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Infectious Disease > ID Exam 2 Immunodeficiency and HIV > Flashcards

ID Exam 2 Immunodeficiency and HIV Flashcards

1
Q

Immunodeficiency = increased incidence and severity of

A
  1. Infection (change in effector)
  2. Malignancy (change in effector)
  3. Autoimmunity (change in regulatory)
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2
Q

Opportunistic pathogens

A 
PCP
Aspergillus, CNS toxo
Listeria
Nocardia
Crytptococcus and sporidium
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3
Q

4 components of immune function

A

Anatomic (skin, mucus)
Phagocytic (PMNs, macs)
Cell mediated: T cells
Humoral: B cells

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4
Q

Public vs. private phenotypes

A

Public: multiple infections with multiple organisms
Ex: agamma, SCID
Private: susceptibility to one infection
Ex: Xlinked lymphoprolif syn (EBV), TLR-3 d/o (HSV encephalitis)

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5
Q

Sources of immunodeficency

A 
Malnutrition
HIV/AIDS
Age
Other (meds, transplant)
Primary
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6
Q

Compromise: primary, secondary, pathogen
Skin
Lung
GI/oral

A

Skin: 1˚ eczema 2˚ burns (pseudo), IV lines -> S. aureus
Lung: 1˚ CF 2˚ post-viral -> pseudo, staph, strep
GI/oral: chemo rx -> e coli, candida

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7
Q 
Chronic granulomatous disease (phagocytic source of immunodeficency:
mech
s/sx
pathogens
dx test
A

Normal phagocyte number but NADPH ox defect
Recurrent skin abscesses, prolonged pneumo, bone
S. aureus, serratia, nocardia, salmonella, aspergillus
NBT test of PMN

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8
Q

Decreased cell mediated immunity

A 
Malnutrition
Oral steroids
Immunotherapy
Chemotherapy
Transplant
HIV/AIDS
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9
Q

Antibody isotype and recognition

A

IgG1: proteins
IgG2: polysaccharide capsule
IgM: blood
IgA: mucosal

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10
Q

Primary antibody deficiencies

A 
IgA deficiency
CVID (low total immunoglobulins)
IgG2 deficiency
Hyper IgE (Job's)
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11
Q

Secondary antibody deficiencies

A

CLL
Multiple myeloma
Renal and GI loss (of ab)

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12
Q

Complement defects and bugs

A

C2 most common
C1-4 (classical): pyogenics
C5-9 (terminal): Neisseria (MAC complex)

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13
Q

CD4 counts in HIV/AIDS

A

> 500: good
200-500: intermediate
<200: advanced, AIDS

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14
Q

What are TRECs?

A

T cell excision circles
Pieces of DNA cut out during intrathymic T cell gene rearrangement
VDJ recombination leads to variation in T cell receptor and excision of TRECs
No TRECs = not making new T cells receptors
Therefore immunodeficient

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15
Q

What if TRECs are low?

A 
Repeat assay
Flow cyto to check different types of T and B cells
CD3, 4, 8 (T cells)
CD16,56 (NK cells)
CD19, 20 (B cells)
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16
Q

Sites for block in lymphocyte development

A

T and B cell receptor re-arrangment
Signaling (cytokines)
Purine metabolism

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17
Q

Newborn screen criteria

A 
Serious
Detectable
Incidence
Treatment and treatment leads to better prognosis
Cost effective to screen
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18
Q

Newborn screen criteria

A 
Serious
Detectable
Incidence
Treatment and treatment leads to better prognosis
Cost effective to screen
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19
Q

S/Sx of immunodeficiency in kids

A 
Failure to thrive
Diarrhea
Opportunistic infections
Absence of lymphoid tissue
Absent thymus on CXR
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20
Q

SCID Treatment

A

Bone marrow transplant

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21
Q

Dx criteria fo CVID

A

Recurrent sinopulm infections
>4 years old
Marked decreased of IgG and IgA with or without low IgM (on two occasions)
Poor vaccine response
B cell phenotype suggests arrest of maturation (no memory)
No profound CD4 defects
R/o 2˚ hypogamma

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22
Q

CVID treatment

A

IVIG

Pulse steroids

23
Q

Types of retroviruses

A

Oncoviruses (HTLV)
Lentiviruses (HIV)
Spumaviruses
Endogenous retroviruses (HERV- autoimmuno assoc.)

