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Aaron-Exit: Championship Rounds > Pathoma Chapter 2C > Flashcards

Pathoma Chapter 2C Flashcards

1
Q

Step 4?Transmigration and Chemotaxis

A
  1. Leukocytes transmigrate across the endothelium of postcapillary venules and move toward chemical attractants (chemotaxis).
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2
Q

Neutrophils are attracted by

A

bacterial products, IL-8, C5a, and LTB4

Remember Platlet Activating Factor (Random Amboss, Question, remember that…)

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3
Q

Step 5?Phagocytosis

A
  1. Consumption of pathogens or necrotic tissue; phagocytosis is enhanced by opsonins (IgG and C3a). 2. Pseudopods extend from leukocytes to form phagosomes, which are internalized and merge with lysosomes to produce phagolysosomes.
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4
Q

Chediak-Higashi syndrome

A

is a protein trafficking defect (autosomal recessive) characterized by impaired phagolysosome formation.

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5
Q

Clinical features of Chediak-Higashi syndrome include

A

Increased risk of pyogenic infections, Neutropenia, Giant granules in leukocytes, Defective primary hemostasia, Albinism, Peripheral neuropathy

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6
Q

Why is there Neutropenia in Chediak Higashi syndrome?

A

(due to intramedullary death of neutrophils)

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7
Q

In chediak higashi there are Giant granules in leukocytes because?

A

due to fusion of granules arising from the Golgi apparatus

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8
Q

In chediak higashi Defective primary hemostasia is due to?

A

abnormal dense granules in platelets

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9
Q

Step 6?Destruction of phagocytosed material

A
  1. O2-dependent killing is the most effective mechanism. 2. HOCl generated by oxidative burst in phagolysosomes destroys phagocytosed microbes.
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10
Q

How does O2 dependant killing occur?

A

O2 is converted to O2. by NADPH oxidase (oxidative burst). O2. is converted to H202, by superoxide dismutase (SOD). H202 is converted to HOCl (bleach) by myeloperoxidase (MPO).

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11
Q

NADPH oxidase

A

O2 is converted to O2. by (oxidative burst).

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12
Q

SOD

A

O2. is converted to H202, by superoxide dismutase

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13
Q

MPO

A

H202 is converted to HOCl (bleach) by myeloperoxidase (MPO).

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14
Q

CGD is characterized by?

A

poor O2-dependent killing.

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15
Q

CGD is Due to?

A

NADPH oxidase defect (X-linked or autosomal recessive)

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16
Q

What does CGD lead to?

A

recurrent infection and granuloma formation with catalase-positive organisms, particularly Staphylococcus aureus, Pseudpmonas cepacia, Serratia marcescens, Nocardia, and Aspergillus

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17
Q

Nitrobiue tetrazolium test

A

is used to screen for CGD. Leukocytes are incubated with NBT dye, which turns blue if NADPH oxidase can convert 02 to O2. but remains colorless if NADPH oxidase is defective.

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18
Q

MPO deficiency results in?

A

defective conversion of H202 to HOCl

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19
Q

MPO deficiency symptoms?

A

Increased risk for Candida infections; however, most patients are asymptomatic.

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20
Q

MPO deficiency and NBT?

A

normal; respiratory burst O2. to H2O2 is intact.

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21
Q

O2-independent killing

A

less effective than O2-dependent killing and occurs via enzymes present in leukocyte secondary granules (e.g., lysozyme in macrophages and major basic protein in eosinophils).

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22
Q

Step 7?Resolution

A

Neutrophils undergo apoptosis and disappear within 24 hours after resolution of the inflammatory stimulus.

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23
Q

Macrophages

A

Macrophages predominate after neutrophils and peak 2-3 days after inflammation begins.

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24
Q

What are macrophages derived from?

A

monocytes in blood

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25
Q

How do macrophages arrive in tissue?

A

via the margination, rolling, adhesion, and transmigration sequence

26
Q

What do macrophages do?

A

Ingest organisms via phagocytosis (augmented by opsonins) and destroy phagocytosed material using enzymes (e.g., lysozyme) in secondary granules (02-independent killing)

27
Q

What are the outcomes for macrophages managing the next step of the inflammatory process?

A

Resolution and healing, 2. Continued acute inflammation, Abscess, Chronic inflammation

28
Q

Macrophages induce Resolution and healing by?

A

Anti-inflammatory cytokines (1L-10 and TGF-(Beta) are produced by macrophages.

29
Q

Macrophages induce Continued acute inflammation by?

A

persistent pus formation; IL-8 from macrophages recruits additional neutrophils.

