Inflammation Flashcards

1
Q

Hyperaemia

A

Active increase in blood flow to an area. First step in acute inflammation

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

Oedema

A

increase fluid (from the vessels) in the interstitial tissue (does not enter cells, however sits in the connective tissue between the cells)

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

2 classifications of oedema

A

Exudate and transudate

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

Describe Exudate

A

Inflammatory extravascular fluid with high protein concentration

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

Describe Transudate

A

Extravascular fluid with low protein concentration

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

Effusions meaning

A

fluid leaks into body cavity

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

Resolution

A

Healing without scarring, restoration of structure & function.
Possible following acute inflammation

Depends on:
Tissue type
Extent of the injury
Presence of factors that can impair repair (infection, nutrition, etc).
Some tissues will never undergo resolution

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

Organisation

A

Healing by scarring/fibrosis.
Possible following acute inflammation
Depends upon:
(Inevitable following chronic inflammation)
Prior to maturation scar tissue is composed of granulation tissue

Granulation tissue:
- Macrophages: signalling and gobbling
-Fibroblasts/Myofibroblasts: make collagen
- Angiogenesis: growth of new capillaries
Mature scar is made of collagen protein

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

Ulcer

A

area of necrosis on surface. a lesion or sore on a body surface like the skin or mucous membranes

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

Abscess

A

Area of necrosis from acute inflammation. If the microbes are gone, the area becomes a cystic space. If the microbes remain, the body walls off area with granulation tissue and becomes chronic abscesses.

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

What form of cell death causes an inflammatory response?

A

Necrosis

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

What are the 3 features of acute inflammation?

A
  1. Hyperaemia
  2. Oedema (exudate)
  3. Neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 3 possible outcomes of acute inflammation?

A
  1. Resolution: healing
  2. Organisation: healing
  3. Chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 3 main components of granulation tissue & their role/purpose in repair?

A
  1. Macrophages remove the debris
  2. Fibroblasts secrete collagen
  3. New vessels grow (angiogenesis) & provide oxygen & nutrients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens following granulation tissue response?

A

Once complete, fibroblasts & macrophages leave, the vessels die by apoptosis leaving the acellular collagen scar, which will contract over time
Just filling a gap where tissue has been lost
Function lost
Distortion of surrounding tissue

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

What are the consequences of healing through organisation?

A
  • Scarring: lost function and healthy tissue
  • Distortion of surrounding tissue
  • Contraction in larger scars can cause pain and discomfort
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 main causes of chronic inflammation?

A
  1. Unresolved acute
  2. Repeated acute
  3. Special cases - no acute response (some infections and diseases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define the 3 components of chronic inflammation?

A
  1. Continued injury/necrosis
  2. Repeated attempts to repair: a. Granulation tissue (3 components) b. Proliferating parenchymal (normal, functional) cells
  3. Lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the possible negative consequences of chronic inflammation.

A
  • Loss of function through scarring

- If epithelial cells are proliferating, more chance of cancer

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

What is meant by sterile & non-sterile sites in the human body? Give examples.

A
Sterile - sites where microbes should not be present. This includes: Blood
Brain & CSF
Bone & Marrow
Lower Respiratory
Upper urogenital
Stomach - unsure

Non-sterile - where microbes can be present. such as- Skin
GIT
Upper Respiratory
Lower urogenital

21
Q

Main differences between the innate & adaptive systems

A

Innate: fast response, not specific, Gremline encoded, cellular (neutrophils, macrophages, NK cells), Humoral: complement components

Acquired/adaptive: Slow response, able to differentiate between targets, learns and remembers memory, cellular (T and B cells), Humoral: antibodies

22
Q

Autoimmune response

A

Healthy cells are attacked by the immune system, causing harm to functional systems

23
Q

Hypersensitivity response

A

Overactive immune system leading to allergies, asthma, anemia, lupus etc.

24
Q

Immune-compromised meaning

A

Individuals’ immune system are underactive.

