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inflammation Flashcards

1
Q

What are the cardinal signs of inflammation?
(Strayer, 2020)

A
  • heat
  • pain
  • redness
  • swelling
  • possible loss of function
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2
Q

What are the three main elements of inflammation?
(Strayer, 2020)

A
  • Vascular
  • Cellular
  • Chemical
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3
Q

What happens in the vascular element of inflammation?
(Strayer, 2020)

A

increased blood flow to the injured area and increased vascular permeability at the site allowing plasma, plasma proteins and cells to infiltrate the site of injury

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4
Q

What happens at the cellular element of inflammation?
(Strayer, 2020)

A

response of the innate immune system cells
* phagocytic cells are first line of defense and clear up cellular debris from damaged or necrtoic cells

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5
Q

What happens at the chemical element of inflammation?
(Strayer, 2020)

A
  • chemical cascades of the compliment system enahce the immune cell response
  • coagulation cascade occurs to minimise blood loss and temporarily repair damage
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6
Q

What happens if there is an unregulated or excessive response of inflammation?
(Strayer, 2020)

A
  • can cause tissue injury and disease e.g. cancer, cardiovascular and respiratory diseases
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7
Q

What happens at the initation stage of inflammation?
(Strayer, 2020)

A
  • first stage
  • chemical mediators are activated by invaders, damaged cells and extracellular matirx
  • these chemical mediators stimulate vascular changes e.g. vasodilation and increased permeability to the area to recruit macrophages
  • this increased vascularity and permeability flood the area with coagulation factors, cytokines, chemokinesm platelets and inflammatory cells e.g. neutrophils
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8
Q

What happens at the amplification stage of inflammation?
(Strayer, 2020)

A

if the injury is more extensive then more white blood cells (leukocytes) and macrophages are attracted to the area by the activated complement system

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9
Q

What happens at the destruction stage of inflammation?
(Strayer, 2020)

A

enzymetic digestion and phagocytosis reduce or remove damaged tissue, debris, foreign material and infectious organisms

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10
Q

What happens at the termination stage of inflammation?
(Strayer, 2020)

A
  • anti-inflammatory mechanisms limit the tissue destruction and damage to normal cells, setting the scene for healing and repair,
  • this occurs by reversing the vascular changes and reducing further fluid and cellular access to the injury site
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11
Q

What is the difference between acute and chroic inflammation?
(Strayer, 2020)

A

Acute:
acute includes activation, amplification, destruction, and termination
* if this is insufficient to resolve the initial damage or remove infectious agents this progresses into chronic inflammation

chronic
this is when further white blood cells infiltrate the area and fibrosis occurs (the deposition of extracellular matix leading the scarring and loss of function)

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12
Q

What are neutrophils?
(Strayer, 2020)

A
  • type of white blood cell (leukocyte) that plays a critical role in the innate immune response
  • most abundant type of white blood cell
  • stored in bone marrow
  • accumulate at sites of injury and infection
  • attract other white blood cells and activate T cells
  • clear up cellular derpus and invading organisms as well as secreting chemical mediatoyrs that steralise and degrade injured tissue
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13
Q

What is phagocytosis?
(Strayer, 2020)

A
  • process of engulfing and destroying unwanted or dangerous material
  • they recognise the material and attach it to the phagocytic cell
  • the bound material is then drawn into the cell and membrane bound extensions crowd around it, engulfing it in the phagocyte
  • lysosomal enzymes are then released into the phagosome and degreate and destroy the material
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14
Q

What are endothelial cells?
(Strayer, 2020)

A
  • create a functional barrier between the intra and extra vascular spaces, lining the blood vessels
  • secrete antiplalelet and antithrombotic cells
  • when the blood vessels are damaged they attract and activate inflammatory cells
  • respond to increased levels of bradykinin, histamine, endotoxins, and cytokines
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15
Q

Name some white blood cell types.
(Strayer, 2020)

A
  • macrophages- clear pathogens and debris, producing inflammatory mediatory
  • dentritic cells- antigen presenting cells, stimulating T cell secretion
  • basophils/ mast cells- release inflammatory mediators
  • platelets- initiate and regulate clotting, aggregate with fibrular collagen forming a plus, produce inflammatory mediators
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16
Q

What are some chemical mediators?
(Strayer, 2020)

A

coagulation
- activation of cascade. activate cells by binding with specific receptors, stimulating further release of chemical mediators and recruiting cells to sites of injury. play a role in amplifying responses by activating cascade mechanisms

kinins
- amplifying inflammation responses

complement
- activation of inflammatory response

17
Q

What are the positive consequences of inflammation?
(Strayer, 2020)

A
  • limit the area of injury
  • clear pathogens and damaged tissue
  • restore tissue integrity
18
Q

What are the local consequences of inflammation?
(Strayer, 2020)

A
  • oedema
  • abscess formation
  • fibrinous exudate- may become collagenous masses or keloid
  • ulceration- due to damage to the epithelium causing layers to be removed and expose underlying tissues
19
Q

What are the systemic consequences of inflammation?
(Strayer, 2020)

A
  • increasead WBC
  • decreases in WBC
  • fever- can inhibit bacteria and viruses
  • pain- as chemical mediators also stimulate nociceptors making more sensitive to stimulation and pain
  • disseminated intravascular coagulation- leading to blockage of vessels or overconsumption of clotting agents resulting in predisposition to bleeding
  • shock- due to large volumes of cytokines released causing widespread vasodilation and a drop in blood pressure
  • sepsis
20
Q

What is the sequence of wound healing?
(Strayer, 2020)

A
  1. inflammatory cell migration
  2. fibrin clot
  3. macrophages recruited
  4. fibroblasts recruited
  5. temporary matrix
  6. final phase
21
Q

