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Immuno 2 Flashcards

1
Q

Which Abx are protein synthesis inhibitors? (5)

A

Aminoglycosides, Tetracyclines (bind to 30s subunit)

Chloramphenicol, Clindamycin, Macrolides (bind to 50s subunit)

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2
Q

MoA of aminoglycosides?

Side effects?

A
  • bind to 30s subunit causing misreading of mRNA

- nephrotoxic, ototoxic

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3
Q

MoA of tetracyclines?

Side effects?

A
  • bind to 30s subunit blocking binding of aminoacyl-tRNA

- teeth discolouration, photosensitivity

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4
Q

MoA of chloramphenicol?

Side effects?

A
  • binds to 50s subunit inhibiting peptidyl transferase

- aplastic anaemia

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5
Q

MoA of clindamycin?

Side effects?

A
  • binds to 50s subunit inhibiting translocation (movement of trna from acceptor site to peptidyl site)
  • common cause of C diff
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6
Q

MoA of macrolides?

side effects?

A
  • bind to 50s subunit inhibiting translocation

- nausea (esp erythromycin), p450 inHIBitor, prolonged QT interval

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7
Q

Exotoxins are usually secreted by Gram +ve bacteria

5 classifications?

A 
Pyrogenic toxins
Enterotoxins
Neurotoxins
tissue Invasive toxins
miScellaneous toxins
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8
Q

What are endotoxins

A

lipopolysaccharides released by Gram -ve bacteria

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9
Q

What are pyrogenic toxins?

Examples?

A
  • superAg which bridge the MHC class II protein on APCs with T cell surface receptors
  • > massive endogenous cytokine release -> fever, rash etc
  • TSST-1 superAg (toxic shock synd toxin)
  • strep pyrogenic exotoxin A & C (scarlet fever)
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10
Q

What are enterotoxins?

Organisms that produce enterotoxins?

A
  • Act on GI tract -> diarrhoeal illness, vomiting illness

- cholera, shigella dysntery, E coli, s aureus, bacillus cereus

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11
Q

How does cholera enterotoxin work?

A
  • activates adenylate cyclase via Gs -> cAMP increase -> inc Cl- secretion, reduced Na absorption
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12
Q

How does shiga toxin work? (shigella)

A
  • inactivated 60s ribosome -> epithelial cell death
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13
Q

How does E. coli heat Labile toxin work?

A
  • activates adenylate cyclase via Gs -> inc cAMP -> watery diarrhoea
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14
Q

How does E. coli heat Stabile toxin work?

A
  • activates guanylate cycles -> inc cGMP -> watery diarrhoea
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15
Q

How long does staph aureus enterotoxin illness last?

A
  • D&V <24h
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16
Q

How does cereulide (bacillus cereus enterotoxin) work?

A
  • it’s a potent cytotoxin that destroys mitochondria -> vomiting illness which may present within 4h ingestion
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17
Q

How does tetanospasmin (clostridium tetani neurotoxin) work?

A
  • acts on nerves
  • blocks release on the inhib NTs GABA & glycine -> continuous motor neuron activity -> continuous muscle contraction -> lockjaw & resp paralysis
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18
Q

How does clostridium botulinum neurotoxin work?

A
  • acts on NMJ

- blocks ACh release -> flaccid paralysis

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19
Q

What is the clostridium perfringens tissue-invasive toxin? What happens?

A
  • alpha-toxin (lecithinase)

- myonecrosis (gas gangrene) & haemolysis

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20
Q

Which organisms produce tissue invasive toxins?

A
  • clostridium perfringens alpha-toxin (gas gangrene, haemolysis)
  • staph aureus exfoliatin (staph scalded skin syndrome)
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21
Q

Staph aureus exfoliatin tissue invasive toxin causes what disease

A

Staph scalded skin syndrome

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22
Q

4 organisms that produce miscellanous toxins

A
  • corynebacterium Diphtheria
  • pseudomonas aer. (exotoxin A)
  • bacillus anthracis (ED oedema factor)
  • bordetella pertussis exotoxin
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23
Q

How does diphtheria toxin work?

A
  • ADP ribosylates EF-2 (elongation factor) -> inhibition -> necrotic mucosal cells -> diphtheric membrane on tonsils
  • systemic distribution may produce necrosis of myocardial, neural & renal tissue
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24
Q

How does pseudomonas exotoxin A work?

A
  • inhibitis EF-2 in same way as diphtheria
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25
Q

How does oedema factor (anthrax) work?

A
  • forms a calmodulin-dependent adenylate cyclase -> inc cAMP -> impaired function of neuts/macrophages -> reduces phagocytosis
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26
Q

How does pertussis exotoxin work?

