PBL's Flashcards

1
Q

VENOUS LEG UCLER

A

Outline the management strategy appropriate for this condition?
- Pt social and medical history
- Assessment of the wound to determine the location, size and number of the wounds.
- Assessment of the arterial supply to leg- ABI
- An ABI of <0.8 requires further investigation with duplex scan to confirm the presence and degree of arterial occlusion
- Clean wound and dress with non woven island dressing + bandage
- Advise pt to check leg for lesions, blisters
- Apply topical antibiotic
- Refer back to GP
- Track wound size
- Leg elevation
- Choose dressings that maintain adequate moisture balance, apply graduated compression bandage after evaluation of the arterial circulation and. Address patients concerns.
What does the appearance of the other leg (shown above) tell you about his past medical history?
- Venous staining- previous venous insuffiency- pooly of blood

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2
Q

Pagets Disease

A

What is Pagets Disease and who does it affect ?
• Characterised by inc bone remodelling, bone hypertrophy and abnormal bone structure that leads to pain and bone deformity and weakening
• Affects elderly
2. What is its natural history (ie how does it progress), what is the prognosis
• 5 year survival rate
• No current cure, but treatment can help relieve e.g. diphosphonates
3. Can it cause foot problems, and if so, what are the signs and symptoms that the clinician should be looking for?
• Fractures due to brittle
• Deformity of bone
• Compression on nerves from enlarged bones- leading to a loss of sensation or movement
4. What can you, as a podiatrist, do for this ?
• Foot mobilisation to restore normal function to joints to reduce pain

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3
Q

Charcot Marie Tooth Disease

A

• Neuromuscular disorder
• Hereditary motor and sensory neuropathy (HMSN), encompasses a clinically and genetically heterogeneous group of disorders characterized by muscle wasting, weakness, and sensory loss usually most severe distally.

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4
Q
  1. What are the potential problems that CMT can cause - from a podiatric perspective
A

• Individuals present with a cavus foot of varying degrees
• Foot drop
• On WB there is minimal change in arch heigh or length
• Sprained ankles, hammertoes, painful callus and corns
• Inversion sprains, shin splints
• Ulcers typically neuropathic in plantar and digital high pressure locations- dependant on deformity and progression of weakness and muscle imbalances
• Neuropathic pain- reduced monofilament sensation
• Gait issues

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5
Q
  1. What can you – as a podiatrist – do about this patient’s foot presentation?
A

• Orthoses
• Foot taping/ strapping
• Supportive footwear- high top shoes can give support for weak ankles
• GP
• Richie braces- offload plantarly

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6
Q
  1. What other potential problems can arise from development of CMT and what are the potential impacts of this condition on the patient’s lifestyles
A

• Impair mobility- exercising, struggle with daily living
• Nerved degeneration- loss of sensation
• Muscle weakness/ wasting
• Chronic fatigue
• Trouble breathing/ swallowing
• Scoliosis

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7
Q
  1. What is the prognosis for someone with CMT?
A

• Not a fatal disease and does not affect normal life expectancy
• Slow progression, varies

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8
Q

What are the signs and symptoms that you (as a podiatry practitioner) would expect to have presented in a patient with likely DVT?

A

• Throbbing or cramping pain in 1 leg (rarely in both legs) usually in calf or thigh
• Measure largest size of calf- 2 and 3cm difference
• Swelling in one leg
• Pain that may worsen
• Warm skin around painful area
• Red or darkened skin around painful area
• Swollen veins that are hard or sore to touch
• Lower extremity DVT can be symptomatic or asymptomatic.
• Pain at rest- painful to walk
Subjective:
- Bed rest, long plane flights
- Chronic venous insuffiency
- Varicose veins- becomes stagnent

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9
Q

What would you do to assist in your diagnosis – from simple to complex (DVT)

A

• Most common test is venous duplex ultrasound
• Well’s score questionnaire – will suggest if further imaging is needed
• Contrast venography
• Positive homo sign
• The biggest complication of DVT is a pulmonary embolism. Symptoms of a pulmonary embolism include difficulty with breathing/shortness of breath, chest pain, syncope and a change in mental status. One can diagnose a pulmonary embolism via a ventilation perfusion scan or a spiral CT.
• DVT in the lower limb can be classified as a) proximal, when the popliteal vein or thigh veins are involved or b) distal, when the calf veins are involved.
• findings from clinical examination are combined with the assessment of DVT medical history (such as trauma, surgery, immobilization, long-distance travel, cancer, hormone treatment, and pregnancy

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10
Q

What are the management strategies employed for DVT? - both short term and longer term?

