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160 Cards in this Set
- Front
- Back
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Phases of hair growth
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Anagen- growing phase, 3-4 years
Catagen- regression of hair follicle; lasts 2-3 weeks, transitional hairs Telogen- resting phase, cessation of all activity. Hairs destined to be shed, lifespan 3 months. |
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Nails
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Hard plates of tightly packed, specialized keratin.
Nail growth- 1 mm/week |
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Eccrine Sweat Glands
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Widely distributed; open directly onto skin surface. Control body temperature
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Apocrine Sweat Glands
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Limited to genitalia, axillae, areolae; stimulated by emotional stress
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Sebacceous Glands
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Found surrounding hair follicles; distributed over entire body EXCEPT palms and soles. Largest glands found on facer and upper back; influenced by androgen secretion
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Infants- Skin
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Skin smoother, less oily
Desquamation of stratum corneum Vernix caseosa Subcutaneous fat poorly developed Lanugo Eccrine glands function after 1 month- poor thermoregulation Aprocrine glands do not function Shedding of hair at 3 months Secretion of sebum may result in cradle cap Numerous skin lesions may be observed, ie. Mongolian spots, nevus flammeus, hemangiomas, milia, erythema, toxicum neonatorum |
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Adolescents- Skin
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Aprocrine glands activated
Increased sebum production; appearance of acne Grow pubic/axillary hair Facial hair in boys |
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Pregnant Women- Skin
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Increased blood flow to the skin
Increased sweat/sebaceous gland activity Fat deposits Stretch marks (striae gravidarum) Vascular spiders Increased pigmentation |
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Older Adults- Skin
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Decreased oil/sweat glands
Decreased elasticity of dermis Decreased subcutaneous tissue Thin, flat epidermis Decreased melanocyte function Decreased axillary hair Decreased body/head hair Increased nasal/ear hair in men Decreased nail growth Increased facial hair in women Specific lesions more common: actinic keratoses, basal cell carcinoma, seborrheic keratoses, stasis ulcers, senile pruritus, keratotic horns |
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KOH Examination
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Microscopic examination of KOH preparation of scraping taken from affected area. Most sensitive office lab test (if performed properly)
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Wood's Lamp
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Flurescent, long wave, UV light
Produces invisible long wave UV radiation- "black light" Commonly used to identify FUNGAL LESIONS, areas of hyperpigmentation, corneal lacerations Microsporium- GREEN fluroescence, Trichophyton- DOES NOT fluoresce, Tinea Versicolor- YELLOW fluoresence, Pseudomonas- GREEN fluoresence |
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Tzank Test
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Used to diagnose herpes infections
Scraping of base of vesicle is applied to microscopic slide; fixed with 95% ETOH and stained with Wright or Giemsa stain. POSITIVE TEST- multinucleated giants cells visible- either herpes simplex or varicella zoster |
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Darier's Sign
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Positive when brown macular or slightly popular lesion of urticaria pigmentosa becomes palpable wheal after being vigorously rubbed with blunt end of instrument
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Auspitz's Sign
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Postive when scratching of scaly lesion reveals punctuate bleeding points within lesion; suggestive of psoriasis
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Skin Biopsy
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Shave, Punch, or Incisional
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General Pigmentation
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Reflects patient's nutritional, hematologic, CV, or pulmonary status
Consistent with genetic background and varies from pinkish tan to ruddy dark tan; callused areas may appear yellow, vascular flush may be noted s/t anxiety or excitement Color hues in dark skin best seen in sclera, conjunctiva, buccal mucosa, tongue, lips, nail beds, palms Freckling of buccal cavity, gums, and tongue- normal phenomenon |
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Temperature of Skin
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Warm to touch
Hypothermia localized with Raynaud's Hyperthermia- infection, hyperthyroidism |
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Moisture
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Dry
Dehydration- evident in oral mucus membranes Diaphorisis |
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Cafe au Lait Spots
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Tan or light brown macules or patches with well-defined borders; vary in diameter from .5-20 cm.
Caused by an increase in the number of basal melanocytes Benign, cosmetic disorder with no malignant potential; when <3 cm in length and <6 in number Presence of > 6- 90% probability of neurofibromatosis No response to bleaching; lasers may eliminate DD: solar lentigines, pigmented nevi |
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Freckles (Ephelides)
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Tan to dark brown small macules; increase with sun exposure and fade during winter.
