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CMOD Week 3 > Pathoma Chapter 2 > Flashcards

Pathoma Chapter 2 Flashcards

1
Q

What is inflammation used for?

A

Allows inflammatory cells, plasma proteins, and fluid to exit blood vessels and enter the interstitial space

acute and chronic

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2
Q

What is acute inflammation characterized by?

A

presence of neutrophils and edema. Arise in response to infection of tissue necrosis (not apoptosis)

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3
Q

How do TLRs work?

A

These are called ‘Toll-Like Receptors’ and are present on cells of the innate immune system (macrophages and dendritic cells) and are activated by PAMPs on binding pathogens.

TLRs are also on the surface of lymphocytes and are thus involved with acquired immunity

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4
Q

What doe activation of TLRs induce?

A

results in regulation of NF-kB pathway that activates transcription of multiple immune mediators

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5
Q

What do PGI2, PGD2, and PGE2 do?

A

cause vasodilation and increased vascular permeability

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6
Q

What else does PGE2 do?

A

mediates pain and fever (PGI2 does as well)

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7
Q

What does LTB4 do?

A

attracts and activates neutrophils

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8
Q

What do LTC4, LTD4, and LTE4 do?

A

vasoconstriction, bronchospasm, and increased vascular permeability

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9
Q

What are mast cells activated by?

A

1) tissue trauma
2) C3a and C5a
3) cross-linking of cell-surface IgE by antigen

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10
Q

What happens when mast cells are activated?

A

Immediate- preformed histamine granules degranulate, causing vasodilation and increased vascular permeability

Delayed-production of AA metabolites, particularly leukotrienes

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11
Q

What effects does bradykinin have on acute inflammation?

A

induces vasodilation and increased vascular permeability (similar to histamine) and pain

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12
Q

The redness (erythema) and warmth (heat) associated with acute inflammation are due to what?

A

vasodilation, resulting in creased blood flow

key mediators are: histamine, prostaglandins, and bradykinin

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13
Q

Swelling associated with acute inflammation is due to what?

A

Due to leakage of fluid from postcapillary venues into the interstitial space (exudate)

key mediators are: histamine, tissue damage (which causes endothelial lining disruption)

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14
Q

Pain associated with acute inflammation is due to what?

A

bradykinin and PGE2 sensitize nerve endings

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15
Q

Fever associated with acute inflammation is due to what?

A

Pyrogens (e.g. LPS from bacteria) cause macrophages to release IL-1 and TNF, which increase cyclooxyrgenase in perivascular cells of the hypothalamus

The increased PGE2 raises temperature set point

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16
Q

What is the first step of how neutrophils leave vasculature and enter inflammed tissue?

A

1) vasodilation slows blood flow in post capillary venues and cells marginate from center of flow to periphery

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17
Q

What is the second step of how neutrophils leave vasculature and enter inflammed tissue?

A

2) Upregulation of P and E Selection facilitate ROLLING of leukocytes at the site of inflammation

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18
Q

P-selectin is released from where?

A

Weibel-Palade bodies (mediated by histamine)

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19
Q

E-selectin up regulation is induced by what?

A

TNF and IL-1

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20
Q

P and E Selectins bind to what on incoming leukocytes?

A

sialyl Lewis X molecules (addressins)

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21
Q

What is the third step of how neutrophils leave vasculature and enter inflammed tissue?

A

cellular adhesion molecules (ICAM and VCAM) are unregulated on endothelium by TNF and IL-1 and attach to integrins on leukocytes

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22
Q

Integrins are unregulated on leukocytes by what?

A

C5a and LTB4

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23
Q

Leukocyte adhesion deficiency

A

autosomal recessive defect on LFA-1 on leukocytes causing delayed umbilical detachment, increased circulating neutrophils (due to impaired adhesion of marginated pool of leukocytes and recurrent bacterial infections that lack pus

24
Q

Neutrophils are attracted by which chemotaxis?

A

IL-8, C5a, and LTB4

This is the fourth step of how neutrophils leave vasculature and enter inflammed tissue

25
Q

What happens when a leukocyte encounters a bacterial pathogen?

A

phagocytosis leading to degradation of pathogen via PRRs. Phagosomes fuse with lysosomes resulting in pathogen uptake, NADPH reaction, etc.

26
Q

What is Chediak-Higashi syndrome?

A

protein trafficking defect (autosomal recessive) characterized by impaired phago-lysosome formation

27
Q

How does Chediak-Higashi syndrome manifest clinically?

A

increased risk of pyrogenic infections

neutropenia

giant granules in leukocytes (due to fusion of granules from Golgi)

abnormal dense granules in platelets

Albinism

Peripheral neuropathy

28
Q

How are pathogens killed by phagocytes?

A

O2 dependent killing is the most effective

fusion of phagosome with lysosome results in oxidative burst resulting in superoxide. Superoxide is converted to hydrogen peroxide by superoxide dismutase. Hydrogen peroxide is converted to bleach by MPO

O2-independant chilien is less effective and occurs via enzymes like lysosyme in macrophages and major basic protein in eosinophils

29
Q

Chronic granulomatous disease

A

Due to NADPH oxidase defect (x-linked or AR)

Leads to recurrent infection and granuloma formation with catalase positive organisms, especially Staph. aureus, Pseudomonas coppice, Serrate marcescens, Aspergillus

30
Q

How is CGD diagnosed?

