Boards Part 2 (2of 2) Flashcards by Danny Hansen

• 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

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Main thing in charcot

Severe PN

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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

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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

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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

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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

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Sanders/Frykberg Classification

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

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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

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3 groups of treatment for charcot

Phyiscal T: offlad, cryo, bone st

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

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total reconstruction of charcot is to restore what angles

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

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genesis of atherosclerosis

 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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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)

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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

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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

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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

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5P’s of acute limb ischemia

Pulselessness
Paralysis
Paresthesia
Pain
Pallor

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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

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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

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venous anatomy le

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

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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

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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

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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.

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

Reticular and Spider Veins

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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

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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 ```

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 legs*and 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 ```