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Fundamentals Of Science > Pathophysiology of inflammation > Flashcards

Pathophysiology of inflammation Flashcards

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1
Q

physiology

A

science of the function of living things

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2
Q

pathophysiology

A

study of the disordered physiological processes that cause, result from, or are otherwise associated with a disease or injury

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3
Q

pathology

A

scientific study of disease itself

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4
Q

disease

A

a condition where the presence of an abnormality is sufficient to cause a loss of normal health

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5
Q

causes of acute inflammation

A

Microbial infection e.g. bacteria, viruses
Allergy e.g. pollen, animals, dust
Physical agents e.g. trauma, ionising radiation, heat, cold
Chemicals e.g. corrosives, acids, alkali, smoke, bacterial toxins
Tissue necrosis e.g. ischaemia (not enough blood getting to tissue) , infarction (no blood getting to tissue)

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6
Q

disease depends on?

A

trigger and location

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7
Q

first 3 steps of inflammation

A

trigger, detection, signalling

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8
Q

inflammatory mediators explain

A

chemical messenger that convey info from one cell to another;operate in the immediate microenvironment (compared with hormones that are released from an endocrine gland & travel to distant targets in the circulation)

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9
Q

inflammatory mediators include:

A

histamines, prostaglandins and leukotrienes
- triggers a cascade that brings in defence forces against trigger, repel it & heal any damage

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10
Q

inflammatory mediators that are eicosanoids

A

prostanoids, leukotrienes, lipoxins, resolvins

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11
Q

inflammatory mediators that are peptides and proteins

A

cytokines, bradykinin

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12
Q

inflammatory mediators that are simple compounds (amines)

A

histamine, serotonin (5HT)

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13
Q

roles of interleukins

A

signal between wbc (and many other functions)
=pro-inflammatory e.g. TNF-a , IL-1
= anti-inflammatory e.g. TGF-beta, IL-4,10,13

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14
Q

Role of interferons (INF)

A

interfere with viral replication
e.g. INF-a, INF-b, INF-y

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15
Q

role of chemokines

A

control the migration of wbc e.g. neutrophils, IL-8, monocytes, eosinophils

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16
Q

role of colony stimulating factors

A

stimulate the formulation of maturing colonies of wbc

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17
Q

cytokines define

A

protein/ polypeptide mediators synthesised & released by cells of the immune system during inflammation; coordinate the inflammatory response

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18
Q

after signalling inflammation pathway leads to—

A

vascular response - and or fluid exudate /cellular exudate

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19
Q

during fluid exudate there are four proteolytic enzyme cascades involved:

A

coagulation cascade
fibrinloytic cascade
kinin cascade
complement cascade

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20
Q

cellular exudate is when?

A

chemokines attract circulating cells
-adhesion molecules (e.g.migration to tissues)
- neutrophils predominate

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21
Q

Drives clotting- stimulates the production of thrombin, which converts fibrinogen to fibrin ?

A

coagulation cascade

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22
Q

Breaks down clots – these systems are balanced

A

fibrinolytic cascade

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23
Q

kinin cascade:

A

maintains & amplifies the process
drives production of bradykinin which is a vasodilator but also mediates pain

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24
Q

complement cascade

A

releases histamines
is chemotactic (attracts cells)
opsonises (tags damages cells & microbes) & lyses bacteria

