Exam II Flashcards
(82 cards)
1
Q
Risk factors for Influenza
A
Old and young age
Underlying organ disease
obesity
pregnancy
2
Q
Influenza Viral Structure
A
Orthomyxovirus family Spherical, enveloped Replicates in nucleus Hemagglutinin: sialic acid binding Neuraminidase: cleaves sialic acid
3
Q
URT Viruses
A
Rhinovirus (common cold)
Coronavirus (common cold)
Adenovirus (sore throat)
Parainfluenza (sore throat)
4
Q
LRT Viruses
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Parainfluenza (bronchitis, croup) Influenza (bronchitis, bronchiolitis) Adenovirus (bronchitis) Metapneumovirus (bronchitis) RSV (bronchiolitis) Coronavirus (bronchitis)
5
Q
Viral Pneumonia
A
Influenza Parainfluenza Rhinovirus (type C) RSV, SARS, MERS coronavirus Adenovirus
6
Q
Rhinovirus and coronavirus
A
Incubation: 2-3 days Symptoms 5-7 days Rhinovirus: naked capsid Coronavirus: enveloped Common cold
7
Q
Adenovirus
A
pharyingitis
dsDNA
8
Q
Parainfluenza
A
Croup (barking cough, improves in cold)
enveloped, ssRNA
9
Q
RSV
A
Infects respiratory epithelial, dendritic cells
Small airway plugging from mucus and inflammation
Enveloped
Most important in 1st year of life
10
Q
Metapneumovirus
A
Mimics RSV
Enveloped
11
Q
Model for Pathogenesis of Viral Respiratory Infection
A
- Virus attaches through receptor mediated endocytosis
- Replication
- Local spread into epithelial cells
- innate sensing of PAMPs
- Interferon, cytokines, chemokines produced
- Stimulation of mucus production
- Recruitment of inflammatory cells
- Death of epithelial cells by lysis and exit of virus (non-enveloped)
12
Q
IgD
A
Membranes of naive B cells Small amount in serum Associated with signaling proteins (BCRs) Helps trigger B cells Lost when class switching
13
Q
IgM
A
Pentameric soluble form or membrane bound
First Ab made
Most efficient at complement activation
14
Q
IgG
A
Most abundant Ab in serum Neutralizes viruses and toxins Opsonizes bacteria Agglutinates and precipitates antigen Activates complement Placental passage
15
Q
IgA
A
Dimeric
Main Ab in secretions
Does NOT activate complement
16
Q
IgE
A
Present at low levels
Binds to Fc receptors on basophils and mast cells
Activates eosinophils, basophils, mast cells
Parasitic and hemolinths
Allergies
Does NOT activate complement
17
Q
MHC Class I
A
Present on all nucleated cells Recognized by CD8+ T cells Important with viruses and parasites Associated with TAP, proteasome, ERAP Polymorphic alpha chain with 3 domains and small invariant subunit (alpha)
18
Q
MHC Class II
A
Present on antigen presenting cells
Recognized by CD4+ T cells
Associated with HLA
Polymorphic beta chain with 2 domains and 2 invariant chains (beta)
19
Q
Bare Lymphocyte Type I
A
Mutation in TAP
Low level of MHC I expression
Leads to few CD8 cells
Chronic bacterial infections, treated with antibiotics, immunoglobulins
20
Q
Bare Lymphocyte Type II
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Mutation in transcription factors for MHC II expression
CD4 T cell development impaired
Deficient antibody response
Fatal unless bone marrow transplant
21
Q
T cell receptor development
A
Somatic gene rearrangement: VDJ recombination in thymus Begin as double positive (CD4 and CD8 +) Positive selection for cells expressing functional TCRs Negative selection (x2) for autoreactive Differentiation into mature T cells
22
Q
TCR VDJ Recombination
A
Valpha and Vbeta undergo VDJ recombination
Coordinated by RAG1 and RAG2 genes
Aire drives expression of tissue specific proteins
23
Q
T Cell Development Problems
A
No RAG1 or RAG2 = SCID (no T or B cells)
No Aire = spontaneous autoimmunity against glands
No thymus = DiGeorge Syndrome (no T cells)
24
Q
Chemokines and T cells
A
IFN-gamma: TH1
TGF-Beta: TH17, Treg
IL-4: TH2
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T cells and cytokines
TH1: IFN-gamma, TNF alpha (intracellular microbes)
TH17: IL-17, IL-21, IL-22 (extracellular pathogens)
TH2: IL-4 (helminths/parasites)
Treg: TGF-beta, IL-10
26
Antibody Structure
4 protein chains: 2 heavy, 2 light with variable and constant regions
Variable region: binds antigen
