Physio VIVA
Stroke risk factors
- Smoking - Drug use - High BP - Cardiac disease - Diabetes mellitis - Abnormal blood lipids - Lack exercise
Prevalence of COPD
1 IN 7 Aussies over 40 Indigenous Australians 2-3 times more likely
RA prevalence
1.9% of Aus populations, 13% of all arthritic conditions, can occur at any age, frequent onset in those aged 35-64, slightly higher prevalence in women, those is low SA areas, indigenous Australians have higher prevalence
OA prevalence
10% of population, incidence rising with ageing population
HF prevalence
4% of the population aged above 45 have HF Aboriginal Australians 2-3 times higher
Osteoporosis definition
A condition where bones becomes fragile, brittle and fracture more easily than normal bones . Even minor incidents can cause bone fracture Characterised by: - low bone mass - Micro-architectural deterioration of bone tissue w resultant increase in fragility and risk of fracture
OA Diagnosis
Able to spot osteophytes, bone remodelling, joint space narrowing, subchondral sclerosis on X-RAYs. Arthroscopy Blood test can rule out RA
Stroke Definition
Acute loss of blood flow to brain due to infarct or hemorrhaging
Stroke management principles
Acute management - Focus on assessment, prevention of complications Rehab - Teaches skills that lost, new skills to compensate for permanent impairment LT management - Consider principles CC management
OA Physio Rx
Address impairments: reduce pain, increase ROM, restore muscle control Role in facilitating self management Unload joints with gait aids, braces, wedges in shoes Electrophysical agents, such as ultrasound Can refer to other specialists Rehab post surgery Prehab pre surgery Initial role in diagnosing OA, then refer
Paget's Demographics
Affects 4% of Australians, >55 years
Physio diabetes management
Assess RF, facilitate behaviour change, be alert for complications, rehab post amputation
RA pathophysiology
Auto immune disease Systemic illness (effects multiple organs in the body) Uncontrolled proliferation of synovial tissue Proliferation of macrophages and fibroblasts Lymphoctyes infiltrate peri vascular regions Proliferation of endothelial cells Blood vessels in area occluse Irregular growth of synovial tissue over time, forming invasive pannus tissue Pannus tissue invades/destroys cartilage and bone RA can involve the -eyes (scleritis) - lungs (can cause difficulty breathing) - heart (pericarditis) (myocarditis) (endocarditis) can cause chest pain and shortness of breath - blood and blood vessels (low levels of white blood cells, RBCs, spleen enlargement, ulcers of skin.
Diabetes Diagnosis
Blood test - Fasting blood plasma glucose test - Glucose tolerance test - Fasting test result, above 7mmol/L, Random test 11.1mmol/L - Haemoglobin at 6.5%+
RA diagnosis
Blood tests: Rheumatoid factor found in 80% of cases Citrulline antibody (anti CCP)- in most pts Antinuclear antibody (ANA) Measuring inflammation Ethrocyte sedimention rate (ESR) C-reactive protein Complete blood count X-RAYS: - early disease (normal or soft tissue swelling only) - Later (bony erosions notable) Joint fluid analysis
Paget's contraindications
Bone fragility represents a precaution for physical activity
OP diagnosis
Bone mass density is a predictor of fracture rate. Also used to monitor fracture rate during treatment. It is assessed via bone densitometry Clinical diagnosis: history of minimal trauma fracture, loss of height in middle aged to elderly, pain. Risk of fracture is assessed by BMD and assessment of risk factors. Established OP can be recognised through X-RAYS
OP pathophysiology
Bone models and remodels throughout life, with increasing age less bone is replaced than that is remodelled. Oestrogen deficiency (w menopause) increases remodelling intensity, which in turn accelerates bone loss. Bone loss is greatest in first 3-6 years post menopause then steadies, then accelerates after 70. Hypogonadism in men can also accelerate bone loss, where there is a gradual decline in testosterone
Paget's Pathophysiology
Bone tissues maintained by cells called osteoblasts and osteoclasts, in PD balance b/w two groups of cells disturbed. Osteoblasts are too much bone tissue produced = enlargement. New bone= weak and unstable
Stroke pathophysiology
Brain cannot get enough blood, brain cells die due to lack of blood and oxygen Ischaemic changes due to loss of blood
OA pathophysiology
Breakdown and eroding of articular cartilage, ligaments, eroding of meniscus, often bony spurs (osteophytes) growing around edge of joint. Bone and synovial involved, joint swelling and inflammatory pain, often bursitis, inflamed tendon junctions.
