Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Principles of Disease > Inflammation > Flashcards

Inflammation Flashcards

(88 cards)

Start Studying
1
Q

What is the main purpose of acute inflammation

A
  • Protect homeostasis

- Response to injury

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

What are the 5 cardinal signs of acute inflammation?

A 
Rubor - redness
Calor - temperature
Tumor - swelling
Dolor - pain
Loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the possible causes of acute inflammation?

A 
Biological (eg microorganisms)
Chemical (acids, alkali, urine, bile)
Physical (extreme cold/heat)
Mechanical (trauma, surgery)
Dead tissue (necrosis irrititates nearby tissue)
Hypersensitivity (reactions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does acute inflammation occur?

A

Localised to affected area, occurs in capillary bed and surrounding ECF

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

What is the pathogenesis of acute inflammation?

A
  1. Increased vessel radius - increased blood flow
  2. Increased vessel permeability - increased exudate (protein leakage)
  3. Neutrophil migration (through vessel and out)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does increased vessel radius cause increased flow in acute inflammation?

A

Increased vessel radius (dilatation, smooth muscle relaxed) –> Pouseuille’s Law: 2x radius increase, x16 increase in flow

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

What type of leaking occurs in acute inflammation?

A

Exudation (high protein content)

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

What is found in the plasma exudate in acute inflammation?

A

Proteins, immunoglobulins (antibodies) and fibrinogen (clotting factor)

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

What happens as a result of increased vessel permeability?

A
  • Exudative process (oedema)

- Increased viscosity and slower flow (stasis)

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

What is the sequence of events in exudate formation?

A

Normally neutrophils are in middle of lumen (surrounded by RBC)
During acute inflammation:
- Margination (neutrophils pushed towards vessel wall
- Pavementation (neutrophils adhere to endothelium)
- Emigration (neutrophils push out through vessel wall)

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

What are the benefits of acute inflammation?

A
  • rapid response to non-specific injury
  • neutrophil action: denature antigens/destroy organisms
  • cardinal signs: short term tissue protection
  • plasma proteins localise inflammation
  • resolution of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the sequence of microvascular changes in acute inflammation?

A
  • Increased radius (increased flow)
  • Increased permeability (exudate)
  • Neutrophil migration out of vessel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of neutrophils in acute inflammation?

A

To phagocytose and destroy foreign organisms

To denature antigens

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

How do neutrophils kill foreign antigens?

A

Phagocytosis - Release of granules (enzymes and oxygen free radicals) - digestion of foreign antigen

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

What is the fate of activated neutrophils?

A

Neutrophils die after having released their granules to digest foreign antigen

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

What is the role of plasma proteins in acute inflammation?

A

Fibrinogen - clotting factor: localises inflammation by walling off the area through production fibrin clots and stopping pus from leaking out of inflamed area
Immunoglobulins - trigger humoral immune response, antigen specific

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

Give examples of some acute inflammation mediators

A

Histamine, serotonin (5HT), prostaglandins and leukotrienes, NO, Platelet-activating factors (PAF), Reactive Oxygen Species (ROS)

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

What is the role of acute inflammation mediators broadly speaking?

A
  • Produced by a number of cells
  • Pro or anti inflammatory properties
  • Vasoconstriction, vasodilatation, vessel permeability
  • Histamine agonists or antagonists
  • Some derived from arachidonic acid (leukotrienes and prostaglandins
  • Some derived from platelets (serotonin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give examples of mediators derived from arachidonic acid

A

Leukotrienes and prostaglandins

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

Where is histamine produced?

A

In mast cells

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

What mediator can stop leukotrienes and prostaglandins from being formed?

A

Omega 3 fatty acids (stop arachidonic acid synthesis)

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

What are some of the immediate and long term systemic effects of acute inflammation?

A

Immediate: pyrexia, malaise/fatigue, neutrophilia

Long term: lymphadenopathy, anorexia, weight loss

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

What is pus?

A

It’s a mixture of neutrophil and organism debris, RBC, exudate, proteins, fibrinogen etc

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

What is an abscess?

