Boards Part 2 (2of 2) Flashcards
• 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
Charcot
Main thing in charcot
Severe PN
etiology of charcot
• 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
clinical presentation of charcot
- 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
how to distinguish between charcot and OM
•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
Eichenholtz radiographic classification of charcot
–Developmental/Acute
•Soft tissue swelling,, osteochondral fragmentation, joint fragmentation, joint dislocation
–Coalescent
•Reduced swelling, bone callus proliferation, fracture consolidation
–Reconstructive
• Bony ankylosis, hypertrophic proliferation
Sanders/Frykberg Classification
I. MTPjs II. TMT III. NC, TN, CC Joints IV. Ankle Joint V. Calcaneus
Goal and treatment of charcot
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
3 groups of treatment for charcot
Phyiscal T: offlad, cryo, bone st
med: bisph, calcitonin
surg: TAL, exostectomy, reconstruct
total reconstruction of charcot is to restore what angles
• Restore lateral talo-first metatarsal angle and Calcaneal inclination angle
genesis of atherosclerosis
Response to Injury
Lipid accumulation
Chronic inflammatory process in the artery
Balance between plaque formation/regression & arterial enlargement
Unstable plaque formation
prevention of atherosclerosis
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)
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
Lower limb ischemia
Peripheral Arterial Occlusive Disease
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
Lower limb ischemia
Acute Limb Ischemia
Primary Causes Secondary Causes
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
5P’s of acute limb ischemia
Pulselessness Paralysis Paresthesia Pain Pallor
what to do when signs of ischemia are present
When these signs are present, do not delay, tissue loss is likely
Compartment syndrome, gangrene, muscle and nerve damage
tx of ischemic limb
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
venous anatomy le
oDeep Venous System • Named with corresponding arteries oSuperficial Venous System • Greater Saphenous • Lesser Saphenous • Tributaries oPerforating or Communicating oValves
Three basic mechanisms that lead to a raised AVP (ambulatory venous pressure) and the signs and symptoms of CVI (chronic venous insufficiency)
- Muscle pump dysfunction
- -age, trauma, etc - Valvular reflux
- -loss of collagen, elastin - Venous obstruction
- -dvt
Clinical Classification of Venous Disease (CEAP)
- Reticular and spider veins
- Varicose veins
- Varicose veins and leg swelling
- Varicose veins and evidence of venous stasis skin changes
- Varicose veins and a healed venous stasis ulceration
- Varicose veins and an open venous ulceration
Clinical Classification of Venous Disease (CEAP) treatments for each
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.
Subcutaneous Varicosities
They form due to increased hydrodynamic pressure.
Symptoms include itching & discomfort pain.
Mainly cosmetic complaints
Reticular and Spider Veins
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.
Varicose Veins
Venous Stasis Skin Changes
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
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
Phlebitis
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
Septic Thrombophlebitis
◦ Antibiotics ◦ Surgery ◦ Extensive hospitalization ◦ ICU See most commonly in ◦ burn patients ◦ steroid usage ◦ intravenous drug use
◦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
DVT
Most frequently used in diagnosis of DVT
Most accurate noninvasive modality
Venous Duplex Ultrasound
◦ Dyspnea ◦ Pleuritic chest pain ◦ Apprehension ◦ Cough ◦ Tachypnea tachycardia
PE
what thrombi are greatest risk for PE
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
gold standard for PE
Spiral chest CT
PE treatment
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
in segmental limb pressures, why use toe pressures
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
segmental limb pressures interpretation
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
index of less than what indicates occulsive arterial disease
.90
. 20-30mmHg drop from one segment to the next or from one side to the opposite side indicates occlusive process
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
Transcutaneous Oxygen Tension Introduction
rare disease of lymphedema
milroys and meige
Secondary Lymphedema
• Acquired defects are those one is not born with but that are the result of
- injury
- surgery
- trauma
- radiation
- infection
- malignancy
Nonatherosclerotic vascular diseases
Vasospastic disorders -Raynaud’s Phenomenon/Disease Vasculitis -Giant cell arteritis -Takayasu’s Disease y --Kawasaki’s Disease Polyarteritis Nodosa Miscellaneous -Buerger’s Disease
