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MOD Exam 1 > Ch. 3: Inflammation and Repair > Flashcards

Ch. 3: Inflammation and Repair Flashcards

1
Q

Define Inflammation

A

a response of vascularized tissues to infections and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents

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2
Q

What are the series of steps for the course of inflammation? (5 R’s)

A

Recognition (of pathogen)

Recruitment (of leukocytes)

Removal (of pathogen or offending substance)

Regulated (termination of Rxn)

Repair (of tissues)

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3
Q

Which of the following pairs of cell types and Cytokines/Immunoglobulins is correctly paired for the condition of chronic or acute asthma?

A. Eosinophils, IgA
B. Eosinophils, Ig E
C. Neutrophils, Ig E
D. Macrophages, IL-17

A

B. Eosinophils, Ig E

table 3-1 (71)

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4
Q

What are the 5 hallmark signs of inflammation

A

Rubor (redness)
Calor (heat)
Dolor (pain)
Tumor (swelling)

Loss of function

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5
Q

A 65 year old patient returns to your office with the same pain in his hands he has had for a while now. The flair up has been more progressive over the last few days. On blood blood test, you notices higher numbers of monocytes, macrophages and lymphocytes. Which type of inflammation is most likely occurring in this patient?

Acute or Chronic?

A

Chronic

Table 3-2 (71)

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6
Q

A 55 y/o man comes to your office with a small ulcer on his foot. He has a hx of T2DM and hyperglycemia. The ulcer has a black ring around it and looks to have purulent discharge. Which of the following causes of inflammation is most prevelent in this patients condition?

A. Infection
B. Necrosis
C. Foreign Bodies
D. Immune reaction (Hypersensitivity)

A

B. Necrosis

p71-72

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7
Q

T/F: Acute inflammation has a higher prevalence of local and systemic signs than chronic inflammation?

A

True

3-2 (71)

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8
Q

What are the main causes of inflammation?

A

Inflammation
Necrosis
Foreign bodies
Immune Reaction

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9
Q

What are the three components of acute inflammation?

A

Dilation of small vessels
Increased permeability of small vessels
Emigration of leukocytes

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10
Q

What is the principle difference between transudate, exudate, pus, and edema

A

Exudate: high protein, may contain some white and RBC

Transudate: Low protein and low cell count

Pus: purulent with high leukocytes (neutrophils), microbes, and cellular debris

Edema: extracellular fluid buildup in tissues can be either exudate or transudate

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11
Q

Which selectins are expressed on the surface of the endothelium?

A

E-selectin
P-selectin
(induced by TNF and IL-1)

L-selectin on leukocytes, Naive T/B cells

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12
Q

Which integrins bind to ICAM-1?

A

LFA-1 (Neutrophils, monocytes, T cells)

MAC-1 (monocytes, DCs)

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13
Q

Which integrins bind to VCAM-1

A

VLA-4 ( Monocytes, T cells)

a4b7 ( Monocytes, T cells)

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14
Q

Which Ig on the surface of endothelial cells and leukocytes is responsible for the transmigration (diapedesis) of leukocytes into the intracellular space?

A

CD31 AKA PECAM-1

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15
Q

How long do neutrophils predominate the cells of early infection?

A

6-24 hrs

Monocytes 24-48 hrs

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16
Q

what are the three steps of phagocytosis

A

Recognition and attachment
engulfment
destruction of microbe

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17
Q

what are the 4 phagocytic receptors and their ligands that aid phagocytes in their recognition abilities

A

G-Protein coupled receptor - lipids, chemokines, N-formyl-methionyl peptidases

Toll-like receptor - Microbial surface proteins

Cytokine receptor - IFN-y

Phagocytic receptor

Fig 3-7

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18
Q

Describe the process of engulfment

A

Once a particle binds, the cell membrane begins to envaginate. The cell sends out extensions of the cytoplasm called pseudopods. This wraps around the particle which forms the phagosome. This then joins a lysosome forming the phagolysosome. This is dependent on actin filament rearrangement.

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19
Q

What is the name of the process that occurs in azurophilic granules of neutrophils in which MPO (myeloperoxidase), in the presence of a halide (Cl) converts H2O2 into OCl2?

A

Halogenation

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20
Q

What the are three types of NO found in the body and which is involved in immune response?

A

endothelial (eNOS)
neuronal (nNOS)
inducible (iNOS) - involved in immunity by IFN-y

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21
Q

What are Neutrophil extracellular traps

A

extracellular fibrillar networks that provide a high concentration of antimicrobial substances at sites of infection and prevent the spread of the microbes by trapping them in the fibrils

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22
Q

What factors contribute most to the short lived action of the immune response?

