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MOD 1: DR > Chapter 3.2 > Flashcards

Chapter 3.2 Flashcards

1
Q

• Triad of Complement Activation

A
  1. Increases vascular permeability
  2. Opsinzation
  3. Chemotaxis
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2
Q

What assists with inflammation in compliment system?

A

Anaphylatoxins: C3a and C5a&raquo_space;» C4a

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3
Q

C5a has 3 functions. what are they

A

anaphylatoxin,
chemoattractant,
activates the lipoxygenase pathway

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4
Q

What assists with opsinization?

A

C3b, promote phagocytosis by neutrophils and mfs

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5
Q

What assists with cell lysis?

A

C5b: binds C6-9 to make the MAC complex, which has alot of C9 => kills bacteria within cell walls, like Niessiera infection

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6
Q

Def in C5b, C6-9 or MAC predisposes to?

A

Nieserra bacteria

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7
Q

Most important step of complement activation?

A

Cleavage of C3 into C3a and C3b

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8
Q

• All three pathways of complement activation lead to the formation of _____

A

C3 convertase

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9
Q

Classical pathway

A

GM makes classic cars

C1 binds IgG and IgM, bound to Ag combine => + path

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10
Q

Alternative pathway

A

+ by microbial surface proteins, like endotoxin or LPS

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11
Q

Lectin pathway

A

MBL binds to carbs on microbes => activates C1

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12
Q

What are the actions of anaphylatoxins?

A

Simulate histamine release form mast cells

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13
Q

Inherited deficiencies in C1 inhibitor lead to what?

A

heriditary angioedema

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14
Q

DAF

A

regulatory protein that prevents formation of C3 convertases

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15
Q

CD59

A

regulatory protein that inhibits formation of MAC complex

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16
Q

Hereditary deficiency of the enzyme that makes GPI anchors on the plasma membrane causes what?

A

a deficiency in DAF and CD59, which are anchored to plasma membrane with GPI anchor

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17
Q

Acquired deficiency of the enzyme that makes GPI anchors is called

A

paroxysmal nocturnal hemoglobinuria => cause excessive activation of compliment and lysis of RBC and more common in F

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18
Q

Inherited deficiencies of compliment

A

increases our chance of getting infections and causes deficiencies in regulatory proteins => causing macular degeneration, hemolytic uremic syndrome

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19
Q

Deficiency in reg proteins

A

causes excessive compliment activation, which causes macular degeneration and hemlolytic uremic syndreme

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20
Q

Platelet activating factor is inflammatory mediator. What does it do and where is it found?

A

PAF is on leukocytes and mast cells.

Platelet aggregation, vasodilation/bronchoconstriction, increases venular permeability at low concentrations

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21
Q

Protease-activated receptors (PARs)

where are they
what activates them
what do they have a role in

A

PARS are located on [platelets and leukocytes activated by thombin].

Role in clotting

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22
Q

Chemokines:

source:
Action:

A

leukocytes, activated MO

chemotaxis, leukocyte activation

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23
Q

Compliment

Source

action

A

Vasodilation (by stimulating mast cells)

Kills target (MAC)

Leukocyte chemotaxis and activation

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24
Q

What are morphological hallmarks of acute inflammatory reactions?

A

dilatlation of BV
Accumulation of leukocytes and fluid in extravascular tissue.

But, special patterns can be superimposed.

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25
Q
  1. Serious inflammation
A

Serious inflammation is protein, leukocyte poor, uninfected effusion that accumulates in body cavities lined by peritnium, pleura or the pericardium.

Seen in acute inflammation

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26
Q

What are examples of serous inflammations

A

skin blisters

viral infection that causes serious accumulation under the skin

27
Q
  1. Fibrinous inflammation
A

In acute inflammation; greater increases in vascular permrability or local procoagualants (cancer cells ) that allow fibrinogen to leak out (fibrin exudate) and form fibrin deposits in tissues or spaces, causes inflammation of body lining like [meninges, pericardium and pleura].

28
Q

Histologically, what do fibrinous inflammation look like?

A

eosinophillic mesh of threads or amorphous substances

29
Q

Can the fibrin deposits in fibrinous inflammation be revmoed

A

yes; macrophages can revemo whoever if they fail; there is ingrowth of fibroblasts and BV => scarring => thickening in pericardium and epicardium which can obliterate the pericardial space

30
Q
  1. Purulent (suppurative) inflammation
A

Purulent (suppurative) inflammation is the production of pus; an exudate from neutophils, debris from necrotic cells and edema that occurs d/t bacterial infections that cause liquifactive necrosis, such as STAPH

31
Q

Staph is referred to as what

A

pyogenic (pus-producing) bacetia

32
Q

What is a common example of Purulent (suppurative) inflammation,

A

occurs in acute pancreatits

33
Q
  1. Absess
A

when pus becomes burried in a tissue, organ or confined space

34
Q

What pattern do we see with absess

A
  1. a central region of dead necrotic leukocytes,
  2. Surrounded by surving neutrophils
  3. Surrounded by vascular dilation and fibroblastic and parenchumal proliferation, clues for chronic inflammation!
35
Q

do absesses remain forever?