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
Raynaud’s
diff between primary and 2ry raynauds
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
treatment for raynauds
Avoid precipitanting factors Avoid caffeine, tobacco Nifedipine Losartan Sympathectomy Amputation
Classification of Vasculitides
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
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
Polyarteritis Nodosa
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
wegener’s granulomatosis
temporal arteritis HA scalp tenderness blindness tA biopsy to confirm
Giant cell arteritis
Pulseless arteritis
Aorta/major branches
Young females
Symptoms in arms and neck
Takayasu
“Mucocutaneous lymph node syndrome” Major cause of acquired heart disease in children Coronary aneurysms Pink eye pathcy rash peeling skin enlarged LN
Kawasaki
“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
Buerger’s Disease
diagnostic criteria of buergers
Smoking history Onset <50 years Infrapopliteal arterial occlusions Upper limb involvement Absence of other atherosclerotic risk factors (except smoking)
“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
eczema
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
contact dermatitis
Leather dyes/tanning chemicals
Spares the web spaces is hallmark
SHOE BOX Contact Derm
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.
Primary Irritant contact dermatitis
Eczema due to a COMBO of chemical + sunlight
Big offender is citrus juice, especially LIME
Perfumes are also common
Photo Allergic Contact Dermatitis
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
Dermatitis Medicamentosa
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
Atopic Dermatitis
skin lesions in atopic derm
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.
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
Lichen Simplex Chronicus
lesions of lichen simplex chronicus
Plaques of well demarcated lichenification
Exaggerated skin lines
May see hyper pigmentation
Initially erythema
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
Nummular eczema
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
Dishydrotic eczema
treatment of venous stasis dermatitis
Wet to damp-Burrows Solution Elevation Compression Unna Boot Topical steroids calcineurin inhibitors Correct medical problem-i.e... CHF
“winter itch” Usually winter Usually elderly ‘ASTEATOTIC ECZEMA-lesions 'crazy paving' Very dry and scaling on erythematous base Legs a common location
ASTEATOTIC ECZEMA
Corticosteroids Potency
– 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%
corticosteroid selection
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
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
hyperhydrosis
hyperhydrosis treatment
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)
(Callus
Diffuse
Non-nucleated
tyloma
heloma molle, durum
corns
nucleated
Core
well-circumscribed
IPK
Neurovasculare PK
very painful
►Skin tags & polyps ►Often found in skin folds or creases ►Increase in middle age ►Usually asymptomatic ►Treatment rarely needed: excision
Acrochordon
►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
Acral Fibrokeratoma
►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
Dermatofibroma
►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
Digital Mucous (Mucoid) Cysts
►Most common cyst ►Few mm to several cm ►Slow growing, may drain ►Cyst wall of squamous epithelium ►No I & D, excision only ►Associated with trauma ►Epidermal cells implanted deep
Epidermal (Inclusion) & Sebaceous Cysts
►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 & juxta-epidermal types
Poroma*
►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
Nevi
3kinds of nevi and explain
Junction - flat, pinpiont
Compound - slightly elevated, dome shaped
Dermal - verrucoid, pedunculated (have stalk)
►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
Dysplastic Nevus
nevus on trik that has hair
beckers
kids
dome shaped nevus
need excision
spitz
►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
Piezogenic* Papules
►Rapidly growing, pink to bright red growth
►Minor trauma & ingrown nails
►Cerebriform highly vascular tumor
►Bleeds easily
►Treat with debridement & cautery plus topical antibiotic
Pyogenic Granuloma
►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
Porokeratosis
►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
Seborrheic Keratosis
►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
Stucco keratosis
onycholysis from proximal to distal
onychomadesis
Transverse nail splitting
• Onychoschizia
(Longitudinal ridging/splitting
• Onychorrhexis
ABCDEF of Melanonychia
