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Pathology > Test 1: 08-09 Chronic Inflammation > Flashcards

Test 1: 08-09 Chronic Inflammation Flashcards

1
Q
  1. What extends chronic inflammation?
A

Causative stimuli persistence

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2
Q
  1. What are 3 morphological features of chronic inflammation
A

i. Infiltration of mononuclear cells
ii. Tissue destruction
iii. attempts at healing by CT tissue replacement, angiogenesis, and fibrosis

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3
Q
  1. How does chronic inflammation begin?
A

Low grade, smoldering response without signs of acute inflammation

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4
Q
  1. Chronic inflammation may be the result of?
A

i. Persistent infections by certain microbes
ii. Immune-mediated inflammatory diseases
iii. Prolonged exposure to toxic exogenous (silica) or endogenous (atherosclerosis) agents

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5
Q
  1. Persistent infections by certain microbes can be difficult to erase. What do they have in common?
A

i. Low toxicity
ii. Evoke delayed hypersensitivity response
iii. Pattern called “granulomatous reaction”

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6
Q
  1. What are causes immune-mediated inflammatory diseases and give an example of each? Pattern?
A

a. Three causes
i. Autoimmune diseases i.e. rheumatoid arthritis, multiple sclerosis
ii. Unregulated immune responses i.e. inflammatory bowel diseases
iii. Allergic response i.e. bronchial asthma
b. Pattern: mixed acute and chronic inflammation, fibrosis may occur

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7
Q
  1. What do macrophages formed from and migrate to? Origin?
A

a. From circulating blood monocytes and migrate out of bloodstream into tissue
b. Bone marrow

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8
Q
  1. What are organs/tissues are macrophages especially concentrated in and what are their names?
A

i. Liver (Kupffer cells)
ii. Spleen and lymph nodes (sinus histiocytosis)
iii. Lungs (alveolar/pulmonary macrophages)
iv. CNS microglia

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9
Q
  1. Macrophages serve as? What is this system called?
A

a) Filter for matter, microbes, senescent (old) cells

b) The mononucleated phagocyte system

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10
Q
  1. Activation signals for macrophages include cytokines, what are these secreted by? Give two more activation signals
A

Sensitized T & NK cells, bacterial endotoxin, other chemical mediators

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11
Q
  1. After activation, macrophages secrete many biologically active proteins whose roles are?
A

Keep pathogens in check, can also cause host injury and fibrosis if inappropriately activated

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12
Q
  1. Give six products secreted by macrophages and a brief description if any
A

i. Acid and neutral proteases (toxic to ECM)
ii. Complement components and coagulation factors
iii. Reactive oxygen species and nitrogen species (toxic to microbes and host cells)
iv. AA metabolites (eicosandoids)
v. Cytokines, (IL-1 & TNF) and chemotactic factors (cause influx of other cells)
vi. Growth factors (cause collagen deposition and angiogenesis)

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13
Q
  1. In chronic inflammation, what happens to macrophages? What mediates one of these processes?
A

a. Macrophages persistently accumulate and proliferate
b. Accumulation mediated by
i. Recruitment of monocytes from circulation
ii. Local proliferation after emigration from bloodstream
iii. Immobilization of macrophages

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14
Q
  1. Tissue damage in chronic inflammation may also be caused by what four things?
A

i. Necrotic tissue
ii. Leukocyte mediators
iii. Liberation of substances from dying tissue
iv. Killing by T lymphocytes

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15
Q
  1. What mobilizes lymphocytes? What relationship do T-lymphocytes and macrophages have?
A

a. Any immune stimulus/non-immune inflammation

b. Reciprocal (bidirectional) relationship

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16
Q
  1. What initially activates T-lymphocytes? What do these activated ones produce? What do these activated ones release?
A

a. Antigen-presenting macrophages
b. Cytokines that recruit monocytes including IFN-y(major activator of macrophages)
c. Cytokines, including IL-4 and TNF further activating lymphocytes/other cell types

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17
Q

a. Antigen-presenting macrophages
b. Cytokines that recruit monocytes including IFN-y(major activator of macrophages)
c. Cytokines, including IL-4 and TNF further activating lymphocytes/other cell types

