ch 19 skin diseases Flashcards
natural defenses of the skin
• Skin : epidermis + dermis
○ Epidermis = keratinized , stratified squamous epithelium
○ Dermis = mostly fibrous CT , collagen and hyaluronic acid
• Hair, sebaceous glands and sweat glands project into dermis
• Dry, layered , acidic, defensins, lysozyme, normal biota on and under the skin surface
○ Staph epi, propionibacterium acnes, lactobacillus , staph aureus (4%) and yeasts such as candida
Acne
• The term “acne” encompasses all follicle-associated skin lesions
• Many contributing factors
○ Exaggerated keratinization clogs pores
○ Over production of sebum (stimulated by hormones) - oil produced by sebacious glands - induced by hormones
P. Acnes ( part of normal biota) releases lipase’s to digest extra oil, breakdown products + bacteria = inflammation
i. Breaks down lipids and creates acidic env. Its not all bad news and we all hav it
• Virulence factors : P. acnes release lipase • Treatments : ○ Topical creams tht enhance sloughing of cells ○ Antibiotics ( contributing to Abx-resistance ) ○ Pore clogged excess hormones . 80 - 90% hav been exposed
Impetigo
- Superficial bacterial infection tht causes skin to flake or peel off
- Not serious , but highly contagious; children are usual victims
- Causative agent: Staph aureus and or streptococcus pyogenes
- Sings and symptoms : itchy peeling skin flaky scabs usually around muth and face
○ Exfoliative toxins , coded by phage DNA
○ Release of (proteins) Exotoxins epithelial cell-cell binding (desmosomes)
○ Hyaluronidae
• Distinguish S. aureus from S. pyogenes by coagulase test
○ Pthogenic S. aureus produce coagulase, an enzyme tht coagulates blood
• Treatment : Abx
Cellulitis
• Fast spreding infection in dermis and hypodermis(below dermis)
• Causative agent : S. aureus and S. pyogenes
○ Usually enter via parenteral route (surgery cutt)
• Signs and symptoms : pain, swelling, warmth , lymphangitis (speading thru lymphatic system
• Treatment : ABx
gas gangrene
• Serious condition tht results in tissue death (necrosis)
• Causative agent : clostridium perfringens
○ Gram-positive , endospore-forming anaerobic bacterium found in soil and GI
• Signs and symptoms : bacteria produce toxins and gas in damaged , necrotic muscle tissue; pain edema , bleeding , fever , blackened necrotic tissue with gas bubbles
• Pathogenesis and virulence factors :
○ Need damaged / dead tissue and anaerobic env.
○ Endosposres germinate, vegetative growth, exotoxins releases
○ Toxins : alpha toxins (exo toxins proteins) (RBC lysis), collagenase, hyaluronidase, Dnase
○ Gas produces from anaerobic fermentation of muscle carbohydrated
• Treatments :
○ Clean wounds and bed sores
○ Debridement of dead tissue
○ Surgery
○ Abx
○ Hyperbaric oxygen therapy - O2 delivered in high pressure chamber Characterized necrotic (dead tissue) anaerobic bacteria entering wound. Wen spores enter wound they can germinate (spores r tough) {anaerobic conditions r present O2 deprived and other aerobic bacteria enter wound also spores germinate hatch which release toxins and eat away at tissues also muscle tissue sometimes they hav fermented muscle carbohydrates produces gas bubbles
chicken pox
• Highly contagious disease tht results in a rash with “pox” lesions
• Mild, unless immunocompromised
○ “chickenpox parties”
• Causative agent agent: human herpesevirus 3 (HHV-3) called varicella cirus or aricella-zoster virus (VZV)
• Signs and symptoms fever rash with lesions tht r itchy and then crust over (no longer contagious) secondary infection possible
• Pathogens : see shingles
Virually caused disease . Envelope human herpes virus many many type of herpes types. Mild disease lesions on the skin puss filled aontageous but once they dry and crust over not contagious .
shingles
- During and after chickenpox, the virus enters sensory neurons and travel to ganglia; enter latency
- Virus can become reativated (stress, x-rays, immunsuppresive drugs, surg. Etc) resulting in shingles (herpes zoster)
- Signs and symptoms : lesions along dermatomes
- Pathogenesis : enter via respiratory tract thru blood to skin and causes cells to fuse and lyse then can enter sensory neurons
- Treatment : prevention via vaccine
Become reactivate chicken pox. Could b stress immunocompromised etc. Virus enters nervous system thru sensory neurons enters the cell body and becomes latent (integrates its genome ) wen virus reactivates goes to skin face and thoracic nerves . Each nerve serves a very specific area of the skin (dermatome )
Virus enter respiratroy tract enter blood skin enter neurons ????????
Chicken pox virus prevented
Shingles are pre exposed to chicken pox but reactivates
measles
- Viral disease tht is still widespread in developing countries
- Causative agent ; measles virus
- Signs and symptoms “ fever koplik’s spots (oral lesions) , red rash spreading from head secondary infections common
- Pathogenesis: enter via respiratory tract travels thry lymph to vlood to skin causes cells to fuse forming synctia
- Treatment : prevention via MMR vaccine
Viral disease extremely contagious . MMR vaccine . Virus causes fever , koplik’s spots (oral lesions) spots in oral cavity
warts
- Benign growths ; also called papollomas are all caused by viruses
- Causative ageny: most commonly human papillomaviruses (HPV)
- Signs and symptoms : usually painless benign skin growths tht can occur anywhere on body
- Pathogenesis : infect basal cells via microtruma ; replicate with keratinocytes and shed when cells exfoliated; viral replication alters epidermal structure, resulting in wart
- Treatment : home treatments , cryosurgery
HPV particles infect deeper lvls of epidermis mitotically active and useful for virus to spread . And as the kerotinocytes is pushed up ??? Changes the growth of these cytes .
cutaneous anthrax
• Most common and least dangerous version of anthrax
• Causative agent : baccillus anthracis
• Primarily a disease of herbivores (cattle sheep goats etx.
○ Spores can exist indefinitely
○ Become infected with spores from animal products
Micro trauma to skin . Leather and hydes of animal
Streptobaccillus
• Symptoms : ○ Fever rash with lesions tht are itchy and crust over black eschar . Secondary infection possible • Pathogenesis ○ Endospores enter skin via parenteral route ○ Edema toxin results in edema in the target tissue ○ Necrotic lesion forms painlesss black eschar
what is coagulase test ? how is it performed and how r the results useful
- Inoculate plasma with staph bacteria and look for coagulation
- Coagulation = coagulase - positive
- Take plasma from animal and look for presence of clotting bcuz plasma will hav all the clotting
- Plasma is inoculated with staphylococcal neg = liquid + = clumping
anatomy of skin
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