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Medicine year 1 semester 2 > Case 7- inflammation > Flashcards

Case 7- inflammation Flashcards

1
Q

Why is acute inflammation important

A

A precursor for the repair processes in damaged tissue. It brings the host’s defence mechanism from circulation to the sites they are needed. They remove necrotic cells and tissues and promote healing and reconstruction of damaged tissure

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2
Q

What triggers inflammation

A

PAMPS (found on the outside of pathogens) and DAMPS (due to localised tissue injury) trigger inflammation.

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3
Q

Characteristics of acute inflammation

A

Rapid onset, short duration, mainly Neutrophils and prominent characteristic response.

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4
Q

Characteristics of chronic inflamation

A

Slow onset (days), long duration (weeks, months), involves Monocytes/ Macrophages/ Lymphocytes, there is a less characteristic response.

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5
Q

Cardinal symptoms of inflammation

A

Redness (rubor), Heat (calor), Swelling (tumor), Pain (dalor) and loss of function.

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6
Q

Acute inflammation- vasodilation of small vessels (neurotransmitter)

A

Relaxation of smooth muscle cells within the vessel walls leading to slowed blood flow. Histamine drives this by binding to H1 receptors, there is decreased blood flow. There will be pooling of blood at the site causing heat and redness.

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7
Q

Acute inflammation- increased vascular permeability of the microvasculature

A

This enables plasma proteins and leukocytes to leave the circulation and enter the interstitial space. Occurs primarily via endothelial cell retraction via the breakdown of adjacent cell gap Junctions. Can also occur indirectly via leukocyte mediated damage, the leukocytes become over excited and attack the endothelial cells, or direct endothelial cell injury (such as burns and trauma). Vascular permeability is driven by Histamine binding to H1 receptors. Causes swelling and pain, the pain is due to the dissociation of the gap junctions and the swelling.

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8
Q

Acute inflammation- emigration of leukocytes

A

Leukocytes move from the circulation to the site of injury and infection. Is a multi-step process. Vasodilation and increased vascular permeability encourages stasis where the blood slows down, so leukocytes can leave the blood

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9
Q

Transudate

A

When the fluid leaves the vasculature but the proteins and Leukocytes dont. Less oncotic then exudate

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10
Q

Exudate

A

The fluid that moves from the vasculature to the interstitial space, contains high protein and Leukocyte levels. More oncotic then transudate

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11
Q

Pus

A

When the fluid leaves the vasculature to the interstitial space containing high protein levels and Leukocytes, in pus the Leukocytes are dead (mainly neutrophils)

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12
Q

The multistep process of the Emigration of Leukocytes

A

1) Margination
2) Rolling
3) Stable adhesion
4) Emigration/ Transmigration/ Diapedesis
5) Chemotaxis

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13
Q

The multistep process of the Emigration of Leukocytes- Margination

A

Leukocytes move from the central part of the blood vessel to the peripheral zone of the blood vessel, directly engaging with the endothelial cells. It is mediated by stasis (slowed blood flow)

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14
Q

The multistep process of the Emigration of Leukocytes- Rolling

A

Leukocytes rolling along the surface of the endothelial layer. Slowed by selectin/glycoprotein and integrin/integrin ligand interactions, which are fragile and easily break. The leukocytes express glycoproteins and the endothelia cells selectins. This slows down the movement of the Leukocyte along the endothelial layer

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15
Q

The multistep process of the Emigration of Leukocytes- stable adhesion

A

Cytokines released from the site of injury increase integrin and integrin receptor binding (affinity) – this stops the leukocyte at site of infection / injury

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16
Q

The multistep process of the Emigration of Leukocytes- emigration/ transmigration/ diapedesis

A

Leukocytes extend their pseudopodia downwards and squeezes through endothelial gap junctions, they are made larger by increased vascular permeability. Emigration is mediated by a protein called PCAM1

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17
Q

The multistep process of the Emigration of Leukocytes- Chemotaxis

A

Leukocytes follow a chemokine gradient to find and locate pathogens –complement proteins C3a & C5a are potent chemokines. They move down the chemotaxic gradient to the site of infection.

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18
Q

The white blood cells which you find in acute inflammation

A

Presence of neutrophils (6-24 hours) which are replaced by Macrophages (24-48 hours). This because Neutrophils have the highest amount of Glycoproteins so they bind the easiest to the endothelial layer.

