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Microbiology > Circulatory, RES & Lymphatics-Viral II > Flashcards

Circulatory, RES & Lymphatics-Viral II Flashcards

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Biology 101 flashcards
1
Q

inflammation of the middle muscular layer of the heart wall leading to ventricular dysfunction

A

myocarditis

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2
Q

myocarditis is more prevalent in

A

men

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3
Q

symptoms of myocarditis

A

shortness of breath, excercise intolerance, fatigue (also chest pain, abdominal pain, palpitations, syncope)

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4
Q

may mimic myocardial infection

A

myocarditis

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5
Q

most US myocarditis cases are associated with

A

viral infection

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6
Q

Most recently, myocarditis is associated with

A

B19 parvovirus, HHV-6

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7
Q

Echovirus, influenza virus, mumps virus, adenoviruses (2/5), and enteroviruses (especially coxsackie B) are associated with

A

myocarditis

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8
Q

Dx: of myocarditis

A

chest cardiograph, electrocardiogram, endomyocardial biopsy, nucleic acid based test

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9
Q

Tx: myocarditis

A

manage symptoms of CHF and arrhytmias (if mild, bed rest and observation)

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10
Q

swollen, tender parotid glands, sometimes accompanied by submandibular gland swelling with a prodrome of malaise and anorexia (1-2 days)

A

Mumps

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11
Q

-ssRNA genome, one serotype, incubation period is 14-18 days, paramyxoviridae family

A

Mumps virus

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12
Q

Age of onset of mumps

A

5-14 yrs (pre-vaccine era)

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13
Q

% of mumps infections that are asymptomatic

A

20%

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14
Q

Complications of mumps

A

meningitis, orchitis, deafness, myocarditis (very rare, often fatal)

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15
Q

how is mumps spread?

A

respiratory secretions, saliva, contaminated fomites

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16
Q

where is mumps spread to after primary viremia

A

salivary glands, testes, ovaries, pancreas, CNS

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17
Q

where is mumps spread to after secondary viremia

A

generalized spread to salivary and other glands and other body sites including the kidneys

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18
Q

Dx:

A

assay to detect viral genomes or serology

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19
Q

Tx: mumps

A

uncomplicated cases resolve on their own

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20
Q

Prevention of mumps

A

live attenuated vaccine (MMR/MMRV vaccine) intramuscular injection

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21
Q

MMRV stands for

A

mumps, measles, rubella, varicella

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22
Q

1st dose of MMRV

A

MMR + varicella for 12-15 month olds

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23
Q

2nd dose of MMRV

A

MMRV 4-6 yrs of age

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24
Q

Give 2 doses of mumps vaccination for adults who are at high risk which include

A

health-care workers, international travelers, students at post–high school educational institutions

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25
Q

cases of mumps are highest in which age group (even amongst vaccinated individuals)

A

18-24

26
Q

patients exhibit cutaneous lesions that are pink, purple, or brown in color, are non-painful, and can become confluent

A

Kaposi’s Sarcoma

27
Q

Cases with visceral lesions present with

A

weight loss or fever

28
Q

kaposi’s sarcoma lesions are caused by

A

increased proliferation of endothelial cells

29
Q

kaposi’s sarcoma histology

A

spindle cell morphology

30
Q

how many types of karposi’s sarcoma are there

A

4

31
Q

rare disease, middle eastern or mediterranean descent, few lesions, rarely life threatening

A

Classic KS

32
Q

equatorial africa, two forms-1 presents like classic KS, 2-aggressive form in pre-pubrescent children, often fatal within 3 years

A

Endemic KS

33
Q

occurs in individuals with immune system suppression after organ transplant, KS regresses after immunosuppressive therapy is discontinued

A

transplant-related KS

34
Q

more widespread lesions than other KS forms, may include other symptoms such as lymph node swelling, fever, weight loss, often fatal when lung involvement occurs

A

AIDS-related KS

35
Q

KS is caused by?

A

Human Herpes Virus 8 (Kaposi’s associated herpesvirus (KSHV))

36
Q

enveloped, dsDNA genome, latent state in KS lesions, contains several homologues of cellular genes (turn on proliferation)

A

human herpes virus 8 (causes kaposi’s sarcoma)

37
Q

KS leads to over proliferation due to

A

cellular homologues

38
Q

transmission of HHV-8/KS

A

blood borne, sexual and needle sharing

39
Q

other HHV-8 associated diseases

A

castleman’s disease, primary effusion lymphomas

40
Q

Tx: KS

A

control immune deficiency

41
Q

Why won’t antivirals have any affect on KS?

A

virus is in latent state in lesions

42
Q

Visceral lesions of KS Tx

A

chemotherapy, radiation, or surgery

43
Q

T-cell origin, presents with lymphadenopathy, hepatosplenomegaly, hypercalcemia, skininfiltration of tumor cells (papules, plaques, tumors, ulcers)

A

Adult T-cell Lymphoma

44
Q

flower cells are identifying for

A

ATL (T-cells)

45
Q

ATL is most common in

A

southern Japan, the Caribbean, and Central Africa

46
Q

median age of onset for ATL

A

55 years

47
Q

median survival time post diagnosis of ATL

A

7 months

48
Q

Dx of ATL

A

detection of antibodies to HUman T-cell leukemia virus 1 (HTLV-1)

49
Q

HAM/Tropic Spastic Paraparesis

A

HTLV-1 associated myelopathy

50
Q

Demyelination of neurons within the spinal cord-likely autoimmune

A

HAM

51
Q

HAM highest incidence in

A

adult women infected by HTLV-1

52
Q

stiff gait, lower extremity weakness, back pain, incontinence are symptoms of

A

HAM

53
Q

infects CD4/CD8 positive T cells

A

HTLV-1 (Human T-cell leukemia virus I)

54
Q

+ssRNA, reverse transcription, retrovirus, enveloped

A

HTLV-1

55
Q

HTLV-1 gets into cell via the

A

GLUT1 receptor

56
Q

has a similar life cycle to HIV

A

HTLV-1

57
Q

Time between infection with HTLV-1 and ATL development

A

30 years

58
Q

greastest risk of ATL

A

childhood transmission

59
Q

Transmission of HTLV-1

A

nursing, blood transfusion, sexual transmission (male to female more efficient)

60
Q

cell-associated virus

A

HTLV-1

61
Q

Tx: of ATL

A

combined chemotherapy (limited effectiveness)

62
Q

prevention of ATL

A

avoid nursing in endemic areas, screen blood supply, reduce unprotected sex

Microbiology (8 decks)

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