Week 10 - soft tissue Flashcards
What structures are included under the term “soft tissue”? (LO1)
- Skin.
- Subcutaneous tissue/fat/fascia.
- Muscles.
- Tendons.
- Ligaments.
- Joint capsule.
- Neurovascular structures (nerves, veins, arteries).
List the types of soft tissue injuries. (LO1)
Soft tissues can be the primary injury but will always be injured in the case of fractures/dislocations. Forms of soft tissue injuries: - Cuts. - Lacerations. - Crushing injuries. - Impalements. - Inflammation.
What is the most common complicating feature of soft tissue injuries? (LO1)
Foreign bodies. Soft tissue injuries can present with foreign bodies in the wound. This can be agricultural, splinters, glass or metal fragments.
Describe the presentation of tendinopathy. (LO1)
- Pain worsened by active movement, particularly against resistance.
- Tenderness of the tendon and insertion.
- Soft tissue swelling and effusion around the area.
Describe the presentation of tenosynovitis. (LO1)
- Pain in the affected tendon region.
- Tends to affect the hands (pollicis brevis tendons and finger flexors).
- Examination shows swollen tendon and crepitus on palpation.
- Nodules on the tendon in response to constriction of tendon sheath.
- Fixed flexion of digit in severe cases.
Describe the presentation of tendon rupture. (LO1)
- Loss of movement at the joint to which the tendon provides power, deformity and sometimes swelling.
- Popeye deformity if bicep tendon ruptures.
Describe the presentation of bursitis. (LO1)
- Red.
- Hot.
- Swelling.
- Localised pain.
Describe the presentation of knee injuries. (LO1)
- Menisci injury - they act as shock absorbers so prone to injuries caused by large forces crossing the knee.
- Acute swelling and instability - indication of ligamentous injury.
- Locked knee.
- Effusion.
- Large acute effusion can be caused by a very peripheral tear - indication of ligament injury or fracture.
- A small chronic effusion is common.
- Joint line tenderness - usually positive in torn menisci patients.
Describe the pre-liminary investigations of a suspected soft tissue injury. (LO1)
- History of presenting complaint.
- Past medical history including drugs and allergies.
- Personal, social, occupation history.
- Examine:
1. Look for deformity/signs of injury.
2. Feel for tenderness and swelling (effusion).
3. Move to assess the range of movement, both active and passive.
4. Special tests such as anterior draw test in knee to test stability and power.
Describe the further investigations of a suspected soft tissue injury. (LO1)
- X-rays.
- Ultrasound.
- CT scan (to investigate associated fracture).
- MRI scan.
List the key differential diagnoses for presentations of soft tissue injuries. (LO1)
- Tendinopathy - pain arises from strain or injury to tendons and their insertion to the bone.
- Tenosynovitis - inflammation of the synovial lining of a tendon sheath.
- Tendon rupture - causes chronic inflammation and degeneration/trauma.
- Bursitis - inflammation of a bursa and pain from the friction of bone.
- Meniscal tear - menisci are two semicircular fibrocartilage structures, causes pain and swelling.
- Ligamentous injuries - damage to ligaments around a joint, e.g. ACL (sports accidents), PCL (dashboard injury - tibia is hit forcefully).
- Dislocation.
- Crush injuries.
- Lacerations.
- Sprains.
Describe the general management of soft tissue injuries. (LO1)
- Analgesia.
- RICE (rest, ice, compress, elevate).
- Immobilise if unstable.
- Physiotherapy.
- Surgical repair.
- Education/information about injury and preventing it getting worse.
Describe the management of tendinopathies. (LO1)
- Rest or avoidance of precipitating cause.
- NSAIDs.
- Physiotherapy local.
- Corticosteroid injections.
- Surgery if no improvement.
Describe the management of tenosynovitis. (LO1)
- Rest.
- Splinting.
- Local corticosteroid injection.
- Surgical decompression of the sheath may be required in some cases.
Describe the management of tendon ruptures. (LO1)
- No intervention required if the function has been preserved, e.g. long head of bicep ruptured.
- Some cases, splinting is all that’s required.
- Surgery often required to restore function.
Describe the management of bursitis. (LO1)
- Rest.
- Aspiration of fluid - but should avoid doing this to prevent making it septic.
- Antibiotic therapy if septic bursitis.
Describe the management of meniscal tears. (LO1)
- Often treated conservatively.
- If symptoms do not improve, repaired by arthroscopic techniques.
Describe the management of ligamentous tears. (LO1)
For ACL:
- RICE.
- Physiotherapy.
- ACL reconstruction for functional stability of the knee.
- Similar to PCL management except PCL less likely to need surgery.
For collateral ligament injuries:
- Usually heal well with conservative measures.
