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223 Cards in this Set

  • Front
  • Back
what two questions should you ask yourself when establishing a tx plan for infection
-is hospitalization required (oral vs IV antibiotics) and is surgical intervention required (OR I&D)
when getting the NLDOCAT of an infected pt, what questions should you ask
-any previous ulcer or infection, any recent antibiotic usage, trauma, last meal, check shoegear for foreign body, F/C/NS/N/V
if a pt with an infection has a history of post -op surgery, what bacteria is responsible
staph aureus
if a pt with an infection has a history of IV line, what bacteria is responsible
staph epidermidis
if a pt with an infection has a history of implant, what bacteria is responsible
staph epidermidis
if a pt with an infection has a history of scratching, what bacteria is responsible
tinea infection with secondary bacterial infection (gram neg)
if a pt with an infection has a history of puncture wound, what bacteria is responsible
-cellulitis can be caused by staph and strep, or osteo can be caused by pseudomonas
if a pt with an infection has a history of IV drug use, what bacteria is responsible
MRSA, MRSE, Pseudomonas
if a pt with an infection has a history of water realted infection, what bacteria is responsible
pseudomonas, aeromonas hydrophilia, vbrio vulnificans,mycobacterium marinum
if a pt with an infection has a history of dog/cat bites, what bacteria is responsible
pasteurella multicida
if a pt with an infection has a history of human bites, what bacteria is responsible
eikenella corrodens
what part of your body regulates body temperature
hypothalamic regulatory center
what stimuli affect the hypothalamus to regulate temperature to cause a fever
endogenous pyrogens secreted by leukocytes and Kupffer cells (also bacterial endotoxins, phagocytosis and certain immune rxns)
what are kupffer cells
-specialized macrophages in the liver
During infection and fever endogenous pyrogen increases the set point of the body and temp is raised; what are 2 signs of increased set point
chills and fever
what should one suspect if a pts post-op temperature is 107
anesthetic hyperthermia
what should one suspect if a pts post-op temperature is 105
blood transfusion rxns
what should one suspect if a pts post-op temperature is 104
closed abscesses
what should one suspect if a pts post-op temperature is 103
atelectasis/pneumonitis.drug rxns/liver disease
what should one suspect if a pts post-op temperature is 102
wound infection
what should one suspect if a pts post-op temperature is 101
draining abscess
what should one suspect if a pts post-op temperature is 100
benign post-op fever, post anesthesia overshoot
what should one suspect if a pts post-op temperature is 98
usual range of normal
what should one suspect if a pts post-op temperature is 96
post op hypothermia
in times of infection, what vital signs will increase in value
-temp, BP, pulse, respiratory rate, BG is diabetic
what are 4 signs of septic patient
elevated temp, hypotensive, tachycardic, tachypnic (rapid breathing)
what is the difference between septicemia and bacteremia
bactermia means there is bacteria in the blood and it can spread to distant foci; septicemia in addition to bacteremia has F/C and represents the failure of the body to localize infection
if pulses are non-audible, check with a doppler; if they are still non-audible or weak...
get n on-invasive arterial studies (PVR's)
what ABI is inadequate for healing in DM
ABI less then 0.45
how many mmHg is needed to heal a digital wound (blood flow)
at least 30 mmHg
when assessing someone with an infection, what questions should you ask yourself during their Derm exam? (think of the 5 cardinal signs of inflammation)
Dolor (most imp, even neuropathic pts will have pain), Rubor, Calor, Tumor, Functio Lasea {pain, red, heat, swelling, loos of fxn}
why do you get rubor and calor at the sight of infection
at the site of inflammation blood vessels dilate and there is increase blood flow to the area
why do you get tumor (swelling) at an infection site
there is extravasation of phagocytes and fluid into the perivascular space resulting in tumor (swelling)
what is extravasation
refers to the leakage of fluid (movt of WBC from the capillaries to the tissues surrounding them)
why does a pt with an infection have dolor and loss of function
the edema from extravasation causes stretching of the cutaneous nerve fibers causing pain, which then causes loss of fxn
fact: always note the intensity of the signs of inflammation (dolr, calor, etc) and compare to the contralateral limb
.
what are the 5 characteristics you should use when evaluating and describing a wound
location, size, base, depth, drainage, odor, margins of wound, surrounding tissue.(MS BOD LSD)
when should size of a wound be measured (before or after debridement)
after debridement
what are the diff kinds of bases you can have in a wound
granular, fibrotic, fatty, necrotic, mascerated
what questions should you ask about depth
does wound probe to bone or track up tendon sheaths or fascial planes, is bone or tendon exposed?
wagner classification doesnt take presence of neuropathy or size of lesion into account; but what are its Grades based on
depth
Wagner Grade 0
no open lesions may have keratosis or cellulitis
Wagner Grade 1
superficial ulcer, doest go beyond skin
Wagner Grade 2
beyond full thickness of skin, Ulcer extends to ligament, tendon, joint capsule or deep fascia without abscess/osteomyelitis
Wagner Grade 3
ulceration to bone, Deep ulcer with abscess, osteomyelitis or joint sepsis
Wagner Grade 4
wet or dry Gangrene localized to forefoot or heel (may or may not have cellultis)
Wagner Grade 5
extensive gangrene to portion of the foot or whole foot, foot salvage is not possible
what types of drainage can you have in a wound
-serous, serosanguinous, hemorrhagic, liquefactive, purulence
what does a fruity wound odor suggest
pseudomonas
what does a foul odor indicate
anerobes
abnormal redness of the skin due to capillary congestion such as inflammation
erythema
acute spreading infection of the skin and CT
cellulitis
how do cellulitis and erythema differ
cellulitis is more wide spread and its boundaries are NOT clearly demarcated
what are the most common bacteria assoc with cellulitis
staph aureus and Group A strept
when checking the surrounding tissue of a wound, what words can you use
erythema, cellulitis,edema, lymphadenopathy, lymphangitis
as edema decreases, what happens to the skin lines
you see an increase in skin lines
what is lymphadenopathy
As infection-fighting cells and fluid accumulate, the lymph nodes enlarge to many times their normal size. the lymph nodes may also be red and warm.
if you suspect lymphadenopathy in a pt, where should you check for swollen lymph nodes
in the groin and behind the knee
lymphangitis
blood poisoning, red streaks up the legs along the lymphatic channels from infection into the blood
what is the #1 cause of lymphangitis
Group A Strept
what is the etiology and process of lymphangitis
-infection is drained from teh body via lymphatics; lymph nodes can bc swollen during this process (lymphadenopathy) due to excess bacteria and inc pressure from edema; when nodes are overwhlemed, lymph drainage can be blocked and red streaks occur
how can bacteremia lead to septicemia
bacteria can seed the blood via the lymphatics which can lead to septicemia
always get an x-ray with an infected pt so you have a baseline, what should you be looking for onthe x-ray
soft tissue swelling, gas in soft tissues, foreign body, trauma, osteomyelitis
when looking for osteo on an infected pts xray; what are you looking for
periosteal reaction, lytic changes with sclerotic border, cortical breaking, osseous destruction, sequestrum, involucrum, cloaca, Brodie's abscess
Periosteal reaction
callus formation or formation of new bone in response to injury; white fuzziness out of line of the normal coritcal bone line
lytic lesion with sclerotic border
dark hole in the bone with a white sclerotic border (seen in osteo)
sequestrum
piece of dead bone that becomes seperated from healthy bone during necrosis (detached necrotic cortical bone)
involucrum
new layer of bone growth outside existing bone, results from the stripping of the periosteum by build up of pus in the bone and new bone growing from the periosteum
cloaca
space in which the dead bone resides
brodie's abscess
subacute osteomyelitis (common in tibia)
what is the lag time for osteo to show on x-ray
10-14 days
Fact: Diagnosis is made by clinical exam, Radiographic studies are ONLY an adjunct!!
