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316 • THE MUSCULOSKELETAL SYSTEM
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This causes a false-positive anterior drawer sign that should
not be interpreted as ACL laxity.
• With your hands behind the upper tibia and both thumbs over
the tibial tuberosity, pull the tibia anteriorly (see Fig. 13.42B).
Significant movement (compared with the opposite knee) indicatesthatthe ACL is lax. Movement of >1.5 cm suggestsACL
rupture. There is often an associated medial ligament injury.
Lachman test
• Flex the knee at 20–30 degrees with the patient supine.
Place one hand behind the tibia and grasp the patient’s
thigh with the other hand. Pull the tibia forward to a ssess
the amount of anterior motion of the tibia in comparison to
the femur. An intact ACL should prevent forward translational movement (‘firm endpoint’),whileadeficient ACL
will allow increased forward translation without a decisive
‘endpoint’.
Posterior drawer test
• Push backwards on the tibia. Posterior movement of the tibia
relative to the femoral condyles suggests posterior cruciate
ligament laxity.
Tests for meniscal tears
Meniscal tears in younger, sporty patients usually r esult from a
twisting injury to the weight-bearing leg. In middle-aged patients, degenerative, horizontal cleavage of the meni sci is
common, with minimal or no histor y of trauma. Meniscal injuries commonly cause slow-onset effusions, especially on
weight bearing or after exe rcise. Associated joint-line tenderness is common.
A simple test for a meniscal tear is to extend the patient’s knee
rapidly from 30 degrees of flexion to full extension. If the patient
experiences medial or lateral pain, this suggests a tear, and
formal testing should take place.
Meniscal provocation test (McMurray test)
Examination sequence (Video 30D)
Ask the patient to lie supine on the couch. Test the medial and
lateral menisci in turn.
Medial meniscus
• Passively flex the patient’s knee to its full extent.
• Externally rotate the patient’s foot and abduct the upper leg
at the hip, keeping the foot towards the midline (that is,
creating a varus stress at the knee).
• Extend the patient’s knee smoothly. In medial meniscus tears, a
click or clunk may be felt or heard, accompanied by discomfort.
Lateral meniscus
• Passively flex the patient’s knee to its full extent.
• Internally rotate the patient’s foot and adduct the leg at the
hip (that is, creating a valgus stress at the knee).
• Extend the patient’s knee smoothly. In lateral meniscus tears, a
click or clunk may be felt or heard, accompanied by discomfort.
Patella
Examination sequence (Video 30E)
• Look for prepatellar bursa swelling.
• Feel around the patella for tenderness suggestive of enthesitis
or tendonitis.
Patellar apprehension test
• With the patient’s knee fully extended, push the patella laterally
and flex the knee slowly. If the patient actively resists flexion,
this suggests previous patellar dislocation or instability.
Other tests for patellofemoral pathology are unreliable and may
be positive in normal individuals.
Ankle and foot
Anatomy
The ankle is a hinge joint. The talus articulates with a three-sided
mortise made up of the tibial plafond and the medial and lateral
malleoli. This allows principally dorsiflexion and plantar flexion,
although some axial rotation can occur at the plantar-flexed
ankle. The bony mortise is the major factor contributing to stability, but the lateral, medial (deltoid) and inferior tibiofibular ligaments are also important (Fig. 13.43).
1
3
9
5
4
Fig. 13.43 Ankle ligaments.
1
Lateral malleolus
2
Medial malleolus
3
Lateral (external) ligament
4
Medial ligament
5
3
6
3
2
9
3
7
4
5
8
Deep fibres of medial ligamen
Navicular
6
Spring ligament
7
Calcaneus
8
Talus
9
Movements of the ankle and foot are summarised in
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Fig. 13.44. Foot movements are inversion and eversion, prin-
cipally occurring at the mid-tarsal (talonavicular/calcaneocuboid)
and subtalar (talocalcaneal) joints.
The history
A ‘twisted’ ankle is a very common injury, and is usually related
to a sporting injury, such as stepping off a kerb or a stair
awkwardly. Establish the exact mechanism of injury and the
precise site of pain. Frequently, there has been a forced inversion injury, stressing the lateral ligament. A sprain occurs when
some fibres are torn but the ligament remains structurally intact.
A complete ligament tear allows excessive talar movement in
the ankle mortise with instability.