A

It’s a collection of pus walled off by a fibrinogen-derived pyogenic membrane (membrane made of fibrin that walls off pus from surrounding area)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is a multiloculated abscess?
An abscess in which pus breaks through the pyogenic membrane and deposits in a new cavity (second abscess) etc
26
What are different conditions related to pus collection in areas of the body?
Abscess - generic term for collection of pus Empyema - pus deposited in body cavity (eg pleura, gall bladder) Pyaemia - pus in the blood
27
What is the term used to describe pus formation?
Suppuration
28
What does the definition granulation mean?
It's the deposition of granulation tissue in reparation of inflamed area
29
What is granulation tissue composed of?
New capillaries (angiogenesis); fibroblasts and collagen; macrophages
30
What is sepsis?
Bacteria growing in the bloodstream causing a systemic acute inflammation response
31
What is bacteraemia?
Bacteria getting into the bloodstream
32
What are the signs of sepsis?
Tachycardia Low blood pressure Pyrexia Haemorragic skin rashes
33
Why does low blood pressure occur in sepsis?
Because a widespread arteriolar vasodilatation (acute inflammatory response) causes the total peripheral resistance to decrease
34
Why does sepsis cause tachycardia?
Because CO is decreased by the fall in TPR, so to maintain it SV or HR have to be increased. SV remains unchanged, so HR compensates instead
35
Why does sepsis lead to death?
Because the body fails to compensate for reduction in CO (caused by reduction in TPR), leading to widespread hypoxia, cell death and multiple organ damage
36
What are the 4 outcomes of acute inflammation?
1. Resolution (healing) 2. Suppuration (pus formation) 3. Organisation (granulation tissue deposition) 4. Dissemination (sepsis)
37
What is disseminated intravascular coagulation (DIC) and why does it happen?
- DIC is the simultaneous haemorraging from vessels due to permeability and clotting action by fibrinogen. - It occurs because fibrinogen is making clots to stop the permeability of vessels, but not fast enough so blood is getting out through the ruptured vessels
38
What processes cause hypoxia in sepsis?
Drop in TPR and reduced CO | Oedema and fluid leakage in ECF creating a barrier for O2 to cross to get to cells and tissues
39
What type of white blood cell is most prevalent in acute inflammation?
Neutrophil
40
What type of white blood cell is most important in chronic inflammation?
Macrophages, B/T lymphocytes, plasma cells, fibroblasts
41
What defines chronic inflammation?
Presence of macrophages, B and T lymphocytes, plasma cells | Presence of necrosis/organ damage and slowly progressive loss of function
42
What are some of the signs of chronic inflammation?
Non-specific malaise, unwell Weight loss Slow/progressive loss of function
43
What are the outcomes of chronic inflammation?
Ongoing tissue damage/necrosis Granulation tissue and angiogenesis Fibrosis and scarring Granuloma formation
44
What are some examples of secondary chronic inflammation?
Acne; peptic ulcers; cholecystitis; osteomyelitis
45
What are some examples of primary chronic inflammation?
``` Autoimmune disorders (connective tissue diseases): SLE, rheumatoid disease, autoimmune thyroiditis Endogenous and exogenous substances (surgical material, digestion-resistant organisms, necrosis) ```
46
What are the most prevalent infective granulomatous diseases globally?
Tuberculosis Leprosy Syphilis
47
What defines a granuloma?
``` Granulomatous inflammation caused by nondigestible pathogen Epithelioid macrophages Giant cells Surround dead tissue Surrounded by lymphocytes ```
48
What are examples of some known types of giant cell found in granulomas?
``` Langhans type (tuberculosis) Warthin-Finkeldy type (measles, rarely) Foreign Body type (pyogenic granulation tissue) Silicone associated (burst implants) ```
49
What are examples of common types of non-infective granulomatous diseases?
Rheumatoid disease Crohn's disease Sarcoidosis
50
What is the sequence of events in wound healing?
Injury Acute inflammation - fibrinogen (clotting) Organisation - granulation tissue Scar formation and healing
51
What promotes wound healing?
``` Good nutrition (vitamin A, C) Clean wound No/minimal bruising Metabolic activity stable and normal Local mediator activity ```
52
What impairs wounds healing?
``` Bad nutrition Dirty gapind wound Lots of hematoma Edges not adjacent Impaired angiogenesis Metabolic imbalance ```
53
What differentiates normal wound healing with fracture healing?
Bone repair as well as tissue repair Granulation tissue contains osteoblasts as well as fibroblasts Macrophages remove dead bone debris
54
What molecule promotes angiogenesis and where is it secreted?
VEGF - vascular endothelial growth factor Promoted by other enzymes secreted by hypoxic cells to promote oxygen supply
