Study your flashcards anywhere!

Download the official Cram app for free >

  • 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

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/155

Click to flip

155 Cards in this Set

  • Front
  • Back
Range of normal orally measured body temperature
36.3-37.5 ℃
(97.3-99.5 ℉)
At what time of day is body temperature higher?
afternoon
Pyrogenic cytokines
-TNF-α
-IL-1
-IFN-γ
Steps for activation of fever
-Rise in core body temperature
-Release of pyrogenic cytokines from leukocytes
-Activation of crcumventricular organs
-Prostaglandins
Relationship between rectal and oral temperature
R = O + 1℉
Exogenous pyrogens
Bacterial:
-antigens
-toxins
-LPS
Which receptor is implicated in fever?
Toll-like receptors
Dx criteria for FUO (Fever of Unknown Origin)
T > 101℉ or 38.3℃ on multiple occasions over a 3 week period AND unknown cause after intense evaluation for 1 week
Type of vaccine: MMR
Live attenuated
Type of vaccine: Varicella
Live attenuated
Type of vaccine: Polio (Sabin)
Live attenuated
Type of vaccine: Polio (Salk)
Killed
Type of vaccine: Influenza
Killed
Type of vaccine: Capsular polysaccharides
Subcellular
Type of vaccine: Surface proteins
Subcellular
Type of vaccine: Toxoids
Subcellular
Type of vaccine: ISG (Immune Serum Globulin)
Passive immunization
Type of vaccine: TIG (Tetanus Ig)
Passive immunization
Type of vaccine: VZIG (Varicella Zoster Ig)
Passive immunization
Type of vaccine: RIG (Rabies Ig)
Passive immunization
Type of vaccine: CMVIG (Cytomegalovirus Ig)
Passive immunization
Type of vaccine: HBIG (Hepatitis B Ig)
Passive immunization
Type of vaccine: Rhogam [Anti Rh (D)]
Passive immunization
Types of Bacteremia
1°: Direct inoculation (Vascular catheters, IVDU, brushing teeth, dental work, defectation)

2°: Translocation from other infected site
Hallmark of endocarditis
Vegetation (thrombi, bacteria)
Pathogenesis of IE (infectious endocarditis)
Valvular endothelium --> Platelet-fibrin deposition --> Nonbacterial thrombotic endocarditis --> Adherence

OR

Mucous membranes --> Trauma --> Bacteremia --> Adherence

THEN

Adherence --> Colonization --> Vegetation
Most common organism in acute IE
S. Aureus
Most common organism in subacute IE
Viridans streptococci
Most common organism in prosthetic valve IE
Early: Staphylococcus epidermidis

Late: Usual pathogens
Most common organism in IVDU-caused IE
-S. aureus
-P. aeruginosa
-C. albicans
Consequences of vegetation in infective endocarditis
-Persistent bacteremia
-Host response (proinflammatory cytokines)
-Tissue destruction by organism (valvular damage)
-Vegetation fragmentation (emboli [large and small (deposited in fingertips, retina, conjunctiva)])
-Immune complex formation
(Deposition in kidneys [glomerulonephritis] or in choroid plexus, spleen, skin)
General principles of antibiotic therapy in infectious endocarditis
-Bactericidal activity
-High antimicrobial concentrations in the vegetation
-Frequent dosing (to prevent regrowth)
-Long-term treatment (4-6 weeks)
Types of spread in osteomyelitis
-Hematogenous spread
-Children (distal femur, proximal tibia)
-Adults (axial skeleton)
-Contiguous spread
-Diabetics with neuropathy
-Vascular insufficiency
Major pathogens in osteomyelitis
Neonates, infants, later: S. aureus

Neonates also Strep

Diabetics: Mixed infections (gram +, gram - and anaerobes)
Osteomyelitis: Treatment
-Individualized based on organism
-Surgical debridement often required
Septic arthritis: Types of spread
-Hematogenous
-Direct inoculation
-Contiguous infection
Why is septic arthritis an emergency?
Synovium destruction is rapid and irreversible.
Upper bowel pathogen types
-Viruses (Norwalk agent, Rotavirus)
-Paraistes
Upper bowel diarrhea characteristics
-Larger volume
-rarely bloody or inflammatory
-more associated with malabsorption and dehydration
Lower bowel pathogen types
Bacterial
-E. Coli
-Salmonella
-Shigella
-Campylobacter
Lower bowel diarrhea characteristics
-Smaller volume
-Usually bloody
-Fecal leukocytes are found
-Dehydration
When are antibiotics recommended for diarrhea treatment?
-Infants
-Immunocompromised hosts
Steps in pathogenesis of urinary tract infection
Fecal e.coli --> Vaginal Introitus (Using p. fibriae and sticky/atrophic epithelium)