- Physiotherapy.
- Brace for 6 weeks.
- Minor tears will heal without bracing.
What is a bursa? (LO2)
Small fluid filled sac that allows muscles, tendons and ligaments to glide over bones. Bursitis is when these sacs become inflamed.
How can bursitis develop? (LO2)
- Normally due to prolonged pressure on a bursa against a bone.
- For example: olecranon bursitis from resting your elbows on a desk for a long time.
- Bursitis can also occur from repetitive movements or trauma.
- The main risk with bursitis is septicaemia, caused by Staphylococcus aureas via direct penetration of the skin. The spread can be haematogenous.
Describe the epidemiology of bursitis. (LO2)
- Equal incidence between men and women.
- Occupational predilections.
- Colloquial names: housemaids knees, student’s elbow.
- Older individuals are often affected by bursitis more due to conditions such as osteoarthritis which increase the likelihood of bursitis.
- Septic bursitis: immunocompromised patients, diabetes, rheumatological disorders, alcoholism are at greater risk of becoming septic.
Describe the clinical presentations of bursitis. (LO2)
Clinical examination:
- Pain at the site of the bursa.
- Swelling.
- Tenderness on palpation.
- Decreased range of motion.
- Low grade temperature (septic).
- Erythema/warmth to touch (septic).
- Presence of risk factors.
Describe the investigations for bursitis. (LO2)
- X-ray - can rule out fractures/dislocations.
- MRI - expensive so not recommended.
- Ultrasound - subjective to clinician.
- Gram stain - septic.
- Aspiration - septic.
- Blood test - septic.
Describe the management of bursitis. (LO2)
- Most cases will heal on their own.
- RICE.
- Analgesia: paracetamol/NSAIDs.
- Education on exacerbating movements and proper padding for occupationally acquired bursitis.
- Corticoid injections often used on deep bursitis but not recommended on superficial bursitis due to the risk of iatrogenic septic bursitis, skin atrophy and tendon damage.
- Corticosteroisd can also delay a differential diagnosis.
Describe the management of septic bursitis. (LO2)
- This is caused by a systemic condition so it is important that the underlying condition is treated first.
- For septic bursitis, systemic antibiotics against gram-positive bacteria should be used.
What is carpal tunnel syndrome? (LO3)
CTS results from compression of the median nerve as it passes through the carpal tunnel at the wrist. The carpal tunnel is formed by the space between the transverse carpal ligament (flexor retinaculum) and the carpal bones.
Describe the epidemiology of carpal tunnel syndrome. (LO3)
- Most common entrapment neuropathy, prevalence between around 1 in 25.
- Most common in women (3:1), particularly at 40-60 years old.
- Usually idiopathic but can be associated with several underlying conditions.
List the risk factors for carpal tunnel syndrome. (LO3)
- Diabetes mellitus.
- Hypothyroidism.
- Rheumatoid arthritis.
- Pregnancy.
- Acromegaly.
- Trauma - wrist fracture.
- Obesity.
Describe the presentation of carpal tunnel syndrome. (LO3)
- Pain/paraesthesia in the median nerve distribution in mainly the palmar aspect.
- Not every patient will complain of pain/numbness as they might be unable to localise their symptoms. Sometimes symptoms will just be whole forearm and hand feeling painful/numb.
- Aching wrist and clumsiness.
- Symptoms usually worse at night and wake a patient from sleep.
Describe the presentation of advanced carpal tunnel syndrome. (LO3)
- Muscle wasting in the thenar eminence.
- Strength of these muscles should be tested.
- The opponens pollicis muscle should also be tested by asking the patient to touch the thumb and little finger to touch and resist separation of the two (opposition of hand).
Describe the investigations of carpal tunnel syndrome. (LO3)
- Phalen’s test: inverted prayer (forced flexion of the joint for 60 seconds).
- Tinel’s test: tap over the median nerve, proximal to the flexoretinaculum.
- A positive finding for either will give symptoms of CTS including Tinel’s sign: paraesthesia.
- Electromyography (EMG) is the most specific and sensitive clinical test. Confirms and localises damage to the median nerve in the carpal tunnel and can categorise severity of damage to the nerve that helps to guide management.
- Ultrasound - identifies structural abnormalities that might be impacting the nerve such as a ganglion cyst or tendinitis. Can also assist in the diagnosis of CTS given that the median nerve might swell and become enlarged when it is damaged. In addition, ultrasound can assist in guiding needle placement for steroid injection into the carpal tunnel.
Describe the management of carpal tunnel syndrome. (LO3)
Conservative:
- Wrist strap/splint.
- Avoid certain movements - wrist flexion, hard grip, vibrating tools or playing instrument.
- Analgesia.
