Week 10 - soft tissue Flashcards
(144 cards)
1
Q
What structures are included under the term “soft tissue”? (LO1)
A
- Skin.
- Subcutaneous tissue/fat/fascia.
- Muscles.
- Tendons.
- Ligaments.
- Joint capsule.
- Neurovascular structures (nerves, veins, arteries).
2
Q
List the types of soft tissue injuries. (LO1)
A
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.
3
Q
What is the most common complicating feature of soft tissue injuries? (LO1)
A
Foreign bodies. Soft tissue injuries can present with foreign bodies in the wound. This can be agricultural, splinters, glass or metal fragments.
4
Q
Describe the presentation of tendinopathy. (LO1)
A
- Pain worsened by active movement, particularly against resistance.
- Tenderness of the tendon and insertion.
- Soft tissue swelling and effusion around the area.
5
Q
Describe the presentation of tenosynovitis. (LO1)
A
- 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.
6
Q
Describe the presentation of tendon rupture. (LO1)
A
- Loss of movement at the joint to which the tendon provides power, deformity and sometimes swelling.
- Popeye deformity if bicep tendon ruptures.
7
Q
Describe the presentation of bursitis. (LO1)
A
- Red.
- Hot.
- Swelling.
- Localised pain.
8
Q
Describe the presentation of knee injuries. (LO1)
A
- 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.
9
Q
Describe the pre-liminary investigations of a suspected soft tissue injury. (LO1)
A
- 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.
10
Q
Describe the further investigations of a suspected soft tissue injury. (LO1)
A
- X-rays.
- Ultrasound.
- CT scan (to investigate associated fracture).
- MRI scan.
11
Q
List the key differential diagnoses for presentations of soft tissue injuries. (LO1)
A
- 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.
12
Q
Describe the general management of soft tissue injuries. (LO1)
A
- Analgesia.
- RICE (rest, ice, compress, elevate).
- Immobilise if unstable.
- Physiotherapy.
- Surgical repair.
- Education/information about injury and preventing it getting worse.
13
Q
Describe the management of tendinopathies. (LO1)
A
- Rest or avoidance of precipitating cause.
- NSAIDs.
- Physiotherapy local.
- Corticosteroid injections.
- Surgery if no improvement.
14
Q
Describe the management of tenosynovitis. (LO1)
A
- Rest.
- Splinting.
- Local corticosteroid injection.
- Surgical decompression of the sheath may be required in some cases.
15
Q
Describe the management of tendon ruptures. (LO1)
A
- 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.
16
Q
Describe the management of bursitis. (LO1)
A
- Rest.
- Aspiration of fluid - but should avoid doing this to prevent making it septic.
- Antibiotic therapy if septic bursitis.
17
Q
Describe the management of meniscal tears. (LO1)
A
- Often treated conservatively.
- If symptoms do not improve, repaired by arthroscopic techniques.
18
Q
Describe the management of ligamentous tears. (LO1)
A
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.
19
Q
What is a bursa? (LO2)
A
Small fluid filled sac that allows muscles, tendons and ligaments to glide over bones. Bursitis is when these sacs become inflamed.
20
Q
How can bursitis develop? (LO2)
A
- 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.
21
Q
Describe the epidemiology of bursitis. (LO2)
A
- 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.
22
Q
Describe the clinical presentations of bursitis. (LO2)
A
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.
23
Q
Describe the investigations for bursitis. (LO2)
A
- X-ray - can rule out fractures/dislocations.
- MRI - expensive so not recommended.
- Ultrasound - subjective to clinician.
- Gram stain - septic.
- Aspiration - septic.
- Blood test - septic.
24
Q
Describe the management of bursitis. (LO2)
A
- 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.
25
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.
26
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.
27
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.
28
List the risk factors for carpal tunnel syndrome. (LO3)
- Diabetes mellitus.
- Hypothyroidism.
- Rheumatoid arthritis.
- Pregnancy.
- Acromegaly.
- Trauma - wrist fracture.
