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Boards Part 2 - Section 1 > Boards Part 2 (2of 2) > Flashcards

Boards Part 2 (2of 2) Flashcards

1
Q

• Neuropathic osteoarthropathy
• A progressive condition characterized by joint dislocation, pathologic fractures, and severe
destruction of the pedal architecture
• May result in debilitating deformity leading to infection or amputation

A

Charcot

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2
Q

Main thing in charcot

A

Severe PN

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3
Q

etiology of charcot

A

• Neurovascular -autonomic neuropathy
• Neurotraumatic–repetitive trauma to an insensatefoot
• Unified theory***
• nuclear factor -B ligand (RANK L)activates osteoclast progenitor cells leading to bone
resorption

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4
Q

clinical presentation of charcot

A
  • Unilateral swelling
  • Increased skin temperature (>10°)
  • Erythema
  • Joint effusion
  • Bone resorption
  • Pain 75%
  • Intact skin vs. concomitant ulcer
  • Often mistaken for cellulitis cellulitis, acute gout, DVT, osteomyelitis
  • Average delay in diagnosis is 29 wks
  • Can be associated with a plantar ulceration
  • Usually admitted through E for IV abx
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5
Q

how to distinguish between charcot and OM

A

•Look for soft tissue defects/ sinus tracts to bone.
•Fluid collections
•Solitary bone vs. diffuse
–– Osteomyelitis usually does not cross joint boundaries
•No deformity with most osteomyelitis
•Location: midfoot vs forefoot
Gold standard
•Bone biopsy
•Be careful of false positive result from contamination

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6
Q

Eichenholtz radiographic classification of charcot

A

–Developmental/Acute
•Soft tissue swelling,, osteochondral fragmentation, joint fragmentation, joint dislocation
–Coalescent
•Reduced swelling, bone callus proliferation, fracture consolidation
–Reconstructive
• Bony ankylosis, hypertrophic proliferation

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7
Q

Sanders/Frykberg Classification

A 
I. MTPjs
II. TMT
III. NC, TN, CC Joints
IV. Ankle Joint
V. Calcaneus
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8
Q

Goal and treatment of charcot

A

Goal - maintain a stable plantigradefoot that is braceable or shoeable and ulcer free!!!
Management
•NON WEIGHT BEARING!!!!
•Immobilization – can use Total Contact Cast
–Can take 18 weeks for temp normalization
•Bone stimulator
•Cryotherapy (Cryocuff/Aircast)
––Be careful
–– 30 min BID
Management
• Make an instant TCC by adding plaster to CAM boot
• Once edema decreasedSkin temp returns to normal, may progress to protected WB
• Mean return to permanent foot wear = 4-6 months
Custom Shoes
CROW Boot(Charcot Restraint Orthotic Walker)
AFO
Rocker Soles
BISPHOSPHONATES

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9
Q

3 groups of treatment for charcot

A

Phyiscal T: offlad, cryo, bone st

med: bisph, calcitonin
surg: TAL, exostectomy, reconstruct

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10
Q

total reconstruction of charcot is to restore what angles

A

• Restore lateral talo-first metatarsal angle and Calcaneal inclination angle

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11
Q

genesis of atherosclerosis

A

 Response to Injury
 Lipid accumulation
 Chronic inflammatory process in the artery
 Balance between plaque formation/regression & arterial enlargement
 Unstable plaque formation

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12
Q

prevention of atherosclerosis

A 
Controlling the risk factors
 DM2, HTN, Smoking etc.
Decrease in LDL or increase in HDL
 Associated with favorable changes in the plaque
 This also lowers the risk of CAD, and PAD
Medication Management
 Statins
How low should we go? Below 200 is good
 Antioxidants (Vitamin E)
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13
Q 
Age related: >65
Intermittent Claudication
Rest Pain
Ulcers
Gangrene
Classic progression: 
1) decreased/absent pulses: asymptomatic
2) intermittent claudication
3) rest pain
4) arterial ulcer or gangrene
A

Lower limb ischemia

Peripheral Arterial Occlusive Disease

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14
Q

Pain at rest:
Cardiac output decreases with sleep
As this progresses, pain becomes constant
May require patient to “dangle” limb
Adjusts the perfusion pressure in the limb due to gravity
Massage or walking also relieves pain

A

Lower limb ischemia

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15
Q

Acute Limb Ischemia

Primary Causes Secondary Causes

A 
Primary Causes 
Embolus (most common cause)
Thrombosis
Pressure Thrombosis
Can occur in patients without pre-existing PVD
Secondary Causes
Infection
Trauma
Pressure
Iatrogenic
Occurs in patients with pre-existing PVD
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16
Q

5P’s of acute limb ischemia

A 
Pulselessness
Paralysis
Paresthesia
Pain
Pallor
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17
Q

what to do when signs of ischemia are present

A

When these signs are present, do not delay, tissue loss is likely
Compartment syndrome, gangrene, muscle and nerve damage

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18
Q

tx of ischemic limb

A

Conservative
Monitor closely
ABIs
Exercise
Risk factor modification
Walking program
Cessation of tobacco
Mange co-morbidities
Education
Medications
Research shows a lack of clinical benefit
Surgical
Controversial for patient with claudication
Is patient compliant with conservative options
Options include stent, plasty, bypass grafting

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19
Q

venous anatomy le

A 
oDeep Venous System
• Named with corresponding arteries
oSuperficial Venous System
• Greater Saphenous
• Lesser Saphenous
• Tributaries
oPerforating or Communicating 
oValves
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20
Q

Three basic mechanisms that lead to a raised AVP (ambulatory venous pressure) and the signs and symptoms of CVI (chronic venous insufficiency)

A
  1. Muscle pump dysfunction
    - -age, trauma, etc
  2. Valvular reflux
    - -loss of collagen, elastin
  3. Venous obstruction
    - -dvt
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21
Q

Clinical Classification of Venous Disease (CEAP)

A
  1. Reticular and spider veins
  2. Varicose veins
  3. Varicose veins and leg swelling
  4. Varicose veins and evidence of venous stasis skin changes
  5. Varicose veins and a healed venous stasis ulceration
  6. Varicose veins and an open venous ulceration
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22
Q

Clinical Classification of Venous Disease (CEAP) treatments for each

A

CEAP 1 — No need to refer for medical treatment, cosmetic problem only.
CEAP 2 — Refer routinely to vascular specialist for duplex ultrasound.
CEAP 3-5— Refer quickly to vascular specialist for duplex ultrasound.
CEAP 6— Refer urgently to vascular specialist for duplex ultrasound & to Wound Care Center for ulcer assessment.

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23
Q

Subcutaneous Varicosities
They form due to increased hydrodynamic pressure.
Symptoms include itching & discomfort pain.
Mainly cosmetic complaints

A

Reticular and Spider Veins

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24
Q

Typically in the legs.
A result of increased pressure.
Twisted (tortuous),bulging, discolored.
Symptoms include
◦ An achy or heavy feeling.
◦ Burning, throbbing, muscle cramping and swelling in your lower legs.
◦ Worsened pain after sitting or standing for a long time.

A

Varicose Veins

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25
Q

Venous Stasis Skin Changes

A 
Corona Phlebectatica
◦ Blue-bleb appearing lesion
Lipodermatosclerosis
◦ Skin is brown (red or purple)
Atrophie blanche
◦ Thin, pale skin
Varicose eczema
Edema/induration
Hemorrhage
Venous Stasis Ulceration
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26
Q

Superficial: affects veins on the skin surface.
The condition is rarely serious
Usually resolves with warm compresses and anti-inflammatory medications.
Can be associated with deep vein thrombophlebitis

A

Phlebitis

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27
Q

Characterized by
◦ venous thrombosis
◦ inflammation
◦ bacteremia
Can see severe systemic infections
Major concern: embolization of infected thrombus to lungs
This leads to multiple septic pulmonary emboli, hypoxia, sepsis, and often death.

treatment and who gets it

A

Septic Thrombophlebitis

◦ Antibiotics
◦ Surgery
◦ Extensive hospitalization 
◦ ICU
See most commonly in 
◦ burn patients
◦ steroid usage
◦ intravenous drug use
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28
Q 
◦Edema- Unilateral
◦Warmth
◦Erythema 
◦Pain/tenderness (50%) 
◦Palpable firm cord
◦Night cramps
 Calf tenderness
◦ Most common location in the lower extremity is in the veins in the calf region
 Homan’s sign
◦ Passive dorsiflexion at ankle causes pain
 Pratt’s sign
◦ Squeezing of calf causes pain
 Low grade fever
 Rapid pulse—tachycardic
A

DVT

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29
Q

Most frequently used in diagnosis of DVT

Most accurate noninvasive modality

A

Venous Duplex Ultrasound

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30
Q 
◦ Dyspnea
◦ Pleuritic chest pain
◦ Apprehension
◦ Cough
◦ Tachypnea tachycardia
A

PE

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31
Q

what thrombi are greatest risk for PE

A

Proximally located (above knee) thrombus are at greatest risk for PE
◦ 5% of calf vein thrombi lead to PE
◦ Nearly 50% iliac vein thrombi lead to PE

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32
Q

gold standard for PE

A

Spiral chest CT

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33
Q

PE treatment

A

 Immediate therapeutic anticoagulation is initiated for patients with suspected DVT or pulmonary embolism. Anticoagulation therapy with heparin reduces mortality rates from 30% to less than 10%.
 Assessment of pulmonary embolism severity, prognosis, and risk of bleeding dictate whether thrombolytic therapy should be started. Thrombolytic therapyis not recommended for most patients
 Current guidelines recommend starting unfractionatedheparin (UFH), low–molecular weight heparin (LMWH), or fondaparinux (all grade 1A) in addition to an oral anticoagulant (warfarin) at the time of diagnosis
◦ Heparin: 800-1500U/hr continuous drip; monitor PTT
◦ Warfarin (Coumadin): 2-10mg po titrate to INR 2-3x normal

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34
Q

in segmental limb pressures, why use toe pressures

A

 Narrow thigh cuffs give artificially elevated high thigh pressures
 Calcified arteries are difficult to compress (e.g. pts with diabetes and adv renal diseased pts)
 Good indication in this case to use toe pressures because digital arteries are seldom calcified

