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PMCOL 344 Exam Latest Update
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PMCOL 344 Exam Latest UpdateGout
what is it?
characteristics? - Answer -metabolic disorder leading to raised plasma uric acid levels
-painful attacks of acute arthritis produced by deposition of sodium urate crystals in
joints (big toe)
urate crystals and immune response - Answer activate PRRs (toll like receptors) to
trigger innate immune response. activation of kinin, complement, generation of
cytokines and accumulation of neutrophils. neutrophils engulf crystals and cause tissue
damage by releasing ROS and proteases.
acute treatment of gout
prophylaxis treatment - Answer - NSAIDS and glucocorticoids
- Inhibitors of uric acid synthesis (allopurinol) and Uricosuric drugs (probenecid)
Allopurinol - Answer acute treatment of gout. inhibits uric acid synthesis
Allopurinol mechanism - Answer analogue of hypoxanthine, converted to alloxanthine by
XO and then irreversibly inhibits XO (product inhibition)
reduces levels of urate and uric acid in plasma, tissues and urine
formation of uric acid - Answer DNA breakdown produces hypoxanthine. converted by
xanthine oxidase into xanthine. converted by xanthine oxidase into uric acid.
Probenecid - Answer - increases excretion of urate by inhibiting reabsorption by URAT-1
in proximal tubule.
- competes with urate for binding.
-not selective, also inhibits excretion of other drugs (can also prolong actions of
penicillin by inhibiting its secretion in kidneys)
infections - Answer invasion and multiplication of organisms
colonization (commensals) - Answer gut bacteria break down food remains, produce
vitamins (vit K), control growth of potentially pathogenic organisms (antimicrobials
cause secondary infections due to decreased normal flora)
classification of bacteria - Answer shape (spheres=cocci, rods=bacilli, spirals)
aerobes and anaerobes
,gram positive, gram negative
gram positive bacteria - Answer one plasma membrane. up to 40 layers of
peptidoglycan layers. purple stain sticks to mesh
gram negative bacteria - Answer 2 plasma membrane layers, makes it harder for drugs
to get into cell. peptidoglycan layers between membranes.
bactericidal - Answer kills bacteria
bacteriostatic - Answer stop bacteria from reproducing or inhibit growth (not kill)
must have active immune system (critical in helping body control and eliminate
infections) no decline in bacteria, can increase once drug removed
antibiotic targets - Answer - biochemical reactions: affect formation of cell wall, protein
synthesis
- structural targets: affect membrane, intracellular organelles
classes of potential biochemical reactions (targets) - Answer Class 1: generation of ATP
and simple carbon compounds (similar in humans therefore poor targets)
Class 2: energy dependent synthesis of amino acids, nucleotides, phospholipids, etc
Class 3: formation of macromolecules RNA, DNA, peptidoglycans
(2 + 3 most important)
Folate in humans vs bacteria - Answer Class 2 reaction.
Folate (FH4) required for DNA synthesis, humans can only get folate from diet, bacteria
cannot take up folate so need de novo synthesis.
sulfonamides as antibiotics - Answer inhibit folate synthesis by competitively inhibiting
dihydropteroate synthetase
broad spectrum
folate synthesis - Answer PABA (p-amino benzoic acid) converted into folate by
dihydropteroate synthetase. folate then converted into tetrahydrofolate (FH4) by
dihydrofolate reductase. FH4 then involved in DNA synthesis (thymidylate).
sulfonamides (examples 3) - Answer SULFAMETHOXAZOLE, sulfasalazine, prusugral
(anti platelet)
sulfamethoxazole - Answer analogue of PABA, compete for binding to dihydropteroate
synthetase.
broad spectrum, effective against gram - and + bacteria
, bacteriostatic (suppress division, no killing)
sulfonamides negative aspects - Answer -occurrence of adverse reactions and
resistance (synthesis of dihydropteroate enzyme that is insensitive to drug)
-effects reduced in presence of tissue breakdown (presence of purines and thymidine
can be used directly by bacteria for DNA synthesis and bypass need for folic acid
human vs bacterial dihydrofolate reductase - Answer differential sensitivity to enzyme
antagonists
trimethoprim - Answer inhibitor of folate synthesis
-very high affinity for bacterial vs human
-bacteriostatic
-given with sulfamethoxazole as co-trimoxazole
-resistance to trimethoprim due to altered dihydrofolate reductase
methotrexate - Answer inhibits both human and bacterial enzyme but bacteria cannot
take it up so it is not effective as an antibiotic
class 3 reactions - Answer bacterial cell wall synthesis
peptidoglycan - Answer -major component of bacterial cell wall, not found in eukaryotic
cells (good drug targets)
-backbone of amino sugars (N-acetyl muramic acid and N-acetylglucosamine
-peptide side chains, crosslinked to form lattice
-essential to resist high internal osmotic pressure (disrupt wall and bacteria die)
peptidoglycan synthesis - Answer bacteria transport building blocks across membrane
using lipid carrier containing 55 carbon atoms (C55)
beta-lactam antibiotics - Answer -inhibit synthesis of bacterial cell wall peptidoglycan
- bacteriocidal
-covalently bind to penicillin-binding proteins (PBPs) in cytoplasmic membrane. inhibit
cross-linking of the peptide chains attached to the peptidoglycan backbone, inactivate
inhibitors of autolysis
penicillin binding proteins - Answer have two enzyme domains: a transpeptidase that
cross links amino acid side chains, and a glycosyltransferase that links subunits of the
glycopeptide polymer. both have to be working to form mesh.
unique to each bacterial species leading to variation in sensitivity to drugs
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