- Obesity.
29
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.
30
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).
31
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.
32
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).
33
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.
34
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.
35
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.
36
What is the resting potential difference between intracellular and extracellular environments? (LO4)
-70mV.
37
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.
38
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.
39
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.
40
Describe the initiation of an action potential. (LO4)
1. Small ionic change due to external potential change or mechanical force raises the resting potential.
2. Threshold voltage for voltage-gated sodium channels (VgNa) is reached.
3. 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.
4. VgNa channels close and VgK channels open.
5. HYPER/REPOLARISATION: K⁺ ions flow out of the cell down the electrochemical gradient, causing repolarisation of the cell from +30mV to -90mV.
5. 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.
41
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.
42
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.
43
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.
44
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.
45
Describe the process of synaptic transmission in the somatic nervous system. (LO5)
1. Action potential arrives at neuromuscular junction.
2. This triggers voltage-gates calcium channels to open at the nerve terminal.
3. 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.
5. 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.
6. 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.
7. 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.
46
What aspects are controlled by the somatic nervous system? (LO5)
Sensory and motor supply to the skin, muscles and joints.
47
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).
48
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:
1. Smooth muscles may contract in response to synaptic transmission or electrical coupling.
- Synaptic transmission - unitary smooth muscles.
- Electrical coupling - multiunit smooth muscles.
2. Smooth muscle cells express a wide variety of neurotransmitter and hormone receptors.
49
How does the synaptic input to smooth muscle differ from that of skeletal muscle. (LO5)
1. The neurons are part of the autonomic nervous system rather than the somatic nervous system.
2. 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.
50
What are the 2 basic types of smooth muscle tissues? (LO5)
Multiunit and single unit.
51
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.
52
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.
53
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).
54
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).
55
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.
56
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.
57
What is vasoconstriction of inactive muscle controlled by during exercise? (LO6)
- CNS central command.
| - Medullary cardiovascular centre.
58
What is increased stroke volume controlled by during exercise and how is it controlled? (LO6)
Skeletal muscle mechanical response:
1. Contracting muscle pumps blood through peripheral veins.
2. Increases venous return to the heart.
3. Right atrium pressure increases, end diastolic pressure and volume increase.
4. Increased stroke volume (Starling's law).
59
What is vasodilation of active muscle controlled by during exercise and how is it controlled? (LO6)
Skeletal muscle chemical response (active muscles):
1. Interstitial fluid metabolites change: O2 and pH drop, CO2, lactic acid, K+ and adenosine levels rise.
2. Increased osmolarity.
3. Blood vessel dilation.
60
What is increased cardiac output controlled by during exercise and how is it controlled? (LO6)
1. Increased sympathetic output to heart (ventricular myocardium and sinoatrial (SA) node) = increased heart rate and stroke volume.
2. Decreased parasympathetic output to sinoatrial (SA) node = increased heart rate.
3. Both of these increase cardiac output.
61
What is Starling's law? (LO6)
The force or tension developed in a muscle fibre depends on the extent to which the fibre is stretched.
So applying it to cardiovascular changes:
As venous return increases, ventricle walls stretch more = ventricular contraction is stronger as recoil returns the muscle cells to their original length.
62
List the factors sustaining reinforcement of cardiovascular changes during exercise. (LO6)
- Exercise pressor reflex.
- Arterial baroreflexes.
- Metabolites.
- Venous return.
- Histamine release.
- Adrenaline release.
- Core body temperature regulation.
63
How does the exercise pressor reflex sustain cardiovascular changes during exercise? (LO6)
1. Neural drive originating in active muscle.
2. Stretch receptors sense muscle contraction.
3. Receptor signals travel through fibres to the spinal cord and medullary cardiovascular control centre.
4. This sustains sympathetic outflow to the heart.
64
How do arterial baroreflexes sustain cardiovascular changes during exercise? (LO6)
The central command resets the arterial baroreflex threshold so that a higher mean arterial pressure is required to slow the heart rate. (Keeps heart rate up).
