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Micro last plus one anatomy 5 > viral infections of the skin soft tissue, bone, muscle and joints I > Flashcards

viral infections of the skin soft tissue, bone, muscle and joints I Flashcards

1
Q

papilloma

A
  • benign growth of the skin or mucous membranes
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2
Q

macule

A
  • small DISCOLORED patch of skin that forms an area distinct from the normal surrounding surface
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3
Q

papule

A
  • CIRCUMSCRIBED RAISED PORTION OF THE SKIN
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4
Q

vesicle

A

-small pouch of CLEAR fluid

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5
Q

pustule

A

full of pus

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6
Q

warts

A
  • hyperkearatotic
  • cutaneous are often painless if cutaneous
  • CAUSED BY HPV
  • LOOK CAULIFLOWER LIKE
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7
Q

Name for common wart
plantar wart
flat warts

A

verruca vulgaris
verruca plantaris
verruca plana

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8
Q

HPV

A
  • nonenvveloped
    dsDNA
    replication depends on differentiation status of the tissue
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9
Q

what layer of the skin would you expect to find a new HPV infection

A

suprabasal

-infected at basal layer, virion matures as moves up

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10
Q

where does the bump come from in warts?

A
  • expanding of all layers due to proliferation
  • proliferation initiated so that the virus can use the cell’s machinery to replicate itself
  • specifically- HPV-7 and HPV-6 are used to inactivate tumor suppressor cells Rb and P53 respectively causing the cells to go into S phase more and reprematurely
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11
Q

what are the main cutaneous HPV viruses divided into common and plantar warts

A
  • common- 2,3,10

- plantar- 1.4

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12
Q

transmission of HPV? incubation of HPV? diagnosis?

A
  • HPV- direct contact or with contact with surfaces
  • 3-4 months
  • diagnosis- appearance-koilodal cells (large nuclei with halo/nonstained around them) and hyperkeratosis
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13
Q

Treatment/prevention for HPV

A
  • common and plantar warts usually spontaneous regress after a few months- 2 yrs
  • wart removal- cryotherapy, cytotoxic, chemicals, surgical removal
  • > NOTE HPV 16, 18, 6, 11: do not protect against cutaneous warts
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14
Q

Molluscum Contagiosum

A
  • painless, pearly, umbilicated, nodules
  • seen in genitals (sexual-for adults), hands on kids via contact
  • has concavity
  • in microscope, it has LARGE AMOUNT IN CELL
  • large eosiophilic cytoplasmic inclusions (molluscum bodies)
  • poxviridae
  • large dsDNA genome
  • replicates within cytoplasm - UNIQUE
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15
Q

incubation and transmission of molluscum contagiosum

A
  • 14-50 days

- transmission via direct contact with lesions or fomaite transmission thru a towel or something

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16
Q

treatment of molluscum contagiosum

A
  • often resolution with in 2-12 months without treatment

- removal thru surgery or cryotherapy

17
Q

Herpes labialis

A
  • cold sores
  • painful/[painless and found in vermillion boarder of lip
  • a reactivation of the herpes simplex virus
  • HOWEVER, AT PRIMARY INFECTION YOU CAN GET A WIDE RAGE OF INFECTIONS LIKE WIDESPREAD INFECTION OF THE MOUTH INCLUDING gingicomastitis (in gums)
  • herpes simplex virus
18
Q

Herpes Simplex keratitis

A
  • leading cause of infectious blindness in US
  • initial infection causes conjunctivitis that takes weeks to heal
  • recurrent disease lead to corneal opacity
  • caused by leading simplex
19
Q

herpes simplex encephalitis

A
  • rare
  • mortality rate over 30% even with antivirals
  • commonly leads to neuro probs
  • caused by herpes simplex virus
20
Q

herpetic whitlow

A
  • lesions in the digits

- from herpes simplex

21
Q

what is the herpes simplex virus

A
  • dsDNA

- latent and lytic phases of the life cycle exist

22
Q

during a herpes outbreak, what is the productive phase of the life cycle?

23
Q

cold sore pathology

A
  • HSV virus comes and infects the epithelium of the mouth, and replication occurs
  • some of the virus gets into the sensory neuron and stays latent there
  • when cold sore goes away and there is stress via emotional or traumatic, we get the virus coming out of neuron for outbreak
24
Q

what is HSV-1 and HSV2 known to cause?

A

1 = mouth lesions
2= genital lesions
90% of the population has them just not everyone shows it

25
Q

what is prescribed for herpes? how does it work?

A

FOSCARNET AND ACYCLOVIR

  • acyclovir works like this:
  • > relies on the viruse’s thymidine kinase to phosphorylate it converting it to acyclovir monophosphate
  • > use cellular kinases to make acyclovir triphosphate which is a nucleotide mimic that allows it to inhibit the viral DNA polymerase incorporation into viral DNA to get CHAIN TERMINATION
26
Q

Varicella

A
  • chicken pox
  • lesions on trunk, scalp and face most
  • fever and lesions last approx. 5 days
27
Q

what is important to note about the lifecycle of varicella?

A
  • it is an evolutionized process
  • starts as vesicles -> pustules -> scabs (healing)
  • GET “CROPS OF LESIONS”- there are multiple evolutionary stages in a single area of the body
28
Q

though varicella is seen all over, where is it NOT?

A
  • soles of feet or palms
29
Q

what are some complications of varicella

A
  • from itching, can inoculate self with bacteria as a secondary infection
  • pneumonia - can be due to the viral infection of the lungs or a secondary bacterial infection -> viral has worse outcome and is attributed to MOST OF THE DEATHS FROM CHICKEN POX
30
Q

chicken pox and pregnancy
first 20 weeks of gestation
vs
infection late gestation

A
  • infection during the first 20 weeks- low birth weight, skin, scarring, encephalitis, chorioretinitis and microcephaly
  • infection late in gestation or right after birth- gives lesions on viscera and disseminated infection =worse!!
31
Q

herpes zoster

A
  • causes shingles- reactivation of VSV
  • epidemiology- elderly and immunosuppressed
  • get paresthesia (pins and needles) before break out
  • GET VESICULAR LESIONS ON FACE AND TRUNK UNILATERALLY
  • FLOWS DERMATOMES
  • get fever and malaise
32
Q

postherpetic neuralia

A
  • herpes zoster

- Shingles outbreak that causes pain long after lesions have resolved

33
Q

what is varicella-zoster virus?

A 
- dsDNA
enveloped
- herpesviradae fam
- LATENT INFECTION- USUALLY IN THE DORSAL ROUTE OR TRIGEMINAL
-one serotype
34
Q

how is varicella-zoster transmitted? incubation time? diagnosis?

A
  • tx- via lesions or respiratory secretions
  • incubation time- 2 wks
  • diagnosed via TZANCK SMEAR, antibodies, clinical analyses
35
Q

varicella vaccine

A
  • PREVENTS PRIMARY INFECTIONS
  • LIVE ATTENUATED
  • grown in tissue culture
  • combined with measles, mumps, rubella
  • first dose - 12-15 months old
  • second dose- 4-6 years old
36
Q

zoster vaccine

A
  • to protect against from VZV REACTIVATIONS
  • SAME LIVE ATTENUATED VACCINE WITH HIGHER TITER
    -recommended for all adults over 60regardless
    -
37
Q

when are anti-herpetic drugs used on patients to treat varicella zoster? what drugs are used?

A
  • when patient obtains a primary infection late in the their life
  • acyclovir
  • varicella is not as susceptible to acyclovir as HSV

Micro last plus one anatomy 5 (8 decks)

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