• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/83

Click to flip

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;

83 Cards in this Set

  • Front
  • Back
paul ehrlich
1880's and 1890's observed chemotherapy in action
grhard domagk
red dye prontosil, metabolized in body into sulfonamide, effective drug against bacterial infections
alexander fleming
discovered P. notatum
antimicrobial chemotherapy
uses chemicals to prevent and treat infections
"Drugs"
antibiotics and synthetic
mutation means
protein structure changed
narrow spectrum
ex. kills only bacteria
broad spectrum
ex. kills fungi and bacteria
penicillins
inhibit cell wall synthesis
aminoglycoside drugs
inhibit protein synthesis
organisms can only produce antibiotics on what surface?
solid
five modes of action of antibiotics:
1. inhibition of cell wall synthesis
2. disruption of cell membrane function
3. inhibit protein synthesis
4. inhibition of nucleic acid synthesis
5. action as antimetabolites
base analogs function as
molecular mimicry: inhibit DNA synthesis by attaching to DNA polymerase
examples of base analogs:
1. PABA
2. sulfanilamide
3. para-amino salicylic acid
solution to resistance to antibiotics:
modify the R group, the enzyme wont recognize the new molecule and no resistance
paul ehrlich
1880's and 1890's observed chemotherapy in action
grhard domagk
red dye prontosil, metabolized in body into sulfonamide, effective drug against bacterial infections
alexander fleming
discovered P. notatum
antimicrobial chemotherapy
uses chemicals to prevent and treat infections
"Drugs"
antibiotics and synthetic
mutation means
protein structure changed
narrow spectrum
ex. kills only bacteria
broad spectrum
ex. kills fungi and bacteria
penicillins
inhibit cell wall synthesis
aminoglycoside drugs
inhibit protein synthesis
organisms can only produce antibiotics on what surface?
solid
five modes of action of antibiotics:
1. inhibition of cell wall synthesis
2. disruption of cell membrane function
3. inhibit protein synthesis
4. inhibition of nucleic acid synthesis
5. action as antimetabolites
base analogs function as
molecular mimicry: inhibit DNA synthesis by attaching to DNA polymerase
examples of base analogs:
1. PABA
2. sulfanilamide
3. para-amino salicylic acid
solution to resistance to antibiotics:
modify the R group, the enzyme wont recognize the new molecule and no resistance
disk diffusion method
disk soaked in antibiotic
MIC
minimum inhibitory concentration- measures potency
serum killing power
test if serum proteins attach to antibiotics
if serum attaches =
antibiotic not good
tetracyline
causes discolaration of baby's teeth if taken during pregnancy
if medicine is stopped early:
drug resistant bacteria will multiply rapidly and the old antibiotic wont work
solution for drug resistance:
double antibiotic therapy
virulent factors in bacteria: (to get inside skin)
1. invasive pathogens reach epithelial surface
2. pathogens produce hyaluronidase
3. pathogens invade deeper tissues
virulent factors in bacteria (inside skin)
1. pathogen produce coagulate
2. blood clots around pathogen
3. pathogens produce streptokinase, dissolving the clot and releasing pathogen into blood stream
incubation period
no signs of symptoms
prodromal phase
vague symptoms
invasive stage
most severe signs and symptoms
decline phase
declining symptoms
convalescence period
patient regains strength
aquired immunity
made by body
innate immunity
genetic (inborn)
aquired active immunity
own antibodies in presence of antigens
passive aquired immunity
ready made antibodies
ex. snake bites
passive natural immunity
maternal antibodies through milk and placenta
passive artificial immunity
antibodies from other sources

es. serum spider bites
rabies
active natural immunity
exposed to infectious aggent
active artificial immunity
immunization before disease attacks
large molecular substance, complex protein
antigen
b cells from
bone marrow
t cells from
thymus
stem cells in fetal liver migrate to
the bone marrow
the cell that recognizes the foreign substance
replicates to fight it
dont want cells that
recognize own body's proteins
clonal selection hypothesis:
how body tells self from non self
clonal deletion of
"self:" antigens during early development
hetrodymer-
binds heavy chains and light chain
antibody structure:
2 non identical peptides
2 identical
Fab fragment is different depending on
type of antigen and antibody
site of bonding to macrophages only occurs after
binds to an antigen
IgG
crosses placenta
Nonsecretory IgA
on cell surface
secretory IgA
on cell surface
IgD
rare
IgE
histamine releaser
IgM
huge molecule
neutralization
ingested by macrophage

ex. IgA
opsonizatoin
ingested by macrophage

ex. IgG
immune complex
bacteria in plasma

lysis and ingestion
MAC
membrane attack complex
first antibody in response
IgM
second antibody in response (high specificity)
IgG
antigen is recognized much earlier after
already being exposed to antigen before
makes antibodies
plama cells
three types of cells in cell mediated immunity:
Helper T Cells
cyctotoxic t cells
memory t cells
present on all cells
MHC I
present only on macrophages only after phagocytosis
MHC II
trypanosoma sp.
continuously changes antigens
passive immunity has no ____ immunity
lag