65
How does histamine release sustain cardiovascular changes during exercise? (LO6)
Histamine is a potent vasodilator.
1. Cells near arterioles release histamine when sympathetic tone wanes (less noradrenaline).
2. Arterioles relax.
3. Muscle capillary pressure rises.
4. Extravasation into muscle tissue (fluid leak).
66
How does adrenaline release sustain cardiovascular changes during exercise? (LO6)
1. Preganglionic sympathetic fibres innervate adrenal medulla.
2. Adrenaline released.
3. Adrenaline acts on cardiac beta-1 adrenoreceptors.
4. This enhances neural effects on the heart.
5. Increased cardiac output.
67
How does core body temperature regulation sustain cardiovascular changes during exercise? (LO6)
1. Increased metabolism.
2. Core body temperature rises.
3. Temperature-sensitive cells in the hypothalamus signal medulla and activate sympathetic cholinergic fibres to innervate sweat glands.
4. Medulla inhibits sympathetic vasoconstrictor outflow to skin.
5. Sweat glands release more sweat with the co-release of neurotransmitters.
6. Cutaneous vessels dilate.
68
Describe the respiratory changes during exercise. (LO6)
- O2 consumption is 200mL/min at rest. Rises to 3000mL/min when exercising (e.g. running 12km/h).
- Must meet demands for higher oxygen consumption in active muscles.
- Arterial blood gases do not change much during this.
69
If arterial blood gases undergo a minimal change, what changes to meet the increased oxygen consumption requirement during exercise? (LO6)
Increased ventilation rate and increased tidal volume. Increased perfusion of blood to alveoli.
- The respiratory system adjusts to main pO2.
- The system works up until the aerobic threshold (VO2max) is reached.
- Once the threshold is reached, anaerobic metabolism begins to reach the energy demand.
- The VO2max can be increased with physical training.
70
What is meant by VO2max? (LO6)
- Oxygen usage under maximal aerobic activity, beyond which anaerobic respiration begins and an oxygen debt builds up.
- Decreases with age: -1% to -4.6% per year in men. -0.5% to -2.4% per year in women.
- On average, men have a higher VO2max than women.
- Threshold can increase with physical training.
71
How do alveolar ventilation and capillary-diffusion capacity change during exercise? (LO6)
- O2 and CO2 diffusion capacity increases during exercise proportional to metabolic rate.
- Stops pCO2 increasing - allowing for quicker removal.
- Stops pO2 decreasing - allowing for greater uptake.
72
List the factors influencing respiratory changes during exercise. (LO6)
- Joint proprioceptors feedback.
- Anticipation of exercise/psychological influences.
- Increased venous return and cardiac output.
- Rising core temperature.
- Increased sensitivity of the peripheral chemoreceptors to oscillations in arterial pH (H+ levels and lactic acid) and pCO2.
- Decreasing O2 levels.
- Pulmonary stretch receptors.
- CNS.
73
Describe the structure and function of cardiac muscle. (LO7)
Structure:
- Only found in the myocardium.
- Branched cells with only centrally located nuclei.
- Intercalated discs.
Function:
- Involuntary movement.
- Synchronised contractions.
74
Describe the structure and function of smooth muscle. (LO7)
Structure:
- Found in organ systems.
- No cross stripes.
- Narrow cells with a single centrally-located nucleus (spindle-shaped).
- Elastic with no sarcomeres.
- Uniform distribution of myosin filaments.
- The cells have a higher actin/myosin ratio than skeletal muscle cells.
Function:
- Involuntary movement.
- Slower contractions but greater stamina than skeletal.
75
Describe the structure and function of skeletal muscle. (LO7)
Structure:
- Attached to bone or skin.
- Don't branch and have multiple nuclei which are on the periphery.
Function:
- Voluntary movement.
- Maintain posture.
- Stabilise joints.
- Generate heat, e.g. shivering.