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19
Q

Causes of chronic inflammation

A
  • Persistent infection- which the body cant get rid of.
  • Hypersensitivity disease- auto antigens (rheumatoid arthritis), microbes (inflammatory bowel disease), allergic disease.
  • Prolonged exposure to toxic agents- exogenous exposure (dust, asbestos particles), can be endogenous like atherosclerosis
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20
Q

The 3 major components of inflammation

A
  • Infiltration with mononuclear cells
  • Tissue destruction, can be due to the presence of a microbial threat. Necrosis is mediated by the continued presence and activation of mononuclear immune cells and inflammatory chemical mediators.
  • Attempts at healing- collagen deposition and fibrosis mediated by fibroblasts.
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21
Q

Cellular mediators of chronic inflammation

A

The two main cellular mediators of chronic inflammation are Macrophages and Lymphocytes. The Macrophages initiate Phagocytosis to get rid of the offending agent, they then initiate tissue repair by secreting growth factors and cytokines which recruit other cellular mediators. The Macrophages activate the Lymphocytes via antigen presentation on the MHC2 complex. The T Lymphocytes then secrete Cytokines/ Chemokines. It also stimulates B cells to secrete antibodies. This then propagates chronic inflammation.

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22
Q

The two complication of chronic inflammation?

A

Granulomatous and Fibrosis

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23
Q

Granulomatous inflammation

A

Cellular attempt to contain an offending agent that is difficult to eradicate. Mediated by Macrophages which differentiate into specialised epithelioid cells which form a “cage” around the offending agent with a necrotic centre.

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24
Q

Types of Granulomatous

A

Depends on the substance which induces granulomatous inflammation:
Immune granulomas- infectious organisms like bacteria and fungi
Foreign body granulomas- foreign objects and suture fragments

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25
Q

Diseases caused by Granulomatous inflammation

A

Tuberculosis, leprosy, sarcoidosis and syphilis

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26
Q

Why does fibrosis occur

A

When the tissue injury is severe or repetitive you get irreversible collagen deposition. Normally the collagen deposited is removed but not in fibrosis. Due to dysregulation of the wound-healing response

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27
Q

Fibrosis

A

Fibrosis is due to the excessive accumulation of fibrous connective tissue (components of the extracellular matrix (ECM) such as collagen and fibronectin) in and around inflamed or damaged tissue, which can lead to permanent scarring → organ malfunction → death. ECM deposition is driven by fibroblasts

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28
Q

Fibrosis mechanism of action

A

1) A persistent stimulus which chronic inflammation
2) Continued Activation of Macrophages and Lymphocytes leads to the secretion of Cytokines (TNF, IL-1, IL-4) and Growth Factors (TGF-b, FGF)
3) This promotes proliferation of Resident Fibroblasts & Recruitment of Bone Marrow Fibroblasts
4) Leading to the excessive synthesis and deposition of ECM Proteins (Collagen)
5) Production of these cytokines leads to a reduction in the breakdown of collagen via Inhibition of MMPs (Matrix metallopeptidase)
6) Continued failure to adequately contain or eliminate the inciting factors can exacerbate the inflammatory response and lead to a chronic wound-healing response, with continued tissue damage, repair and regeneration, ultimately resulting in fibrosis.

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29
Q

Serous inflammation

A

The slow movement of cell fluid into spaces created by cell injury or into body cavities. The fluid is not infected and does not contain a large number of leukocytes. For example, a skin blister from a burn or viral infection. The fluid will be within or immediately beneath the damaged epidermis

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30
Q

Fibrinous inflammation

A

The passage of fibrinogen out of the blood and into the extracellular space after an increase in vascular permeability or procoagulant stimuli (i.e. cancer cells). Appears as an eosinophilic (bright pink) meshwork or amorphous coagulum. Can occur in serous cavities where there is the conversion of fibrinous exudate into a scar between the serous membranes.

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31
Q

Purulent inflammation

A

Characterised by the production of pus consisting of neutrophils, liquefied cellular debris and edema fluid. Commonly due to pyogenic (pus producing) bacterial infections that cause liquefactive tissue necrosis such as Staphylococci. Abscesses are localised collections of purulent inflammatory tissue with a central mass of necrotic leukocytes and tissue cells surrounded by preserved neutrophils. The pus is enclosed by surrounding tissue.

