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X Clin Med III Exam 2 > HIV, Syphilis and STDs > Flashcards

HIV, Syphilis and STDs Flashcards

1
Q

What is HIV itself?

A

Retrovirus that uses reverse transcriptase for reverse transcription (turning RNA into DNA) to integrate material into host cell DNA and new virus is produced

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2
Q

What is responsible for AIDS?

A

HIV-1

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3
Q

What does HIV target?

A 
T cells (particularly CD4 T cells the helpers)
Also infects B lymphocytes and macrophages
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4
Q

What are lymphocytes?

A

WBCs that defend against protozoa, fungi, some bacteria and viruses

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5
Q

Routes of HIV transmission

A

Sexual transmission (infected body fluids)
Injection drug use
Occupational injury (needlestick)
Blood products
HIV mom to infant
(not just casual contact)
*receptive anal intercourse has highest risk of transmission

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6
Q

What is another name for primary HIV infection?

A

Acute HIV/ acute retroviral syndrome

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7
Q

What is acute HIV?

A

2-6 wks after exposure

Mono like or flu like illness (about 2 wks and resolves spontaneously)

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8
Q

Why is acute HIV missed?

A

Routine HIV Ab test is negative so miss it

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9
Q

Lab for acute HIV

A

HIV RNA (viral load( is measurable and usually extremely high >100,000

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10
Q

Common sxs of acute HIV

A

Fever, adenopathy, sore throat, rash and mucocutaneous ulcers, myalgia, arthralgia, HA, diarrhea, n/v

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11
Q

What does the rash look like in acute HIV?

A

Half of pts

Upper trunk, neck and face

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12
Q

Lab abnormalities in acute HIV

A

Elevated transaminases (LFTs)
Leukopenia
Anemia
Thrombocytopenia

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13
Q

When does clinical latency occur?

A

When immune system response to infection (acute illness resolves) and pt seroconverts!!! and becomes antibody positive
Viral load decreases to a set point
CD4 t cell count slowly declines

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14
Q

When do you see full symptomatic infection of HIV?

A

When immune system deteriorates:

  • Lymphnodes and tissue damaged from burnt out
  • Virus may mutate and become more pathogenic
  • Body fails to keep up replacement of CD4
  • viral load increases
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15
Q

All general sxs of HIV

A

Fever, night sweats, LAD, fatigue, arthralgias, weight loss, oral hairy leukoplakia or thrush, prolonged diarrhes, cervical dysplasia, skin disorders, Kaposis, ITP

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16
Q

Normal CD4 t cell count

A

500-1400 cell/mcL

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17
Q

What is the definition when HIV progresses to AIDS?

A

CD4 T cell count <200 cells/mcL
OR
HIV and 1 of 27 AIDS defining conditions (regardless of T cell count)

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18
Q

Types of AIDS defining conditions

A 
PCP
Toxoplasmosis
MAC
CMV
Candidiasis
Kaposis sarcoma
Cervical cancer
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19
Q

What is pneumocystic jiroveci pneumonia?

A

Common opportunistic infection associated with AIDS
Caused by airborne fungus pneumocystis jiroveci
Reactivated dormant infection

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20
Q

Presentation of pneumocystic jiroveci pneumonia

A

Nonspecific: fever, cough, SOB
May have severe hypoxemia (usually younger 20-30)
CXR shows diffuse or perihilar infiltrates

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21
Q

How to diagnose pneumocystic jiroveci pneumonia

A

Sputum sample: see elevated LDH in most

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22
Q

Tx for pneumocystic jiroveci pneumonia

A

Bactrim and supportive

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23
Q

What does toxoplasmosis cause?

A

Encephalitis (most common intracranial lesion in HIV pts)

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24
Q

What causes toxoplasmosis?

A

Single celled parasite toxoplasma gondii

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25
Q

How to get toxoplasmosis

A

Ingestion of cat feces, contaminated rw food or utensils

Immuncompetent doesn’t usually have pts

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26
Q

Presentation of toxoplasmosis in HIV pt

A

HA, focal neurological deficits, seizures, AMS

Maybe retinits or pneumonitis

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27
Q

Imaging for toxoplasmosis

A

Multiple contrast enhancing lesions on brain CT or MRI

Also seropositive for toxoplasmosis

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28
Q

Mycobacterium avium complex

A

May cause pulm infection when immunocompetent

Found in soil or dust inhaled

29
Q

Presentation of MAC

A

Systemic disease in HIV

Night sweats, weight loss, abd pain, diarrhea, anemia

30
Q

How to diagnose MAC

A

Sputum acid fast bacillus stain positive

Positive sputum and blood cultures

31
Q

Most common retinal infection in AIDs

A

CMV retinitis

32
Q

What is CMV?

