Chapter 23 Flashcards
lacerations, contusions,
Laceration: occur when tissue is torn
Contusion: caused by blow that crushed tissues
B) What is collagen, fibronectin, fibrinogen, and fibrin?
Collagen:a firbrous material the main supportive protien of skin
Fibronogen: blood protien
Fibronectin: is a fibrous glycoprotien occurs both in circulation and tissue, and binds cells and other tissue substances together
Fibrin: fibrinogen is converted to bibrine whis forms clots in the damaged vessles.
C) How does wound healing happen? [Figure 23.1]
- cut blood vessels bleed into the wound. fibrin froms clots in severed capillaries
- blood clot forms in the wound and phagocytes destroy microbes
- wound fills with granulation tissue and blood sessels regrow.
- granulation tissue shrinks and fibroblasts secrete collagen, forming scar tissue. Collagen contracts and epithelium regenerates
1) What is granulation tissue?
Tissue made to fill in damaged area it is red, translucent fibrous material.
D) What is an abscess and when do they form? How are they treated?[Figure 23.2]
is a localized collection of pus surounded by inflamed tissue.
Form as a result of the bodies immune defenses. helps localize infection.
Issue: in trying to treat them their chemical nature intereferes with some anitbiotics so they must be surgically drain in order to fix them.
1)What is pus?
a thick yellowish fluid composed of living and dead leukocytes, tissue debres, and protiens
E) What type of wound is more likely to have an anaerobic infection? Which bacteria is usually the culprit?
puncture wounds, small diameter, deep an contaminated with dirt.
A) What are the consequences of a wound becoming infected? [Table 23.1]
Staph aureus
Strep pyogenes
pseudomonas aerugosa
B) Which Staphylococcus species infect human wounds? [Figure 23.3 and 23.4]
aureus
1) What are the symptoms? What does pyogenic mean?
staph aureus
pyogenic: meaning they generate pus.
Symptoms: inflamation, swelling, red, tender, fever
tss can occur is it is toxin producing strain: highfever, drop in bp, and shock
2) What are Staphylococcus aureaus’ virulence factors? What are superantigens?
proteinase, lipase, and hyaluronidases together cause tissue damage. capsules, coagulase, and protein A (is released from bacterial surface and reacts with circulating antibodies and result in complement system and therefore intense inflamatory response) protect cell from attack.
Superantigens: produced by some strains. these endotoxins can react with hleper t cells activating then and cause them to release cytokines leading to toxic shock.
3) How do individual get these infections?
some are carriers, and so can infect themselves or others with open wounds.
4) What is MRSA, VISA, VRSA and what problems for treatment do they pose?
MRSA- methycillin resistant staph a ( all b-lacams), but can be treated with vancomycin, sulfa drugs,tetracyclines, clindamycin
VISA- Vancomycin-intermediate staph a. oxalynidols are effective in treatment
VRSA- Vancomysin resistant staph a.
C) What causes “flesh-eating disease”? [Figure 23.5]
Strep pyogenes
1) What are the symptoms?
strep pyogenes
necoritzing fascitis (inflamation of the facia and deteriorization) severe pain, swelling, fever, and confusion. overlying skin becomes stretched and discolored due to swelling, can lead to shock and death
2) How does this infection progress?
strep pyogenes
-f protien that helps with colonization of a wound.
destroys the subcutaneous tissue and fascia.
Some cases can destroy the m.
Does damage with enzyme
-Strptolysins which break down the blood clots
-Hylurondases- break down connections between cells
- deoxyribonucleases
Necrotizing ones produce
exotoxin A a super antigen that causes shock
exotoxin B protease destroys the tissue.
As tissues break down osmotic pressure inc, and fliuds move to area causing swelling
as the bacteria grow they produce m proties. This binds to fibrinogen. this complex then binds to nuetrophils causing then to release strong inglamatory molecules ( heparine binding protiens) wich increase the permeability of vessels.
Mprotiens also can stop phagocytosis be breaking down C3B.
-SPE: strep pyogenic exotoxins- super antigens, which activate t cells causing them to realease cytokines. high levels in blood stream = tss
3) How does this infection happen? How is it treated?
flesh eating disease
diabetes cancer, and alchohol
treated with surgery/ treatment
D) What are the symptoms of a Pseudomonas aeruginosa infection? What are it’s virulence factors? [Figure 23.6]
chills, fever, skin lesions and shock
virulence factors:
exotoxin a: stops protien synthesis in the host
exoenzyme s: works with protease to break down lechitin, an important lipid in cells.
pigment pycocyann: uses up iron from the environment and inhibits the growth of other bacteria, and inhibits the nasal cillia and repiratory epihlium
1) How are these infections acquired and how are they treated? pseudomonas aerugosa
moisture, so plants, comsmetics etc.
floronquoles, gentamycin, and impenim
A) What are the symptoms of lockjaw? What causes it? What mechanisms does it use to infect? [Figure 23.7, 23.8, 23.9 and Table 23.3]
Clostridium tetani
Symptoms:Bbegins with restlessness, difficulty swallowing,and sometimes seizures. painful and uncontrolable cramp like muscle spasms,spasms begin with jaw muscles.spasms can cause to fractures. many will die of pneumonia from lung damage caused by regurgitated stomach contents into the lung.
Virulance factors: bacteria stays in wound but releases toxins
-tetanospasmin: (ab pprotien) b portion attatches to the receptors of motor neurons then a portion goes in via endocytosis then this caries it to the spinal cord where it prevents the neurons from releasing the inhibitory neurons blocking their actions and causing muscles to sams with no control. Typically spreads from wound to the side opposite to the spinal collumn then downward. If it enters bloodstream it will first affect the brain affecting the jaw first.
2) How is lockjaw acquired?
eating foods with contaminated spores… so fecal contamination. tattoos, splinters, etc
3) What is the treatment? How can it be prevented? [Table 23.2]
tetanus
keeping up on the vaccine/
treatment: tetanus immune globuline: a preperation of antibodies to the toxin. they bind to it ( if unbound ot neuron), but if bound all they can do for that is give m. relaxents.
B) What are the symptoms of clostridial myonecrosis? What causes it? What mechanisms does it use to infect? [Figure 23.10 and Table 23.4]
“gas gangrene”
cause clostridium perfingens.
symptoms: swelling, thin bloody/brown fluid leaks from wounds (may be frothy because of gas bubbles) skin becomes tight and black. then coma
Virulance factors: gorws in poorly oxigenated and dead tissues.
-alpha toxin: destroys lechitin leading to cell lysis in host cells.
-Collagenase
- Hyalurinase:
As ti breaks down food it produces co2 which accumulate in the tissue. if in blood stream can kill rbcs, and damage vessels. not serious until it invades the m for unknown reasons.
1) How does one acquire this infection and how is it treated?
tetanus
dirt and animal feces enter a wound. also found in some vaginas of healthy women, and if they have self abortion can lead to it.
treatment: surgical removal of all dead tissues, penicillins. also hyperbaric oxygen chambers to oxygenate the tissues better.