- Muscles have a belly and tendons at each end. The belly contracts and is wrapped in epimysium (a sheath preventing friction).
76
List the different types of skeletal muscle fibres. (LO7)
- Red/type 1 - slow oxidative (myoglobin).
- Intermediate/type 2 - fast oxidative.
- White/type 2x - fast glycolytic.
77
Describe how red/type 1 skeletal muscle fibres work. (LO7)
- Slow twitch.
- Uses oxygen, glucose and glycogen.
- ATPase hydrolyses ATP slowly.
- Produces lots of ATP through aerobic metabolism.
- Produce weak contractions and don't fatigue easily.
- Can sustain muscle activity for long periods of time - e.g. walking.
78
Describe how intermediate/type 2 skeletal muscle fibres work. (LO7)
- Fast twitch red.
- ATPase hydrolyses ATP quickly.
- High number of sarcomeres.
- Less ATP produced due to oxidative phosphorylation.
79
Describe how white/type 2x skeletal muscle fibres work. (LO7)
- Fast twitch.
- Anaerobic glycolysis is used so they need less oxygen and therefore, have fewer blood vessels.
- Use glycogen as their main form of energy.
- Largest and strongest muscle fibres.
- Mostly sarcomeres.
- These are used when you suddenly become active such as breaking into a sprint.
- They fatigue easily and these muscles start aching when they've used up their glycogen stores.
80
How does the cross-bridge cycling occur in the initiation of muscle contraction? (LO7)
1. The brain sends a signal from an upper motor neurone to the spinal cord, where it synapses in the anterior horn to a lower motor neurone to the axon of the skeletal muscle neuromuscular junction.
2. Action potential travels along the T tubules.
3. Ca2+ channel is opened and influx of Ca2+ into the sarcoplasm from the sarcoplasmic reticulum.
4. Ca2+ binds to troponin C, causing a conformation change in shape.
5. This moves tropomyosin off the actin binding sites.
6. Myosin heads can then bind to actin but need to be ready.
7. Part of the myosin head is ATPase so it can cleave an ATP molecule to ADP which releases energy.
8. Energy used to move myosin head back into high energy.
9. Myosin head then binds to the actin binding site --> formation of the cross-bridge.
10. Energy is released and myosin head moves towards the M-line, leading to a power stroke.
11. The power stroke of all the myosin heads causes sliding of the thin filament along the thick filament.
12. ADP and phosphate leave the myosin head.
13. A new ATP molecule is able to bind, causing the myosin to release itself from the actin.
14. Once the signal from the lower motor neurone stops, the action potential ends and Ca2+ is pumped back, either out of the cell or back into the sarcoplasmic reticulum.
15. No Ca2+ means troponin changes shape and so, tropomyosin recovers the actin binding sites.
81
Describe the types of phasic muscle contraction. (LO7)
1. Isometric - no change in muscle length.
| 2. Isotonic contraction - muscle changes in length. Used to produce body movements. There are 2 types of this.
82
Describe the two types of isotonic muscle contraction. (LO7)
1. Concentric - muscle shortens and produces movement to reduce the angle at the joint.
2. Eccentric - muscle lengthens.
83
List some rules for muscle contraction. (LO7)
- Muscles always pull.
- Muscle crosses a joint.
- Insertion of the muscle moves towards the origin.
- Muscles have at least two points of contact to bone.
84
What is the shoulder girdle and what is its function? (LO8)
The shoulder girdle includes the shoulder joint (glenohumeral joint) and the scapula. The main function of the shoulder girdle is movement of the scapula, which in turn, facilitates movement of the arm. The shoulder girdle includes the acromioclavicular joint, sternoclavicular joint and the scapulothoracic joint as well as the glenohumeral joint.
85
List the muscles of the shoulder girdle. (LO8)
- Pectoralis minor.
- Serratus anterior.
- Trapezius (upper, middle and lower).
- Rhomboid major.
- Rhomboid minor.
- Levatus scapulae.