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35
Q

segmental limb pressures interpretation

A

Normal
 Ankle/Arm Index (Ankle/Brachial Index) is 1.0 or greater in healthy pts (>.95)
 Number derived from segmental pressure divided by the brachial pressure
 High thigh pressure: 20-40mmHg higher than brachial pressure
 Above knee pressure: equal to brachial
 Below knee pressure: equal to or higher than brachial
 Ankle pressure: equal to or higher than brachial
 Toe pressure: Toe/Brachial Index of .60

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36
Q

index of less than what indicates occulsive arterial disease

A

.90

. 20-30mmHg drop from one segment to the next or from one side to the opposite side indicates occlusive process

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37
Q

a measurement of the metabolic state of the tissue being examined
 Sensitive way of assessing skin blood perfusion pressure
 Does not depend on pulsatile flow

A

Transcutaneous Oxygen Tension Introduction

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38
Q

rare disease of lymphedema

A

milroys and meige

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39
Q

Secondary Lymphedema

• Acquired defects are those one is not born with but that are the result of

A
  • injury
  • surgery
  • trauma
  • radiation
  • infection
  • malignancy
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40
Q

Nonatherosclerotic vascular diseases

A 
Vasospastic disorders
-Raynaud’s Phenomenon/Disease
Vasculitis
-Giant cell arteritis
-Takayasu’s Disease y
--Kawasaki’s Disease
Polyarteritis Nodosa
Miscellaneous
-Buerger’s Disease
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41
Q 
 Definition: Episodic vasospasm of the arterioles in the extremities
 Primary (idiopathic) “phenomenon”
 Secondary (underlying cause) “disease”
 Incidence 5%
 Female:Male 9:1
 Genetic predisposition (25% 1orelative)
Raynaud’s Phenomenon Pathophysiology
Vasospasm small muscular arteries and arterioles
Alpha-adrenergic receptors (sympathetic)
Calcitonin gene-related peptide
Activated platelets 
Serotonin
Thromboxane
Raynaud’s: Clinical Factors
Pallor (vasoconstriction)- White
Cyanosis (sluggish blood flow)-Blue
Redness (hyperemia)-Red
Cold/emotional stress
A

Raynaud’s

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42
Q

diff between primary and 2ry raynauds

A 
Primary
< 30
Rare digit gangrene
Normal nail fold capillaries
autoantibodies: neg or low
symmetrical
ESR normal
ANA neg usually
2ry 
> 30
common digit gangrene
nail fold cap - large tort
frequent autoantibodies
scleroderma, RA, SLE
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43
Q

treatment for raynauds

A 
Avoid precipitanting factors
Avoid caffeine, tobacco
Nifedipine
Losartan
Sympathectomy
Amputation
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44
Q

Classification of Vasculitides

A 
Systemic Necrotizing Vasculitis
Polyarteritis nodosa
Churg-Strauss
Overlap syndrome
Wegener’s Granulomatosis
Giant Cell Arteritis
Temporal arteritis
Takayasu’s
Hypersensitivity Vasculitis
Henock-Schonlein
Serum sickness
Drug induced
Miscellaneous Syndromes
Kawasaki’s
Buerger’s 
Behcet’s
Erythema nodosum
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45
Q

Small and medium sized vessels
Classic necrotizing arteritisinvolvinig kidney, heart, liver, GI tract, peripheral nerves, skin (lungs spared)
Allergic angiitis and granulomatosis (Churg-Strauss dz) like above but involves lungs—severe asthma

A

Polyarteritis Nodosa

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46
Q

Involves upper and lower respiratory tracts, glomerulonephritis, and paranasal sinuses, Arthritis
Saddle nose may result
Renal involvement accounts for most deaths
Autoantibodies to proteinase 3
face, lungs, kidney

A

wegener’s granulomatosis

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47
Q 
temporal arteritis
HA
scalp tenderness
blindness
tA biopsy to confirm
A

Giant cell arteritis

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48
Q

Pulseless arteritis
Aorta/major branches
Young females
Symptoms in arms and neck

A

Takayasu

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49
Q 
“Mucocutaneous lymph node syndrome”
Major cause of acquired heart disease in children
Coronary aneurysms
Pink eye
pathcy rash
peeling skin
enlarged LN
A

Kawasaki

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50
Q 
“Thromboangiitis obliterans”
Segmental occlusive disease
Medium size arteries of extremities
Male:Female 5:1
Median age of onset 34
Primary causative factor: Tobacco
Ischemia of distal extremities
Dependent rubor
Rest pain 
Ulceration
Gangrene
Instep claudication
Upper extremity involvement
A

Buerger’s Disease

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51
Q

diagnostic criteria of buergers

A 
Smoking history
Onset <50 years
Infrapopliteal arterial occlusions
Upper limb involvement
Absence of other atherosclerotic risk factors (except smoking)
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52
Q

“Catch all” inflammatory rash
Acute with vesicles, erythema and pruritis
Sub acute with erythema, scaling pruritis and burning
Chronic with pruritis, lichenification fissures and excoriations

A

eczema

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53
Q

Acute/sub-acute chronic eczema caused by external agents or allergic reaction
ETIOLOGY-exposure to agent
 Exposure 24-72 hrs prior IN PRE-EXPOSEDINDIVIDUALS
 Pruritis
 Rash with blisters and red bumps
 Is “spreading”
 Crusting/oozing
 Severe cases may see constitutional symptoms

A

contact dermatitis

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54
Q

Leather dyes/tanning chemicals

Spares the web spaces is hallmark

A

SHOE BOX Contact Derm

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55
Q

 An irritant produces direct local cytotoxic effect on the cells of the epidermis, with a subsequent inflammatory response in the dermis
 Is not delayed
-”dishpan hands”
-diaper rash
-solvents
-hot peppers
 Irritative contact dermatitis affects very young and very old patients more severely. The most common cause of ACD in elderly patients is topical medication.
 Irritative dermatitis is common in infants. The most common cause is diaper dermatitis.

A

Primary Irritant contact dermatitis

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56
Q

Eczema due to a COMBO of chemical + sunlight
Big offender is citrus juice, especially LIME
Perfumes are also common

A

Photo Allergic Contact Dermatitis

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57
Q

Related to over treatment with topical medications
More likely with damaged or fragile skin
May be due to preservatives
Tx is discontinue and use other typical anti-eczema options

A

Dermatitis Medicamentosa

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58
Q 
An acute, subacute but usually chronic, pruritic inflammation of the epidermis and dermis often occurring in association with a personal or family history of hay fever, asthma, allergic rhinitis or atopic dermatitis.
 AD typically manifests in infants aged 1-6 months 
 Is USUALLYoutgrown
 Persistent rash in an infant 
 VERY itchy
 Exacerbations/remissions
 Poor sleep
 Itch  -> Scratch ->  Rash
Dermatagraphism
FLEXOR AREAS
DIRTY NECK SIGN
allergic salute
A

Atopic Dermatitis

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59
Q

skin lesions in atopic derm

A

Acute: erosions with serous exudate with papules and vesicles on an erythematous base.
Sub acute: scaling, excoriated papules, or plaques over erythematous skin.
Chronic: lichenification and pigmentary changes (increased or decreased) with excoriated papules and nodules.

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60
Q

Rather than a disease process, this is more of a cutaneous reaction to repetitive scratching with resultant scaling and skin thickening
Initial pruritis results in compulsive scratching
Mechanical process thickens skin
Significant emotional overlay—anxiety
Thickened epidermis globally
Increased nerve proliferation -> increased sensitivity -> more scratching
Analogous to erogenous zone

A

Lichen Simplex Chronicus

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61
Q

lesions of lichen simplex chronicus

A

Plaques of well demarcated lichenification
Exaggerated skin lines
May see hyper pigmentation
Initially erythema

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62
Q

allergy-related skin disorder causing characteristic itchy, coin-shaped lesions
Older men typical
Cold weather
Very itchy-may disrupt sleep
Red bumps grow together
Exacerbated with cold, wintry weather
Red papules
Coalesced papules form red or violatious “coin shaped” lesions with central clearing
Possible vesicles with drainage
Symmetrical lesions on the legs-may be seen on trunk and feet-NOT head

Comes and goes and may recur in old spots

A

Nummular eczema

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63
Q 
recurrent or chronic relapsing form of vesicular palmoplantar dermatitis of unknown etiology
Also known as POMPHOLYX 
VERY itchy
Came on quickly
Blister-like rash
Stress seems to bring on
“tapioca” on sides of fingers or toes but is considered a palms and soles diseases emphasizing the sides
80% is on hands
Vesicles are deep seated 
Lasts days to weeks
A

Dishydrotic eczema

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64
Q

treatment of venous stasis dermatitis

A 
Wet to damp-Burrows Solution
Elevation
Compression
Unna Boot
Topical steroids
calcineurin inhibitors 
Correct medical problem-i.e... CHF
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65
Q 
“winter itch”
Usually winter
Usually elderly
‘ASTEATOTIC ECZEMA-lesions
'crazy paving' 
Very dry and scaling on erythematous base
Legs a common location
A

ASTEATOTIC ECZEMA

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66
Q

Corticosteroids Potency

A 
– Based on vasoconstrictive properties
– Class I super potent
– Class II & III potent
– Class IV & V intermediate
– Class VI & VII Mild
Clobetasol is 1000 x more potent than hydrocortisone 1%
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67
Q

corticosteroid selection

A

Start low and for as short a time as possible
– Super potent are reserved for severe dermatosis or tough to penetrate areas (soles)
– Intermediate for non-facial mild to moderate disease
– Mild for genital, eye lid or large areas
Best if applied to moist skin (post bath)
Duration
– Super potent – no more than 3 weeks
– Potent & Intermediate – 6-8 weeks
» May still cycle in sensitive areas

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68
Q 
Primary = Essential = Idiopathic
Secondary
 Hyperthyroidism
 Endocrine Tx for Ca
 Severe Psychiatric Disorders
 Obesity
 Menopause
 Febrile Illness
 Medications
Three forms:
 Emotionally Induced
 Localized
 Generalized
Can cause significant emotional distress and occupational disability
A

hyperhydrosis

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69
Q

hyperhydrosis treatment

A 
Primary
Antiperspirants (aluminum chloride)
Topical 20% aluminum chloride 
Iontophoresis
Drugs (sedatives or anticholinergics)
Botulinum toxin
Surgery (gland excision or sympathectomy)
Alternative (e.g. herbs, acupuncture)
Secondary
Treat underlying condition (e.g. anti-estrogens)
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70
Q

