Infection, Cytokines, Immuno Absite Flashcards

Front 1

Amikacin: Bacterostatic or bacteriocidal?

Back 1

Amikacin: BacterioCIDAL
-Aminoglycoside (along with Tobra, Gentamycin)
-Binds 30s ribosomal subunit -> inhib protein synthesis
-For GNRs: Pseudomonas, Acinetobacter, Enterobacter
-Use with beta lactam for febrile neutropenia
NEEDS O2 => NOT for anaerobes, good in LUNG
-Resistance 2/2 modifying enzymes -> decreased active transport
-Synergistic c/ BETA LACTAMS (amp, amox - facilitate penetration) for ENTEROCOCCUS
-SE: nephrotoxicity (reversible), ototoxicity (irreversible)
-Renal dosing

Front 2

Aminoglycoside resistance is 2/2 _

Back 2

Aminoglycosides (amikacin, gentamicin, neomycin, tobramycin):
-bacteriCIDAL via irreversible binding to ribosome
-Resistance is 2/2 ENZYMATIC MODIFICATION OF TRANSPORT proteins -> decreased active transport
-Require O2 for transport
Amp, Amox improve penetration
-Carneicillin, ticarcillin can INTERFERE

Front 3

Aminoglycosides:
-Bactericidal or bacteriostatic
-Mechanism
-Mode of resistance

Back 3

Aminoglycosides:
-bacteriCIDAL via irreversible binding to ribosome
-Resistance is 2/2 enzymatic modification of TRANSPORT proteins -> decreased active transport
-Require O2 for transport
Amp, Amox improve penetration
-Carneicillin, ticarcillin can INTERFERE

Front 4

Don't give Carbenicillin, Ticarcillin with abx class _

Back 4

Carbenicillin, Ticarcillin interfere c/ AMINOGLYCOSIDES (amikacin, gentamicin, neomycin, tobramycin)

Front 5

Ampicillin, Amoxicillin are synergistic with abx class _ for organism _

Back 5

Ampicillin, Amoxicillin are synergistic with AMINOGLYCOSIDES (amikacin, gentamicin, neomycin, tobramycin) for ENTEROCOCCUS

Front 6

AmphotericinL
-Mechanism
-_% get renal impairment
-other side effects...

Back 6

Amphotericin:
-binds sterols to alter fungal cell wall
-80% get renal impairment
-see anemia, fever

Front 7

Necrotizing fasciitis: empiric antibiotic therapy

Back 7

Necrotizing fasciitis:
-Debridement. Penicillin, Vanc, and Clinda
-Type 1 = polymicrobial
-Type 2 =C. perfringens, Grp A step (Pyogenes), MSSA, MRSA, Vibrio, B. frag
-Strep pyogenes SUPERANTIGEN EXOtoxin-> nonspecific T cell activation -> cytokine overproduction

Front 8

Bacteriostatic antibiotics work by mechanism...

Back 8

BacterioSTATIC: reversible binding to ribosome
-Clindamycin
-Tetracycline
-Erythromycin
-BACTRIM

Front 9

is bactrim bacteriostatic or bacteriocidal?

Back 9

Bacteriostatic: Tetracyclines, chloramphenicol, clindamycin, lincomycin, sulfonamides, trimethoprim, dapsone, INH, macrolides (e.g. erythromycin)
Bacteriocidal: Rifampin, quinolones (e.g. ciprofloxacin), Aminoglycosides (e.g. gentamycin)

Front 10

What is the most common bacteria seen in the biliary tract?

Back 10

Organisms implicated in cholangitis are those found in the gut, most commonly Escherichia coli.

Front 11

Pt being treataed for CAP or mild/moderate HAP or bacterial meningitis gets gallbladder sludging, cholestatic jaundice.
What antibiotic caused this?

Back 11

Ceftriaxone:
SE: gallbladder sludging, cholestatic jaundice

Front 12

Chloramphenicol: Bacteriostatic or bacteriocidal?

