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002 - Pathology - (02) - Inflammation > (05) Lecture 5 > Flashcards

(05) Lecture 5 Flashcards

1
Q

(Fibrinous Inflammation)

  1. fibrinogen –> ? –> ?
  2. What is the definition? not associated with what?
A
  1. fibrin; thrombus (intravascular/vessel-associated)
  2. presence of fibrin in extravascular location (occasionaly also within vasculature/heart); hemostasis
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2
Q

(Fibrinous Inflammation)

(Pathogensis)

  1. injury –> ? –> ?
  2. Injury induced “pro-coagulative” milieu in extravascular location… due to effect of what?
A
  1. vascular permeatbily increase; extravasatiion of fibrinogen
  2. cytokines (such as IL-1, TNF-a) on endothelial cells
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3
Q

(Fibrous Inflammation)

(Pathogenesis)

(Consequences)

  1. tissue necrosis due to what?
  2. stimulation of fibrocytes to what? can causs what three things?
  3. Fibrin is a good substrate for what?
A
  1. decreased perfusion
  2. fibroblasts; wound healing, scarring, exuberant granulation tissue formation
  3. for proliferation of certain bacteria
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4
Q

(Fibrous INflammation)

(causes)

  1. Infections with what? that produce what? only minor what? also what?
  2. What other fancy one?
  3. and chemical/physical injury
A
  1. gram negative bacteria; endotoxin (–>pro-coagulative); chemotaxis; secondary bacterial infection (after viral)
  2. immune-complex mediated reaction (type 3 hypersensitivyt)
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5
Q

(Fibrinous Inflammation)

  1. Variably dense eosinophilc (= “protein-rich’) homogenous to fibrillar exudate with relatively low cellularity
  2. What occurs within several days?
A
  1. beginning fibrosis (formation of granulation tissue)
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6
Q

(Fibrinous INflammation: Where does it occur)

  1. in tubular organs mainly with what? Differentiated based on what?
  2. Also found where?
A
  1. single layered epithelium (respiratory, alimentary and on or benetah serosa); extenesion of fibrin into deeper layers (Psuedomembranosus, diptheritic (-necrotizing)
  2. in vascular wall (fibrinoid vascular necrosis)
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7
Q

(Fibrinous Inflammation: Tubular organ/body cavity)

(Pseudomembranosus)

  1. fibrin forms layer on what?
  2. fibrin removeable with or without damage to underlying mucosa/serosa?

(Diphtheritic (necrotizing))

  1. fibrin deposition does what?
  2. Is fibrin removeable without further damage to underlying mucosa/loss of substance?
A
  1. macroscopically (seemingly) intact (usually reddened) epithelium
  2. without (gets reddened though…)
  3. extends beyond basement membrane into deeper layers
  4. no

(then look at this and next two pages)

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8
Q

(Fibrinous Inflammation: Sequela)

(Small accumulations of fibrin)

1-2 what two things occur?

(Large Accumulations of fibrin)

  1. Stimulation of local inactive fibrocytes –> fibroblasts —> formation of what?
A
  1. resorption (dissolved by macrophages/PMNs)
  2. destruction (bacterial proteases)
  3. granulation tissue (fibrinous inflammation –> fibrous adhesions or fibrous/fibrosing inflammation)
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9
Q

(Fibrinous INflammation: Sequela)

(in tubular organs)

  1. after pseudomembranosus inflammation?
  2. after diptheritic inflammation?
A
  1. restitutio ad itegrum (resolution)
  2. loss of fibrin results in ulcer –> scarring/stricture
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10
Q

(Fibrinous Inflammation: Sequela)

(parenchymal organs)

1-2. what two things do you see?

(on serosa)

  1. Adhesions (acute - acellular) can you separate without damage to tissue?
  2. “fibrous tags” (chronic - fibroblastic) must do what to separate?
  3. diffuse contstrictive fibrosing process
A
  1. fibrosis/sclerosis (hardeining of tissue)
  2. seqeuster formation
  3. yes
  4. tear
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11
Q

ROFK

A

the answer id D

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12
Q

(Suppurative Inflammation)

(Etiology - the study of causation)

  1. What’s the big cause?
A
  1. BACTERIAL INFECTION

also the ones in picture

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13
Q

(Suppurative Inflammation)

  1. strong attraction of what?

