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Infectious Disease > HIV: diagnosis and management > Flashcards

HIV: diagnosis and management Flashcards

1
Q

What is the leading infectious cause of death worldwide?

A
  • HIV
  • it is a global pandemic
  • spreading most rapidly in Asia
    U.S. has > 1 mill infected, 25% unaware of infection
  • Resurgence in U.S. among MSM: blacks and hispanics
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2
Q

Mode of transmission of HIV

A

similar to Hep B
- sexual, parenteral, and vertical (perinatal)
Through body fluids: blood products, semen, vaginal fluids, and breast milk

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3
Q

relative risk per encounter

A
  • *receptive anal intercourse: 1:30-1:100
  • insertive anal intercourse: 1:1000
  • Receptive vaginal intercourse: 1:1000
  • insertive vaginal intercourse: 1: 10,000
  • Receptive fellatio: 1:1000
  • *Needlestick from known HIV + source: 1:300
  • *IVDU sharing needles: 1:150
  • Blood transfusion w/ HIV + blood: 95%
  • vertical spread: 25%
  • decreased use of safer sex practices among MSM causing increase in cases
  • increased use of meth among MSM coupled with unsafe practices shows resurgence in this group
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4
Q

How many people are living with HIV in Montana?

A
  • 496

- 22 new cases of HIV since 2009

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5
Q

Where is AIDs spreading the fastest?

A
  • spreading fastest in Asia

- largest infection rate is in Africa

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6
Q

Why is there a new increase in number of HIV positive people in the U.S.?

A
  • because infected are living longer due to HAART
  • sex practices among high risk groups are worsening again
  • % of new infections is growing fastest in females compared with males
  • Hispanics and Blacks in America are disproportionately affected:
    higher risk if IVDU
    higher risk of “closet” MSM behavior
    Poorest medical care and compliance with HAART
    more homeless and less support system
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7
Q

What is the difference between HIV and AIDs?

A

Both are the result of the retrovirus, HIV. When CD4 count gets to a certain low point it is considered AIDs , this usually takes an average of 10 years (w/o tx) to progress to AIDs. So they are just different phases of the disease.

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8
Q

What is HIV?

A
  • Human Immunodeficiency Virus
  • retrovirus, RNA virus capable of infecting cells and with RNA transcriptase is capable of developing ds DNA that is identical to RNA -> rapidly produce viruses once in cell.
  • HIV invades the helper T cells to replicate itself
  • No cure
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9
Q

What is AIDs?

A
  • Acquired Immunodeficiency syndrome
  • HIV is the virus that causes AIDs
  • disease limits the body’s ability to fight infection
  • A person with AIDs has a very weak immune system
  • No cure
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10
Q

increase likelihood of contracting HIV if you?

A
  • sharing needles w/o sterilization
  • intercourse, oral, and anal
  • mother to baby: before birth -> rupture in the placenta (mixing of maternal and fetal blood), during birth and after birth (through breast milk)
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11
Q

Stage 1 of HIV (primary stage)

A
  • short, flu-like illness, occurs 1-6 weeks after infection
  • no sxs at all
  • infected person can infect other people ( probably highest chance b/c of millions of viruses in blood during this phase)
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12
Q

Stage 2 of HIV

A
  • asymptomatic
  • lasts for an avg of 10 years
  • may be swollen glands
  • level of HIV in blood drops to very low levels (b/c it is in the CD4 T cells, highest number of these are in the gut)
  • HIV abs are detectable in blood, ags may detectable too
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13
Q

Stage 3 of HIV - symptomatic

A
  • sxs are mild
  • immune system deteriorates
  • emergence of opportunistic infections and cancers
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14
Q

Pathogenesis of HIV virus

A
  • retrovirus affects CD4 T-cells, macrophages, and dendritic cells
  • reverse transcription of viral RNA genome into dsDNA occurs
  • imported into cell nucleus and integrated into cellular DNA
  • After entering the body, rapid viral replication up to several million virus particles/ml blood
  • this is accompanies by drop on CD4 T cells and activation of CD 8 T cells -> to kill HIV infected cells
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15
Q

What does HIV target?

