Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Medicine Unit 9 UoS > Unit 9 - Inflammation and repair > Flashcards

Unit 9 - Inflammation and repair Flashcards

1
Q

What are the clinical features of inflammation?

A

Calor - heat
Rubor - redness
Tumor - swelling - vasodilation, increasing blood flow, increased vascular permeability, vascualr stasis
Dolor - pain - action of inflammatory mediators on free nerve endings
Functio laesa - loss of function - damage to cells necessary for function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is acute inflammation?

A

Rapid and short lived response to injury
Develops in mins/hours
Persists for few days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the physiological mechanisms of acute inflammation?

A

Vasodilation
Increased vascular permeability
Vascular stasis
Pain
Leuckocyte extravasation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vasodilation

A

Occurs rapidly
Histamine acts on smooth muscle of small blood vessels - arterioles
New capillary beds open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Increased vascular permeability

A

Histamines, bradykinin, prostaglandins and leukotrienes increase vascular permeability.
Endothelial cells contract and tight junctions between are disrupted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Vascular stasis

A

Slowing/cessation of blood flow
Movement of fluid out of blood increases viscosity
Fibrin clots contribute to stasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pain in inflammation

A

Action of prostaglandins, growth factors and cytokines on free nerve endings - activating or sensitising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Leukocyte extravasation

A

Leukocytes are recruited to the site of inflammation by migrating from the vascular lumen into the tissue, then to site of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do cells stop and adhere to capillary endothelium?

A

Stasis allows cells to line up near endothelium - margination
Leukocyte chemokine signalling allows adhesion molecules to have high affinity state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is this cell involved in acute inflammation?

A

Neutrophil
predominant first 6-24 hours before replaced by monocytes
Nucleus has 2-5 lobes
Phagocytose microbes, dying cells, cell debris, produce NETs, secrete cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is this cell involved in acute inflammation? What are its identifying features

A

Monocyte
Large, pale staining cytoplasm, bean shaped nucleus
differentiates into populations of macrophages and dendritic cells to regulate cellular homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What cell is this involved in acute inflammation? Identifying features?

A

Macrophages
Large, pale staining cytoplasm, bean shaped nucleus, more cytoplasm than monocytes
Phagocytic, secrete lots of pro-inflammatory cytokines, can activate T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some non-cellular effectors in acute inflammation?

A

Complement - Components C3a and C5a are peptide mediators of local inflammation, act on leukocytes and endothelial cellsfacilitate the uptake and destruction of pathogens by phagocytic cells.
Enzymes - eg matrix metalloproteinases from macrophages, break down extracellular matrix
NETs - extruded nuclear chromatin and antimicrobial proteins. Immobilise and destroy pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How may systematic inflammation present?

A

Tachycardia
Hypotension
Leukocytosis
Fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do cytokines act to cause systematic inflammation?

A

Longer lasting than histamine
Act on:
Hypothalamus to cause fever
Sympathetic nervous system to induce CV changes
Liver to produce acute phase proteins e.g. CRP
Bone marrow to produce leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are types of acute inflammation?

A

Serous
Fibrinous
Purulent
Ulcerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is serous inflammation?

A

Accumulation of exudate in a cavity e.g. peritoneal/space created by injury
Exudate from plasma or mesothelium
Exudate is sterile and free of leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is fibrinous inflammation?

A

Large deposition of fibrin
Typically at lining of body cavities e.g pleural/pericardial
High vascular leakage + procoagulant stimuli - fibrin deposition
Scar forms if unresolved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is purulent inflammation?

A

Formation of pus - necrotic debris (dead neutrophils, tissue cells and usually bacteria) and tissue fluid
Abscess is localised collection of pus buried in tissue
If chronic, may replace with fibrotic connective tissue
Often caused by pyogenic bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is ulcerative inflammation?

A

Local surface defect in tissue caused by sloughing off/disintergration of inflamed necrotic tissue
near a surface or Where inflammation and necrosis can occur
Acute and chronic inflammation may occur simultaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the outcomes of acute inflammation?

A

Resolution:
cause of inflammation eliminated, no lasting tissue damage, regeneration, returns to normal
Repair by fibrosis:
cause may be eliminated, extensive damage, cannot regenerate, connective tissue replaces
Progression to chronic inflammation:
cause persists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How may acute inflammation be treated?

A

COX inhibitors:
e.g. aspirin, paracetamol
inhibits prostaglandin synthesis
Steroids:
e.g. dexamethasome
binds to glucocorticoid receptors in innate immune cells, inhibiting inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is chronic inflammation?

A

May follow acute, or begin gradually
Weeks or months
Charaterised by simultaneous inflammation, tissue damage, repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are example of chronic inflammation?

