Week 3 Flashcards

1
Q

Which disease does C1-INH deficiency cause? Why?

A

Hereditary angioedema. C1-INH normally inhibits bradykinin formation. Without C1-INH, enzymes make bradykinin like crazy and patients get edema, vasodilation.

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2
Q

What species of bacteria are people who have a C5-C9 deficiency particularly susceptible to?

A

Neisseria species

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3
Q

What is the cause of membranoproliferative glomerulonephritis type II?

A

C3 Nephritic Factor - an autoantibody that prolongs the half-life of C3bBb –> lots of C3a and C3b generation –> immune complexes build up in glomeruli –> inflammation

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4
Q

Your pediatric patient has recurrent bacterial skin infections, and the umbilical stump took 3 weeks to fall off. What is your Dx?

A

LAD-1 (CD18 integrin defect)

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5
Q

What causes atypical hemolytic uremic syndrome?

A

Factor I, Factor H, or MCP deficiency

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6
Q

Which organisms are people with chronic granulomatous disease susceptible to being infected with?

A

Any catalase positive organisms cuz they can deal with the small bit of ROS that are made by phagocytes of people with CGD.

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7
Q

What test is performed to evaluate for chronic granulomatous disease? How does it work?

A

DHR test - flow cytometry measures amount of ROS-induced fluorescence. No fluorescence = no ROS = CGD.

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8
Q

What test is performed to evaluate for complement protein deficiency? How does it work?

A

CH50 test: put a dilution of serum in a test tube with sheep blood and measure the concentration needed to lyse 50% of the sheep RBCs.

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9
Q

How does Factor H work?

A
  1. It competes with Factor B (alternative pathway) to keep C3b from forming the C3 convertase.
  2. Factor H can displace Factor B and inhibit C3bBb after it has formed.
  3. Factor H recognizes oligosaccharides on human cells and gets rid of C3bBb from these cells.
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10
Q

What is Decay Accelerating Factor and what does it do?

A

DAF is membrane-bound to cells and inhibits C4b in the classical pathway from cutting C2 into C2a and C2b.

It can also inhibit C3bBb in the alternative pathway.

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11
Q

What is CD59 and what does it do?

A

Membrane-bound inhibitor of C9 polymerization in the formation of the MAC complex.

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12
Q

What is the difference between a type 1 and type 2 necrotizing soft tissue infection?

A

Type 1 is polymicrobial - grey discharge, stinky, often located in the perineal area.

Type 2 is from Strep pyogenes (or Staph, aureus or Pseudomonas less commonly) - history of blunt trauma is common.

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13
Q

Why should you give clindamycin in addition to penicillin G for treatment of GAS necrotizing fasciitis?

A

Clindamycin is a protein synthesis inhibitor so it will reduce toxin production.

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14
Q

Which organisms that cause necrotizing soft tissue fasciitis are associated with fresh or brackish water exposure?

A

Vibrio species and Aeromonas hydrophilia

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15
Q

What are the two most common bacterial causes of impetigo?

A

Staph aureus and Strep pyogenes

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16
Q

What are the most common bacterial causes of cellulitis?

A

beta-hemolytic strep, Staph aureus, Pseudomonas in diabetics or immunocompromised

17
Q

Which bacteria can cause cellulitis after animal bites?

A

Pastuerlla multocida, Capnocytophagia canimorsus

18
Q

What is more common: bullous impetigo or non-bullous impetigo?

A

Non-bullous (75% of cases)

19
Q

Name a few symptoms that would clue you in to orbital cellulitis as opposed to preseptal cellulitis.

A
  1. Painful eye movement

2. Proptosis (eye bulging out)

20
Q

Defects in early complement proteins put people at risk for…?

A

Infections with encapsulated organisms and autoimmune conditions like lupus and glomerulonephritis.

21
Q

What is the treatment for a mixed aerobic and anaerobic necrotizing soft tissue infection?

A

beta-lactam and lactamase inhibitor combo, or carbapenem

22
Q

What is the treatment for Staph aureus (including MRSA) necrotizing soft tissue infection?

A

Vancomycin

23
Q

What is the treatment for Strep pyogenes necrotizing soft tissue infection? Why?

A

beta lactam + lactamase inhibitor + clindamycin to stop toxin production cuz it inhibits protein synthesis

24
Q

How does Factor I work?

A

It works with membrane-bound MCP to inactivate C3b –> iC3b