OA differential diagnosis
Bursitis, tendinothopy, muscle spasm, damages meniscus, a vascular necrosis, pagers disease, stress fractures etc.
AS Diagnosis
CXrays (commonly normal stages) Blood tests: Gene called HLA-B27 associated w AS
Paget's Clinical features
Can be silent sometime only becomes evident when blood test or X-ray. Symptoms: Pain and aching in bones Deformed or misshapen bones Affected bone warmer If skull affected may experience headaches, vertigo or tinnitus
OP Clinical features
Can be silent, no symptoms in early stages but can be flagged by: - back pain, caused by a fractured or collapsed vertebra - loss of height over time (vertebral fractures can be occult and asymptomatic, postural abnormality) - Fractures can cause prolonged handicap, alter QOL and be costly in terms of health expenditure.
CHD physio management
Cardiac rehab including learning more about condition, resuming more about condition, resuming normal activity, change lifestyle to improve health, manage medicine, know warning signs)
OP contraindications/precautions
Care with musculoskeletal techniques, attend to falls risk
RA aetiology
Cause is unknown however there are some common risk factors: - age (35-64) -family history - Environment (toxic chemical or infection in your environment) - gender (more common in women) - obesity -smoking
HF Aetiology
Causes: Heart attack, CHD (progresses to HF) Risk factors: Diabetes, HIV, thyroid condition Old age CHD, HA, damage to heart muscle (cardiomyopathy) - infection, alcohol abuse, meds Faulty heart valves Arrythmia Pregnancy High BP Myocarditis
COPD Pathophysiology
Changes in the large central airways, small peripheral bronchioles and lung parechyma. The normal inflammatory response increases, increases the number of macrophages, leukocytes which release elastases which causes lung destruction
CHD Clinical features
Chest pain tightness burning breathlessness pins and needles pain (chest, jaw, arms, shoulders, abdomen, sternum) Women's symptoms can be different- nausea, shortness of breath, fatigue, similar pain Symptoms are associated with exertion after a meal, however can be unexpected- ie. symptoms at rest, not eased with medication, unstable angina
RA definition
Chronic inflammation of the joints, can affect other organs, can potentially cause joint destruction and functional disability.
CHD diagnosis
Clinical assessment- raise suspicion of angina Further testing needed outside the scope of physio Coronary angiogram- dye in artery, xrayed ECG- echocardiogram, detects and record electrical activity Stress testing- increase heart rate, test heart Chest X-ray- reveal heart failure, if heart changed shape Blood test- assess RF, fats, sugar, proteins in blood, cholesterol
Coronary Heart Disease Definition
Consequence of narrowing coronary arteries, lack blood flow to heart
OP course and prognosis
Consequences of fractures can be ongoing: - mortality within one year for 20% of those with hip fractures - 50% of females don't return to prev. Functional levels - 20% of people require long term care - risk of future fractures rise with each new fracture (cascade effect)
HF Pathophysiology
Contraction/relaxation of heart inadequate Heart is weak, stiff, or both Accumulation of blood in left side makes breathing hard Accumulate in right side, fluid accumulation in legs, liver etc. Usually affects both sides but can be R/L sided
CHD Pathophysiology
Coronary arteries become less patent- due to plaque build up, athesclerosis (build up of fatty deposits of inner wall coronary arteries, clog arteries and reduce blood flow to heart) Unstable plaque (plaque with more fat, and thin cap which can crack-then sealed with a clot, inflamed) Lack of blood flow to heart- angina
Contraindications/Precautions for RA
Damage to lung tissue- limitations w physical exertion Cardiovascular disease- limitations w physical exertion Upper cervical spine instability, assoc. w/ ligament damage Inflammation of blood vessels can lead to nerve, heart, and brain problems Pericarditis and myocarditis can lead to congestive heart failure For the practitioner: take care w exercise prescription avoid high intensity exercise avoid joint mobilisation/manipulation avoid techniques that stress skin and bones