A
  • selectively targets CD4 helper T cells
  • also infects B cells and macrophages (infected macrophages will be impt in CNS sxs)
  • Acute infection results in over 10 billion HIV visions being produced/day
  • T cells become non-fxnl following infection therefore there is a qualitative defect in T cells which overshadows the simple quantitative defect
  • **the infection of B cells, T cells and macrophages results in a mixed immunodeficiency
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16
Q

What are the 3 mechanisms that will cause a clinical presentation of the syndrome?

A
  • Immunodeficiency: direct result of immunosupression, spectrum of infections and neoplasms, very low incidence of certain infections seen in other causes of immunodeficiency (listeriosis, aspergillosis), higher incidence of other infections (Kaposi’s sarcoma)
  • Autoimmunity: lymphocytic infiltrate of organs (lymphocyte interstitial pneumonitis), auto production (immunologic thrombocytopenia)
  • Allergy/Hypersensitivity rxns: higher rates of allergic runs to unknown allergens (eosinophilic pustular folliculitis), increased rates of hypersensitivity to meds
17
Q

HIV is a continuum, what are the 4 phases of it?

A
  • primary HIV infection
  • asymptomatic infection
  • symptomatic infection
  • AIDs
  • the length and severity of each phase is dependent on host and virus->
    use of antiretroviral therapy
    use of chemoprophylaxis for opportunistic infections

generally: primary - 3-14 days, asymptomatic - 4-8 years, symptomatic - 4-8 years, AIDs os 2-20 years

18
Q

Clinical presentation of primary infection

A
  • brief, mono type of illness
    sxs: fever, sweats, lethargy, malaise, myalgias, arthralgias, HAs, photophobia, diarrhea, sore throat, lymphadenopathy, truncal maculopapular rash
  • sudden onset ( lasts 3-14 days)
  • more than 50% of HIV pts have sxs of primary infection
  • most common neuro sxs: are HA and photophobia
  • most commonly seen sx in all HIV pts is gen. lymphadenopathy
19
Q

Clinical presentation of the asymptomatic phase

A
  • longest of the 4 phases
  • most variable of the 4 phases
  • w/o tx, lasts 4-8 years
  • lack of overt evidence of HIV disease
  • only evidence is sero-positivity
  • pts can easily spread the disease w/o knowing b/c of being asymptomatic
20
Q

Clinical presentation of symptomatic seropositivity (still HIV)

A
  • onset ushers in 1st physical evidence of immune dysfunction
  • persistent gen. lymphadenopathy
  • localized fungal infections: toes, fingernails, mouth, women with recurrent vaginal candidiasis or trichomonal infections
  • oral hairy leukoplakia ( one of most commonly missed signs of HIV) is very prevalent
  • cutaneous manifestations include widespread warts, molluscum, psoriasis, and seborrheic dermatitis, multidermational zoster, and herpes simplex
  • night sweats, wt loss, and diarrhea
21
Q

Clinical presentation of AIDS in general:

A
  • PEs are often normal
  • abnormal physical findings may be non-specific
  • HIV/AIDs is a multi-system disease and therefore a complete H & P becomes very important
  • the official dx of AIDs reqrs a combo of factors based on WHO/CDC guidelines
  • Bottom line: Any “AIDS defining illness” regardless of CD4 count or other opportunistic infections with CD4 count less than 500 is dx
  • Generally best to look past effect on systems
22
Q

Systemic clinical presentation of AIDS

A
  • fever, night sweats, and wt loss
  • persistent fever w/o focal signs requires work up:
    blood cultures, chest X-ray, sinus imaging
  • WT loss: can be quite severe and is generally muscle mass loss.
    anorexia, nausea, vomiting and diarrhea add to wt loss
  • increased metabolic rate due to virus compounds the problem
  • growth hormone and anabolic steroids are used to try to get wt back and marijuana is used for nausea (or rx: dronabinol)
23
Q