A

Herpes virus in general pop (blood, sexually transmittesd, perinatally)

33
Q

Presentation of CMV retinitis

A

Visual disturbances

Can cause blindness when untreated

34
Q

How to diagnose CMV retinitis

A

Perivascular hemorrhages and white fluffy exudates on fundoscopic
Seropositive for CMV

35
Q

Candida and CD4

A

More invasive the candida (like into trachea) the lower the associated CD4 t cell count

36
Q

What CD4 count does kaposis sarcoma occur at?

A

ANY

37
Q

When is kaposis seen classically?

A

Elderly eastern european and mediterranean males

38
Q

When is aids related kaposis sesn most?

A

Homosexual men (lesions multifocal and widespread with LAD)

39
Q

When do you screen for HIV?

A 
Everyone 13-64: voluntary opt out
Anyone in whom TB tx is being initiated
At each presentation for STD
Pts at risk (MSM)
Pregnant
40
Q

Most common screening and diagnostic testing for HIV

A

Combo HIV antibody (4-12 wks after infection-after seroconversion) and antigen (won’t miss the acute) testing

41
Q

Who is treated with antiretroviral therapy?

A

All with HIV, even those in acute infection

42
Q

When to start post exposure prophylaxis for HIV?

A

Within 72 hrs

43
Q

When do people do well usually with CD4

A

> 350

44
Q

Medication based on CD4 count <200

A

Bactrim DS (prophylaxis for PCP)

45
Q

Medication based on CD4 count <100

A

Bactrim DS (prophylaxis for toxoplasma encephalitis)

46
Q

Medication based on CD4 count <50

A

Azithromycin (for disseminated mycobacterim avium complex)

47
Q

What causes syphilis?

A

Treponema pallidum

48
Q

Stages of syphilis

A 
Primary
Secondary
Latent
Tertiary
Neurosyphilis
Ocular syphilis
49
Q

Presentation of primary syphilis

A

Painless chancre that appears at location where syph entered body (4-6 wks)

50
Q

Presentation of secondary syphilis

A

Rash (COMMON): non-pruritis, palms and soles of feet, not contagious
Condyloma lata
Mucous patches: painless flat patches (infectious)
May have malaise LAD
2-6 wks

51
Q

What is condyloma lata?

A

Moist, heaped, wart-like papules
Occur in intertriginous areas (gluteal folds, perianal area)
Contagious

52
Q

Latent phase of syphilis

A

Asymptomatic
No longer sexually transmittable
Years

53
Q

Presentation of tertiary syphilis

A

Most don’t get this (more in untreated)
10-30 yrs after infection
Damage heart, bvs, nervous system

54
Q

What is neurosyphilis?

A

Any stage

Paralysis, difficulty with coordination, dementia

55
Q

What is ocular syphilis?

A

Any stage

Changes in vision or blindness

56
Q

Diagnosis of syphilis

A

Rapid plasma reagin (RPR) or venereal disease lab test (VDRL)–antibody with titer (low may be false positive)

57
Q

What to do to confirm RPR?

A

Treponemal antibody test (FTA-ABS)

58
Q

What to do is suspect neurosyphilis or ocular syphilis?

A

LP (lumbar puncture) or VDRL on spinal fluid to confirm

59
Q

What to do after treat pt for syphilis

A

Confirm success with RPR titer at 3, 6, 12 and 24 mos

4 fold decrease is good response

60
Q

Congenital syphilis

A

Untreated syph in pregnancy can lead to stillbirth, neonatal death, deafness, neuro impairment and bone deformities

61
Q

How to prevent congenital syphilis

A

Screen pregnant woman at 1st prenatal visit

If high risk, screen and get sex history at 28 wks and delivery

62
Q

What causes lymphogranuloma venereum?

A

Chlamydia trachomatic

63
Q

Presentation of lymphogranuloma venereum

A

Unilateral inguinal bubo
Self limited gential ulcer or papule at site of innoculation
Anal discharge and rectal bleeding

64
Q

How to diagnose lymphogranuloma venereum

A

R/o syph
Contact health dept
Maybe specimen swab

65
Q

Tx for lymphogranuloma venereum

A

Erythro or doxy

66
Q

What causes chancroid

A

Haemophilus ducreyi

67
Q

Presentation of chancroid

A

Painful tender genital ulcer
Lesions with foul-smelling discharge
Inguinal adenitis

68
Q

Diagnose chancroid

A

R/o syph and HSV

Contact county health (special culture)

69
Q

Tx for chancroid

A

Azithro, ceftriaxone, cipro

X Clin Med III Exam 2 (9 decks)

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