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FTCM > L6, L9, L12- Inflammation and Repair > Flashcards

L6, L9, L12- Inflammation and Repair Flashcards

1
Q

Inflammation occurs in order to remove (1) via changes in (2) and (3). This is important for setting up (4). The inflammatory reaction is considered apart of (innate/adaptive) immunity.

A

1- injurious agent
2- vascular
3- cell
4- the base for tissue healing and repair
5- innate (although helps prepare the adaptive immune response)

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2
Q

Some negative effects of inflammation include exacerbation of (1) causing (2). If inflammation fails, (3) may occur. Inappropriate inflammation reactions may also occur in response to (4) and (5).

A

1- tissue injury
2- pain
3- abscess / fail to clear infection => further complications
4- nonharmful environmental Ags, allergic disease
5- self-Ags, autoimmunity

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3
Q

list the 5 general steps of the inflammatory response

A

1) offending agent recognized
2) recruitment of leukocytes and plasma proteins (to site of offending agent)
3) leukocytes and proteins activated to eliminate offending agent
4) reaction is controlled and terminated
5) damaged tissue is repaired

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4
Q

define acute inflammation

A
  • initial rapid response: develops w/in mins-hrs, lasts for hrs-days
  • characterized by presence of exudate
  • predominate leukocyte = neutrophils
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5
Q

define chronic inflammation

A
  • develops slowly, lasts for longer duration than acute
  • associated with more tissue destruction
  • predominate leukocyte = lymphocytes and macrophages
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6
Q

list the cardinal signs of inflammation

A
  • rubor (redness)
  • calor (heat)
  • dolor (pain)
  • tumor (swelling)
  • loss of function (function laesa)
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7
Q

list some causes of inflammation

A
  • infections: bacterial, viral, fungal, parasitic
  • trauma / physical agents
  • chemical agents
  • tissue necrosis (any cause)
  • foreign body (ex. sutures)
  • immune rxns
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8
Q

the key cell receptor for microbial recognition is _____ (include some defining characteristics)

A
  • Toll-like receptors (TLRs)
  • distinguish self and foreign
  • when activated, production of certain molecules promote inflammatory reaction
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9
Q

Cells have sensors in the (1) to recognize various molecules, including (2), that are liberated / altered as a result of cell damage. They activate (3) to induce (4).

A

1- cytosol
2- ATP, uric acid, DNA, etc
3- inflammasome formation (multiprotein cytosolic complex)
4- CK production

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10
Q

leukocytes can recognize (1) or (2) surrounding microbes, after a process called (3), which results in release of CKs to initiate (4)

A

1- Abs (IgG)- recognizing its Fc tail
2- complement protein (C3b)
3- opsonization
4- inflammatory response

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11
Q

(1) can recognize microbial sugars / proteins to promote (2) and (3). Examples include (4).

A

1- circulating proteins
2- ingestion
3- complement activation
4- mannose binding lectin, collectins

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12
Q

events of acute inflammation include (1) followed by (2)

A

1- vascular changes

2- cellular events

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13
Q

list the two parts of vascular changes seen in acute inflammation- includes their purpose

A

1) changes in vascular caliper (diameter/dimensions) and blood flow: vasodilation and turbulent flow
2) inc vascular permeability
- purpose is to maximize movement of plasma proteins and leukocytes out of circulation and into site of infection / injury

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14
Q

the escape of fluids from vasculature to interstitial tissue is called (1) and the fluid is referred to as (2)

A

1- exudation

2- exudate

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15
Q

Immediately after an injury or infection, associated vasculature will undergo (1) briefly before (2) occurs due to various mediators, but mostly due to (3). This results in (4) to give rise to the following cardinal signs of inflammation: (5).

A 
1- neurogenic vasoconstriction
2- vasodilation
3- histamine
4- inc blood flow (turbulent flow)
5- heat (calor) + redness (rubor) = erythema
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16
Q

Following vasodilation in area of injury/infection, vasculature will undergo (1) leading to (2) and (3). (4) and (5) of the blood in the microvasculature is evident to cause (6).