Describe what happens when inflammatory cells migrate to the site of injury.
(Strayer, 2020)

A
  • Inflammatory cells are attracted to the area
  • macrophages, fibroblasts, and smooth muscle actin migrate to the wound from surrounding tissue
  • fibronectin, growth factors, chemokines, cell debris, and bacteria are recruited to the wound site (2-4 days)
  • initial phase of repair reaction beings with haemorrhage into the tissues
22
Q

Describe how a fibrin clot is formed.
(Strayer, 2020)

A
  • just after injury, platelets move to the site of injury and become activated releasing chemical signals that recruit more platelets to the injury site
  • once there are enough platelets they stick together, forming a thrombus, or clot at the site of injury. This seals the gap created by the wound preventing loss of plasma and tissue fluid and protecting from infection.
  • coagulation cascade occurs once activated by the tissue factor, exposed by the injury, reacts with clotting factors in the blood
  • a series of enzymatic reactions that lead to the conversion of fibrinogen, a soluble plasma protein, into insoluble fibrin strands.
  • this forms a mesh-like network of insoluble fibrin strands. These fibrin strands, along with aggregated platelets, strengthen the platelet plug and stabilize it to form a more durable blood clot.
  • after the blood clot is formed, platelets contract, pulling the fibrin strands closer together and squeezing out excess fluid
  • over time, the damaged blood vessel is repaired through the action of endothelial cells, which line the inner surface of blood vessels, and the clot is gradually dissolved by fibrinolysis
23
Q

Describe what happens when macrophages are recruited.
(Strayer, 2020)

A
  • macrophages and monocytes are recruited to the wound from the blood, bone marrow and spleen
  • they continue to clear up any remnants and damages extracellular matrix by acting as inflammatory cells
  • they also act in wound healing ways to stop inflammation and secrete factors promoting fibroblast and collagen production to form new blood vessels and heal the wound
24
Q

Describe what happens when fibroblasts are recruited and a temporary matix is formed.
(Strayer, 2020)

A
  • fibroblasts are activated early in the healing process by cytokines, producing collagen, hyaluronan, and proteoglycans in the extracellular matrix
  • they deposit a new extracellular mix during the intermediate phase of repair
  • during this time the fibrin clot is cleared by enzymes
25
Q

Describe what happens in the final stage of wound repair.
(Strayer, 2020)

A
  • fibroblasts convert the production of stiffer, thicker collagen fibres enriched in the temporary matrix
  • this leads to a stronger, definitive matrix, involving many other matrix molecules in the assembly of the collagen network
26
Q

What is angiogenesis?
(Strayer, 2020)

A
  • new blood vessels are formed into the granulation tissue which results in more blood vessels per volume than any other tissue.
  • restoration of the capillary bed is essential for delivery of oxygen and nutrients and the removal of metabolic waste products.
  • the new vessels mainly form by endothelial cells sprouting from existing capillary vessels. It is activated by the release of cytokines and growth factors and the loss or disruption of basement membranes around endothelial cells.
  • proliferation and assembly of the endothelial cells supports the growth of new capillaries. In the process of remodelling, only a few capillaries fully mature the rest are resorbed.
  • the basement membranes are made from a unique set of extracellular matrix molecules. They self-assemble into a sandwich like structure of covalently linked collagen fibres on a laminin network.
  • The basement membrane determines cell shape and contribute to cellular development.
27
Q

What is re-epithelisation?
(Strayer, 2020)

A
  • important to restore the integrity of the epidermis to protect against infection and fluid loss.
  • the epidermis is constantly renewing itself by mitotic division of its basal layer cells which mature as they move out towards the surface before they are eventually shed.
  • for this to occur the basal layer of cells needs to be intact and with its cells in direct contact with each other and the basement membrane.
  • as the epidermis becomes re- established it separates the scab from the newly formed granulation tissue, then resumes its normal cycle of division, maturation and shedding, remodelling through this process.
28
Q

What is wound contracture?
(Strayer, 2020)

A
  • Open wounds contract and deform as they heal depending on how they are attached and move with the underlying tissues.
  • This wound contraction is mediated by myofibroblasts which act like smooth muscle cells.
  • They contain a lot of actin fibres and other fibres that respond to stress and start to appear at the wound site around day 3 and start to contribute force to the contraction of the wound.
29
Q

What is scar remodelling?
(Strayer, 2020)

A

Eventually granulation tissue becomes scar tissue as the balance between collagen formation and breakdown is established.
Fibroblasts will continue to alter the scar appearance for years following the injury.

30
Q

How are wounds with apposed edges healed?
(Strayer, 2020

A
  • by primary intention
  • apposed wound edges are held together with a suture leading to minimal tissue gaping or loss
  • this means there is decreased granulation tissue as the wound only requires minimal cell proliferation and neovascularisation to heal
  • this results in a narrow, linear scar
31
Q

How are wounds with separated edges healed?
(Strayer, 2020)

A
  • by secondary intention
  • the gouged wound is left to remain open
  • this means the edges remain far apart and there is substantial tissue loss
  • the healing process requires wound contraction, extensive cell proliferation, matrix accumulation, and granulation tissue to heal
  • the wound is re-epithelialized from the margins, with collagen fibres deposited throughout the granulation tissue
  • the granulation tissue is eventually reabsorbs, leaving a large collagenous scar.
32
Q

What nurses need to consider in a wound assessment?
(Cox, 2019)

A
  • anatomic location
  • degree of tissue damage
  • type of tissue in the wound
  • wound size
  • infection
  • pain
33
Q

What types of wounds do you get?
(Cox, 2019)

A
  • pressure injury
  • venous ulcer
  • arterial ulcer
  • diabetic ulcer
  • skin tear
  • moisture associated skin damage

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