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Course 1 > immune deficiency/infections > Flashcards

immune deficiency/infections Flashcards

1
Q

what are the 3 types of Abs?

A

neutralizing, opsonizing, complement activating

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2
Q

which Ig can cross the placenta?

A

IgG

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3
Q

where do B cells mature and differentiate?

A

BM

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4
Q

what region is found on the HC but not LC?

A

D

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5
Q

what are processes that contribute to B cell diversity?

A

recombination, chain pairing, junctional diversity, somatic hypermutation

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6
Q

when does negative selection happen for B cells?

A

before leaving BM

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7
Q

where does somatic hypermutation happen?

A

LN

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8
Q

through which receptor do B cells present Ag to Th cell?

A

MHCII

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9
Q

what ligand mediates B/T cell binding?

A

CD40

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10
Q

what are T-independent Ags made of?

A

polysaccharide, lipid

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11
Q

what Ag is produced by T-independent B cells?

A

IgM

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12
Q

what does positive selection in B cells do?

A

select for V-nt variations that lead to better Ag binding

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13
Q

what is the most common PID?

A

humoral

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14
Q

what are the different types of B cell deficiencies?

A

maturation defect, Ab production defect, crosstalk defect

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15
Q

what Ig is impacted by transient hypogammaglobulinemia of infancy?

A

IgG

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16
Q

deficiency in which Ig is the most common?

A

IgA

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17
Q

what infection are pts with selective Ab deficiency at risk for?

A

Strep pneumoniae (no response to pneumovax)

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18
Q

what are examples of encapsulated bacteria?

A

strep, staph, H influenza, N meningitidis, klebsiella, pseudomonas

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19
Q

what are PE signs of agammaglobulinemia?

A

no LN/tonsils

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20
Q

what is the mode of inheritance of agammaglobulinemia?

A

mostly Xlinked through BTK mutation (some AR)

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21
Q

what class of diseases do pts with CVID struggle with?

A

chronic inflammatory diseases (lung, hep, granulomas, IBD)

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22
Q

what is the definition of CVID?

A

decreased levels of 2 Ig types, poor vaccine response, r/o other causes of deficiency

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23
Q

what are hyper IgM pts at risk for?

A

OI (CMV, pneumocystitis), autoimmunity, malignancy

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24
Q

how are pts with humoral deficiencies treated?

A

Ig replacement, antibiotics (prophylaxis), aggressively tx infections, monitor closely

25
Q

where do T cells mature?

A

thymus

26
Q

what are the different types of APC?

A

B cells, dendritic cells, macrophages

27
Q

Which MHC moelcule is used to present to Th cells? Tc?

A

Th-MHCII

Tc-MHCI

28
Q

what is Th1 responsible for? what molecule does it release?

A

intracellular microbe killing (stimulate macrophage and Ab)

IFN-g

29
Q

what is Th2 responsible for? what molecule does it release?

A

stimulate eosinophils to fight parasites, also activate macrophage in tissue repair

IL4, IgE

30
Q

what is Th17 responsible for? what molecule does it release?

A

recruit neutrophil and monocytes for autoimmune diseases

IL17, 22

31
Q

what is T reg responsible for? what molecule does it release?

A

immunosuppression

IL10, TGFb

32
Q

how do cancer cells evade the immune system?

A

look like self Ag, no MHCI, secrete immunosuppressive proteins

33
Q

what is MSDS?

A

defect in IFg and IL12 that cause susceptibility to intracellular organisms

34
Q

what organism causes CMC? What deficiency is this caused by?

A

candida albacans, Th17 deficiency

35
Q

what is SCID?

A

combined deficiency due to maternal engraftment or T cell mutations

36
Q

why can’t live vaccines be given to pts with SCID?

A

no T cells, so can contract disease

37
Q

what are examples of live vaccines?

A

varicella, MMR, rota, flu

38
Q

what is the presentation of Xlinked SCID (common gamma chain defect)?

A

low T/NK, normal B levels but no Igs (maturation defect)

39
Q

what is the triad of wiskott aldrich disease?

A

eczema, recurrent infection, thrombocytopenia

40
Q

what is the presentation of DiGeorge syndrome?

A

absence of thymus, low T cells, cardiac abnormalities, hypocalcemia, cleft palate, learning disability

41
Q

GATA2 deficiency presentation

A

low monocytes, B cells, CD4

HPV infections (NK deficiency)

42
Q

what is the CD4 count in AIDS-defining illness?

A

<200

43
Q

what are the tests for HIV disease status?

A

4th gen test (screening), western blot (confirmation)

44
Q

what is the UN 90-90-90 goal?

A

90% HIV infected know their stat

90% diagnosed on ARV

90% on ARV have suppressed viral loads

45
Q

how are ARV regimens built?

A

3 drugs from different classes: 2 NRTIs, one of NNRTI, protease inhibitor, or integrase inhibitor

46
Q

what infections are pts with complement deficiency at risk for? How is this deficiency confirmed?

A

pyogenic/neisseria infection, or SLE

CH50 test

47
Q

how do we test for oxidative burst capacity in CGD?

A

dihydrorhodamine flow cytometry

48
Q

what are examples of catalase + organisms?

A

staph, Ecoli, klebsiella, pseudomonas, candida, aspergillus

49
Q

what test determines T cell proliferation rate?

A

mitogen

50
Q

what drugs are used to tx a pseudomonas infection?

A

piperacillin, ceftazidime, meropenem, gentamycin, cipro

51
Q

what is the nature of a pseudomonas infection?

A

green pus in burns or cathethers

52
Q

why can’t azoles be used to treat PJP?

A

no ergosterol

53
Q

what is the presentation of PJP?

A

fever, dry cough, chest pain (batwing on XR)

54
Q

what is the tx for cryotococcus neoformans infections?

A

L-amphoterocin, fluconazole

55
Q

what complications are associated with toxoplasma gondii infections?

A

chorioretinitis, brain abscess

56
Q

what does the halo sign indicate in XR?

A

pulmonary aspergillosis

57
Q

what are the DDx for mono?

A

cancer, CMV, toxoplasma gondii

58
Q

seeing the owl eye sign on an IBD biopsy indicates what disease?

A

CMV infection

59
Q

what do gram - cocci pairs indicate in pt that have undergone a splenectomy?

A

nesseria menigitis

Course 1 (6 decks)

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