.
involucrum is a cloak of laminated /spiculated periosteal reaction; does this occur before or after sequestrum
before
what first line tests would you order for a pt with infection upon inital presentation
CBC with diff, Chem Panel
what is included in a Chem panel
BUN, Creatine, Glucose, electrolytes (Na,K, Cl, CO2)
what is included in a CBC with diff
Hgb, Hct, platelet count, WBC count, differential looks at white blood cells into each type: neutrophils (also known as segs, PMNs, granulocytes, grans), lymphocytes, monocytes, eosinophils, and basophils
what second line tests should be performed after intial presentation of infection to monitor progress or rule out other sources of infection
ESR/CRP, blood cultures, urinalysis, urine culture
if a pt has an infection and they need to go to surgery what tests should be ordered
PT, PTT, LFT's, CXR, EKG
PTT
partial thromboplastin time:how long it takes for the blood to clot
PT
Prothrombin time: time it takes for the liquid portion of your blood (plasma) to clot
LFT
liver fxn tests
CXR
chest xray
what WBC count signifies infection
higher then 10,000 (Leukocytosis)
list the types of WBC
Never Let Mom Eat Beans (neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils)
what are 2 other names for neutrophils
PMN (polymorphonuclear cells) or Band cells
what is the diff between a PMN and a band cell
-PMN is a mature neutrophil, band cell is an immature neutrophil
inital killer cell
neutrophil; contains lysozome and lactoferrin
how long does a neutrophils fxn last
-its half life is 6 hours but it lasts 1-2 days
how long does it take for a PMN to mature
14 days
what do basophils contain
heparin, histamine and other substances to contract smooth muscle and inc permeability of BV's
when are eosinophils increased
NAACP- neoplasms, allergies, addisons, collagen and vascular dz, parasites
neutrophils is the 1st line of phagocytic response, what is the second
monocyte (replaces the neutrophil with in 24 hours)
what is a macrophage activated from during an inflammatory state
macrophage
what does a macrophage do
-it is a agressive phagocytic, bacteriocidal, long lived cell that processes antigens and delivers them to lymphocytes for specific antibody prodcution
WBC that posess cellular mediators for immunity (B cells/T cells)
Lymphocytes
cells produced from bonemarrow and produce specific antibody
B cell
cells produced from thymus and produce specific sensitized lymphocytes
T cell
when a pt has infection, why do you get Leukocytosis (inc WBC) w/ a shift to the left (inc band cells)
the body tries to fight infection by inc WBC, specifically neutrophils. But the neutros dont have time to mature to PMN's before they are needed to "kill" the infection and band cells are produced
what does BUN measure
BUN stands for blood urea nitrogen. Urea nitrogen is what forms when protein breaks down.
when is BUN often performed
to test kidney fxn (not as specific as Cr); measures hydration state
best index of renal fxn
creatine clearance; helps to determine proper antibitoic dosages
what does a chem panel include
BUN, creatine, Glucose, Electrolytes (Na, K, Cl, CO2)
normal BUN
7-20 mg/dL
normal creatine
038-1.4 mg/dL
ESR
-erythrocyte sed rate; measures the distance in mm a column of erythrocytes falls in 1 hour
ESR is a non-specific test for..
