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54 Finals > IC10 Physio (Inflammation) > Flashcards

IC10 Physio (Inflammation) Flashcards

1
Q

3 functions of skeleton

A
  1. Main storage for Ca and phosphorous (regulate mineral balance btw bloodstream and bone)
  2. Form, support, stability, movement
  3. Parts of skeletal system: bone, ligament, muscle, tendon, cartilage, other connective tissue
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2
Q

function of bone marrow

A
  1. Red — hematopoeisis
  2. Yellow — fatty connective tissue (source of fat, used in times of starvation)
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3
Q

3 functions of muscles

A
  1. Keep bones in place, role in movement
  2. Skeletal muscles are attached to bones and arranged in opposing groups around joints
  3. Muscles are innervated — nerves conduct electrical currents from the CNS that cause muscles to contract
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4
Q

Tendons vs joints vs ligaments

A
  • Tendon: tough flexible band of fibrous connective tissue, connect muscle to bone
  • Ligament: connect ends of bones together to form a joint, limit joint dislocation and restrict improper hyperextension and hyperflexion
  • Bursae: provide cushions between bones and tendons and/or muscles around a joint
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5
Q

How does immune system respond to non-pathogenic insults

A
  1. During tissue injury/ cell death, DAMPS are released
  2. DAMPS are recognised by PRR on APC -> trigger immune system -> inflammation
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6
Q

what DAMP activates neutrophils to release more DAMPS/ cytokines

A

CXCL8

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7
Q

what DAMP activate monocyte to inflammatory monocyte

A

CCL2

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8
Q

what cytokine stimulate inflammatory monocyte to inflammatory macrophage

A

INF-y, TNF-a, IL-1

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9
Q

what cytokine stimulate stimulate inflammatory macrophages to become tissue repair macrophages

A

IL-4, IL-10, IL-13

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10
Q

Tissue repair macrophages produce (blank) for repair process

A

growth factors PDGF, VEGF, IGF-1

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11
Q

repair processess include…

A
  • Cell mobilisation
  • Proliferation
  • Differentiation
  • Tissue stem cell activation
  • Angiogenesis
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12
Q

(impaired healing, scarring, fibrosis) inflammatory macrophages are stimulated by what cytokine?

A

inflammatory macrophages when stimulated by IL-4 becomes pro-fibrotic macrophage

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13
Q

what does pro-fibrotic macrophage release?

A
  1. MMPs (matrix metalloproteinases) to increase ECM deposition
  2. (growth factors) TGF-ß and PDGF to activate scar forming myofibroblast — important for forming scar in muscles
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13
Q

(regeneration) inflammatory macrophages are stimulated by what cytokine?

A

inflammatory macrophages when stimulated by IL-10 becomes anti-inflammatory anti-fibrotic macrophage → inhibit scarring

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14
Q

Regulatory T cells when stimulated by which cytokine also becomes anti-inflammatory anti-fibrotic macrophage?

A

IL-10

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15
Q

Function of pericyte

A

important for angiogenesis; activate stem/progenitor cell that is important for the renewal of cells during regeneration

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16
Q

IGF-1 (insulin GF-1) function

A

stimulate stem/progenitor cell that is important for the renewal of cells during regeneration

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17
Q

Tx of soft tissue injury

A
  • Tx: anti-inflammatory drugs
    1. NSAID — inhibit COX
    2. Glucocorticoids — inhibit inflammatory response
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18
Q

Causes of OA

A

wear and tear, degeneration, injuries, repeated overuse

19
Q

RF of OA

A

age, physical or sports injuries, obesity

20
Q

Early OA phenotype

A

initial meniscal and hyaline articular cartilage damage

21
Q

Egs of DAMPS and how they are produced in OA

A

DAMPS: alarmins, free FA, dead cells
- initial meniscal and hyaline articular cartilage damage → produce DAMPS

22
Q

How is the complement system activated in OA?

A

PRRs found on macrophages and APC recognise DAMPs and activate the complement system.

23
Q

Activation of macrophages produce what cytokines?