A

Treated with anticoagulants- Monotherapy with rivaroxaban or apixaban
• don’t break up existing blood clots, but prevent clots from getting bigger and reduce risk of developing more clots.
• Long term: compression stockings-graduated compression to reduce leg swelling
o Continue medication
o Keep follow up appoints with doctor

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11
Q

pustular tinea

A
  • Dry between toes properly, clean toes, when did it start, feet stay dry, type of footwear, is it painful, what type of pain is it
  • Has it got better/worse?
  • How often do you change your socks, how often do you clean your feet
  • Family history of it? Is it anywhere else?
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12
Q

4 What would your management plan be? (tinea)

A
  • Antifungal cream, keep feet clean and dry in and after the shower, possible cover and dress to stop infection, clean all socks appropriately
  • Psoriasis  cream, tell GP!!! (if systemic), diet, manage stress levels
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13
Q

Navicular Fractures and their Management
contributory factors in fractures of the navicular?

A
  • High impact sports, trauma to the bone resulting in avascular necrosis
  • Central 1/3 of navicular avascular
  • Chronic trauma from repetitive foot strike
  • Most common in track and field athletes
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14
Q

navicular #
How are they normally treated?

A
  • Radiography, X-ray, triple phase bone scan, CT, MRI
  • May be type I, II or III
  • Non-weight bearing short leg cast for 6-8 weeks/high leg boot
  • Check navicular tenderness on cast removal
    • If still tender  re-cast for 2 weeks
    • If not  functional rehabilitation for 6 weeks, full activity resumes 6 weeks after cast removal
  • Surgery indications 
    • Displaced or fragmented fracture
    • Failed conservative therapy or delayed union/non-union
    • Type III fracture
    • High level athlete for faster return to play
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15
Q

Types of Psoriasis

A

• Plaque psoriasis – also known as vulgaris (most common)
• Guttate psoriasis – small red dots
• Inverse – where skin touches, localised in flexural areas of skin (armpit, groin, etc.)
• Postural (palmoplantar) – sterile vesicles on skin, may be localised to certain areas of body

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16
Q

One has retinopathy
One has glaucoma
One has macular degeneration

A
  • Retinopathy  retinal blood vessels leak fluid or bleed, causing macular oedema (swelling of the macular), common in diabetes – can damage central vision
  • Glaucoma  the nerve connecting the eye to the brain is damaged, usually due to high eye pressure (angle-closure glaucoma), eye-pain, slow vision loss, nausea
  • Macular degeneration  causes loss of central field of vision, center of the retina degenerates (dry), leaky blood vessels grow under the retina (wet)
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17
Q

Psoriasis:

A

• Chronic skin disease marked by periodic flare ups or sharply defined red patches covered in silver flaky skin
• Episodes and remission
• Skin lesions on trunk, limbs, elbows, knees, scalp, skin folds, sacral region and nails
• Lesion may be pustular, scaling, red, raised, demarcated, cracked and itchy
• Aetiology unknown

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18
Q

psoriasis patho

A

• Autoimmune (T cells mistake body proteins as foreign antigens)
• Overactivity of helper T cells, eventually release excess prostaglandin’s (dilating blood vessels)
• Impaired ability to regulate skin cell division
Initiating and aggravating factors
• Stress, trauma, infection, weather, drugs

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19
Q

psoriasis rx

A

• Topical – emollients, coal tar, dithranol, steroids
• Systemic – PUVA, retinoids (Vitamin A – antiaging cream), methotrexate (chemotherapy drug)

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20
Q

Forms of Cutaneous Malignant Neoplasm

A
  1. Melanoma
  2. Basal cell carcinoma
  3. Squamous cell carcinoma
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21
Q

Longitudinal Grooves

A

 Causes:
1. Psoriasis
2. Poor Circulation
3. Frost Bite
4. Radiation
5. RA

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22
Q

Local Anaesthesia

A

Precautions
Allergies
- Procedures where sensation reduction is required:
• Bony procedures (e.g. arthroplasty)
• Nail removal  permanent/temporary
• Foreign body removal
- Local inflammation or infection
- Anticoagulated patients
- Medical/neurological conditions – get clearance
Products
Lignocaine
- Trade name  Xylocaine
- Uni 1% and 2% - 5ml plastic ampoule
Bupivacaine
- Trade name  Marcaine
- Maximum dose:
• Adult  2mg/kg single dose
• 400mg in 24hrs
- Slow acting, long lasting (2-5hours)
- Used when prolonged nerve block is necessary  joint arthroplasty
- Not routinely used in Uni clinics

