WEEK 2 - AGEING VS PATHOLOGY Flashcards

1
Q

Necrosis

A

Process of cellular death, occurring when cells are exposed to extreme conditions. This leads to damage to the internal cellular environment, leading to cell death.

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2
Q

Apoptosis

A

Pre-planned cell death where the cell actively takes part in its own death. Apoptosis is required for regular smooth functioning of the body.

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3
Q

Senescence

A

The permanent arrest of the cell cycle to avoid uncontrolled (cancerous) cell proliferation.

Senescent cells are still metabolically active. They produce molecules known as senescence-associated secretory phenotypes (SASP). These phenotypes mediate inflammation and work towards cell repair.

Too many senescent cells can cause too much inflammation around the body, worsening conditions such as Alzheimers, heart disease and liver fibrosis.

Causes:

  • Damage to DNA
  • Shortening of telomeres
  • Mitochondrial damage
  • Epigenetic factors
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4
Q

Osteoarthritis

A

Description

  • Clinically, symptomatic OA is defined as pain occurring on most days during the past month in addition to radiographic changes (i.e., osteophytes, subchondral sclerosis, and joint space narrowing).
  • Degenerative - caused by a degenerative breakdown of the articular cartilage in a joint
  • Most common
  • causes localised inflammation
  • commonly effects knee, hip, hands and spine (in that order)

Causes/risk factors

  • Factors that can influence OA
    • 50+ years old
    • female gender
    • obesity
    • family history
    • physically demanding lifestyle (job, sport)
  • higher incidence of OA secondary to an aging population and a worldwide obesity epidemic.

Symptoms

  • joint grinding in movement
  • inflammation of joint
  • joint locking or giving way
  • osteophytes, subchondral cysts and minimised joint space
  • articular cartilage erosion
  • pain when used
  • lack of ROM around effected joint

Treatment

  • healthy lifestyle
    • quit smoking
    • correct diet
    • keeping active
    • weight loss
  • medication to manage pain
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5
Q

Rheumatoid Arthritis

A

DESCRIPTION

  • Auto-immune
  • causes inflammation of the synovial space (synovitis)
  • synovium thickens, pushing into joint space and damaging cartilage + bone in joint.

CAUSES/RISK FACTORS

  • causes systemic inflammation
  • Caused by
    • genetic predisposition
    • smoking

SYMPTOMS

Patients may report a ‘flare’

  • Seen as a period of time where their symptoms are heightened.
  • Pain may be increased, fatigue increased, along with other symptoms
  • Can be triggered by change/misuse of medication, or increased stress levels, and sometimes occur at of nowhere.
  • Patients are prompted to rest during their flares.

TREATMENT/MANAGEMENT

  • medicine to subdue pain and inflammation
  • moderate activity to maintian joint mobility and muscle strength (roughly 30 min a day)
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6
Q

Ankylosing spondylitis

A

DESCRIPTION
AUTOIMMUNE
- Inflammation at Enthesis attachment points – ligaments, tendons, capsule
- SIJ & Spine
- mainly localised to spine
- SIJ affected first leading to LBP
- Inflammatory cells (mainly macrophages & lymphocytes) accumulate in joint capsule, fibrocartilage,
periosteum and entheses.
- macrophages & lymphocytes erode bone – increases & activates osteoblasts – lay down new matrix
- New matrix becomes callus and becomes osseous.

CAUSES/RISK FACTORS

  • High Assoc. HLA-B27 – 90-95% (a protein on surface of WBC’s)
  • Strong genetic predisposition
  • Greater in White Male – 90%. Mainly Nth European –
  • 15-20’s peak – 40yrs (Late adolescent – early adulthood)
  • Less rapid progression in females

SYMPTOMS

  • LBP (low back pain) & stiffness
  • LBP & stiffness is Progressive

Early

  • Early 20’s – peak incidence
  • LBP & stiffness decreases with activity – EMS
  • Decreased forward & lateral flexion, rotation before X-ray
    changes seen

Later

  • Lx curvature flattens
  • Thx curvature – increased Kyphotic
  • Hips & shoulders flexed
  • Costosternal, Costovertebral, Costotransverse joints =
    decreases chest mvt t/f chest infections

TREATMENT

Physiotherapy

  • Early diagnosis better – early medical & physical treatment improves functional outcomes
  • Education
  • Continuous Physiotherapy - maintain RoM - spine & peripheral joints
  • Clinical visits & home programs - Monitor patient compliance

Pharmacological

  • NSAIDS: pain relief not prevention
  • Biological response modifying agents – decrease amount of inflammatory cyto/chemokines

Surgical

  • To prevent major deformity
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7
Q

What causes increased SASP presentation

A
  • Mechanical - sedentary behaviour, repeat injury
  • Metabolic - poor diet, (excess sugar/fat) - places mechanical stress on body
  • Chemical (eg, tobacco) - smoking, drugs
  • Radiation - sun
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