A 
1- inc permeability
2- loss of fluid
3- inc vessel diameter
4- slower blood flow (turbulent flow)
5- inc viscosity
6- stasis
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17
Q

what is the purpose of stasis

A
  • blood leukocytes accumulate along vascular endothelium

- easier for leukocytes to adhere to endothelium and then migrate through vascular wall –> interstitial tissue

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18
Q

define exudate

A
  • the fluid present in interstium at site inflammation
  • high protein content
  • some WBCs and RBCs present
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19
Q

describe the 4 mechanism that can increase vascular permeability

A
  • gaps due to endothelial contraction: venules, most common, via vasoactive mediators, fast and short-lived (mins)
  • endothelial injury: arter./capil./venul., toxins/burns/chemicals, fast and long-lived (hrs-days)
  • leukocyte endothelial injury: venules (pulmonary capillaries), late and long lived (hrs)
  • increased transcytosis: venules, vascular endothelium derived growth factor
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20
Q

what is the response of lymphatic vessels in inflammatory process

A
  • dilatation (inc diameter)
  • lymphangitis (inflammation of vessels: dilation, inc permeability)
  • lymphadenitis (enlargement of lymph nodes)
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21
Q

list the two parts of cellular events seen in acute inflammation

A

1) leukocyte recruitment

2) leukocyte activation

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22
Q

list the general steps of leukocyte recruitment in acute inflammatory response [include which leukocytes]

A

[mainly neutrophils]

1) margination, rolling, adhesion to endothelium
2) migration across endothelium + vessel wall (diapedesis)
3) migration in tissue to chemotactic stimulus (chemotaxis)

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23
Q

margination of leukocytes occurs due to (1) in early inflammatory response and since there is a decrease in (2), WBCs assume a (3) position

A

1- slowed blood flow (turbulent flow) / stasis
2- wall shear stress
3- peripheral position along the endothelium

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24
Q

define rolling of leukocytes

A
  • transient adhesion of leukocytes to endothelium

- repeated process of binding and detaching => rolling along vessel wall

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25
Q

the interactions of the following are responsible for rolling of leukocytes

A

(selectins- expression regulated by CKs)

  • L-selectins, leukocytes
  • E-selectins, endothelum
  • P-selectins, platelet + endothlium
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26
Q

The weak rolling interactions of leukocytes and endothelium mediated by (1) help slow leukocytes down enough to allow them to adhere via (2) present on leukocytes and (3) and (4) present on endothelial cells.

A

1- selectins
2- integrins
3- VCAM-1 (vascular cell adhesion molecule)
4- ICAM-1 (intercellular adhesion molecule)

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27
Q

Migration of leukocytes across the endothelium and vessel wall is called (1) and usually occurs in (2) type vessels. (3) is an important adhesion molecule involved. Leukocytes pierce the basement membrane by (4) to enter extravascular tissue.

A

1- transmigration, diapedesis
2- postcapillary venules
3- PECAM-1 (platelet endothelial cell adhesion molecule)
4- secreting collagenases

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28
Q

list the molecules responsible for chemotaxis

A
  • CKs- IL-8
  • C5a
  • LT-B4
  • bacterial products
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29
Q

order the following by which they peak in an acute inflammatory response: edema, monocytes/macrophages, neutrophils

A
  • edema (quickly): recruit leukocytes
  • neutrophils (~1 day): destroy offending agent
  • monocytes/macrophages (~2 days): repair damaged tissue
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30
Q

list the three results of leukocyte activation once they recognize microbes or dead cells

A
  • phagocytosis
  • intracellular killing of engulfed pathogen
  • production of mediators to amplify inflammatory reaction
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31
Q

list the steps of phagocytosis

A

1- recognition + attachment of particle to be ingested by leukocyte
2- engulfment
3- killing/degradation of ingested material (via phagosomal-lysosomal fusion)

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32
Q

the key opsonizers in the immune system are….

A

-IgG
-C3b (complement)
-collectins
(they function to enhance leukocyte attachment to microbial surfaces)

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33
Q

intracellular killing within phagocytes occurs via….