Become apparent between 6-9 years of age; genetic predisposition, accentuated by sun exposure, increase in number and size during pregnancy Respond to bleaching agents DD: lentigo, superficial sebhorrheic keratosis, nevi |
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Melasma (Cholasma, Mask of Pregnancy)
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Mottled brown, blotchy symmetric pigmentation of forehead, cheeks, upper lid, and chin
Types: Epidermal: 70% of cases, VISIBLE UNDER WOODS LAMP Dermal: 15%, NOT VISIBLE under Woods Lamp Indeterminant: occurs primarily in deeply pigmented people Most prevalent in Hispanics May also occur with OCPs or hormonal supplementation Usually occurs during 3-4th month of pregnancy and fades after delivery Responds to hydroquinone 4% bleaching agent DD: Postinflammatory hyperpigmentation |
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Postinflammatory Hyperpigmentation
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Brown or purple macule that occurs at site of previous lesion or trauma
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Solar Lentigo (Age Spots, Liver Spots)
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Macula that is darker and larger than a freckle; does not fade during the winter
Occurs on sun exposed areas Occurs in 90% of white after age 70 Responds to bleaching agents DD: freckles, nevi, lentigo maligna |
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Albinism
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Genetic alteration of melanin pigment system, affecting skin, hair, eyes
Photophobia, visual defects, nystagmus common; otherwise healthy DD: Vitilgo |
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Vitiligo
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Totally white, non-scaling macular patch with convex outline; hair may or may not be hypopigmented
Localized loss of melanocytes from skin and hair; may occur after severe emotional or physical trauma. 10% of patients have coexisting autoimmune conditions (DM, hypothyroidism, Addison's disease) Spontaneous repigmentation in 15% of cases DD: tinea versicolor, pityriasis alba, idiopathic guttate hypomelanosis |
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Postinflammatory Hypopigmentation
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Hypopigmented macules/patches that occur in same location as prior inflammatory lesions
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Pityriasis Alba
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Round to oval hypopigmented patches with fine scales, occurring predominantly on face, upper arms, neck and shoulders.
Lesions spontaneously resolve in months and/or with puberty- TEMPORARY. Result from reduction of active melanocytes in affected skin. DD: Tinea versicolor, tinea alba, vitiligo |
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Idiopathic Guttate Hypomelanosis
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Small, hypopigmented droplike macules wtih sharply defined borders. Surface is smooth; no scaling, scaring, atrophy.
Most common on sun exposed skin, particularly shins and forearms. NEVER ON FACE, TRUNK, Lesions increase in # with age Basic etiology unknown; may be result of trauma or injury or UV exposure More common in females >50 yo; has familial predisposition DD: Vitiligo, chemical depigmentation, tinea versicolor, postinflammatory hypopigmentation |
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Benign Melanocytic Tumors (Melanocytic Nevi)
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Cutaneous hamartoma or benign proliferation of cells
Can be classified based on: Histology: junctional, compound & dermal Appearance: halo nevus, blue nevus, etc Time of presentation: congenital vs. acquired |
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Acquired Melanocytic Nevocellular Nevi (NCN)
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Benign neoplasms composed of nevus cells; derived from melanocytes
Most disappear by age 60 (except dermal NCN) Extremely common; appear on almost everyone. Most adults have about 20; less common in pigmented people Most arise in childhood and adolescence; if present at birth, congenital. Children who have had painful sunburns before age 10 may present with more nevi Puberty and Pregnacny- both the size and number of nevi increase Very few nevi arise after age 40- should be monitored as more likely to become melanoma. Clinical presentation varies, depending on stage of evolution; most lesions are very small (<1 cm) and may occur anywhere. Appear mostly on sun-exposed skin above waist NEVER become malignant s/t manipulation or trauma. |
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Junctional NCN
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Most common form; flat or only very slightly raised, tan, brown, or dark brown macules/patches, round or oval with smooth, regular borders. Color uniform throughout. Skin furrows are preserved, scattered discrete with random distribution. Size is <.6 cm; IF >1.0 cm NEVUS IS CONGENITAL OR DYSPLASTIC NCN
Pigmented nevi of PALMS, SOLES, GENITALIA, & MUCUS MEMBRANES ARE ALMOST ALWAYS JUNCTIONAL NEVI. |
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Compound NCN
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Slightly to markedly raised pigmented papule or nodule; usually dark brown or black; center more pigmented than periphery. Round, dome shaped, occasionally papillomatous or hyperkeratotic, often associated with bristle like terminal hair.
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Dermal NCN
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Dome shaped, soft papule; appears after adolescence
Skin colored, tan, brown or flecks of brown, often with telengiectasia (Small dilated blood vessels near the skin surface) Most common on face and neck; can occur on trunk and extremities Most hairy nevi are dermal |
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Halo NCN
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Nevus surrounded by ring of hypopigmentation
Most common on backs of adolescents and gradually disappear over months to years |
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Blue NCN (Dermal Melanocytoma)
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Acquired, benign, firm, dark-blue to gray-black sharply defined papule or nodule.
Smaller than 1 cm and stable for many years do not need to excise. Malignant melanoma RARELY develops in blue nevi. |
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Spitz Nevus (Benign Juvenile Melanoma)
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Benign melanocytic tumor; onset 3-13 years, most often 3-7 years. Common on face and lower extremities; easily mistaken for hemangioma.
Solitary, firm, slightly scaly, round, dome-shaped nodule; red brown or brown-black; 5-10 mm in size Comes rapidly; fast growth over 6-12 months then stabilizes. Does not regress spontaneously; may bleed when traumatized. |
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Urticaria pigmentosa
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Characterized by few to many brownish spots which itch and when scratched produce welts and reddened skin. Brown spots contain cells with high levels of histamine; may develop flushing and headache from massive release of histamine from these spots. Treatment is contraversial- histology concerning for melanoma; most are benign, metastasis is possible; reccommend excisional biopsy
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Nevus Spilus
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Solitary, nonhairy, flat brown patch of melanization dotted by smaller dark brown to blackish freckle like areas of pigmentation. Size varies from 1-20 cm. Generally present at birth; may appear at any age.