(Callus
Diffuse
Non-nucleated

A

tyloma

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71
Q

heloma molle, durum

A

corns

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72
Q

nucleated
Core
well-circumscribed

A

IPK

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73
Q

Neurovasculare PK

A

very painful

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74
Q 
►Skin tags & polyps
►Often found in skin folds or creases
►Increase in middle age
►Usually asymptomatic
►Treatment rarely needed: excision
A

Acrochordon

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75
Q

►Benign fibrous mass with central keratoma
►Often found at locations of irritation and rubbing
►Raised collar with central keratosis
►Remove central keratin and prevent pressure or rubbing
►Surgical excision/realignment

A

Acral Fibrokeratoma

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76
Q 
►Fibrous histiocytoma
►Inflammatory process
►Often secondary to penetrating trauma or follicle rupture
►Hard, elevated papule or nodule firmly adherent to skin
►Varied colors
►May shrink in timeDermatofibroma
►Dimple sign or Retraction sign
►Usually asymptomatic
►Surgical excision is curative
A

Dermatofibroma

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77
Q

►Benign, soft, smooth, dome-shaped, oval to round, translucentlesion
►Located dorsally on fingers and toes
►White to pink pseudocysts
►Slow growing
►Not a true cyst (no lining)
►Filled with viscous clear fluid—will transilluminate
►Nail fold cysts will damage nail matrix
►DIPJ cysts may be herniations of tendon sheath or joint capsule

A

Digital Mucous (Mucoid) Cysts

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78
Q 
►Most common cyst
►Few mm to several cm
►Slow growing, may drain
►Cyst wall of squamous epithelium
►No I &amp; D, excision only 
►Associated with trauma
►Epidermal cells implanted deep
A

Epidermal (Inclusion) & Sebaceous Cysts

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79
Q 
►Benign, appendageal tumor
►Commonly found on sides and soles of feet
►Involves intraepidermal eccrine sweat ducts
►Skin colored to red
►Solitary, firm
►Surgical excision is curative
►Eccrine
►Apocrine
►Intradermal &amp; juxta-epidermal types
A

Poroma*

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80
Q 
►Benign tumors containing nevus cells derived from melanocytes
►Acquired or congenital
►Acquired appear after 6 months of age
►Most are less than 5mm
►Concentrated on sun-exposed sites
A

Nevi

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81
Q

3kinds of nevi and explain

A

Junction - flat, pinpiont
Compound - slightly elevated, dome shaped
Dermal - verrucoid, pedunculated (have stalk)

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82
Q 
►AKA Atypical mole, Clark’s nevus
►An atypical melanocytic nevus
►Larger with indistinct and irregular borders
►Found on trunk and calves
►More likely to become melanoma
A

Dysplastic Nevus

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83
Q

nevus on trik that has hair

A

beckers

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84
Q

kids
dome shaped nevus
need excision

A

spitz

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85
Q

►Weight-bearing herniations of fatinto the dermis
►Heels, arches, lateral aspects of feet
►Common, skin-colored, soft
►Usually painless
►Treat with heel cups or excision if necessary

A

Piezogenic* Papules

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86
Q

►Rapidly growing, pink to bright red growth
►Minor trauma & ingrown nails
►Cerebriform highly vascular tumor
►Bleeds easily
►Treat with debridement & cautery plus topical antibiotic

A

Pyogenic Granuloma

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87
Q

►Painful, keratotic plug
►Located plantarly
►1-3mm discrete lesion
►Translucent, cone-shaped center
►No bleeding with debridement
►Painful with medial & lateral compression and direct pressure
►Treat with enucleation, topical acid under occlusion, padding, sclerosing injections, excision
►Hypertrophy of stratum corneum about sweat ducts

A

Porokeratosis

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88
Q

►One of the most common benign lesions in geriatrics
►2mm to 3cm diameter
►Deeply pigmented
►Greasy scale
►Onset 5th-6thdecade
►Slow growing
►Treatment rarely needed: curettement + cautery or liquid nitrogen
*Functional disturbance of the sebaceous glands

A

Seborrheic Keratosis

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89
Q

►Small, light-colored, flat, keratotic lesions
►“Stuck on”
►Men >40 years old
►Legs, feet, forearms but never palms or soles
►Treatment rarely needed: curettement or cryotherapy

A

Stucco keratosis

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90
Q

onycholysis from proximal to distal

A

onychomadesis

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91
Q

Transverse nail splitting

A

• Onychoschizia

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92
Q

(Longitudinal ridging/splitting

A

• Onychorrhexis

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93
Q

ABCDEF of Melanonychia

A 
A = Age
B = Brown/black band
C = Change in morphology
D = Digit involved
E = Extension of pigment (Hutchinson’s sign)
F = Family or personal history of dysplastic nevus or melanoma
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94
Q

yellow nail sydrome association

A

cirrhosis

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95
Q 
 Longitudinal extravasation of blood
 Moves with the nail plate
 Common causes
 Trauma
 Drugs
 Dermatologic dz
 Systemic dz (which serious disorder should you be most concerned about??) - Endocarditis
 Idiopathic conditions
A

Splinter Hemorrhages

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96
Q

transverse white bands on nails from arsenic poisoning

A

Mees Lines

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97
Q

transverse white bands on nails from low albumin

A

Muehrcke’s lines

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98
Q

Spoon Nails
 Idiopathic causes
 Hereditary or congenital

most common cuases

A

koilonychia

 Iron deficiency anemia
 Trauma
 Malnutrition

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99
Q

Hippocratic Nails
Lovibond’s Angle
(Increased Unguophalangeal Angle)

most common causes

A

clubbing

 Lung neoplasms
 Hypertrophic osteoarthropathy
 Cardiovascular dz
 Cirrhosis
 Colitis
 Thyroid dz
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100
Q

Caused by trauma or systemic illness or chemo

A

Beaus lines

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101
Q

 Subungualhyperkeratosis
 Keratosis palmaris et plantaris
 Leukokeratosis of oral mucosa
 Familial

A

Pachyonychia Congenita

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102
Q

periungal fibromas associated wtih

A

tuberous sclerosis

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103
Q

Cause unknown
Possible osteochondroma
Must take x-ray
Excision of bone necessary but nail may not return to normal shape

A

Subungual Exostosis

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104
Q

types of papulosquamous disorders

A

psoriasis
Lichen planus
Pityriasis rosea
pityriasis rubra pilaris

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105
Q 
papulosquamous
•Sudden onset of ugly loose scales
•PRURITIS
•Recent strep throat, viral infection, immunization, use of antimalarial drug, or trauma
•Family history of similar rash
•Pain in joints
•Blisters
Patient may feel “ill”
REMISSIONS AND EXACERBATION
KOEBNER’S PHENOMENON 
•Thick, silvery scales that arise from the coalescence of red scaling papules
•Sharp margins
•Salmon pink color base
LOCATION
•Extensor surfaces – elbows, knees
A

Psoriasis

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106
Q

Atypical FLEXOR surfaces

papulosquamous

A

psoriasis inversa

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107
Q
  • Halo or ring of hypo-pigmentation around psoriaic plaque
  • diffusion of an inhibitor of prostaglandin synthesis from the psoriatic plaque during UVR therapy to the adjacent normal skin
A

woronoff ring

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108
Q
  • Strep infection
  • Gutta means drops
  • Trunk/arms/legs
  • Lesions much smaller
  • Scales are finer
  • Less than 2% of psoriasis
  • Usually spares feet
  • Younger individuals
  • Self limited
A

GUTTATE PSORIASIS

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109
Q
  • Life threatening
  • Scaling
  • Fever
  • Onycholysis
  • Huge surface area of the body has bright red scaling
  • > 50 YO male
A

ERYTHRODERMA

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110
Q
  • Often palms and soles
  • Pustules that dry up and turn brown
  • Mimics vesicular tinea pedis
A

pustular psoriasis

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111
Q
  • Rare form of psoriasis generalized pustular psoriasis.
  • Multiple pustules in the flexural areas - the backs of the knees, the insides of the elbows, the armpits and the groin
  • Pustules can coalesce to form lakes of pus which can cause infection
  • Can be life-threatening especially in the elderly
  • Often triggered by stopping steroids rebound
A

VON ZUMBUSCH

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112
Q
  • Papulosquamous condition known for pruritic, violacious, polygonal lesions with a fine scale
  • Very itchy
  • Stress precipitates
  • Insidious
  • 1sthits flexor limbs and spreads
  • Oral lesions may not be noticed or may burn
  • White-lace pattern*
  • Mucus membranes*
  • Anterior legs
  • Flexor arms
  • Genitalia
A

Lichen planus

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113
Q

Wickhams striae associated with what

A

lichen planus

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114
Q

MUCOUS MEMBRANES of Lichen Planus

A

•Possible conversion to SCC
•Usually seen with chronic LP
•May develop painful erosions
Striae

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115
Q

NAILS of LP

A
  • Ridging and grooving from thinning
  • Onycholysis
  • 10% see nail changes
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116
Q
  • Large 2-10 cm reddish patch-HERALD PATCH may be related to fever or infection
  • Trunk that may spread to other areas
  • Lesions may have an associated ring of scales, COLLARETTE
  • Symptomatic care
  • Self-limiting
A

Pityriasis rosea

117
Q
  • Thick scaling with red follicular papules
  • Looks like psoriasis
  • Palms and soles
  • Hyperkeratosis
  • Often seen on joint surfaces
  • Fissuring
  • Moisturizers
  • retinoid
A

Pityriasis rubra pilaris

118
Q

Can metastasize anywhere
Very aggressive and deadly
Higher incidence in blue eyed, fair skinned individuals and/or multiple common nevi
Sun exposure huge risk-especially in individuals not used to sun on day to day….e.g. office worker has higher risk than construction worker
• A mole that changes
• Pigmented lesion that grows, bleeds, ulcerates, itches or hurts
• Family history of MM

A

Malignant Melanoma

119
Q

MELANOMA-ABCDEF

A 
A Asymmetry: halves don’t match
B Border: irregular, ragged, notched or blurred
C Color: mottled and haphazard
D Diameter: >6mm
E Elevation: raised 	
Evolving: undergoing change
F Funny Looking: just looks weird
120
Q

Surgical Excisionmargins melanoma

A
  • Based on depth:
  • In situ: 0.5 cm
  • 1-2mm: 1 cm
  • 3-4mm: 2 cm
  • No benefit going > 2cm
121
Q

Surgical Excisionnodes melanoma

A

Excised as per sentinel node biopsy (SNLB) usually recommended if >1mm depth
Sentinel node is first node tumor drains into
Determined by placing radioisotope and blue dye at tumor site
Sentinel node status (positive or negative) is the most important prognostic factor for recurrence and is the most powerful predictor of survival in melanoma patients.

