Conditions Flashcards

(36 cards)

1
Q

Osteoporosis Definition

A

Reduced bone mass per unit volume

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2
Q

Osteoporosis Risk Factors

A

-Smoking
-alcohol
-low calcium diet (esp as a child)
• Lack of weight bearing exercise in childhood and adolescence
• Vitamin D – it increases calcium transport
• Prevent hormone deficieny- breast, prostate, thyroid cancer and HRT
• Eating disorder
• Malabsorption- coeliac

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3
Q

Osteoporisis Pathophysiology

A
  • Peak bone mass around 30 y.o and then gradual decrease
  • Bone stimulated by PTH, Vit D, TH, interleukin 1
  • Bone inhibited by oestrogen, androgens, progesterone, calcitonin
  • 2.5% bone loss per year post menopausal, women lose 30-40% of peak bone mass in lifetime
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4
Q

Osteoporosis Scan Features

A

T score-
above 1 = normal
-1 to -2.5 = osteopenia
less the -2.5= osteoporosis

is severe if there is a fracture

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5
Q

Osteoporosis Medications (3)

A

-Biophosphonates (e.g Fosamax) increase osteoclastic apoptosis and inhibiting bone resorption
oSelective Oestrogen Receptor Modulators (SERMS), acts like oestrogen to slow l=bone loss and reduce # risk
oHRT- normalize oestrogen and slow bone loss

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6
Q

Osteomyelitis Definition

A

Infection of the bone due to progressive inflammatory destruction- Staphlococus aureus

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7
Q

Osteomyelitis Pathological phases (5)

A

o Inflammation- acute- increase of lymphocytes to medullary bone= increase in intraosseous pressure=pain
o Supparation- pus formation 48-72 hrs- pressure increase can burst through the periosteum into the surrounding ST
o Necrosis- amount of pressure impacts the endosteal blood supply= periosteal stripping=sequestration
o Formation of new bone- 10-14 days- perosteum lays down new bone- onvolucrum surrounds the sequestrum
o Resolution- antibiotic therapy and pressure release

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8
Q

Osteomyelitis SSx adults and children

A

In children-
• Often have ssx prior to radiographic evidence
• Malaise, pain, fever
• Often history of trauma
• Pseudoparalysis (late stage when they cant weight bear)

In adults-
•	Immuno-comprised or old
•	Bone tenderness 
•	Limp or decreased function 
•	Mm spasm or other soft tissue involvement (often initial symptom)
•	Pyrexia and malaise if it has spread
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9
Q

Osteoarthritis Definition

A

Inflammatory, progressive cartilage degeneration

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10
Q

Osteoarthritis causes

A
  • Primary/idopathic- no obvious triggering factor (most common)
  • Secondary- trauma, connective tissue disorder
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11
Q

Osteoarthritis pathophys

A
  • Disease of the articular cartilage
  • Articular cartilage contains chondrocytes to decrease friction, reduce tension and resist heavy compression
  • Chrondrocyte damage (genetic/envri- age, stress, surgery, trauma, inflame)→ Proliferation→ secretion of MMP stimulated by inflame interleukin 1. Collagenase and Protease break down type 2 collagen→ Matric remodeling and degradation→ breakdown, cracking and erosion of cartilage
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12
Q

Osteoarthritis SSx and joint affected

A
•	Women >40 y.o 
•	Usually gradual and slow onset 
•	Weight bearing joitns 
•	Pain-
o	Stiffness in the morning that eases 
o	Worst at the end of the day 
o	Relieved by rest 
o	Worse in the cold 
•	Signs-
o	Bony enlargement 
o	Crepitus
o	Restrited movement
o	Tenderness on palpation 
Joints affected-
•	Distal (DIPS more common) (RA PIPS more often) 
•	Proximal interphalangeal joints (PIPS) 
•	1st metacarpal-trapezium joint 
•	1st metatarsal phalangeal joint 
•	Spine
•	Hips
•	Knee
•	AC
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13
Q

Osteoarthritis Radiological Findings

A
  • Loss of joints space
  • Osteophytic growth
  • Subchondral bone cysts
  • Subchondral sclerosis
  • Asymetrical distribution
  • Intra-articular loose bodies
  • Articular deformity
  • Vacuum phenomenon
  • Decrease density
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14
Q

Osteoarthritis Managment

A
•	Education 
•	Slow release paracetamol 
•	Correct risk factors (weight, injury, overuse)
•	Exercise
•	Manual therapy to address biomechanical compensati
-joint replacement
-NSAIS
_immunomodulatory drugs
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15
Q

Ankolosing Spondylitis Definition

A

chronic inflammatory condition- HLA b27 gene

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16
Q

Ankolosing Spondlitis Pathophys

A
  • Pannus layers over articular cartilage and inflammatory cells infiltrate synovium.
  • Fibrous tissue replaces the bone and fibrocartilage to invade the bone
  • Bone erosion repairs to form spurs
17
Q

Ankolosing Spondylitis SSx

A
  • Progressive, worsening LBP
  • Stiff ache sacrum, buttocks, thigh
  • Diminished chest expansion
  • Worse in morning, evening and night
  • Stiffness and rigid
18
Q

Ankolosing Spndylitis Radiology Findings

A
  • Squaring of vertebral bodies
  • Subchondrol sclerosis
  • Ossifications
  • Syndesmophytes where ligaments insert= bony growth
  • Fusion of facets, SIJ, CV joint
  • Bamboo spine
19
Q

