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immunology > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is the step-by-step pathway of the classical complement pathway?

A

1) Antibody binds to antigen
2) C1q portion of C1 complex (C1q2r2s) binds to Fc portion of antibody
3) Activated C1s cleaves C4 and C2 –> C4a + C4b + C2a + C2b
4) C4b + C2a –> C2a4b (C3 convertase)
5) C3 convertase cleaves C3 –> C3a + C3b
6) Some C3b binds to C4b2a –> C4b2a3b (C5 convertase)
7) C5 convertase cleaves C5 –> C5a + C5b
8) C5b binds to C6-9 = MAC

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2
Q

What is the step-by-step pathway of the alternative complement pathway?

A

1) C3 spontaneously hydrolyzes –> C3a + C3b
2) C3b binds with Factor B C3bB
3) Factor D cleaves C3bB –> C3bBb + Ba
4) C3bBb (C3 convertase) hydrolyzes C3 –> C3a + C3b
5) C3b binds with C3bBb –> C3bBb3B (3B reprsents newly cleaved C3b)
6) C3bBb3B (C5 convertase) cleaves C5 –> C5a + C5b
7) C5b binds to C6-9 = MAC

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3
Q

What are the early pathway steps in the classical complement pathway?

A

C1 complex (C1qr2s2), C2, C4, C3

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4
Q

What are the late pathway steps in the classical and alternative complement pathway?

A

C5 - C9

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5
Q

What consequences are associated with the early complement pathway defects?

A

Invasive infections with encapsulated microbes

Lupus or glomerulonephritis are common issues

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6
Q

What consequences are associated with the late complement pathway defects?

A

Invasive infections with Neisseria species

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7
Q

What is the CH50 test?

A

Test to diagnose late complement pathway defect

AB-coated sheep blood is added to patient’s serum. Look at how many sheep RBCs are lysed

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8
Q

What are the functions of C1-INH? Is it soluble or membrane bound?

A

C1-INH binds to C1r and C1s of the C1 complex, which inhibits cleavage of C4 and C2

C1-INH inhibits the Kinin-Kallikrein System, which is involved in vasodilation, vascular permeability, and blood pressure.

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9
Q

What is the consequence of defective C1-INH?

A

Hereditary angioedema

-Characterized by attacks of rapid swelling in various tissues

Triggered by

  • Trauma
  • Surgery
  • Emotional stress
  • And dental procedures (can be life-threatening)
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10
Q

What is C3 Nephritic Factor (C3NeF)? Is it soluble or membrane bound?

A

Autoantibody that prolongs the half-life of C3bBb

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11
Q

What is the consequence of C3NeF?

A

Membranoproliferative Glomeruloneohritis Type II

-kidney disfunction due to deposits of immune complexes in the glomeruli

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12
Q

What is factor H? it soluble or membrane bound?

A

Competes with factor B by preventing the formation of C3Bb (alternative pathway)

soluble

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13
Q

What is factor I? Type of activity?

A

Has serine protease activity to cleave C3b –> inactive C3b (iC3b)

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14
Q

What is Membrane Cofactor Protein (MCP aka CD46)

A

Membrane bound protein located on self-cell membranes via GPI anchors

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15
Q

What is the consequence of defective Factor H?

A

Hemolytic Uremia Syndrome

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16
Q

What is the consequence of defective Factor H or Factor I or Membrane Cofactor Protein (MCP)?

A

Hemolytic Uremia Syndrome (HUS)

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17
Q

What is leukocyte adhesion deficiency?

A

Inability of leukocytes to migrate to site of infection/inflammation

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18
Q

What is chronic granulomatous disease?

A

Defect with NADPH oxidase complex preventing proper oxidative bursts

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19
Q

What is primary immunodeficiency?

A

congenital immunodeficiency that can affect effector and regulatory arms of immune system

often caused by mutations in specific genes

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20
Q

What is secondary immunodeficiency

A

non-genetic immunodeficiency that is secondary to something else (chemotherapy, malnutrition, burns, HIV, etc)

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21
Q

Type 1 necrotizing soft tissue infection microbe(s) and treatment

A

aerobes and anaerobes

foul odor, grey discharge, crepitus (crackling skin)

surgery
Beta-lactam + Beta-lacatmase inhibitor combo

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22
Q

Type 2 necrotizing soft tissue infection microbe(s) and treatment

A

streptococcus pyogenes

surgery
Beta-lactam + beta-lactamase inhibitor combo PLUS clindamycin for GAS toxin inhibition

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23
Q

Type 3 necrotizing soft tissue infection microbe(s)

A

marine vibrio species

fresh or brackish (salty) water exposure

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24
Q

What are the common etiologies of necrotizing soft tissue infections?

