Chapter 22 Flashcards
A) What two layers compose the skin? What are they composed of? [Figure 22.1]
Epidermis: surface layer. made of multiple layers of flat cells. outermost is made of dead cells filled with Keratin
Dermis: underlayer. vessels and nerves inervate. has ct wich binds to fat and other cells of subcutaneuos layer
B) What is subcutaneous tissue and where is it located?
it is under dermis and it supports layers of the skin
C) What type of bacteria are commonly found on the skin? [Table 22.1]
diptheroids: non motile gram pos rods of corynbacterium and propionibacterium
Staphylococci. gram pos cocci. coagulase neg
Fungi: sm yeasts of Massezia
A) What are the symptoms of acne vulgaris? What causes it? What does it do to the skin?
1) How can it be treated?
enlarged subcuatneous glands and increase secretion of sebum. “back heads and white heads”
Where hair follicle epithelium thickens and sloughs off in lumps gradually blocking sebum from working to the surface.
Cause: propionibacterium acnes.They eat sebum and to get more sebum they grow in to trap the sebum to eat. This attracts neutrophils whose enzymes damage the walls of the follicle.
Treated: limiting with benzoyl peroxide, Acutane reduce sebum production ( for more serious acne)
2) What is an abscess?
When neutrophils attracted to infected site release their enzymes which damage the walls of the follicle causing it to burst and releases it’s contents into surrounding tissue.
B) What are the symptoms of a hair follicle infection? What causes them? By what mechanism do they affect the skin? [Figure 22.2, 22.3 and Table 22.3]
inflamation of hair follicles
Cause: staph areus
Attatches to cells of follicle multiplies and spreads to the sebaceous gland. Producing inflamatory response frorming absesses.
- Some produce polysacharide capsule, or a protiens to prevent phagocytosis.
- Coagulase: activates blood protien prothrombrin to make thrombrin which is converted ot fibrin which forms protiens that make a weblike clot. The bact gets covered in the fibrin allowing it to hide.
- Hylurindase: degrades hyluronic acid which holds host cells together.
- Proteases: degrades collegen
- Lipase: degrades lipids to proved a food source
- Alpha toxin: kills hosts cells by making holes in their membranes.
1) What are the differences between folliculitis, furuncles, and carbuncles?
Folliculitis: inflamation of one or more hair follicles causing red bumps or pimples.
Furuncles: infection goes from folicle to other cells and caused lovalized swelling. This is a boil.
Carbuncles: a large area of redness and pain with several sites of drainng pus. rever can be present
What does protein A do?
cell wall component which messes with phagocytosis.
folicle infections 4 How do you get these types of infections? How are they treated?
Typically live in moist areas like nose and then gets transfered
Treated: with draining pus and oral antibiotics for carbuncles.
5) What type of resistance has S. aureus developed?
resistant to penicillin MRSA
vancoycin VRSA
ha= hospital aquired
ca= community aquired
C) What are the symptoms of SSSS? What causes it? By what mechanism does it affect the skin? [Figure 22.4 and Table 22.4]
2) What is the most common age group affected? How do you get it? 3) How is it treated?
Staphylococcal scalded skin syndrom: redness of skin, malaise, fever. whithin 48 hrs skinbecomes wrinkled and blisters formed and easily peel.
Affect:
-Exfoliatin: destroys material and binds together outer layers of epidermis
– splits under layer of epidermis and so it enters blood stream.
Common among infants.
Spread: from person to person
Treatment: methicillin and dead skin is removes.
D) What are the symptoms of impetigo? What causes it? By what mechanism does it affect the skin? [Figure 22.5 and Table 22.6]
pyoderma: infection characterized by pus prod.
inflamation in patches just beneath dead layer of skin. Thin walled blisters develop then break and ooze, yellowish crusts and plana. enlarged lyph nodes, fever. Result from damage to skin ie bug bites, burns, scrapes
Cause: Strep pyogenes
Affects: hyluranic acid capsule to to conceal it.
M protien which interferes with phagocytosis
and enzymes preoteases, nucleases, and hyaluronidase.
2) Where is impetigo mostly found? How does it spread?
poor kids in hot humid areas. ‘fomites and person to person
3) What are the differences between S. pyogenes and S. aureus? [Table 22.5]
virulance factors
pg 529
4) How can impetigo be treated?
penicillin
E) What are the symptoms of Rocky Mountain Spotted Fever? What causes it? By what mechanism does it affect the skin? [Figure 22.6, 22.7 and Table 22.7]
headache, m, joint pain, fever. Then rash with pink spots start on palms wrists ankles and soles of feet then spreads.
Cause: Rickettsia rickettsii. spread from ticks, lice, mites
Affects:
- force endothelial engulf them. Once inside they multiply and coat themselve in hose actin and use this proteins to move into adjacent host cells. eventually the membrane is so damaged it ruptures, and it goes into blood stream. Infect sm vessels leading to clotting and small areas of necrosis causing the hemmoratic rash. and can also damage kidneys and heart.
- lipopollysacharide endotoxin: in blood leads to shock and bleeding
1) How did RMSF get it’s name?
It was first recocnised in the rock mountain of the US
2) Where are the highest incidents of RMSF? [Figure 22.8]
in the summer. atlantic and south central states.
3) Which types of ticks are known to transmit it? [Figure 22.9] RMSF
wood ticks
4) How can RMSF be treated and prevented?
doxycycline and cloraphenicol
avoid ticks