A
  • inhibits Gi -> inc cAMP -> imp neuts/macro -> reduced phagocytosis
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27
Q 
HLA antigens are encoded by genes on which chromosome ?
class I Ag?
class II Ag?
A

6
I - A, B, C
II - DP, DQ, DR

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28
Q

Ass with HLA-A3

A

haemochromatosis

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29
Q

Ass with HLA-B51

A

Behcet’s disease

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30
Q

Ass with HLA-B27

A

ankylosing spondylitis
Reiter’s syndrome
acute anterior uveitis

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31
Q

Ass with HLA-DQ2/DQ8

A

coeliac disease

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32
Q

Ass with HLA-DR2

A

narcolepsy

Goodpasture’s syndrome

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33
Q

Ass with HLA-DR3

A

dermatitis herpetiformis
Sjogren’s syndrome
1ry biliary cirrhosis

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34
Q

Ass with HLA-DR4

A

T1DM (also dr3)

Rheumatoid arthritis

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35
Q

Th1 cells are involved in which response?

what do they secrete?

A
  • cell-mediated & delayed type IV hypersensitivity

- IFN-gamma, IL2, IL3

36
Q

TH2 cells are involved in which response?

what do they secrete?

A
  • humoral Ab immunity eg stimulating IgE production

- IL4, 5, 6, 10, 13

37
Q

Someone has repeated infections with encapsulated bacteria… raises the suspicion of what? (appropriate Ix?)

A

Immunoglobulin deficiency - check serum Igs

38
Q

Role of reverse transcriptase in HIV infection?

A

It transcribes viral RNA to host DNA - creating dsDNA

39
Q

Protein made in the liver that binds to phosphocholine in bacteria cells AND cells undergoing apoptosis…. then can activate the complement system ?

40
Q

Examples of acute-phase proteins?

A
  • CRP, ferritin, fibrinogen, complement, alpha-1 AT, caeruloplasmin, procalcitonin, serum amyloid A, haptoglobin
41
Q

Examples of negative acute phase proteins (liver decreases production during acute phase response)?

A
  • Albumin, transferrin, transthyretin/prealbumin, retinol-binding protein, cortisol-binding protein
42
Q

A series of proteins that circulate in plasma involved in inflammatory & immune reaction of the body?
what processes are they involved in?

A
  • Complement proteins

- chemotaxis, cell lysis, opsonisation

43
Q

Complement deficiency that causes hereditary angioedema?

A

C1-INH (inhibitor protein deficiency)

  • multifunctional serine protease inhibitor
  • probably by uncontrolled bradykinin release -> tissue oedema
44
Q

Complement deficiency that causes recurrent bacterial infections?

45
Q

Complement deficiency that predisposes to Leiner disease?

A

C5 def - rec diarrhoea, wasting, seb derm

46
Q

Complement deficiency that predisposes to immune complex disease e.g. SLE, HSP?

A

C1q, C1rs, C2, C4 def (classical pathway components)

47
Q

Complement deficiency that leads prone to Neisseria meningitides infection?

A

C5-9 def (encodes MAC: membrane attack complex)

48
Q

Cytokine mainly from macrophages which induces fever, and involved in acute inflammation?

49
Q

Cytokine from Th1 cells that stimulates growth & differentiation of T cell response?

50
Q

Cytokine from activated T helper cells which stimulates differentiation & proliferation of myeloid progenitor cells?

51
Q

Cytokine from Th2 cells which stimulates proliferation & differentiation of B cells?

52
Q

Cytokine from Th2 cells which stimulates production of eosinophils?

53
Q

Cytokine from macrophages which is involved in neutrophil chemotaxis?

54
Q

Cytokine from Th2 cells that inhibits Th1 cytokine production?

A

IL-10
aka human cytokine synthesis inhabit factor
- an anti-inflam cytokine

55
Q

Cytokine from dendritic cells, macrophages & B cells which activates NK cells & stimulates differentiation of naive T cells into Th1 cells?

56
Q

Cytokine from macrophages which induces fever and involved in neutrophil chemotaxis?

57
Q

Cytokine from Th1 cells that activates macrophages?

58
Q

Cytokines released by the body in response to viral infections & neoplasia?

A

Interferons

  • alpha & beta bind to type 1 R’s
  • gamma binds to type 2 R’s
59
Q

Antiviral interferon produced by leukocytes?

adverse effects?

A

IFN-alpha

  • flu-like Sx & depression
  • useful in hep B & C, Kaposi’s sarcoma, metastatic RCC, hairy cell leukaemia
60
Q

Antiviral interferon produced by fibroblasts?

utility?

A

IFN-beta

- reduces frequency of exacerbations in pts with relapsing-remitting MS

61
Q

Interferon produced by T lymphocytes & NK cells?

utility?