Achilles tendon rupture is associatedwith sudden plantar flexion
at the ankle against resistance (e.g. in jumping or lunging). It is
common in middle-aged patients doing unaccustomed activities
such as squash, and it is associated with some medications such
as oral glucocorticoids and fluoroquinolone antibiotics. Sudden
painoccursabove the heel andthereis often a sensationornoiseof
a crack. Patients may feel as if they have been kicked or even shot.
Forefoot pain, often localised to the second metatarsal, after
excessive activity such as trekking, marching or dancing, suggests a stress fracture (Fig. 13.45). Symptoms are relieved by
rest and aggravated by weight bearing.
Non-traumatic conditions
Anterior metatarsalgia with forefoot pain is common, especially
in middle-aged women. Acute joint pain with swelling suggests
an inflammatory arthropathy such as rheumatoid arthritis or
gout. In severe cases, the metatarsal heads become prominent
and walking feels like walking on pebbles or broken glass.
Plantar surface heel pain that is worse in the foot-strike phase
of walking may be caused by plantar fasciitis and tends to affect
middle-aged patients and those with seronegative arthritides.
Posterior heel pain may be caused by Achilles tendonitis or
enthesitis.
Spontaneous lancinating pain in the forefoot radiating to
contiguous sides of adjacent toes occurs with Morton’s
Neutral
Forefoot
adduction
Eversion Inversion
Fig. 13.44 Terminology used for movements of the ankle and foot.
Forefoot
abduction
Dorsiflexion
(extension)
Plantar
(flexion)
Flexion Extension
Detailed examination of the musculoskeletal system • 317
13
Fig. 13.45 Stress fracture of second metatarsal. Fracture site and callus
(arrow).
neuroma. A common site is the interdigital cleft between the third
and fourth toes. This occurs predominantly in women aged 25–
45 years and is aggravated by wearing tight shoes.
The physical examination
Examination sequence (Video 31)
Ask patients to remove their socks and shoes.
Look
• Examine the soles of the shoes for abnormal patterns of
wear.
• Assess gait. Look for:
• increased height of step, indicating ‘foot drop’
• ankle movement (dorsiflexion/plantar flexion)
• position of the foot as it strikes the ground (supinated/
pronated)
• hallux rigidus – loss of movement at the metatarsophalangeal
(MTP) joints.
• From behind and with the patient standing:
• Observe how the heel is aligned (valgus/varus).
• From the side:
• Observe the position of the midfoot, looking particularly at the
medial longitudinal arch. This may be flattened (pes planus –
flat foot) or exaggerated (pes cavus).
• If the arch is flattened, ask the patient to stand on tiptoe. This
restoresthe arch in a mobile deformitybut not in a structural one.
• A ‘splay foot’ has widening at the level of the metatarsal
heads, often associated with MTP joint synovitis.
318 • THE MUSCULOSKELETAL SYSTEM
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Fig. 13.46 Hallux valgus overriding the second toe.
• Examine the ankle and foot for scars, sinuses, swelling,bruising,
callosities (an area of thickened skin at a site of repeated pressure), nail changes, oedema, deformity and position.
• Look for deformities of the toes such as hallux valgus
(Fig. 13.46) or overriding toes.
• Observe any bunion (a soft-tissue bursal swelling) over the
first metatarsal head that may be inflamed or infected.
Feel
• Feel for focal tenderness and heat.
• In an acute ankle injury, palpate the proximal fibula, both
malleoli, the lateral ligament and the base of the fifth metatarsal.
• Gently compress the forefoot. Assess the MTP joints for
swelling and tenderness suggestive of inflammatory arthritis.
Move (see Fig. 13.44)
Active movements
• Assess plantar flexion/dorsiflexion at the ankle, inversion/
eversion of the foot and flexion/extension of the toes.
Passive movements
• Grip the patient’s heel from below with the cup of your left
hand, with your thumb and index finger on the malleoli.
• Put the foot through its arc of movement (normal range 15
degrees dorsiflexion to 45 degrees plantar flexion).
• If dorsiflexion is restricted, assess the contribution of the
gastrocnemius (which acts across both knee and ankle joints)
by measuring ankle dorsiflexion with the knee extended and
flexed. If more dorsiflexion is possible with the knee flexed,
this suggests a gastrocnemius contracture.
Passive foot inversion/eversion
• Examine the subtalar joint in isolation by placing the foot into
dorsiflexion to stabilise the talus in the ankle mortise.
