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26 Cards in this Set
- Front
- Back
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Define Acne vulagris
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Eruption involving pilosebaceous units.
Predominantly on face, upper back, and chest. Composed of: -comedones (plug clogging skin pore) -cysts (closed sac) -papules (small inflammed elevation of skin, non-suppurative or pus-ish) -pustules (blister with pus) May be non-inflammatory, or progress to inflammatory. |
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Why does acne vulgaris primarily occur in puberty adolescence?
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Androgenic stimulation of sebaceous gland size and sebum secretion
With follicles plugged by hyperkeratinisation (genetic cause) (leads to proliferation of Propionibacterium acnes) |
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What is the difference between blackheads and whiteheads?
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Black = open comedones (sebum turns black in contact with air)
White = white comedones |
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What mediates non-inflammatory acne into inflammatory types?
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Propionibacterium acnes: Lipase action - metabolises sebum lipids to yield fatty acids, which is PRO-INFLAMMATORY.
Closed comedones also possible to become inflamed. |
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What are qualities of inflammatory acne?
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Erythematous (abnormal redness)
- papules (inflamed eleveation of skin, no pus) - nodules (kinda hard, spherical abnormal structure) - pustules (inflamed eleveation of skin, has pus) - cysts (closed sac) |
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Name 4 key reasons of Acne vulgaris
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Poral occlusion;(Hyperkeratinisation, occulusion via cosmetic oils and tar, genetic influence)
Bacterial colonisation of duct;(by Propionobacterium acnes) Dermal inflammation (due to release of mediator and contetents of ruptured comedone) Increased sebum rate (androgen-dependent) (oral contraceptives containing progestogens, genetic influence) |
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Define abcesses.
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*Localised* collection of purulent inflammatory tissue, accumulated in cavity, formed on the basis of an infectious process (Staphylococcus aureus) (Propionibacteria too weak to cause abcess)
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Name the 7 virulence factors of Staphylococcus aureus
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Coagulase
(turns fibrogen into fibrin = protective barrier) Catalase (H2O2 -> H2O & O2) (resists oxidative burst = raised survival in m-phages) Protein A (binds antibody Fc region = prevents IgG-mediated clearance) Exotoxins - Leukocidin (kills WBC's) - Haemolysin (kills RBC's) - TSST (Toxic Shock Syndrome) - 5 enterotoxins (targets intestinal mucosa) - Exfoliative toxin (causes staphylococcal scalded skin syndrome) Capsule (resists opsinisation and phagocytosis) Adhesins (Elastin, collagen-binging proteins = resists physical removal) Other secreted products - Hyaluronidase - Fibrinolysin - Deoxyribonuclease |
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Name and describe Staph aureus exotoxins
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- Leukocidin (kills WBC's)
- Haemolysin (kills RBC's) - TSST (Toxic Shock Syndrome) - 5 enterotoxins (targets intestinal mucosa) - Exfoliative toxin (causes staphylococcal scalded skin syndrome) |
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Which layer do thin skin lack?
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Stratum lucidum (layer 2 in thick skin)
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Name and describe the 5 layers of thick skin.
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Stratum corneum (corny)
Flat, dead, piled-up, anuclear Packed with keratin filaments Stratum lucidum (luke's) thick skin only Nuclear degeneration complete Stratum granulosm (grand) Has granules (densely-staining) Nuclear deneneration begins Stratum spinosum (spy) Cells begin to flatten/elongate, and stock keratin Stratum basale (base) Actively dividing (some stem/progenitor cells) |
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Contrast eccrine and apocrine cells
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Eccrine cells secrete without releasing part of the cell. Apocrine does.
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What do abcesses result from?
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Invasion by aggressive pathogens like Staph aureus, which cause tissue necrosis and lead to walled off abcess cavity.
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7 Functions of skin
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Waterproofing
Thermal regulation Sensation Protection (mechanical, chemical, microbial) Metabolism (fat storage, vitamen D) Excretion (sweat) Communication (colour, odour) |
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4 possible consequences of acute inflammation
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Resolution
Organisation (Scarring) Abcess Chronic inflammation |
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Name the 5 cardinal signs of acute inflammation
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Rubor (redness)
Dolor (pain) Tumor Calor (heat) Loss of function |
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Acute inflammation:
What do compliments do? Name some. |
Increases vessel permeability, chemotaxis
C3a, C5a, LTC4/D4/E4, chemokines (esp. IL-8) |
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Acute inflammation:
What do cytokines do? Name some. |
Promotes diapedesis (WBC pass through intact capillary walls and into surrounding tissues)
IL-1, TNF alpha (tumor necrosis factor) |
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Acute inflammation:
What do vasoactive amines do? Name some. |
Vasodilation
Nitric oxide, histamine, serotonin |
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What do vasoactive amines, cytokines, and compliments, all cause?
And what processes does this cause? |
Leukocyte activation, =
Phagocytosis Reactive oxygen species Recognition of opsonins (IgG, C3b) Lysosomal enzymes |
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What is the treatment for abcesses?
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Lancing and draining
= PUS REMOVAL (allows healing) |
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Alone, how effective are antibiotics for abscesses?
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Antibiotics don't penetrate abscess wall effectively (great work, Staph aureus coagulase)
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What are the 4 conventional treatments for acne vulgaris?
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Decrease keratinisation: benzoyl peroxide, retinoids, azelaic acid,
- Or dissolve keratin Anti-bacterial (Propionobacterium acnes): benzoyl peroxide, azelaic acid, antibiotics Decrease sebum production: hormonal treatments Decrease inflammation: Retinoids, azelaic acid, anti-inflammatory drugs |
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Pharmaceutical benefits scheme (PBS):
What happens if the Pharmaceutical Benefits Advisory Committee (PBAC) doesn't approve the drug? |
Drug not part of PBS = private script (not government-subsidised)
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Pharmaceutical benefits scheme (PBS):
Which 4 parties must approve the drug for it to become government-subsidised (under PBS)? |
Australian Drug Evaluation Committee (ADEC)
Pharmaceutical Benefits Advisory Committee (PBAC) Pharmaceutical Benefits Pricing Authority (PBPA) Minister of Health and Ageing |
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List the factors of gram -ve bacteria (often more virulent than gram +ve)
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Stains red not purple
Has outer membrane Thinner peptidoglycan layer Has lipopolysaccharide (LPS) Has endotoxin (released on death) No teichoic acid Capsule sometimes present (same with +ve) Lysosome-resistant More resistant to penicillin |
