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135 Cards in this Set
- Front
- Back
Why are arterial thombi more problematic than venous emboli?
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The vessles that venous emboli originate from are usually smaller than the ones that they flow into
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What causes most fat emboli?
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broken long bones
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Why do divers have problems when they go from low pressure to high?
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It realeases nitrogen that causes air emboli that plug up microvasulature
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How do you prove that there is air in the heart?
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You fill the paracardium with water and then puncture the heart and bubbles come up
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Shock?
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hypoperfussion of the entire body
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3 ways to develop shock?
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Hypovolemic, Cardiogenic, and vascular
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3 types of vasular shock
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Neurogenic
septic anaphylactic |
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What does lactic acidosis usually lead to?
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vasodialation and increased vascular permeability.
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How does shock build on itself?
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decreased output leads to hyposia which leads to lactic acidosis which leads to vasodialation and permeability which leads to pooling and decreased blood flow and volume which further deacreases output and the problem gets worse
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How do you fix shock?
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You need to narrow the problem to a site on the shock cycle.
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Which tissues are most sensitive to shock?
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Those that whould be most affected by lose of oxygen
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What are 5 tissue effects of shock?
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1. cerebral neuronal necrosis
2. Acute renal tubular necrosis 3. Centrilobular hepatic necrosis, (liver necrosis) 4.Gastrointestinal necrosis 5.diffuse alveolar damage |
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What are 4 clinical signs of shock?
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1. tachycardia
2. ineffective blood volume 3. oliguria 4. metabolic acidosis |
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eosin?
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red dye that stains protine
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eosinophils are used to combat?
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paracites
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basophils are very blue because?
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It's granulas stain dark blue
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Basophils are also called?
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mast cells
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What does a plams cell look like under the microscope?
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oval shaped cell with the nucleus at one end.
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What is the distinguishing feature of a macrphage under the microscope?
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bean shaped nucleous
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What are the primary cells involved in actue inflamation?
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neutrophiles
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What are the cells found at the begining of the chronic inflamatory phase?
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lymphocytes and macrophages
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What cells follow lyphocytes and macrophages i healing?
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fibroblasts
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What are the cardinal signs of inflammation?
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heat, redness, swelling, pain, lose of function
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What are the sequence of events in inflammation?
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1.vasoconstriction
2.vasdialation 3. increased permiability 4. hemoconcentration and stasis 5. leukocyte adhesion 6. emigration 7. chemotaxis 8. aggresgation 9 phagocytosis |
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Selective Toxicity?
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knockout disease tissue without harming patient tissue
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Bacteriostatic?
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reversible inhibition of bacterial growth, requires more rigorous attention to blood levels, eradication requires host system
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Bactericidal
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direct killing of bacteria
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facultative anaerobe?
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grows in +or - oxygen
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Antibacterial spectrum?
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usually designated by gram stain.
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narrow spectrum?
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Gram + OR Gram -
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braod spectrum?
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Gram + and -
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Extended spectrum?
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intermediates between + and -
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Chemotherapeutic agent?
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sytheticly produced
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Antiseptic?
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used in skin
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Disinfectants?
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used for objects
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A peninillin?
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Inhibition of cell wall synthysis
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A Tetracyclin?
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Inhibition of protien synthesis
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An Azole?
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Destruction of cell membrane function. Anti-fungal
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Floroquinolone?
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Alters nucleic acid synthesis
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Metronidazole?
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miscellaneous. knowone knows
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MIC?
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Minimum inhibitory concentration. lowest concentration of an antimicrobial that inhibits the visable growth of a microorganism after overnight incubation.
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What is the treatment goal for MIC?
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to keep the concentration above the MIC
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why is mixing bacteriostatic and bacteriocidal drug ineffective?
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because bacteriocidal drug often require growth for them to take action
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What is the most common toxic effect of antimicrobials?
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miscellaneous GI effects. You get infections becuase you've knocked out flour that was keeping stuff in check like candidiasis and colitis caused by clostridium difficile.
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Whcih areas are hard to get drugs into?
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abscesses, bone, prostate, joints, alveoli, eye
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time-dependent killing?
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amount of time the serum concentration is about the MIC.