30
Q

Macrophages induce Abscess by?

A

acute inflammation surrounded by fibrosis; macrophages mediate fibrosis via fibrogenic growth factors and cytokines.

31
Q

Macrophages induce chronic inflammation by?

A

Macrophages present antigen to activate CD4+ helper T cells, which secrete cytokines that promote chronic inflammation

32
Q

Chronic inflammation is characterized by?

A

presence of lymphocytes and plasma cells in tissue, its a delayed response but more specific (adaptive immunity) than acute inflammation

33
Q

Chronic inflammation stimuli include

A

(1) persistent infection (most common cause); (2) infection with viruses, mycobacteria, parasites, and fungi; (3) autoimmune disease; (4) foreign material; and (5) some cancers.

34
Q

T lymphocytes are produced where?

A

Produced in bone marrow as progenitor T cells

35
Q

Where are T lymphocytes further developed?

A

Further develop in the thymus where the T-cell receptor (TCR) undergoes rearrangement and progenitor cells become CD4+ helper T cells or CD8 cytotoxic T cells

36
Q

T cells use TCR complex for?

A

(TCR and CD3) for antigen surveillance

37
Q

What does the TCR complex do?

A

recognizes antigen presented on MHC molecules i. CD4+ T cells?MHC class II, CD8+ T cells?MHC class I

38
Q

Activation of T cells requires what?

A

(1) binding of antigen/MHC complex and (2) an additional 2nd signal.

39
Q

CD4+ helper T-cell activation

A

Extracellular antigen (e.g., foreign protein) is phagocytosed, processed, and presented on MHC class II, which is expressed by antigen presenting cells (APCs) - B7 on APC binds CD28 on CD4+ helper T cells providing 2nd activation signal.

40
Q

Activated CD4+ helper T cells do what?

A

secrete cytokines that help inflammation and are divided into two subsets.

41
Q

What are the subsets of activated CD4+?

A

TH1 and TH2

42
Q

TH1 subset

A

secretes IL-2 (T cell growth factor and CD8+ T cell activator) and IFN-gamma (macrophage activator)

43
Q

TH2 subset

A

IL-4, IL-5, IL-10

44
Q

TH2 subset secretes IL-4 which results in?

A

facilitates B-cell class switching to IgG and IgE

45
Q

TH2 subset secretes IL-5 which results in?

A

eosinophil chemotaxis and activation, maturation of B cells to plasma cells, and class switching to IgA

46
Q

TH2 subset secretes IL-10 which?

A

inhibits TH1 phenotype

47
Q

How does CD8+ cytotoxic T-cell activation occur?

A

Intracellular antigen (derived from proteins in the cytoplasm) is processed and presented on MHC class I, which is expressed by all nucleated cells and platelets.

48
Q

What provides the 2nd activation signal for CD8+?

A

IL-2 from CD4+ TH1 cell

49
Q

Cytotoxic T cells are activated for?

A

killing

50
Q

SLE is characterized by

A

antinudear antibody ANA; sensitive, but not specific and anti dsDNA antibodies (highly specific)

51
Q

Antihistone antibody is characteristic of?

A

drug-induced SLE.

52
Q

What are some common causes of drug induced SLE?

A
  1. Hydralazine, procainamide, and isoniazid are common causes 2. Removal of drug usually results in remission.
53
Q

30% of what cases are associated with SLE?

A

Antiphospholipid antibody syndrome

54
Q

Antiphospholipid antibody syndrome is characterized by?

A

autoantibody against proteins bound to phospholipids. 2.

55
Q

In antiphospholipid antibody syndrome what are the most common antibodies?

A

Anticardiolipin and lupus anticoagulant

56
Q

In antiphospholipid antibody syndrome what tests are disrupted?

A

Leads to false-positive syphilis test and falsely-elevated PTT lab studies, respectively

57
Q

What does antiphospholipid antibody syndrome result in?

A

arterial and venous thrombosis including deep venous thrombosis, hepatic vein thrombosis, placental thrombosis (recurrent pregnancy loss), and stroke

58
Q

What does antiphospholipid antibody syndrome require?

A

lifelong anticoagulation

59
Q

What is sjogren syndrome?

A

Autoimmune destruction of lacrimal and salivary glands, lymphocyte-mediated damage (type IV hypersensitivity) with fibrosis

60
Q

How does sjogren syndrome classically present?

A

as dry eyes (keratoconjunctivitis), dry mouth (xerostomia), and recurrent dental carries in an older woman (50-60 years)?Can’t chew a cracker, dirt in my eyes

Aaron-Exit: Championship Rounds (27 decks)

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