Rheumatoid Arthritis Definition

A

Generalised connective tissue disorder

20
Q

Rheumatoid Arthritis Pathophsy

A

Inflammation of synovium (oedema and effusion)
• Formation of pannus at the bare area that spreads over bone and cartilage
• Bone destruction as pannus erodes in bare area and into subchondral bone= subchondral cysts

21
Q

Rheumatoid Arthritis SSx

A
•	Females>males
•	Onset 20-60
•	Periodic episodes
•	Joint pain 
•	Swelling 
•	Stiffness
•	Loss of function 
•	Bilateral joint involment 
•	MCP and PIPS 
Often affect the Cx
22
Q

Systemic Lupus Erythematosus Definition

A

Auto-immune, connective tissue disease→ dysfunctional immune system→ overproduction of autoantibodies

23
Q

SLE risk factors

A
  • Genetic
  • UV overexposure
  • EBV
  • Drug induced
  • High Oestrogen
  • OCP
  • 1st trimester pregnancy
24
Q

SLE pathophys

A

• T cells work with the B cells to make autoantibodies which are deposited into various areas e.g. joints and kidneys, leading to apoctosis (cell death) and that’s when symptoms occur

25
SLE SSx
* Women of childbearing age 15-35 years * Asian and Indigenous populations * Presents with a combination of joint, skin and mucosal symptoms * Cutaneous manifestations (malar/butterfly or discoid rash) * Oral ulcers * Arthritis occurs in 95% of patients * Renal manifestations- Lupus nephritis * Haematlogical- anaemia, thrombocytopenia * Serositis- pericarditis, pleuricy * Fever * Malaise * Headache
26
SLE management
* Blood test for Antinuclear antibodies (ANA), double stranded DNA, ENA antibodies etc * There is a SLE criteria where they must tick off minimum 4 between the clinical and lab criteria * Reduce environmental triggers (UV, HRT) * NSAIDS * Antimalarials * In severe cases, corticosteroids and when they cannot be used due to osteoporosis risk, immunosuppressive drugs
27
Gout definition
Monosodium urate crystal disorder
28
Gout risk factors
* Long term renal disease * Long term medication use of duirectics and salicylates * High purine diets (meat and shellfish) * High alcohol and soft drinkconsumption
29
Gout pathophys
• Abnormality of uric acid metabolism resulting in urate crystal deposition usually in joints, soft tissue (tophi) and urinary tract • Hyperuricemia= saturation in synovial fluid and soft tissue leading to crystal build up - Xanthine oxidase --> uric acid which is usually excreted but when in excess builds crystals
30
Gout stage (4)
• Stage 1- Asymptomatic Hyperuriceaemia- o Elevated serum uric acid o Usually no clinical manifestations and no treatment necessary other than lifestyle modifications • Stage 2- Acute Gouty Arthritis- o Acute attack of sever pain, usually the great toe but can bee knees, other toes etc o Often in early hours of the morning and wakes the patient o Skin over joint is red, shiny, hot, swollen and tender to touch (often the bedsheet is too much) o May be precipitated by alcohol or dietary excess, starvation, surgery o Subsides in 3-10 days • Stage 3- Intercritical Gout- o Time between the attacks o Low to no pain o Low level inflammation causes joint destruction o Time for aggressive management strategies (lifestyle, medications to prevent chronicity) • Stage 4- Chronic Tophacious Gout- o Tophi- monosodium deposits that are usually painless in the soft tissue, synovial tissue or bone (ears, elbows, toes, fingers) o Occurs in the more chronic stages when uric acid levels remain high over a number of years o More frequent and pain painful attacks o Permanent joint destruction
31
Gout Management
* Synovial fluid aspirate to check for uric acid crystals which is the only real diagnostic feature * Elevated serum uric acid * Xray to see punched out joint erosions * Lifestyle changes- decrease co-morbidities of obesity and alcoholism * Education about diet * Increase H20to help with kidney function * Corticosteroids for chronic inflammation * Allopurinol- Xanthine Oxidase inhibitor- it is indicated when there are frequent attacks and in the presence of tophi
32
Calcium Pytophosapahte Deposition Disease Definition
Crystal deposition in the joint and soft tissue which is almost exclusive to articular cartilage = inflammation and tissue damage
33
CPPD risk factors
* Most common in over 65 y.o * OA * Previous joint trauma * Metabolic disease (diabetes) * Family History
34
CPPD pathophys
* Largely unknown | * Main theory is an excess of pyrophosphate production in cartilage
35
CPPD SSx
* Acute attacks minics gout * One or multiple joitns * Pain in the larger joints usually (knee, 2nd and 3rd MCP, wrist and shoulder) * Synovitis with tenderness * Swelling * Systemic features
36
CPPD management
* Can also miic gout, tendonitis of RC or achillies, RA, OA * Synovial fluid analysis (CPPD crystals are rhomboids whereas gout are rod shaped) * Xray for chondrocalcinosis- hyperwhite line along cartilage, joint space narrowing and subchondral new bone * Treat the ssx of the attack * Often once diagnosed cortisone injection into the joint is 1st line to prevent further inflammation and joint destruction * Additionally managed with paracetamol and or corticosteroids depending on the patient