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General Pathology > inflammation > Flashcards

inflammation Flashcards

1
Q

Definition of acute inflammation

A

well-organized cascade of vascular and cellular changes within living vascularized tissue

(zachary)

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2
Q

Aim of acute inflammation

A

LOCALIZATION of destructive effect in the site of entry

ELIMINATION of exo- and endogenous agents + necrotic tissues and cells.

Keeping INTEGRITY of organism, initiation of tissue REPAIR (growth factors)

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3
Q

4 signs of inflammation

A

Rubor (redness),
Tumor (swelling),
Calor (heat)
Dolor (pain)

Loss of function - 5th sign

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4
Q

3 phases of acute inflammation

A

Fluidic, cellular, reparative

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5
Q

Aim of fluidic phase of acute inflammation?

A

To dilute, isolate and trap the stimulus of damage, so limiting the extent of involvement adjacent normal cells and tissue

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6
Q

Why signs of inflammation occur?

A

Increased blood flow, vasodilation, fluid accumulation

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7
Q

What is the difference between acute and chronic inflammation?

A

Chronic:

  • longer duration
  • response is mainly by lymphocytes and macrophages, tissue necrosis
  • tissue repair: healing, fibrosis and granulation tissue formation

(zachary)

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8
Q

How to distinguish vascular and cellular response during inflammation?

A

Vascular - what is going before WBCs actually fighting the agent

Cellular - actual fighting

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9
Q

How does acute inflammation starts (for example in case of bacteria infection)

A
  1. Tissue damage -› cell membrane damage -› arachidonic acid -› prostaglandins (by COX) and leukotriens (by lypooxygenase)
  2. Activation of mast cells
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10
Q

What do mast cells release in the case of inflammation?

A

Histamines, Leukotriens, Prostaglandins. They are preformed, so release is very quick!

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11
Q

Importance of arachidonic acid in inflammation?

A

Starting material for prostaglandins (COX) and leukotriens (lipooxygenase)

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12
Q

How do cytokines (PGs, leukotriens, histamines) act on endothelial cells and smooth muscle?

A
  • stimulate contraction of endothelial cells (gaps between cells appear)
  • stimulate endothelial cells to expose selectin proteins (adhesion of white blood cells)
  • vasodilation of smooth muscle -› increase of blood flow
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13
Q

What is margination?

A

migration of white blood cells (WBCs) toward the endothelium during blood flow. -› Slowing down -› rolling -› adhesion -› diapedesis

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14
Q

What is diapedesis?

A

squeezing of WBCs out of the bloodstream into surrounding tissues through gaps between endothelial cells

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15
Q

What do macrophages secrete?

A

Interleukines and TNFs

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16
Q

How WBCs entering the tissue know where is site of injury?

A

Positive chemotaxis

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17
Q

oxidative burst

A

release of reactive oxygen species (free radicals) to degrade pathogen. Also can be harmful to the cell itself

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18
Q

What cells are antigen presenting cells?

A

macrophages, dendritic cells, B cells

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19
Q

What are the only cells that can have MHC-1 ?

A

Antigen presenting cells

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20
Q

Panniculitis - ?

A

Inflammation of adipose tissue

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21
Q

Two components of inflammatory response?

A

VASCULAR response and CELLULAR response

Parallel processes!

22
Q

What are toll-like receptors (TLRs)?

A

TLRs are class of pattern recognition receptors (PRRs) that initiate innate immune response

23
Q

What are interferons?

A

molecules secreted by cells invaded by viruses that stimulate other cells to help defend against viruses

24
Q

What receptors “identify” inflammatory stimuli?

A

Toll-like receptors and other pattern recognition receptors (PRRs) of macrophages, dendritic cells, mast cells, B-lymphocytes, neutrophils

25
Q

What patterns do pattern recognition receptors recognise?

A

Pathogen-associated molecular patterns (PAMPs)
Damage-associated molecular patterns (DAMPs) (non-index inflammatory response)

26
Q

What are many DAMPs?

A

Nuclear or cytosolic proteins. Damage/death of cell -> release

27
Q

Vascular response.

A

Vasodilation, increased blood flow

28
Q

By what vasodilation is induced?