inflammation, infection, malignancy, renal disease, connective tissue disease and age
used as a baseline to monitor effectiveness of tx, how often should it be taken
5-7 days
C reactive protein is similar to ESR but more difficult to perform and more expensive;
CRP is produced by the liver and increases during inflammation
if a pt has leukocytes and nitrates in the urine
probably UTI
what are good antibiotic choices to start before culture and sensitivity results
Ancef/Flagyl or Bactrim/Flagyl or Unasyn
I&D of infected wound
dont use a touniquet (need to differentiate btwn healthy bleeding tissue and necrotic tissue), incise down to bone and do not seperate tissue planes) ..see pg 29
what soft tissue cultures should you take of a infected wound you are I&D ing
soft tissue swabs for gram stain, aerobic, anaerobic, fungal and acid fast
what bone cultures should you take of an infected wound
take bone pieces for bipsy and culture, also request sensitivites for all tissue and bone cultures
when irrigating an infected wound:
pulse lavage or 60 cc syringe wiht an 18 gauge blunt tip needle; use normal saline
I&D wounds s hould be packed open, when can they be closed
when all signs of infection are gone, usually 3-4 days after I&D
why should you use a wet to dry dressing for daily wound care of an open wound
it absorbs fluid exudates, faciliates debridement upon removal
what solutions can be used for a wet to dry dressing
saline, betadine, dilute betadine, Dakins, Acetic acid
why use saline in dressing
isotonic and drying
why use betadine in a dressing
drying, antimicrobial, but can be caustic to tissues (dilute betadine is less drying and caustic)
what is Dakins and why use it in a dressing
(.25% hypochlorate); it is antimicrobial and promoets granulation tissue
when should you use acetic acid in a wound dressing
antimicrobial and good for pseudomonas
with respect to wound healing, should the limbs be elevated
yes, this encourages venous and lymphatic drainage to reduce edema and improve local blood flow (DO Not elevate in pts with compromised circulation)
when an I&D was performed on an infected wound with necrotic tissue, what type of wound closure should be employed
Delayed Primary Closure; usually 3-4 days after intial I&D
intentions of wound healing
primary intention, in which all tissues, including the skin, are closed with suture material after completion of the operation; secondary intention, in which the wound is left open and closes naturally; and third intention, in which the wound is left open for a number of days and then closed if it is found to be clean.
what are 3 classifications of osteomyelitis (Waldvogel)
hematogenous, contiguous, vascualr impairment, chronic osteomyelitis
hematogenous osteomyelitis
usually staph aureus or strep in neonates
contiguous osteomyelitis
direct infection bone from exogenous source or spread of infection from a near by infected focus (prosthesis, implants, open fx)
why do pts with vascular compromise get osteo
-these pts have difficulty mounting an inflammatory response and have poor delivery of antibiotic to the site (vacularity needs to be addressed to insure healing)
piece of necrotic tissue, usually bone that has become seperated from surrounding healthy tissue
sequestrum
the sheath of new bone that forms around a sequestrum
involucrum
a chronic abscess of boe surrounded by dense fibrous tissue and sclerotic bone
brodie's absces
acute osteomylelitis
supperative infection with edema, vascular congestion and small vesssel thrombosis
what causes the symptoms of acute osteomyelitis
the acute inflammation causes an increase in osseous pressure and intravascualr thrombosis; the suppuration produces sub-periosteal abscess that may discharge into surrounding tissues
chronic osteomyelitis
infected dead bone or scar tissue, ischemic soft tissue envelope and a refractory clinical course (reoccurs despite surgical and antibotic intervention)
Clerny-Mader classifies osteomyelitis based on anatomic and physiologic stage; what are the anatomic stages
medullary, superficial, localized and diffuse
Clerny-Mader classifies osteomyelitis based on anatomic and physiologic stage; what are the physiologic stages; these are the factors that may compromise their healing
A: Normal Host
BS: Systemically compromised Host
BL: locally compromised host
C: tx is worse then the disease
how much resorption is needed to detect osseous changes of osteomyelitis on x-ray; how long does this take