Clinical features of stroke
Depends on location of stroke eg: lesion to broca's speech area can lead to diffculty producing speech
HF Diagnosis
ECG- assess rhythm, duration, underlying conditions Chest X-ray- look at fluid congestion or other causes
Diabetes multi D team
Endocrinologist Podiatrist Dietition Diabetes nurse educator Renal physician Vascular surgeon Ophthalmologist Physio
AS Pathophysiology
Enthesitis: inflammation where soft tissue attaches to bone Common sites: tendo achilles, Costco Chondral joints, plantar fascia
RA physio Rx
Facilitate balance b/w rest and activity During quiet periods- ROM exercises, aquatic therapy, balance etc. Devices to assist ADLs Self management facilitation incl. risk management Referral- medical review, OT, podiatry
Paget's Management principles
Falls prevention, manage impairments Support self management Medication: Biphosphonates- slow progression, control bone building process to normal bone growth Pain killers (analgesics), non steroidal anti inflammatory drugs (NSAIDs) Calcium and Vit D- for bone health Surgery- for complication of Paget's disease
Paget's Disease Physio management
Falls prevention, manage impairments Support self management
Paget's Disease Definition
Focal areas of excessive osteoclasts bone reabsorption accompanied by a secondary increase in osteoblasts bone formation. Can manifest as bone or joint pain
OA participation restrictions
Gardening, playing golf etc.
CHD Differential diagnosis
Heartburn Indigestion Lung issues Symptoms of angina w shoulder, arm (ask about exertion, present at rest, symptoms associated with arm movements, impairments such as loss of ROM, loss muscle tone, strength-indicate muscle tissue)
Diabetes aetiology
Hypoglycemia (too much glucose is blood) can lead to: Nephropathy- decreased effectiveness of kidney, may need dialysis or transplant Retinopathy- disease of eye can lead to vision loss Peripheral vascular disease- affect legs, feet, progessive, result in poor healing, skin lesions, amputation Neuropathy- loss of nerve function, in both diabetes types - can be sensory, autonomic, motor, slow progression, limb threatening
OP management principles
Identify and manage risk of falls through pharmacological interventions, lifestyle modifications). Rehabilitate after fracture Liaison with GP re bone density Exercise- weight bearing, high impact, strength, balance) Medication (biophosphonates, vit d, calcium) stop smoking Reduce alcohol intake Risk factor screening
Stroke aetiology
Infarction: -athesclerosis - thrombi (blood clots that stay there) -emboli (blood clots that move to another location) - small vessel occulation Heamorrage (bleed on brain): - hypertension - anticoagulation therapy -tumour erosing blood vessles - trauma
Ankylosing Spondylitis Definition
Inflammatory arthritis affecting the spine and large joints. Causes stiffness and pain in neck, back and pelvis as well as hips shoulders, eyes , skin, bowel and lungs
Stroke course and prognosis
Is variable can have no change or slow improvement Neuroplasticity and re education needed Most dramatic recovery takes place in initial days following stroke as swelling decreases
Osteoarthritis definition
Joint disease, breakdown of articular cartilage, deterioration of ligaments, often bony spurs grow around edge of joint.
Symptoms of RA
Joint swelling, pain, redness, stiffness (multiple joints often affected symmetrically) Fatigue (anemia due to reduces RBCs) Lack of appetite Low emotional affect Stiffness, prolonged Deformity of joints due to destruction of cartilage Deformity incl. hallucinate vagus, hammer toes, rheumatoid nodule Swelling Dryness of eyes/mouth (inflammation of glands) Chest pain Predisposition to infection (enlarged spleen) Rheumatoid nodules (lumps under skin) Ulcers
OA comorbidities
Lack of sleep, depression, fatigue, negative mindset or emotions, helplessness
CHD Demographics
Leading cause of death in Australia 20 Aus die every day
Diabetes prognosis
Leads to secondary complications including amputation etc.
