THE PEDIATRIC DIAGNOSTIC EXAMINATION - PART 8 pdf

Brown, circular, some Anywhere, more on I, C, A Tinea corporis, cruris, or capitis scaling, clear center; may thighs, crural area, ringworm be red; hair loss and trunkDiaper rash, red to

2 Intertrigo Bright red, some scaling Obese pts., rubbing A, C Mistaken for monilia

skin

3 Petechiae Location of trauma, Pt generally A, C, I Accidental, self-inflicted, abuse,

capillaries; facial petechiaewith severe coughing orvomiting

II Blue macules

be papular

nonuniform pigment, areasvariegated color, >4 cm in

diameter

3 Tattoo Artistic pattern, but may be Anywhere A, C History of trauma, FB (e.g.,

III Purple macules

Ecchymoses/ Traumatic in normal patient, Anywhere I, C, A Review “Petechiae” abovepurpura but also consider all causes

under “Petechiae” above

(Continued)

TABLE 16–1 Macules (Continued)

IV Brown macules

hyperpigmentation

1 Endocrine Stria (Cushing), oral Anywhere, more in A, C, I Addison, Cushing,

(Addison), vitiligo,proptosis, goiter (↑ thyroid)

disease sx (Wilson), hair and nail

changes (hemochromatosis)

xanthomata

medications

B Localized

hyperpigmentation

1 Acanthosis Brown to black; may be Axillae, neck, A, C, I Insulin resistance, polycystic

obesity and insulin elbowsresistance; amenorrhea,

hirsuitism

2 Nevi Uniform, regular border, Anywhere A, C, rarely I Watch for malignant change

round

Lentigo, ECG abn., ocularhypertelorism, pulm

stenosis, abnormal genitalia, retardation,deafness

Lentigo, GI polyps, Peutz-Jeghers syndromepremature puberty

4 Becker nevus Brown to black, irregular Shoulder and trunk A, C

pigmentation, satellites,contains hairs

5 Café-au-lait spot Tan, regular, >0.5 cm, >five, Diffuse A, C Neurofibromatosis type I

axillary freckles, Lischnodules, optic gliomas,neurofibromasTan, irregular, unilateral, Unilateral, single McCune-Albright syndromeprecocious puberty, bone or multiple

TABLE 16–1 Macules (Continued)

7 Fungal infection Brown, circular, some Anywhere, more on I, C, A Tinea corporis, cruris, or capitis

scaling, clear center; may thighs, crural area, (ringworm)

be red; hair loss and trunkDiaper rash, red to brown Penis, scrotum labial Monilial diaper rash

with satellite lesionsStreaky rash, lightly Shoulder, neck C, A Tinea versicolor

to hypopigmented,occasional scales

V White macules

A Diffuse (total) Total body pigment loss Diffuse I, C, A Eye findings: nystagmus,

photophobia,↑ skin ca,

1 Albinism Melanin loss, eczematous Diffuse I, C, A Retardation (MR), seizures

rash

2 Phenylketonuria Albinism

3 Hematologic Total pigment loss, sharply Diffuse I, C, A

B Localized

proximal May be associated with deafness

and symmetrical forelock, heterotropia of iris)

2 Tuberous Multiple small Diffuse C, A, often not Seizures, MR

patches (raised plaques),Angiofibromas on face Face, nasolabial

Sebaceum)

3 Incontinentia Diffuse, preceded by Swirling pattern I, C, A Developmental delay, usually

4 Nevus Large areas of Linear pattern C, A, rarely I Usually isolated, but rarely

5 Halo nevus Pigmented center, surrounding Anywhere C, A Benign, depigmented area of

6 Pityriasis alba Discrete, may be scaling Face and neck A, C, rarely I Associated with atopy

7 Postinflammatory Localized to areas of original Anywhere A, C, I Multiple causes, allergic, toxic,

postinflammatoryhyperpigmentation

9 Vitiligo Diffuse, sharp, milk-white Anywhere, A, C, I Absent melanocytes, may be

immune disorder

Abbreviations: HSM = hepatosplenomegaly; CMV = cytomegalovirus; TSST = toxic shock syndrome toxin; DIC = disseminated intravascular coagulation;

Pts = patients; Assoc = associated; Abn = abnormal.

TABLE 16–2 Papules

I Red papules

A Infectious

1 Folliculitis Pinpoint, in hair follicules, Hair location, esp A, C, rarely I Staph Pseudomonas from pools

2 Scarlet fever Pinpoint “sandpapery,” red Diffuse, ↑ in axilla C, A Group A strep rarely viral

Strawberry tongue, Pastia’slines antecubital fossa area

3 Lyme disease Eryth chronicum migrans, Location of tick bite A, C Borrelia burgdorferi, assoc.

4 Fungal See Table 16–1 Scales Anywhere, abscess A, C Tinea cruris (groin), barbis

feet, and scalp

6 Warts Pink, scaly, or keratotic; Anywhere, plantar, C, A Papilloma virus

hypopigmented; may periungual

be flesh

7 Gianotti-Crosti Small red papules Face, extremities, C, occ I Viral prodrome, HSM,

8 Scabies Papules with burrows, Web of fingers, groin A, C less in I Sarcoptes scabii, pruritus

may form vesicles more diffuse in

infants

B Allergic

1 Papular Small raised papules, Anywhere C, A, I Pruritic, self-limited, also may

polymorphous w/clear centers (E multiforme)