• Move the heel into inversion (normal 20 degrees) and eversion
(normal 10 degrees).
• Examine the combined mid-tarsal joints by fixing the heel with
your left hand and moving the forefoot with your right hand
into dorsiflexion, plantar flexion, adduction, abduction, supination and pronation.
Passive hallux and lesser toe movements
• Assess flexion and extension at MTP and interphalangeal joints.
Pain and stiffness at the first MTP joint suggest hallux rigidus.
• If there is toe deformity, assess impingement on the other
toes. Claw toes result from dorsiflexion at MTP joints and
plantar flexion at PIP and DIP joints. Hammer toes are due to
dorsiflexion at MTP and DIP joints and plantar flexion at PIP
joints. Mallet toes describe plantar flexion at DIP joints.
Special tests
Achilles tendon
Examination sequence
• Ask the patient to kneel with both knees on a chair.
• Palpate the gastrocnemius muscle and the Achilles tendon for
focal tenderness and soft-tissue swelling. Achilles tendon
rupture is often palpable as a discrete gap in the tendon about
5 cm above the calcaneal insertion (Fig. 13.47A).
A
Fig. 13.47 Ruptured Achilles tendon. A Site of a palpable defect in the
Achilles tendon (arrow).
when the calf is squeezed is pathognomonic of an acute rupture of the
Achilles tendon.
B Thomson’s test. Failure of the foot to plantar-flex
Fractures, dislocations and trauma • 319
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Thomson’s (Simmond’s) test
Examination sequence
Squeeze the calf just distal to the level of maximum circumference. If the Achilles tendon is intact, plantar flexion of the foot will
occur (see Fig. 13.47B).
Mulder’s sign for Morton’s neuroma
Examination sequence
• Squeeze the metatarsal heads together with one hand while
at the same time putting pressure on the interdigital space
with your other hand. The pain of the neuroma will be localised to the plantar surface of the interdigital space and may
be accompanied by a ‘clunk’ as the neuroma slides between
the metatarsal heads. Paraesthesia will radiate into the
affected toes.
Fractures, dislocations and trauma
A fracture is a breach in the structural integrity of a bone. This
may arise in:
• normal bone from excessive force
• normal bone fromrepetitive load-bearingactivity (stressfracture)
• bone of abnormal structure with minimal or no trauma.
The epidemiology of fractures varies geographically. There is a
predicted epidemic of osteoporotic fractures because of the
increasing size of elderly populations. Although any osteoporotic
bone can fracture, common sites are the distal radius
(Fig. 13.48), neck of femur (see Fig. 13.34), proximal humerus
and spinal vertebrae.
Fractures resulting from road traffic accidents and falls are
decreasing because of legislative and preventive measures such
as seat belts, air bags and improved roads. A fracture may occur
in the context of severe trauma.
The history
13
Establish the mechanism of injury. For example, a patient who
has fallen from a height on to their heels may have obvious
fractures of the calcaneal bones in their ankles but is also at risk
of fractures of the proximal femur, pelvis and vertebral column.
The physical examination
A
B
Fig. 13.48 Colles’ fracture. A Clinical appearance of a dinner-fork
deformity.
B x-ray appearance.
Use the ‘Look – feel – move’ approach. Observe patients closely
to see if they move the affected part and are able to weight-bear.
Examination sequence
Look
• See if the skin is intact. If there is a breach in the skin and the
wound communicates with the fracture, the fracture is open
or compound; otherwise, it is closed.
• Look for associated bruising, deformity, swelling or wound
infection (Fig. 13.49).
AB
Fig. 13.49 Ankle deformity. A Clinical appearance. B Lateral x-ray view
showing tibiotalar fracture dislocation.
320 • THE MUSCULOSKELETAL SYSTEM
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Feel
• Gently feel for local tenderness.
• Feel distal to the suspected fracture to establish if sensation
and pulses are present.
Move
• Establish whether the patient can move joints distal and
proximal to the fracture.
• Do not move a fracture site to see if crepitus is present; this
causes additional pain and bleeding.
Describe the fracture according to Box 13.19. Each suspected
fracture requires an X-ray with orthogonal views, which involves
two views (at least) at perpendicular planes of the affected bone.
The joints above and below should also be imaged.
Investigations
Common investigations in patients with musculoskeletal disease
are summarised in Box 13.20.