Genetic
Drugs/treatment - RT can kill haemopoetic cells. Diabetes can make you immunocompromised
Comorbid conditions

25
Q

What are the general features of chronic inflammation

A

Later onset (days)
Longer duration (weeks- years)
Involves lymphocytes & macrophages
Involves further injury & repeated attempts to repair
Always results in organisation (scarring)

26
Q

Types of microorganisms

A
• Parasites - largest, multiple celled 
• Yeast & fungi 
• Bacteria - intra or extra cellular
• Viruses - intracellular parasites, survive within host unlike other microorganisms 
Prions - smaller than virus
27
Q

What are the two types of defences?

A

Innate and acquired

28
Q

Where in the body is the innate defence more dominant?

A

Epithelium, mucous, cilia on epithelium, hair, keratin, bacteria and the conditions they induce (e.g. the low pH of the female ectocervix), reflex coughing

29
Q

Where is the acquired system more dominant?

A

immune system = lymphocytes

Prolonged “treatment” and “battle” against antigens

30
Q

Microbiology

A

Study of infectious diseases

31
Q

What factors do infections depend on?

A
  1. The host & principally the host response to infection
  2. Site of infection
  3. Characteristics of the organism principally the intrinsic virulence (power to cause disease) of the organism
32
Q

How do microbes cause disease?

A
  • Overcome defenses
  • Damage host cells
  • Alter host cells &/or cytokine production
  • Adhesive/invasive factors, capsules, slime, fimbriae, pili, enzymes
  • Toxins (exotoxins, endotoxins, enterotoxins etc)
  • Cause damage & impair host defense
    Overall, establish infection causing disease
33
Q

Monocyte

A

immature macrophage (phagocyte)

34
Q

Congestion

A

passive build up of blood within vessels

35
Q

Pus

A

like exudate, purulent inflammatory exudate high in neutrophils, cell debris & sometimes pyogenic organisms

36
Q

Inflammation

A

The body’s general response to injury (necrosis) and infection.
Acute inflammation is the start of repair although it can lead to further injury.
Chronic inflammation is not part of repair.

37
Q

5 signs of Acute Inflammation

A

Heat - hyperaemia
Redness - hyperaemia
Swelling (exudate)– oedema due to hyperaemia & increased permeability
Pain – Stretch receptors & chemical mediators
Loss of function – swelling & pain

38
Q

Chemical mediators of inflammation

A

Cause pain and conducts the process
Vast majority of plasma proteins are made in liver (important for inflammatory response)
Some mediators released from cells (special cells)

39
Q

Chemotaxis

A

Locomotion according to a chemical gradient

40
Q

Chemokine

A

Agent that induces chemotaxis (type of cytokine)

41
Q

Cytokine

A

Hormone of the Immune system

42
Q

Process of Extravasation in acute inflammation

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Diapedesis
  5. Migration
43
Q

Process of phagocytosis in acute inflammation

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing and degradation
44
Q

Steps following necrosis and infection

A
  1. Release of chemical mediators creating a vascular and cellular response
  2. Vascular response: hyperaemia (vasodialition and increase in permeability), oedema (exudate)
  3. Leukocyte activation and recruitment leads to attack by neutrophils
45
Q

Fibrinous exudate

A

Increases chance of organisation
Occurs following acute inflammation within linings of the body (meninges, pleural, pericardial and peritoneal)
May be removed by fibrolysis & phagocytosis
Otherwise may lead to the ingrowth of granulation tissue & scarring

46
Q

Role of lymphocytes in the acquired immune system

A

• T cells
• B cells à Plasma cells à Antibodies
• Feature in chronic inflammation where the immune system is causing problems
• Autoimmune disorders
• Hypersensitivity disorders
• Involves lymphocytes macrophages & fibroblasts
• Involves continued injury, inflammation & repeated attempts to repair
Healing inevitably by organization

47
Q

Roles of Immune System

A

Defense against infections
Defense against tumors
Recognition of foreign proteins & tissues
Recognition of other foreign substances (lipids, carbohydrates)

48
Q

4 parts of the immune response

A
  1. Non-specific INNATE
  2. Specific response (slower) ADAPTIVE
  3. Non-specific reinforcement INNATE
  4. Memory ADAPTIVE