Light Chain: 1 v, 1 c
Heavy Chain: 1v, 3-4 c
CDR loops of variable region determines specificity (encoded by VDJ)
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Antibody Diversity
VDJ recombination
Heavy chain first
Recombination events including cleavage, hairpin formation lead to a lot of combinations
28
NK Cells
Invariant activating and inhibitory receptors
Recognize "missing self" (absence MHC I)
No preactivation required
No memory
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CD8 Cells
Express CD8 and TCR
Recognize MHC I presentations
Preactivaion and differentiation required
Memory
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CD8/NK Cell Similarities
Shared purpose: protect host from pathogens, destroy malignant cells
Shared mechanism: granzyme/perforin pathway, death receptor pathway (Fas/FasL), INF-gamma, TNF
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Measles Exanthem
Erythematous macules and papules
| Starts on face, spreads cephalocaudally
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Measles Enanthem
Koplik spots
| Present 2 days before and after rash
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Scarlet Fever Exanthem
Facial erythema with circumoral pallor
Sand paper rash
Intense at creases
Causes desquamation
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Scarlet Fever Enenthem
Strawberry tongue
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Rubella Exanthem
Pink to red macules and papules
| Spreads in 24 hours (faster than measles)
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Rubella Enanthem
Petichiae on palate and uvula (Forcheimer's spots)
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5th Disease Exanthem
Erythema infectiosum
Slapped cheek appearance
Reticulated, lacy rash on extremities
No enanthem
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Roseola Exanthem
Sudden onset of rash after fever
Begins on trunk
Nonpruritic (fades in hours/2 days)
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Roseola Enanthem
Nagayama spots: red papules in soft palate and uvula
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Inactivated/Killed Vaccine
Inactivates whole pathogen (heat or chemical)
No risk of reactivation
Ex: Polio (IPV), HAV, Rabies
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Toxoid Vaccine
Made from inactivated toxin
Requires intermittent booster
Ex: tetanus, diptheria
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Subunit Vaccine
Specific component isolated
May be mixed with adjuvant
Ex: HBV, HPV, Pertussis, Influznea (shot)
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Conjugate Vaccine
Encapsulated organisms coated in polysaccharides
Enhance reaction by combining with protein (diphtheria toxin)
Ex: Haemophilus influenzae, pneumococcal conjugate
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Live, attenuated Vaccine
Live, attenuated organism infected (MMR, varicella, BCG) or ingested (Rotavirus, OPV) or sprayed
Grow pathogen in chick embryos (can reactivate)
Contraindication for immnocompromised
Ex: MMR, varicella, rotavirus, influenza (nasal), OPV, yellow fever, BCG (only in other countries)
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HPV
High Risk: 16, 18, 31, 33
High number of sexual partners associated with oropharyngeal cancer
Produces E6 and E7 proteins that disable suppressors (Rb, p53)
Pathology: koilocytes
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Measles
4 day prodrome
Pathology: Warthin-Finkeldy Giant Cells
Skin rash with cough, coryza, conjunctivitis
Koplik spots
No treatment - SSPE complication years later
Highly contagious (90%)
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Rubella
Skin rash milder than measles
Palatal petechiae, red tonsils, soft palate
Congenital can cause stillbirth, blueberry muffin lesions
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Mumps
Epidemic parotitis
Contagious 1-2 days before onset
Meningitis can occur
Orchitis: inflammation of testes
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HIV Epidemiology