A

IL-1ß, IL-8. TNF, chemokine

24
Q

Progression of OA phenotype

A
  • Synovitis (inflammation of the joints)
  • Chondrocyte (cartilage cells) activation -> Inflammation signal transduction, MMPs, oxidative stress, viability loss (cell death), cartilage erosion
25
Q

Non-pharm for OA

A
  • physical therapy
  • occupational therapy
  • transcutaneous electric nerve stimulation (TENS)
  • synovectomy (surgical removal of synovial membrane)
  • tendon repair
  • realigning bones
  • joint fusion
  • total joint replacement
26
Q

Causes of RA

A

autoimmune disorder (recognition of self antigen in the joints causes immune-mediated damage to synovial joints)

27
Q

RF of RA

A

obesity, PMH/FH of autoimmune diseases

28
Q

Dx of RA

A
  • high CRP — inflammation more than OA
  • rheumatoid factor and anti-CCP antibodies positive — autoimmune disorder
29
Q

Cytokines involved in RA

A
  • TNF (most important) -> produced from macrophages from myocytes
  • IL-1 -> produce MMP
  • IL-6 -> cause bone destruction
30
Q

tx of RA

A
  • Anti-inflammatory — NSIADs, glucocorticoids
  • DMARDS
  • Biologics (EAT)
31
Q

eg of bDMARDs

A
  • TNF inhibitor — etanercept
  • IL-1R antagonist — anakinra
  • anti-IL-6R antibody — tocilizumab
32
Q

Causes of gouty arthritis

A

high uric acid

33
Q

most important cytokine causing gout

A

IL-1

34
Q

IL-1 production by MSU crystals (activation of innate immune cells)

A
  1. MSU crystals bind to TLR (toll-like receptors) → production of inflammasome components
  2. MSU crystals activate inflammasome. Efflux of K+ out of cell occurs. Mitochondria produce ROS.
  3. Inflammasome activates caspase-1 enzyme.
35
Q

function of caspase-1 enzyme

A
  1. catalyse pro-IL-1ß to IL-1ß
  2. cleavage of gasdermin D to N-terminal cleavage product → cause pyroptosis (formation of pyroptotic pore) → allows IL-1ß to leak out & other substances to leak in → cell death
36
Q

Effect of IL-1ß

A
  1. IL-1ß bind to IL-1ß receptors in endothelial cells and synoviocytes and activate the cells via phosphorylation
  2. Activation of NF-kB (nuclear factor Kappa B eg p65, p50) → transcription of cytokines and chemokines → increase inflammatory cascade and neutrophil influx
37
Q

Tx of gout arthritis

A
  • Allopurinol, febuxostat
  • Colchicine or MCC950 — inhibit inflammasome
  • SC anakinra — IL-1R inhibitor
  • SC canakinumab — IL1ß inhibitor
  • ß-hydroxybutyrate — block K+ efflux
  • Epigallocatechin gallate — inhibit ROS
  • IL-1ß processing inhibitors — VX-765, AAT-Fc
38
Q

Cause of osteoporosis

A

bone loss is faster than bone generation

39
Q

Sx of osteoporosis

A

weak and brittle bones (easy to break), stooped posture, back pain

40
Q

RF of osteoporosis

A

age, menopause (decr Ca in bones), steroid use, long term PPI use

41
Q

Definition of Osteoblasts, Osteocytes, Osteoclasts

A
  • Osteoblasts: derived from mesenchymal stem cells, for bone matrix synthesis and mineralisation
  • Osteocytes: are osteoblasts that become incorporated within the newly formed osteoid, involved in formation and resorption processes
  • Osteoclasts: large multinucleated cells like macrophages, for resorption of mineralised tissue, found attached to the bone surface at sites of active bone resorption
42
Q

Bone remodelling and renewal process (4 phases)

A
  1. Activation and resorption: pro-osteoclast are stimulated and differentiated by cytokines and growth factors into mature active osteoclasts → digest mineral matrix of old bones
  2. Reversal: end of resorption
  3. Formation: osteoblasts synthesise new bone matrix
  4. Quiescence: osteoblasts become resting bone lining cells on the newly formed bone surface
43
Q

Why do old age cause osteoporosis?

A

During old age: less osteoblast, more osteoclast → decrease renewal of bones

44
Q

Drug that cause causing secondary osteoporosis and how it occur

A

Glucocorticoids
- GC affects function and numbers of osteoclasts, osteoblasts, and osteocytes
- Induces the decrease in osteoblast differentiation (less synthesis) and increase death of both osteoblasts and osteocytes
- Effect: less synthesis of new bones

45
Q

Prevention of osteoporosis

A
  • nutrition: calcium and vit D
  • Low impact exercises

54 Finals (7 decks)

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