Stroke physio management
Learn new ways to do activities affected by stroke Aim to stimulate brain to adapt Rehab should be scheduled therapy 2-3 hours a day, 2 hours active task practice ADL Sit-stand etc
CHD management principles
Lifestyle changes (slow down more rest, avoid large meals, avoid stress, smoke free, increase physical activity, healthy weight) Medication as prescribed (nitrates- relax, widens blood vessels allows more blood to heart), cholesterol lowering drugs, anticoagulants (reduce stress on heart)
Stroke prevalence
Major cause of death in Aus Hemorrhaging= 80% of deaths
OA Aetiology
More common in females and older individuals More common in lower SE areas
Anky Spon Prevalence
More common in males Symptoms of AS usually b/w 15-45 years
Osteoporosis demographics/ prevalence
More than 1 million people have OP, more common in females than males, prev. Increases w age Problem worsening w ageing population
RA Rx principles
No cure exists: - reduce joint inflammation - maximise joint destruction - reconstruct joints -rehabilitate Combination of -medication (1st line: aspirin, cortisone reduce pain/inflammation, 2nd line: disease modifying anti-rheumatic drugs, corticosteroids, biological DMARDs) - rest -strengthening exercises - joint protection -self management - surgery to repair or replace joints
OA course and prognosis
No direct cure, degenerative (worsening condition), some treatments can control the consequences
OA Rx Principles
Non pharmacological: Self management, exercise (obesity RF), pacing activity, joint protection, weight reduction, unload joints, laser, transcutaneous nerve stimulation, ultrasound, acupuncture. Pharmacological: Panadeine, stronger alangesia, non steroid anti inflammatory spies, glucosamine/chrondoitin (conflicting evidence), intra articular injection. Surgical: Osteotomy, joint replacement, fusion
RA Course and Prognosis
Often begins slowly - minor joint pain - stiffness -fatigue (chronic) Pts can experience periods w/o symptoms and periods of exacerbation, usual course involves joint destruction and functional disability. No cure
RA differential diagnosis
Often mistaken for other inflammatory conditions eg: - systemic lupus ether arises - ankolysing spondylitis - septic arthritis - tuberculous arthritis etc...
COPD course and prognosis
Often undiagnosed, think just normal part of ageing
COPD definition
Ongoing disorder to do with narrowing of airways, long term lung disease. Covers diseases such as bronchitis, emphysema
AS course and prognosis
Onset early adulthood, progressive (w progressive consequences- such as flexed spinal posture, and complications that occur secondarily eg breathing difficulties).
AS differential diagnosis
Other inflammatory diseases (eg. RA)
AS management principles
Physiotherapy (eg. Aquatic therapy) to keep the spine flexible/improve posture Medication such as analgesics, non-steroidal anti-inflammatory drugs, corticosteroid medicines or injections, disease modifying anti-rheumatic drugs (DMARDs). A rheumatologist can diagnose AS and prescribe treatment (self management)
AS Aetiology
Predisposing factors are mostly unknown, potentially genetic
CHD Aetiology
Predisposing factors: Unhealthy eating Inactivity Overweight High BP, cholesterol Smoker Diabetes Lack of good social support Male Family history Ethnicity
COPD Aetiology
RF: smoking, exposure to irritants in the environment, genetics, parental smoking, asthma
Paget's Aetiology
Reason for accelerated bone growth unknown (potentially could be genetic and environmental factors, such as virus) Risk factors: ethnicity (more common in people from England, Scotland, Central Europe and Greece) Age (increasing age) Genetics (more likely if family history)
Physio COPD management
Respiratory physio: Techniques include airway clearance, breathing techniques, percussion, promote physical activity, prescribe breathing machines
OP Aetiology
Risk factors: - Advanced age - Family history - small or thin build - obesity - low levels of oestrogen - delayed puberty or early menopause - low levels of testosterone - low calcium intake - vit d deficiency - low physical activity levels - smoking - excessive alcohol intake - RA - chronic diseases - Steroid, gonadotropin releasing agonists, anti epileptics, anti depressants - malabsorption - organ and bone marrow transplant - inflammatory bowel disease - type 1 and 2 diabetes
OP Physiotherapy Management
Screening risk factors and manage RF. Referral for screening and management (BMD, pharmacology, vision correction, drug review etc) that is outside scope of physio Falls prevention Provision of gait aids Prescription of hip protectors
OP risk factors
Smoking, alcohol exposure, low BMI, corticosteroid use, fracture, prev. Fragility fracture.
