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Pathomorphology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the stages of acute inflammation? Can these stages be further subcategorised? If so, how?

A

There are two main stages of acute inflammation:

  • vascular events
  • cellular events

Vascular events can be further divided into:

  • hemodynamic changes
  • changed vascular permeability

cellular events can be further categorised into:

  • exudation of WBC
  • phagocytosis
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2
Q

What is the function of inflammation?

A

Deliver WBC/leukocytes to site of injury and activate them

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3
Q

What is meant by margination?

A

The accumulation of leukocytes/WBC at the periphery of the blood vessel.

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4
Q

During acute inflammation (cellular events), leukocytes/WBC stick to the endothelium of the blood vessel. what is this process called? How is it achieved?

A

Adhesion
The leukocytes/WBC stick to the blood vessel endothelium by the use of adhesins; the following adhesins are employed in this process:

  • L-selectin (brings WBC to lymph nodes)
  • E-selectin (used in both rolling and adhesion)
  • P-selectin (involved in rolling)
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5
Q

How many types of exudate are there? Explain the difference.

A

There are 5 types of exudate:

  1. serous (watery and serum-like ie. blister in burns)
  2. purulent (creamy-pus)
  3. fibrinous (rich in fibrinogen and fibrin)
  4. haemorrhagic (damage to blood vessels)
  5. catarrhal (increased mucus secretion)
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6
Q

What is the difference in appearance of new and old pus microscopically?

A

New pus - dead and alive WBC, RBCs, fibrin, tissue fragments

Old pus - same as above + crystals of cholesterol and macrophages

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7
Q

Elaborate on what is an abscess and the types of abscess.

A

Increased neutrophil infiltrate in inflamed tissue + necrosis = cavity formed with pus (abscess).

The process of forming an abscess is suppuration and is caused by pyogenic bacteria.

Types of abscesses are:

  • carbuncle (abscess in soft tissues of neck and dermis - typically found in diabetics)
  • furuncle (acute inflammation of hair follicles in dermal tissues)
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8
Q

What are the systemic effects of chronic inflammation?

A
  • Fever
  • Anemia
  • Leukocytosis
  • Increased ESR
  • Secondary systemic amyloidosis
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9
Q

What are the types of chronic inflammation?

A
  1. chronic non-specific inflammation

2. chronic granulomatous inflammation

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10
Q

What is empyema?

A

purulent inflammation with build up of pus in relatively or completely isolated anatomical cavities or cavities that don’t drain well ie.

  • pleural cavity
  • pericardial cavity
  • abdominal cavity
  • galbladder
  • pyosalpinx (infalmmation + pus build up in fallopian tube
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11
Q

What is a phlegmon?

A

diffuse purulent inflammation that spreads diffusely between the tissue elements ie. interfascial, intermuscular spaces or between membranes of hollow organs)

  • may be soft (diffuse appearance, no clear boundaries, doughy conistsency, turbid purulent fluid flows from site of incision)
  • dense (necrosis present in area of inflammation, no clear boundaroes, dead tissues are gradually separated, dense consistency)
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12
Q

What is rhinoscleroma? What is the causative agent?

A

chronic destructive inflammatory lesion of the nose and upper respiratoory airways.

Typically caused by diplobacilli Klebsiella rhinoscleromatis

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13
Q

What is interstitial productive inflammation? What are the consequences?

A

formation of widespread inflammatory immune cell infiltrate in the stroma of the organ, ie. the layers of connective tissue b/w specialised microstructures and cells

examples are:
interstitial myocarditis
interstitial hepatitis
interstitial nephritis
interstitial pancreatitis
interstitial pneumonia

The consequences are:

  • sclerosis (fibrosis) in the stroma of the organs
  • cirrhosis: growth of connective scar tissue, causing organ deformation
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14
Q

What are the three ways in which chronic inflammation can occur?

A
  1. chronic inflammation proceeding acute inflammation
  2. recurrent attacks of acute inflammation
  3. chronic inflammation de novo (aka from scratch)
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15
Q

How does chronic inflammation following acute inflammation occur?