2 Insect bites Similar to pap urt., entry Exposed areas C, A, I Pruritic, self-limited

site, excoriations fromscratching

3 Drug eruption Pink-red, may be scaly Symmetric, oral A, C, I Occ pruritic, unrelated to

4 Eczema Pink, scaly plaque, secondary Antecubital and I, C, A Pruritic, remissions and flares,

to weeping, excoriation, popliteal fossae; associated with asthma;

healing; may be nummular hands; more diffuse adolescents(coin-like), pin point and on cheeks in

follicular in dark skin pt infants

5 Contact Papules initially, may form Exposed areas; pattern C, A, I Very pruritic, does not spread dermatitis crusts, plaques & vesicles of contact (streaks by scratching unless antigen

umbilicus for nickelfrom belt buckle)

(Continued)

TABLE 16–2 Papules (Continued)

C Inflammatory

1 Miliaria Tiny red papules; occ vesicle Neck and back; I, C, A Red-miliaria rubra,

2 Acne Red or flesh papules Face, forehead, back A, C Plugged oil glands (whiteheads)

pustular

3 Vasculitis

a Blanching

1 Juvenile rheum Discrete red evanescent macules Anywhere I, C, A Arthritis, lymphadenopathy,

2 Lupus Red papules with scale; over Sun-exposed or malar A, C Multisystem disease, psych

atrophy, telangiectasia

3 Kawasaki Papular/macular Anywhere; erythema I, C Persistent fever,

involvement

b Petechial See “Petechiae,” TABLE 16–1 See “Petechiae,” See “Petechiae,” TABLE 16–1

TABLE 16–1

4 Granulomatous

disease

a Common

1 Granuloma Ring, clear center, rubbery Dorsum hands and, A, C Often mistaken for ringworm

surfaces

2 Pyogenic Red, vascular, friable Anywhere, often of C, A Bleed easily Needs excision

3 Foreign body Red brown papules Location of FB I, C, A Remove foreign body

(FB)

TB and atypical mycobacteria

1 Seborrhea Scaly, greasy, occ crusts Scalp, eyebrows, I, C, A “Cradle cap” in infants

intertriginous areas

2 Keratosis Perifollicular, pinpoint, pink, Extensor surface of A, C, I Assoc with dry skin (eczema,

3 Pityriasis, Large herald patch, salmon Trunk, proximal A, C Mild itching, self-limiting

4 Psoriasis Red plaques, may be pustular, Anywhere, but often A, C Chronic or recurrent, mild itch,

sharp margins, white-silvery extensor surfaces, often mistaken for eczema,

Often mistaken for eczema

(Continued)

TABLE 16–2 Papules (Continued)

5 Eczematoid

rashes

a Dyshidrosis Papules, peeling, Hands, feet, big toes A, C, I Areas of sweating, excessive

burning

b Eczema Umbilicated vesicles Preexisting eczema C, I, A Herpes simplex present aka

c Lip-smacking Irritated, scale, fissure, Perioral, cheilitis C, A History of lip licking

d Wiskott-Aldrich Eczematous or seborrheic, Anywhere I, C, A Immunodeficiency, draining ears,

e Acrodermatitis Patches with crusting, Acral areas, tip of I Zinc deficiency

enteropathica weeping, excoriations, nose perioral

diaper area

regress; turn gray whenresolving

II Flesh-colored

papules

1 Acne, warts See under “Red Papules”

2 Molluscum Smooth, domed, umbilicated, Anywhere C, A Poxvirus, contain eosinophilscontagiosum white plug

3 Neurofibromatosis See under “Brown Macules” Anywhere C, A, I Fleshy neurofibromas

4 Tuberous See under “White Macules” Angiofibromas of C, A, I

5 Nevi See under “Brown Macules” Anywhere A, C, fewer in I Watch for malignant change

6 Keloids Shiny, bulging, sharp border Area of injury A, C Dark-skinned pts, female > male

7 Lichen sclerosus May be macular, scaly, in Anywhere, often A, C

et atrophicus plaques or atrophic genitalia

8 Lichen striatus Linear, scaly, sometimes Blaschko’s lines A, C Self-limiting, may be genetic,

9 Lichen nitidus Pinpoint, may coalesce, non Arms, genitalia, A, C Koebner phenomenon, male

III Brown papules

A Single

1 Mastocytosis See “Red Macules/Allergies”

2 Melanoma Changing mole, spreading, Sun-exposed areas A, C (rarely) “ABCD” mnemonic, asymmetry,

variability

(Continued)

TABLE 16–2 Papules (Continued)

B Multiple

1 Multiple atypical May be macular, some color Sun-exposed areas, A, C Watch for malignant changes

patients

2 Langerhans May be yellow or macular, Trunk, axilla, groin A, C, I Systemic involvement, bone

2 Ecthyma Blue to black center; may Anywhere, often I, C, A Malignancy or

3 Blue nevi See “Blue Macules”

4 Foreign body See “Blue Macules”

B Multiple

1 Lichen planus Some scales, hyperkeratosis, Flexural surfaces, A, rarely C “Four p’s” purple, pruritic

hyper/hypopigmentation, mucosa, genitalia polygonal papules

V Purple papules See “Purple Macules”

1 Subacute Osler’s nodes (tender), Fingers and toes A, C, I Fever, changing heart murmurbacterial Janeway lesions (nontender) Palms

endocarditis Splinter hemorrhages Subungual

VI Yellow papules

1 Xanthomas May be eruptive (surrounding Eruptive, anywhere A, C Severe hyperlipidemia, liver

erythema), noneruptive, or Noneruptive, disease, nephrotic syndrome,

tendons eyelids(xanthelasma)

2 Pseudoxanthoma Pale, grouped, interspersed Flexural areas, neck A, C Diffuse arterial disease, premature

Abbreviations: HSM = hepatosplenomegaly; PKU = phenylketonuria; mos = months; TB = tuberculosis; w/ = with; occ = occasional; psych = psychological;

Pt = patient; E = erythema; esp = especially; neurol = neurological.