A
  • O2 dependent killing (ROS)

- O2 non-dependent enzymatic killing (+ RNS)

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34
Q

list methods where leukocytes can cause tissue damage

A

(leakage of lysosomal contents into extracellular space)

  • Phagosome leakage: regurgitation during feeding
  • attempting to phagocytose large molecules (futile phagocytosis)
  • engulfment of cytotoxic material => phagocyte disintegration
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35
Q

list the benefits from cellular infiltrates in acute inflammation

A
  • phagocytosis
  • microbial killing
  • release of mediators
36
Q

list the benefits from fluid exudate in acute inflammation

A
  • dilute toxins
  • Ig delivery
  • fibrin formation (fibrinogen)
  • activate plasma mediator system
  • cell nutrition
  • promotes immunity
37
Q

list the 4 types of acute inflammation

A
  • serous infla.
  • fibrinous infla.
  • suppurative / purulent infla.
  • ulcers
38
Q

(1) inflammation is marked by exudation of cell poor fluid, which is typically (not/infected); examples include: (3)

A

1- serous
2- not infected
3- blisters (burns / viral infection), pleural/pericardial effusions, ascites

39
Q

(1) inflammation develops following vascular leakage; (2) leaks out into extracellular space and (3) is formed/deposited. This inflammation usually occurs in (4).

A

1- fibrinous
2- fibrinogen
3- fibrin
4- linings of body cavities; ex. meninges, pericardium, pleura

40
Q

(1) inflammation is marked exudation of cell rich fluid, consisting of (2). This inflammation is usually caused by (3) and also leads to (4) necrosis. Examples include (5).

A 
1- suppuritive / purulent
2- neutrophils, liquified debris of necrotic cells, edema fluid
3- pyogenic bacteria
4- liquefactive necrosis
5- boils, furuncles, abscess
41
Q

(1) is a local defect / excavation on the surface of an organ or tissue that is produced by (2). It usually affects the following: (3).

A

1- ulcers
2- sloughing of inflamed necrotic tissue
3- mucosa of mouth, stomach, intestines, genitourinary tract

Note- in response to acute and chronic inflammation

42
Q

list the outcomes of acute inflammation

A
  • complete resolution: clearance, repair, return to normal function
  • progression to chronic inflammation: mononuclear cell infiltration + fibrosis
  • abscess formation: pus formation (–> eventually leads to fibrosis)
  • scarring / fibrosis: loss of function
43
Q

Chemical mediators of inflammation are derived from (1) or (2). They are deactivated by the following mechanisms: (3), (4), (5), (6)

A

1/2- plasma (liver) or cell derived (at site of inflammation)
3- spontaneous decay (PGs)
4- enzymatic degradation (kinin via kininase)
5- elimination (ROS + antioxidants)
6- inhibition (complement inhibitory proteins)

44
Q

list the sources of cell derived mediators of acute inflammation

A
  • endothelial cells (at site)
  • tissue macrophages
  • mast cells
  • recruited leukocytes
45
Q

list the cell derived mediators of acute inflammation

A
  • vasoactive amines
  • arachidonic acid metabolites: PGs, LTs, TXs
  • CKs
  • ROS
  • lysosomal enzymes
46
Q

list the sources of plasma derived mediators of acute inflammation

A
  • Complement system: C5a/C3a, C3b, MAC
  • Coagulation / Fibrinolytic system: Hageman factor / factor XII
  • Kinin system: bradykinin (pain)
47
Q

list some causes of chronic inflammation

A
  • progression from acute inflammation due to i) persistent infection, ii) prolonged exposure to injurious agent
  • recurrent bouts of acute inflammation
  • chronic inflammatory response from the onset
48
Q

list the features of chronic inflammation (3)

A
  • infiltration of mononuclear cells
  • tissue destruction
  • attempted healing with new vessel formation and fibrosis
49
Q

list the cells of chronic inflammation

A
  • macrophages
  • lymphocytes
  • eosinophils, mast cells, few neutrophils
50
Q

define epithelioid cells

A
  • form of activated macrophages
  • resemble endothelial cells, abundant cytoplasm
  • limited phagocytic activity, mainly secretory function
51
Q

define Giant Cells

A

-fused activated macrophages (multinucleated)

  • Langerhans Giant Cell: nuclei in U-shape
  • Foreign Body Giant Cell: randomly arranged nuclei (clustered/clumped)
52
Q

M1 macrophages, aka (1), are induced by (2) and have (3) and (4) as the main functions

A

1- classically activated macrophages
2- IFN-γ, microbes
3- microbicidal actions: phagocytosis + killing (ROS, RNS, NO, lysosomal enzymes)
4- inflammation (IL-1, IL-12, IL-23, CKs)

Note- they inhibit M2 macrophages

53
Q

M2 macrophages, aka (2), are induced by (2) and have (3) and (4) as the main functions

