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Cardiopulmonary Renal > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is the function of inflammation?

A
  • Remove the initial cause of injury
    • Ex. Microbes & toxins

-Remove necrotic cells & tissues

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2
Q

What is inflammation?

A

Protective: response to cell & tissue injury

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3
Q

What are the components of general information?

A

Vascular & leukocyte reactions

-Activated in response to the inflammatory stimulus

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4
Q

Give an overview of Acute inflammation

A

Rapid onset
-Typically within onset

Short duration
-hours or a few days

Characteristics
5 cardial signs
Neutrophil migration

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5
Q

What is the overview of chronic inflammation ?

A
  • May follow acute inflammation if the stimulus persists
  • May also be an insidious, low- grade response without acute reaction
  • Long duration
    • Weeks or months

Characteristics:

  • macrophages & lymphocytes
  • proliferation of blood vessels
  • fibrosis
  • tissue destruction
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6
Q

What are the cardial signs of inflammation?

A

4 cardinal signs of acute inflammation (celsus):

  1. Redness (rubor)-hyperemia
  2. Swelling (tumor)- fluid exudation and hyperemia
  3. Heat (calor)- hyperemia
  4. Pain (dolor)- release of bradykinin and PGE2

5th sign added by Virchow:
5. Loss of function (functio laesa)- combined effects, mainly swelling and pain

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7
Q

Summarize the nomenclature of inflammation

A

The nomenclature used to describe inflammation in different tissues . ALMOST always employs the tissue name plus the suffix- it is

-Inflammation of the appendix = appendicitis, inflammation of the Fallopian tube= salpingitis and inflammation of the pericardium = pericarditis

Exception include pleurisy (inflammation of the pleura) and acute cellulitis (infection causing inflammation of subcutaneous tissues)

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8
Q

Explain the 3 components of acute inflammation

A
  1. Vascular dilation- relaxation of vascular smooth muscle results in engorgement of tissue with blood
    • hyperemia
  2. Endothelial activation
    • increased endothelium permeability allows leakage of plasma proteins
      • edema
      • expression of adhesion molecules
      • production of factors that cause vascular dilation
  3. Neutrophil activation & migration
    - Increased expression of adhesion molecules
    - Increased motility
    - Increased capacity for bacterial killing
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9
Q

Explain the events of neutrophil migration

A
  • Neutrophils express cell-cell recognition molecules
  • Neutrophils are slowed down by selectin receptors on endothelial receptors on endothelial cells
  • Neutrophils begin to roll on the surface
    • Endothelial secretions induce the expression of other molecules on the neutrophil
      • integrins
  • Integrins- ICAM-1 interactions provide firm adhesion to the endothelium
  • Neutrophil extends pseudopod between endothelial cells
  • Neutrophil exits circulation & enters connective tissue
    • Migration directed by chemoattractant molecules
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10
Q

Explain development of acute inflammatory exudate

A
  1. Early vascular changes- dilation of vessels (engirged capillaries) and adhesion of neutrophils to endothelium (pavementing); fluid accumulation in interstitium
  2. Migration of neutrophils- neutrophils pass through vessel walls (pseudopods extend between adjacent endothelial cells), then penetrate the endothelial basement membrane and migrate into perivascular connective tissue
  3. Early formation of exudate - In the tissue, neutrophils are attached to the site of tissue damage by inflammatory chemical mediators, such as complement component C5a and LTB4, and migrate actively towards higher concentrations of these agents (chemotaxis)

Several other plasma proteins are present in the tissue space- evidenced by fibrin (from plasma fibrinogen)

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11
Q

What plasma proteins are found within the tissue of lysosomes?

A
  • components of the coagulation cascade (fibrinogen, prothrombin, factor VIII, von Willebrand factor)
  • Acute phase reactants (C-reactive proteins)
  • complement proteins (C3a, C5a)

Circulating immunoglobins (antibodies)

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12
Q

What is opsonization?

A

Neutrophils play an important role in destruction of microorganisms- phagocytosis of organisms is promoted by a coating of immunoglobin and complement

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13
Q

What are the morphological types of acute inflammation?