122
Q 
Melanoma
•	Female 30-50
•	YUPIE
•	Most common-70% of MM
•	Upper back-males
•	Legs-women
A

SUPERFICIAL SPREADING MELANOMA

123
Q 
Melanoma
•	65 year old+
•	Slow growing but often large
•	Head, neck and arms
•	Macular to nodular
•	May have areas of hypopigmentation
•	4-10% of MM
A

LENTIGO MALIGNIA

124
Q 
•	Palms/soles*/digits/nails
Melanoma
•	Most common in dark skin patients
•	2-8% of MM in whites
•	50%+ in dark skinned individuals
•	Considered very aggressive
•	*most common site in dark skin patient
A

Acral Lentiginous

125
Q 
melanoma
Men 40-50 on Legs and trunk
Most aggressive/most deadly
Rapid growth*
“blueberry” color
15-30% of MM
Grows down
A

nodular

126
Q
  • UV mediated..rare Arsenic
  • Single pink macule that grows and is well demarcated as it enlarges, becomes {raised} plaque
  • Can become malignant
  • Pre-SCC (SCC In situ) is intra-epidermal carcinoma-basement membrane is intact
  • Treatment is excisional biopsy
A

bowens disease

127
Q 
•	Most common soft tissue malignancy of the foot
•	Fair complexion at higher risk
•	Proximity to equator 
•	UV associated
Varied
Pink/red/tan
Plaques or nodules
Erosions/Ulcers/Scaling
Can be associated with a cutaneous horn
•	Can be aggressive, invading tissues and metastasize to nodes: rate is about 4% in general but climbs to 30% in lower extremities 
•	Can be fatal
•	Cure is 90% + with early recognition
A

SCC

128
Q
  • SCC due to old skin damage, such as a chronic ulcer, chronic osteomyelitis or old burn-60% found on lower extremity
  • Mechanism may be toxins from ulcer or cycle of damage-irritation-repair at ulcer site can result in malignant transformation
A

MARJOLIN ULCERS of SCC

129
Q

SQUAMOUS CELL CARCINOMA treatment

A
  • Wide Surgical Excision 4mm margins for non-invasive and10mm for invasive lesions
  • Mohs is gold standard for SCC ulcers
  • Radiation
130
Q
  • # 1 skin cancer
  • “Rodent bite” ulcer
  • Sore that won’t heal
  • “pearly” papule
  • Crusty
  • Waxy
  • Bleeds easily
  • Can look like Bowen’s
  • Locally destructive but not aggressive
  • Slow growing
  • Metastasis
A

Basal Cell carcinoma

131
Q
  • Pink, hyper- or hypo-pigmented patches
  • Fine scale
  • Upper back/young adults
  • M. globosa common lipophilic yeast
  • Flouresce with Wood’s lamp
  • AKA pityrosporum ovale, Malassezia furfur
  • 2-8% of the U.S. population
  • Common in warm, humid climates
  • “spaghetti and meatball” hyphal pattern
  • Treat with selenium sulfide or ketoconazole shampoo. May need oral therapy or prophylactic treatment.
A

Pityriasis (Tinea) Versicolor

132
Q

 The most challenging type of tinea pedis
 T. rubrum most common
 Often not responsive to topical agents
 1-2 weeks of oral antifungal will eradicate infection
 Do not use gels or sprays

A

Hyperkeratotic Tinea

133
Q

 Intertriginous infections caused by dermatophytes that are not complicated by bacterial overgrowth
 Simple topical antifungal creams BID x 1-4 weeks usually sufficient

A

Dermatophytosis Simplex

134
Q

 Intertriginous infections caused by dermatophytes complicated by moisture and bacterial overgrowth
 Often mascerated
 Usually white but may be discolored due to certain bacteria
 Often malodorous
 Requires drying and antibacterial therapy as well as antifungal therapy

A

Dermatophytosis Complex

135
Q

T. mentagrophytes var. interdigitale
Vesicles caused by immune reaction
May culture the fluid or the roof of the blisters
 Vesicles often located in non-weightbearing areas
 Topical antifungal therapy is usually sufficient

A

Vesiculobullous Tinea Pedis

136
Q

 Chronic dermatophytosis
 Often unilateral-usually the dominant hand
 Usually associated with t. pedis
 Must eradicate co-existing skin and nail fungal infections to prevent recurrence

A

Tinea Manuum

137
Q
  • Topical antifungal BID x 4 weeks
  • Often requires oral antifungals
  • Usually annular with central clearing
  • Sometimes pustular
  • Sometimes geographic shapes
A

Tinea Corporis (Ringworm)

138
Q 
 Invasion of hair follicles produces inflammation
 Trychophyton species
 Treatment 
 Shaving or depilatories
 Antifungal shampoos or lotions
 Oral antifungals
A

Tinea Barbae

139
Q

Infection caused by Phaeoannellomyceswernickii
Pigmented scalylesions
Differential diagnosis?
Only topical antifungals needed
 Infection caused by Hortaea(Phaeoannellomyces) wernickii
 Pigmented scaly lesions
 Differential diagnosis?
 Topical antifungals and keratolytics after skin scraping

A

Tinea Nigra

140
Q

 Deep fungal infection of the follicle (t. rubrum)
 AKA: granuloma trychophyticum
 Commonly occurs on the lower leg in young women who shave or on lesions inappropriately treated with potent steroids
 Granulomatous papules with inflammation and scaling
 KOH pos, may need biopsy
 Will not respond to topical antifungals–use oral antifungals 4-6 weeks***

A

Majocchi Granuloma

141
Q

 Scale without inflammation on one hand (tinea manuum)
 Bilateral tinea pedis
 Nail involvement on one hand is pathognomonic
 Oral antifungals required

A

Two Foot One Hand

142
Q

 Most common orally (thrush) in young kids
 Antibiotic use and immunodeficiency are predisposing factors
 White creamy papules & plaques on mucosa
 Occlusion and moisture promotes it
 Satellite pustules are characteristic
 Common pediatric manifestation?

A

Candidiasis (Candidosis)

143
Q

Treatment for Oral Thrush

A

Gentian Violet

144
Q

Primary immune deficiency syndrome.
Recurring infections of paronychial areas, skin, mucosa.
Onset in infancy or childhood.

A

Mucocutaneous Candidiasis

145
Q 
Most occur in childhood
Followed by immunity
Poor morphologic specificity 
Maculopapular rashes
Morbilliform(measles like) rashes
Group name
A

Exanthems

146
Q

Parvovirus B19
“Slapped cheeks”*
Lace-like erythema on legsand buttocks
Usually in children (serious complications in adults)
May confirm serologically
Three stages
 2-4 days of bright red erythema on the cheeks
 Macular to morbilliformeruption on the extremities
 3d. to 3 wks of reticular rash
Treatment: reassurance, fluid, acetominophen

A

Erythema Infectiosum (Fifth Disease

147
Q 
Maculopapular or morbilliform eruption
RNA paramyxovirus
MMR vaccine failure or unvaccinated
 Respiratory transmission (76%)
 Incubation 10-14 days
 Prodrome of fever, malaise, and three C’s = cough, coryza, conjunctivitis
 Koplik spots precede rash
 2 week course
 Vitamin A suppl. for kids
A

Measles (Rubeola)

148
Q 
Initial high fever
Fever breaks as rash erupts*
1-5 mm macules and papules
Herpes virus 6 & 7
Lasts hours to days
Presents aged 6-18 months
Supportive therapy
A

Roseola (Exanthem Subitum)

149
Q 
 Rash may be mild
 Similar to roseola
 Facial erythema spreads to trunk involvement*
 1-2 mm raised lesions
 Cervical and occipital adenopathy
 Arthritis &amp; fever
 RNA togavirus
 Supportive therapy
A

Rubella

150
Q

 Coxsackie virus A16 & Enterovirus 71
 3-8 mm grey-white oval vesicles
 Involves mouth, hands, feet, and buttocks
 Fecal-oral route
 Epidemics common—very contagious
 Rare fatalities
 No treatment needed but isolation recommended
Aphthous erosions in oral cavity
 Oral mouthwash solutions available for symptom relief
Silver-grey vesicles on dorsal foot
Generally resolves in 7-10 days

A

Hand Foot and Mouth Disease

151
Q 
 Caused by varicellazostervirus
 Airborne transmission
 Children primarily
 Incubates 14-21 days
 Involves trunk, face, extremities, oral mucosa
 Headache, malaise, fever
 May cause scarring
 IgG antibodies confer immunity
Dew drop on rose petal
Diagnosis with Tzank smear
May isolate virus in culture
Symptomatic tx in kids
Oral antivirals in adults
A

Chicken Pox (Varicella)

152
Q

 Pink or flesh-colored papules with central dell
 Often linear
 Skin to skin contact or shared equipment
 Often associated with eczematous eruptions
 Molluscum contagiosumvirus (MCV) attacks keratinocytes
 In adults is considered a sexually transmitted disease
Treatment: tape strip the core, blistering compounds, or curettage. Cryotherapy or imiquimod may be used.
Self-limited in immunocompetent individuals but very contagious.
Facial lesions in adults suggest HIV infection
The hallmark is the intracytoplasmic inclusion body called “molluscum body”
The incidence is rising

