic - Maternal grandmother has similar lesions Her exam shows well-demarcated pink-red scaly plaques on the elbows, knees and trunk. What is the most likely diagnosis? a) Atopic dermatitis b) Chronic plaque psoriasis c) Tinea corporis d) Allergic contact dermatitis e) Impetigo |
Chronic Plaque Psoriasis
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What is the most common variant of Psoriasis?
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Chronic Plaque Psoriasis
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What is the typical appearance of Chronic Plaque Psoriasis? Locations?
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- Sharply defined plaques with silvery-white scales, often symmetric
- Most common locations: elbows, knees, scalp, presacrum, hands and feet - Genitalia involved in up to 30% of patients |
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What is Psoriasis associated with?
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- 20-30% of patients have arthritis
- Increased risk of metabolic syndrome and CVD - Several other variants, more than one may co-exist simultaneously |
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What kind of lesion is this?
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Plaque psoriasis on elbows (well-demarcated)
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What kind of lesion is this?
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Scalp psoriasis - well demarcated plaques with silvery white scales
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What kind of lesion is this?
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Palmoplantar Psoriasis
- Palms and soles can be involved in isolation or with other areas |
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What kind of lesion is this?
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Pustular Psoriasis
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What kind of lesion is this?
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Nail Psoriasis
- Isolated finding or in association with cutaneous findings |
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What kind of lesion is this?
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Psoriasis: Erythroderma
- Wide-spread erythema can be similar to a severe drug eruption, but it appears with history of psoriasis |
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Psoriasis is predominantly mediated by which of the following T-cell subsets?
a) Type 1 helper (Th1) T cells b) Type 2 helper (Th2) T cells c) Cytotoxic T cells d) Regulatory T cells e) Natural killer T cells |
Type 1 helper (Th1) T cells
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What cytokines are involved in mediating psoriasis?
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Type 1 helper (Th1) T cells:
- Increased: IL-2, IL-12, IFN-γ, TNF-α - Decreased: IL-1 and IL-10 |
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What kind of cells are found to be involved in the pathogenesis of Psoriasis?
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* Type 1 helper (Th1) T cells
- Also Th17 and Th22 cells |
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Which of the following medications could be used to treat psoriasis?
a) Interferon b) Lithium c) Methotrexate d) Terbinafine e) Minocycline |
Methotrexate
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How do you design treatment for Psoriasis?
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Treatment individualized balancing extent and severity of disease, patient's perception of severity and side effects of treatment
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What are the types of treatment strategies used for Psoriasis?
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- Topical treatments
- Phototherapy - Systemic therapy |
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What are the types of topical therapies for Psoriasis?
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- Corticosteroids
- Topical vitamin D analogs - Tar-based therapies - Topical retinoids |
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What are the phototherapy for Psoriasis?
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- PUVA (for hand/foot involvement)
- NBUVB (for diffuse disease) - Excimer laser (for localized disease) |
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What are the types of systemic therapies for Psoriasis?
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- Methotrexate
- Cyclosporine - Retinoids - Biologic agents (eg, inhibit TNF-α, IL-17, etc) |
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What is the mechanism of Methotrexate?
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- Synthetic analog of folic acid
- Competitively inhibits DHFR (dihydrofolate reductase) which is necessary for pyrimidine and purine synthesis - Inhibits conversion of Folate to Dihydrofolate on to Tetrahydrofolate |
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What are the adverse effects of Methotrexate?
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- Nausea, anorexia, fatigue
- Alopecia - Stomatitis - Leukopenia and thrombocytopenia - Hepatotoxicity |
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What med may be used in methotrexate overdose?
a) Methylene blue b) Activated charcoal c) Naloxone d) Leucovorin e) Epinephrine |
Leucovorin
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What is the mechanism of Leucovorin? Use?
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- 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 |
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Case 5:
- 53 yo man w/ 2 day history of pruritic eruption on torso and extremities - PMH of hypertension, treated with atenolol How would you describe this rash? |
- Diffuse, confluent erythematous papular rash
- Red blanching macules and papules |
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Case 5:
- 53 yo man w/ 2 day history of pruritic eruption on torso and extremities - PMH of hypertension, treated with atenolol Mr. Ryan’s exam shows red blanching macules and papules on the torso and extremities. How would you describe this eruption? a) Acral b) Arcuate c) Dermatomal d) Intertriginous e) Morbilliform |
Morbilliform
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What word describes this rash?
