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Foundations III > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Potential negative consequences of antibiotic use

A

toxicity, allergic reactions, resistance

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2
Q

Common toxicities associated with antibiotics

A

Beta-lactams: allergic reactions, anaphylaxis
Aminoglycosides: nephrotoxicity
Vancomycin: Red Man’s Syndrome
Fluoroquinolones: Achilles tendon rupture
Linezolid: bone marrow suppression
Daptomycin: myopathy
Trimethoprim-sulfamethoxazole: Stevens-Johnson Syndrome

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3
Q

Factors driving resistance

A

treatment of human illnesses with antibiotics, fecal/oral, carniverous consumption

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4
Q

Resistance mech.

A

efflux pumps, alteration of porins, microbial enzymes, mutations of target molecules, increase in binding sites (weaken availability for active site), transformation of prodrugs into moieties

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5
Q

Describe 2 laboratory methods used to establish whether an organism is sensitive or resistant to a specific antibiotic

A
  1. Kirby Bauer Method (measures MIC, uses zones of growth inhibition)
  2. Broth dilution test (can get MIC and MBC)
  3. E-test (with antibiotic gradient in a strip)
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6
Q

Describe what it means for beta-lactam agents to have time-dependent killing and how this characteristic influences how we dose them

A

Antibiotics with time dependence: beta-lactams, clindamycin, linezolid, vancomycin
Calculated as Time/MIC
How to dose- does several times a day, short infusion periods across the day

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7
Q

Describe what it means for an aminoglycoside to have concentration-dependent killing and how this characteristic influences how we dose them

A

Antibiotics with concentration-dependence: aminoglycosides
Calculated as AUC/MIC
How to dose- one big dose per day

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8
Q

Epidemiology of malaria

A

3% of world population infected (~220 million)
Endemic in 100+ nations
Congo and Nigeria ~40% of cases worldwide
90% of malaria-related deaths in sub-saharan africa

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9
Q

Identify the mammalian life cycle stages for Plasmodium spp.

A

Vector- Anopheles mosquito
Sporoziotes injected in blood meal, infection of Kupffer resident macrophages, release of merozoites, differentiation into trophozoite upon invasion of rbc’s, then schizont, then merozite or gemotcyte which is taken back into mosquito gut via bloodmeal to complete sexual cycle

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10
Q

Kupffer cell invasion and evasion of the immune repsonse

A

Kupffer cell invasion- thrombospondin and properdin receptors
RBC invasion- surface glycoproteins and lectins
Evasion of the immune response-
1) cytoadherence to endothelial cells evades clearance (ICAM-1, VCAM
1, CD36, and E-selectin)
2) mimotropes alter T cell behavior
3) cytokine production (TNF, IFN-gamma, IL-1) decrease parsitic specific immune response

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11
Q

Clinical findings and organ system involvement

A 
Hepatocyte injury (jaundice synthetic, and metabolic dysfunction), Renal failure, acidosis, hypoglycemia, hyponatremia, CNS injury (p. falciparum)
Blackwater fever
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12
Q

Prevention and treatment of malaria

A

Prophylaxis- quinolones (chloroquine, mefloquine, primaquine), antifols and sulfas (pyrimethamine, trimethoprim), artemisinins,doxycyclin

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13
Q

Pathophysiology of malaria

A

Infected RBC–> decrease in HB–> increase in rbc destruction–> cytokine release–> SIRS–> decreased red blood cell production–> endothelial dysfunction–> lose liquid–> DIC (clotting)–> capillary leak syndrome–> splenomegaly+hepatic+renal dysfunction

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14
Q

Toxiplasmosis life cycle

A 
Dormant cysts (bradyzoites) are consumed by wild animals and release tachyzoites (lytic active form), oocytes secreted in cat feces infect via the fecal-oral route then release sporozoites which turn into tachyzoites which replicate in skeletal muscle and brain
Cysts are resistant to many things
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15
Q

Toxaplasmosis clinical features

A

CNS infection, lymphadenopathy, pneumonia, rash, encephalitis, Parkinson’s
or Torch symptoms from transplacental transmission

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16
Q

Fungal virulence factors

A

Thermotolerance- the more adaptible a bacteria is to growing in colder body temp. from the soil the better ex. Crytococcus neoformans
Enzymes- proteases, lipases, phosholipases to break through mucous membranes or epithelium
Cell wall- sugars are immunogenic but are difficult to clear