55
What happens in callus formation?
Osteoblasts deposit woven bone with cartilage Osteoclasts remove dead bone Bone remodelling: Woven bone and cartilage replaced with lamellar bone
56
Give some examples of when angiogenesis occurs
Thrombosis - bypass occluded vessel Cancer - provide steady oxygen supply to cancer cells Wound healing
57
What is hypersensitivity?
Excessive/inappropriate response to antigens which would not normally cause an inflammatory response
58
What causes the damage in hypersensitivity reactions?
The inflammatory reaction to the antigen by the body, not the antigen itself
59
How many types of hypersensitivity are there?
4
60
What is Type 1 Hypersensitivity?
Allergy: excessive IgE production along with other factors
61
What is atopy?
It's the physiological increase in IgE production without showing the allergy hypersensitivity
62
What are the different ways allergens can come in contact with immune system?
through ingestion, inhalation, injection and physical contact
63
What molecule in the immune system is responsible for allergic reactions and why?
T Helper Cells, because they trigger inappropriate IgE production from B cells
64
Where are histamine and other mediators released from during a Type 1 Hypersensitivity reaction?
Mast cells
65
What are the reasons for the early and late phase of a Type 1 Hypersensitivity reaction?
The release of premade (early phase - histamine, heparin) and newly synthesised (late phase - prostaglandins, leukotrienes) inflammatory mediators
66
What is Type 2 Hypersensitivity?
An activation of IgM/IgG to antigens on cell surfaces or tissues, which may be self or foreign
67
What processes cause damage in Type 2 Hypersensitivity and what is the end result?
Complement pathway activation --> cell lysis Fc receptor binding to IgM/IgG causes phagocytosis Antibody-dependent cellular cytotoxicity Results in damage of cell function (inhibition or stimulation of cell)
68
What is Type 3 Hypersensitivity?
Hypersensitivity reaction to pathological production of antibody/antigen immune complexes
69
What antibodies are normally involved in Type 3 Hypersensitivity reactions?
IgM, IgG or a combination of the two
70
What are the possible presentations of a Type 3 Hypersensitivity reactions?
Serum sickness - systemic deposition of immune complexes causing hypersensitivity reaction Arthus reaction - localised reaction to immune complex deposition
71
What are the possible predisposing factors determining a Type 3 Hypersensitivity Reaction?
Predisposition to antigen, or abnormal immune reaction to antigen
72
What differentiates Hypersensitivity reaction 4 from 1-3?
It is T helper cell mediated rather than antibody mediated
73
What is another name for Type 4 Hypersensitivity?
delayed-type reaction
74
What normally causes Type 4 Hypersensitivity?
- Low molecular weight antigens which on their own cause no reaction, only when attached to a carrier protein - organisms which evade digestion/destruction by immune system
75
What is a low molecular weight antigen called that causes Type 4 Hypersensitivity reactions?
Hapten
76
What is the overlap between type 4 hypersensitivity reactions and chronic inflammation?
- inability to remove an antigen | - the aggregation of giant cells and formation of granulomas
77
What is tolerance in the context of the immune system?
It's the ability of lymphocytes to ignore self/auto antigens
78
How is tolerance ensured in the body?
By killing off lymphocytes which are activated by self antigens, and "training" B cells (in bone marrow) and T cells (in thymus) to ignore self antigens
79
What is autoimmunity?
lymphocytes being activated by self antigens in the body and attacking them
80
What triggers autoimmunity?
A combination of predisposing factors and a breakdown in tolerance
81
What factors can contribute to autoimmunity?
Genetics Environmental Hormonal Immune regulation
82
Broadly speaking, what are the two main categories of autoimmune diseases?
Organ specific (localised) and non-organ specific (widespread)
83
What types of radionuclides are usedin PET scanning, and what are their half lives?
F18 - 110min C11 - 20 min N13 - 10min O15 - 2min
84
What are the ideal properties for a nuclear isotope?
- Half life long enough for length of investigation - Emits gamma rays - Readily available in hospital - Easily bound to pharmaceutical molecules for tracking
85
What are the main types of nuclear imaging?
PET and SPECT
86
What are the properties of nuclear imaging?
- Pick up gamma rays emitted by radioisotopes in body | - Show functional/biological activity
87
What is 99m Technetium used for?
Bound to pharmaceutical molecules for bone, brain, lung, kidney and heart scans
88
What is an important consideration to make in nuclear imaging?
Exposure to ionising radiation

Principles of Disease (3 decks)

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