30-50% resorption occurs in 10-14 days
as far as radiographic signs of osteomyelitis go; list the 3 signs and the order in which they appear
soft tissue swelling, periosteal rection (thickening or elevation), focal osteopenia
how can osteomyelitis be diagnosed
bone biopsy; hematogenous osteo can be dx by a positive blood culture and a positive bone scan
what are the primary goals of I&D of infected wounds
1. adequate drainage
2. thorough drainage
3. obliteration of dead space
4. antimicrobial coverage
what are the 4 steps of surgical tx of infected wounds
1. debridement of nonviable and marginally viable tissue
2. antibiotic PMMA impregnated beads
3. Ingress-Egress Systems
4. bypass surgery (vasc consult)
what is PMMA
PMMA is a clear plastic (Polymethylmethacrylate )impregnated beads
what is ingress-egress system used in surgical wound tx
Closed suction irrigation: closed system w/ continula flushing of the wound via inflow tubing (ingress) and outflow tubing (egress)
what antibiotic is generally used with PMMA beads and why
gentamycin; because it is NOT heat labile and the curing process of the PMMA is an exothermic process
Gentamycin is a heat stabile antibiotic used with PMMA beads, what are some other antibiotics used
Cephalasporins (Cefazolin,Moxalactam,Cefotaxime)
Tobramycin, Vancomycin, Ticarcillin
how long should antibiotic impregnated beads be left in a wound
2-4 weeks
primary surgical tx of an infected wound includes debridement and irrigation, what does secondary surgical tx include
reconstruction of bone and tissue with bone grafts/tissue grafts and deplayed primary closure
after surgical tx of an infected wound, how long should the pt remain on antibiotics
6-8 weeks
how often should a post surgical infected wound pt be scheduled for follow up care
For first 6 mths, every month.
6 mths-1 year, every 3 months.
1 yr-2 yr, every 5 months.
what criteria should the antibiotic used for localized dose at specific target tissue sites
water soluble, non-toxic to tissue, bactericidal, available in powder form, heat stable if used with PMMA
Systemic antibiotic therapy alone does not usually eradicate bacteria because of poor penetration into bone; Local application of antibiotics can provide high drug concentrations at the site of infection and can avoid systemic effects; other then PMMA beads what else can be antibiotic carriers
cancellous bone graft, demineralized bone matrix, Ca hydroxyapatite, plaster of paris
how are PMMA antibiotic beads made
-monomer(liquid) and polymer(powder) are mixed together with a powdered antibiotic. then small beads are formed and placed on a 26 or 28 gauge wire like a beaded necklace.
where are PMMA antibiotic beads used normally
they are implanted into a dead space, typically in an area of debrided osteomyelitic bone
if you have a 40-60 gram pack of PMMA; how much cefazolin powder do you add
4-8 grams
if you have a 40-60 gram pack of PMMA; how much cefotaxime powder do you add
4-8 grams
if you have a 40-60 gram pack of PMMA; how much nafcillin powder do you add
4-8 grams
if you have a 40-60 gram pack of PMMA; how much Tobramycin powder do you add
5-10 grams
if you have a 40-60 gram pack of PMMA; how much vancomycin powder do you add
4-8 grams
if you have a 40-60 gram pack of PMMA; how much Ticarcillinpowder do you add
6-13 grams
if you have a 40-60 gram pack of PMMA; how much clindamycin powder do you add
4-8 grams
what is the general ratio of antibitoic powder to bead ratio suggested by Cierny
1:5
what is one major disadvantage of PMMA beads
have to remove them after 10-14 days
a multitude of bacteria, viruses, mycobacteria and fungi have been associated with this type of CURABLE arthritis
Septic arthritis
list the mechanisms of septic arthritis (how the pt gets it)
1. direct joint invasion by the microbe
2. joints can be indirectly affected by immune response of the host (ex. Hep B and gonococal arthritis)
3. other unknown causes from enteric gram negatives like shigella and yersinia
what are some predsposing factors for acute bacterial arthritis
1.RA
2.crystal induced arthritis
3.osteoarthritis,charcot jts,hemarthroses(bleeding into jt spaces)
4.chronic systemic dz (SLE,sickle cell,cancer)
Why are RA pts susceptible to acute bacterial arthritis
damaged joint is a good nidus for infection
most acute bacterial arthritis occurs from hematogenous dissemination from a primary source of infection, by also from...