A

Factors like IL-10 and TGF-B

as well as the natural short half life of the inflammatory cells and their products which are degraded rapidly after the insulting agent is removed.

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23
Q

What are the most important mediators of acute inflammation?

A 
Vasoactive amines (histamine)
lipid products (prostaglandins and leukotrienes)
Cytokines (including chemokines and compliment)
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24
Q

what are the major types of cells that produce the mediators for acute inflammation?

A

Sentinel cells
Mast Cells, DCs, Macrophages

other cells can be induced to produce those mediators.

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25
Q

What is the class of enzyme the produce prostaglandins and from what is it synthesized?

A

Cyclooxygenase (COX-1 COX-2)

synthesized from arachadonic acid

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26
Q

Which eicosanoids are responsible for vasodilation?

A

PGI2, PGE1, PGE2, PGD2

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27
Q

Which eicosanoids are responsible for vasoconstriction?

A

Thromboxane A2, Leukotrienes C4, D4, E4

Leukotrienes also cause increased vascular permeability

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28
Q

if you wanted to prescribe an anti-inflammatory drug which COX enzyme would be, theoretically, more beneficial to block due to the other’s high involvement in homeostasis?

A

COX-2 specific inhibitor

COX-1 is involved dramatically in ion regulation which is why chronic use of things such as Ibuprofen and Aspirin (block both COX1/2) can lead to ulceration and bleeding

However it also seems COX-2 specific blockers increase brain injury potential so fuck me ammi right?

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29
Q

Inhibition of what enzyme will prevent the formation of leukotrienes and be beneficial in the treatment of asthma.

A

5-lipoxygenase.

note*
12-lipoxygenase makes Lipoxins A4 and B4 which are anti-inflammatory

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30
Q

What naturally found substance could you offer to a patient to reduce inflammation due to its poor substrate ability to be used by cycloxygenase and lipoxygenase pathways?

A

polyunsaturated fats in fish oil.

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31
Q

Where is TNF made and what is its function

A

Macrophages, Mast Cells, T lymphocytes

Stimulates expression of endothelial adhesion molecules and secretion of cytokines, systemic rxn

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32
Q

Where is IL-1 made and what is its function

A

Macrophages, Endothelial cells, some epithelial cells

Stimulates expression of endothelial adhesion molecules and secretion of cytokines, systemic rxn
FEVER!!!

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33
Q

Where is IL-6 produced and its main function

A

Macrophages, other cells

acute phase response

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34
Q

Someone presents to the hospital with muscle wasting, anorexia and appears cachexic. Which cytokine would be most predominant in this presentation?

A

TNF

functions to regulate energy use and suppress appetite.

35
Q

What produces IL-17, what is its function, and is it more prominent in acute or chronic inflammation

A

T Lymphocytes

Recruitment of neutrophils and monocytes

BOTH acute and chronic

36
Q

What produces IL-12 and what is its function?

A

DCs and Macrophages

induce IFN-y

37
Q

What produces IFN-y and what is its function?

A

T cells

NK cells

38
Q

Which of the following Chemokines is most influential in recruiting neutrophils?

A. C-X-C
B. C-C
C. C
D. CX3C

A

A. C-X-C

39
Q

What are the three pathways of compliment?

A

Classical - IgM or IgG bind C1

Alternative - microbial surface molecules (shnyra always said spontaneous…)

the Lectin - Mannose-binding-lectin binds to carbohydrates and activates C1

40
Q

To what step in compliment do all pathways lead to?

A

formation of C3 convertase which cleavs C3 to C3a and C3b. this in turn forms C5 convertase which cleaves C5 into C5a and C5b. C5b joins C6-9 to form the MAC

41
Q

Which of the following components of compliment serve as a chemotactic agent for neutrophils, monocytes, eosinophils, and basophils?

A. C5a
B. C3a
C. C5b
D. C4a

A

A. C5a

inactive C3b (iC3b) serves as an opsonin.

42
Q

Deficiency in compliment controller C1 inhibitor leads to what condition?

A

hereditary angioedema

43
Q

Describe the actions of DAF and CD59

A

DAF: inhibits the formation of CD3 convertase (deficiency results in paroxysmal nocturnal hemoglobinuria)

CD59: inhibits formation of MAC

44
Q

What are the morphogenic hallmarks of acute inflammation?

A

dilation of small vessels

accumulation of leukocytes

Fluid in extravascular tissue

45
Q

Describe the hallmarks of serous inflammation

A

exudation of cell-poor fluid into spaces created by cell injury or into body cavities lined by the peritoneum, pleura or pericardium

46
Q

Describe the hallmarks of fibrous inflammation

A

fibrinous exudate develops when the vascular leaks are large or there is a local procoagulant stimulus (ie cancer)

mostly in pericardium and meninges

47
Q

Describe purulent inflammation

A

production of pus, and exudate containing neutrophils and liquified debris of necrotic cells and edematous fluid.