13.20 Common musculoskeletal investigations
13.19 Describing a fracture
• Which bone(s) is/are involved?
• Is the fracture open (compound) or closed?
• Is the fracture complete or incomplete?
• Where is the bone fractured (intra-articular/epiphysis/physis/meta-
physis/diaphysis)?
• What is the fracture’s configuration (transverse/oblique/spiral/commi-
nuted (multifragmentary)/butterfly fragment)?
• What components of deformity are present?
• Translation is the shift of the distal fragment in relation to the
proximal bone. The direction is defined by the movement of the
distal fragment (e.g. dorsal or volar) and is measured as a percentage of the overall diameter of the bone described.
• Angulation is the angle formed by the deflection of the distal
fragment relative to the proximal fragment, measured in degrees.
• Rotation is measured in degrees along the longitudinal axis of the
bone (e.g. for spiral fracture of the tibia or phalanges).
• Shortening: proximal migration of the distal fragment can cause
shortening (e.g. in an oblique fracture). Shortening may also occur if
there has been impaction at the fracture site (e.g. a Colles’ fracture
of the distal radius).
• Is there distal nerve or vascular deficit?
• What is the state of the tissues associated with the fracture (soft
tissues and joints [e.g. fracture blisters, dislocation])?
Investigation Indication/comment
Urinalysis
Protein Glomerular disease (e.g. SLE, vasculitis)
Blood Glomerular disease (e.g. SLE, vasculitis)
Haematological
Full blood count Anaemia in inflammatory arthritis, blood loss after trauma
Erythrocyte sedimentation rate/plasma viscosity Non-specific indicator of inflammation or sepsis
C-reactive protein Acute-phase protein
Biochemical
Urea and creatinine [ in renal impairment (e.g. secondary amyloid in RA or adverse drug effect)
Uric acid May be [ in gout. Levels may be normal during an acute attack
Calcium Y in osteomalacia; normal in osteoporosis
Alkaline phosphatase [ in Paget’s disease, metastases, osteomalacia and immediately after fractures
Angiotensin-converting enzyme [ in sarcoidosis
Urinary albumin : creatinine ratio Glomerular disease (e.g. vasculitis, SLE)
Serological
Immunoglobulin M rheumatoid factor [ titres in 60–70% of cases of RA; occasionally, low titres in other connective diseases. Present in up
Anti-cyclic citrullinated peptide antibody (ACPA) Present in 60–70% of cases of RA and up to 10 years before onset of disease. Highly specific for RA.
Secondary amyloid in RA and other chronic arthropathies
Drug adverse effects (e.g. myocrisin, penicillamine)
Neutrophilia in sepsis and very acute inflammation, e.g. acute gout
Leucopenia in SLE, Felty’s syndrome and adverse effects of antirheumatic drug therapy
to 15% of normal population. Superseded by anti-cyclic citrullinated peptide antibodies
Occasionally found in Sjögren’s syndrome
Investigations • 321
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13.20 Common musculoskeletal investigationsdcont’d
Investigation Indication/comment
Antinuclear factors [ titres in most cases of SLE; low titres in other connective tissue diseases and RA
Anti-Ro, Anti-La Sjögren’s syndrome
Anti-double-stranded DNA SLE
Anti-Sm SLE
Anti-ribonucleoprotein Mixed connective tissue disease
Lupus anticoagulant, anti-cardiolipin antibodies,
anti- b
glycoprotein 1
2
Antineutrophil cytoplasmic antibodies Granulomatosis with polyangiitis, polyarteritis nodosa, Churg–Strauss vasculitis
Other
Schirmer tear test, salivary flow test Keratoconjunctivitis sicca (dry eyes), Sjögren’s syndrome
Imaging
Plain radiography (x-ray) Fractures, erosions in RA and psoriatic arthritis, osteophytes and joint-space loss in osteoarthritis, bone
Ultrasonography Detection of effusion, synovitis, cartilage breaks, enthesitis and erosions in inflammatory arthritis.