A

1- alternatively activated macrophages
2- IL-13, IL-4
3- tissue repair / fibrosis (GFs, TGF-β)
4- anti-inflammatory effects (IL-10, TGF-β)

Note- they inhibit M1 macrophages

54
Q

list the lymphocytes involved in chronic inflammation

A
  • Th cells (Th1, Th2, Th17)
  • Tc cells
  • Plasma cells
55
Q

Th1 cells produce (1) to activate (2)

Th2 cells produce (3) to recruit (4), activate (5)

Th17 cells produce (6) to recruit (7)

A

1- IFN-γ
2- M1

3- IL-4, IL-5, IL-13
4- eosinophils
5- M2

6- IL-17
7- neutrophils

56
Q

eosinophilic granules contain (1) and have an important role in (2)

A

1- major basic protein

2- parasitic / allergic reactions

57
Q

if arachidonic acid undergoes COX (= (1)) pathway, (2) can form to yield (3) and (4) can form to yield (5)

A

1- cyclooxygenase
2/3- PGs: vasodilation, inhibits platelet aggregation
4/5- TXs (TX-A2): vasoconstriction, promotes platelet aggregation

58
Q

if arachidonic acid undergoes 5-lipoxygenase pathway, (1) forms leading to (2)

A

LTs- chemotaxis (LT-B4, LT-A), bronchospasm + inc vascular permeability (LT-C,D,E 4)

59
Q

list the components of the mononuclear phagocytic system

A
  • monocytes (blood)
  • resident tissue macrophages
  • free macrophages
  • epithelioid cells
  • giant cells (langerhans, foreign body)
60
Q

granulomatous inflammation is generated by (1) in the (2) form with the assistance from (3)

A

1- macrophages (activated)
2- epithelioid of giant cell form
3- Th1 cells

61
Q

list the 6 causes of granulomatous inflammation, include associated microbe

A
  • tuberculosis (mycobacterium tuberculosis) [the only caseating granuloma]
  • leprosy (mycobacterium leprae)
  • syphilis (treponema pallidum)
  • cat-scratch disease (bartonella sp.)
  • indigestible material (talcosis, berylliosis)
  • idiopathic (sarcoidosis, Crohn’s)
62
Q

list some morphological features of chronic inflammation

A
  • fistula formation
  • sinus
  • chronic ulcer
  • chronic abscess
  • thickening of a hollow viscus
  • stricture formation (abnormal narrowing)
63
Q

(fistula/sinus) connects a cavity lined with granulation tissue and an epithelial surface, the other is defined as (2)

A

1- sinus (cavity + epithelial surface; blind-ended sac)

2- fistula = connection between 2 epithelial-lined surfaces

64
Q

list the systemic effects of an inflammatory reaction (include the cause)

A

(caused by CKs)

  • fever
  • leukocytosis
  • acute phase proteins
  • other manifestations
65
Q

describe fever as an inflammatory response (include its mediator)

A

-raise of body temperature by 1-4 C
-most frequent feature
-caused by pyrogens (exogenous and endogenous)
-mediated by TNF
[-complex mechanism: bacteria stimulate leukocytes, release CKs, inc PGs –> acts on hypothalamus]

66
Q

Leukocytosis = (1), with a rise of (2).

  • (3) occurs in bacterial infections
  • (4) occurs in viral infections
  • (5) occurs in parasitic infections
  • (6) occurs in typhoid fever
A 
1- inc WBC count
2- 15000-20000 cells/mL
3- neutrophilia
4- lymphocytosis
5- eosinophilia
6- leukopenia
67
Q

In the acute phase protein response from inflammation, there is a decrease in (1) synthesis and an increase (2), (3) [which if prolonged may cause (4)], and (5) [which leads to (6)]

A

1- albumin
2- CRP (C-reactive protein)
3/4- serum amyloid AA –> amyloidosis (amyloid deposition)
5/6- fibrinogen –> Rouleaux formation (RBC stacking) + inc ESR (erythrocyte sedimentation rate- ability for RBC to settle in a column)

68
Q

these three CKs, (1), are responsible for activating (2) to produce the following acute phase proteins: (3)

