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Unit 9 > Week 1: Inflammation and repair 1 > Flashcards

Week 1: Inflammation and repair 1 Flashcards

1
Q

Define inflammation

A

A localised response resulting color,tumor, rubor, dolor and function laesa due to infection or injury.

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2
Q

What is the purpose of inflammation?

A

Protective response against damage/pathogens
Trigger homeostasis

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3
Q

What is the mechanism behind calor, rubor and tumour in inflammation?

A

Vasodilation increases blood flow
Increased vascular permeability and causes vascular status
More blood closer to the surface

Friction from diapedisis may also contribute to heat

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4
Q

What is the mechanism behind dolor from inflammation?

A

Action of inflammatory mediators on free nerve endings to activate or sensitize the endings.
Typically prostaglandins (leukocyte release) and bradykinin released from mast cells.

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4
Q

What causes functio de laesa during inflammation?

A

Damage to cells necessary for tissue function including parenchymal and stromal cells

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4
Q

What are the kinetics of acute inflammation?

A

Rapid and short lived reponse to injury.
Develops over minutes/hours
May persist over a few days
Starting with edema, neutrophil infiltrate the monocyte/macrophage infiltrate

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4
Q

What is the process behind vasodilation in inflammation?

A

Microbes/ nectrotic tissue release PAMPs/DAMPs that are recongised by PRR on tissue resident immune cells.
Results in the release of inflammatory mediators
In particular histmane release from mast cells.
Histamine binds to H1 receptors on endothelial cells, results in the production of NOx. NOx results in the relaxation of smooth muscle in capillary walls - acting as a vasodilator

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4
Q

What are the key phsyiological features of acute inflammation?

A

Vasodilation
Increased vascular permeability
Vascular statis
Pain

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4
Q

What is the mechanism behind increased vascular permeability during inflammation?

A

Vasodilation
Inflammatory mediators such as histamine, prostaglandins and leukotrienes cause endothelial cells to contract, disrupting the tight junctions to widen the gaps.

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5
Q

What is the mechanism behind vascular statis in acute inflammation?

A

Increased vascular permeability - loss of fluid from blood plasma
This increases the viscosity of blood hence slower flow
Fibrin clots may also form - due to increased pro-coagulant factors such as fibrinogen and thromboxane

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5
Q

What is the process of leukocyte extraversion in inflammation?

A

Vasodilation and increased vascular permeability from inflammatory mediators.
Vascular stasis allows immune cells to lone up near endothelium (imagination)
Leukocyte forms low affinity bonds with the endothelial walls by E-selectin on endothelial cells and sialyl-Lewis on leukocyte, alongside L selecting on leukocyte walls and ligand on endothelial cells.
Breaking and reformation of these bonds allows the leukocyte to roll along endothelium.
Chemokine signalling in leukocyte cause a higher affinity adhesion molecule, this tighter bond is where the leukocyte will pass through widened gaps in the endothelial layer (from endothelial cell contraction), squeezing into intersitial fluid by diapedesis (may secrete collagenases to help degrade BM)
Follows chemokine gradient to site of injury, chemokines rearrange the cytoskeleton of the lymphocyte to allow it to move forward.

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5
Q
A

Basophil

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5
Q

What is the process by which a macrophage can lead to pain sensation?

A

A resident activated macrophage releases inflammatory mediators such as TNF and PGE2, which bind to cytokine receptors on the surface of nociceptor terminals.
Leads to a cascade of signalling inside the nocicpetor including the activation of adenylate cyclase.
This leads to increased Ca2+ mobilisation
Increased voltage or ligand gated channel activation
Increased neuropeptide transcription and release
Increased transcription or receptor and channel proteins.
Leads to sensitisation to or activation of a pain signal

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6
Q
A

Lymphocyte

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7
Q
A

Monocyte

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8
Q
A

Macrophage

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9
Q
A

Eosinophil

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10
Q

What are the main cell types involved in acute inflammation?

A

Neutrophils
May be followed by monocytes and macrophages (typically in smaller numbers)

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11
Q

What is the role of neutrophils in acute inflammation?

A

Dominate for 6-24 hours
Die and replaced by monocytes

Phagocytose pathogens, debris and dead cells, will secrete cytokines and produce NETs

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12
Q

What is the key way to distinguish between histological monocytes and macrophages?

A

Macrophages tend to have more cytoplasm (and lack of rbcs in background)

13
Q

What is the role of macrophages in acute inflammation?

A

Phagocytic
Secrete cytokines
Activate T cells

14
Q

What are the Non-cellular effectors in acute inflammation?

A

Complement
Enzymes
NETs

15
Q

What is the key role of complement?

A

Activated by:
Classical pathway - C1 binds to antigen antibody complex on pathogen surface
Lectin Pathway - C4/C2 binds to sugars on pathogen surface e.g MBL binds to mannose on surface
Alternative - C3b binds directly to pathogen surface

Enzyme cascade - compliment proteins are cleaved to be activated

Outcomes:
C3a and C5a recruit phagocytic cells by chemotaxis and promote inflammation!!!!!!!! acute inflammation
C3b - membrane attack complex
C3b - opsonisation

16
Q

What is the role of NETs in acute inflammation?

A

Netosis in. neutrophils released NETs
Consist of antimicrobial proteins and nuclear chromatin to immobiliser and destroy pathogens

17
Q

What is the role of MMP in acute inflammation?