86
What are the movements of the scapula? (LO8)
- Protraction - happens when punching or hunching of the shoulder, the scapula moves anteriorly.
- Retraction - happens when pulling shoulders back towards the midline, scapula moves posteriorly (winging of the scapula).
- Elevation - happens when raising shoulders (shrugging), scapula moves superiorly.
- Depression - lowering of the shoulders, scapula moves inferiorly.
- Lateral rotation - top of the scapula moves medially, bottom of the scapula moves laterally.
- Medial rotation - top of the scapula moves laterally, bottom of the scapula moves medially.
87
What is the function pectoralis minor? (LO8)
Protraction of the scapula.
| Holds the scapula against the posterior chest wall.
88
What is the function of serratus anterior? (LO8)
Protraction of the scapula.
*Clinical note: serratus anterior is supplied by the long thoracic nerve which comes off the brachial plexus and runs down the lateral side of the chest wall and when damaged, usually by a side injury, it causes winging of the scapula.
89
What type of injury would cause winging of the scapula? (LO8)
Injury to the long thoracic nerve due to trauma to the lateral chest wall. This would affect innervation to the serratus anterior which opposes the winging motion.
90
What is the function of the trapezius? (LO8)
```
Upper:
- Elevation of the scapula.
Middle:
- Retraction of the scapula.
Lower:
- Depression of the scapula.
All fibres contracting together:
- Lateral rotation of the scapula.
```
91
What is the function of the rhomboid major? (LO8)
Retraction of the scapula.
| Medial rotation of the scapula.
92
What is the function of the rhomboid minor? (LO8)
Retraction of the scapula.
| Medial rotation of the scapula.
93
What is the function of the levatus scapulae? (LO8)
Elevation of the scapula.
94
What are the movements of the shoulder joint (glenohumeral joint)? (LO8)
- Extension.
- Flexion.
- Abduction.
- Adduction.
- Internal rotation.
- External rotation.
95
List the muscles of the shoulder joint. (LO8)
- Deltoid.
- Pectoralis major.
- Latissimus dorsi.
- Teres major.
- Coracobrachialis and biceps brachii.
Rotator cuff muscles: SITS
- Supraspinatus.
- Infraspinatus.
- Teres minor.
- Subscapularis.
96
What is the function of the deltoid? (LO8)
```
Anterior:
- Flexion of the shoulder.
Middle:
- Abduction of the shoulder - first 15º.
Posterior:
- Extension of the shoulder.
```
97
What is the function of the pectoralis major? (LO8)
Flexion of the shoulder.
Adduction of the shoulder.
Internal rotation of the shoulder.
98
What is the function of the latissimus dorsi? (LO8)
Extension of the shoulder.
Adduction of the shoulder.
Internal rotation of the shoulder.
99
What is the function of the teres major? (LO8)
Extension of the shoulder.
Adduction of the shoulder.
Internal rotation of the shoulder.
100
What is the function of the coracobrachialis and biceps brachii? (LO8)
Flexion of the shoulder (very minor role so if these muscles are damaged, you can still flex your shoulder).
101
What is the function of the supraspinatus? (LO8)
Abduction of the shoulder.
102
What is the function of the infraspinatus? (LO8)
External rotation of the shoulder - main muscle with this role.
103
What is the function of the teres minor? (LO8)
External rotation of the shoulder - minor role so cannot isolate and test this muscle. Lends a hand to all the movements of the rotator cuff but mainly external rotation.
104
What is the function of the subscapularis? (LO8)
Internal rotation of the shoulder.
105
List the two main benefits of exercise. (LO9)
Reduces risk of:
- Dementia by up to 30%.
- Hip fractures by up to 68%.
- Depression by up to 30%.
- All-cause mortality by 30%.
- Cardiovascular disease by up to 35%.
- Type 2 diabetes by up to 40%.
- Colon cancer by 30%.
106
How does physical activity help reduce the risk of cardiovascular disease? (LO9)
- Reduced blood pressure.
- Increases circulating HSL and reduces triglycerides.
