Immunology Flashcards

1
Q

Lymph node structures:
Follicle
Paracortex
Medulla

A

Follicle: B cells (in outer cortex). Primary follicles dense, dormant; 2ndary active and have germinal centers

Paracortex: T cells, high endothelial venules (allow T and B cells to enter from blood). Enlarges w/ viral infxn, poorly dvlped w/ DiGeorge

Medulla:

  • medullary cords: lymphocytes, plasma cells
  • medullary sinuses: reticular cells, macrophages; communicate w/ efferent lymphatics
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2
Q

Selective IgA deficiency

A

Most common primary immunodeficiency; most asymptomatic, but can see airway and GI infxns (giardia), AI disease (celiac), atopy, anaphylaxis to IgA containing products (e.g. blood transfusions which contain small amounts of IgA)

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3
Q

What steps of protein synthesis do each of these block?

Aminoglycosides
Tetracyclines
Chloramphenicol
Clindamycin
Macrolides
Linezolid
A

Linezolid: 50 initiation
Aminoglycosides: 30s initiation; also cause misreading of mRNA
Tetracyclines: 30s elongation
Chloramphenicol: 23s peptidyl transferase of the 50s subunit (catalyzes peptide bond formation/transfers growing polypeptide onto amino acid during elongation)
Macrolides: 50s translocation
Clindamycin: 50s translocation

LA TC MC (initiation, elongation, termination): “come to LA, Their Chipotle’s More Cultured”

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4
Q

Common serum tumor markers:

  • AFP
  • CA 19-9
  • CA 125
  • CEA
  • hCG
  • PSA
A
  • AFP: HCC, germ cell tumors
  • CA 19-9: pancreatic
  • CA 125: ovarian
  • CEA: GI (e.g. colorectal)
  • hCG: choriocarcinoma, germ cell tumors, testicular cancer (can stimulate TSH receptors and cause PNPS hyperthyroidism)
  • PSA: prostate
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5
Q

Antifungal targets

  • Terbinafine
  • Azoles
  • Echinocandins
  • Polyenes
  • Flucytosine
A
  • Terbinafine: lanosterol synthesis (squalene epoxidase)
  • Azoles: ergosterol synthesis (14-a-demethylase)
  • Echinocandins (e.g. caspofungin): cell wall synth (beta glucan)
  • Polyenes (ampho B, nystatin): cell membrane integrity. directly act on ergosterol in membrane
  • Flucytosine: DNA/RNA synthesis in nucleus
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6
Q

Antigenic shift vs. drift

A
  • Antigenic shift: reassortment of viral genome e.g. when segments of human flu A virus reassort w/ swine flu A virus –> can cause a pandemic (more severe)
  • Antigenic drift: minor changes based on random mutation in HA or NA genes; can cause epidemics
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7
Q

Neonatal conjunctivitis in NG vs. Chlamydia

A
  • NG: purulent, occurs earlier (within 5 days)…“after 5 days, it’s gonnawaya (gonorrhea)!”
  • Chlamydia (serovars D-K): watery, occurs later (1-2 wks)
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8
Q

Filgrastim, Sargramostim

A

aka GM-CSF. Used in leukopenia to recover granulocyte and monocyte counts

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9
Q

IL-2 as immunotherapy

A

Used for RCC and metastatic melanoma

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10
Q

Uses of IFN-alpha, beta, gamma as immunotherapy

A
  • IFN-alpha: for chronic hep C (not preferred) and B, RCC, hairy cell leukemia and malignant melanoma, kaposi sarcoma, condyloma accuminata (HPV)
  • IFN-beta: for MS
  • IFN-Gamma: chronic Granulomatous disease
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11
Q

Actions of endogenous IFN-alpha, beta and gamma

A
  • IFN-gamma: made by NK and T cellls in response to macrophages/IL-12 or Ag. Increases macrophage intracellular killing ability & MHC II xprssn
  • IFN-alpha/beta: made by most human cells in response to viral infxn. Halt protein synthesis & promote apoptosis of infected cells to limit viral replication and spread
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12
Q