TABLE 16–3 Nodules and Cysts

I Cysts

A Epidermal

1 Epidermoid cyst Single or multiple, white Face, scalp, neck, C, A, milia in Gardner syndrome (polyps,

2 Vellus hair cyst Small, 1–2 mm, from vellus Anywhere C, A May be genetic

follicle

3 Steatocystoma 1–3 cm, yellowish, sebaceous Chest, arms, face C, A Autosomal dominant type

4 Syringomas 1–2 mm; flesh to brown, Face, eyelids, cheeks, A Females > males; ↑ in Down

5 Trichoepithelioma Skin-colored up to 8 mm Cheeks, lips, labial C, A large and multiple = autosomal

B Dermal

1 Dermoid cyst Congenital, firm, attached Eyes, head, neck I, C, A Contains dermal structures

C Subdermal cysts

1 Synovial Over tendon, feels tense Wrist, anywhere, A, C Enlarge after trauma or bleeding

3 Neurofibroma “White macules,” Face, lips, oral A, C

neurofibromatosis but mucosa I, C, Amay be sporadic and

solitary

neoplasia

(Continued)

TABLE 16–3 Nodules and Cysts (Continued)

C Inflamed red

nodules

1 Carbuncle Red, warm, fluctuant Areas with hair A, C, I Pus, culture for bacterial etiology

2 Hydradenitis Develops from pustules, Groin, axilla A, occ C Inflammation of apocrine gland;

complication

3 Erythema Red-blue, tender 1–5 cm Pretibial area A, C, Associated with strep.,

allergy, oral contraception,collagen-vascular disease

4 Panniculitis

a Cold Red, indurated, nontender, Cheeks, or other I, C Crystallization and rupture of

exposed

b Subcutaneous Similar to cold panniculitis, Anywhere I Self-limiting

fat necrosis spontaneous

c Lupus Purplish, painless, 1–5 cm Face, extremities, A, C Resistant to treatment, may

TABLE 16–4 Blisters (Vesicles) and Bullae

I Vesicles and bullae

A Vesicles

6 Varicella Umbilicated, red base, Proximal → distal, Fever, pruritus

(chickenpox) eventually form crusts centrifugal, mucosal

surfaces

7 Eczema herpeticum See “Papules”

8 Herpes simplex I, Vesicles → crusts Oral mucosa, gingivae, I, C Fever, → diminished intake,

9 HSV I recurrent “Cold sores” Oral mucosa, face C, A Recur same location, stings

“whitlow” on finger initially, associated with

illness or stress

10 Herpes zoster Umbilicated vesicles Dermatomal, also eye A, C Sting or burn initially, mistaken

or secondary; observe fortransmission to newborn

(Continued)

TABLE 16–4 Blisters (Vesicles) and Bullae (Continued)

B Bullae, traumatic

1 Second-degree See “Macules” for Dependent pressure I, C, A Consider abuse based on

(rubbing)

C Bullae, infectious

1 Impetigo Yellow crust, weeping, Anywhere, esp face I, C, A Bullae most likely staph infection

satellite lesions, mouth, noseerosions, yellow

crusts, pustules

2 Staph.-scalded Diffuse erythema, Generalized +Nikolsky I ,C, A SSSS toxin

3 Dermatophyte Red erosion, scale Palms, soles, fingers A, C Originally a blister

D Bullae-immunologic

1 Pemphigus Severe, large bullae, Start on scalp, oral A, C Severely ill, can be fatal, due to

to desmoglein

2 Pemphigus Similar in appearance, Similar to PV A, C Not as ill as PV, may be

3 Linear IgA Tense small bullae, may Lower trunk, legs, C, A Varying degree of illness Biopsybullous dermatosis, be linear or annular but may spread with PMN and eosinophils

of childhood)

4 Bullous Tense blisters >2 cm, Similar to CBDC, C, A Subepidermal bullae, IgG and C3

5 Epidermolysis Similar to BP; more Acral initially, but A, C IgG deposits at base of blister;

collagen-vascular disease

E Bullae, other

1 Epidermolysis Mild, recurrent Acral, elbows, knees I, C Autosomal dominant

improves with age

2 Epidermolysis Severe associated with At birth, anywhere, I, C Autosomal recessive may bebullosa letalis atrophy and dystrophy; but generally spares lethal, severe mucous

(Continued)

TABLE 16–4 Blisters (Vesicles) and Bullae (Continued)

3 Stevens-Johnson Severe mucous membrane Starts as red macules A, C Prodrome of fever, flulikesyndrome (SJS) involvement, extensive, on head, spreading symptoms, severely ill, may

confluent blisters, down and forming get secondary sepsis, scarring,thin-walled, + Nikolsky blisters after 1–3 days and permanent damage to

4 Toxic epidermal Severe end of spectrum See SJS above A, C More severe than SJS, higher

5 Erythema multifome Formally thought as Anywhere, mild A, C Infectious causes, mycoplasma,

spectrum; hivelike involvementlesions with some

target formation, mayform blisters

Abbreviations: STD = sexually transmitted disease; IBD = inflammatory bowel disease; assoc = associated; PMN = polymorphonuclear neutrophils; esp =

especially; w/ = with.