A

Histamine, serotonin (mast cells, basophils, platelets)
Prostaglandins, nitric oxide (mast cell, platelets)

29
Q

Cytokines - ? ЧТО ЭТО ВООБЩЕ НАХУЙ ЗА ОПРЕДЕЛЕНИЕ

A

Category of small proteins that are important in cell signalling

30
Q

Cytokines are produced by …?

A

Macrophages, b- and t-lymphocytes, mast cells, endothelial cells, fiibroblasts and stromal cells

31
Q

Cytokines include … ?

A

Chemokines, interferons, interleukins, lymphokines and tumor necrosis factors but generally NOT HORMONES OR GROWTH FACTORS

32
Q

What do cytokines do in inflammation?

A

They signal immune cells to travel to the site of infection, activate those cells and stimulate to produce more cytokines. This feedback loop is controlled by the body.

33
Q

Vascular changed in acute inflammation

A

1) Haemostasis

2) Venula-hyperpermability

3) Micro vascular exsudation

34
Q

Why haemostats happens?

A

Vasodilation + loss of fluid -> concentration of blood in vessels of microcirculation, increased viscosity, slower blood flow

35
Q

For how long does haemostasis occur?

A

Few minutes (severe injury)
15-30 minutes with mild stimuli

36
Q

Vascular leakage

A

Leads to escape of protein rich fluid (exudate) into the extravascular tissue (inflammatory edema)

Leads to increased interstitial hydrostatic pressure and endothelial dysfunction.

37
Q

Types of endothelial permeability increase:

A
  1. Formation of ENDOTHELIAL GAPS in POSTCAPILLARY VENULES due to endothelial construction (histamine, leukotriens, 10-15 mins) most common
  2. DIRECT ENDOTHELIAL INJURY (everywhere, hours to day)
  3. LEUKOCYTE MEDIATED ENDOTHELIAL INJIRY (late response, hours)
38
Q

Sequence of leukocyte extravasation:

A

1 - margination and adhesion to vascular lumen
2 -transmigration across endothelium (= leukocytadiapedesis)
3 - migration in the interstitium (chemotactic stimulus)
4 - leukocyte activation, phagocytosis
5 - IC degradation

39
Q

What are the names of main adhesion molecules?

A

Selectin (weak adhesion)
integrin (strong connection)

40
Q

Leukocyte adhesion deficiency - ?

A

Decreased expression of adhesion molecules on the surface of leukocytes -> leukocytes can’t cross vascular walls properly

41
Q

What breeds are predisposed to LAD (leukocytes adhesion deficiency) ?

A

Holstein calves (bovine LAD, beta-2 integrin deficiency)
Irish setters (canine LAD)

42
Q

Symptoms of bovine leukocyte adhesion deficiency

A
  • gingivitis
  • tooth loss
  • ulcers (oral, enteric, cutaneous)
  • abscesses without pus
  • leukocytosis
  • pneumonia
  • death within few days after birth
43
Q

Leukocytediapedesis - ?

A

= extravasation. Movement of leukocytes into interstitial-extravascular connective tissue

44
Q

What cells predominate in the first 24 to 48 hours of acute inflammation?

A

Neutrophils

45
Q

By what cells are neutrophils replaced later in acute inflammation?

A

Macrophages (extravasation takes longer than neutrophils)

46
Q

Substances that cause chemotaxis are called … ?

A

Chemoattractants

47
Q

Examples of chemoattractants

A

Exo: bacterial products
Endothelial: components of complement system, cytokines, arachidonuc acid metabolites

48
Q

Sequence of phagocytosis:

A
  • recognition and attachment
  • engulfment, formation of phagocytosis vacuole
  • degradation of ingested material
49
Q

Types of intracellular degradation

A

Oxygen dependent (ROS) and independent (proteolytic enzymes)

50
Q

What happens to neutrophils after they phagocyte the agent?

A

Undergo apoptosis and ingested by macrophages

51
Q

Specificity of inflammation in dogs?

A

INCREASED ERYTHROCYTE-DIAPEDESIS. (RBCs extravasation) -> haemorrhagic appearance of the purulent inflammatory fluid.

General Pathology (19 decks)

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