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32
Q

Ulcers

A

A local defect or excavation of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflamed necrotic tissue. Occurs when tissue necrosis and resultant inflammation is on or near a surface. It is most commonly encountered in the mucosa of the mouth, stomach, intestines, or genitourinary tract, and the skin and subcutaneous tissue of the lower extremities in older persons who have circulatory disturbances that predispose them to extensive ischemic necrosis.

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33
Q

Histamine inflammation table

A

Mast cell/ basophil
Vasodilation
Increased permeability

34
Q

Plasma proteins inflammation table

A

Liver
Vasodilation
Increased permeability
Leukocyte recruitment

35
Q

Prostaglandins

A

Mast cell/ basophil/ Nuetrophil
Vasodilation
Increased permeability

36
Q

Leukotrienes

A

Mast cell/ basophil/ neutrophil
Increased permeability
Increased Leukocyte recruitment

37
Q

Cytokines

A

Mast cells/ Macrophages
Vasodilation
Increased permeability
Leukocyte recruitment

38
Q

Chemokines

A

Mast cell / Macrophages

Leukocyte recruitment

39
Q

Bradykinin

A

Made from kininogens (plasma proteins) produced by the liver. It increases vascular permeability by gap junction dissociation and increased histamine release from mast cells. It increases local endothelial eicosanoid production

40
Q

Eicosanoids

A

Prostaglandins and Leukotrienes. Made from oxidation of Arichodonic acid

41
Q

How are Prostaglandins and Thromboxane’s produced

A

Membrane phospholipids -> Arachidonic acid using the enzyme Phosphilpase A2. Arachidonic acid -> Prostglandins and Thromboxanes using the enzyme Cyclooxygenase

42
Q

How is Leukotriene A4 produced

A

Membrane phospholipids -> Arachidonic acid using the enzyme Phospholipase A2. Arachidonic acid -> Leukotriene A4 using the enzyme 5-lipoxygenase and FLAP

43
Q

How is Leukotriene B4 produced

A

Membrane phospholipids -> Arachidonic acid using the enzyme Phosphilpase A2. Arachidonic acid -> Leukotriene A4 using the enzyme 5-lipoxygenase and FLAP. Leukotriene A4 -> Leukotriene B4 using the enzyme Epoxide hydrolase.

44
Q

How is Leukotriene C4 produced

A

Membrane phospholipids -> Arachidonic acid using the enzyme Phosphilpase A2. Arachidonic acid -> Leukotriene A4 using the enzyme 5-lipoxygenase and FLAP. Leukotriene A4 -> Leukotriene C4 using the enzyme Leukotriene C4 synthase

45
Q

The main systemic effects of inflammation

A

1) Fever (pyrexia)
2) Increase in acute phase proteins.
3) Increase in Leukocyte cell number
4) Sepsis

46
Q

What causes fever in inflammation

A

It is mediated by pyrogenic microorganisms and the Prostaglandin E2 production

47
Q

Pyrogens

A

Components from microorganisms that induce fever, i.e. LPS which is found on the outside of gram negative bacteria. They act like pathogen-associated molecular patterns (PAMP) and bind to Toll-Like Receptors

48
Q

Pyrogen mediated mechanism of action of fever

A

1) Pyrogens on the surface of Gram Negative Bacteria, bind to the PRR on macrophages
2) Pyrogen/PRR binding results in the production and secretion of cytokines IL-6, IL-1b , TNF-a into the blood
3) These cytokines migrate to the Blood Brain Barrier and bind to receptors on Brain Endothelial Cells
4) This activates Prostaglandin E2 Synthesis. Phospholipids in the membrane of blood brain barrier endothelial cells → Arachidonic acid (by the enzyme Phospholipase A2) → Prostaglandin E2 (PGE2) Synthesis (by Cyclooxygenase).
5) PGE2 enters the brain vasculature and binds to receptors in the hypothalamus, which raises the body temperature.

49
Q

Why is a fever useful?

A

Bacteria work best at the bodies normal temperature, so by increasing the temperature you reduce bacteria reproduction. A high temperature also causes hyperproliferation of leukocytes i.e. Macrophages. You can treat fever by blocking the enzymes from working.

50
Q

What causes the increase in acute phase proteins in inflammation?