TABLE 16–5 Primary Scales

I Ichthyoses

A Lamellar Collodion baby, large More on legs and scalp; I, C, A ↑ water loss, temp instability,ichthyosis thick brown scales after facial involvement autosomal recessive, 1:100,000

B Ichthyosiform Similar to lamellar Similar to lamellar I, C, A Autosomal recessive, 1:100,000 erythroderma ichthyosis, erythematous, ichthyosis; flexural incidence

bullous and nonbullous and intertriginous

C Ichthyosis Mild scaling Diffuse, spares flexural I, C, A Starts around 3 mos., improves

dominant, incidence 1:250;association with atopicdermatitis

D X-linked Large “dirty” scales, mild Similar to ichthyosis I, C, A Starts around 3 mos., improves

2:6000 males, assoc withcryptorchidism, Kallmann and Poland syndromes

(Continued

TABLE 16–5 Primary Scales (Continued)

E Epidermolytic Diffuse scaling, blisters Generalized, esp I, C, A Autosomal dominant or sporadic,

overgrowth

II Syndromes

with ichthyosis

A Netherton Hair shaft abnormality, Anywhere I, C, A Autosomal recessive, failure to

B Refsum Similar to ichthyosis Similar to ichthyosis A Blindness, deafness, ataxia,

phytanic acid metabolism

C Sjögren-Larsson Lamellar ichthyosis Similar to lamellar I, C, A Spasticity, MR, seizures, tooth

D KID syndrome Keratosis, ichthyosis, Extremities, head I, C, A Keratoconjunctivitis

deafness

nevi, limb defects; also heartand renal defects

F Conradi Ichthyosis, erythroderma, See “Ichthyosiform I, C, A Chondrodysplasia punctata,

TABLE 16–6 Induration, Sclerosis, Atrophy

I Induration and

sclerosis

A More common

1 Urticaria See “Red macules” Generalized, more I, C, A More severe cases

2 Scleredema Induration, diffuse, red Chest and back A, C Post strep infection

3 Scleroderma Poorly defined, variable Acral → proximal A, C Ulceration of fingertips; calcinosis

calcifications

porphyria, graft-vs.-host,leprosy, mucopolysaccharidosis,hypothyroidism (myxedema),PKU, progeria

II Atrophy

A More common

1 Lichen sclerosus See “Flesh-colored papules”

et atrophicus

2 Lupus Red, scaly, telangiectasia, Sun-exposed areas, A, C, I Females > males, multisystem

(Continued)

TABLE 16–6 Induration, Sclerosis, Atrophy (Continued)

3 Morphea White-yellow, circumscribed Trunk, proximal A, C Females > males, nonprogressive

4 Poikiloderma Atrophic, scaly, mottled, Face, neck, trunk I, C Associated with malignancies

wrinkly

5 Ehlers-Danlos Wrinkly, “cigarette-paper,” Areas of trauma C, A Hyperextensibility, collagen

6 Striae Linear, usually vertical; Areas of growth A, C Females > males, assoc with

colored red, white, purple and stretch pregnancy, weightlifting,

obesity, Cushing syndrome,steroid toxicity

7 Necrobiosis Red-yellow plaques, ulcer Anywhere, especially A Long-standing diabetes, can be

diabeticorum

8 Trauma Depressed areas Trauma or injection A, C Insulin, steroid, or other

9 Scarring Depressed, hypopigmented Site of inflammation A, C, I Varicella, shingles, smallpox,

B Rarer

1 Progeria Induration, sclerosis, atrophy Diffuse I, C, A Alopecia, birdlike, early

atherosclerosis

2 Lawrence-Seip Dystrophy, acanthosis Generalized, severe I, C, A Multiple endocrine abnormalities,

3 Werner Scleroderma-like, calcifying More on face A Diabetes, hypogonadism, early

Abbreviations: PKU = phenylketonuria; CNS = central nervous system; assoc = associated; esp = especially; mos = months; MR = mental retardation; Temp =

temperature.

Configuration Pattern and Clinical Etiology and Associated Systemic

I Painless

A Neuropathic Sharp, heaped edges Areas of trauma, A, C, I Sensation loss (spina bifida,

ingestion, diabetes)

II Painful

A Ischemic

1 Vasculitis Small, sharp edges, Acral, but spread A, C, I Consumptive coagulopathy (e.g.,

cutis, Behçet’s,cryoglobulinemia, Hgb SS,ergotism

B Granulomas Similar to ischemic, may Midline, nasal, oral, A, C Inflammatory bowel disease, TB

C Mechanical

1 Decubital Undermined, spread in Pressure areas, bony A, C, I Bedridden patients, e g.,

2 Traumatic Configuration of area of Location of trauma Burns, cold, corrosives

trauma, possible gangrene

(Continued)

TABLE 16–7 Ulcers (Continued)

3 Radiation Bullae → shaggy ulcers → Location of radiation A, C, I Cancer patients

sharp ulcers if chronic, therapyvariable pigmentation,

telangiectasia

synd.), adolescents withpsychiatric problems (rubbing,cutting)

D Infectious

1 Puncture wounds Indurated and yellow, Area of bite, abscess A, C, I Determine bacterial etiology

bite, others)

Pseudomonas (ecthyma

a Cat scratch fever May present only as Arm, hand, face, A, C Bartonella henselae, cat scratch,

b Tularemia Oculoglandular type Face, eyes, and A, C, I Pasturella tularensis, rodent or

c Sporotrichosis Ulcer, nodules along Finger, hand A, C Sporothrix schenckii, roses, timber,

c Primary syphilis Chancre, single, punched-out, Male and female A If in child, sexual abuse until

indurated base, ± pain, (often missed) proven otherwise, Treponema

d Gonorrhea Mild erosions → small Male and female A If in child, sexual abuse until

ulcer, marked exudate (often missed) proven otherwise; Neisseria

gonorrhoeae

PCR; in child, think sexualabuse but not always

A, C, I Condyloma lata, secondary

syphilis, sexual abuse inchildren until proven otherwise

Abbreviations: DIC = disseminated intravascular coagulation; Hgb SS = sickle cell anemia; MRSA = methicillin-resistant Staphylococcus aureus; PCR = polymerase

chain reaction; HPV = human papilloma virus; synd = syndrome; TB = tuberculosis.