48
Q

Describe the hallmarks of ulcers

A

a local defect or excavation of the surface of an organ or tissue that is produced by the sloughing of inflamed necrotic tissue.

49
Q

What are the three possible outcomes of acute inflammation?

A

Complete resolution (all cells are replaced and inflammation removed)

Healing by connective tissue (scarring, fibrosis) - no regeneration, abundance of fibrin exudation

Progression to chronic inflammation - maintenance of inflammatory response, and angiogenesis.

50
Q

What are the main causes of chronic inflammation?

A

Persistent infection

Hypersensitivity reaction

Prolonged exposure to potentially toxic agents (out or in)

51
Q

What morphologic characteristics are prevalent in chronic inflammation?

A

Infiltration with mononuclear cells

Tissue destruction

Attempts at healing

52
Q

Which of the following describes a macrophage in the liver?

A. histiocytes
B. kupffer cells
C. microglia
D. alveolar macrophages

A

B. kupffer cells

A. histiocytes - lymph node and spleen
C. microglia - CNS
D. alveolar macrophages - Lungs

53
Q

What is the difference between classically activated M1 macrophages and alternatively activated M2 macrophages.

A

classical activation is accomplished by IFN-y as well as microbial peptides engaging TLR and T cell receptors

Alternative activation is accomplished by IL-13 and IL-4. and inhibit classical activation; anti inflammatory

54
Q

What are the two possible outcomes from macrophage activation?

A

1) elimination of injurious stimuli and initiation of repair mechanisms
2) persistence of macrophage activation leading to further inflammatory responses in chronic inflammation

55
Q

T cells, predominantly CD4+ T cells, have a wide variety of actions they can take depending on their subtypes and induction. What are the three subtypes of CD4+ T cell and what are their functions?

A

Th1 - inflammation through IFN-y -> classical activation of macrophages

Th2 - secrete IL-4, IL-5, and IL-13 which recruit and activate eosinophils and perform alternative macrophage activation

Th17 - IL-17 secretion which induce cytokines that recruit neutrophils

56
Q

Describe the function and immunologic pattern of eopsinophils

A

They are abundant in immune reactions involving IgE and parasites. Their granules contain major basic protein

57
Q

Describe the function and immunologic pattern of mast cells

A

widely distributed in connective tissue and participate in acute and chronic inflammation. they express the receptor FCeRI that cross links with IgE -> allergic reaction

58
Q

What are the two types of granuloma?

A

Foreign body granulomas - absence of T cells; form around foreign bodies such as talc or sutures

Immune granulomas - persistent T-cell mediated response, macrophages -> IL-2 -> T-cells -> macrophages

59
Q

The biopsy of a woman who has TB was taken. There was a note of cells with indistinct borders, pink cytoplasm called epithelioid cells. There are also multinucleated, giant cells between 40-50 um in diameter (langhans giant cells). Grossely, caseous necrosis is also observed. Morphologically, what type of specific inflammation is seen here?

A

Granulomatous inflammation

pg 98

crohn’s disease and sarcoidosis have less necrotic centers and more fibrous centers.

60
Q

Look at table 3-8 I couldnt make an effective question, plus he says its intro

A

HEY BUSTER! DID YOU EVEN LOOK!? I didnt think so!

61
Q

Describe the acute phase response

A

cytokine-induced systemic reactions, notable IL-1, TNF,, and IL-6 as well as Type I interferons

62
Q

Describe how exogenous and endogenous pyrogens influence the development of fever

A

LPS (or other exogenous pyrogen) stimulates IL-1 or TNF (endogenous pyrogen) release from leukocytes. This induces cycloxygenase to produce prostaglandins (PGE2) which set the temp point higher in the hippo-thala-moose

63
Q

Name and describe the three best know acute phase proteins

A

C-reactive protein (CRP) - Induce IL-6, bind microbial cell walls as opsonins

Fibrinogen - Induce IL-6, binds RBCs cause rouleaux formation (erythrocyte sedimentation)

serum amyloid A (SAA) - Induce TNF and IL-1, bind microbial cell walls as opsonins

64
Q

Which of the following proteins produced during an acute phase response is responsible for the depletion of iron in chronic inflammation?

A. CRP
B. Fibrinogen
C. Hepcidin
D. SAA
E. Ferritin
A

C. Hepcidin

65
Q

What is a major distinguishing factor between a leukemoid reaction and leukemia?

A

presence of left shift/increase in band cells.

the leukemoid reaction is associated with the rapid increase in leukocytes meaning more immature leukocytes are released.

