OP03 AIDS Flashcards

(43 cards)

1
Q

How does HIV fulfil Koch’s postulates as a cause of AIDS?

A

Epidemiological association
Isolation
Transmission pathogenesis

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2
Q

Read this slide on evidence that HIV causes AIDS - dont memorise

A

o AIDS and HIV infection are invariably linked in time, place and population group
o A single factor, HIV, predicts whether a person will develop AIDS,
o In cohort studies, severe immunosuppression and AIDS-defining illnesses occur almost exclusively in individuals who are HIV-infected
o Before HIV epidemic, AIDS-related diseases were rare in developed countries; today, they are common in HIV-infected individuals
o HIV can be detected in virtually everyone with AIDS.
o Newborn infants have no behavioural risk factors for AIDS, yet many children born to HIV-infected mothers have developed AIDS and died.
o The HIV-infected twin develops AIDS while the uninfected twin does not
o HIV causes the death and dysfunction of CD4+ T lymphocytes in vitro and in vivo.

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3
Q

What is the structure of HIV virus?

A

gp120 and gp41 attach to receptors in human cells
P17 makes the capsid envelope of the virus
P24
Inside is 2 pairs of RNA - integrase and reverse transcriptase

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4
Q

What do integrase and reverse transcriptase in the HIV virus do?

A

Integrase integrates the viral genome into human cells
Reverse transcriptase produces DNA at the expense of the RNA in the virus

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5
Q

How does HIV replicate?

A
  • Virus entry into host (into CD4, macrophages, Fc receptors) eg CD4 cells have chemokine receptors which HIV attaches to
  • Envelope and capsid attach to cell membrane and breakdown
  • RT and viral RNA are reverse transcribed into DNA
  • DNA integrated into host DNA using viral integrase
  • Host RNA polymerase transcribed viral DNA to create more RNA and RT. Translation of envelope, capsid and RT.
  • Assembly, and viral budding out of cells to infect other cells
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6
Q

What is the typical course of a HIV infection?

A

a) Transmitted through exchange of blood of bodily fluids: sexual contact, injection, perinatal
b) Primary acute infection with a characteristic clinical picture
c) Prolonged period without obvious visible symptoms
d) A severe immunodeficiency resulting in the development of secondary opportunistic infections and tumours that cause death in AIDS patients

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7
Q

Stages of HIV infection - time course

A
  • Primary HIV infection
  • 3-6 weeks: Acute HIV syndrome mononucleosis-like plasma viremia
  • 1week-3months: HIV-specific immune response, seroconversion
  • 1-2weeks: clinical latency, decline CD4 cell count, PGL
  • 10years: Clinically apparent disease, AIDS-defining illness, ARC
  • 2 years: Death from AIDS
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8
Q

What is seroconversion?

A

Immune system reacts to the presence of the virus and starts making antibodies to the virus

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9
Q

When can you detect the virus?

A

1 week - 3 months

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10
Q

What is PGL?

A

Persistent generalised lymphadenopathy = swollen palpable lymph nodes that persist in many places in the body

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11
Q

What are normal values for CD4 count?

A

500-1400/mm^3

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12
Q

What is the CD4 count in HIV and AIDS??

A

HIV: T-cell count 200-400/mm^3
AIDS: <200/mm^3

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13
Q

What are constitutional symptoms of AIDS?

A

Fever, weight loss, fatigure, night sweats, Diarrhoea, persistent generalised lymphadenopathy

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14
Q

AIDS defining conditions - what opportunistic infections can arise?

A

 Mycobacterium tuberculosis, avium intracellulare
 Pneumocystis carinii pneumonia
 Candidiasis (trachea, bronchi, lungs, oesophagus)
 Herpes simplex
 Cryptococcosis
 Cytomegalovirus
 Histoplasmosis
 Salmonella

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15
Q

AIDS defining conditions - what neoplastic disease can arise?