Wiskott-Aldrich syndrome

A

Mutated WASp gene; leukocytes and plt unable to reorganize actin cytoskel –> defective Ag presentation. XLR. Increased risk of AI dz & cancer. Decreased to normal IgG/M, increased IgE/A

WATER: Wiskott-Aldrich, Thrombocytopenia (fewer & smaller), Eczema, Recurrent (pyogenic) infxns. E and A in “wAtEr” for increased IgE/A

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13
Q

Respiratory vs. non-respiratory fluoroquinolones; which are active against pseudomonas

A

Levo and Moxi are respiratory (active against CAP, atypical pneumonia); Cipro is non-respiratory

Cipro and Levo are active against pseudomonas

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14
Q

Characteristics in each stage of syphilis

A
  1. painless chancre
  2. palm/sole maculopapular rash, condyloma lata (painless, warty white genital lesions)
  3. gumma (chronic granulomas), aortitis, argyll-robertson pupil (accomodates but unreactive to light); neurosyphilis (tabes dorsalis) common late manifestation but can occur at ANY stage
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15
Q

Congenital syphillis

A

snuffles, saddle nose, rhagades (linear scars at angles of mouth), hutchinson notched teeth, mulberry molars, sensorineural deafness. Tx mom in FIRST tri w/ Pen G

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16
Q

Organisms that cause infection with small dose

A

Shigella (10-500 cells)
C. jejuni (500 cells)
E. histolytica (1-10 organisms)
Giardia lamblia (10 organisms)

17
Q

Side effects of amphotericin B

A
  • Fever/chills
  • Hypotension
  • Nephrotoxicity (distal RTA and low GFR; reduce w/ hydration) –> arrhythmias (hypoK/Mg d/t increased DCT permeability), anemia (decreased Epo)
  • IV phlebitis

Less side fx w/ liposomal amphotericin

18
Q

Beta-lactams vs. vanco: mechanism of action

A
  • Beta-lactams bind PBPs (e.g. transpeptidases) and prevent cross-linking of peptidoglycan in the cell wall
  • Vanco binds terminal D-ala residues of cell wall glycoproteins and prevents transpeptidases from forming cross-links
19
Q

Primary CNS lymphoma

A

AIDS-defining illness, pathogenesis involves EBV infection (but unlike abnormal T cells on peripheral smear, will see abnormal population of B cells in brain biopsy). May be ring-enhancing/must distinguish from Toxo via CSF/other lab tests

20
Q

Primary vs. secondary TB

A
  • Primary: hilar nodes + ghon focus (usually mid-lower lobes) = ghon complex. Either heals by fibrosis and calcification (Ranke complex) or progresses (e.g. w/ AIDS, malnutrition - insuff immune response) –> miliary TB (widespread dissemination
  • Secondary: fibrocaseous cavitary lesion usually in upper lobes; can cause caseation and scarring in lung, kidney caseation, etc (localized destructive disease)
21
Q

Apoptosis pathways

A
  • Intrinsic (mitochondrial): inactivation of bcl2 –> cyt c leaks out of cell to activate caspases
  • Extrinsic (receptor-ligand): FASL binds FAS (CD95) on target cell, or TNF-a binds its receptor on target cell activating caspases.
  • Cytotoxic (cell-mediated): perforins create memb pores; granzyme enters pores –> activates caspases. Occurs w/ viral infected cells

Caspase activation –> activation of protease (destroys cytoskeleton) and endonuclease (destroys DNA)

22
Q

IPEX syndrome

A

Genetic deficiency of FOXP3 on Treg cells. Immune dysregulation, Polyendocrinopathy (thyroiditis or T1DM), Enteropathy (diarrhea), X-linked (male infants). Also p/w AI dermatologic conditions e.g. eczema

23
Q

Diagnostic features of Sjogren syndrome

A

2/3 criteria:

  • dry eyes/mouth
  • ANA and antiSSA or antiSSB or RF
  • lymphocytic sialadenitis

Also at increased risk for B cell (marginal zone) lymphoma; late in dz course

24
Q

Factors released by mast cells upon degranulation

A

Histamine, heparin, tryptase (can use as marker for mast cell activation; relatively specific), eosinophil chemotactic factors