2-4. by what three things?

  1. What is the hallmark macroscopically?
  2. microscopically?
A
  1. neutrophils
  2. mediators (chemokines)
  3. bacterial products
  4. injured tissue
  5. PUS
  6. neutrophils (viable and degenerate)
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14
Q

(Suppurative Inflammation)

(Pathogenesis)

(mildly aggressive insult)

  1. characterized by what?
  2. removal of occasional dead neutrophil by what?

(More aggressive insult)

  1. large number of what with release of large quantities of what? leads to what?
  2. what does pus =?
A
  1. viable neutrophils
  2. macrophages
  3. degenerate (+/- viable) neutrophils with release of large quantities of lytic enzymes; tissue lysis
  4. degenerate neutrophils and bacteria
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15
Q

(Suppurative Inflammation)

(Cause)

  1. what is the major one?

2-3. what are the two little ones?

A
  1. pus-producing (pyogenic) bacteria (eg arcanobacterium PYOGENES, strep, staph, etc)
  2. sterile chemical injury
  3. autoimmune disease (type II and III)
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16
Q

(Suppurative Inflammation)

(Where does it occur?)

(in a body cavity/tubular organ without drainage)

1-2. can get either what or what?

(tubular organ with drainage)

  1. why is it difficult to recognize?

(intraepithelial accumulation in multi-layered epithelium)

  1. forms a what?
A
  1. small quantity of exudate (purluent pleuritis)

or

  1. Large quantity of exudate (empyema, pyothorax, pyometra, hypopion)
  2. exudate doesn’t accumulate
  3. pustule
17
Q

(Suppurative Inflammation: where does it occur cont.)

(Parenchymal organ - “interstitial”)

(Good immune function and weak injury)

  1. will you get tissue lysis?

(Good immune function and aggressive injury)

  1. will you get tissue lysis?

3-4. what two things will you see?

A
  1. no (frequently not detecable macroscopically)
  2. yes
  3. microabcesses (only detectable histologically) and macroabcesses
  4. individual/multiple large abcesses

(plus learn these two slides)

18
Q

(Suppurative Inflammation: Abscess - “aposteme”)

(Abscess development)

  1. what happens first?
  2. then progression until what?
  3. then what?
  4. is it a cyst?
A
  1. tissue lysis (with accumulation of neutrophils)
  2. immune response overcomes injurious stimulus
  3. granulation tissue forms connective tissue capsule (“maturation of abcess)
  4. NO
19
Q

(Suppurative Inflammation: Abscess - aposteme)

(Histology)

  1. What do you see in the center?
  2. in the periphery?
  3. at the interface?
A
  1. degenerate neutrophils (possibly with bacterial or fungal agents)
  2. capsule of connective tissue
  3. “pyogenic membrane” with inner layer (viable neutrophils) and outer layer of granulation tissue with interspersed inflammatory cells
20
Q

(Suppurative Inflammation: Fistule)

  1. what type of suppurative inflammation?
  2. with draining tract to what?
  3. What happens first? with accumulation of what?
  4. progression until what occurs?
  5. then what?
A
  1. chronic
  2. body surface, body cavity, lumen of tubular organ
  3. tissue lysis; neutrophils
  4. immune response overcomes injurious stimulus
  5. granulation tissue formation (bordering draining tract)
21
Q

(Suppurative Inflammation: “Phlegmone”/phlegmonous inflammation)

(Subcutis and Skeletal muscle)

  1. Under what conditions does this occur?
  2. rapid spread along fascia without what?
A
  1. when poor immune function and aggressive injurious stimulus
  2. tendency of demarcation
22
Q

(Chronic Suppurative Inflammation)

  1. Histologic lesion of chronic suppurative inflammation (in tubular organs) or body cavities may be dominated by what with only a few what?
A
  1. dominated by lymphocytes and plasma cells with only a few neutrophils (Eg pyometra)

+ figure this out

002 - Pathology - (02) - Inflammation (6 decks)

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