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
yellow nail sydrome association
cirrhosis
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
Splinter Hemorrhages
transverse white bands on nails from arsenic poisoning
Mees Lines
transverse white bands on nails from low albumin
Muehrcke’s lines
Spoon Nails
Idiopathic causes
Hereditary or congenital
most common cuases
koilonychia
Iron deficiency anemia
Trauma
Malnutrition
Hippocratic Nails
Lovibond’s Angle
(Increased Unguophalangeal Angle)
most common causes
clubbing
Lung neoplasms Hypertrophic osteoarthropathy Cardiovascular dz Cirrhosis Colitis Thyroid dz
Caused by trauma or systemic illness or chemo
Beaus lines
Subungualhyperkeratosis
Keratosis palmaris et plantaris
Leukokeratosis of oral mucosa
Familial
Pachyonychia Congenita
periungal fibromas associated wtih
tuberous sclerosis
Cause unknown
Possible osteochondroma
Must take x-ray
Excision of bone necessary but nail may not return to normal shape
Subungual Exostosis
types of papulosquamous disorders
psoriasis
Lichen planus
Pityriasis rosea
pityriasis rubra pilaris
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
Psoriasis
Atypical FLEXOR surfaces
papulosquamous
psoriasis inversa
- 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
woronoff ring
- 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
GUTTATE PSORIASIS
- Life threatening
- Scaling
- Fever
- Onycholysis
- Huge surface area of the body has bright red scaling
- > 50 YO male
ERYTHRODERMA
- Often palms and soles
- Pustules that dry up and turn brown
- Mimics vesicular tinea pedis
pustular psoriasis
- 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
VON ZUMBUSCH
- 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
Lichen planus
Wickhams striae associated with what
lichen planus
MUCOUS MEMBRANES of Lichen Planus
•Possible conversion to SCC
•Usually seen with chronic LP
•May develop painful erosions
Striae
NAILS of LP
- Ridging and grooving from thinning
- Onycholysis
- 10% see nail changes
- 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
Pityriasis rosea
- Thick scaling with red follicular papules
- Looks like psoriasis
- Palms and soles
- Hyperkeratosis
- Often seen on joint surfaces
- Fissuring
- Moisturizers
- retinoid
Pityriasis rubra pilaris
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
Malignant Melanoma
MELANOMA-ABCDEF
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
Surgical Excisionmargins melanoma
- Based on depth:
- In situ: 0.5 cm
- 1-2mm: 1 cm
- 3-4mm: 2 cm
- No benefit going > 2cm
Surgical Excisionnodes melanoma
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.
Melanoma • Female 30-50 • YUPIE • Most common-70% of MM • Upper back-males • Legs-women
SUPERFICIAL SPREADING MELANOMA
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
LENTIGO MALIGNIA
• 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
Acral Lentiginous
melanoma Men 40-50 on Legs and trunk Most aggressive/most deadly Rapid growth* “blueberry” color 15-30% of MM Grows down
nodular
- 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
bowens disease
• 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
SCC
- 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
MARJOLIN ULCERS of SCC
SQUAMOUS CELL CARCINOMA treatment
- Wide Surgical Excision 4mm margins for non-invasive and10mm for invasive lesions
- Mohs is gold standard for SCC ulcers
- Radiation
- # 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
Basal Cell carcinoma
- 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.
Pityriasis (Tinea) Versicolor
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
Hyperkeratotic Tinea
Intertriginous infections caused by dermatophytes that are not complicated by bacterial overgrowth
Simple topical antifungal creams BID x 1-4 weeks usually sufficient
Dermatophytosis Simplex
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
Dermatophytosis Complex
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
Vesiculobullous Tinea Pedis
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
Tinea Manuum
- Topical antifungal BID x 4 weeks
- Often requires oral antifungals
- Usually annular with central clearing
- Sometimes pustular
- Sometimes geographic shapes
Tinea Corporis (Ringworm)
Invasion of hair follicles produces inflammation Trychophyton species Treatment Shaving or depilatories Antifungal shampoos or lotions Oral antifungals
Tinea Barbae
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
Tinea Nigra
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***
Majocchi Granuloma
Scale without inflammation on one hand (tinea manuum)
Bilateral tinea pedis
Nail involvement on one hand is pathognomonic
Oral antifungals required
Two Foot One Hand
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?