Magnetic resonance imaging Joint and bone structure; soft-tissue imaging
Computed tomography High-resolution scans of thorax for pulmonary fibrosis, neck scan in trauma
Dual-energy x-ray absorptiometry Gold standard for determining osteoporosis. Usual scans are of lumbar spine, hip and lateral vertebral
Isotope bone scan Increased uptake in Paget’s disease, bone tumour, infection, fracture. Infrequently used due to high
Joint aspiration/biopsy
Synovial fluid microscopy Inflammatory cells (e.g. [ neutrophils in bacterial infection)
Polarised light microscopy Positively birefringent rhomboidal crystals – calcium pyrophosphate (pseudogout)
Bacteriological culture Organism may be isolated from synovial aspirates
Biopsy and histology Synovitis – RA and other inflammatory arthritides
SLE, antiphospholipid syndrome
changes in Paget’s disease, pseudofractures (Looser’s zones) in osteomalacia
Double contour sign in gout
Detection of bursae, tendon pathology and osteophytes
assessment for fractures
radiation dose.
Negatively birefringent needle-shaped crystals – monosodium urate monohydrate (gout)
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RA, Rheumatoid arthritis; SLE, systemic lupus erythematosus.
322 • THE MUSCULOSKELETAL SYSTEM
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OSCE example 1: Right shoulder pain
Mr Hunt, 38 years old, has a 2-month history of right shoulder pain, with no history of trauma.
Please examine the shoulder
• Introduce yourself and clean your hands.
• Expose both of the patient’s shoulders and arms.
• Comment on acromioclavicular deformity and muscle wasting; look for winging of the scapula.
• Compare the right shoulder to the normal left shoulder.
• Perform active and passive movements. In particular, look for frozen shoulder, which is diagnosed by limitation of external rotation and flexion.
• Finally, examine the arm, looking for conditions such as biceps rupture.
• If all movements of the shoulder are normal, conduct a full examination of the neck.
• Thank the patient and clean your hands.
Summarise your findings
The patient reports pain between 120 and 60 degrees of abduction when lowering the abducted shoulder. Pain is reproduced upon abduction against
resistance.
Suggest a differential diagnosis
The most common cause of these symptoms is impingement syndrome, which can be confirmed by carrying out special tests (Neer and Hawkins–Kennedy).
Differentials include frozen shoulder, calcific tendonitis, acromioclavicular joint pain, arthritis (osteoarthritis, rheumatoid arthritis or posttraumatic), long head
of biceps rupture and referred pain from the neck.
Suggested investigations
X-ray will reveal degenerative changes in osteoarthritis or tendon calcification. Ultrasound may demonstrate effusions, calcific deposits and tendon damage/
rupture.
OSCE example 2: Painful hands
Mrs Hill, 46 years old, presents with an 8-week history of insidious onset of pain, stiffness and swelling of her hands. She smokes 15 cigarettes per day.
Please examine her hands
• Introduce yourself and clean your hands.
• Look:
• In this case, there is swelling of two MCP joints on the right, and one PIP joint on the left.
• Normal nails and skin (therefore psoriatic arthropathy is unlikely).
• Feel:
• Ask first what is sore and seek permission to examine gently.
• Tender, soft swelling of the MCP and PIP joints in the hands and left elbow.
• In feet: tender across her MTP joints on squeeze test but no palpable swelling.
• Move:
• Painful MCP joints in right hand on active and passive flexion, reducing handgrip and fine movements.
• Left elbow does not fully straighten
Summarise your findings
The patient has tender, soft swelling of two MCP joints and one PIP joint. There is pain associated with active and passive movement of the affected joints,
resulting in limitation of hand and elbow function.
Suggest a differential diagnosis
The pattern of joint involvement, patient’s gender, duration of symptoms and history of smoking support a clinical diagnosis of rheumatoid arthritis. The
differential diagnosis of psoriatic arthropathy is less likely because of her normal nails and lack of the typical skin changes of psoriasis.
Suggest initial investigations
Full blood count, renal function tests, calcium, phosphate and liver function tests are carried out to assess for anaemia of chronic disease and to determine
suitability for disease-modifying antirheumatic drugs; C-reactive protein to assess the degree of systemic inflammation; anti-CCP antibody to confirm whether
seropositive rheumatoid arthritis is present; application of the 2010 American College of Rheumatology/European League Against Rheumatism criteria (see
Box 13.14) for classification of rheumatoid arthritis; hand and foot X-rays to detect any bony erosions; chest x-ray to look for rheumatoid lung disease.
Investigations • 323
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Integrated examination sequence for the locomotor system
• Ask the patient to undress to their underwear.
• Ask the GALS (gait, arms, legs, spine) questions and perform the GALS screen.
• Identify which of the joints require more detailed examination:
• What is the pattern of joint involvement?