A

Break down extracellular matrix.

18
Q

What are the symptoms of systemic inflammation?

A

Tachycardia
Hypotension
Leukocytosis
Fever

19
Q

What brings on the effects of systemic inflammation?

A

Cytokines, particularly IL-1beta, TNFalpha and IL-6, all of which have longer lasting effects than histamine

Act on hypothalamus to cause fever
SNS to cause cardiovascular changes
Liver - to release APP such as CRP
Bone marrow - to produce more leukocytes

20
Q

Identify the key features of acute inflammation in this histological image

A

Dilated and congested blood vessels
Neutrophils in the tissue
Tissue oedema (white space)

21
Q

What are the different types of acute inflammation?
How are they different?

A

Serous
Fibrinois
Purulent
Ulcerative

All have different morphological features

22
Q

What are the key features of serous inflammation?

A

Accumulation of exudate in a cavity
Cavity may be natural e.g peritoneum or created by an injury (under epithelium)
Exudate originates from plasma or mesothelium
Exudate is sterile and free of leukocytes

E.g skin blister

23
Q

What are the key features of fibrous inflammation?

A

High deposition of fibrin
Occurs at lining of body cavities
Normally after highly vascular leakage and a procoagulant stimuli resulting in fibrin deposition.
If not resolved scar formation disrupts function

24
Q

What are the key features of purulent/suppurative inflammation?

A

Formation of pus - necrotic debris and tissue fluid (causes liquifaction on necrosis)
Usually caused by a pyogenic bacteria (staphylococci aureus)
In chronic inflammation the abcess may be surrounded by fibrotic connective tissue

25
Q

What is an abscess?

A

Localised collection of pus inside a tissue
Type of purulent inflammation

26
Q

What are the key features of ulcerative inflammation?

A

Local defect in tissue from disintigration of inflamed necrotic tissue
Found where inflammation occurs at or near a surface
May have areas of acute and chronic inflammation.

27
Q

Describe what is depicted in the histological image?

A

Loss of mucosal layer
A - artery close to hemorrhage
F - is a fibrous scar shown by high collagen deposits

28
Q

What are the different outcomes of acute inflammation?

A

Resolution - cause eliminate and no tissue damage, normal function restored
Healing/repair by fibrosis - extensive tissue damage results in connective tissue replacing functional tissue, can not regenerate
Progression to chronic inflammation

29
Q

What medication typically used to treat acute inflammation?

A

Cox-inhibitors: prevent prostaglandin production, relieve pain
Steroids: such as dexamethasome, binds to intracellular glocorticoid receptor, acts as transcription factor to decrease pro-inflammatory cytokines and increase anti-inflammatory cytokines

30
Q

What are the key features of chronic inflammation?

A

Prolonged inflammatory response of weeks or months
Characterised by simultaneous inflammation, tissue damage and attempts at repait

31
Q

What are the origins of chronic inflammation?

A

Follow acute or begin insidiously

  1. Persistent infection
  2. Unresolved inflammation
  3. Continuing exposure to a stimuli (e.g dog hair or asbestos)
  4. Hypersensitivity diseases (inappropriate activation of immune system)
32
Q

What conditions can be classified as acute inflammation?

A

Allergic reactions
Chemical irritants
infection
trauma injury
Burns
Laceration, cuts, wounds.
Frostbites

33
Q

What conditions may be classified as chronic inflammation?

A

Cardiovascular disease
Neurological disease
Autoimmune disease
Rheumatoid arthiritis
Cancer
Fibromyalgia
Chronic Fatigue Syndrome

34
Q

What are the morpholigical features of chronic inflammation?

A

Tissue infiltrate - is mainly mononuclear cells (macrophages, lymphocytes and dendritic cells)
Destruction of normal tissue architecture leading to loss of tissue function
Angiogenesis and fibrosis - as part of ongoing repair attempts

35
Q

What cell type is present?

A

Plasma cell
Eccentrically placed nucleus
Chromatin collects near nuclear membrane giving a clock face appearance.

36
Q

What are the features of chronic inflammation in this slide?

A

Lymphocytes
Plasma cells
Macrophages
Lots of collagen deposits
Loss of normal structures - such as hair follicles and sweat glands in the skin (replaced by scar tissue)

37
Q

What are the outcomes of chronic inflammation?

A

Healing by fibrosis
Immune Mediated Inflammatory Disease.

38
Q

What are some of the causes of a disregulated inflammatory response?

A

Genetic
Acquired - cancer, disease etc

39
Q

What medications may be given to treat chronic inflammation conditions?

A

NSAIDs - e.g ankylosing spondylitis
Corticosteroids - e.g inhaled budesonide for chronic asthma
Immunosuppressants - methotrexate for rheumatoid arthiritis
Biologics - adalimumab for severe active chrons disease.

40
Q

What is the process of complete resolution of an acute inflammatory response?

A

Causes localised and low grade damage to cells – hence cells retain ability to regenerate and stem cell population survives – combined with low grade damage to the ECM – tissue is able to regenerate when stimulated by growth factors released by macrophage. Combined with the reabsoprtion of exudate into lymphatics and macrophages clearing pathogen and necrotic tissue. Inflammation is said to be completely resolved.

**exam answer should include detailed from resolution of inflammation year 1.

Unit 9 (15 decks)

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