6rh leading cause of death
25 million have died worldwide
33.4 million as of 2008
20% not aware of infection
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HIV Pathogenesis
Envelope fuses with CD4 membrane
gp120 binds to CD4 and gp41 is transmembrane protein
Reverse transcriptase incorporates virus into host DNA (healthier patient = less virus replication)
New viruses assemble and bud from infected cells
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HIV Stages of Infection
Acute: asymptomatic 2-3 weeks monolike illness
Latent: up to 10 years; persistent lymphadenopathy may develop
AIDS: CD4
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Oral Manifestations HIV
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Dry mouth
Candidiasis
Oral hairy leukoplakia
Kaposi sarcoma
HPV warts
Herpes
Aphthous ulcers
Squamous cell carcinoma
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HHV1
Herpes Simplex Oral I
Primary and chronic
Herpes labialis
Secretion contact, esp. oral
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HHV2
Herpes Simplex Genital II
Primary and chronic
Herpes genitalis, neonatal
Secretion contact, esp. genital
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HHV3
Varicella-Zoster Virus
Primary (chickenpox) and chronic (Shingles)
Contact with infected skin lesions
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HHV4
Epstein Barr Virus
Primary (mono) and chronic (risks various)
Infectious mono, multiorgan manifestations
Contact with oral secretions, blood, transplanted organs
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HHV5
Cytomegalovirus (CMV)
Primary and chronic
Infectious mono, prolonged fever
Contact with oral or genital secretions, urine, breast milk, blood, transplant
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HHV8
Kaposi Sarcoma
| Contact with bodily secretions
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OI with CD
Thrush: C. Albicans; fluconazole
VZV: dermatome; Acyclovir
TB: M. tuberculosis; RIPE
S. pneumoniae (community acquired); ceftriaxone
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OI with CD
PCP (pneumocystis jiroveci); TMP/SMX
HSV: acyclovir
Cryptosporidium: protozoa; antiretroviral therapy
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OI with CD
Candida esophagitis: C. albicans; fluconazole
Toxoplasmosis: toxoplasma gondii; sulfadiazine + pyrimethamine
Histoplasmosis: H. capsulatum; itraconazole
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OI with CD
CMV retinitis: CMV; ganciclovir
Disseminated MAC: mycobacterium avium-intracellulare complex; azithromycin, rifampin
Cryptococcal meningitis: cyptococcus neoformans; amphotericin
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HIV associated Malignancies
Kaposi's Sarcoma (HHV 8)
Cervical Cancer (HPV)
Non-hodgkin lymphoma (EBV; HHV4)
Primary CNS Lymphoma (EBV; HHV4)
64
Hep A
Virus: non-enveloped, ssRNA
Cause: fecal/oral spread
Pathogenesis: stool viral shedding; 28 day incubation
Diagnosis: serum antibodies
Prognosis: self-limiting (10-15% severe disease)
Prevention: increase sanitization, vaccine
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Hep E
Virus: non-enveloped, ssRNA
Cause: fecal/oral spread
Pathogenesis: stool viral shedding; 40 day incubation
Diagnosis: serum antibodies
Prognosis: self-limiting (bad in pregnant women)
Prevention: sanitation, vaccine in China
66
Hep B
Virus: enveloped dsDNA
Cause: blood transmission
Pathogenesis: noncytolytic with reverse transcriptase; incubation 1-6 months
Symptoms: viral symptoms; immune system causes damage
Diagnosis: HbsAb (vaccine or previous), HBcAb (previous), HBeAg (active virus)
Prognosis: acute (resolved infection or vaccination) and chronic (90% perinatal)
Prevention: vaccination; antiviral medications
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Hep D
Virus: enveloped ssRNA
Cause: HBV infection (uses HBsAg)
Pathogenesis: coinfection with HBV or superinfection (HBV first, HDV second)
Diagnosis: serology, PCR
Prognosis: superinfections 5-15% mortality
Prevention: vaccinate against HBV