A

Molluscum Contagiosum

153
Q 
 Primary infection at many locations
 Orofacial (coldsore) HSV-1
 Genital HSV-2
 Characterized by
 Neurovirulence
 Latency
 Reactivation
 May be triggered by stress, immune suppression, illness
 Highly contagious-spread by close personal contact
 Higher prevalence in blacks
Pustular vesicles
Crusted vesicles
Diagnosis by identification of the virus in tissue culture, polymerase chain reaction, or direct flourescent antigen
Treatment with antivirals
A

Herpes Simplex

154
Q 
AKA: Mat pox, wrestler’s herpes, scrumpox
Highly contagious
Contact sports
Herpes simplex 1
Latent virus causes recurrence
Acyclovir or Valtrex
A

Herpes Gladiatorum

155
Q

Herpes simplex infection of the digit

A

Herpetic Whitlow

156
Q
  • First line of therapy for onychomycosis
  • Direct comparative trials vs. itraconazole
  • demonstrates superiority for onychomycosis
  • Defer til after pregnancy
  • Not for lactation
  • Abnormal liver enzymes
  • Diarrhea
A

Terbinifine

157
Q
  • Take capsules with food to increase absorption
  • CI in pregrant
  • FDA warning on risk of CHF
  • Intense CYP 3A4 Inhibition
  • Numerous drug interactions
A

Itraconoazole

158
Q
  • Most commonly used for Cocci and Cryptococcal meningitis
  • Neprhotoxicity
  • Anemia
  • Antidote to rigors in Meperidine
A

Amphotericin B

159
Q 
Infestation of lice (pediculus humanus)
Live on hair but feed from skin
Transmitted through direct contact
Itching is common
Nits (eggs) are often easier to see than the louse
Treatment for head lice
Premethrin 1% or gamma benzene hexachloride shampoo/comb/rinse
Wash or bag all linens and clothing
A

Pediculosis

160
Q

Infestation by mite Sarcoptes scabiei
Creates burrows, lays eggs and poops
Intense itching follows immune recognition
Prolonged physical contact required for transfer
Only lives on humans
Look for linear burrows with black dot at the end
Eggs and feces
Eggs in burrow
Scabies often leads to excoriation

A

Scabies

161
Q

Crusted Scabies

A

In typical scabies approximately 20 mites infest the host.
In crusted scabies thousands of mites are present.
Scabies may cause hand dermatitis
Nodular Scabies possible

162
Q

Treatment for Scabies

A

Premethrin cream (more potent compound than that used for head lice)
Apply from the neck down everywhere and leave on overnight
Treat all family and intimate contacts
Wash all clothing and linens in hot water and dry in dryer or store for several days
Corticosteroids may help prolonged itching after treatment.
Oral ivermectin may be used (200ug/kg)

163
Q

Caused by L. brasiliensis or L. mexicana (sand fly)
Papulonodules progress to crusting, ulceration, scarring
Nontender and nonpruritic
DX with scraping, biopsy, or needle aspirate, look for amastigotes (parasite)
Ulcers are common in Leishmaniasis
Severe disfigurement is possible with mucosal spread of L. brasiliensis
Lack of treatment may lead to disfiguring scars

A

Cutaneous Leishmaniasis

164
Q

Treatment for Leishmaniasis

A

Systemic antimonial sodium stibogluconate (20mg/kg x 20 days
Add allopurinol
One study of fluconazole
Local heating, curettage, or topical meglumine antimoniate
Imiquimod topically may hasten healing
Severe scarring

165
Q

AKA creeping eruption
Dog or cat hookworm (Ancylostoma caninum or A. braziliense)
Acquired from wet sand or dirt contaminated with feces
Red, pruritic, serpiginous eruption
Treat with ivermectin 200 ug/kg in single oral dose or topical thiobendazole

A

Cutaneous Larva Migrans

166
Q

Earliest sign is painless subcutaneous swelling. May have a history of penetrating injury at site
Years later a subcutaneous nodule appears
Massive swelling with induration, skin rupture, and sinus tract formation
Characterized by formation of grains containing aggregates of causative organisms that discharge through multiple sinuses
Lymphadenopathy is unusual. Lymphedema can occur

A

Mycetoma (Madura Foot)

167
Q 
Rapid growing fungus
White, wooly colonies
Grayish brown w/ age
Simple long/short conidiophore
Single conidium/small groups
A

Pseudallescheria boydii which cause eucytoma

168
Q

treatment for madura foot

A 
Actinomycetoma
2 drugs in 5 week cycles (may repeat once or twice)
TMP-SMZ, dapsone, streptomycin, Amikacin, Rifampin
Eumycetoma
Voriconazole (Pseudallerscheria boydii)
Ketoconazole (Madurella mycetomatis)
Itraconazole
Amphotericin B
10 months!
169
Q

Most common vector borne disease in the United States
Vector: deer tick Ixodes scapularis
Etiology: gram negative spirochete Borrelia burgdorferi
36-48 hours of attachment required for transmission

A

Lyme Disease (Lyme Borreliosis)

170
Q

Lyme Disease Stages

A

Stage 1
Localized infection
Erythema migrans (expanding annular ring) 90%
Stage 2
Dissemination
Secondary rings of EM
Lethargy and fatigue, transient neurologic sx
Stage 3
Persistent infection over months to years
Migratory arthritis
Chronic neurologic symptoms

171
Q 
Often confused with t. pedis
Interdigital maceration and pruritis. 
May be cellulitis
Flouresces “coral red”
Corynebacterium minutissimum
A

Erythrasma

172
Q

Erythrasma tx

A

Oral erythromycin 1gm/day
May try macrolides
Topical treatment may be sufficient
Drying agents useful

173
Q

May appear on any weight bearing area while sitting
Erythematous papule that progresses to pustule, furuncle, or carbuncle
S. aureus and P. aeruginosa
Try local compresses
Mupirocin for staph
Systemic antibiotics rarely indicated-no evidence of improvement in pseudomonal folliculitis

A

Hot Tub Dermatitis (Folliculitis)

174
Q 
Progression of basic folliculitis
Commonly known as “boils”
Groups of furuncles form carbuncles
Compresses often sufficient
Carbuncles require surgical drainage
A

Furuncles and Carbuncles

175
Q

Typically found in children on face and upper extremity
May also be found in adults on the foot and leg.
Very superficial, highly contagious
Classic golden crusts beginning as vesicles
May develop creamy drainage.
Group A strep and S. aureus (including MRSA) are causative

tx

A

Impetigo

Topical mupirocin
Oral antibiotics rarely needed: cover staph and strep

176
Q

 Uncommon in LE but may follow surgery
 Common in infants and young children
 Fever, tenderness, large flaccid bullae
 Get wound cultures, biopsy definitive
 Septicemia may result but uncommon
 Blood cultures may be required-S. aureus
 Fluid and electrolyte management
 Parenteral antibiotics aimed at eradicating the source of the infection-cloxacillin
 Healing usually complete in 5-7 days

A

Staphylococcal Scalded Skin Syndrome

177
Q

Occurs more frequently on the LE at sites of excoriation, insect bites, dermatitis
Deeper lesion than Impetigo, involving dermis, and may cause scarring
Punched out ulcers with greenish/yellow crusts develop from pustules
Streptococci most common, pseudomonas found with Ecthyma gangrenosum
Treatment same as Impetigo

A

Ecthyma

178
Q 
Cellulitis involving lymphatic blockage
Typically on the face but also on LE
Sharply demarcated geographic cellulitis with a raised border
Fever, pain, leukocytosis common
Tough to culture
Group A streptococcus
Parenteral or oral penicillin
A

Erysepilas

179
Q 
Severe, constant pain
Bullae
Skin necrosis or ecchymosis
Gas in the soft tissues
Edema extending beyond erythema
Cutaneous anesthesia
Systemic toxicity
Rapid spread
Acute, severe, and rapidly progressive disease affecting superficial and deep fascia
Easy dissection of fascial planes
Follows trauma or surgery
High mortality rate

tx

A

necrotizing fasciitis

Make initial smaller incision, proceed with aggressive surgical debridement if
Necrosis of tissues is seen
No response to antibiotics
Profound toxicity, fever, hypotension
Easy planal dissection
The presence of gas
180
Q

 Rapidly progressive
 Most commonly follows trauma
 Acute onset 6 hours to 3 days post injury
 Pain and toxemia are hallmarks
 Fever, hypotension and tachycardia common
 Foul smelling watery brown/red drainage
 Gas and crepitus in tissues, in planes
 Clostridium species (most common is perfringens) are infecting organisms
 Positive blood cultures not common
Air in soft tissues

A

Clostridial Myonecrosis (Gas Gangrene)

181
Q

Clostridial Myonecrosis (Gas Gangrene) tx

A 
Prompt I & D and debridement
Excise necrotic muscle
Decompression of fascial compartments
Penicillin G 24 million U/day plus Clindamycin 600-900mg q 8h
Carbapenems empirically
182
Q

VRE: Vancomycin Resistant Enteroccus antibiotic

A 
No cephalosporins are effective
Linezolid
Tigecycline
Daptomycin
Quinupristin/dalfopristin
183
Q

drugs for severe diabetic infection

A 
Beta-lactamase inhibitor compounds
– Ampicillin/sulbactam (Unasyn®) ±a quinolone
– Ticarcillin/clavulanic acid (Timentin®)
– Piperacillin/tazobactam (Zosyn®)
Clindamycin + a gram-negative agent
Ertapenem
Broad-spectrum quinolones
Linezolid
184
Q

4 kinds of Immunologic Responses

A

Type I: immediate hypersensitivity
IgE antibodies, histamines & kinins, urticaria
Type II: cytotoxic hypersensitivity
IgG or IgM, platelet destruction, purpura
Type III: immune complex sensitivity
Antibody complexes with complement causing vasculitis
Type IV: cell‐mediated reactions
Antigen reacts with Langerhans’ cells, macrophages, T lymphocytes, contact dermatitis

185
Q 
 Wheals (evanescent edematous papules and plaques)  Pruritic!
 Acute vs chronic (>6 weeks)
 Acute
 IgE‐dependent or complement mediated
 Large wheals often associated with angioedema
 Often atopic background
 More common in children
 Chronic
 Rarely IgE‐dependent, may be autoimmune
 Cause unknown in 80%
 More common in adults and women
 Diagnosis
 Clinical picture obvious
 Dermographism
A