Pulmonary clincal presentation of AIDS

A
  • pneumocystis pneumonia is the most common opportunistic infection seen in AIDs (people w/o AIDs don’t get this)
  • community acquired pneumonia is most common cause of pulmonary disease in HIV infected pt: bacterial, mycobacterial, and viral
  • TB occurs in 4% of HIV + people in US
  • non-infectious causes of lung disease: kaposi’s, non-Hodgkins lymphoma, interstitial pneumonitis
  • sinusitis: both acute and chronic
24
Q

CNS clinical presentation of AIDS

A
  • toxoplasmosis: most common space occupying lesion in HIV, focal near deficits, seizures, altered mental status, dx by CT or MRI
  • CNS lymphoma: 2nd most common space occupying lesion in HIV, imaging may be able to differentiate, may need brain bx
  • AIDs dementia complex: dx of exclusion based on brain imaging and CSF eval, difficulty w/ cognitive skills and diminished motor speed, sxs may wax and wane
25
Q

CNS clinical presentation of AIDS continued……

A
  • cryptococcal meningitis: fever and HA w/ less than 20% having meningismus, dx based on + latex agglutination of CSF, + latex agglutination (CRAG) of serum is + in 70-90%
  • HIV myelopathy: leg weakness and incontinence due to spinal cord impairment, spastic paresis and ataxia are seen on PE, dx of exclusion so need LP, and MRI
  • Progressive multifocal leukoencephalopathy (PML): viral infection of white matter of the brain, aphasia, hemiparesis, and cortical blindness
26
Q

PNS clinical presentation of AIDS

A
  • inflammatory demyelinating polyneuropathy: similar to Guillan-Barre
  • Transverse myelitis due to herpes zoster or CMV
  • Peripherial neuropathy common in many HIV pts: numbness, tingling, pain in LEs, ***may be drug induced due to some HAART drugs
  • CMV can cause an ascending polyradiculopathy: LE weakness, neutrophilic ploeocytosis in CSF with negative bacterial cultures
27
Q

Rheumatologic manifestations in AIDS

A
  • Arthritis is very common (may look like RA)
    single or mult. joints, w/ or w/o effusions, involvement of large joints most common
  • several inflammatory syndromes have been reported: Reiter’s syndrome, psoriatic arthritis, SICCA syndrome (dry eyes and mouth), SLE
  • Avascular necrosis of femoral head
28
Q

Ocular manifestations of AIDS

A
  • complaints of visual changes must be evaluated in +HIV pt
  • CMV retinitis: perivascular hemorrhages and white fluffy exudates, most common retinal infection in HIV and is rapidly progressive, need immediate referral to ophtho
  • Herpes infection common
  • toxoplasmosis is frequently recurrent
29
Q

GI manifestations in AIDS

A
  • candidal esophagitis: very common in HIV pts, suggestive sxs are treated and only non-responsive pts are given endoscopy
  • hepatic disease: autopsy shows liver is very frequent site for disease/neoplasms, many of these are subclinical, co-infection with Hep B and C is common, low-level hepatic disease may be cause for persistent N/V
  • Biliary Disease: acalculous cholecystitis with sclerosing cholangitis
  • Enterocolitis: very common in HIV pts, may be due directly to HIV macrophage infection, secondary causes include bacteria, viruses, and protozoans. More severe and chronic sxs than non-HIV pts, may present with high fever and severe abdominal pain. Need repeat stool cultures and stool for ova and parasites. If repeat stool studies negative, endoscopy is indicated. Sxs for > 1 month and no identifiable cause, presumptive for AIDS enteropathy
30
Q