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25
why is pus green?
as neutrophils die, they release myeloperoxidase which gives pus its green colour
26
harms of inflammatory
Digestion of normal tissues E.g. proteases released from lysis of neutrophils Swelling E.g. of airway, in brain may be harmful Inappropriate inflammatory response where stimulus is 'harmless' Hypersensitivity
27
example of antigen presenting cell (APC)
dendritic cell : detect pathogens , activate adaptive immunity macrophages: engulf tissue debris, dead cells, microorganism
28
difference between macrophage (M1/M2)
M1- Pro-inflammatory M2- tissue repair and healing
29
APC travel where?
in the lymphatic system to the lymphoid tissue, where they present the AT to the cell lymphocytes
30
what mature in the bone marrow, make antibodies?
B cells
31
what mature in the thymus, cell mediated immunity ?
T cells
32
Cytokine example
Interleukins, interferons (INF) , chemokines, colony stimulating factors (CSF)
33
What happens at vascular response stage(
Inflammatory mediators released Vasodilation= increase blood flow (rubor calor) Increased vascular leakiness (tumor)
34
What happens at vascular response stage?
Inflammatory mediators released Vasodilation = increased good flow (rubor, calor) Increased vascular leakiness (tumor) - all lead to this and cellular exudate
35
3 types of examples of granulocytes
Basophil, eosinophil, neutrophil
36
3 types of example phagocytes
Neutrophil Macrophage Dendritic cell
37
What happens at cellular exudate?
Chemokines attract circulating cells Adhesion molecules involved : can increase adherence to endothelial cells , allowing migration into tissues Neutrophils predominate
38
Phagocyte process to APC
1. Interaction between phagocyte and pathogen promoted by opsonisation 2. Pathogen interacts with phagocyte receptors 3. Phagocyte pathogen envelops: lysosomes contain proteolytic enzymes and hydrogen peroxide 4. Pathogen digested 5. Pathogen breaks down into proteins and other molecules 6. Becomes APC
39
Benefits of inflammatory response
Delivery of: antibodies, nutrients and oxygen, drugs e.g. Antibiotics Dilution of toxins Fibrin formation: trapping bacteria, forming matrix of granulation tissue Stimulates adaptive immunity
40
Example of pro-inflammatory
M1
41
Role of M2.
Tissue repair and healing
42
Macrophage role
Engulf tissue debris, dead cells, microorganism Then antigen present
43
Dendritic cell role
Detect pathogens Antigen present-activate adaptive immunity
44
How is an antigen presented?
Processed by cell and presented with major histocompatibility complex Proteins found on surfaces of cell help the immune system recognise foreign substances
45
APC travel where to present the antigen?
Travel in the lymphatic system to the lymphoid tissue
46
Difference between B and T cell
B cells: mature in the bone marrow, make antibodies T clue: mature in the thymus, cell mediated immunity
47
Memory antibody
IgG
48
Acute antibody
IgM
49
Allergic antibody
IgE
50
Antibody in body fluids e.g. Saliva, snot
IgA
51
Adaptive immunity involves
Humoral immunity: B cell make antibodies Effective in intracellular fluid Cell mediated immunity: Cytotoxic T cells kill intracellular microorganisms Activate macrophages
52
Systemic effects of inflammation
Constitutional symptoms e.g. Fatigue Lymph node enlargement Increased circulating WBC Liver-release acute phase response proteins (C-reactive protein) Hypothalamus-pyrogens from leukocytes e.g.IL2 cause fever Inflammation
53
Suppuration
Continuos fight between the bacteria and the immune system- abscess or collection of pus
54
Different classes of MHC
MHC 1 MHC 2 Trigger different pathways
55
Drugs to treat inflammation
Non steroidal anti-inflammatory drugs e.g. Aspirin, ibuprofen Corticosteroids eg prednisolone
56
Role of NSAIDs
Inhibit synthesis of the prostaglandin mediators, therefore prevent activation of the inflammatory pathway
57
What can be used for acute or subacute inflammation?
Corticosteroids But in the long term, have severe side effects which limit their use for chronic inflammation
58
If trigger persists in the inflammation response it can lead to?
Chronic inflammation and tissue destruction
59
Autoimmune disease
A process where we have abnormal detection of self; fail to recognise self, therefore antibodies/ cytotoxic cell against self— can lead to chronic inflammation and tissue destruction
60
Example of autoimmune disease: thyroid
Graves' disease
61
Example of autoimmune disease: bones
Rheumatoid arthritis
62
Example of autoimmune disease: muscles.
Muscular dystrophy
63
Example of autoimmune disease: skin
Eczema Vitiligo
64
Example of autoimmune disease: lung
Fibromyalgia
65
Example of autoimmune disease: nerves
Peripheral and diabetic neuropathy
66
Example of autoimmune disease: gi tract
Crohn's disease Celiacs disease Diabetes type 1
67
Example of autoimmune disease: blood
Leukaemia
68
Example of autoimmune disease: brain
Autism Multiple sclerosis
69
When treating autoimmune disease, the aim of treatment is to?
Reduce symptoms- anti-inflammatory drugs Prevent long term tissue damage- disease modifying drugs Maintain function: physiotherapy
70
Why is treatment for auto- immune disease targeted at inflammation? And not cause
Cause is largely unknown
71
DMARDs
Disease modifying anti-rheumatic drugs
72
Biologics
Subset of DMARDs Synthetic antibodies that can be antibodies against a specific protein
73
Hypersensitivity
An excessive and potentially harmful immune reaction t0 a foreign substance not otherwise considered to be noxious ( harmful or injurious to health)
74
Role of DMARDs
Immunosuppressants that damp down the immune system to stop it from attacking the joints
75
How many types of hypersensitivity are there?
4
76
Immediate/anaphylactic hypersensitivity
Type 1
77
One key difference between hypersensitivity and acute inflammation is?
That mediating cell is called an eosinophil in cellular exudate Stains red with certain stain under microscope
78
Laryngeal edema LE
Vocal cords in the larynx are incredibly swollen
79
Adrenaline is what agonist?
Adrenoceptor agonist
80
Effect of adrenaline on alpha and beta receptors
Vasoconstriction = alpha receptors Vasodilation = beta receptors
81
How to treat anaphylaxis
Anti-histamine Corticosteroids Adrenaline injection -> alpha- constriction b/c of hypertension B adrenoceptor agonist = vasodilation, increases in bp, reduce swollen airways and breathe
82
How to treat chronic type I hypersensitivity
Prevention: Maintain immune suppression so there isn't inflammation via desensitisation / corticosteroids Treatment: control flares/attacks asap with corticosteroids eg eczema topical steroid cream
83
Type 2 hypersensitivity is known as
Antibody-dependent cytotoxic hypersensitivity
84
What happens in type 2 hypersensitivity
Antibody-dependent reaction Antibodies (IgG or IgM) attach to cellular antigen E.g. rbc from transfusion Happen- cell protein combined with drug Opsonise cells, activate complement, own cells are phagocytes
85
Type 3 hypersensitivity also known as?
Complex-mediated hypersensitivity
86
What happens in type 3 hypersensitivity?
IgM or IgG antibodies form complexes with soluble antigen e.g in foreign serum Complexes become deposited in tissues where they activate inflammation, causing tissue damage Eg. Occurs in blood vessels, kidney, joints
87
Type 4 hypersensitivity also known as
Cell - mediated or delayed hypersensitivity
88
What happens in type 4 hypersensitivity
Pathological reactions to environmental chemicals or persistent microbes (eg tuberculosis)
89
How to treat hypersensitivity?
Anti-histamines Leukofriene receptor antagonists Monoclonal antibodies Corticosteroids have multiple actions
90
Benefits of treating hypersensitivity
Relieve symptoms of inflammation : pain, swelling Reduce tissue damage due to chronic inflammation
91
Adverse effects of treating hypersensitivity
Anti-inflammatories may prevent healing by: impairing resolution of inflammation Allowing activity by suppressing pain Immunosuppressants suppress other inflammatory responses e.g. Infection may be more severe

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