Urticaria and Angioedema

186
Q

Panniculitis
Red, painful subcutaneous nodules
Shins, extensor surfaces of UE, dorsum of feet
Peak incidence 3rddecade
Fever, malaise, arthralgia (50%) esp. ankles
Self‐limited, 4‐6 wk duration
Caused by drugs, infections, inflammatory dz

tx

A

erythema nodosum

 Bed rest/compression
 ASA, NSAIDS
 Steroids only with known etiology and no infection

187
Q

Self‐limiting (1 mo)
Target lesions
Symmetrical, round, red or purple
Caused by infections and drugs
Treat by removing drug and giving steroids
Severe variant = Stevens‐Johnson Syndrome

A

erythema multiforme

188
Q

Mild, exfoliative changes to hands & feet
No erythema
Rapid healing when drug has been eliminated

A

acroexfoliative dermatitis

189
Q 
Acute onset with rapid progression
Reaction to drugs and disease
Exfoliation with erythematous base
All meds must be stopped
Steroids begun ASAP
E.E. Syndrome is full body and can be life‐threatening
A

Exfoliative Erythroderma

190
Q

AKA Erythema Multiforme Major
Mucocutaneous tenderness and erythema followed by necrosis and sloughing
Potential for severe morbidity and death
Immune complex mediated hypersensitivity
Etiology: viral infections, drugs, malignancies
Treat as severe burn
Toxic epidermal necrolysis (Lyell’s Disease) is most severe variant
Nikolsky’s sign common (skin wrinkles, slides, separates with slight pressure

A

SJS

191
Q

Arsenic & lithium well known causes
Multiple, small, punctate hyperkeratoses on the palms and soles
May convert to SCC**
May treat with sharp debridement, cryotherapy, electrodessication

A

Drug‐induced Plantar Keratoses

192
Q

Pruritic reaction
Vesicles and papules
Crusting and scaling if drug use continues
Stop drug!

A

Eczematous Drug Reaction

193
Q

Well‐defined, sharply marginated lesion
Occurs in the same location each time the patient is exposed to the sensitizing medication
Dermatitis develops within minutes of exposure
Remove drug and treat itching

A

fixed drug reaction

194
Q

Caused by ultraviolet light exposure after taking certain medications
Sunburn‐like erythema, papules, vesicles are possible
Present only in sun exposed areas
Prevent sun exposure and/or stop drug exposure
Common photosensitizers
Antibiotics
NSAIDS
Diuretics
Hypoglycemics
Antifungals

A

Photosensitivity Reaction

195
Q

Benign, inflammatory, granulomatous condition of the dermis of unknown origin
Occurs in all age groups but most common in young women

A

Granuloma Annulare

196
Q

 Typical red macule/papule/nodule on leg* or foot-grows, especially pre-tibial
 Ulcer results with purulent base and overhanging violaceous border
Immune system dysregulation
Inflammatory bowel disease*
Classic-legs
Atypical-hands
 Ulcers tend to be deep

A

Pyoderma Gangrenosum

197
Q

Pyoderma Gangrosum tx

A

Oral steroids
Immunosuppressive agents
Typical ulcer care
Heal slow and when good and ready with and pigment changes

198
Q

 Soles and to a lesser degree the palms become hyperkeratotic
 Hits pressure areas of the soles first
 Onset in the 40s
 obese
 Painful fissures
 Tx with low dose etretinate moisturizers, keratolytics and debridement

A

KERATODERMA CLIMACTERICUM (Haxthausen’s Disease)

199
Q 
 Systemic condition affecting any organ
-lungs #1
-lymph nodes/chest cavity #2
 noncaseating epithelioid granulomas form in tissue and will compromise the organ 
African Americans (especially women) 
Erythema Nodosum
-lower legs
-most significant cutaneous finding with sarcoidosis
-acute
-self limiting
-tx often not required
A

sarcoid

200
Q 
Proximal muscle weakness-progressive
Elevated muscle enzymes
Abnormal EKG finding
Abnormal muscle biopsy
Skin findings
* Major diagnostic criteria
Gottron’s papules
Heliotrope Rash (peri-orbital violaceous discoloration) 
Peri-ungual Telangectasias
 Rash is pruritic and in exposed areas
Pathognomonicfor DM
>40 yo adults and 5-10 for children
Females 2X more affected
Association with Vasculitis/CVD/malignancy
Poikiloderma
Mottled pigmentation especially on the neck from sun exposure
A

Dermatomyosis

201
Q 
Red or violaceous papules over the knuckles (mcpj, pipj and dipjs)
Can look like lichen planus lesions
Can also be over elbows, knees and feet
Raised, smooth and flat topped
Pathognomonicfor DM
With Dermatomyositis
A

Gottron’s papules

202
Q

dermatomyositis tx

A

oral steroids

avoid sun

203
Q

Reddish macule/papule evolves to a pustule that to a keratotic plaque
Toes and soles
Reiters

A

Keratoderma blennorrhagicum

204
Q

Member of the genetic blistering diseases
Enzyme deficiency leads to lack of normal collagen and blisters form, mainly in areas of trauma
Improves with aging/outgrow ?
 Nikolsky sign
 Asboe-Hansen sign
 Treatment is wound care based and infection prevention and management

A

EPIDERMOLYSIS BULLOSA SIMPLEX (EBS)

205
Q

 ESB sub type located on palms and soles
 Exacerbated with heat and increased sweating
 Slow healing and thick walled bullae
 Tx is avoiding trauma or friction
 Avoid de-roofing blisters

A

WEBER-COCKAYNE SYNDROME

206
Q

Autoimmune blistering diseases
Autoantibodies attack the keratinocyte cell surface
Keratinocytes can no longer adhere to each other
Severe, life-threatening blistering results
Mucosa especially affected
All races
Male=female
Onset 50+ yo
Nikolsky Sign
Asboe-Hansen sign

A

Pemphigus

207
Q 
Inherited keratinization disorder
abnormal epidermal differentiation or metabolism 
Fine scales
Scales protrude and make skin rough
Extensor surfaces
A

ICHTHYOSIS

208
Q 
Tiny, uniform papules
Makes skin very rough
Adolescence
Upper arms
Dry, chapped skin
Very common, 40% +
Lacti-care 
retinoids
A

KERATOSIS PILARIS

209
Q

 Severe thickening of palms and soles
 Hereditary
 Associated fissures
 Dystrophic nails

A

PALMARPLANTARKERATODERMA

210
Q 
 Inherited papulosquamous disorder
 Papules are pink with waxy scale/predominant on seborrhoeic areas 
 Pits on palms and soles
 May see plaques/crusting/infection
 Reduce heat, UV and humidity
 Dermabrasion 
“V” nick at end of nail
Long bands of white and red
A

DARIER’S DISEASE - keratosis follicularis

211
Q 
Inherited
 diagnostic criteria
Café-au-lait macules
Neurofibromas
Axillary/inguinal freckles (Crowe’s Sign)
Lisch nodules
Bi-lateral optic nerve gliomas
1stdegree family member with Dx
A

NEUROFIBROMATOSIS - von recklinghausen’s disease

212
Q

melanocytic hamartomas, clear yellow to brown, well defined, dome shaped elevations projecting from the surface of the iris
NF

A

Lisch Nodules

213
Q

– P revalence/ I ncidence: common in the foot and ankle
– Description: well circumscribed, soft or indurated based on duration–cystic consistency, fluid filled, freely movable in sub-q tissue “Weak spot on an inner tube” associated with joint or synovial sheath
– Location: dorsum of foot; often attached to extensor tendon or joint capsule
– Tissue Origin: myxoid degeneration of the connective tissue of either tendon sheath or pericapsular tissue
– Clinical Presentation/ Diagnosis: asymptomatic or pain with rubbing in shoe gear; transillumnation, aspiration
Treatment: marginal local excision; 70% recurrence rate
• aspiration
•Goal surgically, is to excise without breaking it

A

ganglion cyst

214
Q

– Prevalence/ Incidence: most common STT in the body; obese middle aged
– Description: soft, movable asymptomatic mass
•Cutaneous lipoma (superficial): most common; well circumscribed; static
•Deep-seated lipoma: rare; margins difficult to identify; not static
– Location: most often about heel
– Tissue Origin: globule of fat separated by a thin fibrous capsule
– Clinical Presentation/ Diagnosis: asymptomatic
– Treatment: extracapsular marginal excision

A

Lipoma

215
Q

– Prevalence/ Incidence: relatively rare-Autosomaldominant
– Description: solitary or multiple
• If multiple: von Recklinghausen’s disease; malignant potential; café au lait spots
• May be associated with fibrous dysplasia and bowing deformities
– Location: cutaneous arising from sensory or autonomic fibers; or deep from major nerve structures
– Tissue Origin: spindle cells of peripheral nerves
– Clinical Presentation/ Diagnosis: soft, non-tender; if painful then needs treatment
– Treatment: cutaneous form is easily excised; extra capsular marginal local excision - deeper may be well invested in the nerve (may be difficult to excise)
 expect loss of neurological functionfibrous dysplasia
Neurofibromatosis- café au lait spots

A

Neurofibroma

216
Q

–Prevalence/ Incidence: middle aged
–Description: involves a major nerve; well encapsulated fusiform nodule which arises from within the nerve
–Location: varies
–Tissue Origin: peripheral nerve sheath
–Clinical Presentation/ Diagnosis: tender, palpable nodule; neurogenic pain/paresthesias when compressed or traumatized-LOOK FOR TINNELS
–Treatment: marginal local excision; curative
-Think ear canal for these too

A

Neurilemmoma (schwannoma)

217
Q

– Prevalence/ Incidence: childhood/adolescence
– Description:
•Capillary hemangiomas: masses of capillaries; most common in the foot
•Cavernous hemangiomas: large, dilated, tortuous, endothelial cavities
– Location: in skin, sub-q tissue, fascia, muscle
– Tissue Origin: blood vessel
– Clinical Presentation/ Diagnosis:
•superficial type: painless with bluish color, overlying skin is warm
•Deeper type: painful; increasing pain with exertion
– Treatment: symptomatic tx; compression therapy, surgical excision is difficult because of no true psuedocapsule; high local recurrence rate
•Pre-op angiogram
•MRI with contrast

