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MPharm2 SL22105 > Inflammation > Flashcards

Inflammation Flashcards

Acute inflam Adhesion and chemotaxis Manipulation

1
Q

What is inflammation?

A

Normal part of immunity in response to tissue injury
Repair damaged tissue
Self-limiting and beneficial

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2
Q

What are the three stages of inflammation?

A
  • tissue injury (release of histamine)
  • dilation and increased leaking capilliaries
  • phagocytes consume bacteria and debris
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3
Q

Why are infections warm and red?

A

Arteriolar dilatation
Increased blood flow to inflamed tissue

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4
Q

Why do infections swell both acutely and chronically?

A

Leakage of plasma from blood vessels into the tissue
- Plasma extravasation
More chronically
- Cellular accumulation
- Tissue remodelling
- Fibrin deposition

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5
Q

What are the 3 causes of loss of function in long term injuries?

A

Tissue remodelling
Tissue destruction
Fibrin deposition

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6
Q

What are mast cells?

A

Like circulating basophils
Widely distributed throughout connective tissue and mucosal surfaces
- Synthesise and release ‘inflammatory mediators’

Stimuli:
- Mechanical injury to skin
- Type 1 immediate hypersensitivity via IgE (allergy)
- Chemicals: eg. insect bites

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7
Q

What are endothelial cells and their three functions?

A

Blood vessels are lined with endothelial cells
Functions:
- Filteration of fluids
- Blood vessel size regulation (endothelial-derived NO causes arteriolar dilatation)
- hemostasis

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8
Q

What are the 3 points about chemical mediators of inflammation?

A
  • Act on microvasculature and tissues
  • Lowspecificity
  • Synthesised and released from cells and tissues when required
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9
Q

What are the two roles of histamines on blood vessels?

A
  • relaxes arteriolar smooth muscle
  • contraction of venular endothelium = increased permeability
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10
Q

What are the two Eicosanoids and what do they do?

A

Lipid-based signaling molecules that play a role in innate immune response
- Prostaglandins
- Leukotrienes

Prostaglandins involved in vasodilation, pain and fever
Target for commonly used anti-inflammatory medications (eg. aspirin, ibuprofen)

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11
Q

What are Prostaglandins in Fever?

A

Fever results from elevation of the hypothalamic ‘thermostat’

Regulated by production and action of PGE2 in the hypothalamus

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12
Q

What are leukotrienes?

A

Activate the immune system after infection, injury, or contact with allergens
Oedema
- LTC4, LTD4and LTB4 stimulate increased vascular permeability

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13
Q

Why is inflammation beneficial?

A

Increased supply of cells and chemical mediators to site of inflammation and tells body to rest

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14
Q

What is leukocyte migration?

A
  • Leukocytes move from the blood to sites of inflammation and immune activation
  • Directional control is co-ordinated by tissue expression of adhesion molecules
  • On arrival at site they participate in host defence, inflammation and repair
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15
Q

What are the 4 stages of leukocyte diapedesis?

A
  1. circulating
  2. tethering/rolling
  3. firm adhesion
  4. transmigration
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16
Q

What are selectins?

A

Cell adhesion molecules that are glycoproteins

Important in initial ‘tethering’ of leukocytes to vascular cells

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17
Q

What is L-selectin?

A

A key adhesion molecule that regulates both the migration of leukocytes at sites of inflammation and the recirculation of lymphocytes between blood and tissues

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18
Q

What are P-selectins?

A

Key roles in mediating inflammation through promoting adherence of leukocytes to activated platelets and endothelium

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19
Q

What are E-selectins?

A

An adhesion receptor involved in slowing down leukocyte rolling

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20
Q

What are integrins?

A

Integrins are the principal receptors used to bind to the extracellular matrix. They function as transmembrane linkers between the extracellular matrix and the actin cytoskeleton. A cell can regulate the adhesive activity of its integrins from within.

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21
Q

What are integrin ligands?