T>MIC is best predictor of efficency |
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Concentration-dependent killing?
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Killing increases as concentration increases abouve MIC.
AUC and Cmax/MIC are best predictirs |
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beta-lactam antibiotics?
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most important class of cell wall inhibitors. have beta lactam ring.
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What do beta-lactams bind to?
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Penicillin binding protiens, mostly parts of the peptidoglycan layer
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What is beta-lactam major toxicity?
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allergic reactions
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Are beta-lactams bacteriocidal or bacteriostatic?
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bacteriocidal
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arebeta-lactams time or concentration dependent?
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Time
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Are beta-lactams metabolized?
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No, you pee them out
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How is resistance aquired for beta-lactams?
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clevage of the beta lactam ring
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The general structure of a penicillin?
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2 rings and they differ by a R group.
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How discovered penicillin?
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Alexander Fleming
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How is penecillin metabolized?
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It's not
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penicillin's spectrum?
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Gram positive
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4 groups of penicllin?
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1. Pen G
2. beta-lacamase resistant penicillins 3. Extended specrum penicillins 4. extended spectrum penicillins with beta-lactamase inhibitors |
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Pen G is given by?
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injection
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Half life of Pen G?
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around 30 min
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Pen V?
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Is the same as Pen G but can be taken oraly
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Why arn't beta-lactimase resistant peniciliins used much?
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resistance to them
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2 types of extended specrum penicillins?
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1. ampicillin
2. Amoxicillin |
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Main use for amoxicillin?
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kildren usually is taken oraly
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Ticarcillin?
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anti-pseudomonal penicillin, been replaced because it hade Na+ overload problems
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Poperacillin?
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A braoder spectrum antibiotic-Best drug against pseudomonas.
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Inprotant factos for penicillin absorption?
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deacreased by food. take 1 to 2 hours before a meal
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3 types of penicillin allergic reactions?
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Immediate- anaphylaxix ethin 15-30 min
Accelerated-- 1-72 hrs.skin eruptions whheezing Delayed- days to weeks after exposure |
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What auses the allergic reaction of penicillin?
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The ring breaks and attaches to other protines
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Ampicillin rash?
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In patients with mono and lymphatuc leukemia that is non-allergic
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3 beta lactamase inhibitors?
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1. clavulanic acid
2. sulbactam 3. Tazobactam |
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Augmentin?
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a combination of clavulanic acid and amoxixillin
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Why do you need to give beta lacamase inhibitors along with penicillins?
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because beta-lactamace inhibitors do not have inherent antimicrobial activity
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When are beta-lactamase inhibitors used?
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Mixed anerobic and aerobic infections
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Cephalosporin?
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similar to penicillin with a few wrinkles. broader spectrum and more resistance to beta-lactamase
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What causes the many different pharmaco kinetics in cephalosporins?
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They have 3 R group locations
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In Cephalosporin when you get more gram - activity what happends to gram + activity?
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It goes down
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How is a cephaloporin metabolized?
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It's not
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Cefazolin?
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a cephalosporin used for surgical prophylaxis. has good tissue penetration.
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2nd gerenration cephalosporins?
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have extended spectrums and can kill anaerobes.
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Cefoxitin?
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a 2nd generation cephalosporin that is used manily for abdominal surgury because the abdomin has many anaerobic microbes
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4 notable uses for 2nd generation cephalosporins?
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1. surgical prophylaxis
2. sinusitis 3. Otitis media 4. lower respiratory tract infections |
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Advantages to 3rd and 4th generation cephalosporins?
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braod spectrum, can get into the CSF
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Toxic effects of cephalosporin?
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allergic, ususally not a problem for people that are allergic to penicillin but still not a good idea.
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Why are NMTT side chain a problem?
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they causes bleeding abnormalities and alchohol intolerance.
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Ceftriaxone should not be mixed with?
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Ca
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3 Carbapenem?
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Imipenem
Meropenem Erapenem |
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Carbapenem?
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extreamly broad spectrum, inactivates beta-lactamase
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carbapenems are mostly used for?
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enterbacter infections
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1 Monobactam?
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Aztreonam
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Why is aztreonam is unique because?
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It only has 1 ring
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Only haveing one ring is an advantage for aztreonam because?
