Chapter 6 pt 4

Question 1

HIV affects B cells how?

Answer 1

HIV infected MO => release IL6 => B cell proliferation => can cause non-hodgkins lympnh (d.t EBV?)

Hypergammaglobinemia, but decreaese isotype switching

cannot mount immune response

Question 2

what is acute retroviral syndrome

sx?

Answer 2

flu like sx of HIV that occurs; 3-6 weeks after exposure and stops sponanteously 2-4 weeks after bc we reach viral set point

rash, cervical adenopathy, fever, weight loss, sore throat, V/D, malagia and fatigue

Question 3

What helps to predict how fast we go from HIV => AIDS?

Answer 3

viral set point

higher= earlier onset

Question 4

For clinical managment of HIV, blood levels of what are the most reliable SHORT TERM indicator of disease progression?

what is used to tell us when to start anti-retroviral therapy?

Answer 4

CD4+ T-cell counts

CD4+ Tcell counts

Question 5

Where are the sites of continuous HIV replication and cell destruction during the clinical latency period?

Answer 5

Spleen

LN

Question 6

Viral load at the end of the acute phase of HIV infection reflects which equilibrium?

How is this related to the prognosis?

Answer 6

the viral load we reach at the end of the acute phase is the equillibrium between the HIV and our body fighting it off

creates our viral set point, which tells us the progression of the disease and the rate if decline of DC4+ T cells

Question 7

Which test result would be the most reassuring of negative HIV?

Answer 7

negative HIV nucleic acid test (NAT)

Question 8

When do we see the following in our blood:

HIV RNA

HIV p24?

HIV Ab?

Answer 8

Day 11 (tested by NAT)

Day 17

Day 22; seroconversion occured and anti-HIV ab are present

Question 9

Pt reports feeling feverish abd body aches and he didn’t know if it was a stress response from anxiety. Which accounts for this phenomenon?

Answer 9

HIV viremic spike

Question 10

in HIV when does viremia occur

when do people start to serovonvert

Answer 10

7-14 days

7-21 days

Question 11

What occurs during chronic infection of HIV?

Answer 11

1. Clinical latency= no symptoms, but the virus is still replicating (mainly in LN and spleen)
2. CD4+ cells are declining

Question 12

how long does chronic infection last?

Answer 12

Typically, 7-10 years. but in fast progressors 2-3

Question 13

Ppl in clinical latency are assymotoms, but they can develop minor opportunisitc infections like?

Answer 13

oral/vaginal candidiathis,
herpes

autoimmune thromboctypenia

Question 14

• What are the clinical manifestations of AIDS?

Answer 14

opportunistic infections,
Kaposi sarcoma,
B-cell lymphomas,
CNS abnormalities

Question 15

When is someone said to have AIDS?

Answer 15

less than 200 CD4+ /mm3

Question 16

What accounts for the majority of deaths in patients with untreated AIDS?

Answer 16

Opportunistic infections

Question 17

Most common fungal infection in patients with AIDS?

Answer 17

Candidiasis

Other: Pneumocystis jirove

Question 18

CMV retinitis occurs almost exclusively in patients with?

what is affected

Answer 18

CD4+ T cell counts less than 50 per microliter =>

eyes and GI tract are effected

Question 19

Patients with AIDS have a high incidence of which tumors?

Answer 19

1. Kaposi sarcoma (KS)
2. B-cell lymphoma
3. Cervical squamous cancer (woman)
4. Anal cancer (men)

Question 20

Most common neoplasm in patients with AIDS?

Caused by what virus

Answer 20

• Kaposi Sarcoma, a vascular tumor

- Human herpes`virus 8 (HHV8)

Question 21

Immune reconstitution inflammatory syndrome may occur with what?

Answer 21

HAaHAART treatment given to some patients with advanced disease

Question 22

What are the adverse side effects of HAART?

Answer 22

• Lipoatrophy (loss of facial fat)
• Lipoaccumulation (excess fat deposition centrally)
• high lipids
• Insulin resistance
• Peripheral neuropathy
• Premature cardiovascular, kidney, and liver disease

-

Question 23

What are the adverse side effects of HAART?

combo of 3 drugs that blocks HIV; can supress viral levels bwloe detected, stop loss of CD4+ cells and overtime, increase them to normal

Answer 23

• Lipoatrophy (loss of facial fat)
• Lipoaccumulation (excess fat deposition centrally)
• high lipids
• Insulin resistance
• Peripheral neuropathy
• Premature cardiovascular, kidney, and liver disease

-

Question 24

• How is amyloidosis characterized?

Answer 24

amyloidosis is a disorder characterized by the extracellular deposits of misfolded proteins that aggregate => insoluble fibrils

Question 25

• What are the three ways that proteins may deposit as amyloid?

Answer 25

1. make too many proteins that are prone to misfolding and aggregation
2. mutations that make proteins that cannot fold properly and tend to aggregate
3. defective or incomplete proteolytic degradation of extracellular proteins

Question 26

• How do amyloid deposits damage tissue?

Answer 26

• pressure atrophy

Question 27

• Do amyloids evoke an inflammatory response?

Answer 27

• No