Candidiasis (Candidosis)
Treatment for Oral Thrush
Gentian Violet
Primary immune deficiency syndrome.
Recurring infections of paronychial areas, skin, mucosa.
Onset in infancy or childhood.
Mucocutaneous Candidiasis
Most occur in childhood Followed by immunity Poor morphologic specificity Maculopapular rashes Morbilliform(measles like) rashes Group name
Exanthems
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
Erythema Infectiosum (Fifth Disease
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
Measles (Rubeola)
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
Roseola (Exanthem Subitum)
Rash may be mild Similar to roseola Facial erythema spreads to trunk involvement* 1-2 mm raised lesions Cervical and occipital adenopathy Arthritis & fever RNA togavirus Supportive therapy
Rubella
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
Hand Foot and Mouth Disease
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
Chicken Pox (Varicella)
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
Molluscum Contagiosum
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
Herpes Simplex
AKA: Mat pox, wrestler’s herpes, scrumpox Highly contagious Contact sports Herpes simplex 1 Latent virus causes recurrence Acyclovir or Valtrex
Herpes Gladiatorum
Herpes simplex infection of the digit
Herpetic Whitlow
- 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
Terbinifine
- Take capsules with food to increase absorption
- CI in pregrant
- FDA warning on risk of CHF
- Intense CYP 3A4 Inhibition
- Numerous drug interactions
Itraconoazole
- Most commonly used for Cocci and Cryptococcal meningitis
- Neprhotoxicity
- Anemia
- Antidote to rigors in Meperidine
Amphotericin B
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
Pediculosis
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
Scabies
Crusted Scabies
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
Treatment for Scabies
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)
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
Cutaneous Leishmaniasis
Treatment for Leishmaniasis
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
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
Cutaneous Larva Migrans
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
Mycetoma (Madura Foot)
Rapid growing fungus White, wooly colonies Grayish brown w/ age Simple long/short conidiophore Single conidium/small groups
Pseudallescheria boydii which cause eucytoma
treatment for madura foot
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!
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
Lyme Disease (Lyme Borreliosis)
Lyme Disease Stages
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
Often confused with t. pedis Interdigital maceration and pruritis. May be cellulitis Flouresces “coral red” Corynebacterium minutissimum
Erythrasma
Erythrasma tx
Oral erythromycin 1gm/day
May try macrolides
Topical treatment may be sufficient
Drying agents useful
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
Hot Tub Dermatitis (Folliculitis)
Progression of basic folliculitis Commonly known as “boils” Groups of furuncles form carbuncles Compresses often sufficient Carbuncles require surgical drainage
Furuncles and Carbuncles
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
Impetigo
Topical mupirocin
Oral antibiotics rarely needed: cover staph and strep
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
Staphylococcal Scalded Skin Syndrome
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
Ecthyma
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
Erysepilas
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
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
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
Clostridial Myonecrosis (Gas Gangrene)
Clostridial Myonecrosis (Gas Gangrene) tx
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
VRE: Vancomycin Resistant Enteroccus antibiotic
No cephalosporins are effective Linezolid Tigecycline Daptomycin Quinupristin/dalfopristin
drugs for severe diabetic infection
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
4 kinds of Immunologic Responses
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
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
Urticaria and Angioedema
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
erythema nodosum
Bed rest/compression
ASA, NSAIDS
Steroids only with known etiology and no infection
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
erythema multiforme
Mild, exfoliative changes to hands & feet
No erythema
Rapid healing when drug has been eliminated
acroexfoliative dermatitis
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
Exfoliative Erythroderma
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
SJS
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
Drug‐induced Plantar Keratoses
Pruritic reaction
Vesicles and papules
Crusting and scaling if drug use continues
Stop drug!