17
Q

Differences between fungal and mammalian eukaryotic cells

A

ergosterol vs cholesterol, cell wall with glucans, chitin, and cellulose

18
Q

Antifungal agents

A

Polyenes (amphotericin B)- binds ergosterol, destabilizes the fungal cell membrane, no resistant
Azole- inhibit fungal cytochrome p450 to interupt ergosterol synthesis, but hurts human p450 so there are a lot of drug interactions
Flucytosine (5-FC)- permease that enters fungal cell and is converted into 5-fluorouracil to disrupt genome
Echinocandins- impair cell wall via 1,3 beta glucan
Griseofulvin- targets microtububles/keratins (hair/nails), inhibits mitosis

19
Q

Importance of appropriate specimen collection for infections disease testing

A

contamination which will affect hospital stay, antibiotic use, additional tests, and hopsital bill

20
Q

Factors affecting turnaround time for microbiological assays

A

type of assay: blood culture, serological assay, susceptibility to antibiotics, rapid antigen detection, PCR, biochemical profile
type of organism being tested for

21
Q

Molecular methods of diagnosis

Advantages vs disadvantages

A

PCR and probe hybridization
Advantages- short turnaround time
Disadvantage- Do not detect more true positives than Gram stain, No impact on therapy for true positives, False positives resulted increased costs, hospital stay, and no clinical benefits

22
Q

Protein structure of Ab

A

5 isotypes of Ig’s (M/D/G/E/A), heterotetramer with 2 identical heavy and light chains
Heavy has variable (N-terminal) and constant regions; CDR regions of variable regions is the antigen-binding site
Light has variable regions
Membrane-bound or secreted

23
Q

Protein structure of TCR’s

A

Dimer with alpha and beta chains, variable and constant regions with variable region where the antigen binds
Always membrane bound

24
Q

Mech. of diversity in antigen binding sites

A

VDJ recombination in heavy chains; VJ recombination in light chains
Junctional diversity- N region addition, P region diversification
Isotype switching (changing constant region)
Somatic hypermutation

25
Q

Mech. for antibody secretion and change in effector mutation

A

antibody secretion- splicing out of transmembrane and cytoplasmic tail exons

26
Q

MHC Class I and II

Structure

A

Class I- polymorphic alpha chain non-covalently associated with beta-2 secreted protein (HLA-A, HLA-B, HLA-C)
Class II- polymorphic alpha and beta chains non-covalently associated with non-polymorphic protein (HLA-DR, HLA-DP, HLA-DQ)

27
Q

MHC Class I and II

Function

A

Class I binds CD 8 cytotoxic cells (alpha 3), endogenous shorter peptide
Class II binds CD4 Thelper cells (beta 2), exogenous longer peptide

28
Q

Polymorphisms of MHC

A

6 possible MHC Class I alleles and 12 possible MHC Class II alleles
Polymormphisms and polygeny
MHC alleles are expressed codominantly

29
Q

2 mech. of antigen processing and presentation

A

Type I: IC pathogen–> Proteosome–> ER via TAP-> associate with MHC Type I–> vesicle transport to membrane
Type II: Phagocytosis of pathogen–> phagocytosis –> fusion with lysosome–>digested into peptide–> associates with type II in the cytosol and through vesicle transport goes to the membrane
Note- to prevent type II from engage in non-specific binding in the cytosol, protein LI/invariant chain binds type II in ER to occlude, as MHC type II moves to the cytosol proteases cleave LI into CLIP which is removed by MHC protein HLA-DM

30
Q

Classification for the different types of tissue damage caused by immune system

A 
Type 1- IgE-mediated, immediate (minutes), binds to FcR on mast cells or basophils, reintroduction of antigen causes mast cell degranulation
Type 2- IgG antibody activation against cell surface/EC matrix antigens, leading to complement and Fc mediated upregulation of macrophages and neutrophils, leading to opsonization, tissue damage, or cellular dysfuncion (hormone receptor)
Type 3- IgG soluble immune complexes, deposited in kidney, synovium, and vessels, usually systemic
Type 4- CD4 or CD8 Th cells lead to inflammatory (DTH) or cytotoxic response to self or foreign antigen, contact dermatitis/celiac's disease, superantigens bind to both TcR's and MHC class II's
31
Q

Live versus inactivated vaccine

A

Live- attenuated form of wild virus/bacteria put through multiple subculture to compromise its virulence, able to replicate inside host, immunity usually develops in one dose, interference due to circulating antibodies, must be handled with care
Inactivated- whole killed or fractional, cannot replicate, may require many vaccinations or booster follow-ups

32
Q

Polysaccharide conjugated fractional vaccine

A
  1. Stimulates T-dependent immunity
  2. Enhanced antibody production especially in young children
  3. Elicit booster response per dose
    Ex. Pneumococcal vaccine polysaccharide capsule conjugated with non-toxic Diptheria toxin

Foundations III (5 decks)

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