A

If tissue destruction is intensive or bacteria survive and remain in small numbers at the site of acute inflammation, this can lead to chronic inflammation.

Such examples are:

  • osteomyelitis
  • pneumonia as a result of lung abscess
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16
Q

In which cases, do recurrent attacks of acute inflammation cause chronic inflammation?

A
  • recurrent urinary tract infection may lead to chronic pyelonephritis
  • repeated infection of gallbladder may lead to chroni cholecystitis
17
Q

When is chronic inflammation de novo seen?

A
  • infection with a microbe that has low pathgoenicity from the start ie. Mycobacterium tuberculosis
18
Q

What is croupous inflammation? What are the consequences?

A

subtype of fibrinous inflammation, characterised by:
- development on mucous membranes covered with a cylindrical epithelium at shallow necrosis, or serous membranes covered with a single-layered flat epithelium - mesothelium, where the epithelium base has loose connection with the underlying tissue.

Resulting pellicles can be easily separated from the epithelium, even with deep impregnation of fibrin.

Examples of croupous inflammation are:

  • tracheitis, bronchitis
  • croupous pneumonia
  • fibrinous pericarditis
  • firbinous pleuritis
  • fibrinous peritonitis

When pellicles are removed, there is hyperemia of mucous membrane and an erosion forms.

  • complete regeneration of the epithelium
  • adhesive pleurisy (connection(s) between visceral and parietal pleura leave) due to reorganisation of fibrin.
19
Q

What are the features of chronic inflammation?

A
  1. mononuclear cell infiltration ie. phagocytes, lymphoid cells. Phagocytes include circulating moncoytes, tissue macrophages and epithelioid cells and multi-nucleated giant cells
  2. necrosis - most chronic inflammatory lesions are characterised by necrosis (activated macrophages release biologically active substances that cause this ie. proteases, elastases, NO etc.)
  3. proliferative changes (blood vessels and fibroblasts proliferate due to necrosis, as a result inflammatory granulation tissue is seen)
20
Q

What is a granuloma?

A
  • circular, tiny lession ca. 1mm in diameter

- comprised mainly modified macrophages aka epithelioid cells and at the periphery there is a rim of lymphoid cells

21
Q

What are the possible outcomes after acute inflammation?

A
  1. resolution (tissue returns back to normal ie. lobar pneumonia)
  2. healing - if tissue loss after acute inflammation is superficial, the tissue is regenerated; if tissue destruction is a lot, healing occurs by fibrosis
  3. suppuration - formation of an abscess (if the abscess is not drained, it may undergo calcification later on)
  4. chronic inflammation - not ideal!
22
Q

What is the pathogenesis of a granuloma?

A
  1. phagocytosis (macrophages engulf antigen/pathogen, but cannot break it down, as a result they transform into epithelioid cells)
  2. CD4+ T cells (macrophages are so desperate, they present antigen to CD4+ T cells - this activates them
  3. cytokines - activated CD4+ T cells release cytokines that do the following:
    - IL-1 , IL-2 stimulate more division of more T-cells
    - interferon - y activates macrophages
    - TNF-a promotes fibroblast prolif. and activated endothelium to secrete prostaglandins
    - growth factors trigger growth of fibroblast
23
Q

What bacterial diseases can cause granulomatous inflammation? Identify the bacteria responsible and key histological features.

A

Tuberculosis (Mycobacterium tuberculosis); histologically, we see tuberculous granulomas with central caseation necrosis; acid-fast bacili

Leprosy (Mycobacterium leprae); histologically, we see foamy histiocytes + acid-fast bacili and epithelioid cell granulomas (tuberculoid)

Syphilis (Treponema pallidum); histologically, we see gummas made of histiocytes, plasma cell infiltration and central necrosis

Granuloma inguinale (C. donovani); histologically, we see anal and genital lesions, macrophages and neutrophils show Donovan bodies

Brucellosis (Brucella abortus); histologically we see dairy infection in humans, enlarged lyph nodes, spleen, bone marrow and non-specific granulomas

Tularemia (Francisella tularensis); histologically we see necrosis and acute suppuration; tubercles hard (or with tiny central necrosis)

Pathomorphology (5 decks)

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