- Changes in arterial wall homeostasis reduces atherosclerotic disease.
- Improved aortic valve function and reduction in calcification.
- Increases ventricular chamber wall thickness.
- Increases number of red cells to a point.
- Changes in cardiac vasculature to increase oxygen availability.
- Induces changes in body composition.
107
How does physical activity help manage depression? (LO9)
- Moderate clinical effect in declining depression.
- Long term follow-up on mood found in favour of exercise.
- No more effective than other physiological/pharmacological treatments.
- Important for those who don't want pharmacological treatment.
108
How does physical activity help reduce the risk of type 2 diabetes? (LO9)
Reduces insulin resistance which reduces the chance of developing diabetes.
109
Describe the presentation of muscle pain. (LO10)
- Proximal muscle weakness.
| - Worsening symptoms on exercise and post-exertional cramps.
110
List some presentations and features of muscle pain on history-taking and explain the differentials for them. (LO10)
- Proximal muscle weakness: myopathy (muscle disease), myositis (muscle inflammation).
- Worsening symptoms on exercise and post-exertional cramps: metabolic myopathy (glycogen storage disease).
- Strong family history and childhood/early adulthood onset: muscular dystrophy.
- Alcohol excess: inflammatory myositis and atrophy of type 2 muscle fibres.
- History of glucocorticoid therapy or prolonged/severe hypercalcaemia or osteomalacia: proximal myopathy.
Myopathy and myositis can also occur with many drugs and viral infections like HIV and/or its treatment: polymyositis and dermatomyositis are associated with co-existing/co-presenting malignancy.
111
Describe the clinical examination for muscle pain. (LO10)
Clinical examination should document the presence, pattern and severity of muscle weakness. Use the Medical Research Council (MRC) scale: no power (0) to full power (5).
112
Describe the initial investigations for muscle pain. (LO10)
Routine biochemistry and haematology:
- ESR.
- CRP.
- Creatine kinase.
- Serum 25(OH)-vitamin D.
- PTH.
Pathology:
- Parvovirus.
- Hep B.
- HIV.
- Streptococcus.
Others:
- Urine protein electrophoresis.
- Serum ACE.
- ANAs/ENAs.
- RF.
- Complement.
- Myositis-specific autoantibodies (Jo-1).
- Open muscle biopsy.
- Electromyography.
- Imaging for malignancy (CT scan).
113
Describe the management of muscle pain. (LO10)
- Usually determined by the cause but all patients should benefit from physio and graded exercise to maximise muscle function after the initial inflammation has been controlled.
Basic therapeutic aims:
1. Educate the patient on disease.
2. Control pain.
3. Optimise function.
4. Modify disease process where possible.
5. Identify comorbidity.
114
Describe the general interventions for muscle pain. (LO10)
- Education.
- Aerobic conditioning.
- Muscle strengthening.
- Simple analgesics.
- Disease modifying therapy.
- Reduction of adverse mechanical factors.
- Pacing of activities.
- Appropriate footwear.
- Weight reduction if obese.
115
List the exercises that may benefit a patient with muscle pain. (LO10)
Aerobic fitness training:
- Can produce long-term reduction in pain and disability.
Local strengthening exercise:
- Muscles that act over compromised joints.
- Reduces pain and disability.
- Improves muscle strength, proprioception, coordination and balance.
- Small amounts are often better.
Weight-bearing exercise:
- Can increase bone density and slow bone loss.
116
List the key considerations when managing a patient with muscle pain in a holistic manner. (LO10)
- Patients activity requirements and occupational and recreational aspirations.
- Risk factors that may influence disease.
- Patient's perceptions and knowledge of the condition.
- Medications and coping strategies tried already.
- Comorbid disease and therapy.
- Availability/cost, etc.
117
List the main nerves of the upper limb. (LO11)
- Axillary nerve.
- Musculocutaneous nerve.
- Median nerve.
- Radial nerve.
- Ulnar nerve.