24
Q

Retrovirus structural proteins

A

Envelop (gp 41, 120) (wizard pipe, transmem and outer)
Matrix (p17) -> Gag
Capsid (p24) -> Gag (sundial on hat)

25
Retroviral enzymes and encoding gene
Reverse transcriptase (inhibited by AZT) (spell book) Integrase (integrate into host DNA) Protease (produce mature virion, inhibited by ritonavir) Encoded by pol (Paul's Smithy)
26
HIV accessory genes (outside Gag, pol)
Tat: transactivator (Tax in HTLV) Rev: nuclear exporter (Rex in HTLV)
27
Long terminal repeats
cis elements required for: | RT, gene transcription, integration, packaging etc
28
AIDS defining cancer (viral co-infections)
Kaposi's sarcoma (HHV-8) Non-hodgkin's lymphoma (EBV, HHV-8) Cervical cancer (HPV) Have all decreased incidence (compared to anal, lung, liver)
29
HIV positive vs negative cancer presentation | Contributing factors
``` Develops younger Faster progression Atypical pathology More aggressive, poorer outcomes Higher rate of relapse ``` ``` Behavioral risk factors (MSM) Direct effects of HIV 1. Tat transactivation of proto-oncogenes 2. Suppression of p53 3. Pro-angiogenesis ```
30
Should HAART be continued through chemo?
Yes, but pick chemo agents to avoid exacerbation toxicities
31
HTLV
Infects T lymphs | Causes lymphoproliferative disorders
32
HTLV associated diseases
Adult T cell leukemia/lymphoma HTLV assoc myelopathy (HAM, tropical spastic paralysis) Uveitis
33
HTLV associated myelopahty (HAM)
Resembles MS | Possible autoimmune destruction of neural cells
34
What influences if HTLV will produce ATL or HAM?
Immune response: Evasion -> ATL (minimal Tax) Strong reaction -> HAM (increased Tax)
35
Important HIV genes
Gag: matrix (p17), capsid (p24) Pol: RT, protease Env: envelope (gp 41, 120)
36
Important HIV drug target via gene
Pol: RT -> NRTI (phos required), NNRTI Pol: protease -> -navir Pol: integrase -> raltegravir (HALTegravir, halt at the nuc) Env: gp 120 -> maraviroc (CCR5 inhib) Env: gp 41 -> enfuviritide (fusion inhib)
37
Natural history of illness in HIV and CD4 counts
>200: Thrush, oral hairy leuko, TB <200: PCP, histo, toxo, crypto <100: esophagitis due to candida <50: CMV, MB avium
38
T Cell receptors important in HIV | Mutations
CD4 CCR5 (early bind) CXCR4 (late bind) CCR5 delta32 mutation: increased resistance and improved prognosis
39
1˚ infection and s/sx
Mono-like with or without asceptic meningitis 2-3 wks post exposure 50% unrecognized S/Sx: maculopapular rash, oral ulcers, mono sx
40
Classic HIV opportunistic infections
Kaposi's Thrush (extension into esophagus) CMV retinitis CNS toxoplasmosis (ring enhancing abcess w/ edema)
41
Factors that contribute to HIV evolution/resistance
Genetic diversity (lots of mutations) Fast replication rate Selective pressures Therefore use multi-drug therapy
42
Pre-exposure prophylaxis
HIV negative patient using treatment | Tenofovir DF-emtricitabine
43
Post-exposure prophylaxis
is a thing. Rad.
44
Basic principle of HAART
Backbone of 2 NRTI Plus base of integrase inhibitor (RALTegravir) Base can also be NNRTI or protease inhibitor
45
PEP Recommendations
Started within 72 hours Continued for 4 weeks Follow up ab testing at 4 weeks up to 6 months
46
NRTI examples and mechanism of action
``` Lamivudine Zidovudine Stavudine Didanosine Abacavir Emtricitabine All activated by intracellular kinase: nucleoSIDE, bind/block RT Tenofovir: nucleoTIDE Tenofovir alafenamide: better plasma levels, less AR ```
47
NRTI side effects
``` Mito tox Anemia Granulocytopenia Neuropathy (stocking, glove) Lactic acidosis ```
48
NNRTI examples and mechanism of action
Eevirapine Efavirenz Delaviradine Not activated by kinase, bind and block RT
49
HIV protease inhibitors
-avir Indinavir Ritonovir (can boost other levels via CYP inhib) Darunavir (rash and SJS) Resistance is harder, need multiple mutations
50
HIV PI side effects
``` GI intolerance Central adiposity Hyperglycemia Hyperlipidemia Kidney stones with indinavir ```
51
Integrase inhibitors
-gravir Raltegravir Dolutegravir (high resistance to mutations) Elvitegravir (CYP3A4 substrate, admin with booster) GReat compared to protease inhibitors (AVIR)
52
Integrase inhibitors side effects
WELL TOLERATED | Other than maybe some rhabdo
53
Entry inhibitors
Maraviroc: CCR5 binder/inhibitor (co-receptor binding) Enfuvirtide: gp41 inhibitor (fusion inhibitor)

Infectious Disease (13 decks)

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