Week 2 Flashcards

1
Q

clinical presentation of influenza pneumonia

A

· Fever, cough, or sore throat (referred to as influenza-like illness [ILI])
· Uncomfortable or lethargic appearance
· Prominent dry cough (rarely hemoptysis)
· Flushed integument and erythematous mucous membranes
· Rales or rhonchi
· Wheezing
· Tachycardia
· tachypnea
· decreased breath sounds

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2
Q

Treatment of influenza pneumonia

A
  • supportive care: maintain oxygen, hydration, rest, meet increased calorie need
  • meds: Oseltamivir orPeramiviror Zanamivir
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3
Q

influenza vaccines

  • types
  • contraindications
A
  • Quadrivalent/ Trivalent (H1N1, H3N2 and B)

- History of severe allergic reaction to any vaccine component (H1N1, H3N2 and 2 B)

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4
Q

immune response to influenza vaccine

  • onset
  • duration of efficacy
A
  • antibodies are formed two weeks after vaccine is given
  • seasonal flu vaccine protects against the influenza viruses that research indicates will be most common during the upcoming season
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5
Q

appropriate administration of antibiotics following an influenza infection in relation to secondary and/or concomitant bacterial infections.

A
  • Infection with the influenza virus impairs T lymphocytes, neutrophils, and macrophage function, which leads to impairment of host defenses and may foster bacterial infection of normally sterile areas
  • Antibiotics should only be used if there is a bacterial complication of the flu
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6
Q

epidemiology of influenza

A
  • pregnant women, children under 59 months, the elderly, individuals with chronic medical conditions, individuals with immunosuppressive condition, individuals who work in healthcare
  • mainly during winter
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7
Q

pathogenesis of influenza

A
  • IAV infect respiratory epithelial cells or alveolar macrophages,
  • single-stranded RNA of the influenza virus is recognized by toll-like receptor (TLR) 7 and retinoic acid-inducible gene-I (RIG-I) but the virus can secrete NS1 to inhibit function of tripartite motif (TRIM) in the ubiquitination of RIG-I
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8
Q

Diagnosing flu

A
  • Rapid influenza : RT-PCR
  • sputum and blood culture
  • chest x-ray
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9
Q

Varicella zoster clinical presentation

A

Fever, headache, malaise, abdominal pain, vesicular pruritic rash

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10
Q

progression of chicken pox

A

• Symptoms occur 2 weeks after virus enters the body. - skin lesions start out as flat, red itchy spots but become elevated and develop into papules then into small fluid filled vesicles. Within 1-2 days, vesicles crust over and become scabs. After 5 days, scabs fall off.
-New lesions continue to form on the body every 3-5 days, so you see lesions in different phases at the same time

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11
Q

mode of transmission of chickenpox

A
  • inhalation of respiratory droplets and aerosols generated by skin lesions
  • direct contact with droplets or vesicular fluid from skin lesions
  • transplacental spread
  • blood transfusions (rare)
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12
Q

risk of cellulitis development as a complication of chickenpox

A

-Secondary bacterial infections of the skin, usually caused by group A Streptococcus and S. aureus,

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13
Q

Varicella virus

A
  • live attenuated vaccine
  • routine 2-dose vaccination in children > 12 months old - first dose at age 12-15 months and second dose at age 4-6 years
  • generally contraindicated in individuals with primary or acquired immunodeficiencies or those receiving immunosuppressive therapy
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14
Q

Pathogenesis of varicella

A
  • Virus initially enters respiratory epithelial cells. They fuse with the membrane and inject their capsid into it. Capsid binds to nucleus and injects it with DNA where it’s copied. The viral DNA is transcribed into RNA then goes to ribosome where they are translated into capsid proteins. Capsid and viral DNA fuse together. They go to Golgi then leave the cell, leaving behind a dead cell.
  • Virus replicates in epithelial cells and eventually picked up by immune cells and taken to lymph nodes, now causes primary infection-varicella (chicken pox) which consists of primary and secondary viremia
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15
Q

Dx of VZV

A
  • made on clinical grounds alone

- best confirmed by real time PCR

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16
Q

Management of VZV

A
  • disease is usually self-limiting and antiviral medication usually not needed
  • symptom directed treatment include acetaminophen/ibuprofen for fever, headache, aches, pain; soothing cream to relieve pruritus; fluid and electrolytes to maintain hydration
  • post-exposure prophylaxis includes the varicella zoster igG
17
Q

risks and pathophys of ZVZ reactivation

A
  • Immunocompromised people, older people, and people who experience high stress are at risk for VZV reactivation
  • viral particles remain in the dorsal root or other sensory ganglia, where they may lay dormant for years to decades
  • In this latent period, host immunologic mechanisms suppress replication of the virus, but VZV reactivates when the host mechanisms fail to contain the virus.