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Pathology > 4th Exam - Viral Diseases > Flashcards

4th Exam - Viral Diseases Flashcards

1
Q

Viral affinity for one cell type:

A

tropism

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2
Q

Consequences of viral infection:

A

no injury, tissue destruction, inflammation, weaken host defense, cell proliferation, neoplasia

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3
Q

Virus that causes tissue destruction:

A

Hep B

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4
Q

What causes tissue destruction in Hep B infection?

A

immune-mediated, not the virus

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5
Q

Infiltration type with viral infections:

A

lymphocytic

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6
Q

Viral infection often leads to:

A

bacterial infection

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7
Q

Case: pregnancy, illness at 7wks gestation, small head, cataracts, heart murmer:

A

Rubella infection during pregnancy

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8
Q

Define teratogenic:

A

induce birth defects

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9
Q

Developing fetus, most vulnerable to intrauterine infection during this period:

A

1st trimester

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10
Q

Is the fetus primarily or secondarily infected in congenital rubella syndrome?

A

secondarily

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11
Q

Evidence of active congenital rubella syndrome infection at birth:

A

none, no inclusion bodies, no inflammation

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12
Q

Main symptoms of baby born with congenital rubella syndrome (CRS):

A

microcephaly, ventricular septal defects, cataracts, microencephaly, deafness

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13
Q

Part of brain most commonly affected in CRS:

A

cerebrum

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14
Q

Hep B transmission:

A

Parental route (any body fluids) or as STD

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15
Q

Hep B virus is found here:

A

blood, body fluids

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16
Q

6 forms of Hep B infection:

A

subclinical, acute, fulminant (wide spread necrosis of liver), persistent infection, hepatocelllular carcinoma, AI vasculitits (pts w history of Hep B, like pts w PAN)

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17
Q

AI vasculitis connected to Hep B infection is related to this disease:

A

PAN

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18
Q

Pre-icteric phase (HBV)

A

Anorexia, fever, fatigue

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19
Q

Icteric phase:

A

jaundice, hepatomegaly, 90% recovery

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20
Q

TF? HBV is cytolytic.

A

F. body’s immune system goes against its hepatocytes (immune-mediated)

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21
Q

How do a person’s cytotoxic T cells kill hepatocytes in HBV?

A

T cell rec binds cell w both HBcAg (Hep B core antigen: usually indicates person is infectious) and Class 1 MHC, T cell releases perforins, punctures cell membrane, cell dies

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22
Q

Infection type assoc w PMN’s:

A

bacterial

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23
Q

Indicative of viral lymphocytosis:

A

Lymphocytic inflammation, Antibody producing B cells, T cells

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24
Q

Smoldering HBV infection with lymphocytic inflammation:

A

piecemeal necrosis, edges of portal zones chewed up – cirrhosis –> hepatoma

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25
Q

Arterial lesions of a person w AI vasculitis contain:

A

HBV, complement, and Ig

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26
Q

What induces the AI response in AI vasculitis?

A

virus in lesion

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27
Q

Red, generalized, maculopapular rash is assoc w:

A

Measles

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28
Q

Multiple white lesions are assoc w:

A

Measles, Koplik spots (pathogneumonic finding)

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29
Q

What cell type is assoc w measles:

A

PMN

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30
Q

What precedes measles by 2-3d?

A

rash, Koplik spots, often on buccal mucosa

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31
Q

Pathoognomic for measles:

A

Koplik spots

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32
Q

What virus causes Hand Foot Mouth Disease?

A

Coxsackievirus, A16 most often

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33
Q

TF? There is a vaccine for Hand Foot Mouth Disease.

A

F

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34
Q

Itchy, maculopapular rash that becomes a vesicular, water-filled, lesion later

A

Hand Foot Mouth Disease

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35
Q

This disease presents similarly to syphilis:

A

Hand Foot Mouth Disease

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36
Q

Fever is assoc w:

A

Hand Foot Mouth Disease, Acute Hep, Mumps, Varicella Zoster, Mono

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37
Q

How is the cell killed in acute Hep?