Back 12

Chloramphenicol: BacterioSTATIC
-binds 50s ribosomal subunit -> inhib protein synthesis
-used for anaerobes (but broad spectrum coverage)
-SE: grey baby syndrome, bone marrow suppresion (direct toxic effect, usually reversible), apastic anemia (rare, unpredictable, unrelated to dose, generally fatal)

Front 13

Cilastatin prevents renal hydrolysis of abx class _ -> increases 1/2 life

Back 13

Cilastatin prevents renal hydrolysis of CARBAPENEMS (meropenem, imipenem
-> increases 1/2 life

Front 14

Clindamycin: Bacteriostatic or bacteriocidal?

Back 14

Clindamycin: BacterioSTATIC
-binds 50s ribosomal subunit-> inhib ribosomal translocation-> inhib protein synthesis
-used for anerobes (at resp tract, skin, soft tissue) , some GPCs (e.g. bone/joint infections caused by Staph aureus)
-good for aspiration PNA
-can be used for Clostridium perfringens
SE: C diff colitis

Front 15

Type _ = predomindant type of collagen in the body

Back 15

Type 1 = predomindant type of collagen in the body
-priniciple cartilage in late scars
-Type 3 becomes type 1 with maturation, ~week 3

Front 16

Type _ = predomindant type of collagen being synthesized in 1st 48 hrs of wound healing

Back 16

Type 3 = predomindant type of collagen being synthesized in 1st 48 hrs of wound healing
-Low in Ehler-Danlos
-becomes type 1 with maturation, ~ week 3

Front 17

Max amount of collagen in a wound is at what time period?

Back 17

Collagen production starts on day 3, max at 2-3 WEEKS
-After that point, collagen amount stays the same, but cross-linking improves strength

Front 18

Predominant type of collagen in cartilage = _

Back 18

Predominant type of collagen in cartilage = Type 2

Front 19

type _ collagen = in basement membranes

Back 19

Type 4 collagen = in basement membranes

Front 20

types _ and _ collagen are in cartilage

Back 20

Types 2 and 6 collagen = in cartilage

Front 21

Collagen = glycine x3
-alpha-ketoglutarate, vit C, O2, iron needed for enzyme _

Back 21

Collagen = glycine x3
-alpha-ketoglutarate, vit C, O2, iron needed for propyl hydroxylase

Front 22

Complement cascade:
-_, _ are anaphylatoxins
-C_-_ = membrane attack complex

Back 22

Complement cascade:
-C3a, C5a are anaphylatoxins
-C5-9 = membrane attack complex
-Classic path initiated by antibodies; Alternate path initiated by bacteria
-Classic + Alt paths converge on C3

Front 23

Complement cascade:
-C3a, C5a are anaphylatoxins
-C5-9 = membrane attack complex
-Classic path initiated by _; Alternate path initiated by _
-Classic + Alt paths converge on C3

Back 23

Complement cascade:
-C3a, C5a are anaphylatoxins
-C5-9 = membrane attack complex
-Classic path initiated by antibodies; Alternate path initiated by bacteria
-Classic + Alt paths converge on C3

Front 24

Complement cascade:
-C3a, C5a are anaphylatoxins
-C5-9 = membrane attack complex
-Classic path initiated by antibodies; Alternate path initiated by bacteria
-Classic + Alt paths converge on _

Back 24

Complement cascade:
-C3a, C5a are anaphylatoxins
-C5-9 = membrane attack complex
-Classic path initiated by antibodies; Alternate path initiated by bacteria
-Classic + Alt paths converge on C3

Front 25

__ type chemokines:
-chemotactic; important in angiogenesis, wound healing

Back 25

CXC chemokines:
-chemotactic, angiogenesis, wound healing
-C stands for cysteine
ELR(+) CXC chemokines induce neutropil migration, interact with chemokine receptors CXCR1 and CXCR2. E.g. interleukin-8 (IL-8),
-ELR (-) CXC chemokines tend to be chemoattractant for lymphocytes.

Front 26

initial cytokine response to injury is based on 4 cytokines...

Back 26

Initial cytokine response to injury/infection dependent on TNF/IL-1 (synergistic), CXC, IL6

Front 27

Ehler-Danlos:
Deficinecy in type _ collagen

Back 27

Type 3 = predomindant type of collagen being synthesized in 1st 48 hrs of wound healing
-Low in Ehler-Danlos

Front 28

_ = lipopolysaccharide A from gram (-) bacteria

Back 28

Endotoxin = lipopolysaccharide A from gram (-) bacteria

Front 29

Enterococcal blood stream infection (not VRE);
-default antibiotic

Back 29

Enterococcal blood stream infection (not VRE) => AMPICILIN = default
NOT covered by TMP/SMX or cephalosporins

Front 30

Pt being treated for acute brochitis exacerbation or UTI gets Erythema Multiforme.
What antibiotic was used?