Clinical interventions:
- Glucocorticoid injections - reduce swelling around nerve (for those with moderate symptoms of CTS).
- Surgical decompression/release (for severe cases or when steroid injections and splints have failed).
Describe the prognosis of carpal tunnel syndrome. (LO3)
- Can spontaneously improve in 1/3 of patients (especially in young women and if pregnancy induced).
- 70% improvement with wrist splints.
- 60-70% success rate with corticosteroid injections.
- 80-90% success rate with carpal tunnel release surgery.
Describe the possible complications of carpal tunnel syndrome. (LO3)
- Wrist-splinting paraesthesia can occur in some patients when wearing a splint that is too tight or doesn’t fit properly.
- Reoccurrences after surgery can occur in around 5% of patients.
What are the relative concentrations of Na⁺ and K⁺ ions across the plasma membrane? (LO4)
- Low concentration of Na⁺ ions inside cell: 14mM.
- High concentration of Na⁺ ions outside cell: 145mM.
- High concentration of K⁺ ions inside cell: 140mM.
- Low concentration of K⁺ ions outside cell: 4mM.
- The cell is more permeable to K⁺ than Na⁺ so only K⁺ ions can freely move between environments.
What is the resting potential difference between intracellular and extracellular environments? (LO4)
-70mV.
How is the resting membrane potential maintained? (LO4)
- K⁺ ions move out of the cell down the electrochemical gradient.
- This leaves a negative charge inside the cell.
- Na⁺ ions moves into the cell down the voltage gradient.
- Sodium-potassium pumps perform active transport: 2 K⁺ moved into the cell in exchange for 3 Na⁺ ions moved out.
- This leaves a negative change on the inside of the cell.
- If only K⁺ ions moved across the membrane, the system would eventually run down and reach true equilibrium with a membrane potential of 0mV.
What is saltatory conduction? (LO4)
- Neurones are wrapped in myelin sheath, made up of Schwann cells.
- Nodes of Ranvier are gaps in the sheath.
- Impulse jumps from node to node rather than the entire length of the axon.
- Allows for faster impulse transmission.
Give an example of saltatory conduction. (Hint: pain)(LO4)
Aδ fibres are myelinated and so much faster at transmitting pain than C fibres which are not myelinated.
Describe the initiation of an action potential. (LO4)
- Small ionic change due to external potential change or mechanical force raises the resting potential.
- Threshold voltage for voltage-gated sodium channels (VgNa) is reached.
- DEPOLARISATION: VgNa channels open for 1ms and the cell is more permeable to Na⁺ ions than K⁺ ions. Na⁺ ions flow into the cell down the electrochemical gradient causing depolarisation of the cell from -70mV to +30mV.
- VgNa channels close and VgK channels open.
- HYPER/REPOLARISATION: K⁺ ions flow out of the cell down the electrochemical gradient, causing repolarisation of the cell from +30mV to -90mV.
- REFRACTORY PERIOD: voltage-gated channels for Na⁺ and K⁺ become inactive, allowing the membrane potential to increase from -90mV to -70mV. No action potentials can be transmitted in this period.
What is meant by “all or none” when talking about action potentials? (LO4)
Once the action potential has started, it has to be completed in an “all or none” response. This is due to the regenerative opening of the VgNa channels which means that once one Na⁺ channel opens, others follow which then leads to the opening of K⁺ channels.
Define propagation with relation to action potentials. (LO4)
The unidirectional transmission of the action potential along the axon of the neurone from the cell body of the neuron where it originates.
Describe propagation of action potentials. (LO4)
- Allows impulses to be transmitted to the target tissue, no matter how far from the neuronal body without any loss of amplitude. This is a digital signal.
- Action potentials can amplify an initial small potential change. This is to compensate for the poor cable structure of an axon.
- A large potential change can propagate along the axon without loss of amplitude.
- Propagation is unidirectional due to the refractory period of the VgNa channels. This is a significant limitation so requires a large number of different nerves serving different specific functions.
- The code is digital and largely dependent on the frequency of firing rates.
Describe the propagation of an action potential under anaesthesia. (LO4)
- If entry of Na⁺ ions are blocked with a local anaesthetic, reducing the axon to a simple cable, then a minimum length must be paralysed to prevent propagation.
- The high potential change of the action potential can propagate by passive spread over small distances.
- There is a high margin of safety.
Describe the process of synaptic transmission in the somatic nervous system. (LO5)
- Action potential arrives at neuromuscular junction.
- This triggers voltage-gates calcium channels to open at the nerve terminal.
- Ca²⁺ ions enter the nerve terminal and trigger a cascade of reactions, leading to vesicles of acetylcholine (ACh) to integrate with the presynaptic membrane, releasing more than 60 quanta of ACh.
