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