A

CVD, neurological disease, autoimmune disease, rheumatoid arthritis, cancer, fibromyalgia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are causes of chronic inflammation?
Persistent infection e.g. H pylori Unresolved acute inflammation after injury Continuing exposure to stimulus Hypersensitivity diseases
26
What are the features of chronic inflammation?
- Tissue infiltration - Destruction of normal tissue architecture - Angiogenesis and fibrosis
27
What cells infiltrate tissue in chronic inflam?
Mononuclear cells - monocytes, macrophages, dendritic cells and lymphocytes incl plasma cells
28
What destroys normal tissue architecture in chronic inflam?
Persisting offending agent or immune cells. Potential functio laesa
29
What does angiogenesis and fibrosis consist of?
Characteristic of ongoing repair process Production of new blood vessels Excessive deposition of collagen and other ECM = connective tissue - contributing to loss of function
30
What cell is this thats involved in chronic inflam?
Lymphocyte Small Thin edge of cytoplasm Secretes cytokines
31
What cell is this that is involved in chronic inflam?
Plasma cells Random placed nucleus Secrete antibodies
32
What are the outcomes of chronic inflam?
Repair by fibrosis ->can cause further issues e.g. bile duct strictures, constrictive pericarditis
33
What may cause chronic inflam?
Genetics Acquired conditions e.g. cancer, metabolic and infectious disease Character of immune-mediated inflammatory disease
34
How can chronic inflammation be treated?
NSAIDs e.g. naproxen Corticosteroids e.g. budesonide Immunosuppressants e.g. methotrexate Biologics e.g. adalimumab
35
What is granulomatous inflammation? What are the features?
Chronic inflammation Response to agent difficult to eradicate -Organised collection of immune cells and others - Aggregation of activated macrophages
36
Foreign-body granuloma
Reaction to inert foreign material No T cell mediated immune response
37
Immune granuloma
Caused by agents that can cause T cell mediated response Can be caused by mycobacterial, fungal and parasitic infections
38
What are examples of granulomas without foreign bodies in non-infectious disease?
Chron's disease Sarcoidosis
39
What cell types are found in granulomatous inflammation?
Macrophages/monocytes Multinucleate giant cells Lymphocytes
40
What are caseating granulomas?
Granulomas with necrotic centre - looks soft and 'cheesy' Free radical mediated injury and hypoxia -> death by necrosis
41
What is the outcome of granulomatous inflammation?
Heal by fibrosis = Tissue and organ damage Can calcify in certain tissues - type of scarring
42
What are the outcomes of tissue repair?
Regeneration - after mild, superficial injury -stem cells regenerate epithelium Scar formation - after severe injury Or combination of both
43
What are the stages to repair? (4)
-Hemostasis: immediate, blood vessels constrict, clotting activated - Inflammatory: Starts quickly, lasts few days - Proliferative: fibroblasts and endothelial cells prolif. Collagen produced - Remodelling: ECM reorganises, variable replacement of normal tissue
44
What are the different tissue type that regenerate to different degrees?
Labile tissue: continually dividing in normal state, easily regenerate if stem cells are still present Stable tissue: capable of regeneration in response to injury Permanent tissue: terminally differentiated, unable to regenerate
45
How does regeneration occur?
Surviving functional cells proliferate Stem cells located in specific niches in tissue differentiate Growth factors produced by macrophages, epithelial cells and fibroblasts drive regeneration
46
TGF-B
Transforming growth factor beta Function: Fibroblast migration, collagen synthesis, monocyte migration
47
PDGF
48
VEGF
49
EGF
50
FGF
51
What role does ECM have in tissue repair?
Needed for full regeneration Damaged ECM -> scarring Cells use integrins to bind to ECM Interaction signals cells -> cell survival and proliferation
52
Scar formation
When damage is severe, tissue unable to regenerate No return to full function Granulation tissue forms within 3-5 days
53
What are the stages of scar formation?
Angiogenesis - vascular endothelial cells proliferate in response to GF, new blood vessels sprout Fibroblast migration and proliferation - stimulated by GF and cytokines Deposition of ECM - fibronectin dominates first, then collagen Decreased cellularity, progressive vascular regeneration - macrophages, fibroblasts and vascularity decline Myofibroblast differentiation, contraction of scar Remodelling of new connective tissue - Organisation of collagen. MMPs
53
What are histological features of scars?
Dense fibrous tissue No adnexal structures e.g. glands Re-epithelialisation
53
What factors influence tissue repair?
Infection Disease Nutritional status Glucocorticoids Mechanical factors Perfusion Foreign bodies Injury type and extent
53
Why does infection and disease affect tissue repair?
Infection: prolongs inflammation and may increase damage Disease: poor perfusion, impaired leukocyte function, ongoing low level systemic inflammation
54
Why does nutritional status and glucocorticoids affect tissue repair?
Nutritional status: protein deficiency, vitamin C deficiency (collagen synthesis) Glucocorticoids: reduce inflammation and impact repair process
55
Why do mechanical factors, poor perfusion foreign bodies and injury type and extent affect tissue repair?
Mechanical factors: physical disruption of repairing tissue Poor perfusion: reduced delivery of materials/cells Foreign bodies: persistence of stimulus Injury type and extent: extensive injury will result in at least partial loos of function
56
What are different types of scars?
Hypertrophic scar, keloid, excess granulation tissue, wound rupture/ulceration, contracture
57
What type of scar is this? why is it formed?
Hypertrophic scar Due to excessive collagen generation and accumulation
58
What type of scar is this? why is it formed?
Keloid Due to excessive collagen generation and accumulation
59
What type of scar/wound is this? Why is it formed?
Excess granulation tissue Can block further healing re-epithelialisation
60
What type of scar/wound is this? Why is it formed?
Wound rupture or ulceration After inadequate formation of granulation tissue/scar Due to repeated trauma/continuing infection
61
What type of scar is this? Why is it formed?
Contracture Excessive contraction of a scar leads to restricted movement or deformity
62
What are some causes of systemic chronic inflammation (low-grade)?
Ageing: immunosenescence and mitochondrial dysfunction likely to contribute Poor diet: alteration of gut microbiome and excess adipose tissue Stress: prolonged cortisol levels promotes inflammation and attenuates tissue repair
63
What are some consequences of low grade systemic chronic inflammation?
Sickness behaviours and physiological responses: fatigue, raised BP Breakdown of tolerance leading to autoimmune disease and IMID Dysregulation of normal cellular and tissue physiology, predisposing to metabolic diseases and cancer

Medicine Unit 9 UoS (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions