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Personal ESA2 MSK > Session 11 > Flashcards

Session 11 Flashcards

1
Q

What is “Old Age”?

A
  • No consistent definition - issue between chronicity and physiology
  • WHO Criteria
  • Age > 65 years (developed countries)

Biological

Demographic

Sociological

In a less developed country with a lower age expectancy, old age may be younger than 65 years.

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2
Q

What is the function of MSK?

A
  • Locomotion: enable efficient movement
  • Endoskeleton: protects and supports soft tissues
  • Homeostasis: Ca2+ regulation, temperature regulation, energy storage
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3
Q

Discuss Ageing and the Musculoskeletal System

A
  • Ageing begins when adulthood reached - bone mineral declines steadily after the age of 30 years
  • Rate of loss is ~0.5-1% per year
  • Peak bone density depends on exercise and diet etc. The higher the peak bone density, the better protected you are in old age.
  • Involves a loss of cells, reduction in cells ability to repair, increased genetic mutations (hence why cancer risk increases as you ger older)
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4
Q

What are the physical changes and their consequences of ageing?

A
  • Physical Changes; sarcpopenia, decreased bone mineral density
  • Consequences:

-Loss of muscle strength and endurance

Loss of bone strength

Increased fall risk

Increased fracture risk

Reduction in ability to perform ADL’s (activities of daily living e.g. bathing, eating, walking, dressing etc_

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5
Q

How is bone mineral density loss accelerated?

A

Loss accelerated with low reproductive hormone levels, poor calcium and/or vitamin D status, inactivity, endocrine or gastrointestinal pathologies.

Loss of bone mineral is often accompanired by changes in trabecular architecture making the bone less strong both as a material and as a structure. Trabecular patterns become more wispy, haphazard, less structured

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6
Q

What is Sarcopenia?

A

Loss of muscle mass due to loss of muscle fibers and reduced muscle cross-sectional area

Loss of muscle contractility

Loss of neuronal innervation (possibly higher in Type II fibres innervated by large alpha motor neurons)

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7
Q

Why do Falls occur?

A
  • Decreased mobility
  • MSK-related posture and gait changes e.g. due to hip replacement
  • Neuro-related gait and proprioception changes
  • Environmental hazards

These all increase fall risk which along with increased bone weakness –> fractures

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8
Q

What is Osteoporosis?

A
  • Women lose bone mass faster after menopause but it happens to men too.
  • A skeletal disease characterised by:

Low bone mass per unit volume

Deterioration of micro-architecture

Increased bone fragility

Increased suceptibility to low trauma fractures

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9
Q

Describe how bone mineral density is measured

A

Measured against population mean in young adults

  • Normal: within 1 Standard Deviation of mean
  • Osteopenia (low bone mass): 1-2.5 Standard Deviation below mean
  • Osteoporosis: >2.5 Standard Deviation below mean
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10
Q

What is a DEXA scan?

A
  • Dual Energy Xray Absorptiometry
  • Assess bone mineral density
  • Xrays of 2 different energies
  • Aimed at femur and L-spine (L3)
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11
Q

What are T and Z scores?

A

T score: number of SD below mean for SEX and RACE matched healthy young adult population (25-35y age)

Z Score: number of SD below mean for an AGE, SEX, and RACE matched young adult population

  • The difference between your measurement and that of a young healthy adult is known as a T score.*
  • The difference between your measurement and that of someone of the same age is known as a Z score.*
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12
Q

Risk Factors for Osteoporosis

A
  • Age
  • Low Bone Mass
  • Caucasian/Asian
  • Previous Fragility Fracture
  • Positive Family History
  • Low BMI (<19 kg/m2) e.g. due to anorexia
  • Lifestyle (smoking, alcohol, diet
  • Early menopause
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13
Q

What are Bisphosphonates?

A

Anti-resorptive agents

Effect osteoclasts (bone resorption)

Effect on bone:

  • decrease bone turnover
  • increase bone mineralisation
  • minimal effect on bone volume
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14
Q

How do Bisphosphonates work?

A

Taken up by osteoclasts

Inhibits mevalonate pathway

Osteoclasts lose ruffled border

Osteoclasts become inactivated (apoptosis) - stop working

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15
Q

Describe normal bone physiology

A

Normal Bone Physiology

  • Resorption: osteoclasts break down bone mineral and matrix creating an erosion
  • Reversal: mononuclear cells prepare bone surface for new osteoblasts to begin building bone
  • Formation: osteoblasts form a matrix to replace resorbed bone with new bone
  • Resting: a prolonged resting phase until a new remodelling cycle begins.
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16
Q

What is the pathophysiology of osteoporosis?

A

Bone resorption > bone formation

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17
Q

What is Type 1 and Type 2 Osteoporosis?

A

Type 1

  • Post-menopausal
  • Loss of Oestrogen - accelerated loss (2-3%) over next 6-10 years

Type 2

  • Senile
  • Age related, hyperparathyroidism, Ca2+ deficiency
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18
Q

What are the Consequences of Hip Fractures?

A
  • High mortality rate (up to 30% at 1 year)
  • High morbidity rate
  • PE/DVT/CVA (stroke)/MI
  • Pressure sores
  • Chest infections / UTIs
  • Reduced mobility (only 50-60% regain their pre-injury ambulatory status) - 20% never walk again
  • Confusion
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19
Q

What is OA?

A

Disorder of synovial joints that is characterized by

  • Focal areas of damage to the articular cartilage
  • Remodelling of underlying bone and the formation of osteophytes - new bone at joint margins (bone’s unsuccessful attempt to heal itself)
  • Mild synovitis (synovium becomes inflamed)
  • Eventually everybody will get OA! (80% of >80 year olds)
20
Q

What are the clinical feautres of OA?

A
  • Pain
  • Stiffness
  • Deformity
  • Join swelling
21
Q

What are the Radiological features of OA?

A
  • Decreased joint space
  • Sclerosis
  • Osteophytes
  • Bone cysts
22
Q

What is the Non-operative treatment for OA?

A
  • Weight loss
  • Exercise / Physiotherapy (increase muscle mass, increase proprioceptors)
  • Analgesia / NSAIDs
  • Joitn injection
23
Q

What is the Operative treatment of OAs?

A

Arthroscopy (joint keyhole surgery)

Osteotomies (a formal cut in bone –. helps offload pressure in the medial compartment of the leg)

Arthrodesis (bones are fused together - good for pain relief, bad for function)

24
Q

Why perform a hip replacement?

A
  • Relief of Pain
  • Get back to work
  • Improve function
  • Return to leisure activities
  • Better range of motion
25
Q

What are local complications of a knee replacement?

A
  • Leg length inequality (slight difference)
  • Dislocation (3%)
  • Infection (2-3%)
  • Loosening (usually after 10-15 years(
  • Neurovascular damage
  • Sciatic/femoral nerve, common peroneal nerve
26
Q

Describe the femoral artery

A

The femoral artery is a continuation of external iliac artery (when the external iliac artery crosses under the inguinal ligament, it becomes the femoral artery)

The femoral artery continues down the anterior surface of the thigh, via the adductor canal. During its descent the artery supplies the anterior thigh muscles. The adductor canal ends at an opening in the adductor magnus, called the adductor hiatus. The femoral artery moves through this opening and becomes the popliteal artery after entering popliteal fossa.

27
Q

Describe the deep artery of the thigh

A

Femoral artery gives off a branch called the deep artery of the thigh which in turn gives off three main branches: perforating branches (3 or 4 arteries that perforate the adductor magnus, contributing to the supply of the muscles in the medial and posterior thigh), lateral femoral circumflex arteryand medial femoral circumflex artery.

28
Q

What does the popliteal artery birfucate into?

A

Anterior and Posterior Tibial arteries

29
Q

Describe the Obturator Artery

A

The obturator artery, branch of internal iliac artery and enters thigh through obturator foramen and descends via the obturator canal to enter the medial thigh, bifurcating into two branches:

~Anterior branch supplies the pectineus, obturator externus, adductor muscles and gracilis.

~Posterior branch supplies some of the deep gluteal muscles.

The gluteal region is largely supplied by the superior and inferior gluteal arteries.

These arteries also arise from the internal iliac artery, entering the gluteal region via the greater sciatic foramen. In addition to the gluteal muscles, the inferior gluteal artery also contributes towards the vasculature of the posterior thigh.

30
Q

Why is there a risk of intracapsular fracture of neck of femur?

A

Due to rupture of retinacular arteries (mostly from medial circumflex femoral artery)

The artery to the head of femur (branch of obturator artery) is more important in children à less important blood supply in adults

To find the femoral pulse, place little finger on ASIS and thumb on Pubic Tubercle. The femoral pulse should be palpated 2 or 3 fingers just below inguinal ligament. The femoral artery is a common site for insertion of catheter to gain access to left side of the heart – for a coronary artery.

NOTE: brachial or radial arteries could also be used.

Use the femoral vein to access the right side of heart.

31
Q

What could acute ischaemia be due to?

A

Thrombus

Embolism

Haemorrhage and Compartment Syndrome

32
Q

What are the common sites of atherosclerosis formation?

A

Abdominal aorta and iliac arteries

Proximal coronary arteries

Thoracic aorta, femoral and popliteal arteries

Internal carotid arteries

Internal carotid arteries

Vertebral, basilar and middle cerebral arteries

33
Q

How would you assess arterial occlusion in the lower limb?

A

Comparison of lower limb pulses (femoral, popliteal, posterior tibial, dorsalis pedis) – compare pulses.

Doppler ultrasound

Arteriogram – X-ray following injection of radio-opaque contrast dye

34
Q

How does Occlusion limit blood flow?

A

When pressure is constant: flow is proportional to radius4

If you reduce the radius of the vessel by one half, flow will be reduced to 1/16th

Partial occlusion = stenosis

35
Q

What are the Consequences of Peripheral Artery Disease (Signs of poor perfusion)?

A

Skin problems

Lack of hair

Ulcers

Infection

Skin necrosis

Loss of pulses

Cold to touch

36
Q

Describe Treatment for Peripheral Artery Disease

A

Antiplatelet therapy: aspirin

Risk factor modification: lipid lowering therapy, smoking cessation, BP control, diabetes control, increased exercise levels

37
Q

How can acute ischaemia be due to compartment syndrome?

A

Muscles and neurovascular structures in the leg are in compartments bound by strong fascia (quite inextensible)

Arterial bleed increases pressure

Comrpession of arteries – ischaemia

May also be caused by infection or trauma which causes swelling.

May have to surgically cut fascia to relieve pressure.

38
Q

Explain about a Popliteal Aneurysm or Haemorrhage

A

(Abnormal dilation of popliteal artery)

Oedema and pain in popliteal fossa

Mass with pulpable sensation – may also hear a bruit on auscultation

Popliteal artery can be at risk of rupture with fracture of distal femur or dislocation of the knee

39
Q

What is the course of the Great Saphenous Vein?

A

Arises from dorsal venous arch of foot

Courses anterior to the medial malleolus

Passes the media aspect of the knee – hand’s breath from patella

Passes through the fascia lata at the saphenous opening to drain into the femoral vein in the femoral triangle

40
Q

What is the course of the Small Saphenous Vein?

A

Arises from the lateral marginal vein of foot

Passes posterior to the lateral malleolus

Course up the posterior aspect of the calf

Drains into the popliteal vein at the popliteal fossa

41
Q

What is meant by Saphenous Cutdown?

A

Emergency situation when it is difficult to find a vein for venepuncture or cannula insertion

Great saphenous vein can be located anterior to the medial malleolus by making a skin incision at this location: risk of saphenous nerve injury which travels great saphenous vein and pain along medial border of foot.

Sural nerve normally travels with short saphenous vein

42
Q

Describe the deep veins of the lower limb

A

Deep veins accompany all major arteries often as paired venae comitantes

43
Q

Explain about Venous Drainage and Muscle Pumping

A

Blood drains from superficial to deep via perforating veins

The superficial, deep and perforating veins of the limbs all have valves which prevent backflow.

Venous return is assisted by contraction of the calf muscles: contracted muscles compress the deep veins and propel blood to the heart. The blood pushed downwards will cause the lower valve to close, preventing blood flow away from the heart.

44
Q

Explain about Varicose Veins

A

Dilated tortuous superficial veins

Valve flaps fail to meet or become damaged and incompetent – fail to prevent backflow

If there is incompetency in perforated veins, blood can flow backwards

Venous insufficiency (walls are weakened, damaged valves, veins stay filled with blood especially when standing) –. Venous insufficiency ulcers typically around medial malleolus occur.

45
Q

Explain about Deep Vein Thrombosis

A

Risk factors: Virchow’s triad (stasis, hypercoaguability, vascular damage)

Sites: (most common initial site, but can propagate), also – popliteal, femoral iliac

Signs: tender swollen calf, warmth and erythema (red) of affected limb

Consequences: risk of pulmonary embolism, postphlebitic syndrome

46
Q

What is Post-Phlebitic Syndrome?

A

Chronic deep venous insufficiency –> increased venous pressure in distal part of limb –> increased capillary hydrostatic pressure –> lymphoedma

Damage to venous valves

Lymphoedema

47
Q

What are the structures lying posterior to medial malleolus?

A

Posterior ankle tendons (mnemonic): posterior to medial malleolus, Anterior to Posterior; Tom, Dick and Very Nervous Harry

tendon of Tibialis posterior

tendon of flexor Digitorum longus

tibial Artery

< >

tibial Nerve

flexor Hallucis Longus

Personal ESA2 MSK (22 decks)

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