Vaginal introitus --> Bladder (through intercourse, diaphragm or spermicide)

Bladder --> Kidney (if stasis or obstruction)
Urinary tract infection: Treatment
Quinolones or TMP-SMX are superior to β-lactams
Urinary tract infection: Most common pathogens
SEEK PP

-Staphylococcus Saprophyticus (2nd most common)
-E. Coli (Most common)
-Enterococcus
-Klebsiella pneumoniae
-Proteus
-Pseudomonas
Urinary tract infections: Duration of treatment
Cystitis (superficial): 3 days

Pyelonephritis (invasive): 14 days
Cystitis: Symptoms
-Dysuria
-Urgency
-Frequency
Pyelonephritis: Symptoms
-Fever
-Chills
-Flank pain
-Tenderness
-⇧WBC
Urinary tract infection: relapse versus reinfection
Relapse: same organism, interval < 2 weeks. Longer course of antibiotics and x-ray

Reinfection: different organism or interval > 2 weeks. discontinue diaphragm, and use estriol cream or prophylactic antibiotics.
Definition: Complicated urinary tract infection
UTI in patient with anatomic abnormality:
-foley catheter
-obstructive lesion (tumor, stone)
Asymptomatic bacteriuria: Who to treat/not treat
Treat: pregnant, newborns, urologic manipulation

Don't treat: elderly, diabetic, foley catheter
Pneumonia: Routes of infection
Inhalation
-In healthy/younger people
-Viruses/atypical agents

Aspiration
-In elderly/debilitated
-Bacterial

Hematogenous
-Rare
Pulmonary defenses against pathogens
Non-specific (Gag reflex, mucociliary elevator, alveolar macrophage)

Immune (Humoral, Cell-mediated)
Community acquired pneumonia - Pathogens
-Influenza A
-M. pneumoniae
Community acquired pneumonia - Host factors
Healthy, not immune
Community acquired pneumonia - Route of infection
Inhalation
Community acquired pneumonia - Microbial factors
Adhesins
Pneumococcal pneumonia - Pathogens
S. pneumoniae
Pneumococcal pneumonia - Host factors
-Healthy, not immune
-N-P colonization
-viral infection?
Pneumococcal pneumonia - Route of infection
Aspiration
Pneumococcal pneumonia - Microbial Factors
Capsule
Hospital-acquired pneumonia - Pathogens
Gram - bacilli
Hospital-acquired pneumonia - Host factors
-Debilitated
-⇩Clearance
-N-P colonization
Hospital-acquired pneumonia - Route of infection
Aspiration
Hospital-acquired pneumonia - Microbial factors
None
Community-acquired pneumonia - Outpatient treatment
Younger: Macrolide
Older: Quinolone
Doxycycline

(Macrolides and Quinolones are active versus atypicals (such as mycoplasma))
Community-acquired pneumonia - Inpatient treatment
IV antibiotics

β-lactam and macrolide

OR

Fluoroquinolone

(Macrolides are active versus atypicals. Fluoroquinolones are active versus penicillin-resistant pneumococci and gram negatives)
Community-acquired pneumonia - Prevention (and who recieves it)
Vaccination

Indicated for elderly or heart/lung/metabolic disease


-yearly Influenza
-once and 5 year boost: pneumococcal
Hospital-acquired pneumonia - Prevention
Semirecumbent position
Tuberculosis: Primary infection pathogenesis route
-Inhalation --> Lower lobe
-Silent bacillemia seeds organs
-Cell mediated immunity (healing, ppd+, ghon complex)
Tuberculosis: Recrudescent infection (Risk factors/location/importance)
-⇩ Cell-mediated immunity (eg HIV)
-Apex of lung
-Contagious
Tuberculosis in HIV: Rate, location
8% per year