The normal hair cycle consists of the following phases:

Anagen This represents active growth, where the hair follicle begins in

the deep dermis and wraps itself around the dermal papilla Theloose previous hair of that follicle is pushed out This phase gener-ally lasts 2 to 3 years

Catagen This is a transitional phase lasting about 3 weeks Hair growth

ceases, and the hair bulb dislodges itself from the dermal papilla.The end of the hair now has a blunt club shape to it

Telogen This is the resting phase, which lasts 3 to 4 months The hair

now assumes a mace-like shape at the base and dislodges itself withthe onset of the new anagen phase

At any given time 70 percent or more of hair is in the anagen phase,

so ongoing hair loss is not noticeable

Problems

Although most of dermatology is morphology-driven, there are still keyhistorical points to cover:

• Time of onset? Congenital or acquired?

• How does the condition progress? Does it wax and wane? Is itbecoming steadily worse?

• Is there a patient history of systemic illness that may explain theproblem?

• Is there a family history of a similar condition?

• Are there associated systemic symptoms and signs with the presentcondition?

• Is the patient exposed to medications or toxins that may cause hairloss?

• Is there any pain, stinging, or pruritus?

• Is there a history of injury or underlying allergy or infection?

• How is the patient’s emotional stability? Is there a history of mutilation or hair pulling?

self-Findings

Hair problems are due to hair loss (alopecia), excess hair chosis), or abnormalities of the hair shaft Examination of hair is byobservation and palpation Key findings related to each of the problemsare enumerated below

(hypertri-590 Chapter 16: The Integument System—Skin, Hair, Nails

Hair Loss

Pattern

Is the hair completely or partially absent? Is the shaft intact or abnormal?

Is there a differential in length of hairs that are present? Is the hair loss inpatches or diffuse? What is the shape of the patch? Are there abnormalities

of the skin underlying the area of hair loss such as inflammation or scarring,

or is the underlying skin smooth? Are there hair stubbles present?

Distribution

Is the hair loss focal or diffuse? Did it begin focal and spread, or has italways been diffuse? What specific areas are involved?

General Physical Examination

Are there any abnormalities of other ectodermally derived structures(CNS, eyes, and teeth)? Is there difficulty with temperature control, asmanifest by excessively warm skin or lack of perspiration? Does the gen-eral physical examination lead to any other systemic conditions?

Synthesizing a Diagnosis

The best approach is to use the patient history to categorize whether thecondition is congenital/genetic, metabolic/toxic, infectious/inflamma-tory, or traumatic We will take each category and build on it with keyfindings to arrive at a diagnosis

Congenital/Genetic

Check the underlying scalp for abnormalities Cutis aplasia and tinentia pigmenti cause scarring Nevi or hemangiomas will retard hairgrowth in the involved areas It is helpful to examine hair shafts under

incon-magnification In monilethrix the hair has a beaded appearance, whereas

in pili torti the shaft is twisted In trichorrhexis invaginata the hair appears like bamboo, and in trichothiodystrophy the hair appears ribbon-like.

TABLE 16–8 demonstrates differential diagnoses that are congenitaland/or genetic in origin

Metabolic/Toxic

Is there a family history of metabolic disorders? Hyperthyroidism is ciated with hair loss Consider homocystinuria, often associated with Mar- fanoid habitus, ectopia lentis, and blood clot formation Johanson-Blizzard

asso-syndrome consists of hypothyroidism, pancreatic insufficiency, genitaldefects, craniofacial malformations, and developmental delay Toxinsmay cause hair loss by direct damage with associated scarring Examplesare alkali burns, thermal burns, radiation, surgery, allergens, and heavymetal intoxication such as thallium and arsenic

KEY FINDING

TABLE 16–8 Congenital Hair Loss

Localized

I Nonscarring

A Underlying skin

abnormality Nevus, sebaceous nevus, hemangioma, hamartoma

II Scarring Incontinentia pigmenti, cutis aplasia

Generalized

I No underlying skin

abnormality

B Syndromic Menkes kinky hair syndrome (pili torti, severe retardation), woolly hair syndrome (pili torti),

trichothiodystrophy (retardation, hypogonadism, progeria-like), progeria (thinning of skin, senilepigmentary changes), cartilage-hair hypoplasia syndrome (leg bowing, wide metaphyses, shortstature), trichorhino phalangeal syndrome (mild loose skin, protruding ears, bulbous nose, bonyabnormalities, mild retardation), Hallermann-Streiff syndrome (short stature, frontal bossing, thinnose, parrot-like, eye defects)

II Underlying skin Ectodermal dysplasia syndromes associated with eye, CNS, hypohidrosis; dyskeratosis congenitaabnormality (poikiloderma, reticulate pigmentation, telangiectasia, atrophy), CHILD syndrome (hemidysplasia,(syndromic) ichthyosis, limb defects)