• Is it likely to be inflammatory or degenerative?
• Examine gait and spine in more detail first, if appropriate, then position the patient on the couch for detailed joint examination.
• Assess the general appearance:
• Look for pallor, rashes, skin tightness, evidence of weight or muscle loss, obvious deformities.
• Check the surroundings for a temperature chart, walking aids and splints, if appropriate.
• Examine the relevant joint, or all joints if systemic disease suspected:
• Ask about tenderness before examining the patient.
• Look at the skin, nails, subcutaneous tissues, muscles and bony outlines.
• Feel for warmth, swelling, tenderness and reducibility of deformities.
• Move:
• Active movements first: demonstrate to the patient then ask them to perform the movements. Is there pain or crepitus upon movement?
• Passive movements second: determine the patient’s range of movement. Measure with a goniometer. What is the end-feel like? Describe the deformities.
• If systemic disease is suspected, go on to examine all other systems fully.
• Consider what investigations are required:
• Basic blood tests.
• Inflammatory markers.
• Immunology.
• Ultrasound.
• x-rays, CT, MRI.
• Special tests.
• Joint aspiration for synovial fluid analysis or culture.
13
Michael J Tidman
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Alice SM Tidman
14
The skin, hair and nails
Anatomy and physiology 326
Skin 326
Hair 327
Nails 327
The history 327
Common presenting symptoms 327
Past medical and drug history 328
Family and social history 328
The physical examination 328
Distribution of a rash 328
Morphology of a rash 329
Colour 330
Specific features 332
Morphology of lesions 332
Mouth, hair and nail signs 335
Supplementary examination techniques 336
Investigations 336
OSCE Example 1: Pruritus 337
OSCE Example 2: Pigmented lesion 337
Integrated examination sequence for the skin 337
326 • THE SKIN, HAIR A ND NAILS
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Dermatological conditions are very common (10–15% of
general practice consultations) and p resent to h ealthca re
professionals in all specialties. In the UK, 50% are lesions
(‘lumps and bumps’), including skin cancers, and most of the
remainder are acute and chronic inflammatory disorders
(‘rashes’), including infections, with genetic conditions accounting for a small minority; this ratio will vary across the
world, although the pri nciples of skin assessment are the
same globally.
Dermatological diagnosis c an be challenging. Not only are
there a vast number of distinct skin diseases, but also each
may present with a great variety of morphologies and patt erns
determined by intrinsic genetic factors, including the degree of
skin pigmentation, with the diagnostic waters muddied st ill
further by external influences such as rubbing and scratching,
infection, and well-meaning attempts at topical and systemic
treatment. Even in one individual, lesions with the same pathology can have a very variable appearance (e.g., melanocytic
naevi, seborrhoeic keratoses and basal cell carcinomas).
Many skin findings will have no clinical significance,butitis
important to be able to examine the skin properly in order to
identify tumours and rashe s, and to recognise cutaneous
signs of underlying systemic conditions. The adage that the
skin is a window into the inner workings of the body is entirely
true, and an examination of the integument will often provide
the discerning clinician with important clues about internal
disease processes, as well as information about the physical
and psychological wel lbeing of an individual.
Anatomy and physiology
Skin
The skin is the largest of the human organs, with a complex
anatomy (Fig. 14.1) and a number of essential functions
(Box 14.1). It has three layers, the most superficial of which is the
epidermis, a stratified squamous epithelium containing melanocytes (pigment-producing cells) within its basal layer and Langerhans cells (antigen-presenting immune cells) throughout. The
packaging and distribution of melanin within the epidermal cells
determines the depth of skin pigmentation.
The dermis is the middle and most anatomically complex layer,
containing vascular channels, sensory nerve endings, numerous
cell types (including fibroblasts, macrophages, adipocytes and
smooth muscle), hair follicles and glandular structures (eccrine,
sebaceous and apocrine), all enmeshed in collagen and elastic
tissue, within a matrix comprising glycosaminoglycan, proteoglycan and glycoprotein.
Opening of sweat duct
Subpapillary vascular plexus
Sebaceous gland
Arrector pili muscle
Subcutaneous adipose tissue
Deep cutaneous vascular plexus
Fig. 14.1 Structures of the skin.
Shaft of hair
Epidermis
Sweat duct
Dermis
Sweat gland
Hair follicle
Subcutis
Muscle layer
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