A
  1. Supportive or purulent (pus-containing, exudative) inflammation
  2. Fibrinous inflammation
  3. Serous inflammation
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14
Q

What is suppurative inflammation?

A

Pus is a semi-solid containing neutrophils, fluid and necrotic tissue

An abscess is a circumscribed collection of pus

Thus, the exudate in purulent inflammation is rich in neutrophils- this commonly results from bacterial infection

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15
Q

What causes suppurative/ purulent inflammation?

A

Bacteria that promote inflammation are called “pyogenic” bacteria

Typical pyogenic bacteria include:

  • Staphylococci
  • Streptococci such as S. Pyogenes and S. pneumonia

Common examples of purulent inflammation include:

  • lobar pneumonia
  • bronchopneumonia
  • Acute appendicitis
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16
Q

Explain the histological findings of lobar pneumonia

A

Consolidation= alveoli obliterated by filling with WBCs (mainly neutrophils), fibrin and fluid

Relatively unaffected lobe
-inflammatory response is involving only the alveoli immediately adjacent to the interlobar fissure

Consolidated alveoli at higher magnification shows:

  • neutrophils
  • macrophages
  • fibrin and fluid are filling the air spaces
17
Q

Explain fibrous inflammation in acute inflammation

A
  • The exudate in fibrous inflammation has a high plasma protein content
  • Fibrinogen, a plasma protein, is converted to fibrin and deposited in tissues
  • Usually associated with serous membrane-lined cavities (pleural, pericardial and peritoneal)
  • Fibrin strands form a mat, often causing adhesion between adjacent surfaces
18
Q

Contrast fibrinous and purulent acute inflammation

A

Purulent - exudate with neutrophils as main component

Fibrinous- exudate with fibrin as main component and few neutrophils

19
Q

Explain serous inflammation in acute inflammation

A

In this pattern of acute inflammation the main tissue response is accumulation of fluid with a low plasma protein and cell content (transudate)

Transudate- specific gravity < 0.12 or protein content < 0.25 g/L

Exudate- specific gravity > 1.020 and protein content >25 g/L

Serous inflammation can be seen in the skin in response to a burn, and in serous membrane-lined cavities

Pleural effusions are commonly classified as transdative versus exudative- providing a clue as to likely causes

20
Q

What are the outcomes of acute inflammation? What factors determine these outcomes?

A

4 main outcomes:

  1. Resolution
  2. Healing by fibrosis
  3. Abscess formation
  4. Progression to chronic inflammation

Factors that determine these outcome:
a) Severity of tissue damage

b) Capacity of stem cells within the tissue to replace the specialized cells (regeneration)
c) type of agent causing the damage

21
Q

Explain resolution as an outcome of acute inflammation

A

Complete resistution of normal tissue architecture and function; can only occur when the connective tissue framework is intact and the tissue has the capacity to regenerate

Neutrophils and necrotic tissue are removed by phagocytosis (macrophages) which leave the tissue via the lymphatic drainage

Example: following pneumonia, re-growth of alveolar lining cells depends on resident stem cells To divide and differentiate

Recovery from sunburn (acute inflammatory response in the skin secondary to UV radiation) is another example

22
Q

Explain healing by fibrosis as an outcome of acute inflammation

A

Occurs with substantial damage to connective tissue framework and/or in tissues that lack ability to regenerate specialized cells

  • Necrotic debris and acute inflammatory exudate are first removed by macrophages
  • The defect becomes filled by in growth of granulation tissue (called organization)
  • Granulation is gradually replaced by collagen to form a fibrous (collagenous) scar
  • Structural integrity is re-established
23
Q

Explain abscess formation as an outcome of acute inflammation

A

A localized of pus usually following extensive tissue damage and pyogenic bacteria

Acute abscess
-Expansion is limited by organization & repair at the margins

Chronic abscess
The abscess may become encapsulated by granulation & fibrous tissue

24
Q

What are the factors affecting increased risk of chronic inflammation?