A

liver cell membranes are altered

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38
Q

TF? The basement membrane is stimulated to make more PMNs in acute Hep.

A

F. more lymphos

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39
Q

Cause of lymphocytic inflammation in tissue:

A

Antibody producing b cells, T cells

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40
Q

Smoldering infection is assoc with:

A

lymphocytic inflammation, piecemeal necrosis, edges of portal zones chewed up

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41
Q

30% of pts w AI vasculitis/ PAN have this in their blood:

A

HBAg

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42
Q

Arterial lesions of AI vasculitis/ PAN contain:

A

HBV, complement and Ig

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43
Q

enlargement of the parotid gland, tender, painful to palpation is assoc w:

A

mumps, usually unilateral

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44
Q

TF? Herpes labialis is assoc w fever.

A

F

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45
Q

Herpes labialis lays dormant here:

A

trigeminal neuron

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46
Q

Type 2 herpes simplex infection:

A

genital, STD assoc w uterine, cervcial inflammation and dysplasia

47
Q

Assoc w herpetiform rash:

A

herpes simplex encephalitis (cluster of vesicles)

48
Q

Describe the 1st and 2nd infection of HSV 1:

A

1st: subclinical if young, 2nd: recurrent blisters/ vesicular lesions

49
Q

Assoc w inclusions in ganglion:

A

HSV 1, Herpes zoster, HPV warts

50
Q

Viruses that cause vesicular lesions:

A

HSV 1, herpes zoster, Chx pox, small pox

51
Q

Blisters are found in this skin layer in HSv 1 infection:

A

epidermis or mucosa (HPV is epidermis)

52
Q

Edema of epi cells in HSV infection can lead to:

A

necrosis, several epidermal cells can fuse together to form mulitnucleated cell

53
Q

Cell type assoc w HSV infection:

A

PMNs, like measles

54
Q

TF? A vaccine is available for Varicella-Zoster.

55
Q

Varicella-Zoster rash begins here:

56
Q

Latent Herpes Zoster infection can hide here:

A

Trigeminal ganglion, posterior root, sensory ganglia esp. (sensory nerves)

57
Q

Latent Herpes Zoster infection can be reactivated bc of:

A

lower immunity: HIV, aging, cancer

58
Q

Assoc w neuropathy of sensory nerves:

A

Herpes Zoster

59
Q

TF? Herpes Zoster is most often bilateral.

A

F. unilateral in one dermatome

60
Q

necrosis or hemorrhage in ganglia is assoc w:

A

Herpes Zoster (shingles), band like distribution in dermatome)(

61
Q

This presents just like Strep throat:

A

mono, inflammed, cervical nodes

62
Q

Headache, swollen glands, fever, very tired:

A

mono, strep throat (check)

63
Q

Mono is assoc w an increase in this cell type:

A

PMN and lymphos (62%)

64
Q

Productive EBV infection:

65
Q

Ddx of EBV infection:

A

Leukemia, Burkitt’s lymphoma, Hodgkin’s

66
Q

EBV infects what cell type?

A

B cells of humans only

67
Q

Form of EBV that is more typical of U.S. and underdeveloped countries:

A

U.S.: clinical, underdeveloped: subclinical

68
Q

Antibody produced by acute mono:

A

heterophie antibody, nonspecific IgM reacts w sheep or horse RBC’s, causes agglutintation

69
Q

TF? + heterophilic antibody test (+HAT) is diagnostic for mono:

A

F. highly suggestive

70
Q

Atypical lymphocytes/ cytotoxic t-cells are aka:

A

Downey, huge cells, lots of cytoplasm, big, hyperchromomatic nuclei, T cells reacting TO the presence of B cells (recognize as antigen) of the pt that are proliferating

71
Q

Downey Cells:

A

Reactive, non-infected CD+ cells, attach to B cell and try to get rid of them, sensitized to infected B cells, cytotoxic T cells kill the infected B cells, proliferate in ln, spleen or other lymphoid tissue, pseudoneoplastic T cell proliferation. can get large spleen or LN’s

72
Q

What type of virus is HPV?