extension of an adjacent soft tissue infection or adjoining osteomyelitis
there are three stages of cartilage destruction, what is the inital phase
liberation of lysozomal enzymes from PMN's and synovial lining cells result in loss of proteoglycan from cartilage
what is the 2nd stage of cartilage destruction of a joint
increased mechanical stress and inadequate nutrition result in chondrocyte damage
what is the final stage of cartialge destruction of a joint
enzymes released from PMN's and synovial lining cells with the altered joint mechanics destroy the collagen network
what are the clinical features of a septic arthritic joint
1.red, hot, swollen and acutely painful; usually affects one joint
2. low grade fever
3. infectious focus involving any site (skin,nasopharynx,sinuses,lungs,cervix,rectum)
what are the main three joints where acute bacterial arthritis is seen
knee, hip, ankle (with knee the most common)
what are the lab tests of a pt with acute bacterial arthritis
leukocytosis, elevated ESR, synovial fluid white count >50,000 cells/cm and more then 90% PMN's
what tests are obligatory when septic arthritis is suspected
gram stain and synovial fluid culture
gram negative cocci with high incidence in acute bacterial arthritis
gram neg cocci (n. gonorrhea)
Tx of acute bacterial arthritis
1. antibiotics based on synovial gram stain
2. aspiration of joint daily
3. open surgical drainage if lack of response to ab therapy
4. immobilize and rest joint
what is the most common form or cause of acute bacterial arthritis
disseminated gonococcal arthritis to the joints from a prmary source
most pts with disseminated gonococcal infections are <40 with promiscuity; where are the primary sites of infection
the urethra in men, the cervix in women and the rectum and pharynx of both sexes
what are the clinical symptoms of gonococcal arthritis pts
fevers, chills, malaise, migratory arthritis, periarticular pain and swelling, tenosynovitis, skin lesions
what is the appearance of the skin lesions in gonococcal arthritis
small red macules that can dvlp into pustule lesions; characterized by a gray, necrotic center with a hemhorrhagic base
how is gonococcal arthritis diagnosed
by clinical symptoms and by primary source cultures, joint cultures and synovial fluid cultures
how is gonococcal arthritis treated
1. IV antibiotics (Ceftriaxone,Ceftizoxime,Cefotaxme) then PO antibiotics(Ceftin, Augmentin,Cipro)
2. joint aspiration
3. joint immobilization
what is augmentin made of
amoxicillin and clavulanate
viral arthritis has non-specific symptoms and is relatively short lived and rarely causes joint damage; list 4 common causes of viral arthritis
Hep B, Rubella, Parvovirus B19, HIV related arthropathy
type of arthritis that is usually monoarticular and in the large weight bearing joints
fingal arthritis
Superficial fungi that can cause fungal arthritis
Sporothrix schenckii, Candida albicans, Actinomyces israelii, maduromycoses
deep fungi that can cause fungal arthritis
aspergillus fumigatus, histoplasma capsulatum, cryptococcus neoformans, Coccidiodes, blastomyces
what can cause mycobacterial bone and joint infections
Extrapulmonary TB caused by dissemination of bacilli by hematagenous spread or lymphatic drainage from another area of TB
what does synovial pathology of a pt with TB mycobacterial joint infections show
chronic granulomatous reaction with giant Langerhan-type cell infiltration; acid fast stain of the synovium or surrounding tissue may reveal organisms
what is the most imp reason to perform a synovial fluid analysis
to rule out bacterial infection in a severely inflamed joint; to help differ btwn septic arthritis and crystal induced arthritis
Arthrocentesis
-removal of joint fluid that is therapeutic by relieving pressure and also diagnostic
complications of arthrocentesis
iatrogenic infectioon of a previously sterile joint, bleeding at puncture site and within the joint, possible injury to cartilage by needle, vasovagal episode during/after procedure