A

Intercellular adhesion molecule (ICAM) that help the cell to endure pulling forces without being ripped out
- ICAM-2 – basally expressed on endothelium
- ICAM-1 – induced by cytokines IL-1, TNF

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22
Q

What are matrix metalloproteinases?

A

A family of zinc-dependent extracellular matrix (ECM) remodeling endopeptidases that have the capacity to degrade almost every component of the ECM

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23
Q

What are chemotaxins?

A

Stimulate directed leukocyte movement

Source of chemotaxins = site of inflammation

Chemotaxins stimulate increased inflammatory cell migration in the tissues, and these inflammatory cells increase the inflammatory cascade.

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24
Q

What are chemokines?

A

Produced in response to IL-1, TNF, bacteria
A large family of small, secreted proteins that signal through cell surface G protein-coupled heptahelical chemokine receptors

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25
What are H1 receptor antagonists?
Block H1 receptors Anti-histamines Used for allergies, conjunctivitis, reactions to insect bites
26
What is cyclo-oxygenase?
target enzyme of aspirin COX-1 Constitutive “Housekeeping enzyme”  - products important in normal function of stomach, intestine, kidney and platelets - produced at low levels in all tissues COX-2   Induced - inresponse to injury
27
What are the 3 side effects of NSAIDs?
1. Gastric irritation 2. Bleeding 3. Renal toxicity 
28
What are the 2 anti-thrombotic effects of aspirin?
- impair platelet aggregation - decreased thrombus formation by inhibiting COX
29
What are the 3 ways that anti-inflammatory steroids work?
- Suppress T cell activation and cytokine production - Suppress mast cell degranulation - Decrease capillary permeability indirectly by inhibiting mast cells and basophils
30
What is the MoA of steroids?
Glucocorticoids inhibit neutrophil apoptosis and demargination Glucocorticoids bind to glucocorticoid receptors, inhibits histone acetyltransferase and represses inflammatory gene expression, increase expression of anti-inflammatory genes
31
What is the prevalence of RA?
RA is approximately 3 times more prevalent in woman than in men The overall prevalence of RA in the UK is 0.81% 1.16% for women and 0.44% for men
32
What are the 3 predisposing factors associated with RA?
- Genetic factors - Environmental factors - Hormones or hormonal deficiencies
33
What are anti-citrullinated protein antibodies?
- ACPAs are autoantibidies common in RA - They can be found up to 14 years before onset of symptoms - ACPAs can accurately predict the development of RA
34
What are the 5 common symptoms of RA?
- Painful, stiff joints due to inflammatory synovitis - Symmetrical swelling in small joints - Fatigue - Flu-like symptoms - Morning stiffness
35
What are some of the extra-articular manifestations of RA?
Heart and pericardium - pericardial effusion - ischaemic heart disease Blood - anaemia (haemolytic) - neutropenia kidneys - amyloid disease lung and pleura - pleural disease - pulmonary disease
36
What are the 3 assessment tools for RA?
Radiology - sharp score - larsen index Blood tests - CRP - ESR Disease activity - ACR - EULAR response criteria
37
What are 3 radiological signs of early RA?
- Soft tissue swelling - Periarticular osteopenia - Loss of cartilage
38
What are the 2 radiological signs of severe RA?
- Radial deviation of the carpus and ulnar deviation of the digits - Severe erosive damage of MTP Joints of feet
39
What is the outcome of untreated RA?
Severe disability Life expectancy of patients with RA is reduced by an average of 3–18 years
40
What are the poor prognosis markers of RA?
Genetics - The HLA-DRB1 genotype is associated with more severe forms of RA Laboratory - High ESR or CRP level at outset - Positive RF and ACPA Other - Early visible erosions - Adverse socio-economic status - Smoking
41
What are the 5 categories of RA treatment?