Synthesizing a Diagnosis 593

Hair loss from chemotherapy is nonscarring and results from cessation

of the anagen phase of hair growth

Infectious/Inflammatory

Tinea capitis, or scalp fungus, is endemic among African-American

chil-dren It starts with mild, red, scaly patches of the scalp, and hair lossensues The pattern is typically with stubble formation owing to hairbreakage Lesions are annular but also can be diffuse The scalp lesionsmay become inflamed, forming pustules that often are misconstrued forimpetigo Occasionally, the inflammation becomes more intense andforms raised, boggy plaques (kerions)

Alopecia areata presents as localized round patches of hair loss with

perfectly smooth skin They vary in size and on rare occasions will

progress to alopecia totalis (entire scalp) or alopecia universalis (entire

body) Hairs from the periphery of the area of loss will resemble mation points under magnification Although there is no outwardevidence of inflammation, skin biopsies do indicate evidence of lym-phocytic infiltration and antigen-antibody complexes

excla-Telogen and anagen effluvium results from the arrest of the hair cycle at

either stage This is often a consequence of a high fever, infection, stresssuch as surgery, and certain drugs There is loss of hair over a 3- to 5-monthperiod Although distressing, the hair invariably grows back over several

months Presence of club-shaped hairs supports this diagnosis Anagen effluvium is the result of chemotherapy and heavy metal intoxication

In small infants, particularly with the present “back to sleep” ment, many have a large occipital patch of hair loss owing to constantexertion of pressure on that area This is a self-limiting condition thatresolves as the infant sits and spends less time on his or her back

move-Hypertrichosis or Hirsutism

Hypertrichosis refers to localized patches of increased hair growth ples in children are nevi and hamartomas It also may be a consequence

Exam-of localized application Exam-of steroids, particular androgenic, or become

more extensive owing to hypothyroidism, porphyria, or exposure to other drugs such as phenytoin, cyclosporine, and minoxidil

Hirsutism refers to excessive hair growth in a child or a woman

in a male pattern This often results from endocrine dysfunction,

examples of which are Cushing, adrenogenital, and polycystic ovary syndromes.

Hirsutism may be congenital and can be either genetic (syndromic)

or the result of exposure to toxins such as phenytoin and alcohol

Exam-ples of syndromes include Coffin-Siris syndrome, mucopolysaccharidoses, leprechaunism, trisomy 18, Marshall-Smith syndrome, and others Consult

a text on dysmorphology for further detail

NAILS

The goals of this section are

1 To review developmental anatomy of the nails

2 To enumerate key historical and physical findings

3 To develop differential diagnoses for nail abnormalities

Developmental Anatomy

The nails begin development at 10 to 11 weeks of gestation with a skinfold, out of which develops the nail matrix The matrix is the area ofgrowth, producing the more visible distal nail plate The white crescent

at the base of the nail (lunula) is the distal end of the nail matrix A mal newborn has fully developed nails

nor-Problems

Nail disorders are either congenital or acquired Thus a full history isparamount to arriving at a diagnosis Key historical points are

• When did the patient or caregiver first notice this abnormality?

• Is there a family history of any dermatologic or nail disorders?

• Are there any exposures to infections, medications, or toxins(include travels)?

• Is there a past history of any dermatologic illness, including but notlimited to psoriasis, alopecia areata, lichen planus, and atopy?

• Is there a past history of systemic illness such as lupus sus, immunodeficiency, uremia, or endocrine disorder?

erythemato-• Is there any history of trauma?

594 Chapter 16: The Integument System—Skin, Hair, Nails

Descriptions of key nail abnormalities are as follows:

• Absence, atrophy, or dysplasia

• Hypertrophy of nail bed (onychauxis, pachyonychia)

• Spoon nail (koilonychia)

• Clubbing (angle between nail bed and plate greater than 20 degrees)

• Nail pitting (psoriasis, alopecia areata)

• Brittle nail plates (onychorrhexis)

• Separation of the nail (onycholysis)

• Discolored nail plates (yellow, red, blue, white)

• Subungual hemorrhage or hematoma

• Nail ridging (transverse of longitudinal)

• Transverse lines or ridges (Mees lines, Beau lines)

Synthesizing a Diagnosis

Nail disorders are divided into congenital/genetic and acquired.Acquired disorders may be metabolic/toxic/nutritional, infectious/inflammatory, traumatic, or associated with many chronic illnesses.Sometimes they are idiopathic Diagnoses below and their key histori-cal points and findings are discussed below

Congenital

See TABLE 16–9

Acquired

• Metabolic/toxic/nutritional Congenital metabolic disorders such as

Lesch-Nyhan syndrome manifest hypoplasia of nails owing to ruricemia and nail abnormalities owing to self-inflicted trauma Nail

hype-dystrophy is prominent in acrodermatitis enteropathica (zinc ciency) and diabetes Also, uremia produces whitening of the prox- imal nail bed Always be mindful of nail hypoplasia caused by in utero exposure to anticonvulsants, warfarin, and alcohol Malnutrition

defi-and specific deficiencies manifest as nail abnormalities The nails ofgeneralized malnutrition are dry and brittle and may contain trans-verse ridges They are also friable and appear laminated (onychor-

rhexis) Iron deficiency or hemachromatosis may cause koilonychia Chronic poisoning by heavy metals such as thallium, and arsenic or fluoride, may cause transverse white bands (Mees nails) Chronic

tetracycline exposure, more likely in adolescents, may cause cholysis Changes in nail color may be due to tetracycline exposure

