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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
Q

Retroviral enzymes and encoding gene

A

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
Q

HIV accessory genes (outside Gag, pol)

A

Tat: transactivator (Tax in HTLV)
Rev: nuclear exporter (Rex in HTLV)

27
Q

Long terminal repeats

A

cis elements required for:

RT, gene transcription, integration, packaging etc

28
Q

AIDS defining cancer (viral co-infections)

A

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
Q

HIV positive vs negative cancer presentation

Contributing factors

A 
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
Q

Should HAART be continued through chemo?

A

Yes, but pick chemo agents to avoid exacerbation toxicities

31
Q

HTLV

A

Infects T lymphs

Causes lymphoproliferative disorders

32
Q

HTLV associated diseases

A

Adult T cell leukemia/lymphoma
HTLV assoc myelopathy (HAM, tropical spastic paralysis)
Uveitis

33
Q

HTLV associated myelopahty (HAM)

A

Resembles MS

Possible autoimmune destruction of neural cells

34
Q

What influences if HTLV will produce ATL or HAM?

A

Immune response:
Evasion -> ATL (minimal Tax)
Strong reaction -> HAM (increased Tax)

35
Q

Important HIV genes

A

Gag: matrix (p17), capsid (p24)
Pol: RT, protease
Env: envelope (gp 41, 120)

36
Q

Important HIV drug target via gene

A

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
Q

Natural history of illness in HIV and CD4 counts

A

> 200: Thrush, oral hairy leuko, TB
<200: PCP, histo, toxo, crypto
<100: esophagitis due to candida
<50: CMV, MB avium

38
Q

T Cell receptors important in HIV

Mutations

A

CD4
CCR5 (early bind)
CXCR4 (late bind)
CCR5 delta32 mutation: increased resistance and improved prognosis

39
Q

1˚ infection and s/sx

A

Mono-like with or without asceptic meningitis
2-3 wks post exposure
50% unrecognized
S/Sx: maculopapular rash, oral ulcers, mono sx

40
Q

Classic HIV opportunistic infections

A

Kaposi’s
Thrush (extension into esophagus)
CMV retinitis
CNS toxoplasmosis (ring enhancing abcess w/ edema)

41
Q

Factors that contribute to HIV evolution/resistance

A

Genetic diversity (lots of mutations)
Fast replication rate
Selective pressures
Therefore use multi-drug therapy

42
Q

Pre-exposure prophylaxis

A

HIV negative patient using treatment

Tenofovir DF-emtricitabine

43
Q

Post-exposure prophylaxis

A

is a thing. Rad.

44
Q

Basic principle of HAART

A

Backbone of 2 NRTI
Plus base of integrase inhibitor (RALTegravir)
Base can also be NNRTI or protease inhibitor

45
Q

PEP Recommendations

A

Started within 72 hours
Continued for 4 weeks
Follow up ab testing at 4 weeks up to 6 months

46
Q

NRTI examples and mechanism of action

A 
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
Q

NRTI side effects

A 
Mito tox
Anemia
Granulocytopenia
Neuropathy (stocking, glove)
Lactic acidosis
48
Q

NNRTI examples and mechanism of action

A

Eevirapine
Efavirenz
Delaviradine
Not activated by kinase, bind and block RT

49
Q

HIV protease inhibitors

A

-avir
Indinavir
Ritonovir (can boost other levels via CYP inhib)
Darunavir (rash and SJS)
Resistance is harder, need multiple mutations

50
Q

HIV PI side effects

A 
GI intolerance
Central adiposity
Hyperglycemia
Hyperlipidemia
Kidney stones with indinavir
51
Q

Integrase inhibitors

A

-gravir
Raltegravir
Dolutegravir (high resistance to mutations)
Elvitegravir (CYP3A4 substrate, admin with booster)

GReat compared to protease inhibitors (AVIR)

52
Q

Integrase inhibitors side effects

A

WELL TOLERATED

Other than maybe some rhabdo

53
Q

Entry inhibitors

A

Maraviroc: CCR5 binder/inhibitor (co-receptor binding)
Enfuvirtide: gp41 inhibitor (fusion inhibitor)

Infectious Disease (13 decks)

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