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Flashcards in 4th Exam - Viral Diseases Deck (113)
1

Viral affinity for one cell type:

tropism

2

Consequences of viral infection:

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

3

Virus that causes tissue destruction:

Hep B

4

What causes tissue destruction in Hep B infection?

immune-mediated, not the virus

5

Infiltration type with viral infections:

lymphocytic

6

Viral infection often leads to:

bacterial infection

7

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

Rubella infection during pregnancy

8

Define teratogenic:

induce birth defects

9

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

1st trimester

10

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

secondarily

11

Evidence of active congenital rubella syndrome infection at birth:

none, no inclusion bodies, no inflammation

12

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

microcephaly, ventricular septal defects, cataracts, microencephaly, deafness

13

Part of brain most commonly affected in CRS:

cerebrum

14

Hep B transmission:

Parental route (any body fluids) or as STD

15

Hep B virus is found here:

blood, body fluids

16

6 forms of Hep B infection:

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

17

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

PAN

18

Pre-icteric phase (HBV)

Anorexia, fever, fatigue

19

Icteric phase:

jaundice, hepatomegaly, 90% recovery

20

TF? HBV is cytolytic.

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

21

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

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

22

Infection type assoc w PMN's:

bacterial

23

Indicative of viral lymphocytosis:

Lymphocytic inflammation, Antibody producing B cells, T cells

24

Smoldering HBV infection with lymphocytic inflammation:

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

25

Arterial lesions of a person w AI vasculitis contain:

HBV, complement, and Ig

26

What induces the AI response in AI vasculitis?

virus in lesion

27

Red, generalized, maculopapular rash is assoc w:

Measles

28

Multiple white lesions are assoc w:

Measles, Koplik spots (pathogneumonic finding)

29

What cell type is assoc w measles:

PMN

30

What precedes measles by 2-3d?

rash, Koplik spots, often on buccal mucosa

31

Pathoognomic for measles:

Koplik spots

32

What virus causes Hand Foot Mouth Disease?

Coxsackievirus, A16 most often

33

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

F

34

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

Hand Foot Mouth Disease

35

This disease presents similarly to syphilis:

Hand Foot Mouth Disease

36

Fever is assoc w:

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

37

How is the cell killed in acute Hep?

liver cell membranes are altered

38

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

F. more lymphos

39

Cause of lymphocytic inflammation in tissue:

Antibody producing b cells, T cells

40

Smoldering infection is assoc with:

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

41

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

HBAg

42

Arterial lesions of AI vasculitis/ PAN contain:

HBV, complement and Ig

43

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

mumps, usually unilateral

44

TF? Herpes labialis is assoc w fever.

F

45

Herpes labialis lays dormant here:

trigeminal neuron

46

Type 2 herpes simplex infection:

genital, STD assoc w uterine, cervcial inflammation and dysplasia

47

Assoc w herpetiform rash:

herpes simplex encephalitis (cluster of vesicles)

48

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

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

49

Assoc w inclusions in ganglion:

HSV 1, Herpes zoster, HPV warts

50

Viruses that cause vesicular lesions:

HSV 1, herpes zoster, Chx pox, small pox

51

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

epidermis or mucosa (HPV is epidermis)

52

Edema of epi cells in HSV infection can lead to:

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

53

Cell type assoc w HSV infection:

PMNs, like measles

54

TF? A vaccine is available for Varicella-Zoster.

T

55

Varicella-Zoster rash begins here:

trunk

56

Latent Herpes Zoster infection can hide here:

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

57

Latent Herpes Zoster infection can be reactivated bc of:

lower immunity: HIV, aging, cancer

58

Assoc w neuropathy of sensory nerves:

Herpes Zoster

59

TF? Herpes Zoster is most often bilateral.

F. unilateral in one dermatome

60

necrosis or hemorrhage in ganglia is assoc w:

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

61

This presents just like Strep throat:

mono, inflammed, cervical nodes

62

Headache, swollen glands, fever, very tired:

mono, strep throat (check)

63

Mono is assoc w an increase in this cell type:

PMN and lymphos (62%)

64

Productive EBV infection:

mono

65

Ddx of EBV infection:

Leukemia, Burkitt's lymphoma, Hodgkin's

66

EBV infects what cell type?

B cells of humans only

67

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

U.S.: clinical, underdeveloped: subclinical

68

Antibody produced by acute mono:

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

69

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

F. highly suggestive

70

Atypical lymphocytes/ cytotoxic t-cells are aka:

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

Downey Cells:

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

What type of virus is HPV?

oncogenic, DNA

73

Tissue layer affected by HPV:

epi

74

How is HPV spread?

contact, autoinnoculation

75

Types of HPV:

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

76

Are HPV lesions typically single or multiple?

either

77

HPV warts:

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

78

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

HPV

79

HPV viral genes that enter host genome code for:

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

80

baby born w small head:

zicca virus, rubbela

81

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

F. active organogenesi, though

82

PAN:

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

83

Hand Foot Mouth disease usually lasts

1-2 wk

84

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

Yes

85

TF? Herpes labialis is typically accompanied by fever?

F

86

Oral form of herpes is type:

1

87

TF? You can get oral herpes on your fingers.

T. dentist wo gloves

88

How does the herpes virus get to the tongue?

via CNV, can stay in this nerve for a lifetime

89

Population most likely to be effected by varicella:

kids 2-8yo

90

Varicella is a ____ rash.

vesicular

91

Curse of developed nations:

mono

92

Which lasts longer, strep or mono?

mono, wks - mos

93

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

bacterial, viral

94

Productive infections cause:

cell destrucion

95

Is latent mono productive or non-productive?

non-poductive, B cells proliferate, lympohomas

96

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

F, but you can develop Burkitt's from EBV

97

Is EBV more common in developed or underdeveloped nations?

underdeveloped

98

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

T

99

Is mono more common in developed or underdeveloped countries?

developed

100

Subclinical EBV disease is more common here:

underdeveloped countries, not so clean

101

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

mono

102

Latent, non-productive infection resides here:

B cells

103

LMP-1 binds to:

Tnf-R associated factors

104

FUnction of TRAF's:

activate TF's (NF-kB)

105

Function of NF-kB:

enters nucleus to promote cell proliferation

106

Downey cells are assoc w:

mono

107

Cells infected w mono have this protein:

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

TF? LMP-1 binds to TNF-factors.

F. TNF assoc factors

109

Define autoinoculation:

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

110

Herpes and warts both involve ___ nuclear inclusions.

intra, in skin cells, virial infection

111

p53 protein causes:

apoptosis

112

Rb protein causes:

growth arrest

113

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

p53 and Rb protein routes