A

Type I, Type II, Type II, and MRSA

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25
Q

What is folliculitis?

A

infection or inflammation of hair follicles

papules or pustules centered upon hair follicles

26
Q

MRSA necrotizing soft tissue infection treatment

A

Vancomycin

27
Q

What is an abscess?

A

purulent collection in dermis and subcutaneous tissue

28
Q

What is a furuncle?

A

Boil; purulent abscess associated with hair follicles

29
Q

What is a carbuncle?

A

Multiple furuncles that coalesce and form sinus tracts

30
Q

What is Decay Accelerating Factor (DAF)? Is it soluble or membrane bound?

A

DAF is found on self cell membranes via GPI anchors that prevents the formation of C3 convertase in both classical (C2a4b) and alternative (C3bBb) pathways

31
Q

What is the effector arm of the immune system?

A

carries out the immune response

32
Q

What is the regulatory arm of the immune system?

A

regulates the effector arm of the immune system

33
Q

What is a macule?

A

change in skin color <1cm

34
Q

What is a patch?

A

a macule >1 cm at it’s widest aspect

35
Q

what is a papule?

A

Solid raised lesion that has distinct borders and is less than 1 cm in diameter

36
Q

What is a plaque?

A

Solid raised flat-topped lesion >1 cm in diameter

37
Q

What is a nodule?

A

Solid raised NON-flat-topped lesion >1 cm in diameter

38
Q

What is a vesicle?

A

Raised lesion up to 1 cm in diameter, filled with clear fluid

39
Q

What is a bulla?

A

Raised lesion >1 cm in diameter, filled with clear fluid

40
Q

What is a pustule?

A

Raised lesion filled with pus

41
Q

What is a wheal?

A

Evanescent papule or plaque, often with erythematous borders and pale center

42
Q

What is a scale?

A

Visible fragments of the stratum corneum as it is shed from the skin

43
Q

What is a crust?

A

Liquid debris (serum or pus) that has dried on the surface of the skin

44
Q

What is lichenification?

A

Thickening of epidermis, with resulting accentutation of skin lines, often as a result of scratching

45
Q

What is a fissure?

A

Sharply-defined, linear or wedge-shaped tears in the epidermis

46
Q

What is an erosion?

A

Loss of superficial layers of upper epidermis by friction or pressure

47
Q

What is an ulcer?

A

Epidermis and some dermis have been loss

48
Q

What are the clinical symptoms of neutropenia?

A 
fever
infections/sepsis
peri-rectal pain and abscesses
skin infections
mouth sores
49
Q

What organisms would cause problems with complement deficiency?

A

encapsulated organisms

50
Q

What organisms would cause problems with neutrophil/phagocytosis deficiency?

A

catalase + organisms

51
Q

What is chronic granulomatous disease? How do you test for it?

A

Defect wit NADPH oxidase complex

			Dihydrorhodamine 123 (DHR) dye
Cells that have proper functioning oxidative burst will cause the cell to turn green
52
Q

What are clinical features of necrotizing soft tissue infections

A

infections that spread rapidly along subcutaneous tissue planes, leading to tissue death (fascia, muscles and their associated nerves), and severe systemic toxicity

53
Q

What are the risk factors for necrotizing soft tissue infections?

A

Immunocompromised

  • primary
  • secondary
    • diabetes
    • burns
    • peripheral vascular disease
54
Q

What is the common cause of necrotizing soft tissue infections? second?

A

type 1
aerobes + anaerobes

second is Staph a

55
Q

What is impetigo? What are the two bugs that can cause it?

A

infection of epidermis

Staph a (most common) and strep pyogenes

56
Q

What is the topical of choice for skin infections?

A

Mupricin 2%

57
Q

What causes erysipelas cellulitis?

A

Typically strep pyogenes

58
Q

What causes mastoiditis?

A

complications of otitis media

59
Q

What is sinusitis?

A

Inflammation of the ostia that drain the mucus from each sinus

60
Q

What is orbital cellulitis?

A

inflammation of the sinus passage results in the movement of bacteria from the sinus spaces into the orbital space via the lamina paprycea

61
Q

Septic jugular thrombophlebitis

A

infection of the jugular vein that occurs from pharyngitis that progresses to tonsilitis that progresses to peritonsillar abscesses

immunology (7 decks)

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