Back 30

Bactrim = TMP/SMX
-SE: allergy, nephrotoxicity, Stevens-Johnson (erythema multiforme = IgM immune complex dz of superficial microvasculature), hemolysis in G6PD deficiency
-BacteroSTATIC -
TMP and SMX work synergistically in steps of folate synthesis pathway
(Sulfonamides = PABA analogs, inhibit dihydropteroate synthetase; TMP inhibits diydrfolate reductase)
- for GNRs +/- GPCs
-NOT for Enterococcus,

Front 31

Erythrommycin: Bacterostatic or bacteriocidal?

Back 31

Erythrommycin: BacterioSTATIC
-Macrolide. binds 50s ribosomal subunit ->inhib translocation A -> P site
-for GPCs, esp CAP, atypical (mycoplasma, Lengionellosis) -
Slightly wider spectrum than penicillin
-SE: PO=> nausea, IV=> cholestasis
-Binds motilin R => prokinetic
Eliminated by liver > kidney

Front 32

Pt being treated for TB gets retrobulbar neuritis
-Which antibiotic is to blame?

Back 32

Ethambutol:
-SE = retrobulbar neuritis
-Not hepatotoxic (unlike Isoniazid, Rifampin, Pyrazinamide)

Front 33

Fluoroquinolones: Bacteriostatic or bacteriocidal?

Back 33

Fluoroquinolones: BacterioCIDAL
-Inhibit DNA gyrase
-For GPCs, mostly GNRs (Pseudomonas, Acinetobacter Serratia)
-NOT for enterococcus
-40% of MRSA is sensitive
-Same efficacy PO and IV

Front 34

"

Back 34

Fluoroquinolones (e.g. ciprofloxacin, levofloxacin) are bactericidal agents inhibiting DNA gyrase.

Front 35

Gentamycin: Bacterostatic or bacteriocidal?

Back 35

Gentamycin: BacterioCIDAL
Aminoglycoside (along with Tobra, Amikacin)
Binds 30s ribosomal subunit -> inhib protein synthesis
-Peak 6-10 ug/mL, trough <1 ug/mL
For GNRs. NOT for Neiserria gnorrhoae/meningitidis, Legionalla pneumophilia 2/2 Lipid A endotoxin => shock
-NEEDS O2 => NOT for anaerobes, good in LUNG
-Resistance 2/2 modifying enzymes -> decreased active transport
-Synergistic c/ BETA LACTAMS (amp, amox - facilitate penetration) for ENTEROCOCCUS
-SE: nephrotoxicity (reversible), ototoxicity (irreversible)

Front 36

Gentamycin:
-Peak level: _-_ -
Trough level: _-_

Back 36

Gentamycin:
-Peak level: 5-10 -
Trough level:<1
Important in pts c/ renal failure

Front 37

_ = source of histamine in blood
_ = source of histamine in tissue

Back 37

Basophils = source of histamine in blood
Mast cells = source of histamine in tissue

Front 38

IgE:
-in allergic rxns, type _ hypersensitivity, histamine release (2 main cell types ...), parasites

Back 38

IgE:
-in allergic rxns, type 1 hypersensitivity, histamine release (mast cell, basophil), parasites

Front 39

IL-_:
-from macrophages/monocytes
synergistic c/ TNF
-responsible for fever
-increases Il-6 (acute phase response)
-increases endothelium adherence via selectins, ICAM, VCAM

Back 39

IL-1:
-from macrophages/monocytes
-Initial cytokine response to injury/infection dependent on TNF/IL-1 (synergistic), CXC, IL6
-responsible for fever
-increases Il-6 (acute phase response)
-increases endothelium adherence via selectins, ICAM, VCAM

Front 40

IL-2:
-Made by _, stimulated by _
-Converts __ cells to lymphokine activated killers

Back 40

IL-2:
-Made by helper T cells, stimulated by IL-1
-Converts natural killer cells to lymphokine activated killers

Front 41

IL-_ stimulates B cells to become plasma cells -> secrete Ab

Back 41

IL4 simulates B cells to become plasma cells -> secrete Ab

Front 42

Where are the 4 possible locations for intra-abdominal abscess?