Risk of falls Modifiable Risk Factors
Smoking, eyesight, nutrition, multi medication, tripping hazards)
COPD diagnosis
Spirometry- measures the speed at which lungs can filled and emptied
OA clinical features
Stiffness is joints after sitting down, after sleeping, slow sit to stand, pain in joints. Gait disturbance due to pain, potential limp, may have hair aid, inability to fully extend, difficulty to perform daily tasks. Not uncommon to see swelling and deformity in joint (varus and valgus deformity).
OP differential diagnosis
Symptoms associated with undiagnosed fracture need to be differentiated from other musculoskeletal presentations
Diabetes clinical features
Symptoms: Type 2 can be silent excessive thirst and urine fatigue, hunger, blurred vision, mood swings, sudden weight loss Type 1 has sudden onset and marked symptoms 4 T's- tiredness, toilet, thinner, thirsty
HF clinical features
Symptoms: bloated stomach chest pain coughing hard breathing, shortness of breath dizziness heart pounding, palpation appetite loss, nausea, fatigue, poor sleep, weakness
AS Physiotherapy management
Therapy to keep spine flexible/improve posture Education Exercise Access to support groups
COPD management principles
To optimize function: -stop smoking - pulmonary rehab (inc. physical activity) Medicine: -treat symptoms Pulmonary rehab: - decrease fatigue, hospitalization, dyspnea - Improve QOL, exercise capacity etc. Decrease deterioration: - Flu vaccinations - oxygen therapy
HF management principles
Treat disorder that causes HF Lifestyle changes: Weight, alcohol, smoking, diet, exercise, medication, drugs, surgery
Diabetes management principles
Type 1: - Insulin replacement - injections, pump - Monitoring - Regular activity, eating, weight loss Type 2: - Lifestyle changes - Is progressive - so may need to progess to medication, insulin Prediabetes: - Lifestyle changes: exercise, diet, weight loss - Eating - regular meals, high in fibre, low in fat and sodium - Dietician support - Regular activity
Diabetes prevalence
Type 1: Younger onset Type 2: later onset Males have higher prevalence Indigenous Australians have higher prevalence
HF Course and prognosis
Usually no symptoms to begin, shortness breath, fatigue develops prognosis- only 50% diagnosed will be alive 5 years later
Paget's Course and Prognosis
Usually slow progression Complications: OA in joints near bones affected by Paget's Fractures Hearing loss (pressure on nerves in ear) Paraesthesia: impinged spinal nerves Heart disease: increase no of blood vessels in affected bones, heart has to work harder
AS clinical features
Variable, pain and stiffness in the back, buttocks or neck. Symptoms worst after rest (for eg. Early morning) and relieved w exercise. Pain in tendons and ligaments, commonly anterior chest, heel or under the foot. Approx 5% of LBP is attributed to AS
Heart failure definition
When heart is incapable of accomodating venous return to meet the requirements of the body. Leads to reduced blood flow, congestion of blood in veins
Diabetes definition
Where body is unable to autonomically regulate blood glucose leading to too much glucose in blood Type 1: Body produces inadequate insulin as beta cells have been destroyed (autoimmune) Type 2: Decreases ability to use insulin, still created but not effective (insulin resistant)
COPD clinical features
Worsening dyspnea, progressive exercise intolerance, altered mental status Chronic bronchitis (blue bloater): Productive cough , progresses to intermittent dyspnea Frequent pulmonary infections Cardiac/respiratory failure over time Frequent cough Use accessory muscles for respiration Emphysema (pink puffer) Progressive dyspnea, late non productive cough Eventual loss of muscle bulk, respiratory failure Patients thin, little dry cough Assisted breathing with pursed lips, use of accessory muscles May have wheezing
Paget's Diagnosis
X-rays. Can be confirmed by bone scans or blood test that checks for an enzyme crucial to bone growth called alkaline phosphate