A

no, they can be replaced by CT

36
Q

What are ulcers

A

breaks in the surface of organ or tissue that are made by the sloughing off of inflammed necrotic tissue that often occur in mucosa of GI tract and in LE of DM patients

37
Q

Describe acute stage of peptic ulcer and chronic

A

acute: vascular dilation and immune cell infiltration

chronic stage: fibroblastic proliferation, scarring and accumilation of lymphocytes, MO and plasma cells

38
Q

what are outcomes of acute inflammation

A
  1. complete resolution: debris is removed by macrophages and lymphatic system absorbs edema
  2. Scarring or fibrosis occurs when CT grows over tissue and undergoes organization (converts to mass of fibrous tissue)
  3. PRogresses to chronic inflammation when it cannot be healed or injury is persistant
39
Q

In chronic inflammation, what cells infiltrate the tissue days after inflammation?

A
  1. lymphocytes
  2. plasma cells (B cells)
  3. Monocytes and Macrophages
40
Q

in chronic inflammation, Tissue injury and fibrosis is often ________

A

severe and progressive

41
Q

________, _____ and _______ all coexist with chronic inflammation.

A

inflammation
tissue injury
attempts to repair

42
Q

What allows chronic inflammation to be, chronic?

A

Activation of lymphocytes.

The bi-directional interaction between the MO and T cells: macrophages display Ags to T cells, express mem molecs, and cause T cell responses.

T cells then make TNF, IL1 and chemokines that recruit and activate MORE macrophages.

43
Q

the most common cause of chronic inflammation is persistant infections from microbes that are hard to kill.

What kind of hypersensitivity reaction is this and what can it lead to?

A

delayed type

can lead to granulomatous reaction

44
Q

2nd cause of chronic inflammttion is hypersensitivity diseases. what are these

A

Immune system is excessively and inapprop activated d/t autoimmune diseases

or unregulated activation of or immune system to microbes (IBD) or environmental thinfs

45
Q

What kind of symptoms do hypersensitivity diseases show

A

acute and chronic

46
Q

What is the last 3rd cause of chronic inflammation?

A

prlonged exposure to endogenous or toxic agents: exogenous (silca) -> inflamm lung diases called silicosis

Lipids/cholesterol => arteriosclerosis

47
Q

What are the 3 morphological changes we see in chronic inflammation?

A
  1. Infiltration of chronic immune cells (mononuclear cells: macrophages, lymphocytes and plasma cells)
  2. tissue damage
  3. attempts to health by CT replacement, angiogenesis and fibrosis
48
Q

What is the most dominant cell in chronic inflammation; which

secretes cytokines and GF,
causes phagocytosis
and activates other T-cell.

A

macrophages

49
Q

Macrophages are tissue cells derived from _______ in the ______ and progenitors from ________. They circulate in the blood as ________ (half life of 1 day), however once the arrive to the tissue they differentiate into macrophages (half-life ________).

A

hematopoeitc stem cells
yolk sac and fetal liver

monocytes

months-years

50
Q

Macrophages in the liver are called what?

A

kupffer cells

51
Q

Macrophages in the spleen and LN are called what?

A

sinus histiocytes

52
Q

Macrophages in the CNS are called what?

A

microglia

53
Q

Macrophages in the lung are called what?

A

alveolar macrophages (dust cells)

54
Q

_______ predominate after neutrophils and peak ____days after inflammation begins.

A

macrophages

2-3

55
Q

Classical activation of macrophages produces what kind of macrophages?

A

M1: pro-inflammatory

56
Q

Alternative activation of macrophages produces what kind of macrophages

A

M2: anti-inflammatory involved in tissue repair

57
Q

Classical activation of macrophages

A
    • by endotoxin/TLR, IFN-gamma (inhibit alt act), foreign substances
  2. IFN-y –> macrophages –> IL-12 –> macrophages
  3. Produce ROS and RNS and increase lysosomal enzymes – kill ingested organisms
  4. Produces IL-1, IL-12, and IL-23 causes inflammation
58
Q

• Alternative activation of macrophages (M2, anti-inflammatory, tissue repair)

A
    • by IL-4 and IL-13 which also inhibit the classical pathway.
  2. GF and TGF -B => angiogenesis, activates fibroblasts, and + collagen synthesis
  3. IL-10 and TGF-β cause antiinflammatory affects
59
Q

_____ activated occurs first to destroy the offender, then the _____ to initiate repair

A

Classical activated occurs first to destroy the offender, then the alternative to initiate repair

60
Q

o CD4+ helper T cells secrete cytokines that amplify inflammation & are divided into 3 kinds:

  1. Th1
  2. Th2
  3. Th17

what do each do?

A
  1. Th1 secrete IFN-y and IL2 => + M1 macrophages or intracellular bacteria, fungi and viruses
  2. Th2 secrete IL4/5/13 => activate M2 MO, esophionophils and basophils for parasites
  3. Th17 secrete IL-1, recruit neutrophils and monocytes for EXTRACELLULAR bacteria and fungi.
61
Q

_______are made by accumulation of lymphocytes, APCs, and plasma cells in chronic inflammation.

A

Tertiary lymphoid organs ; perpetualte immune reaction

62
Q

______ contain granules with major basic protein that is very cationic, toxic to parasites and causes lysis to mammalian epithelial cells.

What immune reactions are they abundant in?

A

eosinophils

IgE and parasites

63
Q

______ are found in connective tissue and activation causes release of histamine and prostaglandins in allergic reactions

A

mast cells

64
Q

_______ are induced by persistent microbes or mediators prod by activated mfs and T cells

A

neutrophils

MOD 1: DR (11 decks)

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