Back 42

4 locations for intraabdominal abscess:
-sub-diaphragmatic
-sub-hepatic
-inter-loop
-pelvic

Front 43

Infection w/in hours post-op => suspect 2 organisms

Back 43

Beta-strep and clostridium can present w/in hours post-op

Front 44

_ = best test for cell-mediated immunity

Back 44

Intradermal skin test = best test for cell-mediated immunity

Front 45

Pt being treated for TB gets liver failure + B6 deficiency
-Which antibiotic is to blame?

Back 45

Isoniazid:
-Inhibits mycolic acids
-SE: hepatotoxicity, B6 deficiency

Front 46

Keloids can be treated c/ 3 things…

Back 46

Keloids can be treated c/:
steroids, silicone injections, XRT
-unlike hypertrophic scar tissue, keloids are not confined to the orginal scar area

Front 47

Lipid A = toxic portion of lipopolysaccharide complex, found with gram (-) sepsis
-Potent stimulant for release of TNF ALPHA

Back 47

Lipid A = toxic portion of lipopolysaccharide complex, found with gram (-) sepsis
-Potent stimulant for release of _

Front 48

what is the major side effect of metronidazole

Back 48

peripheral neuropathy = SE of METRONIDAZOLE

Front 49

Metronidazole:
Bacteriostatic or bacteriocidal?
-Mechanism is …

Back 49

Metronidazole: BacterioCIDAL
-Produces O2 radicals -> break up DNA
-For anaerobes
-SE: disulfiram-like rxn, peripheral neuropathy

Front 50

Metronidazole:
Anaerobes
SE: peripheral neuropathy, disulfiram-like reaction

Back 50

Metronidazole:
Anaerobes
SE: peripheral neuropathy, disulfiram-like reaction

Front 51

MHC _:
-CD8 activation; on all nucleated cells, single chain

Back 51

MHC 1:
-CD8 activation; on all nucleated cells, single chain

MHC 2:
-CD4 activation; on all B cells, dendrites, monocytes, 2 chains

Front 52

MHC _:
-CD4 activation; on all B cells, dendrites, monocytes, 2 chains

Back 52

MHC 1:
-CD8 activation; on all nucleated cells, single chain

MHC 2:
-CD4 activation; on all B cells, dendrites, monocytes, 2 chains

Front 53

TNF:
-Exaggerated response = __
-main source = macrophage/monocyte
-Endotoxin (LPS a) = most potent stimulator of production
-overall pro-coagulant effect
-responsible for wasting, cachexia in cancer patients; by lipolysis, glycolysis, anorexia
-recruits + activates neutrophils => more cytokines, free radicals

Back 53

TNF:
-main source = macrophage/monocyte
-Endotoxin (LPS a) = most potent stimulator of production
-overall pro-coagulant effect
-responsible for wasting, cachexia in cancer patients; by lipolysis, glycolysis, anorexia
-recruits + activates neutrophils => more cytokines, free radicals
-exaggerated response => MOSF

Front 54

MRSA:
-mechanism of resistance = _

Back 54

MRSA:
-Resistance is 2/2 change in bacteria binding protein
(not 2/2 beta-lactamase)

Front 55

__ type immune cells:
-neither B nor T cells.
-no antigen presentation needed.
-recognize cells s/ self-MHC

Back 55

Natural killer cells:
-neither B nor T cells.
-no antigen presentation needed.
-recognize cells s/ self-MHC
-IL-2 converts NK cells to lymphokine activated killer

Front 56

IgM, IgG are _, are able to fix complement
-2 IgGs or IgM needed

Back 56

IgM, IgG are opsonins, are able to fix complement
-2 IgGs or IgM needed

Front 57

Cyokine __:
-attracts fibroblasts and increases sm muscle (active agent in Regranex) to speed matrix deposition and collagen formation

Back 57

PDGF:
-attracts fibroblasts and increases sm muscle (active agent in Regranex) to speed matrix deposition and collagen formation