23
Q

Risks in LA administration

A
  • Vaso vagal (fainting)
    • Lay patient back, minimise stress/anxiety
    • Epi Pen to be held in practice, CPR
24
Q

Lignocaine – Maximum dose calculation

A
  • Dependant on weight  HOWEVER 200mg is maximum dose
    Injection Lignocaine 1% = 3mg x weight (kg) / 10 (10%)
  • 3mg x 70kg = 210mg / 10 = 21ml = 20ml (200mg) is maximum dose  can’t use 21ml
  • 3mg x 45kg = 135mg % 10 = 13.5ml
    Injection Lignocaine 2% = 3mg x weight (kg) / 20 (20%)
  • 3mg x 80kg = 240mg / 20 = 12ml = 10ml (200mg) is maximum dose  can’t use more than 10 in 2%
  • 3mg x 50kg = 150mg % 20 = 7.5ml
    Aim to steer clear of maximum dose
    Generally, 5ml of 1% lignocaine in the hallux is sufficient
25
Q

Clindamycin
- Indications:

A

• Can be used for patients with immediate hypersensitivity to penicillin or cephalosporin
• Good bone penetration
When would we use it?
- Indications similar to flucoxacillin and cephalexin, but has better bone penetration
- Skin infections in patients with immediate hypersensitivity to penicillin
- Indicated for osteomyelitis (in combination with ciprofloxacin) for DFI

26
Q

Antimycotic
Antifungal agents in podiatric setting

A

Topical vs. Oral
- Must consider effects of taking the medicine and the risk vs. benefit of doing so
- Also, must consider the efficacy of treatment
• No point recommending agent that has no effect
- Generally, keep topical agents for skin and superficial nail infection and oral agents for nail infections
• More severe/unresponsive skin infections may require oral antifungal agents. Try to limit for 2-6 weeks of oral therapy

Topical
Azoles
- Indications
• Inhibit fungal growth and are indicated in tinea pedis + cutaneous candidiasis.
• Patient must continue using 2 weeks after symptoms have gone
Tinea Pedis
- Terbinafine (1/day for 1 week) more expensive
Onychomycosis
- Amorolfine (once/week, not to be used during pregnancy
Oral (Tell GP antifungal therapy has commenced to monitor systemically)
- Terbinafine and Griseofluvin
- Indications
• Onychomycosis
• Dermatophyte infection of skin, feet, when topical treatment ineffective or inappropriate

27
Q

Terbinafine

A
  • Mode of action
    • Fungicidal, fungistatic, inhibits fungal ergosterol synthesis by inhibiting squalene epoxidase, leading to membrane disruption and cell death

Practice points
- Treatment of choice for dermatophyte onychomycosis
- May be used for other forms of tinea where griseofluvin is ineffective; treat for > 4-6 weeks
- Stop treatment if hepatotoxicity occurs or a rash worsens
- Fewer drug interactions than azole antifungals

28
Q

The “Triple Whammy”

A

The term “triple whammy” refers to the risk of acute kidney injury when an ACE inhibitor or Angiotensionreceptor blocker (usually used for hypertenision) is combined with a diuretic and NSAID. This combination might be seen in a patient with hypertension, congestive heart failure, or renal disease who has arthritis or other mild to moderate pain.

29
Q

Melanoma

A

• ABCDE
• A = Asymmetrical
• B = Boarder
• C = Colour
• D = Diameter (>5mm)
• E = Elevation

30
Q

Vascular Disease in Podiatry

A

• Vascular diseases frequently encountered  PVD, diabetes, Reynaud’s, arterial disease
• Vascular beds = cerebrovascular disease (CVA), coronary arterial disease (CAD), PVD and PAD

31
Q

Peripheral Vascular Disease

A

• Functional – no organic cause. No defects in blood vessel structure. Usually short term ‘spasm’ – e.g. Raynaud’s  triggered by cold, stress, smoking, occupation
• Organic – structural change in blood vessels  inflammation and tissue damage. E.g. PAD, caused by atherosclerotic changes
• PAD  atherosclerotic process
• Assessment: appearance, pulses/Doppler, ABI (<0.5 = severe occlusion), toe pressure, angiogram
 Doppler – claudication, gangrene, rest pain, pain in leg, non-healing ulceration, preoperative, numbness, inability to palpate pulses

