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Fundamentals Of Science > Pathophysiology of inflammation > Flashcards

Pathophysiology of inflammation Flashcards

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Biology 101 flashcards
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
Q

why is pus green?

A

as neutrophils die, they release myeloperoxidase which gives pus its green colour

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26
Q

harms of inflammatory

A

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

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27
Q

example of antigen presenting cell (APC)

A

dendritic cell : detect pathogens , activate adaptive immunity
macrophages: engulf tissue debris, dead cells, microorganism

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28
Q

difference between macrophage (M1/M2)

A

M1- Pro-inflammatory
M2- tissue repair and healing

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29
Q

APC travel where?

A

in the lymphatic system to the lymphoid tissue, where they present the AT to the cell lymphocytes

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30
Q

what mature in the bone marrow, make antibodies?

A

B cells

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31
Q

what mature in the thymus, cell mediated immunity ?

A

T cells

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32
Q

Cytokine example

A

Interleukins, interferons (INF) , chemokines, colony stimulating factors (CSF)

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33
Q

What happens at vascular response stage(

A

Inflammatory mediators released
Vasodilation= increase blood flow (rubor calor)
Increased vascular leakiness (tumor)

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34
Q

What happens at vascular response stage?

A

Inflammatory mediators released
Vasodilation = increased good flow (rubor, calor)
Increased vascular leakiness (tumor)
- all lead to this and cellular exudate

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35
Q

3 types of examples of granulocytes

A

Basophil, eosinophil, neutrophil

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36
Q

3 types of example phagocytes

A

Neutrophil
Macrophage
Dendritic cell

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37
Q

What happens at cellular exudate?

A

Chemokines attract circulating cells
Adhesion molecules involved : can increase adherence to endothelial cells , allowing migration into tissues
Neutrophils predominate

38
Q

Phagocyte process to APC

A
  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
Q

Benefits of inflammatory response

A

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
Q

Example of pro-inflammatory

A

M1

41
Q

Role of M2.

A

Tissue repair and healing

42
Q

Macrophage role

A

Engulf tissue debris, dead cells, microorganism
Then antigen present

43
Q

Dendritic cell role

A

Detect pathogens
Antigen present-activate adaptive immunity

44
Q

How is an antigen presented?

A

Processed by cell and presented with major histocompatibility complex

Proteins found on surfaces of cell help the immune system recognise foreign substances

45
Q

APC travel where to present the antigen?

A

Travel in the lymphatic system to the lymphoid tissue

46
Q

Difference between B and T cell

A

B cells: mature in the bone marrow, make antibodies
T clue: mature in the thymus, cell mediated immunity

47
Q

Memory antibody

A

IgG

48
Q

Acute antibody

A

IgM

49
Q

Allergic antibody

A

IgE

50
Q

Antibody in body fluids e.g. Saliva, snot

A

IgA

51
Q

Adaptive immunity involves

A

Humoral immunity: B cell make antibodies
Effective in intracellular fluid

Cell mediated immunity: Cytotoxic T cells kill intracellular microorganisms
Activate macrophages

52
Q

Systemic effects of inflammation

A

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
Q

Suppuration

A

Continuos fight between the bacteria and the immune system- abscess or collection of pus

54
Q

Different classes of MHC

A

MHC 1
MHC 2

Trigger different pathways

55
Q

Drugs to treat inflammation

A

Non steroidal anti-inflammatory drugs e.g. Aspirin, ibuprofen
Corticosteroids eg prednisolone

56
Q

Role of NSAIDs

A

Inhibit synthesis of the prostaglandin mediators, therefore prevent activation of the inflammatory pathway

57
Q

What can be used for acute or subacute inflammation?

A

Corticosteroids
But in the long term, have severe side effects which limit their use for chronic inflammation

58
Q

If trigger persists in the inflammation response it can lead to?

A

Chronic inflammation and tissue destruction

59
Q

Autoimmune disease

A

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
Q

Example of autoimmune disease: thyroid

A

Graves’ disease

61
Q

Example of autoimmune disease: bones

A

Rheumatoid arthritis

62
Q

Example of autoimmune disease: muscles.

A

Muscular dystrophy

63
Q

Example of autoimmune disease: skin

A

Eczema
Vitiligo

64
Q

Example of autoimmune disease: lung

A

Fibromyalgia

65
Q

Example of autoimmune disease: nerves

A

Peripheral and diabetic neuropathy

66
Q

Example of autoimmune disease: gi tract

A

Crohn’s disease
Celiacs disease
Diabetes type 1

67
Q

Example of autoimmune disease: blood

A

Leukaemia

68
Q

Example of autoimmune disease: brain

A

Autism
Multiple sclerosis

69
Q

When treating autoimmune disease, the aim of treatment is to?

A

Reduce symptoms- anti-inflammatory drugs
Prevent long term tissue damage- disease modifying drugs
Maintain function: physiotherapy

70
Q

Why is treatment for auto- immune disease targeted at inflammation? And not cause

A

Cause is largely unknown

71
Q

DMARDs

A

Disease modifying anti-rheumatic drugs

72
Q

Biologics

A

Subset of DMARDs
Synthetic antibodies that can be antibodies against a specific protein

73
Q

Hypersensitivity

A

An excessive and potentially harmful immune reaction t0 a foreign substance not otherwise considered to be noxious ( harmful or injurious to health)

74
Q

Role of DMARDs

A

Immunosuppressants that damp down the immune system to stop it from attacking the joints

75
Q

How many types of hypersensitivity are there?

A

4

76
Q

Immediate/anaphylactic hypersensitivity

A

Type 1

77
Q

One key difference between hypersensitivity and acute inflammation is?

A

That mediating cell is called an eosinophil in cellular exudate

Stains red with certain stain under microscope

78
Q

Laryngeal edema LE

A

Vocal cords in the larynx are incredibly swollen

79
Q

Adrenaline is what agonist?

A

Adrenoceptor agonist

80
Q

Effect of adrenaline on alpha and beta receptors

A

Vasoconstriction = alpha receptors
Vasodilation = beta receptors

81
Q

How to treat anaphylaxis

A

Anti-histamine
Corticosteroids
Adrenaline injection -> alpha- constriction b/c of hypertension
B adrenoceptor agonist = vasodilation, increases in bp, reduce swollen airways and breathe

82
Q

How to treat chronic type I hypersensitivity

A

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
Q

Type 2 hypersensitivity is known as

A

Antibody-dependent cytotoxic hypersensitivity

84
Q

What happens in type 2 hypersensitivity

A

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
Q

Type 3 hypersensitivity also known as?

A

Complex-mediated hypersensitivity

86
Q

What happens in type 3 hypersensitivity?

A

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
Q

Type 4 hypersensitivity also known as

A

Cell - mediated or delayed hypersensitivity

88
Q

What happens in type 4 hypersensitivity

A

Pathological reactions to environmental chemicals or persistent microbes (eg tuberculosis)

89
Q

How to treat hypersensitivity?

A

Anti-histamines
Leukofriene receptor antagonists
Monoclonal antibodies
Corticosteroids have multiple actions

90
Q

Benefits of treating hypersensitivity

A

Relieve symptoms of inflammation : pain, swelling
Reduce tissue damage due to chronic inflammation

91
Q

Adverse effects of treating hypersensitivity

A

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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