A

oncogenic, DNA

73
Q

Tissue layer affected by HPV:

74
Q

How is HPV spread?

A

contact, autoinnoculation

75
Q

Types of HPV:

A

1, 2, 4, 7, not every HPV virus causes warts!

76
Q

Are HPV lesions typically single or multiple?

77
Q

HPV warts:

A

painless, non-vesicular, waxy, raised gray or brown, may look like tumor, can be in mouth and resemble a tumor

78
Q

Papilomatosis (projections form ski surface along w too much keratin) is assoc w:

79
Q

HPV viral genes that enter host genome code for:

A

E6 and E7, bind p53 and Rbp respectively leading to their degradation

80
Q

baby born w small head:

A

zicca virus, rubbela

81
Q

TF. teratogenic fetal infection in utero often present w active viral inflammation.

A

F. active organogenesi, though

82
Q

PAN:

A

30% have HBV infection, ab complexes w Ag, vessel damaged, affects muscular arteries in men, produces aneurysms in bvs’, esp abdominal arteries

83
Q

Hand Foot Mouth disease usually lasts

84
Q

Can you have Ab’s to measles in you body and not have clinical symptoms?

85
Q

TF? Herpes labialis is typically accompanied by fever?

86
Q

Oral form of herpes is type:

87
Q

TF? You can get oral herpes on your fingers.

A

T. dentist wo gloves

88
Q

How does the herpes virus get to the tongue?

A

via CNV, can stay in this nerve for a lifetime

89
Q

Population most likely to be effected by varicella:

A

kids 2-8yo

90
Q

Varicella is a ____ rash.

91
Q

Curse of developed nations:

92
Q

Which lasts longer, strep or mono?

A

mono, wks - mos

93
Q

Strep is a __ infection, mono is a __ infection.

A

bacterial, viral

94
Q

Productive infections cause:

A

cell destrucion

95
Q

Is latent mono productive or non-productive?

A

non-poductive, B cells proliferate, lympohomas

96
Q

TF? A pt must have mono before getting Burkitt’s lymphoma.

A

F, but you can develop Burkitt’s from EBV

97
Q

Is EBV more common in developed or underdeveloped nations?

A

underdeveloped

98
Q

TF? When we do get exposed to EBV we get mono bc we are in a developed country

99
Q

Is mono more common in developed or underdeveloped countries?

100
Q

Subclinical EBV disease is more common here:

A

underdeveloped countries, not so clean

101
Q

Clumping of BC’s in the heterophilic antibody test indicative of:

102
Q

Latent, non-productive infection resides here:

103
Q

LMP-1 binds to:

A

Tnf-R associated factors

104
Q

FUnction of TRAF’s:

A

activate TF’s (NF-kB)

105
Q

Function of NF-kB:

A

enters nucleus to promote cell proliferation

106
Q

Downey cells are assoc w:

107
Q

Cells infected w mono have this protein:

A

latent membrane protein-1, LMP-1 binds to Tnf-R associated factors, TRAF’s activate TF’s (NF-kB), NF-kB enters nucleus to promote cell proliferation, leas to lymphocytosis

108
Q

TF? LMP-1 binds to TNF-factors.

A

F. TNF assoc factors

109
Q

Define autoinoculation:

A

If a person has a lesion on the body and they touch that lesion, it can spread

110
Q

Herpes and warts both involve ___ nuclear inclusions.

A

intra, in skin cells, virial infection

111
Q

p53 protein causes:

112
Q

Rb protein causes:

A

growth arrest

113
Q

What 2 mechanisms does the HPV infection have to lead to neoplasia:

A

p53 and Rb protein routes

Pathology (23 decks)

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