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Block 3 Found Sci > 2-Chronic Inflammatory > Flashcards

2-Chronic Inflammatory Flashcards

1
Q

chronic inflamm

def

A

must be > 2 weeks, low grade smoldering resp either after acute or from repeated episodes of acute

must have 1. inflamm 2. tissue destruction 3. attempts at repair
-inflamm with mononucleocytes
-repair with fibroblasts

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2
Q

causes

A
  1. persistent microbial infections- low pathogenicity so not kill you right away so delayed hypersensitivity and hard to eradicate
  2. immune related inflamm disease- autoimmune, unregulated responses, allergic vs environ antigens
  3. prolonged exposure to toxins - exo or endogenous (inc plasma lipid components)
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3
Q

morphological features

A
  1. infiltration with mononuclear cells aka macrophages, lymphocytes, plasma cells
  2. tissue destruction- induced by persistent stimulus or inflamm cells
  3. attempts healing- CT replace damaged tissue, new vessel prolif aka angiogenesis and fibrosis (collagen)
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4
Q

role of macrophages

A

key cell in chronic and granulomatous inflamm
-filter and sentinels for lympho stimulation

from circulating blood monocytes that emigrate to site of injury 24-48 hrs after onset

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5
Q

different types of macros

A

@ liver = Kupffer cells
@ spleen, LNs, lungs = pulmonary or alveolar macros
@ CNS = microglia
@ bone = osteoclasts

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6
Q

features for activated macros

A
  1. inc size (look large and flat like squamous)
  2. inc number lysosomes
  3. inc amount of lyso enz
  4. inc ability to kill orgs

compared to monocytes

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7
Q

activation signals macros

A
  1. cytokines from act T cells and NK cells
  2. bacterial endotoxins, gram neg
  3. microbial products
  4. other inflamm mediators
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8
Q

macro activation pathway

A
  1. circulating mono will extravate into tissue
  2. interact with act IFN-gamma or microbes from T cell > inflamm OR IL4/cyotkines > repair
  3. if inflamm then ROS, proteases, cytokines, coag factors, AA metabolites
  4. if repair then growth factors, fibrogenic cytokines, angeiogenic factors, remodelling
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9
Q

macrophage products

inflamm

A

1.

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10
Q

macrophage products

repair

A
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11
Q

persistence of macros

A
  1. cont recruitment of new
  2. local prolif of existing at site of inflamm
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12
Q

local effects of macros

A

from TNF/IL1 activation
1. vascular endo inc procoagulant activity and IL1 cytokines = inflam
2. act leukocytes to produce cytokines = inflam
3. fibroblast act and inc collagen= repair

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13
Q

systemic effects of macros

A
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14
Q

lymphocytes

A

mobilized in setting of specific immune stim like infections and non-immune inflamm like trauma

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15
Q

reciprocal relationship

macro-T cell

A

activated T cell expresses TNF, IL17, chemokines to recruit neutrophils or macros that get activated by IFN-gamma

act macrophage secretes IL1 and TNF-alpha

antigen presentation to T cells by IL12 (TH1)

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16
Q

plasma cells

A

terminal product of B cell act that prod antibodies vs persistent antigens @ inflamm site or vs altered tissue components

can see golgi ghost and large dense nucleus

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17
Q

eosinophils

A

parasitic infections or immune rxn by IgE with allergies

recruitment dep on chemokine eotaxin

granules have major basic protein toxic to parasites but also can epithelial cell lysis

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18
Q

mast cells

A

both acute and chronic inflamm

armed w/ IgE to certain antigens and will release histamine and PG so central for anaphylactic rxns

helpful in parasitic infections bc may produce cytokines like TNF for fibrosis

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19
Q

neutrophils

A

in chronic bc of persistent microbes or mediators enhanced by macrophages, necrotic cells, T cells

acute and chronic can co-exist as chronic active inflamm

key cell of acute

20
Q

results of chronic

A

cont tissue damage

ongoing

21
Q

lifestyle factors

A
  1. smoking
  2. xs alc intake
  3. physical emo stress
  4. obesity
  5. lack of exercise
  6. diet
22
Q

granulomatous inflamm

A

distinctive pattern of chronic in limited # of infections

23
Q

granulom inflamm characteristics

A

aggs of act macroswith squamous cell appearance aka epithelioid, focal area of the inflamm is granuloma surrounded by collar of mononuclear leuks (lymphocytes, plasma cells)