66
Q

Match the shift in cell counts based on the type of infection

  1. Bacteria A. Eosinophilia
  2. Virus B. Neutrophilia
  3. allergies/ parasites C. absolute lymphocytosis
A
  1. B
  2. C
  3. A
67
Q

What condition of over stimulation of the inflammatory response is outlined by the following symptoms.

hyperglycemia
fever
hypotension
disseminated intravascular coagulation
elevated cytokines
A

Septic Shock

68
Q

What are the two forms of tissue repair reactions?

A

Regeneration - some tissues able to replaced damage and essentially return to normal (skin, intestines, liver)

Connective tissue deposition - if damage is too severe or tissue can’t regenerate, fibrous tissue is layed down to repair it. Called fibrosis

*note - if fibrosis develops in a tissue space occupied by inflammatory exudate, its called organization

69
Q

The ability of tissues to be able to regenerate is based on their intrinsic proliferative capacity. Therefore, name and describe the three categories of tissue and their associated proliferative capacity

A

Labile (continuously dividing tissue) - tissue always being lost and replaced such as hematopoietic tissue and surface epithelia

Stable tissues - these tissues are quiescent and have minimal proliferative activity. Most solid tissues, liver, kidney, and pancreas. Exception of liver, tissues have minimal regenerative capacity

Permanent tissues - considered to be terminally differentiated and non proliferative. Majority of neurons and cardiac muscle cells belong to this category.

70
Q

What are the steps in scar formation?

A

Angiogenesis

Formation of granulation base

Remodeling of CT

71
Q

How do macrophages inform the repair of tissues by scar tissues?

A

clearing offending agents and dead tissue

providing growth factors for the proliferation of various cells

Secreting cytokines that stimulate fibroblast proliferation, CT synthesis and deposition

72
Q

Explain how angiogenesis aids the repair of tissues by scar tissues.

A

Vasodilation in response to NO and increase permeability due to vascular endothelial growth factor (VEGF).

Breakdown of basement membrane allows for vessel sprout to form

Migration and proliferation of endothelial cells behind tip leading to remodelling of capillary tubes.

Pg 104 for more info

73
Q

What are the two steps of connective tissue deposition

A

migration and proliferation of fibroblasts into the site of injury

Deposition of ECM proteins produced by these cells

74
Q

What cytokine is the most important for synthesis and deposition of CT and why?

A

TGF-B

stimulates fibroblast migration and proliferation, increased synthesis of collagen and fibronectin and decreased degradation of ECM due to inhibition of metalloproteinases

75
Q

What fiber contributes to the contraction of scar tissue over time?

A

myofibroblasts

76
Q

what is connective tissue remodeling influenced by?

A

it is a balance between synthesis and degradation of ECM proteins

77
Q

What influences tissue repair?

A 
Infection
Diabetes
Nutritional status (vit C deficiency)
Glucocorticoids (inhibition of TGF-B)
Mechanical factors
Poor perfusion
Foreign Bodies
Type and extent of injury
Location of injury
78
Q

Describe healing by first intention

A

injury only involved epithelial layer, principle mechanism of repair is epithelial regeneration.

EX. clean surgical incision approximated by sutures

  • wound rapidly activates coagulation pathways -> scab
  • within 24 hrs neutrophils at incision margin -> 24 - 48 hrs epithelial cells proliferate
  • day 3, neutrophils replaced by macrophages -> collagen fibers and epithelial proliferation continues
  • day 5 has neovascularization
79
Q

Describe healing by second intention

A

cell or tissue loss is more extensive such as in large wounds, abscesses, ulceration, and ischemic necrosis in parenchymal tissues. Repair is regeneration and scarring

development of abundant granulation tissue, accumulation of ECM and formation of large scar and wound contraction by action of myofibroblasts.

At first there is a matrix of type III collagen but by 2 weeks this is replaced by type I collagen.

80
Q

Fibrosis in parenchymal organs is predominantly due to what cytokine?

A

TGF-B

Chronic inflammation and insult to these organs perpetuated the cycle of injury and repair which recruits TGF-B to recruit fibroblasts and other cells to deposit collagen and connective tissue

ie cirrhosis

81
Q

What can inadequate formation of granulation tissue or scar formation lead to?

A

dehiscence - reopening of a wound most secondary to surgery

ulceration - poor blood supply such as in diabetes

82
Q

What can too much scar deposition lead to

A

hypertrophic scars and keloids

-predominant in AA community
accumulation of excessive collagen

83
Q

Excessive granulation causes what problem for wound repair?

A

excessive granulation protrudes around the surrounding skin and block reepithelialization.

MOD Exam 1 (5 decks)

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