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Morbilliform
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Case 5:
- 53 yo man w/ 2 day history of pruritic eruption on torso and extremities - PMH of hypertension, treated with atenolol What additional information would be most important in this patient’s history? a) Recent house guests b) History of atopic dermatitis c) Recent stroke d) Medications started in the past month e) New pet dog at home |
Medications started in the past month
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Case 5:
- 53 yo man w/ 2 day history of pruritic eruption on torso and extremities - PMH of hypertension, treated with atenolol Mr. Ryan reveals he just finished a 10 day course of penicillin for a dental abscess. He has no oral or mucosal lesions. CBC and CMP are within normal limits and he is otherwise feeling well. What is the most likely diagnosis? a) Allergic contact dermatitis to poison ivy b) Exanthematous drug eruption c) Stevens-Johnson syndrome d) Atopic dermatitis e) Drug rash with eosinophilia and systemic symptoms |
Exanthematous drug reaction
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What is the other name for exanthematous drug reaction? Cause?
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Morbilliform Drug Eruption:
- Drug-induced eruption - Likely immunologic, often thought to be delayed (type IV) hypersensitivity reaction |
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When does an Exanthematous drug reaction occur? How long does it last?
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- Usually presents 7-14 days after a drug is started
- Spontaneously resolves in 1-2 weeks - Low grade fever may be present |
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What can commonly cause an Exanthematous drug reaction?
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- Aminopenicillins
- Sulfonamides - Cephalosporins - Anti-convulsants |
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What are the signs of possible severe cutaneous reaction?
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- Mucus membrane involvement
- Temperature above 38.5°C - Blisters - Facial edema and erythema - Lymphadenopathy - Painful skin lesions - Marked peripheral blood eosinophilia |
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What are the names of the severe drug skin reactions?
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Stevens Johnson Syndrome / Toxic Epidermal Necrolysis (SJS / TEN)
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When does Stevens Johnson Syndrome / Toxic Epidermal Necrolysis (SJS / TEN) present?
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Onset between 1-3 weeks after drug initiation
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What is the appearance of skin lesions in Stevens Johnson Syndrome / Toxic Epidermal Necrolysis (SJS / TEN)? Location? Other manifestations?
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- Tender dusky red or purpuric macules that progress to flaccid bullae and erosions
- Involves buccal, ocular, and genital mucosae in >90% - Respiratory tract involved in 25% - Often fever, LAD, hepatitis, and cytopenias |
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What are the most common causes of Stevens Johnson Syndrome / Toxic Epidermal Necrolysis (SJS / TEN)?
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- Allopurinol
- Anti-convulsants - Antibiotics - NSAIDs |
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How do you differentiate Stevens Johnson Syndrome from Toxic Epidermal Necrolysis (SJS / TEN)?
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- Stevens Johnson Syndrome covers <10% of body
- Toxic Epidermal Necrolysis >30% of body Between 10-30% of body is SJS/TEN overlap |
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Describe this patient's lesions?
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More erosions, mucus membranes involved (nose and lips)
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What is wrong with this patients?
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Toxic Epidermal Necrolysis (>30% of skin)
- More extensive involvement; erosions; flaccid bullae |
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What sign is present in this patient's skin?
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Nikolsky's Sign: apply lateral compression to skin and epidermis will slide off
(indicates SJS or TEN) |
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Which of the following is a poor prognostic indicator in this condition?
a) Age <40 b) Serum glucose level > 14 mmol/L c) Serum bicarbonate level > 20 mmol/l d) Serum urea level < 10 mmol/l e) Body surface area on day 1 < 10% |
Serum glucose level > 14 mmol/L
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How does age affect the prognosis for patients with Toxic Epidermal Necrolysis (TEN)?
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Age >40 years = poor prognosis
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How does HR affect the prognosis for patients with Toxic Epidermal Necrolysis (TEN)?
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HR >120 bpm = poor prognosis
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How does malignancy affect the prognosis for patients with Toxic Epidermal Necrolysis (TEN)?
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Presence of cancer or hematologic malignancy = poor prognosis
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How does body surface area involved on day 1 affect the prognosis for patients with Toxic Epidermal Necrolysis (TEN)?
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Body surface area on day 1 >10% = poor prognosis
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How does serum urea level affect the prognosis for patients with Toxic Epidermal Necrolysis (TEN)?
