0.2 Tissue response to Injury Flashcards

1
Q

What is necrosis?

A

Evidence of cell death in a living body

Callular leakage leading to inflammation which removes cellular debris

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2
Q

What is coagulative necrosis associated with?

A

Ischemia (reduced blood flow / lack of oxygen)

Pyknosis, Karyorrhexis, and Karyolysis

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3
Q

What is liquefactive necrosis associated with?

A

Related to microbial growth

Tissue transformed into liquid / viscous mass (microbes eat biological tissue turning stucture into liquid / pus)

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4
Q

What is caseous necrosis associated with and how does it visually appear macroscopically and microscopically?

A

Specific to TB, syphilis, and some fungi

Macroscopically = cheesy tan/white

Microscopically = pink, proteinaceous mass encapsulated by granulomatous processes

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5
Q

What is apoptosis?

A

Programmed cell death

No cell leakage, no inflammation

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6
Q

What is acute inflammation?

A

Coordinated host response to injury

Preprogrammed = similar for all causes

Mostly vascular and local changes

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7
Q

What is chronic inflammation?

A

Next progression, if acute inflammation is unable to deal with bacterial load

Long standing response to long standing injury in which injury and repair occur simultaneously

Different patterns depending on case, but feature emigration of monocytes/lymphocytes into tissues

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8
Q

Wound healing can be undertaken by regeneration or repair. What is the difference between them?

A

Regeneration = replacement of tissue with original tissue eg liver

Repair = blood clot or nectrotic tissue replaced with granulation tissue (matures to scar/bone/adipose)

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9
Q

What are the two types of immunity?

A
  1. Non-specific / innate
  2. Specific / adaptive
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10
Q

What are the characteristics of non-specific / innate immunity?

A
  1. Not targeted to specific organsims
  2. Does not increase after first exposure to organism
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11
Q

What are the characteristics of specific / adaptive immunity?

A
  1. Targeted to specific organisms
  2. Increases following exposure
  3. Confers future protection against organism
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12
Q

What are the four classical signs of acute inflammation?

A
  1. Swelling
  2. Pain
  3. Redness
  4. Heat
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13
Q

The major changes for acute inflammation are vascular to better get blood into tissues with leukocytes and plasma protective factors. How do these changes relate to the classical signs of acute inflammation?

A
  1. Vascular leakage = swelling
  2. Limited movement = pain
  3. Vasodilation = Redness + heat
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14
Q

What are the 3 morphological types of acute inflammation?

A
  1. Suppurative = pus formation
  2. Serous = voluminous clear fluid produced
  3. Fibrinous = fibrin deposited on a surface
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15
Q

Opening of vasculature brings blood to the body surface, which is normally cooler than the core temperature, resulting in redness and heat. What are the steps behind vascular dilation?

A
  1. Increased blood flow = arteriole + venule dilation and the expansion of capillary bed
  2. Leads to edema = swelling + leakage of plasma/proteins in ECM
  3. Neutrophils emigrate into EM (normally only occasional lymphocytes + macrophages)
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16
Q

What are Starling’s forces?

A

Relationship between hydrostatic and oncotic pressure

17
Q

What is the process behind vascular leakage?

A

Inflammatory mediators increase endothelial permeability

Protein leaks out, water follows = protein rich exudate / inflammatory oedema

18
Q

Swelling in acute inflammation is caused by increased vascular permeability and vascular leakage. Starling’s forces play a key role in this. Explain how.

A
  1. Net Flow shifts from normal to outward via increased hydrostatic pressure
  2. Vessel dilates to accomodate pressure changes
  3. Pressure changes allow plasma proteins + water to leak out in rich exudate (oedema)
19
Q

Oedema plays an important role in acute inflammation. What is it?

A
  1. Oedema dilutes toxins and increases lymph flow
  2. Lymph flow takes toxins / bacterial products out of area
  3. Bacterial antigens + toxins presented to lymph nodes for development of immune response