A

nitroblue tetrazolium test used to screen. Turns blue is NADPH oxidase is present

31
Q

MPO deficiency would lead to what?

A

not able to convert H2O2 to HOCl

32
Q

How long do neutrophils live for?

A

about 1 day, neutrophils undergo apoptosis and disappear within 24 hours after resolution of the inflammatory stimulus

33
Q

What cells predominate after neutrophils die?

A

macrophages peak 2-3 days after inflammation begins

34
Q

What role do macrophages have in acute inflammation?

A

macrophages are derived from monocytes in blood and arrive in tissue via the same processes as neutrophils and destroy opsonized pathogens via oxygen species and granules (lysosymes)

Macrophages also work to manage the next step in the inflammatory process

35
Q

Outcomes of acute inflammation:

A

1) Resolution and healing- anti-inflammatory cytokines (e.g. IL-10 and TGF-B) are produced by macrophages
2) Continued acute inflammation- marked by persistent pus formation; IL-8 recruits additional macrophages
3) Abscess- acute inflammation surrounded by fibrosis; macrophages mediate fibrosis via fibrogenic growth factors and cytokines
4) Chronic inflammation; macrophages present antigen to activated CD4+ T cells which produce cytokines that promote chronic inflammation

36
Q

Chronic Inflammation

A

characterized by the presence of lymphocytes and plasma cells in tissue

delayed response but more acquired (specific) than cute inflammation

37
Q

What cytokines do TH1 helper T cells produce?

A

IFN-y (activated macrophages, promotes B-cell class switching to IgG1 and IgG3, and promotes Th1 phenotype)

38
Q

What cytokines do TH2 helper T cells produce?

A

IL-4 (promotes B-cell class switching to IgE), IL-5 (promotes eosinophil chemotaxis and activation and IgA class switching), and IL-13 (similar to IL-4)

39
Q

How can CTLs induce cell death?

A

Fas ligand binds to initiate apoptosis and secretion of perforin and granzyme

40
Q

What is granulomatous inflammation?

A

granuloma forming with giant macrophages in interior and TH1 on exterior

subtypes: caseating and non-caseating

41
Q

What are non-caseating granulomas?

A

lack central necrosis. caused by foreign material, sarcoidosis, Crohn disease, cat scratch fever, and beryllium exposure

42
Q

What are caseating granulomas?

A

exhibit central necrosis and are characteristic of TB and fungal infections

43
Q

Steps in granuloma formation:

A

1) Macrophages process and present antigen via MHC class II to CD4 helper T cells
2) Interaction leads macrophages to secrete IL-12, inducing TH1 differentiation
3) TH1 secrete IFn-y, which converts macrophages to epithelioid histiocytes and giant cells

44
Q

What happens in DiGeorge syndrome?

A

Developmental failure of 3rd and 4th pharyngeal pouches leading to lack of thymus (T cell), etc.

45
Q

X-linked Agammaglobulinemia

A

Complete lack of immunoglobulin due to disordered B cell maturation due to mutation of BTK leading to cell arrest during pre-B cell phase

46
Q

Clinical presentation of X-linked Agammaglobulinemia

A

presents after 6 months of life with recurrent bacterial, enterovirus, and Giardia lamblia infections; maternal antibodies present during first 6 months of life are protective

live vaccines must be avoided

47
Q

What is Hyper IgM syndrome caused by?

A

defected in CD40L on T cells or CD40 on B-cells. Thus, B cells cannot be activated and cytokine class-switching cannot occur

low IgA, IgE, and IgG result in current pyogenic infections (due to poor opsonization), specially at mucosal sites

48
Q

A deficiency in the MAC complex (or any of C5-C9) would leave a patient susceptible to what?

A

Neisseria infection (meningitidis or gonorrhoeae)

49
Q

Tissues are divided into what three types based on regeneration ability?

A

Labile, Stable, or Permanent

50
Q

What are labile tissues?

A

these possess stem cells that continuously cycle to regenerate the tissue

51
Q

Examples of labile tissue

A

small and large bowel, skin, bone marrow, cervix

52
Q

What is the difference between primary and secondary intention

A

Primary- wound edges are brought together (e.g. suturing of a surgical incision); leads to minimal scar formation

Secondary- edges are not approximated granulation tissue fills the defect myofibroblasts then contract the wound, forming a scar.

53
Q

What things would cause a delay in wound healing?

A

Infection (Staph. aureus)

Vitamin C, copper, or zinc deficiency

presence of foreign body, ischemia, diabetes, or malnutrition

54
Q

Why would vitamin C be needed for proper wound healing?

A

vitamin C is an important cofactor in the hydroxylation of proline and lysine pro collagen residues; hydroxylation is needed for eventual collagen cross-linking

55
Q

Why would copper be needed for proper wound healing?

A

a cofactor for lysyl oxidase, which cross-links lysine and hydroxylysine to from stable collagen

56
Q

Why would zinc be needed for proper wound healing?

A

a cofactor for collagenase which replaces type III collagen or granulation tissue with stronger type I collagen in classic wound healing

57
Q

What are the steps of wound repair?

A

1) Replacement of damaged tissue with fibrous scar
2) Formation of granulation tissue consisting of fibroblasts, myofibroblasts, type III collagen, and capillaries
3) Type I replacement of type III collagen via collegians using zinc as a cofactor (stronger)

CMOD Week 3 (10 decks)

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