A

a. B-cell activation
b. Antibodies against persistent antigens
c. Patterns of organogenesis, resembling lymphoid organs

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18
Q
  1. Eosinophils are seen? One of the most powerful chemokines recruiting eosinophils is? What eosinophils contain and what does this cause?
A

a. Parasitic infections or immune reactions mediated with IgE (allergies)
b. Eotaxin
c. Granules with major basic protein (MBP), cationic protein toxic to paratsites but also causes epithelial cell lysis

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19
Q
  1. Mast cells participate in? “Armed” with? Releases? 3 roles?
A

a. Both acute and chronic inflammation
b. IgE to certain antigens
c. Histamines and prostaglandins
d. Roles
i. Anaphylactic shock
ii. Infections
iii. Elaborating cytokines (TNF) contributes to fibrosis

20
Q
  1. Neutrophils appear where? Also called?
A

a. Both acute and chronic inflammation

b. Acute chronic inflammation or chronic active inflammation

21
Q
  1. What is granulomatous inflammation? Mechanism dealing with? Activator of? Activation of which leads to?
A

fill in

22
Q
  1. What is responsible for persistent macrophage activation in granulomatous inflammation? What is a granuloma and what are the types?
A

a. T-cell derived cytokines
b. Granuloma: focus of chronic inflammation of macrophage aggregation turned into epithelium like cells surrounded by mononuclear leukocytes (mainly lymphocytes and sometimes plasma cells)
c. Foreign body granuloma and immune granuloma

23
Q
  1. Foreign body granulomas form as a response to? Form when? What forms as a result? In the end usually granulomas function as?
A

a. Response to usually inert foreign bodies
b. When foreign material is too large for a single macrophage and does not incite inflammation/immune response
c. Epithelioid cells and giant cells
d. Walls off offending object so may be defense

24
Q
  1. Immune granulomas are caused by a variety of agents capable of? Usually occurs when? Process? Give four settings in which granulomas may form
A

a. Cell-mediated response
b. Insoluble particles
c. Macrophages take in and present to appropriate T-lymphocytes leading to T-lymph activation
d. Persistent T-cell responses to certain microbes such as:
i. Treponema pallidum (syphilitic gumma)
ii. Certain fungi
iii. Mycobacterium tuberculosis

25
Q
  1. Morphologically how do macrophages in granulomas appear in H&E sections? When it ages what do granulomas form and how is it formed?
A

a. Activated macrophages in granulomas have pink, granular cytoplasm and indistinct boundaries
b. Rim of fibroblasts and CT due to cytokines secreted by activated macrophages

26
Q
  1. Sometimes multinucleated giant cells appear; what are they derived from? How are these they arranged?
A

a. Fusion of macrophages

b. Peripherally (Langhans-type giant cells) or haphazardly (foreign body-type giant cells)

27
Q
  1. In some infections (TB) there may be a central zone of necrosis in the granuloma, what is this caused by? How does it appear grossly? What is the name for this appearance? What is needed for granulomas to form?
A

a. Hypoxia and free radical injury
b. Cheesy, granular appearance
c. Caseous necrosis
d. Poorly digestible irritants/T-cell mediated immunity

28
Q
  1. Lymphatics provide defense by? Purpose of lymph flow in inflammation? Significance of valves? Drainage may transport the offending agent and lymphatics may become?
A

a. Filtering and policing extravascular fluid
b. Drainage from extravascular space
c. Lymph flow only proximally
d. Lymphatics inflamed (lymphangitis), lymph nodes (lymphadenitis)

29
Q
  1. If the secondary barriers of inflammation defense are overwhelmed, what may this lead to?
    What is the next line of defense? What may form when the pathogens enter the heart vavles, meninges, kidneys, and joints?
A

a. Pathogen access to circulation leading to bacteremia (sepsis)
b. Phagocytic cells of liver, spleen, and bone marrow
c. Organs and massive infection names:
i. Heart valves: endocarditis
ii. Meninges: meningitis
iii. Kidneys: renal abscesses
iv. Joints: septic arthritis