118
Which vertebrae does the axillary nerve stem from? (LO11)
C5, C6.
119
Which muscles (and motor functions) does the axillary nerve innervate? (LO11)
Abduction:
- Teres minor.
- Deltoid.
120
Which part of the skin (sensory) is innervated by the axillary nerve? (LO11)
Skin over the lower deltoid "regimental badge area" - innervated by the upper lateral cutaneous nerve of the arm.
121
What injuries cause axillary nerve damage and how does this present? (LO11)
Injury:
- Trauma to the proximal humerus (surgical neck of humerus fracture).
- Trauma to shoulder girdle (dislocation).
Presentation:
- Inability to abduct the affected limb beyond 15 degrees (deltoid and teres minor innervation).
- Loss of sensation over the inferior deltoid region of skin.
122
What is the quadrangular space and how can it be injured? (LO11)
- Serves as a passageway for the axillary nerve and posterior humeral circumflex artery (PHCA).
- Quadrangular/quadrilateral space syndrome (QSS) can occur secondary to compressive injuries - common in athletes who perform over-head exercises. Can occur due to trauma, hypertrophy or a lesion in the space.
123
Which vertebrae does the musculocutaneous nerve stem from? (LO11)
C5, C6, C7.
124
Which muscles (and motor functions) does the musculocutaneous nerve innervate? (LO11)
Flexion:
- Coracobrachialis.
- Biceps brachii.
- Brachialis.
125
Which part of the skin (sensory) in innervated by the musculocutaneous nerve? (LO11)
Lateral forearm - innervated by the lateral cutaneous nerve of the forearm.
126
What injuries cause musculocutaneous nerve damage and how does this present? (LO11)
Injury:
- Injuries to this nerve are uncommon as it is well-protected within the axilla.
- A stabbing injury would be a possible mechanism of injury.
Presentation:
- Weakened flexion at the shoulder (would still be able to perform flexion due to the functioning pectoralis major and brachioradialis.
- Weakened supination of the forearm.
- Loss of sensation over lateral forearm.
127
Which vertebrae does the median nerve stem from? (LO11)
C6, C7, C8, T1.
128
Which muscles (and motor functions) does the median nerve innervate? (LO11)
Flexion:
- Palmaris longus.
- Flexor carpi radialis.
- Flexor digitorum superficialis.
- Flexor pollicis longus.
- Flexor digitorum profundus (lateral half).
Pronation:
- Pronator teres.
- Pronator quadratus.
Flexion of MCP and extension of IP's index and middle:
- Thenar eminence.
- Lateral 2 lumbricals.
129
Which part of the skin (sensory) in innervated by the median nerve? (LO11)
Lateral aspect of the palm - innervated by the palmar cutaneous branch.
Lateral 3.5 fingers on palmar hand - innervated by the digital cutaneous branch.
130
What injuries cause median nerve damage? (LO11)
- At the elbow - supracondylar fracture of the humerus.
| - At the wrist - laceration proximal to the flexor retinaculum (distal median nerve injury).
131
Describe the presentation of a supracondylar fracture with relation to median nerve function. (LO11)
- Constant supination of the forearm.
- Weakened flexion at the wrist, thumb and MCP joints.
- Inability to extend the IP joints of the index and middle fingers.
- Possible thenar eminence wasting.
- "Hand of benediction" - when trying to make a fist, only little finger able to flex completely.
- Loss of sensation in median nerve innervated areas: lateral palm, lateral 3.5 fingers on palmar hand.
132
Describe the presentation of a laceration proximal to the flexor retinaculum with relation to median nerve function. (LO11)
- Inability to oppose thumb.
- Inability to flex index and middle fingers.
- Hand may present similarly to elbow injury but forearm is unaffected - so not constantly in supination or adducted and the wrist should be able to flex.
133
Which vertebrae does the radial nerve stem from? (LO11)
C5, C6, C7, C8, T1.
134
Which muscles (and motor functions) does the radial nerve innervate? (LO11)
Extension - radial nerve:
- Triceps brachii.