32
Q

Diabetes

A

• Vascular complications:
- Atherosclerotic process more common – bilateral thrombus and occlusion = reduced blood flow and less nutrients to extremities
- Microvascular disease more common – thickening of basement membrane inhibits nutrients crossing cell wall
- Innervation loss to arterioles and venules = abnormal shunting of blood with loss of normal tissue integrity even though macrovascular palpable
• High risk of ulcers – prone to infection – amputation

33
Q

Raynaud’s

A

• Phenomenon or syndrome
• Asphyxia – lack of oxygen supply
• Episodic attacks of demarcated colour changes in fingers/toes following cold exposure

34
Q

Beurger’s

A

• Acute inflammation and thrombosis (clotting) of arteries and veins that affect hands and feet
• Symptoms: claudication in feet and or hands (on rest), numbness, tingling, Raynaud’s phenomenon, skin ulcerations and gangrene, pain dependant on affected region

35
Q

Venous Disease

A

• Varicose veins, deep vein thrombosis, chronic venous insufficiency
• Varicose Veins: valve dysfunction of superficial veins (legs), retro flow occurs, build-up of pressure crating large – torturous veins  Treatment: compression, stripping, laser
• Deep Vein Thrombosis: painful, swollen, red, superficial veins engorged  Risks: hospital, surgery, immobilisation, smoking, obesity, age, drugs – risk of pulmonary embolism
• Chronic Venous Insufficiency: dysfunction of valves, may lead to stasis dermatitis

36
Q

Neuropathies – Common fibular nerve

A
  • Footdrop
    • Cause = injury to fibular head, prolonged squatting, space occupying lesion
    • Clinical diagnosis = weakness of toe and foot dorsiflexors, sensory deficit over web (1st and 2nd toes), weakness of the evertors, sensory changes over dorsal aspect (foot)
37
Q

Neuropathies – Tibial Nerve

A

• Cause = tarsal tunnel syndrome, space occupying lesion popliteal fossa, Morton’s neuroma
• Inability to plantarflex

38
Q

Sural Nerve and Saphenous Nerve – Neuropathies

A

• Superficial sensory loss to skin

39
Q

Spasticity

A

• Form of increased muscle tone (nerve activation) caused by CNS disease
• Preferentially flexor muscles in upper and extensor muscles in lower limb

40
Q

Spastic Disorders – Classifications

A

• Spastic – hemiplegia, monoplegia, diplegia, quadriplegia
• 4 common foot deformities – Talipes (equinovarus, Varus, planovalgus) and toe flexion

41
Q

Cerebral Palsy

A

• From lesion of immature brain that is non-progressive
• Results in disorder of posture and movement that is permanent but not necessarily unchanging

42
Q

Multiple Sclerosis

A

• Autoimmune disorder, demyelination of CNS

43
Q

Guillain-Barre Syndrome

A

• Acute inflammatory demyelinating polyneuropathy, autoimmune response to infectious agent, recovery possible

44
Q

Poliomyelitis (Polio)

A

• Entero-virus infection called poliovirus
• Leads to muscle weakness and acute flaccid paralysis
• Few symptoms

45
Q

Parkinson’s disease

A

• Disorder of basal ganglia affection older patients
• Insufficient dopamine
• Movement disorder
• Tremor, rigidity, bradykinesia, shuffling gait, flexed posture

46
Q

Motor Neuron Disease

A

• Degeneration of both UMN and LMN, onset 40-60yrs, muscle wasting
• Muscle fasciculation’s, spasticity or stiffness in arms and legs and overactive tendon reflexes

47
Q

Myasthenia Gravis

A

• Autoimmune disorder, affects N-M junction, causing weakness and fatigue, onset sudden and symptoms intermittent

48
Q

• Anhidrosis

A

inability to sweat normally

49
Q

• Acanthosis

A

thickening of the skin (epidermal hyperplasia)

50
Q

• Spongiosis

A

intercellular oedema (accumulation of fluid) in epidermis

51
Q

• Hyperkeratosis

A

thickening of stratum corneum (increased keratin)

52
Q

• Intraderma

A

within the layers of skin

53
Q
A

body odour normal)