A

IFN-gamma

- immunomodulatory role esp macrophage activation - e.g. chronic granulomatous disease & osteopetrosis

62
Q

Coagulase- positive staph

A

staph aureus

e.g. skin infections, abscess, osteomyelitis

63
Q

Coagulase negative staph

A

staph epidermidis

e.g. central line infections, infective endocarditis

64
Q

What does IgG do?

shape?

A
  1. enhances phagocytosis of bacteria & viruses
  2. fixes complement & passes to the fetal circulation
    - monomer
    - most abundant isotope in blood 75%
65
Q

What does IgA do?
How is it transported?
Where is it found?
shape?

A

Provides localised protection on mucous membranes

  • transported across interior of cell via transcytosis
  • the predominant Ig in breast milk; also found in digestive, rest & urogen tracts & systems
  • monomer/dimer
  • most commonly Produced Ig in the body
66
Q

What does IgM do?

shape?

A
  1. 1st Ig to be secreted in response to infection
  2. Fixes complement but doesn’t pass to fetal circulation
    - Anti-A, B blood Ab
    - pentamer
67
Q

What does IgD do?

shape?

A
  1. Involved in B cell activation but role in immune system largely unknown
    - monomer
68
Q

What does IgE do?

shape?

A
  1. Mediates type 1 hypersensitivity reactions
  2. Binds to Fc receptors on surface of mast cells & basophils
  3. Provides immunity to parasites e.g. helminths
    - monomer
69
Q

2 regions of Ab/Igs?

A
  1. Fab: Ag-binding fragment

2. Fc: fragment crystallizable region - tail region of Ab interacts with cell surface receptors

70
Q

How are leukotrienes produced:

  • what are they formed from?
  • what are they secreted by ?
  • role in nsaids/asthma?
A
  • from arachidonic acid by action of lipoxygenase
  • secreted by leukocytes
  • nsaid-induced bronchospasm in asthmatics possibly 2ry to express production of leukotrienes due to inhibition of prostaglandin synthetase
71
Q

MoA of Rifampicin?

A

Inhibits RNA synthesis

72
Q

Which Abx inhibit DNA synthesis?

A

Quinolones e.g. ciprfloxacin
Metronidazole
Sulphonamides
Trimethoprim

73
Q

Which Abx inhibit cell wall formation?

A

Penicillins

Cephalosporins

74
Q

Which 4 cells are involved in the adaptive immune response?

A

Helper T cells
Cytotoxic T cells
B cells
Plasma cells

75
Q

Cell of the adaptive immune response that is a major cell of the humeral response, mediates hyper acute organ rejection and acts as an Ag presenting cell?

76
Q

Cell of the adaptive immune response that is differentiated from B cells and produces large amounts of Ab specific to a particular Ag?

A

Plasma cells

77
Q

Cell of the adaptive immune response that is involved in the cell-mediated immune response, recognises Ags presented by MHC class I molecules, induces apoptosis in virally infected & tumour cells, expresses CD8, CD3, TCR and mediates acute & chronic organ rejection?

A

Cytotoxic T cells

78
Q

Cell of the adaptive immune response that is involved in the cell-mediated immune response, recognises Ags presented by MHC class II molecules, expresses CD4, CD3, TCR & CD28, is a major source of IL-2 and helps mediate acute & chronic organ rejection?

A

Helper T cells

79
Q

What type of organism is Klebsiella pneumonias?

A

Gran-negative rod part of normal gut flora

- typically aspiration pneumonia & UTIs

80
Q

Features of Klebsiella pneumonia?
complications?
Prognosis?

A
  • may occur after aspiration
  • more common in etoh & diabetics
  • red-currant jelly sputum
  • often affects upper lobes
  • commonly causes lung abscess formation & empyema
  • mortality 30-50%
81
Q

What are Rickettsiae?
Dx?
Rx?

A

Gram negative obligate intracellular parasites
- typically cause fever, headache, rash (except Q fever which causes pneumonia)

Weil-Felix reaction is positive in all except Q fever

Rx with Tetracyclines

82
Q 
Cause of rocky mountain fever?
Vector = tick
headache, fever
rash starting at peripheries before spreading centrally, initially maculopapular then vasculitic
endemic to east coast US
A

Rickettsia ricketsii

83
Q

Cause of Q fever?
no vector
no rash
causes pneumonia

A

Coxiella burnettie (rickettsiae)

84
Q

Cause of endemic typhus?
vector = flea
rash typically starts centrally then spreads to peripheries

A

Rickettsia typhi

85
Q

Cause of epidemic typhus?

vector = human body louse

A

Rickettsia prowazekii

EXAM (21 decks)

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