Eczematous Drug Reaction
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
fixed drug reaction
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
Photosensitivity Reaction
Benign, inflammatory, granulomatous condition of the dermis of unknown origin
Occurs in all age groups but most common in young women
Granuloma Annulare
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
Pyoderma Gangrenosum
Pyoderma Gangrosum tx
Oral steroids
Immunosuppressive agents
Typical ulcer care
Heal slow and when good and ready with and pigment changes
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
KERATODERMA CLIMACTERICUM (Haxthausen’s Disease)
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
sarcoid
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
Dermatomyosis
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
Gottron’s papules
dermatomyositis tx
oral steroids
avoid sun
Reddish macule/papule evolves to a pustule that to a keratotic plaque
Toes and soles
Reiters
Keratoderma blennorrhagicum
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
EPIDERMOLYSIS BULLOSA SIMPLEX (EBS)
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
WEBER-COCKAYNE SYNDROME
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
Pemphigus
Inherited keratinization disorder abnormal epidermal differentiation or metabolism Fine scales Scales protrude and make skin rough Extensor surfaces
ICHTHYOSIS
Tiny, uniform papules Makes skin very rough Adolescence Upper arms Dry, chapped skin Very common, 40% + Lacti-care retinoids
KERATOSIS PILARIS
Severe thickening of palms and soles
Hereditary
Associated fissures
Dystrophic nails
PALMARPLANTARKERATODERMA
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
DARIER’S DISEASE - keratosis follicularis
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
NEUROFIBROMATOSIS - von recklinghausen’s disease
melanocytic hamartomas, clear yellow to brown, well defined, dome shaped elevations projecting from the surface of the iris
NF
Lisch Nodules
– 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
ganglion cyst
– 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
Lipoma
– 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
Neurofibroma
–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
Neurilemmoma (schwannoma)
– 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
Hemangioma
– 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
Glomus Tumor
– 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
Angioleiomyoma
– 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
Giant cell tumor of the tendon sheath
– 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
Synovial Sarcomas
– 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
Malignant Fibrous Histiocytoma
– 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
Fibrosarcoma
– 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:
Liposarcoma
bone tumors by location
diaphysis osteoid osteoma chondromyxoid fibroma ewing fibrous dysplasia fibrosarcoma
metaphysis
osteosarcoma
osteochondroma
enchondroma
epiphysis
chondroblastoma
GCT - E,M
Cysts - E,M,D
buttressing of bone, form many layers of periosteum
Pagets
bone tumors that can convert to malignant
Giant cell
osteochondroma
‡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
OSTEOID OSTEOMA
‡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
ENCHONDROMA
‡Young adult male
‡Can appear destructive
‡Expansile
‡Frequently involves the leg (70%)
CHONDROMYXOID FIBROMA
‡Male child ‡Most common bone tumor..35% of all ‡Miniature physeal region growing away from the joint ‡Malignant transformation is possible ‡ Mushroom cloud appearance
OSTEOCHONDROMA
‡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
OSTEOGENIC SARCOMA
‡Over 40 male ‡Spotty calcifications “popcorn” or “salt and pepper” ‡Knee is a common locale ‡Result of transformation ‡Can have associated soft tissue growth
CHONDROSARCOMA
‡Young males avg. 12yo , usually white
‡“Onion skin”
‡Pain/mass/”sick” (Think sick kids)
EWING’S SARCOMA
‡Young male
‡Grows during growth
‡Won’t expand
‡Not destructive but can see pathological fracture “fallen fragment sign
SOLITARY BONE CYST(simple or unicameral)
‡Young person ‡Long bones ‡Large/expansile ‡“soap bubble” ‡Easy to confuse with malignant
ANEURYSMAL BONE CYST
‡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
FIBROUS DYSPLASIA
‡Quasi-malignant ‡Middle-age female ‡Knee region ‡Large, expansile, moth-eaten ‡“soap bubble”
GIANT CELL TUMOR
- Deformed bones causing bone pain
- Elevated Alk phos
- Viral/genetic causes
pagets
LBP concerns for cancer
- 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.