Front 58

Penicillin resistance is 2/2 _

Back 58

Penicillin resistance is 2/2 plasmids coding for beta lactamase

Front 59

Cytokine __:
-platelet inhibition
-vasodilation
-bronchodilation

Back 59

PGI2 (prostacyclin):
-platelet inhibition
-vasodilation
-bronchodilation

Front 60

Pyrazinamide:
Main SE

Back 60

Pyrazinamide:
SE: hepatotoxic

Front 61

Quinolones:
-mechanism

Back 61

Quinolones:
-DNA gyrase inhibition
-PO and IV equivalent

Front 62

Pt being treated for TB gets liver failure + GI sx
-Which antibiotic is to blame?

Back 62

Rifampin:
-Inhibits RNA polymerase
-SE: hepatotoxicity, GI sx
-High rate of resistance

Front 63

SvO2:
-Normal _-_%
-High => 2 things...
-Low: 2 things...

Back 63

SvO2:
-Normal 66-77%
-High => sepsis, CN poisoning
-Low: decreased CO, decreased SaO2

Front 64

Tetracycline: Bacteriostatic or bacteriocidal?

Back 64

Tetracycline (and Doxycycline, Minocycline, Dimeclocycline): BacterioSTATIC
-bind 30s ribosomal subunit -> inhib docking of amino-acylated tRNA
-for GPCs, GNRs, syphilis
-Rocky Mtn spotted fever = Riskettsia, Q fever = Coxsiella, Psittacosis, Lymphogranuloma venereum = Chlamydia, eradicate nasal meningococci, Malaria chemoprophylaxis
-SE: pediatric tooth discoloration > drug-induced lupus, hepatitis
Interfere c/ BETA LACTAMS, methotrexate.
-Inactivated by Ca, Al, Fe, Zn => don't take c/ tums, dairy!

Front 65

Don’'t give Tetracyclines with abx class _

Back 65

Tetracyclines interfere c/ BETA LACTAMS

Front 66

Cytokine __:
stimulates fibroblasts
-too much/long => fibrosis (cirrhosis, pulm fibrosis)
-also chemotactic for neutrophils
-speeds healing

Back 66

TGF-beta:
stimulates fibroblasts
-too much/long => fibrosis (cirrhosis, pulm fibrosis)
-also chemotactic for neutrophils
-speeds healing

Front 67

A 30 year old male has had acute suppurative appendicitis for 24 hours prior to presentation in the Emergency Room. The patient has WBC 14 and mild thrombocytopenia on admission labs. What is the cause of his thrombocytopenia?

Back 67

Bacteria-induced platelet aggregation
The body’s systemic response to infection leads to a bacterial-platelet interaction as platelets migrate to the site of infection. The sticky platelets can form aggregates as layers of fibrin and platelets sandwich between bacterial colonies.

Front 68

Bactrim: Bacterostatic or bacteriocidal?

Back 68

Bactrim = TMP/SMX: BacteroSTATIC -
TMP and SMX work synergistically in steps of folate synthesis pathway
(Sulfonamides = PABA analogs, inhibit dihydropteroate synthetase; TMP inhibits diydrfolate reductase)
- for GNRs +/- GPCs
-NOT for Enterococcus, Pseudomonas, Acinetobacter, Serratia
-SE: teratogen, allergy, renal damage, Stevens-Johnson (erythema multiforme - IgM immune complex deposition in superficial vasculature), hemolysis in G6PD deficiency
(in UK, limited to Pneuimocystis PNA, Toxoplasmosis, Nocardiosis, and acute exacerbation of bronchitis / UTIs / pediatric otitis media when there is good rationale for use)

Front 69

Cytokine __:
-main source = macrophage/monocyte
-Endotoxin (LPS a) = most potent stimulator of production
-overall pro-coagulant effect
-responsible for wasting, cachexia in cancer patients; by lipolysis, glycolysis, anorexia
-recruits + activates neutrophils => more cytokines, free radicals
-exaggerated response => MOSF

Back 69

TNF:
-main source = macrophage/monocyte
-Initial cytokine response to injury/infection dependent on TNF/IL-1 (synergistic), CXC, IL6
-Endotoxin (LPS a) = most potent stimulator of production
-overall pro-coagulant effect
-responsible for wasting, cachexia in cancer patients; by lipolysis, glycolysis, anorexia
-recruits + activates neutrophils => more cytokines, free radicals
-exaggerated response => MOSF

Front 70

Tobramycin: Bacterostatic or bacteriocidal?