Often extrapulmonary
Atypical mycobacteria: contagion
Not person-to-person (no need to isolate patient)
Atypical mycobacteria: organisms
-M. marinum (fishtank cleaners)
-MAC (HIV, biofilms)
Meningitis vs. Encephalitis: Causative organisms
Meningitis: A variety of organisms

Encephalitis: Virii
Meningitis vs. Encephalitis: Symptoms
meningitis: fever, headache, stiff neck, photophobia, abnormal CSF

encephalitis: cerebral disturbance (somnolence, seizures, focal findings)
CSF profile: Purulent
-PMNs, low glucose
-Acute

Common cause: bacteria
CSF profile: Lymphocytic low glucose
-Subacute

Common causes:
-TB
-fungi
-spirochetes
-sarcoidosis
-cancer
The CSF profiles
-Purulent
-Lymphocytic low glucose
-Lymphocytic normal glucose
CSF profile: Lymphocytic normal glucose
Common cause: viral
Causes of bacterial meningitis in: neonates
-E. coli
-Group B streptococci
-Listeria

All from birth canal
Causes of bacterial meningitis in: young adults
-Meningococcus
-Pneumococcus
Causes of bacterial meningitis in: older adults
-Pneumococcus
-Meningococcus
Causes of bacterial meningitis in: immunosuppressed people
-Cryptococcus
-Listeria
Causes of bacterial meningitis in: Traumatic
-Pneumococcus
-S. aureus
-Gram negative bacteria
Common infections in immunocompromised (cell-mediated) hosts
-CMV
-Aspergillus
-Pneumocystis jiroveci
-Nocardia
Definition: nosocomial/iatrogenic infections
Infections acquired in hospital or health-care setting which were not present or incubating at admission
Anthrax: X-ray finding
Mediastinal widening
Anthrax: organism information
Bacillus anthracis

Gram-positive spore forming rod.
Anthrax: factos in toxin production
-Edema factor
-Lethal factor
Small pox: organism
DNA virus
Small pox: route of entry
Air droplets/aerosols from highly infectious viral shedding skin lesions
Difference between clinical presentation of small pox and chicken pox
Small pox: lesions all in the same stage
West Nile virus: organism
RNA flavivirus
West Nile virus: Route of entry
Culex mosquito vector
West Nile Virus: Syndromes
CNS
-encephalitis
-meningitis
-meningoencephalitis
-polio-like syndrome
H5N1 Influenza A: Treatment
Neuraminidase inhibitors?
Community Acquired MRSA: Manifestations
-Skin and soft tissue infections
-Pneumonia
Basic mechanism: Cycloserine
Attacks cell wall synthesis
Basic mechanism: Vancomycin
Attacks cell wall synthesis
Basic mechanism: Bacitracin
Attacks cell wall synthesis
Basic mechanism: Fosfomycin
Attacks cell wall synthesis
Basic mechanism: Penicillins
Attacks cell wall synthesis
Basic mechanism: Cephalosporins
Attacks cell wall synthesis
Basic mechanism: Monobactams
Attacks cell wall synthesis
Basic mechanism: Carbapenems
Attacks bacterial cell wall synthesis
Basic mechanism: TMP-SMX (Trimethoprim Sulfate)
Attacks bacterial folic acid metabolism
Basic mechanism: Sulfonamides
Attacks bacterial folic acid metabolism
Basic mechanism: Polymyxins
Attacks bacterial cell membrane
Basic mechanism: Nalidixic acid
Attacks bacterial DNA replication (DNA gyrase)
Basic mechanism: Quinolones
Attacks bacterial DNA replication (DNA gyrase)
Basic mechanism: Metronidazole
Attacks bacterial DNA-dependent RNA polymerase
Basic mechanism: Rifampin
Attacks bacterial DNA-dependent RNA polymerase
Basic mechanism: Macrolides (Erythromycin, Clarithromycin, Azithromycin)
Attacks bacterial protein synthesis (50S ribosome subunit inhibitor)
Basic mechanism: Chloramphenicol
Attacks bacterial protein synthesis (50S ribosome subunit inhibitor)
Basic mechanism: Clindamycin
Attacks bacterial protein synthesis (50S ribosome subunit inhibitor)
Basic mechanism: Tetracycline
Attacks bacterial protein synthesis (30S ribosome subunit inhibitor)
Basic mechanism: Spectinomycin
Attacks bacterial protein synthesis (30S ribosome subunit inhibitor)
Basic mechanism: Streptomycin
Attacks bacterial protein synthesis (30S ribosome subunit inhibitor)
Basic mechanism: Gentamicin
Attacks bacterial protein synthesis (30S ribosome subunit inhibitor)
Basic mechanism: Tobramycin
Attacks bacterial protein synthesis (30S ribosome subunit inhibitor)
Basic mechanism: Amikacin
Attacks bacterial protein synthesis (30S ribosome subunit inhibitor)
Bactericidal or Bacteriostatic: β-lactams
Bactericidal
Bactericidal or Bacteriostatic: Sulfonamides
Bacteriostatic
Bactericidal or Bacteriostatic: Quinolones
Bactericidal
Bugs attacked by: Narrow-spectrum β-lactams
-Streptococci
-Enterococci
-Spirochetes
-Gram negative diplococci
Bugs attacked by: Intermediate-spectrum β-lactams
-Enterococci
-H. flu
-E. coli
-Proteus
-Shigella
-Salmonella
Bugs attacked by: Broad-spectrum β-lactams
Beta-lactamase inhibitors: Carbapenems