- Various ions (mainly Na⁺ ions) flow into the muscle fibre and depolarise the muscle membrane in the same as in an axon. The generated action potential is also called excitatory post-synaptic potential.
- A muscle action potential is therefore propagated over the sarcolemma and through T tubules to inner aspects of muscle fibre in a similar fashion to the propagation of nerve action potential.
- ACh molecules are hydrolysed by acetylcholinesterase into choline and acetate and these two are diffused back across the synaptic cleft into the pre-synaptive neurone where they are reused.
What aspects are controlled by the somatic nervous system? (LO5)
Sensory and motor supply to the skin, muscles and joints.
What aspects are controlled by the autonomic nervous system? (LO5)
Supplies smooth muscles, glands and specialised effector cells (e.g. pacemaker cells in the heart).
How does synaptic transmission in the autonomic system differ from the somatic system? (LO5)
- Similar process to the synaptic transmission in the somatic nervous system.
- Type of neurotransmitter involved varies and may not be acetylcholine (ACh).
Differences:
- Smooth muscles may contract in response to synaptic transmission or electrical coupling.
- Synaptic transmission - unitary smooth muscles.
- Electrical coupling - multiunit smooth muscles. - Smooth muscle cells express a wide variety of neurotransmitter and hormone receptors.
How does the synaptic input to smooth muscle differ from that of skeletal muscle. (LO5)
- The neurons are part of the autonomic nervous system rather than the somatic nervous system.
- The neuron makes multiple synaptic contacts with a smooth muscle cell in a series of varicosities (swellings). These varicosities contain the pre-synaptic machinery release of the transmitter via vesicles. Each varicosity is close to the post-synaptic membrane of the smooth muscle cell, but there is relatively little specialisation of the post-synaptic membrane.
The mechanisms of intracellular communication between smooth muscle cells vary widely between tissues.
What are the 2 basic types of smooth muscle tissues? (LO5)
Multiunit and single unit.
What is meant by multiunit smooth muscle? (LO5)
- Smooth muscle that behaves like multiple, independent cells or groups of cells.
- Each smooth muscle cell contracts independently of its neighbour.
- Each smooth muscle cell receives synaptic input but there is little electrical coupling between cells due to fewer gap junctions.
- Multiunit smooth muscles are capable of fine control, e.g. in the iris and ciliary body of the eye, and in the piloerector muscles of the skin.
What is meant by single unit smooth muscle? (LO5)
- Also known as unitary/visceral.
- A group of cells that work as a syncytium.
- This is because the gap junctions provide electrical and chemical communication between neighbouring cells.
- Direct electrical coupling allows coordinated contraction of many cells.
- Gap junctions also allow ions and small molecules to diffuse between cells, which gives rise to spreading Ca²⁺ waves among coupled cells.
Where is single unit/unitary/visceral smooth msucle found? (LO5)
- Walls of visceral organs: GI, urinary tracts, uterus, many blood vessels.
- In certain organs, adjacent smooth-muscle cells are physically connected by adhering junctions that provide mechanical stability to the tissue.
- Functional size of the unit depends on the strength of intercellular coupling.
- E.g. in the bladder walls, extensive coupling defines large functional units, allowing the walls of the bladder to contract in synchrony.
- E.g. in vessel walls, less coupling defines smaller, independently functioning units (not unlike multiunit muscle).
Describe the variation in receptors in smooth muscle cells. (LO5)
- Different types of cell-surface receptors.
- In general: smooth muscle cells express a variety of such receptors and receptor stimulation may lead to either contraction or relaxation.
- For example, some receptors may be ligand-gated ion channels (e.g. Ca²⁺ channel), G-protein coupled receptors (e.g. adrenergic β₂, muscarinic M₂) that act directly on targets or act via intracellular second messengers (e.g. cAMP, cGMP, IP₃ and DAG).
Describe how smooth muscle cells vary when responding to neurotransmitters/hormones. (LO5)
- The list of neurotransmitters, hormones, environmental factors of vascular smooth muscle alone is vast.
- Identical stimuli may result in very different physiological responses by smooth muscle in different locations.
- Example: systemic arterial smooth muscle cells relax when the oxygen concentration around them decreases. Pulmonary arterial smooth muscle contracts when local oxygen concentration does.
Describe the general cardiovascular changes during exercise. (LO6)
- Vasoconstriction of inactive muscles, splanchnic, renal and cutaneous circulation.
- Vasodilation of active muscles.
- Increased heart rate x3.
- Increased cardiac output x4-5
- Increased stroke volume x1.5.
What is vasoconstriction of inactive muscle controlled by during exercise? (LO6)
- CNS central command.
- Medullary cardiovascular centre.