TABLE 16–9 Congenital/Genetic Disorders of Nails

I Isolated

A Koilonychia No other abnormalities Spooning, clubbing, autosomal dominant, benign

C Congenital clubbing No cardiac or pulmonary Isolated and benign

problems

II Ectodermal dysplasias

Pachyonychia congenita Deafness, blindness, keratoses Nail thickening, yellow-brown discoloration

Dyskeratosis congenita See TABLE 16–8 Similar to pachyonychia congenita

III Hereditary disorders

w/systemic involvement

A Nail-patella syndrome Not limited to nails, +family Autosomal dominant, absence or hypoplasia of nail and

B Tuberous sclerosis Retardation, +family history Periungual fibromas; see “White macules,” “Flesh-colored

papules,” and “Cysts” above

C Ichthyosis See primary scales table

D Chromosomal abn Retardation, multiple anomalies Hyperplastic nails

E Rarer syndromes Hallermann-Streiff, others, koilonychia in trichothiodystrophy,

incontinentia pigmenti

Confirmatory Laboratory Studies 597

(yellow), chlorine or bromine exposure (green), carbon monoxideexposure (deep red), and phenothiazine or antimalarial exposure(blue-gray)

• Infectious The most common condition seen in childhood and lescence is a paronychia, which is usually acute and appears as a painful red swelling of the proximal or lateral nail folds Staphylo- coccus aureus is the most common cause The condition may be

ado-chronic, caused by Monilia, or may be a manifestation of an

under-lying immunodeficiency Chronic fungal infections (onychomycoses)

may appear more frequently in adolescence

• Neoplastic These conditions are rare in children and adolescents Melanoma will cause brown-black discolorations Sometimes benign lentigienes, isolated or syndromic (e.g., Peutz-Jeghers syndrome), will

cause this discoloration

• Traumatic The most common nail trauma seen in day-to-day tice involves subungual hematomas: blue, painful accumulation of

prac-blood under the nail; avulsions and fragility (onychorrhexis, cholysis); and fraying or dystrophy from picking and chronic biting

ony-Subungual hemorrhages may be spontaneous or induced by minimal trauma and often are due to embolic phenomena, endocarditis, sepsis, and vasculitis.

• Chronic disease Recovery from any severe illness, e.g., sickle cell sis, may produce transverse ridges (Beau lines) Look for clubbing

cri-and cyanosis associated with chronic cardiac or pulmonary disease

Half-and-half (Lindsay) nails and white proximal nails present in mia and chronic liver and heart disease Telangiectasia and splinter hem- orrhages with or without trauma always should raise suspicion for endocarditis Chronic conditions may produce significant changes in nail color Brown discoloration is due to Addison disease Yellow nails are associated with jaundice and carotenemia, and blue or gray nails occur in Wilson disease.

ure-• Idiopathic Sometimes nail abnormalities will be diffuse but not ciated with any underlying condition Examples include twenty-nail dystrophy, characterized by yellow, dystrophic, friable nails (all of

asso-them) This condition may last several years but usually resolves

Frequently, onychorrhexis may be idiopathic or benign and familial.

Reedy nails and longitudinal striations appear as an exaggeration

of a normal nail and rarely have any significant cause

Confirmatory Laboratory Studies

After making a diagnosis, the following laboratory aids are often ful to confirm or negate the hypothesis These should be available in aprimary care office setting

use-• Gram stain This is helpful to determine the content of lesions such

as polymorphonuclear cells, eosinophils, and bacteria

• KOH (potassium hydroxide) preparation for fungi Look for hyphae for fungal infections, budding yeast for Candida, or a “meatballs and spaghetti” pattern of tinea versicolor A KOH prep will demonstrate oval opalescent bodies of molluscum contagiosum.

• Low-power microscopy to identify lice, eggs.

• Tzanck smear to identify varicella and herpes simplex Note the

pres-ence of multinucleated giant cells

• Wood’s lamp This is helpful for diagnosis of certain fungal infections, specifically Microsporum Unfortunately, this accounts for only about

10 percent of fungal skin infections Tinea versicolor yields a green fluorescence, as will Pseudomonas infections Pigmented skin

yellow-absorbs ultraviolet light; nonpigmented skin reflects it Thus the Wood’s

lamp is often helpful to detect vitiligo in a fair-skinned individual or tuberous sclerosis in infants with earliest onset of depigmentation

598 Chapter 16: The Integument System—Skin, Hair, Nails

The Psychodiagnostic Examination

17

Chapter

Joseph L Calles

The goals of this chapter are

1 To learn the key elements of the psychiatric history and mental statusexamination and how they may be modified to match the develop-mental level of the patient

2 To classify the psychiatric disorders encountered in younger patients

by the major domains of impairment, i.e., disturbances of thought,feeling, and/or behavior

3 To outline the criteria used in arriving at specific psychiatric diagnoses

4 To learn when to pursue medical, neurologic, and/or cal evaluations/consultations in order to clarify or confirm diagnoses

psychologi-Psychiatric History and Mental

Status Examination

Psychiatric History

For several generations, a medical adage has stated that “80 percent ofdiagnosis is made by the history,” and this has certainly held true in the

field of psychiatry Although we may observe certain physical signs of

illness in our patients (e.g., the characteristic tics of Tourette disorder),

it is generally the symptoms elicited during the clinical interview that

guide the diagnostic process

In order to obtain information (from patients and their caregivers)that is relevant, useful, and complete, it is helpful to follow a consistentformat for data gathering This can and will be modified to correspond

to the quality and quantity of the information received, the source ofinformation (e.g., patient versus parent), and the chronological anddevelopmental age of the patient

Here are the elements that should be included in a standard atric history:

psychi-1 Source of information Is the patient able to describe his or her

symp-toms, or does the caregiver have to provide the information? Hasthe caregiver known the patient all of his or her life, or has therebeen limited (e.g., in a foster-care setting) or sporadic (e.g., changes

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in custody) contact? Is the information reliable, i.e., is it providedout of concern for the child, or is there another agenda, such as get-ting medications to “quiet” the patient or to qualify for disabilitycompensation? Is the information intelligible, or are there speech/language impediments to the process, including having to conductthe interview through an interpreter?