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Serum urea level >10 mmol/L = poor prognosis
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How does serum bicarbonate level affect the prognosis for patients with Toxic Epidermal Necrolysis (TEN)?
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Serum bicarbonate level < 20 mmol/L = poor prognosis
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How does serum glucose level affect the prognosis for patients with Toxic Epidermal Necrolysis (TEN)?
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Serum glucose level >14 mmol/L = poor prognosis
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16 yo F w/ fever, pharyngitis, and LAD is started on amoxicillin for presumed Strep pharyngitis. Five days later she develops pink-red macules and papules on the trunk and extremities?
What is the underlying infection associated with this reaction? a) Herpes simplex virus b) Steptococcus pneumoniae c) Epstein-Barr virus d) Staphylococcus aureus e) Varicella zoster virus |
Epstein-Barr Virus (EBV)
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What can happen in patients with EBV-induced infectious mononucleosis treated with amoxicillin or ampicillin (less often PCN or cephalosporins)?
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Up to 90% of patients get a hypersensitivity reaction:
- Occurs 7-10 days after starting meds - Exact mechanism unknown - Reactive drug metabolites may disturb the balance between cytotoxic and regulatory T cells, allows cytotoxicity against viral infected keratinocytes |
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What type of virus is EBV?
a) dsDNA b) dsRNA c) ssDNA d) ssRNA |
dsDNA
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Case 6:
- 3 yo male has 1 year history of worsening pruritic rash on arms and legs - Takes benadryl as necessary, albuterol nebulizer as necessary with URIs - Father and paternal grandmother have eczema and father has asthma Describe these findings? |
- Left: erythematous papules with secondary excoriation
- Right: erythematous plaques with lichenification |
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What secondary change is observed?
a) Lichenification b) Scar c) Atrophy d) Burrow |
Lichenification
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What kind of lesion is this?
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- Thickening of skin d/t chronic rubbing
- Patient with pruritic lesions may scratch them causing the skin to thicken, which accentuates the lines of the skin |
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What kind of lesion is this?
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Lichenification
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Case 6:
- 3 yo male has 1 year history of worsening pruritic rash on arms and legs His exam shows pink, lichenified plaques with mild scale and excoriations in the bilateral antecubital and popliteal fossae. What is the likely diagnosis? a) Allergic contact dermatits b) Exanthematous drug eruption c) Viral exanthem d) Psoriasis e) Atopic dermatitis |
Atopic Dermatitis (aka Eczema)
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Many children with atopic dermatitis have or will eventually develop which of the following?
a) Cutaneous lymphoma b) Asthma c) Immunodeficiency syndromes d) Food allergies e) Psoriasis |
Asthma
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What are the stages of Atopic Dermatitis?
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- Infantile stage
- Childhood stage - Adult stage |
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What are the characteristics of the infantile stage of atopic dermatitis?
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- More acute
- Involves face, scalp, extensor surfaces of the extremities - Diaper area spared - Secondary impetiginization common |
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What are the characteristics of the childhood stage of atopic dermatitis?
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- More chronic
- Involves flexural folds and extremities - More lichenification |
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What are the characteristics of the adult stage of atopic dermatitis?
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- Variable course
- Hand dermatitis common |
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What kind of lesion is this?
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Excoriation
- Linear loss of epidermis, does not extend into the dermis like an ulcer would - This is more angular because it is self-induced whereas an erosion would be more circular |
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What kind of lesion is this?
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Excoriation - tops of papules are removed by
scratching |
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What kind of lesion is this?
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Impetiginization - yellow crusting in areas of atopic dermatitis
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What does this baby have?
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Infantile Eczema - red, acute looking, oozing, can be yellow and crusty by secondary infection
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What does this baby have?
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Infantile Eczema - scalp involvement
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What does this person have?
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Adult Eczema - very variable, but often just hand dermatitis
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What kind of cells mediate Eczema?
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Type 2 helper T cells
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What cytokines are elevated / decreased in Eczema?
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Type 2 helper T cells
- Increased: IL-4, IL-5, IL-13 - Decreased: IL-2, IFN-γ |
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What is wrong in the skin in eczema?
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Defects in the epidermal skin barrier:
- Decreased essential fatty acids - Fillagrin mutations - Increased susceptability to allergens - Increased water loss |
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What is wrong in the skin in immunity?