A

1- IL-1, IL-6, TNF
2- liver
3- CRP, serum amyloid, fibrinogen, haptoglobin, C3

69
Q

list the other / less common systemic manifestations of inflammation

A
  • inc HR, BP
  • chills / rigor
  • dec or inc sweating
  • lethargy / altered sleep pattern
  • sepsis / septic shock
70
Q

list the three common outcomes of chronic inflammation

A
  • healing by fibrosis (fibroblasts), to replace ECM (most common outcome)
  • lack of resolution and persistance of inflammatory process
  • loss of function: due to abnormal ECM or fibrosis
71
Q

describe the consequences of chronic inflammation that persists and doesn’t resolve

A
  • metaplasia –> dysplasia –> malignancy

- prolonged serum amyloid A production –> secondary amyloidosis (amyloid deposition causing various Sxs)

72
Q

list some long-term effects of persistent chronic inflammation

A
  • ill health / weight loss (cachexia)
  • arrest of growth
  • anemia of chronic disease
73
Q

Cardinal Signs of Inflammation:

  • (1) causes redness/heat
  • (2) causes swelling
  • (3) causes pain
  • (4) causes tenderness
  • (5) causes lack of function
A

1- vasodilation
2- edema + cell infiltrates
3- direct stimulation of nociceptors (K+, bradykinin, PGs, substance P)
4- dec nociceptor threshold (IL-1/6/8, TNF-α) & inc tension (ex. abcess)
5- no resolution from chronic inflammation

74
Q

pain from inflammation is caused by direct nociceptor stimulation by (1) with tenderness caused by a decrease in nociceptor threshold due to (2) and increased (3)

A

1- K+ (necrosis), bradykinin (mast cell), PGs (mast cell), substance P (neurotransmitter)
2- IL-1, IL-6, IL-8, TNF-α (Th1 cells)
3- tension (ex. abscesses)

75
Q

define regeneration

A
  • restoration of damaged components to the normal state

- via proliferation of cells that survived injury and retain capacity to proliferate

76
Q

(1) occurs if injured tissues aren’t capable of complete restitution. It can occur as fibrosis, which is defined as (2) or as an organization defined as (3).

A

1- scar formation (structure is somewhat normal, usually return of majority of function)
2- fibrous tissue creation in background of chronic inflammation
3- develops in tissue space filled with inflammatory exudates

77
Q

ECM has either a (1) form or a (2) form. It components include the following: (3).

A

(extracellular matrix)
1- basement membrane
2- interstitial matrix
3- fibriller proteins (collagen, elastin), adhesive molecules, hydrated gel

78
Q

describe the fibriller proteins found in the ECM

A

Collagen- most abundant protein, mechanical support to maintain body shape / locomotion, different types for different organs, amount is balance between synthesis/degradation

Elastin- non-rigid tertiary structure, provides tissues with elastic recoil

79
Q

describe the function of adhesive molecules in ECM and provide some examples

A
  • connects cells and ECM components to each other (cell-cell, cell-ECM, ECM-ECM)
  • delivers signals about cell proliferation / differentiation
  • Ex: laminin, fibronectin
80
Q

describe the makeup and function of hydrated gels in the ECM

A
  • glycoaminoglycans and proteoglycans
  • rich in Neg. electrical charges
  • provides organs tugor (ability to return to shape if transiently disrupted), lubrication, resilience
  • stores GFs
81
Q

list functions of ECM

A
  • mechanical support
  • cell growth + maintenance of cell differentiation
  • provides scaffolding during tissue repair
82
Q

granulomatous inflammation is chronic inflammation with (1) cells in (2) form and (3) cells; the presence of (4) defines the granuloma as (5) or (6)

A 
1- macrophages
2- epithelioid, giants cells
3- lymphocytes
4- central necrosis
5- caseating (present)
6- non-caseating (not present)
83
Q

caseating granuloma is the key sign of….

A

TB

84
Q

list the cells that predominately proliferate during tissue repair (include what controls this)

A
  • remnants of injured cells
  • fibroblasts
  • vascular endothelial cells

-controlled by Cell Cycle via Growth Factor and other interactions with ECM (auto-, para-, endo-crine signals)

85
Q

(1) are the most important source of GFs, including the following: (2)

A

1- macrophages

2- platelet derived (PDGF), epidermal (EGF) and transforming (TGF-α), hepatocyte (HGF), vascular endothelial (VEGF)

FTCM (16 decks)

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