what is the technique for an arthrocentesis
1. move the joint through ROM to resuspend its contents
2. outline anatomic joint outlines
3.mark the area to be aspirated with the retracted end of a pen
4. cleanse skin and use local anesthetic
5. betadine scrub, then alcohol
6. use a gauge > 20
7. stretch the skin and aspirate slowly
what happens to the viscosity of synovial fluid during inflammation
its viscosity decreases and it can flow from the aspiration syringe like water
what is the normal viscosity of synovial fluid like
it stretches one inche before seperating
what happens to the color and clarity of synovial fluid during inflammation
clarity decreases (cant read newspaper through it),
what does normal synovial fluid look like
transparent straw or yellow color depending on the amt of albumin or bilirubin present
microscopic analysis of synovial fluid can include wet mounts, crystal analysis and stains: what stains can be used
gram stain, prussian blue stain, Ziel-Nielson stain, Congo red stain, Alizarin stain
Polarizing light microscope is used to look at joint crystals in synovial fluid; what do monosodium urate crystals look like (Gout)
needle shaped or long with blunt ends and display a negative befringence
what is negative birefringence
Negative birefringence – yellow when is parallel to the light, and blue when is perpendicular( 2 "l''s" in yellow and paralell)
which joint crystals have a postive birefringence
CPPD-Calcium Pyrophosphate Dihydrate Deposition Disease
what is birefringence
having two indices of refraciton
pseudogout
CPPD-Calcium Pyrophosphate Dihydrate Deposition Disease
what are calcium oxalate crystals associated with
renal failure
what are crystals of protein associated with
dysprotenemic states
what are cholesterol crystals associated with
chronic inflammatory disease
Prussian blue stain is a stain for iron, when will iron show up in synovium
pigmented villonodular synovitis or hemochromatosis
hemochromatosis
iron buildup
what is Ziel Nielson stain useful for evaluating
tuberculosis
what is congo red stain useful for evaluating
amyloid deposits show an apple-green birefringence on polarized light examination
what is Alizarin Red S stain used for
calcium stain for apatite crystals
what is a mucin clot test
several drops of synovial fluid are added to 20 mL of 5% acetic acid, allowing 1 minute for a clot to form
when do you get a "good clot" from a mucin clot test
firm mass that does not fragment on shaking (comes from a normal or osteoarthritis fluid)
when do you get a "poor clot" from a mucin clot test
easily forms flakes, shreds, cloudiness (comes from inflammatory fluids)
a good mucin clot reflects the normal integrity of what compound
hyaluronate
synovial fluid glucose concentration is normally slightly less then that of blood glucose, what glucose level suggests joint infection
a very low level of gluose in the synovial fluid
what factors contribute to the increasing incidence and risk of TB
supression of the immune system, dvlpment of drug resistant strains of mycobacterium, aging population, inc # of healthcare workers who are exposed
what pre-exisitng disease has the leading risk for reactivation of laten TB infection
HIV
which organism is responsible for TB infections in the US
Mycobacterium tuberculosis
what is Pott's disease
TB of the vertebra
what are the steps of tx for TB
1. pt is isolated
2. contact CDC and infection specialist
3. minimum of 3 antibiotics, one of which should be bactericidal
4. tx for 6-9 mths if only pulmonary involvement, tx for 12-18 mths if extrapulmonary TB
what are some possible antibiotic choices for TB and their doses
Isoniazid (3-5 mg/kg/day)
Pyridoxine (10 mg QD)
Rifampin (10mg/kg/day)
Pyrazinamide (20-25 mg/kg/day)
Ethambutol (15-25 mg/kg/day)
Streptomycin (15-20 mg/kg/day)
a human retrovirus that infects lymphocyets and other cells bearing the CD4 surface marker
HIV