A

Hemangioma

218
Q

– Prevalence/ Incidence: F:M (3:1), 20-40 y/o
– Description: vascular tumors
– Location: subungual
– Tissue Origin: blood vessel
– Clinical Presentation/ Diagnosis: bright red to bluish discoloration beneath nail bed; painful-often throbbing, worsens with cold exposure and direct pressure; radiographs may reveal bony erosion
– Treatment: marginal excision; need to avulse nail, recurrence is unusual

A

Glomus Tumor

219
Q

– Prevalence/ Incidence: 2x more likely in females; middle aged
– Description: solitary, encapsulated mass; freely mobile
– Location: lower legs are most common site
– Tissue Origin: smooth muscle layers of blood vessels
– Clinical Presentation/ Diagnosis:painful, increase in size of the swelling with physical activity of the involved part
– Treatment: marginal local excision

A

Angioleiomyoma

220
Q

– Prevalence/ Incidence: slightly higher in females, 30-50 yo, malignancy rare but possible
– Description: locally aggressive-can erode adjacent bone
• Nodular: Extracapsular tenosynovial giant cell tumor; most common
• Diffuse: villous, pigmented, rare and looks just like PVNS
– Location:
• Nodular – Typically flexor surfaces of hand
• Diffuse – About large joints like knee and ankle
– Tissue Origin: synovial membrane about tendon sheaths and joints;
– Clinical Presentation/ Diagnosis:
• Extracapsular tenosynovial giant cell tumor
– Small, painless mass, slowly growing, possible hx of trauma
• Diffuse, villous, pigmented
– Painful, swelling, limitation of ROM of affected joint, palpable mass about joint
– Joint aspirate: serosanguinous brownish fluid
– Degenerative changes on radiographs; get an MRI

A

Giant cell tumor of the tendon sheath

221
Q

– Prevalence/ Incidence: young adults ; M>F70% found in lower extremity
– Description: large, slow growing and deep seated, painful and often with defined margins so may be misdiagnosed as benign, 2-5 years to Dx. Rare
– Location: about joints, especially the knee..deep in tissue
– Tissue Origin: mesenchymal or CT-not necessarily synovial
– Clinical Presentation/ Diagnosis: pain, tenderness and swelling; calcifications on X-ray
– Treatment: radical resection, amputation, radiation, chemotherapy,
– Prognosis: High recurrence with 35-75% 5 year survival rate

A

Synovial Sarcomas

222
Q

– Prevalence/ Incidence: most common, males 50-70 (except angiomatoid which are more prevalent in adolescents)
•5 year survival rate is 73% if location is distal to the knee
– Description: types: pleomorphic*, myxoid, giant cell, inflammatory, angiomatoid
– Location: mostly LE especially the thigh
– Tissue Origin: fibrous connective tissue
– Clinical Presentation/ Diagnosis: painless mass or lump
– Treatment: wide excision
– Prognosis: 5 year survival rate excellent if tumor is

A

Malignant Fibrous Histiocytoma

223
Q

– P revalence/ Incidence: rare, males 35-55
– Description: metastatic potential
– Location: LE especially around the knee
– Tissue Origin: fibroblasts and collagen
– Clinical Presentation/ Diagnosis: painless, deep mass
– Treatment: amputation; if lesion is located deep plantar compartment then BK
– Prognosis: 40-60% 5 year survival rate

A

Fibrosarcoma

224
Q

– Prevalence/ Incidence: most common sarcoma in adults , males >females, rare in foot but common in lower extremity
– Location: limbs and retroperitoneum
– Tissue Origin: fat cells
– Clinical Presentation/ Diagnosis: palpable mass, slowly enlarging and painless, may become very large, may ulcerate
– Treatment: wide excision, amputation
– Prognosis:

A

Liposarcoma

225
Q

bone tumors by location

A 
diaphysis
osteoid osteoma
chondromyxoid fibroma
ewing
fibrous dysplasia
fibrosarcoma

metaphysis
osteosarcoma
osteochondroma
enchondroma

epiphysis
chondroblastoma

GCT - E,M
Cysts - E,M,D

226
Q

buttressing of bone, form many layers of periosteum

A

Pagets

227
Q

bone tumors that can convert to malignant

A

Giant cell

osteochondroma

228
Q 
‡Pre-teen male 3:1 male to female
‡Pain at night relieved by ASA 
‡Nidus-must remove
‡Very Vascular
‡May see swelling and erythema
‡Tiny prostaglandin factory
A

OSTEOID OSTEOMA

229
Q

‡Benign
‡Young adult, usually female
‡Oval & expansile
‡Phalanges
‡Multiple lesions (enchondromatosis) is Ollier’s Disease
‡Multiple lesions + hemangiomatosis is Maffucci’s Disease
‡Look like grapes

A

ENCHONDROMA

230
Q

‡Young adult male
‡Can appear destructive
‡Expansile
‡Frequently involves the leg (70%)

A

CHONDROMYXOID FIBROMA

231
Q 
‡Male child 
‡Most common bone tumor..35% of all
‡Miniature physeal region growing away from the joint
‡Malignant transformation is possible
‡ Mushroom cloud appearance
A

OSTEOCHONDROMA

232
Q 
‡Malignant and 
‡Adolescent males
‡Knee region 60% 
‡#2 most common primary malignant bone tumor after multiple myeloma
‡Sunburst pattern
‡Codman’s Triangle
‡Hair on end
‡Destructive
A

OSTEOGENIC SARCOMA

233
Q 
‡Over 40 male 
‡Spotty calcifications “popcorn” or “salt and pepper”
‡Knee is a common locale
‡Result of transformation
‡Can have associated soft tissue growth
A

CHONDROSARCOMA

234
Q

‡Young males avg. 12yo , usually white
‡“Onion skin”
‡Pain/mass/”sick” (Think sick kids)

A

EWING’S SARCOMA

235
Q

‡Young male
‡Grows during growth
‡Won’t expand
‡Not destructive but can see pathological fracture “fallen fragment sign

A

SOLITARY BONE CYST(simple or unicameral)

236
Q 
‡Young person
‡Long bones
‡Large/expansile
‡“soap bubble”
‡Easy to confuse with malignant
A

ANEURYSMAL BONE CYST

237
Q 
‡Preadolescent
‡Bone replaced by fibrous tissue
‡Long bones
‡“ground glass”matrix 
‡No pain unless pathological fracture
‡Bowing deformities
‡Can convert
‡Can be associated with ALBRIGHT’S DISEASE
A

FIBROUS DYSPLASIA

238
Q 
‡Quasi-malignant 
‡Middle-age female
‡Knee region 
‡Large, expansile, moth-eaten
‡“soap bubble”
A

GIANT CELL TUMOR

239
Q
  • Deformed bones causing bone pain
  • Elevated Alk phos
  • Viral/genetic causes
A

pagets

240
Q

LBP concerns for cancer

A
  • Age >50
  • Prior cancer history
  • Unexplained weight loss.
  • Pain lasting more than one month often intractable and unrelieved with rest (note: most back pain patients feel better with exercise or stretching).
  • No improvement following conservative therapy.
241
Q

nerve sens and motor in LE

A 
– DTR’s Achilles – S1, Patellar – L4
– Sensory: 
• L1, L2, L3 – from lateral to medial along anterior thigh
• L4 – anterior leg
• L5 - big toe
• S1 – lateral foot, posterior leg
– Motor: 
• Extensor hallicus longus L5 (extend big toe)
• Anterior tibialis L4 (walk on heels)
• Gastrocnemius S1 (walk on toes)
242
Q

-Paramedian Herniations

A
  • Male>Female
  • 30’s-40’s
  • L5-S1 most common
  • Pain worse with increasing intrathecal pressure
243
Q

“Which is the most common type ( or location ) of a HNP?” (Herniated disc)

A

Posterolateral herniation is the most common overall ( ie L4-L5 level )

244
Q

bilateral extremity sensory loss, loss of rectal sphincter tone, loss of bowel/bladder function, saddle numbness with severe lower extremity motor weakness.
• Treatment: EMERGENT surgical decompression

A

cauda equina syndrome

245
Q

Connective tissue and bone overgrowth reducing the size of the vertebral foramina
• The main cause is the degeneration and remodeling caused by the normal aging process / arthritis.
• Most common in people over age 60.
• Chronically progressive
• Often bilateral and poorly localized
• Pain radiates to buttocks, thighs, legs
• Worsened with extension (stand, walk)
• Improves with flexion (sit, stoop)
• Stopping ambulation may not improve symptoms, unlike vascular claudication.

A

spinal stenosis

246
Q 
• Chronically progressive
• Other risk factors/vascular disease:
– Smoking, DM, hyperlipidemia, FMHX.
• Uni- or bilateral, poorly localized
• Worse with any LE exertion
• Stopping ambulation will improve
• Physical exam reveals diminished pulses and capillary refill with cyanotic cool extremities.
A

PVD Claudication

247
Q
  • Term used to describe osteoarthritis around the vertebra
  • Also referred to as a bone spur
  • A specific way of describing vertebral osteoarthiritis
A

Spondylosis

248
Q

A separation of the pars interarticularis of the vertebral arch (Scottie dog collar shows defect)

A

Spondylolysis

249
Q

Slippage of one vertebral body onto the next.
• Bilateral spondylolysis must occur first in order for vertebral body slippage to occur.
• Most common at L5/S1.
• Associated with hyperextension injuries.
• Often seen in football lineman and gymnastic participants.
• Pain is often worse with extension and compressive loads
• Grade I – 25% displacement.
• Grade II – 50 % displacement.
• Grade III – 75 % displacement.
• Grade IV 100% displacement.