30
Q
  1. Sepsis causes activation of? Inflammation symptoms attributed to? Most prominent systemic manifestation of inflammation and process?
A

a. Mediator systems in plasma and inflammatory cells
b. Cytokines
c. Hypothalamic-pituitary-adrenal axis, leukocytes/acute phase response, fever and shock

31
Q
  1. Systemic effects of inflammation are called?
A

Acute-phase response or systemic inflammatory response syndrome (SIRS)

32
Q
  1. What is the acute-phase response characterized by (5)? Give the cause and its stimulation?
A

a. Symptoms
i. Fever
ii. Leukocytosis
iii. Decreased appetite
iv. Altered sleep patterns
v. Changes of plasma in acute phase proteins
b. Cytokines whose production stimulated by bacterial products like LPS etc.

33
Q
  1. Fever is produced in response to? Give examples
A

Exogenous pyrogens (bacteria LPS) or endogenous pyrogens (cytokines such as IL-1 and TNF)

34
Q
  1. What do cytokines stimulate in the hypothalamic thermoregulatory centers that increase fever? This in turn, has production stimulated by?
    What inhibits the fever response and how?
A

a. Cytokines stimulate prostaglandin synthesis
b. IL-1 and TNF increase the enzymes (cyclooxygenase) that convert AA into prostaglandins
c. Inhibitors of cyclooxygenase (i.e. aspirin) by inhibiting prostaglandin synthesis in the hypothalamus

35
Q
  1. Acute-phase proteins are plasma proteins that are mostly synthesized in? What changes the plasma levels of this?
A

a. Liver

b. IL-1, IL-6, and TNF-α

36
Q
  1. Give three famous acute phase proteins. Role? Markers/indicators for what test(s)?
A

a. Acute phase proteins:
i. C-reactive protein (CRP)
ii. Fibrinogen
iii. Serum amyloid A protein (cause 2° amyloidosis)
b. Bind to microbial cell walls acting as opsonins and fix complements
c. Indicators
i. Elevated CRP: risk of myocardial infarction
ii. Rise in fibrinogen levels (makes RBCs stick and form stacks called rouleaux) is basis of test called Erythrocyte Sedimentation Rate (ESR) = presence of systemic inflammatory response

37
Q
  1. Leukocytosis is common in inflammatory reactions. What are three characteristics of it?
A

i. Neutrophilia: increase of neutrophils
ii. Lymphocytosis: increase of lymphocytes
iii. Eosinophila

38
Q
  1. In neutrophilia, what are high WBC counts called?
A

Leukemoid reactions

39
Q
  1. Why does leukocytosis occur?
A

An accelerated release of cells from bone marrow and rise of immature neutrophils in blood

40
Q
  1. Lymphocytosis is an? Seen in?
A

Increase number of lymphocytes seen in infectious mononucleosis, mumps, and German measles

41
Q
  1. When does eosinophilia occur?
A

Bronchial asthma, hay fever, and parasitic infections

42
Q
  1. Leukopenia is?
A

Decrease in number of white cells

43
Q
  1. What are two other manifestations of leukopenia?
A

i. Autonomic: increase pulse and blood pressure, decreased sweating, redirect blood flow from shallow to deep beds
ii. Behavioral: shivering, chills, anorexia, somnolence, and malaise

44
Q
  1. In severe bacterial infections (sepsis), large quantities of what is produced? High levels of these change what?
A

a. Cytokines
b. Host response changes:
i. Disseminated intravascular coagulation (DIC)
ii. Thrombosis
iii. Liver injury
iv. Overproduction of NO

45
Q
  1. What does overproduction of NO do?
A

Leads to heart failure, drop in blood pressure (hemodynamic shock)

46
Q
  1. Septic shock is a triad of?
A

i. DIC
ii. Hypoglycemia
iii. Cardiovascular failure

47
Q

what are two consequences of defective(3)/excessive inflammation(2)?

A

a. Defective
i. Increase susceptibility of infections
ii. Delayed healing of wounds
iii. Tissue damage
b. Excessive
i. Basis of many diseases
ii. Non primary immune disorders (e.g. cancer, atherosclerosis, ischemic heart disease, and some neurodegenerative diseases, chronic infectious metabolic and other diseases)

Pathology (6 decks)

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