-P. aeruginosa
-Resistant gram-
-Mixed infections
Bugs attacked by: Sulfonamides
-E. coli
-Pneumocystis Jiroveci
-Toxoplasma gondii
Bugs attacked by: Quinolones
-Gram negatives (pseudomonas)
-Mycoplasma
-Legionella
-PCN-R
-Strep. pneumo
Bugs attacked by: 1st generation cephalosporins
Gram+
Bugs attacked by: 2nd generation cephalosporins
Anaerobes
Bugs attacked by: 3rd generation cephalosporins
Weakly gram+ and gram-
Bugs attacked by: 4th generation cephalosporins
Gram negative
Cephalosporins that attack Pseudomonas
Ceftazidime(3rd-gen)
Cefipime (4th-gen)
Basic Mechanism: Linezolid
Attacks bacterial protein synthesis (Initiation complex)
Bugs susceptible to: M2 inhibitors
Influenza A
Bugs susceptible to: Neuraminidases
Influenza A&B
(H5N1 activity)
Basic Mechanism: Herpes drugs
Attack viral DNA polymerase
-(clovirs) do it using viral/host cell thymidine kinases)
-Foscarnet does not require phosphorylation
Treatable Herpesvirus syndromes
-Herpes simplex 1 and 2
-Varicella
-Primary in adults
-Zoster
-early in course
-if immunocompromised
-CMV

BUT NOT EBV!!
Post-exposure treatment for Hepatitis B
-Vaccinate
-Passive immunization (HBIG)
-Treatment (Entecavir, Adefovir)
Drugs for treatment of HSV-1 and HSV-2
-Acyclovir
-Valacyclovir
-Famciclovir
Treatment for: HSV Encephalitis
IV Acyclovir
Four classes of antiretrovirals
-NRTIs (Nucleoside Reverse Transcriptase Inhibitors)
-NNRTIs (Non-nucleoside reverse transcriptase inhibitors)
-PIs (Protease Inhibitors)
-Fusion Inhibitors
Mechanism: NRTIs
Analogues of naturally occuring deoxynucleotides lacking a 3' hydroxyl group on deoxyribose moiety --> chain termination
Mechanism: NNRTIs
Allosteric inhibition of reverse transcriptase
Mechanism: PIs
Prevent cleavage of nascent proteins for final assembly of new virions
Mechanism: Fusion inhibitors
Block HIV from fusing with a cell's membrane to enter and infect it
Basic idea behind antiretroviral drug-regimen
NRTI: backbone
NNRTI/PI: assistant
Antimicrobials that are strong inhibitors of Cytochrome P450-3A
-Ketoconazole
-Itraconazole
-Voriconazole
-Ritonavir
Antimicrobials that are moderate inhibitors of Cytochrome P450-3A
-Fluconazole
-Saquinavir
-Nelfinavir
-Atazanavir
-Erythromycin
-Clarithromycin
(NOT azithromycin)
Antimicrobials that are strong inducers of Cytochrome P450-3A
Rifampin
Antimicrobials that are moderate inhibitors of Cytochrome P450-3A
Efavirenz
Ritonavir
Cytochrome P450 inducer: High levels or low levels (Quick!)
Low levels
Cytochrome P450 inhibitor: High levels or low levels (Quick!)
High levels