A

Spondylolithesis

250
Q

• Bursa or Tendon Inflammation
– Most common shoulder diagnosis
– Fluid sac and adjacent tendons
• Causes
– Injury, rheumatic condition, infection, repetitive overuse
• SSX
– Posterior lateral shoulder pain, tenderness to palpation at the insertion of the tendon or in the muscle belly
– worse with overhead motion and abduction
• Treatment
– RICE, NSAIDS, PT/OMT, steroid injection

A

Subacromial Bursitis and Rotator Cuff Tendonitis

251
Q

• Impingement of the rotator cuff tendons between the humerus and acromion
• Related to injury of the Shoulder ligaments, weak scapular stabalizers,tendonitis,or altered acromion
• Treatment
– RICE, NSAIDS, PT/OMT, steroid injection

A

Impingement Syndrome

252
Q
  • Inflammation of the bicep tendon
  • SSX: anterior shoulder pain, tenderness at the bicipital groove. Can lead to Bicep tendon rupture
  • Tx: RICE, NSAIDS, PT/OMT, care with injection
A

Bicep Tendonitis

253
Q 
• “Frozen Shoulder”
– Inflammation of the rotator cuff leading to calcific tendonitis
• Causes:
– Prolonged shoulder immobility
– Repetitive overuse
– Trauma followed by disuse
• SSX
– Severally decreased ROM, stiffness, pain
– Gradual onset
– Gradual relief over years
• Treatment
– Physical:PT/OMT
– Medical: Steroid injections, anti-inflammatory
– Surgery
A

Adhesive Capsulitis

254
Q 
• Tear 
– Tendon separates from bone
• Causes
– Overuse
– Instability
– Microtrauma
• SSX
– Pain into deltoid
– Often at night
– Weakness
• TX
– PT, NSAID, Steroid injection, surgery
– Tears requiring surgery are less common
A

Rotator Cuff Tear

255
Q 
• AC Joint Separation
• Causes
– Direct trauma
– FOOSH
• SSX
– Pain!
• Treatment 
– Ice, NSAID
– Rest (Sling)
– PT
– Surgery (grade dependent)
A

Shoulder Separation

256
Q 
• Displaced humeral head 
– With regard to the scapula 
• Anterior
– Humerus anterior to scapula
• Posterior
– 5% of dislocations
• Causes
– Fall, sports injury
• SSX
– Pain
– Arm held at side
– Anatomy changes
• Diagnosis:  Positive Apprehension Test
• Treatment
– Reduction, rest
– Strengthening, surgery
A

Shoulder Dislocation

257
Q

Tennis elbow)

A

Lateral Epicondylitis

258
Q
  • Most common dislocated joint in children, adults second only to shoulder and finger
  • Typically occurs after a fall on an outstretched hand. More than 80% are posterior. Lateral collateral ligament always disrupted. Can have concomitant fx of the radial head/coronoid
  • SSX: pain, swelling, inability to bend the elbow
A

dislocation of elbow

259
Q

Fall on outstretched Hand
• SSX: Pain and edema are present at the lateral elbow with tenderness over the radial head.
• Tx: type 1 sling/splint with early mobilization. Type 2 depends on the severity of displacement. Type 3 is ORIF

A

Radial Head Fracture

260
Q
  • Pain and parasthesias of the first 3.5 digits.
  • Can also have pain in the hand and forearm radially.
  • Often worse at night or with provocative positioning
  • May feel clumsy or drop objects
A

CTS

261
Q
  • One of the most common fx in adults
  • Collies Fx: distal radius displaces dorsally. May also involve fx of the ulnar styloid process
  • Smith Fx: Distal radius displaces volar
  • Usually involves fall on outstretched hand
  • SSX: pain, edema, deformity of distal radius
  • Tx: reduction with splinting for most closed fx. Than a short arm cast
A

Distal Radius Fx

262
Q

a nodular thickening and contraction of the palmar fascia
• The disease has a dominant genetic component, northern European descent
• SSX: one or more painless nodules near the distal palmar crease. Evolves to contracture
• Tx: Self OMT, splinting to delay progression. Surgery of cords. May recur. Requires OT after de Quervain Tenosynovitis
• Etiology: swelling or stenosis of the sheath that surrounds the abductor pollicis longus and extensor pollicis brevis tendons at the wrist.

A

Dupuytren’s Contracture

263
Q

For displaced femoral neck use

A

bipolar hemiarthroplasty

264
Q

Sub-trochanteric Hip FX

A

Use gamma IM nails

265
Q
  • May occur with or without femur fracture
  • Ring fracture
  • Very painful!
  • Self-limiting
  • Surgery rare for isolated injury
  • Treatment
  • Weightbearing as tolerated with walker
  • Pain management
  • Narcotics
  • Analgesics
A

pubic rami fracture

266
Q
  • Temporary interruption of blood to the proximal epiphysis.
  • Occurs between ages 3-12.
  • Affects boys 3-5x more often than girls.
  • May present with a limp and referred pain to thigh or knee.
  • Gradual onset groin, hip, or knee pain
  • Decreased abduction of hip
  • Decreased hip internal rotation
  • Trendelenberg gait
A

legg calve perthes

267
Q
  • Femoral capital epiphysis displaces off the femoral neck.
  • “Ice cream scoop slipping off of cone.”
  • Occurs between ages 12-15 years of age.
  • More common in males than females.
  • Occurs in overweight adolescents.
  • Presents as pain,that may be referred to the thigh or knee.
  • Slow onset of limp.
  • 20 - 40% bilateral within 18 months
A

Slipped Capital Femoral Epiphysis

268
Q

Slipped Capital Femoral Epiphysis tx

A
  • Surgical fixation
  • Protected weightbearing
  • Physiotherapy
269
Q
  • Typically unilateral
  • Boys > Girls
  • Age: 3 – 10 years old
  • Viral v. Antecedent infection
  • Signs & Symptoms
  • Pain
  • Antalgic gait
  • Hip pain w/PROM
  • Knee pain
A

pediatric hip synovitis

no antibiotics

270
Q

grades of knee sprains

A
  • Grade I – tear of few fibers, no instability.
  • Grade II – disruption of more fibers (25-50%) with some loss of function and some instability.
  • Grade III – complete disruption (50 -100%) of ligament with gross instability.
271
Q 
• Mal-alignment of patella causing abnormal tracking in femoral groove.
AKA Chondromalacia Patella
Causes
• Patella position
• Patella alta, patella baja, genu varum, genu valgum
• Wide Q-angle
• Muscle tightness
• Hamstrings v. Quads
• Muscle Imbalance 
• Weak VMO
A

Patellofemoral Syndrome

272
Q
  • Swelling
  • Hot
  • +/- Pain
  • Decreased ROM
  • Suprapatellar
  • Infrapatellar
  • Prepatellar
A

knee bursitis

273
Q
  • Inflammatory process that leads to tendon degeneration.
  • May occur from a single episode or more commonly from repetitive movement.
  • Stages
  • I – Pain after activity.
  • II – Pain during and after activity.
  • III – Pain during activity and prolonged after activity.
  • IV – Tendon ruptures.
A

Patellar tendinitis (Jumper’s Knee)

274
Q
  • Common insertion of muscles Sartorious, Gracilis, & Semitendinous into tibia.
  • Results from genu valgum, weak VMO, and running on uneven slope for distance.
  • Treatment
  • Correction of leg and foot alignment.
  • NSAID’s
  • Steroid Injection
  • RICE
  • Modalities
  • Changing running surfaces.
A

Pes Anserine Tendinitis/Bursitis

275
Q
  • Apophysitis of inferior pole of the patella.
  • Similar to Osgood-Schlatter.
  • “Growing pains”
A

Sinding Larsen-Johansson Syndrome

276
Q
  • AKA Tibia varum
  • Disorder of posterior tibial physis
  • Most common
  • Males
  • African American
  • Obese
  • Infantile
  • Usually bilateral
  • Internal tibial torsion
  • Adolescent
  • Unilateral
  • Less severe
A

Blount’s Disease

277
Q

Malar Rash
Discoid Rash
Photosensitivity
Oral Ulcers – Observed
Arthritis
Serositis: Pleurisy – pain, rub or effusion pericarditis by EKG or rub or effusion
Renal disease: proteinuria > 0.5 gm/day or cellular casts
Neurologic disease: seizures or psychosis
Hematologic disorder: hemolytic anemia or leukopenia

A

SLE

278
Q 
Discrete plaques
Usually in sun exposed areas
Usually erythematous c induration at periphery
Central atrophic scarring
Irreversible alopecia
A

discoid lupus

279
Q

SLE therapy

A

NSAIDs
Corticosteroids
Hydroxychloroquine*
Immunosuppressives: azathioprine, cyclophosphamide, mycophenolic acid
Monoclonal antibodies including rituxamub and belimumab

280
Q

SLE summary

A

Prototype of autoimmune disease
Can involve virtually every organ
Remarkably variable course and prognosis
Should be ANA +
Anti-dS DNA most specific autoantibody
Arthritis/arthralgias most common manifestation
DPGN most devastating manifestation
Infection is probably major cause of death
Increased progression of atherosclerosis

281
Q 
Pain and stiffness- usually proximal and symmetric
Gel phenomenon
Fever
Wt. loss
Fatigue
Depression
Symptoms either very sudden or very gradual onset 
Muscle tenderness
Synovitis especially hands and wrists 
PMR: Notably Absent Findings 
Muscle weakness
Muscle atrophy
Abnormal EMG
Elevated CPK
A

PMR

282
Q

PMR labs

A

Elevated ESR*
Elevated CRP
Anemia: usually NCNC
Mildly elevated LFTs

283
Q

PMR: Prognosis

A

Average length of disease said to be 3 years
Exacerbations common as steroid dose tapered
Relapse may occur after long periods of inactivity
Major change in our impression- length of illness

284
Q

PMR Therapy

A

Low dose corticosteroids*

285
Q 
Age of onset > 50
New onset H/A
ESR > 50mm by Westergren
TA abnormality either decreased pulse or tenderness
Abnormal TA biopsy showing vasculitis
Elevated ESR, CRP
Elevated IL- 6 levels
Anemia- usually NCNC
Decreased albumin
Mild abnormalities in LFTs
ANA, RF neg except must consider age
A

temporal arteritis

286
Q

TA- Biopsy

A

Try to get the biopsy within 14 days of therapy but do not delay Rx if Dx strongly suspected
Get adequate biopsy- 2cm
Do transverse sections
Surgical risk very low

287
Q

TA Rx-

A

Prognosis is excellent c therapy
Corticosteroids are mainstay of Rx
Many patients can get off steroids in 2-3 years but not all
Usefullness of following ESR is ?
Need to watch for long term complications even when off steroids including thoracic or abdominal aneurysm

288
Q

Classification of Scleroderma

A 
SSc
•	dSSc
•	lSSc
•	Overlap syndromes
Localized
•	Morhpea
•	Localized linear
Chemically induced

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