Skin manifestations in AIDS

A
  • HSV infection: occur more frequently and tend to be more severe, due to risk of dissemination, all must be treated with oral medications
  • Herpes zoster: occur more frequently and tend to be more severe, due to risk of dissemination, all must be treated with oral meds
  • Molluscum contagiosum: tend to spread widely, doesn’t disseminate, tx with liquid nitrogen
  • Folliculitis/Furuncles: staph most common bacterial cause of skin infections in HIV pts, due to risk of dissemination, must tx aggressively. Always assume it is MRSA- tx accordingly
  • Bacillary angiomatosis: Bartonella henselae and Bartonella quintana, zoonotic infection from fleas of domesticated cats, raised, red, high vesicular lesions that can mimic Kaposi’s, fever is common with bone, lymph node and liver involvement (more flesh-violet colored)
31
Q

HIV malignancies of AIDS

A
  • Kaposi’s sarcoma: lesions may appear anywhere, careful exam of eyelids, conjunctiva, pinnae, palate and toe webs. Visceral disease will present in 40% of pts with skin lesions
  • Non-Hodgkin’s lymphoma: usually of B-cell origin and are large cell tumors ( kids -> Burkitt’s lymphoma), >70% are extra nodal, depending on advancement of disease and CD4 count, prognosis may be for only few months survival
32
Q

GYN manifestations on AIDS

A
  • recurrent vaginal candidiasis is very common
  • cervical dysplasia is present in >40% of women -> pap every 6 months
  • Cervical neoplasia much more aggressive in HIV+, most women die from cervical cancer, not HIV, cervical neoplasia is so common in HIV, added to CDC definition of AIDS in 1995
  • PID: more common in HIV women, bacteria are same as those seen in non-HIV women
33
Q

T cell activation: co–stimulation

A
  • requires T cell binding to other surface receptors on an APC: dendritic cells and macrophages produce surface B7 proteins when innate defenses are mobilized, B7 binding with CD28 receptor on T cell is crucial co-stim signal, Cytokines: interleukin 1 and 2 from APC’s or T cells, trigger proliferation and differentiation of activated T cell w/o co-stimulation anergy (no rxn to AG) occurs:
  • T cells become tolerate to AG, are unable to divide, don’t secrete cytokines
  • T cels that are activated: enlarge, proliferate, and form clones, differentiate and perform functions according to their T cell class
34
Q

When does primary T cell response peak?

A
  • within a week
  • T cell apoptosis occurs b/t days 7 and 30
  • effector activity wanes as amount of ag declines
  • benefits of apoptosis: activated T cells are a hazard
  • memory T cells remain and mediate secondary responses
35
Q

Cytokines

A
  • mediate cell development, differentiation, and responses in the immune system
  • include interleukins and interferons
  • IL-1 released by macrophages co-stimulates bound T cells
  • IL-2 is a key growth factor, acting on cells that release it and other T cells
  • Other cytokines and or cheekiness (CCR5) amplify and regulate innate and adaptive responses
36
Q

Roles of Helper T cells

A
  • play a central role in the adaptive immune response
  • once primed by APC presentation of AG, they:
    help activate T and B cells, induce T and B cell proliferation, activate macrophages and recruit other immune cells
  • w/o Th there is no immune response
37
Q

Roles of Cytotoxic T cells

A
  • directly attack and kill other cells
  • activated T c cells circulate in blood and lymph and lymphoid organs in search of body cells displaying AG they recognize
  • targets:
    virus-infected cells
    cells w/ intracellular bacteria or parasites
    cancer cells
    foreign cells (transfusion or transplants)
38
Q

Natural killer cells

A
  • recognize other signs of abnormality:
    lack of class 1 MHC
    AB coating a target cell
    different surface marker on stressed cells
  • Use the same key mechanisms as Tc cells for killing their target cells
39
Q

Regulatory T cells

A
  • dampen the immune response by direct contact or inhibitory cytokines
  • important in preventing autoimmune reactions

Infectious Disease (27 decks)

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