A

Mediated by cytokine released by macrophages (IL1, and IL6, and TNFα) which stimulate the Liver to produce acute phase proteins like C-reactive proteins.

51
Q

Why is the increase in acute phase proteins useful in inflammation?

A

C-reactive protein (CRP) can bind to bacterial and fungal cell envelopes. This can cause opsonisation (attracting phagocytic Macrophages). It can also promote the classical complement activation which drives the recruitment of other phagocytic leukocytes and drives the destruction of bacteria and fungi using the membrane attack complex.

52
Q

Clinical blood biomarkers of inflammation?

A

↑ C-Reactive Protein (CRP)
↑ Fibrinogen- relies on the use of the Erythrocyte Sedimentation rate test (ESR), the more inflammation there is the higher ESR is because there is more fibrinogen

53
Q

Inflammation- increase in cell number

A

Caused by micro-organism exposure (PAMP/PRR binding). This causes increased Cytokine production by macrophages (IL-1, IL-6, IL-8) which stimulate haematopoietic stems cells in the bone marrow to proliferate and differentiate into leukocytes, usually neutrophils. The Leukocytes are then released into circulation and increased white cell count (WCC). Typically rises to 20,000 cells per ml and up to 100,000 cells per ml.

54
Q

Why do you get s drop in blood pressure in sepsis?

A

Sustained and increasing microbiological stimulus can lead to continued activation of macrophages and other immune cells (PAMP / Toll like receptors binding). It can lead to a hyperinflammatory response leading to the production of inflammatory cytokines (cytokine storm). The cytokines and ROS from phagocytic leukocytes drives the damage of endothelial vasculature. This can increase vascular permeability, causing the efflux of blood plasma out of the circulation and into the interstitial space.

55
Q

Sepsis- clots

A

In sepsis you get disseminated intravascular coagulation (DIC) where blood clots form throughout the body, blocking small blood vessels. This is caused by the hypersecretion of acute phase proteins.

56
Q

Local factors that effect wound healing

A

Type, size location of wound
Infection and contamination
Growth factors and cellular mediators
Local blood flow, effected by co-morbidities

57
Q

Systemic factors that effect wound healing

A

Increasing age
Nutritional status (especially vitamin C)
Co-morbidities, especially diabetes or CV disease
Drug treatments, especially chronic glucocorticoids

58
Q

Wound healing- extent and location if injury

A

There are two main types of wound healing, primary intention and secondary intention. In both types, there are four stages which occur; haemostasis (process to prevent and stop bleeding), inflammation, proliferation, and remodelling.

59
Q

Healing by primary intention

A

Less collagen deposition and more epithelialisation. Occurs in small traumatic and surgical wounds (scalpel incision) where the dermal edges are close together. There will be clearance of the injurious stimuli as well as mediators and neutrophils

60
Q

Healing by secondary intention

A

More collagen deposition less epithelialisation. Typical in larger traumatic wounds (dog bite) and occurs when the sides of the wound are not opposed, therefore healing must occur from the bottom of the wound upwards. There may be connective tissue replacement and loss of function

61
Q

Wound healing- infection

A

Persistent infections and failure to remove the offending agents impairs wound healing

62
Q

Wound healing- production of local growth factors

A
  • Transforming Growth Factor (TGF) Beta – Activates fibroblast to deposit collagen
  • Vascular Endothelial Growth Factor (VEGF) – Neoangiogenesis (new blood vessels)
  • Fibroblast Growth Factor (FGF)– Fibroblast proliferation
  • Epidermal Growth Factor – Epithelization
63
Q

Wound healing old age

A

The inflammatory response is decreased or delayed, as is the proliferative response. Remodelling occurs, but to a lesser degree, and the collagen formed is qualitatively different.

64
Q

Wound healing- nutrients

A

Poor nutrient status will compromised the patient’s ability to heal and prolong wound healing. Vitamin C play an important role in collagen synthesis and is required for collagen deposition and scar formation.

65
Q

Wound healing- diabetes mellitus

A

Causes the peripheral vasculature to become stiff and rigid, impairing local blood flow throughout the small vessels at the surface of the wound. It inhibits leukocyte recruitment and activation at the site of infection. Can lead to gangrene and amputation. This is due to impaired NO signalling which is needed in vasodilation. The narrowing of the blood vessels leads to a higher blood pressure which limits circulation to the lower extremities.