cellular attempt to contain offending agent diff to eradicate like indigestible substances

extensive tissue destruction (caseous necrosis) sometimes

24
Q

conditions

A
  1. bacterial infection- tuberculosis (caseous necrosis)
  2. fungal
  3. parasitic
  4. autoinflamm- sarcoidosis
  5. foreign materials

settings of persistent T cell respons to certainmicrobes and fungi

25
Q

granulomatous mechanism

A
  1. Th1 cells secret gamma-IFN to act macros
  2. TNF-alpha from macro induce and maintain granuloma

anti TNF drugs can sequester granuloma to break down and disseminate disease, test for TB before starting

26
Q

granulation tissue

characteristics

A
  1. prolif of fibroblasts
  2. new thin walled delicate capillaries bc trying to repair
  3. fibros and caps are in loose ECM
  4. scattered macros and other inflamm cells, esp early stage
27
Q

granulomas

A

epithelioid cells (aggs of macros) + collar of lymphocytes and plasma cells

surrounding rim of fibroblasts and CT in older ones

fuse to form multinucleated giant cells (langhans type if peripheral ring pattern or foreign body type if haphazard arrangement)

NOT the same as langerhan cells

28
Q

foreign body granulomas

A

form in resp to inert foregin bodies like splinters, sutures, breast implant, glass
-will be inside of granuloma since walled off

form when material too large to be phagocytosed

29
Q

lymphangitis

A

inflamm of lymphatic channel
leuks and cell debris in lymphatics
-blood poisoning (red streaks up arm) seen

30
Q

reactive lymphadenitis

A

inflamm of draining lymph node

may gain access to blood stream if overwhelm LN = bacteremia

31
Q

systemic effects clinical signs

acute phase response or SIRS

A
  1. fever
  2. change serum acute phase proteins
  3. inc WBCs
  4. dec appetite
  5. altered sleep patterns
32
Q

systemic effects - fever

A

inc 1-4 degrees when due to infection

LPS from bacterial product (exogenous pyrogen) stim prod of IL1 and TNF (endogenous pyrogens)

IL1 and TNF = inc COX and PG syn via AA @ hypothalamic thermoreg center aka vascular cells and perivascular
-PGE2 resets body temp

33
Q

fever effects

A

improve

34
Q

acute phase proteins

A

syn in liver
-CRP
-ceruloplasmin
-haptoglobin
-fibrinogen
-serum amyloid A protein

35
Q

acute phase proteins mechanisms

A

syn upreg by IL1,6,TNF-alpha

36
Q

leukocytosis

A

inc total WBC count to 15,000-20,000
-normally 4,000-10,000

if >

37
Q

systemic shift left

A

inc immature WBC

38
Q

neutrophilia

A

inc absolute # of neutros in most bacterial infections

39
Q

lymphocytosis

A

inc in absolute # of lymphs in viral infections
-mononucleosis, mumps, german measles/rubella

T cells, B cells, plasma cells

40
Q

eosinophilia

A

inc abs # of eosins in asthma, hay fever, parasitic infections

41
Q

leukopenia

A

dec absolute # of WBC in typhoid fever, debilitated hosts or overwhelming infection, some viral infectionszxxx

42
Q

other manifestations of systemic inflamm

A
  1. ANS- inc pulse and BP, dec sweating after redirected blood flow from cutaneous to deep vascular beds to min heat loss
  2. behavioral- shivering, chills, anorexia, somnolence, malaise
43
Q

sepsis

A

severe bacterial infections with large # LPS and micro-orgs = large quantity of cytokines esp TNF and IL1

xs cytokines = cardiovasc failure, microthrombi (DIC), liver injury form hypoglycemia
-if all 3 then septic shock

44
Q

defective inflamm

A

inc susceptibility to infections + delayed wound healing

45
Q

excessive inflamm

A

severe and/or long time inflamm

basis of many diseases esp cancer
-also autoimmune, atherosclerosis, ischemic heart disease, neurodegenerative

longer inflamm persist = inc risk cancer

46
Q

cancer

A

ROS and RNS (inflam mediators) can damage cells membrane and proteins
-also DNA breakage and promote deamination of DNA = mutagenic events

Block 3 Found Sci (60 decks)

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