2 Identifying information What is the name (including preferred name,

such as a nickname), age (in years and months), gender, race/ethnicity, school name and grade (if applicable), and living situa-tion (e.g., where and with whom) of the patient? Who referred thepatient for the evaluation?

3 Chief complaint What is the referring person, the caregiver (if different

from the referrer), and (if possible) the patient himself or herself cerned about? This important issue will appear in the next section

con-4 History of present illness (HPI) All good stories involve a timeline, and

this one—the patient’s story—is no different The sequence of howproblems developed is the frame onto which to attach other details.The purpose of this section is not only to document symptoms to make

a diagnosis but also—and more important—to get a sense of how ness has affected that patient and those around him or her Importantelements in this section, to be addressed for each problem, include

ill-• Temporal factors When did the problem begin? Has it been

contin-uous or episodic? How often does it occur? When does it occur (e.g.,time of day, day of week, time of year)? How long does it last? What

is the longest period of time that the problem was absent before itrecurred?

• Spatial factors Where did the problem begin? Where does it

com-monly occur now? Are there any settings in which the problemdoes not occur?

• Modifying factors What initially precipitated the problem? Does it

still trigger an episode? Does anything make the problem worse?Does anything make it better? How do people in the immediateenvironment respond when the problem is evident?

• Severity What is the most serious thing that the patient ever did

during an episode? Compared with when the problem firststarted, is it better, worse, or about the same?

• Quality If worse, in what ways? If better, in what ways?

The general and specific symptoms to inquire about appear inthe sections on classification and diagnosis

5 Past psychiatric history Has the patient ever had formal psychiatric

or psychological evaluations? If yes, when, where, and by whom?What were the diagnoses, and were recommendations made? Didthe patient follow them? If so, what were the responses? Is the patientcurrently in therapy, or was the patient in therapy in the past? If yes,what type, how often, for how long, and with whom? Did the ther-apy help? If yes, in what ways? Is the patient taking psychotropicmedications? Has the patient ever been in a psychiatric in-patientunit? Day (partial) hospital program? Residential treatment center?Respite program? Runaway shelter? Any other treatment setting? Ifyes to any of these, what were the circumstances?

600 Chapter 17: The Psychodiagnostic Examination

Psychiatric History and Mental Status Examination 601

TABLE 17–1 is a guide to get details about the medication history,and the caregiver or patient, as part of the preappointment paper-work, can fill it out

6 Past medical history Is the patient currently in treatment for any acute

or chronic medical conditions? Who is the primary care physician?Are there any medical specialists involved in his or her care? Is thereany history of hospitalizations? Surgeries? Trauma (especially headinjury)? Seizure activity (especially nonfebrile)? Serious infections(especially of the CNS)? Are immunizations up to date? Any adversereactions to vaccinations? Any adverse reactions to medications?Any allergies? If currently on any nonpsychotropic medications, listthe names, dosages, indications, and responses Has the patient beensexually active (including oral and anal intercourse)? Did he or sheuse contraception? Is there concern about or history of sexuallytransmitted diseases?

7 For females, obstetric and gynecologic history At what age was

menar-che? Are menses regular? When was the last menstrual period? Arethey painful to the point of being unable to function? Does moodchange before menses to the point of being less able to function? Inwhat way does mood change? Has the patient ever been pregnant?

If yes, how many times? What were the outcomes?

8 Substance use history Does the patient use tobacco or alcohol? Does

the patient use illicit substances, such as marijuana, cocaine, heroin,etc.? If so, what are the routes of use (including intravenous)? Doesthe patient misuse licit substances, such as prescription medications,over-the-counter medications, weight-gain or weight-loss products,nutritional products, herbal products, or “energy” beverages (includ-ing coffee and other caffeinated drinks)? Does the patient ever inhalevolatile compounds (such as gasoline, paint thinner, correction fluid,various sprays, etc.) to get “high?” (This practice is sometimes

referred to as huffing.)

If the patient answers “Yes” to any of these items, at what agedid the activity start? When was the last use? How often does thepatient use it? How much? Any adverse consequences, such as

“blackouts,” memory loss, withdrawal, or other physical symptoms?How about behavioral consequences, such as engaging in unwantedand/or unprotected sex?

9 Developmental history Was it a planned pregnancy? Was the patient

wanted? Were there any complications during the pregnancy? Werethere exposures to any drugs (licit or illicit), alcohol, nicotine, toxins,

or radiation? Was the baby born at term, prematurely, or postdates?Were there any complications at the time of birth or shortly there-after? What were the Apgar scores? Did the baby require bilirubinlights? Were any neonatal screening test results abnormal? Breast-fed, bottle-fed, or both? For how long? How was the feeding expe-rience for both mother and child? Did the child’s growth (length,weight, and head circumference) follow standardized curves, orwere there significant deviations? Were developmental milestones

on time, early, or late? At any point were there concerns about thepatient’s development? At what age was the patient able to sleep