Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
39 Cards in this Set
- Front
- Back
list and briefly describe the 6 types of necrosis |
|
|
role of c3a, c34, c35 c3b
|
C3a - recruits inflammatory cells to site of infection (as with C4a and C5a)
C3b - opsonisation - tags cells pathogen for destruction
C5a - neutrophil chemotaxis
C5b-9 - forms membrane attack complex |
|
What are some of the systemic effects of the inflammatory mediators IL-6 and TNF-alpha |
liver - produce acute phase proteins - C-reactive protein, mannose binding lectin Bone marrow - mobilisation of neutrophils hypothalamus - increased body temperature fat/ muscle - protein energy mobilisationfor increased temp dendritic cells - tnf alpha stimulates migration to lymph nodes and maturation leading to activation of the adaptive immune response |
|
What does C-reactive Protein do? |
binds phosphocholine on bacterial surfaces, acting as an opsonin, and also activates complement. |
|
what does Mannose binding lectin do? |
binds mannose residues on bacterial surfaces, acting as an opsonin and also activating complement. |
|
what changes does TNF-alpha cause at the site of inflammation |
changes in vascular endothelium, expression of E and P selectin, increased gap in cell junctions resulting in increased vessel permeability. |
|
Describe the potential outcomes of inflammation. |
Resolution - process short lived, little tissue damage - neutralisation/ decay of chemical mediators, apoptosis of neutrophils/ phagiocytosis by macrophages, excess tissue fluids, proteins and debris phaged by MO's or removed by lymphatic vessels. Repair - organisation, large amounts of fibrin forms exudates that cannot be resorbed and there is subsequent growth of connective tissue into the fibrinous exudate. happens in areas of substantial tissue loss where there is limiteed ability of cells to regenerate. |
|
define chronic inflammation |
inflammation of prolonged duration where active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously. arises with persistent infection, prolonged exposure to noxious stimulus and in autoimmunity. |
|
What categories of Antibiotic inhibit cell wall synthesis |
Beta-lactams - penicillins - cephalosporins - Carbapenems - Monobactams Glycopeptides |
|
MOA of beta lactams |
preventing the cross‐linkage between the linear peptidoglycanpolymer chains that make up the cell wall |
|
Penicillin's |
mainly active against Gram + organisms many bacteria including most staphlococci are resistent to pencillians as they produce beta-lactamases. |
|
List common Gram + bacteria |
Spherical (Coccus)
|
|
Common Gram negative Bacteria? |
Spherical
Enterics
|
|
Flucloxacillin should be used for? Why? |
Beta lactamase producing staphlococci. Synthetically modified structure sterically hinders access of penicillinase enzyme but it is less active than benzyl penicillin. should not be used alone so as to prevent resistance. |
|
Which penicillins are active against gram positive and also some gram negative bacteria?? |
Broad spectrum Penicillins - amoxicillin and ampicillin - they are more hydrophillic so can cross across more rapidly into gram neg bacteria. penicillinase producing MO's resistent to amoxicillin and ampicillin. amoxicillin better absorbed orally ampicillin better parentally |
|
what AB's are given for pseudomonal infections? |
Piperacillin and ticarcillin - only available with combined be clavulanic acid |
|
what AB can be given to Treat Methicillin resistant S. aureus? |
Vancomyocin NB: also active against most gram positives but negatives are not susceptible. |
|
The first generation Cephalosporins have excellent active against ____________ and some __________ |
Gram positive bacteria - commonly used for uncomplicated skin and soft tissue infections which are usually due to staphylococci and streptococci some gram negative activity against e.coli, proteus, klebsiella |
|
Second generation cephalosporins are slightly ______ active than the first generation against gram positive and they have some activity against ______ |
some activity against gram negative bacteria and bacilli Higher generations generally have expanded spectra against aerobic gram-negative bacilli |
|
describe the activity of third generationn cephalosporins |
poor activity against gram positive 3rd and 4th generations are often used for Polymicrobial infections involving gram-negative bacilli and gram-positive cocci (eg, intra-abdominal sepsis, decubitus ulcers, diabetic foot infections) and When necessary, used with other drugs to cover anaerobes or enterococci |
|
Which generation of cephalosporin is used to tx methicillin-resistant S. aureus (MRSA) and E. faecalis |
5th Generation Activity against other gram-positive cocci and gram-negative bacilli is similar to that of 3rd-generation cephalosporins |
|
Bacterial ribosomes consist of ____ & ___ subunit while mammalian ribsomes consist of _____ & _____? |
Bacterial: 50s and 30s Mammalian: 60s and 40s |
|
which antibiotics affect protein synthesis? |
Aminoglycosides, Tetracyclines, Macrolides, Cholamphenicol |
|
Examples of aminoglycosides |
|
|
what is an important side effect of aminoglycosides not to be forgotten?! |
Damage to the 8th cranial nerve (Vestibulocochlear) and associated ototoxicity. Narrow therapeutic window. Also may impair neuromuscular transmission andare therefore contraindicated in patients with myasthenia gravis. |
|
Main use of gentmyacin? |
Acute Tx of life threatening Gram neg infections may use peak and trough dosing - allows toxicity to dissipate with use of a cell wall inhibitor (penicillin) as base. gentomyocin is a concentration dependant AB. |
|
List some properties of Tetracyclines |
|
|
examples of tetracyclines |
|
|
Side effects of tetracyclines |
don't give to pregnant mothers or children under 8
|
|
Macrolide properties |
|
|
MOA of aminoglycosides, tetracylines and macrolides |
|
|
What are anaerobic bacteria list examples. |
They lack catalase and/ superoxide dismutase and thus are susceptible to oxidative damage. generally foul smelling "Anaerobes can't breath fresh Air" Clostridium Bacteroides Fusobacterium Actinomyces |
|
List Mechanisms by whcich MO's resist antibiotics |
|
|
Differentiate gram negative vs Gram positive. |
GRAM POSITIVE •Thickpeptidoglycan layer (formed by transpeptidase- blocked by penicillin) •Purple/bluegram stain (holds crystal violet)•Lysozymesensitive •LipoteichoicAcid •Exotoxins GRAM NEGATIVE •Lipopolysaccharide (Lipid A + O Antigen)/ Endotoxin •SEPTIC SHOCK!!!! •Pink Gram Stain (Doesn’t hold crystal violet) •Lysosome Resistant •Also produce Exotoxins |
|
Distinguish passive vs Active immunity |
Passive
Active
|
|
Summarise the process of hematopoesisi |
|
|
Stages of wound repair |
|
|
Factors affecting healing |
nutrition mechanical iritation secondary infection foreign bodies edema ischemia/ low perfusion (diabetes) moisture |
|
role of cag-a and vac- a |
Cag-a - induceshost cells to release pro-inflammatory cytokines, but is not present in allstrains. Results in metaplasia and cancer, and disrupts cell integrity. Vac-A - inducesvacuolation(holes) in epithelial cells |