A

Kaposi’s sarcoma
Non-Hodgkin lymphoma
Cervical carcinoma

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16
Q

AIDS defining conditions - other

A

 HIV encephalopathy (AIDS dementia)
 Wasting syndrome due to HIV
 Thrombocytopoenic purpura
 Progressive multifocal leukoencephalopathy

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17
Q

What associated oral manifestations are there with AIDS? (doesn’t define but should make suspicious)

A

Candidal infections
Hairy leukoplakia
Kaposi’s sarcoma
AIDS related periodontal disease
ANUG
Recurrent herpetic infection
Other forms of malignant disease

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18
Q

What is the most frequent oral manifestation of HIV?

A

Candidal infections

19
Q

How does candida present in HIV/AIDS patients?

A

Pseudomembraneous in any site
Erythematous mostly in palate and tongue dorsum
Hyperplastic cheeks, commissures rarely involved (unlike in HIV-seronegative)

20
Q

What is hairy leukoplakia?

A

Asymptomatic white patch often found bilateral in the lateral border of the tongue, with hair-like corrugated appearance.

21
Q

What cells are involved in hairy leukoplakia?

A

No associated inflammatory cells due to depletion of the Langerhan’s cells (APCs)

22
Q

What is the aetiological virus causing hairy leukoplakia?

A

EBV is identifiable in epithelial cell nuclei

23
Q

Is hairy leukoplakia premalignant?

24
Q

How often in HIV patients does hairy leukoplakia occur?

A

20-30% of HIV patients, otherwise in other immunosuppressed patients

25
What is the cause and its role of Kaposi's sarcoma?
Human herpesvirus 8 - the suppression of the immune system by HIV allows its invasion
26
What is Kaposi's sarcoma?
Painless skin or mucosa patches red to violet Become larger and darker with time
27
Where are Kaposi's sarcoma commonly found?
Face - tip of nose Oral - palate > gingiva > tongue
28
What is the commonest tumour associated with HIV?
Kaposi's sarcoma
29
What is the histology of Kaposi's sarcoma?
Endothelial proliferation, cleft-like vascular channels, erythrocytes, hemosiderin, inflammatory cells, atypical spindle cells
30
What is the cure for Kaposi's sarcoma?
No cure, may respond to radio/chemotherapy
31
Whats the associated between HIV/AIDS and periodontal diseases?
(controversial, similar subgingival flora in HIV+ and HIV-) Increased attachment loss in HIV+ CD$ <200mm^3
32
What factors cause acute necrotising ulcerative gingivitis (ANUG)?
Immunosuppression/deficiency, stress, diet, bad hygiene, smoking
33
What microbes cause ANUG?
Fusospirochetal complex
34
How does ANUG present?
Necrosis of interdental papilla Pain, bleeding, metallic taste, marked halitosis Malaise, cervical adenopathy, fever
35
What happens to the oral cavity when ANUG is resolved?
Healing with disappearance of the interdental papillae
36
What happens in recurrent herpetic infection by HSV1 and/or HSV2?
Numerous vesicles that ulcerate Perioral lesions crusting (serum coagulation) - nail bed --> herpetic whitlow; eyes --> herpetic keratitis
37
What are the oral manifestations of recurrent herpetic infection?
Intraepithelial blister Ballooning degeneration
38
Where does the virus for recurrent herpes labialis lesions reside?
Trigeminal ganglion
39
How can HSV recur?
Mild infections, UV light, trauma, stress, menstruation, immunosuppression/deficiency
40
What other forms of malignant disease could be associated with AIDS?
Non-hodgkin lymphoma (EBV?) Kaposi's sarcoma Squamous cell carcinoma (tongue) Ano-rectal carcinoma (HPV)
41
What is HAART - highly active anti-retroviral therapy?
o Reverse transcriptase inhibitors (eg AZT) prevent RNA reverse transcription o Protease inhibitors prevent cleavage of newly synthesised HIV proteins o Some oral lesions might regress, warts tend to increase. Non-Hodgkin Lymphoma less likely to develop, increased cervical cancer o Dry mouth, oral melanosis, perioral dysaesthesia
42
Why does HAART usually fail?
o It is expensive (unavailable to most HIV+ in the world) o Possible poor compliance o Severe side effects o HIV resistance is becoming more common
43
What does malignant transformation in AIDS lead to?
The expression of cell-membrane antigens (CEA, alpha-fetoprotein, PSA)