- Analgesics - NSAIDS - Glucocorticoids - csDMARDS - bDMARDS
42
What are 3 csDMARDS?
- Methotrexate - Sulfasalazine - Hydroxychloroquine
43
What is methotrexate?
Dose - Dose ranges from 7.5 to 25 mg, once a week Onset of Action - 6-8 weeks Avoid - Pregnancy – Teratogenic - Alcohol - Sulfa Antibiotics (Sulfasalazine is ok) Affects cells that rapidly turn over - Immune cells - Mucosal cells - Hair follicles
44
What are 2 common and 3 rare side effects of methotrexate?
Common - Malaise - Nausea Rare - Fever - cough - SOB
45
What is hydroxychloroquine?
Anti-malarial medication found useful for the treatment of inflammatory arthritis Increases intracellular pH Interferes with cell’s ability to degrade and process proteins Dose & Administration - Dose ranges from 200 – 400 mg per day
46
What are 3 common and 2 rare side effects of hydroxychloroquine?
Common - Rash - nausea - cognitive effects Rare S/E - Ocular - heart
47
What is sulphasalazine?
Anti-inflammatory: Salicylic Acid Antibiotic: Sulfapyridine Takes 6-8 weeks to work
48
What are 4 common and 2 rare side effects of sulphasalazine?
Common S/E: - Nausea, - Abd pain - Rash - Headaches Rare S/E: - Hypersensitivity reaction
49
What is leflunomide?
Newer csDMARD A pro-drug that inhibits the activity of dihydro-orotate dehydrogenase, used for de novo synthesis of pyrimidines. Given daily – ranges from 10-20 mg per day
50
What are 4 common side effects of leflunomide?
Common S/E - GI upset - Hypertension - Alopecia - Rash
51
What are the 6 types of biologics?
- TNF Inhibitors - T-Cell Co-Stimulatory Blockade - IL-6 Inhibition - IL-1 Inhibition - JAK Inhibition - B-Cell Depletion
52
What are the risks of TNFs?
High risk of infections
53
What is rituximab?
B cell depleting monoclonal anti-CD20 antibody - B cell apoptosis
54
What is abatacept?
Binds to the costimulatory molecules on antigen-presenting cells, thereby blocking interaction with T cells
55
What are the 3 types of surgery for RA?
- Synovectomy - Arthroplasty - Spinal stabilisation
56
What is steroidal structure?
Steroids have a basic 4 ring structure (6:6:6:5) with side-chains.
57
What are glucocorticoids?
Cortisol and cortisone are a stress hormones. They promote gluconeogenesis. Prednisolone and methylprednisolone are synthetic derivatives. Excessive used can result in Cushing’s Syndrome, whilst sudden withdraw can result in adrenal insufficiency.
58
What are NSAIDs?
NSAIDs are anti-inflammatory drugs which reduce the production of leukotrienes (lipids used to mediate the inflammatory response) They work by inhibiting COX-1 and -2
59
What is Aspirin?
Aspirin is an irreversible, selective COX-1 inhibitor. Drug disappears from the blood rapidly but extended duration of action. Effect is potentiated by caffeine. Long-term low doses reduces blood clotting Not recommended for use in children due to risk of Reyes’ syndrome
60
What is ibuprofen?
Reversible inhibitor of COX-1 and -2. Analgesic, anti-inflammatory and antipyretic activity is largely due to COX-2 inhibition. Only the S-enantiomer is active (the enantiomer which is shown). Naproxen is manufactured as the S-enantiomer, all others as the racemate. Some risk of ulcers (due to COX-1 inhibition).
61
How is ibuprofen activated?
Ibuprofen is given as a racemic mixture, conversion is specifically R to S. Acyl-CoA esters can acylate other proteins (gives rise to allergic reactions and other toxicities)
62
What is diclofenac?
Diclofenac shows is a stronger inhibitor of COX-2 than COX-1 (~10x) Use increases risk of cardiovascular complications Reduced risk of ulcers (due to lower activity against COX-1) Duration of action is 6-8 hours (despite a short half-life)
63
What are selective COX 2 inhibitors?
Increased risk of cardiovascular complications. Effectiveness for pain-relief is similar to that of Ibuprofen, Naproxen, and Aspirin. Naproxen has a lower cardiovascular risk (and is much cheaper) but less widely used.

MPharm2 SL22105 (8 decks)

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