- Brachioradialis.
- Extensor carpi radialis longus.
Forearm extension and supination - deep branch:
- Extensor pollicis longus.
- Abductor pollicis longus.
- Extensor pollicis brevis.
- Extensor carpi radialis.
- Extensor carpi ulnaris.
- Extensor digitorum.
- Extensor digiti minimi.
- Supinator.
135
Which part of the skin (sensory) in innervated by the radial nerve? (LO11)
Lateral arm and inferior deltoid - innervated by the lower lateral cutaneous nerve of the arm.
Posterior arm - innervated by the posterior cutaneous nerve of the arm.
Middle strip of posterior forearm - innervated by the posterior cutaneous nerve of the forearm.
Dorsolateral hand, dorsal lateral 3.5 digits - innervated by the superficial branch.
136
What injuries cause radial nerve damage? (LO11)
At the axilla:
- Dislocation at the shoulder joint.
- Fracture to the proximal humerus.
At the radial groove:
- Humeral shaft fracture.
At the forearm: 2 mechanisms that can affect the 2 branches in the forearm.
- Stabbing/laceration of the forearm - sensory loss (superficial branch).
- Fracture of radial head - motor loss (deep branch).
- Posterior dislocation of radius - motor loss (deep branch).
137
Describe the presentation of a dislocation at the shoulder joint or fracture to the proximal humerus with relation to radial nerve function. (LO11)
- Inability to extend the forearm, wrist and fingers.
- Paralysis of triceps brachii and posterior muscles - leads to wrist drop.
- All four cutaneous branches will be affected.
- Loss of sensation in the lateral and posterior arm, posterior forearm and dorsal hand, including the lateral 3.5 fingers.
138
Describe the presentation of a humeral shaft fracture with relation to radial nerve function. (LO11)
- Radial nerve damage is it travels in the radial groove.
- Triceps brachii weakness (not paralysis).
- Inability to extend wrist and fingers - leads to wrist drop.
- Damage to the superficial branch means the sensory branch is affected.
- Loss of sensation in dorsal hand and dorsolateral 3.5 fingers.
139
Which vertebrae does the ulnar nerve stem from? (LO11)
C8, T1.
140
Which muscles (and motor functions) does the ulnar nerve innervate? (LO11)
- Flexor carpi ulnaris.
- Medial half of flexor digitorum profundus.
- Hypothenar muscles.
- Medial 2 lumbricals.
- Adductor pollicis.
- Palmar and dorsal interossei.
- Palmaris brevis.
141
Which part of the skin (sensory) in innervated by the ulnar nerve? (LO11)
Medial half of the palm - innervated by the palmar cutaneous branch.
Dorsal medial 1.5 digits and dorsal hand - dorsal cutaneous branch.
Medial 1.5 digits - superficial branch.
142
What injuries cause ulnar nerve damage? (LO11)
At the elbow:
- Trauma at medial epicondylitis (fracture).
- Compression at cubital tunnel.
At the wrist:
- Laceration to anterior wrist.
143
Describe the presentation of a medial epicondyle fracture or compression at the cubital tunnel with relation to ulnar nerve function. (LO11)
- Abduction of the wrist when flexing - paralysis of flexor carpi ulnaris and medial flexor digitorum profundus.
- Inability to abduct or adduct fingers (interossei muscles affected)
- Impaired movement of 4th and 5th digits - lumbricals and hypothenar affected.
- Impaired adduction of thumb - adductor pollicis affected.
- Positive "Froment's sign" - patient cannot hold paper between fingers when pulled away.
- Hypothenar eminence wasting.
144
Describe the presentation of a laceration to the anterior wrist with relation to ulnar nerve function. (LO11)
- Inability to abduct or adduct fingers.
- Impaired movement of 4th and 5th digits.
- Positive "Froment's sign" - impaired adduction of thumb.
- Loss of sensation over palmar side of medial 1.5 digits only as the dorsal branch is unaffected.
