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39 Cards in this Set

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list and briefly describe the 6 types of necrosis

  • Coagulative - due to ischemia/ infarct, protiens denature, then enzymatic degradation. cell structure maintained
  • liquefactive - bacterial abscess, brain infarcts, neutrophils release lysosomal enxymes that digest tissue . cavitation
  • Caseous - Macrophages wall off infecting organism. e.g. TB, fungi - fragmented cells and debris surrounded by lymphocytes and macrophages.
  • Fat necrosis - damaged cells release lipase which breaks down TGL in fat cells - outlines of dead fat cells w/o peripheral nuclei, appears blue on H&E stain.
  • Fibrinoid - immune complexes combine with fibrin causing vessel wall damage. - thick and pink vessels.
  • Gangrenous.
  • also Haemorhagic

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)



  • Staphyloccocus
  • Streptococcus


Rod (Baccillus)


  • Bacillus
  • clostridium
  • Cornybacterium
  • Lactobacillus
  • Listeria
  • Mycobacterium
  • Propionibacterium
branching filamentous


  • Acintomyces


Common Gram negative Bacteria?

Spherical



  • Moraxella catarrhalis
  • Neisseria
Rod

Enterics



  • Bacteroides
  • camphylobacter
  • E coli
  • enterobacter
  • helicobacter
  • klebsiella
  • proteus
  • Pseudomonas
  • salmonella
  • serratia
  • Shigella
  • Vibrio
  • Yersinia
Respiratory


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



  • gentamicin
  • netilmicin
  • tobramycin
  • amikacin
  • streptomycin
  • neomycin

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


  • broad spectrum gram +/- but have relatively low activity
  • Bacteriostatic only
  • increasing levels of bacterial resistence
  • Penetrate macrophages well, e.g. Chlamydia (nonspecificurethritis, trachoma, psittacosis), rickettsia (Q‐fever)and Borrelia burgdorferi (Lyme disease).

examples of tetracyclines


  • tetracycline
  • minocycline
  • doxycycline
  • tigecycline

Side effects of tetracyclines

don't give to pregnant mothers or children under 8


  • Staining of teeth,
  • hypoplasia of dental enamel, and
  • abnormal bone growth in children < 8 yr and in fetuses
  • cause photosensitivity in adults (e.g doxycyline)
  • diarhoea and nausea
  • candida overgrowth leading to thrush

Macrolide properties


  • Narrow spectrum, mainly active against gram positive organisms (similar to benzyl penicillin) - therefore can be used as alternative drugs in penicillin sensitive patients.
  • also indicated in Mycoplasma pneumoniae and Legionnaires' disease

MOA of aminoglycosides, tetracylines and macrolides


  • aminoglycosides, tetracylines - bind to 30s subunit inhibiting binding of aminoacyl TRNS
  • Macrolides - bind to 50s subunit


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


  1. Prevent entry - lack of entry transporter, decreased membrane permeability, or efflux pumps
  2. Destroy antibiotic - enzymatic e.g beta lactamase, Amp C cephlasporinase
  3. Change the structure of the antibiotic target - Pointmutations to change the ribosomal subunit
  4. Overproduce the Target - over produce the binding site, overproduce DHFR, DHPS to become resistent to trimoxazole

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



  • Receiving preformed antibodies and bloodbourne factors e.g complement
  • IGA i breast milk. IgG crossing placenta.
  • physical barriers
  • phagocytosis



Active



  • exposure to foreign antigens
  • slow
  • Long lasting protection
  • cell mediated - t cells
  • humoral - b cells

Summarise the process of hematopoesisi


  • Pluripotent stem cell can differentiate into two main common progenitor cells the common myeloid progenitor or the common lyphoid cell
  • The myeloid progenitor is responsible for the eventual production of platelets, Red blood cells, mast cells, basinophils, eosinophils and moncytes.
  • The lymphoid progenitor produces NK cells, t and B cells.
  • from the myeloid line you first develop precursor cells - proerythroblast, megakaryocyte,
  • myeloblast goes on to form basinophils, neutrophils, eosinophils, and moncytes - MO and dendritc cells
  • erythoblast goes on to reticulocyte then mature erythrocyte
  • CLP - forms lymphoblast which forms immature t and b cells.

Stages of wound repair

  1. hemostasis - fibrin plugs provides medium for proliferative cells to move across.
  2. inflammation - PDGF, FGF AND TGF-B recruits fibroblaasts
  3. proliferation - angiogenesis stimulate by VEGF secreted by tissues in response to hypoxia, collagen deposition, granulation, epitheliasation, wund contraction. fibroblasts lay down fibrin strands as framework for cellular migration
  4. Remodelling - metalloprotinases remodel by degrading ECM. Type III collagen replaced by type 1

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