A
  • large numbers of virulent bacteria
  • organization & repair become overwhelmed
  • expansion of abscess and surrounding tissue damage
25
Q

What are the hallmark features of chronic inflammation?

A

-Ongoing tissue damage

  • Chromic inflammatory infiltrate
    1. Macrophage
    2. Lymphocytes
    3. Plasma cells
    4. Eosinophils, mast cells, & fibroblasts (May see a few neutrophils)

Fibrosis

26
Q

What are the subdivisions of chronic inflammation ?

A

Non-specific
-Arises following an episode of acute inflammation when the response was not adequate to neutralize the noxious stimulus

Specific

  • Typical causes
    • immunological agents
      • virus-infected cells, fungi, Protozoa, hypersensitivity, reactions & autoimmune conditions
    • nonimmunological stimuli
      • foreign body reactions, inert noxious materials
27
Q

What are the 2 types of specific chronic inflammation ?

A
  1. Non-granulomatous
  2. Granulomatous
    • characterized by presence of granulomas
    • presence of epithelium macrophaspges & Multinucleated giant cells
28
Q

What immunological agents stimulate specific chronic inflammation ?

A
  • low toxicity organisms such as Treponema sp. (Syphilis and yaws)
  • infective organisms that grow within cells( viruses, Mycobacteria sp.)
  • Hypersensitivity reactions (extrinsic allergic alveolitis)
  • Autoimmune conditions (systemic lupus-erythromatous- SLE)
  • Infections by fungi, protozoa and parasites
29
Q

What non-immunological agents cause specific chronic inflammation?

A
  • suture material
  • wood/vegetable matter
  • metal or glass splinters
  • Inorganic materials such as silica and beryllium
  • A number of foreign materials may excite a chronic inflammatory response with or without discrete granuloma formation
30
Q

Summarize infiltrate of chronic inflammation.

A

Inflammatory cells kill organisms and secrete a wide variety of soluble factors that regulate the inflammatory and healing process

Plasma cells

Lymphocytes

Macrophages

Eosinophils

Fibroblasts

31
Q

What is the histology of plasma cells in chronic inflammation?

A

Purpilish cytoplasm and eccentric clock face nuclei. Plasma cells are differentiated B lymphocytes
L

32
Q

What is the histology of lymphocytes in chronic inflammation ?

A

Have dark, round nuclei with a thin rim of basophilic cytoplasm. These include both helper and cytotoxic T cells as well as B cells

33
Q

What is the histology of macrophages in chronic inflammation?

A

Have oval or kidney bean shaped nuclei and pale cytoplasm -phagocytic and antigen-presenting

34
Q

What is the histology of eosinophils in chronic inflammation?

A

Have bilobed nuclei and brightly eosinophilic cytoplasmic granules. When stimulated, eosinophils release granule contents, including major basic protein-effective in killing parasites

35
Q

What are the histological findings of fibroblasts in chronic inflammation?

A

Secrete extracellular matrix including collagen. After the injurious stimulus has been removed these cells progressively disappear from the tissue over weeks/months.

36
Q

Explain chronic granulomatous inflammation

A

Distinct pattern of chronjc inflammation in a relatively limited number of conditions

A granuloma is a cellular attempt to contain a persistent agent that is diffuctly to eradicate

Characterized by presence of activated epitheloid macrophages & multinucleate giant cells

- epitheloid macrophages fuse to form multinucleated giant cells
- Large mass of cytoplasm containing > 20 nuclei

2 types of giant cells:

a) foreign body giant cells (typical of non-immunological agents)
- nuclei centrally grouped

b) Langhan’s giant cells (typical of immunological giants)
- nuclei arranged in a horse-shoe at the periphery
- Ex. Tuberculosis, sarcoidosis, leprosy

37
Q

What causes tuberculosis granuloma?

A

mycobacterium tuberculosis

38
Q

What is the morphology of tuberculosis granuloma?

A
  • Caseating granuloma
  • Central necrosis
  • Epitheloid macrophages
  • Langerhans giant cells
  • lymphocytes

Cardiopulmonary Renal (35 decks)

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