Back 70

Tobramycin: BacterioCIDAL
Aminoglycoside (along with Gentamycin, Amikacin)
-Binds 30s ribosomal subunit -> inhib protein synthesis
-For GNRs: Pseudomonas, Acinetobacter, Serratia
NEEDS O2 => NOT for anaerobes, good in LUNG
-Resistance 2/2 modifying enzymes -> decreased active transport
-Synergistic c/ BETA LACTAMS (amp, amox - facilitate penetration) for ENTEROCOCCUS
-SE: nephrotoxicity (reversible), ototoxicity (irreversible)
-Weight-based dosing

Front 71

Cytokine __:
-from platelets => platelet aggregation, vasoconstriction

Back 71

TxA2:
-from platelets => platelet aggregation, vasoconstriction

Front 72

Vancomycin resistance is 2/2 _

Back 72

Vancomycin resistance is 2/2 changes in CELL WALL BINDING PROTEIN

Front 73

Vancomycin:
-Peak level: _-_ -
Trough level: _-_

Back 73

Vancomycin:
-Peak level:20-40 -
Trough level: 5-10
-Important in pts c/ renal failure

Front 74

Vancomycin:
-Mechanism
-Mode of resistance

Back 74

Vancomycin:
-Blinds plasma membrane
-Resistance is 2/2 altered cell wall
-Peak level:20-40; Trough level: 5-10

Front 75

what is the mechanism of vancomycin resistance?

Back 75

resistance to vancomycin involves change in cell wall protein

Front 76

Vitamin _ prevents the negative effects of steroids on wound healing

Back 76

Vitamin A prevents the negative effects of steroids on wound healing

Front 77

On days 0-2 of wound healing, #1 cell type = _

Back 77

On days 0-2 of wound healing, #1 cell type = PMNs

Front 78

At days 3-4 of wound healing, predominant cell type = _

Back 78

At days 3-4 of wound healing, predominant cell type = MACROPHAGES

Front 79

Predominant cell type from day 5 onward of wound healing = _

Back 79

Predominant cell type from day 5 onward of wound healing = FIBROBLASTS

Front 80

Most important cell type for wound healing = _

Back 80

Most important cell type for wound healing = MACROPHAGES
-Cytokines
-Growth factors

Front 81

Max tensile strength in a wound is at time point _

Back 81

8 WEEKS: max tensile strength in a wound

Front 82

Peripheral nerves regenerate at _mm/day

Back 82

Peripheral nerves regenerate at 1 mm/day

Front 83

_ = most important factor in healing of wounds by secondary intention
-This depends on _

Back 83

epithelial integrity = most important factor in healing of wounds by secondary intention
(keeping epithelium intact over wound avoids leakage of proteins, serum => avoid infection)
Epithelial cells migrate primarily from hair follicle beds, also from wound edges and sweat glands

Front 84

_ = most important factor in healing of wounds by primary intention
-This is provided by the process of _

Back 84

tensile strength of wound ( = most important factor in healing of wounds by primary intention
-Tensile strength is created by collagen cross-linking
-Sutures hold wound together until the cross-linking occurs

Front 85

opening a wound 5 days after healing has started results in slower or faster healing?

Back 85

opening a 5-day old wound => faster healing b/c cells and products already in place

Front 86

what can't beta lactams be used for mycoplasma?

Back 86

Mycoplasma sp. does not have a cell wall, any β-lactam antibiotic would not be expected to have activity against this group of microorganisms.

Front 87

_ = type I transmembrane proteins involved in innate immunity by recognizing microbial conserved structures.

Back 87

Toll-like receptors = type I transmembrane proteins involved in innate immunity by recognizing microbial conserved structures.

Front 88

"

Back 88

Fluoroquinolones (e.g. ciprofloxacin, levofloxacin) are bactericidal agents inhibiting DNA gyrase.

Front 89

What is the mechanism of fluoroquinolones?

Back 89

Fluoroquinolones (e.g. ciprofloxacin, levofloxacin) are bactericidal agents inhibiting DNA gyrase.