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Defects in cell mediated immunity
- Increased susceptibility to viral, bacterial, and fungal infections of the skin |
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The majority of patients with atopic dermatitis have colonization of lesional, and often non-lesional, skin with which of the following?
a) Streptococcus pyogenes b) Staphylococcus aureus c) Escherichia coli d) Streptococcus pneumoniae e) Psuedomonas aeruginosa |
S. aureus
Kids are often colonized with S. aureus which can then secondarily infect their skin lesions; so often treatment is aimed at treating S. aureus super-infection |
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Which of the following antibiotics could be used to treat Staphylococcus aureus superinfection?
a) Cephalexin b) Ciprofloxacin c) Rifampin d) Clarithromycin e) Gentamicin |
Cephalexin
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What is the mechanism of action of the cephalosporin class of antibiotics?
a) Inhibit 50S ribosomal subunit during protien synthesis b) Inhibit 30S ribosomal subunit during protein synthesis c) Block bacterial cell wall synthesis through inhibition of penicillin-binding proteins d) Inhibit DNA gyrase e) Inhibit RNA synthesis by inhibiting DNA-dependent RNA polymerase |
Block bacterial cell wall synthesis through inhibition of penicillin-binding proteins
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Who is most likely to get infected with Molluscum Contagiosum?
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Most common in children; increased risk with atopic dermatitis
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When does Molluscum Contagiosum appear? Appearance?
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- Appears 7 weeks after exposure to virus (poxvirus)
- Firm, small, pink or flesh-colored dome-shaped papules |
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How do you spread Molluscum Contagiosum?
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Spread by contact with infected skin or clothing
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How long does Molluscum Contagiosum infection last?
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Clears in 2-4 months
- Lesion persists and are more numerous in those with weakened immune systems |
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What is the cause of Molluscum Contagiosum? Structure?
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Molluscum Contagiosum: type of Poxvirus
- Very large double stranded DNA virus - Virion is ovoid to brick shaped, complex structure with several membranes |
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What are the characteristics of Molluscum Contagiosum replication?
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- Replicates exclusively in the cytoplasm of infected cells (a unique feature of a DNA virus - most are in nucleus)
- Single life cycle: lytic replication |
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What does Molluscum Contagiosum look like histologically?
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- Molluscum bodies: large eosinophilic inclusions in cytoplasm = viral factories
- Very little inflammation b/c they have immunomodulatory responses that stop all of our defenses |
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What kind of lesions are these?
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Molluscum Contagiosum
- Usually not very inflammatory, unassuming lesions - Typically described as umbilicated (central depression) |
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What kind of lesions are these?
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Molluscum Contagiosum
- Usually not very inflammatory, unassuming lesions - Typically described as umbilicated (central depression) |
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What is the other name for Eczema Herpeticum?
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Kaposi Varicelliform Eruption
- Refers to viral infection of a pre-existing dermatosis |
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What is the appearance of Eczema Herpeticum? What other symptoms?
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- Sudden eruption of painful, edematous, crusted vesicles, pustules and erosions
- May be associated with high temperature, malaise, LAD |
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Eczema herpeticum is most commonly caused by what?
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Disseminated HSV infection in patients with atopic dermatitis and referred to as eczema herpeticum
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How do you treat eczema herpeticum?
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IV Acyclovir
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What is this an image of?
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Eczema Herpeticum aka Kaposi Varicelliform Eruption (refers to viral infection of a pre-existing dermatosis
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What is the mechanism of action of methotrexate?
a) Inhibits dihydrofolate reductase b) Inhibits IMP dehydrogenase c) Inhibits ribonucleotide reductase d) Produces DNA cross-linkages e) Inhibits calcineurin by forming a complex with cyclophilin |
Inhibits Dihydrofolate Reductase
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The presence of which of the following would indicate a more serious drug-induced eruption?
a) Mild peripheral eosinophilia b) Severe pruritus c) Involvement of the proximal extremities d) Mucous membrane lesions e) Low grade fever |
Mucous membrane lesions
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Atopic dermatitis is predominantly mediated by which of the following T-cell subsets?
a) Type 1 helper (Th1) T cells b) Type 2 helper (Th2) T cells c) Cytotoxic T cells d) Regulatory T cells e) Natural killer T cells |
Type 2 helper (Th2) T cells
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