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little cross-activation
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5 summeriy points for the beta-lactams?
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1. high degree of selective toxicity
2. most bacteria respond 3. high degree of allergic reactions 4. excreted though urin 5. CNS symptoms occure at high levels |
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Vancomycin?
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glycopeptide antibiotic that also blocks cell wall synthysis. narrow spectrum gram +. good for staph and flacobacterium
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How is vacomycin givin?
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IV slowly
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Nephrotoxic?
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toxic to the kidney
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Main use for vancomycin?
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MRSA infections and antibiotic-associated colitis
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Bacitracin?
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another cell wall inhibitor, used for lesions. very toxic
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Fosfomycin?
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cell wall inhibitor that is given to pregnat women with urinary tract infections
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protien inhibitors useually work by?
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inhibition of the ribosome
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The class of Abs that work agains the 30s subunit?
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tetracyclines
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The class of abs that work against the 50s subunit?
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Macrolides, lincosamides, and chloramphenicol
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are protien inhibitor abs. bacteriostatic or bacteriocidic?
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bacteriostatic
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Macrolide means?
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large ring
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What is the specrum of macrolides?
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extended spectrum
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How are macrolides metabolized?
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through the liver through the p450 system.
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3 macrolides of note?
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Erythromycin, clarithromycin and azithromycin
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Why do we not want to give erythromycin to pregant women?
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It can reach the baby
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what is the best absorpbed salt?
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estolate salt.
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Most toxic effect?
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GI upset and acute cholestatic hepatitis
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Advantages to clarithromycin?
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more potent, acid stabe, better absorbed amd longer half life
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Advantage to azithromycin to the others?
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longer halflife, not metabolized by the liver, Goes to the tissues exreamly quickly.
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Clindamycin is effective against?
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anaerobes
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Why is clindamycin problematic?
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It's good at knocking out you GI floura, leading to antibiotic-associated colitus
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2 most affective drugs for anaerobic infections?
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clindamycin, metronidazole
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4 main targets of antimicrobials?
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cell wall, cell membrain, protien synthesis, nucleic acid synthesis
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Polyenes and azoles target?
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fungal cell walls
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4 ways that microbes gain resistance?
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Mutation, Conjugation, Trasnduction, Transformation
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5 ways to restrict the spread of resistance?
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1. Use only when indicated
2. adaquate dose and duration 3. council patient to use aproprietly 4. use narrow spectrum instead of broad. 5. restrict use of new stuff to difficult stuff. |
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What 2 drugs most often cause antibiotic-associated colitis? CDAD?
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clindamycin, and ampicillin
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How do you treat for CDAD?
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stop using the first antibiotic, fluids, Cholestryramine to block the toxic effects of the clostridium dificile, 1 exposure treat with metronidazole, sever or 2nd expose treat with vancomycin
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Type 1 antibiotics?
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are effective at high concentrations
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type 2 antibiotics?
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effective at high exposure and time
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typr 3 antibiotics?
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are effective at both high concentrations and time
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Anionic Detergents?
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effective against gram +, rapid onset, non -irritating, low toxicity.
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Cationic Detergents?
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substituted ammonium choride derivitives. broad specrum, effective at higher ph but do not kill bacterio spores.
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Phelols?
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same mechanism as detergents. usually to weak and to toxic.
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Cresol?
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a methylphenol 3x more potent than phenol but no more toxic. common household disinfectant
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Hexachlorophene?
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2 chlorinated phenols hooked together. goes into solution well, leaves a risidual layer that is antimicrobial. absorption leads to CNS toxicity. bacteriostatic against gram +
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Chlorhexidine?
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broad spectrum. More rapid onset and is not deactivated in blood. does not cause CNS problems.
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Alcohols?
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Used at 70%. low surface tention allows it to get into tight spaces. must stay i contact 30-60 sec. Isopropyl alcohol is more potent
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Chlorine?
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turned into hypoclouse acid. ph dependent, does not kill TB. dissolves blood clots.
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Chloramines?
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comparable to chlorhexidine but does not dissovle blood clots.
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Iodine?
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added to ethanol. is bacteriocidal. well tolerated but a few people are allergic. comparable to chlorohexine.
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