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Hep C
Virus: 7 genotypes, non-enveloped ssRNA
Cause: blood transmission, body fluids
Pathogenesis: non-cytolytic, immune system causes damage
Diagnosis: enzyme immunoassay, RNA PCR, LFTs (may be normal in chronic)
Prognosis: most common blood borne infection in US (80% or more develop chronic)
Prevention: no vaccine, oral pills for type 1
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Acute Viral Hepatitis
Symptoms: asymptomatic in majority, but flu-like symptoms in some
Signs: jaundice, tenderness swelling liver
Labs: high LFTs (>1000 IU/L)
toxins can accumulate, hormone dysregulation
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Chronic Viral Hepatitis
Cirrhosis, immune complex disease, HCC
May be asymptomatic for years
LFTs normal or mildly elevated
Complications develop 15-40 years after infection
Risk and timing of progression varies on type of infection and comorbidities (HIV, EtOH)
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Liver Enzyme Changes with Heptatitis
Increase in AST, ALT (>1000 IU/L)
Increase in GGT, AlkPhos later
Chronic hepatitis may have normal liver enzymes
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Ethics with Tuskegee Study
1930s study involving men with syphilis
Did not give treatment when penicillin came out
Did not give informed consent
Bodies of oversight now exist to avoid studies like this
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Metronidazole
Mechanism: interferes with bacterial DNA replication
Adverse Effects: glossitis, metallic taste, stomatitis, xerostomia, furry tongue
Interactions: ethanol or disulfram; inhibits CYP3A4
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Aminoglycosides
Mechanism: broad spectrum bactericidal; binds 30S
Adverse effects: resistance; high toxicity to kidney, ear, neuromuscular, GI disruption
Interactions: penicillin, non-depolarizing neuromuscular blockers, antidiruetcis and antivirals
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Tetracyclines
Mechanism: binds 30S
Adverse Effects: binds 80S subunit of eukaryote, resistance, enamel hypoplasia and permanent tooth discoloration
Interactions: buffered aspirin, retinoic acid, digoxin, methoxyflurane
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Clindamycin
Mechanism: binds 50S subunit
Adverse Effects: diarrhea, nausea and vomiting, abdominal pain, esophagitis, glossitis, stomatitis, myelosuppression, metallic taste
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Macrolides
Mechanism: binds 50S
Adverse Effects: prolongs QT interval, oral candidiasis, rash, abdominal pain, diarrhea, nausea, pancreatitis
Interactions: amiodarone, quinine, pimozide, Ca channel blockers (heart), atorvastatin (rhabdo)
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Polyene Macrolides
Example: amphotericin
Structure: polar lactone ring
Mechanism: binds ergosterol (10:1 preference), forms pores
Adverse Effects: chills, fever, headache, malaise, anorexia, delirium, malaise, nausea
79
Azoles
Examples: fluconazole, itraconazole
Structure: 5-membered azole ring
Mechanism: lanosterol 14alpha demethylase (inhibits ergosterol synthesis)
Adverse Effects: headache, GI distress, nausea, photophobia, blurred vision
Interactions: warfarin, phenotoin
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Echinocandins
Examples: caspofungin, micafungin, anidulafungin
Mechanism: inhibits synthesis of beta(1,3) glucan (cell wall)
Use: treat fluconazole resistant candida
Adverse Effects: hypotension, peripheral edema, tachycardia, hypokalemia, diarrhea
81
Flucytosine
Mechanism: converted to 5-FU to interfere with RNA synthesis
Use: treat systemic candida and cryptococcus
Adverse Effects: renal, haptic and bone marrow toxicities
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Griesofulvin
Mechanism: inhibits fungal cell mitosis and metaphase; binds human keratin to resist colonization
Use: treat tinea (skin, nails, hair)
Adverse Effects: hepatotoxicity, rash, dizziness, confusion, insomnia, headache, CYP3A4 inducer (decrease hydrocodone)