66
Q

Wound healing- chronic glucocorticoid treatment

A

Suppresses inflammation. Glucocorticoid receptors and nuclear hormone receptors produce proteins which inhibit the inflammatory response. Inhibits TGF beta which is the main growth factor for stimulating fibroblast secretion of collagen. It also destroys the collagen which is already there

67
Q

The mechanism in which Glucocorticoid inhibits the inflammatory response

A

1) Production of Lipocortin which inhibits Phospholipase A2 – ultimately inhibiting the production of proinflammatory mediators prostaglandin and leukotrienes
2) Directly and indirectly Inhibits the transcription factor NFKB – which serves to inhibits toll like receptor signaling and cytokine production in macrophages
3) Inhibits the recruitment and activation of leukocytes

68
Q

How is tissue repaired?

A

It is either regenerated or the scar formation/collagen deposition

69
Q

Regeneration- Labile tissue

A

The tissue is continuously dividing so it regenerates rapidly after injury. I.e. mucous membranes (easily damaged as exposed to outside environment), Lymphoid cells and Haematopoietic cells.

70
Q

Regeneration- stable tissue

A

Long lifespan, “capable” of rapid division following injury when they receive the correct growth factors. (Smooth muscle cell, kidney, lung, fibroblasts and endothelial cells).

71
Q

Regeneration- permanent tissuse

A

Very limited regenerative ability - may regenerate portions of the cell (neurons, cardiac muscle cells, Lens epithlium).

72
Q

How the extent of tissue injury effect tissue regeneration?

A

The integrity of the extracellular matrix and underlying basement membrane is important in regenerative capacity. The basement membrane is needed for growth factor production which allows the cells to progress through the cell cycle and proliferate. There are also stem cells within the basal layer which are in direct contact with the basement membrane. If the basement membrane is damaged, stem cells cant be stimulated to divide impairing regenerative capacity

73
Q

Why is the Liver so good at regeneration?

A

The Liver is able to regenerate due to proliferation of remaining hepatocytes (triggered by cytokines and growth factors) and repopulation from progenitor cells which occurs when hepatocyte proliferation is impaired.

74
Q

Why does collagen deposition occur?

A

Occurs when regeneration isn’t possible because the basement membrane is damaged and the stem cell niche is destroyed. Instead there is proliferation of resident and bone marrow fibroblasts which make the collagen and connective tissue. This provides tensile strength to the damaged tissue

75
Q

Regeneration- acute inflammatory phase

A

Removes injurious agents by recruitment of phagocytic leukocytes (neutrophils), limiting tissue damage. Prepares the wound environment for repair – Macrophages produce Cytokines and Growth Factors (such as TGF beta which tells the fibroblast to produce collagen). The Cytokines and growth factors also cause cellular recruitment and proliferation of fibroblasts from the bone marrow.

76
Q

Stages in tissue regeneration

A

1) A tissue injury
2) Acute inflammatory response
3) Proliferative phase
4) Remodelling phase

77
Q

Tissue regeneration- Proliferative phase

A

1) Angiogenesis
2) Granulocyte tissue formation
3) Epithelialisation

78
Q

Tissue regeneration- Granulocyte tissue formation

A
  • TGFb is secreted from Macrophages, this promotes resident fibroblast activation and bone marrow fibroblast recruitment
  • The fibroblasts are stimulated by TGF-beta to start synthesising and laying down collagen to fill the wound. This forms loose connective tissue.
  • Granulation tissue is pink, soft and very fragile. Intermediate stage before scar tissue formation.
  • Macrophages also produce fibroblast growth factor (FGF) which promotes fibroblast proliferation.
79
Q

Tissue regeneration- Epithelialisation

A

Cells surrounding the injury release epidermal growth factors (EGF) which stimulates epithelial cell growth to close the wound

80
Q

Tissue regeneration- Remodelling phase

A

Maturation & reorganisation of connective tissue by Matrix Metalloproteinases (enzymes which breakdown collagen). The blood vessels which were produced are now destroyed, this is called avascularisation. The scar increases in tensile strength over the next 3-6 months and the wound balances due to avascularisation (regression of new blood vessels formed during the proliferative phase). The Leukocyte’s and fibroblasts depart, those that remain become inactive.

Medicine year 1 semester 2 (61 decks)

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