nerve sens and motor in LE
– 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)
-Paramedian Herniations
- Male>Female
- 30’s-40’s
- L5-S1 most common
- Pain worse with increasing intrathecal pressure
“Which is the most common type ( or location ) of a HNP?” (Herniated disc)
Posterolateral herniation is the most common overall ( ie L4-L5 level )
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
cauda equina syndrome
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.
spinal stenosis
• 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.
PVD Claudication
- Term used to describe osteoarthritis around the vertebra
- Also referred to as a bone spur
- A specific way of describing vertebral osteoarthiritis
Spondylosis
A separation of the pars interarticularis of the vertebral arch (Scottie dog collar shows defect)
Spondylolysis
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.
Spondylolithesis
• 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
Subacromial Bursitis and Rotator Cuff Tendonitis
• 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
Impingement Syndrome
- 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
Bicep Tendonitis
• “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
Adhesive Capsulitis
• 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
Rotator Cuff Tear
• AC Joint Separation • Causes – Direct trauma – FOOSH • SSX – Pain! • Treatment – Ice, NSAID – Rest (Sling) – PT – Surgery (grade dependent)
Shoulder Separation
• 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
Shoulder Dislocation
Tennis elbow)
Lateral Epicondylitis
- 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
dislocation of elbow
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
Radial Head Fracture
- 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
CTS
- 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
Distal Radius Fx
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.
Dupuytren’s Contracture
For displaced femoral neck use
bipolar hemiarthroplasty
Sub-trochanteric Hip FX
Use gamma IM nails
- 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
pubic rami fracture
- 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
legg calve perthes
- 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
Slipped Capital Femoral Epiphysis
Slipped Capital Femoral Epiphysis tx
- Surgical fixation
- Protected weightbearing
- Physiotherapy
- Typically unilateral
- Boys > Girls
- Age: 3 – 10 years old
- Viral v. Antecedent infection
- Signs & Symptoms
- Pain
- Antalgic gait
- Hip pain w/PROM
- Knee pain
pediatric hip synovitis
no antibiotics
grades of knee sprains
- 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.
• 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
Patellofemoral Syndrome
- Swelling
- Hot
- +/- Pain
- Decreased ROM
- Suprapatellar
- Infrapatellar
- Prepatellar
knee bursitis
- 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.
Patellar tendinitis (Jumper’s Knee)
- 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.
Pes Anserine Tendinitis/Bursitis
- Apophysitis of inferior pole of the patella.
- Similar to Osgood-Schlatter.
- “Growing pains”
Sinding Larsen-Johansson Syndrome
- AKA Tibia varum
- Disorder of posterior tibial physis
- Most common
- Males
- African American
- Obese
- Infantile
- Usually bilateral
- Internal tibial torsion
- Adolescent
- Unilateral
- Less severe
Blount’s Disease
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
SLE
Discrete plaques Usually in sun exposed areas Usually erythematous c induration at periphery Central atrophic scarring Irreversible alopecia
discoid lupus
SLE therapy
NSAIDs
Corticosteroids
Hydroxychloroquine*
Immunosuppressives: azathioprine, cyclophosphamide, mycophenolic acid
Monoclonal antibodies including rituxamub and belimumab
SLE summary
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
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
PMR
PMR labs
Elevated ESR*
Elevated CRP
Anemia: usually NCNC
Mildly elevated LFTs
PMR: Prognosis
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
PMR Therapy
Low dose corticosteroids*
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
temporal arteritis
TA- Biopsy
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
TA Rx-
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
Classification of Scleroderma
SSc • dSSc • lSSc • Overlap syndromes Localized • Morhpea • Localized linear Chemically induced