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Becker's Nevus (Nevus Spilus Tardus)
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Irregular macular hyperpigmentation characteristically seen on shoulders, anterior chest, or scapular region of adolescent males. Grows up to 10-15 cm; after a period of time (often 1-2 years) coarse hair appears in the region of the pigmented area.
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Juvenile Xanthogranuloma
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Dome shaped, yellow, pink, orange, or brown nodules that vary in size from a few mm to 4cm in diameter. Usually present at birth or appear within 6-9 months of life. Affected children otherwise normal and have normal lipid levels.
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Dermatofibroma
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Very common; can be found at any age
Possibly scar-like reaction to insect bite Slow growing, round to oval, firm nodule; deeper component attached to overlying skin. Few mm to several cm in size. Pink to brown- may be darker in center. Most common on LEGS, ARMS, TRUNK |
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Fitzpatrick's (retraction) sign
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Skin dimples downward with lateral retraction.
Confirms Dermatofibroma |
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Cherry Angioma (Senile Angioma)
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1-8 mm in diameter, asymmetric/symmetric, bright red to purple papule
Almost universal with aging Most common sites: TRUNK and PROXIMAL EXTREMITIES Histology: clusters of tightly packed, small blood vessels in upper dermis |
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Sebaceous Gland Hyperplasia
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Most common site: TRUNK AND PROXIMAL EXTREMITIES. Also- forehead, cheeks, nose, vulva
Common in middle age and elderly people In patients with RARE FAMIAL FORMS begins during puberty. Soft, yellow, dome shaped papules, some of which are centrally umbilicated 2-4 mm in diameter No clinical significance |
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Nevus Sebaceous
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Congenital hamartoma of the skin; malformation of skin with abundance of sebaceous glands.
Fairly uncommon; no gender differences Sharply circumscribed solitary, yellow-orange oval to linear verrucous papule/nodule. 5mm-several cm Frequently present at birth; becomes more verrucous and yellow in puberty Most commonly located on head and neck in 5-20% of cases, BASAL CELL CARCINOMA OCCURS in portion of lesion. Treatment: excision before puberty or if >1 cm in infancy |
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Dermatofibroma
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Very common; can be found at any age
Possibly scar-like reaction to insect bite Slow growing, round to oval, firm nodule; deeper component attached to overlying skin. Few mm to several cm in size. Pink to brown- may be darker in center. Most common on LEGS, ARMS, TRUNK |
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Fitzpatrick's (retraction) sign
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Skin dimples downward with lateral retraction.
Confirms Dermatofibroma |
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Cherry Angioma (Senile Angioma)
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1-8 mm in diameter, asymmetric/symmetric, bright red to purple papule
Almost universal with aging Most common sites: TRUNK and PROXIMAL EXTREMITIES Histology: clusters of tightly packed, small blood vessels in upper dermis |
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Sebaceous Gland Hyperplasia
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Most common site: TRUNK AND PROXIMAL EXTREMITIES. Also- forehead, cheeks, nose, vulva
Common in middle age and elderly people In patients with RARE FAMIAL FORMS begins during puberty. Soft, yellow, dome shaped papules, some of which are centrally umbilicated 2-4 mm in diameter No clinical significance |
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Nevus Sebaceous
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Congenital hamartoma of the skin; malformation of skin with abundance of sebaceous glands.
Fairly uncommon; no gender differences Sharply circumscribed solitary, yellow-orange oval to linear verrucous papule/nodule. 5mm-several cm Frequently present at birth; becomes more verrucous and yellow in puberty Most commonly located on head and neck in 5-20% of cases, BASAL CELL CARCINOMA OCCURS in portion of lesion. Treatment: excision before puberty or if >1 cm in infancy |
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Dysplastic Melanocytic Nevus (Clark's Melanocytic Nevus)
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Potential Precursor of melanoma and markers of person at risk for developing primary malignant melanoma
Red to brown macular-papular lesion with indistinct, irregular border; occurs most often on trunk and extremities. First appears in middlechildhood and develops Has hereditary tendency; autosomal dominant inheritance. Has relation to sunlight exposure. |
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ABCDE
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A: Asymmetry in shape
B: Border is irregular C: Color is mottled- haphazard display of colors; shades of brown, black, gray, red D: Diameter is usually large; greater than the tip of a pencil eraser E: Elevation is almost always present- surface distortion is assessed by side-lighting. Enlargement- a history of an increase in the size of the lesion is one of the most important signs of malignant melanoma |
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MMRISK
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M: Moles- atypical Moles (more than 10)
M: Moles- common Moles (numerous) R: Red hair and freckles I: Inability to tan; skin phototypes I and II S: Sunburn, severe sunburn before age 14 K: Kindred, family history of melanoma |
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Malignant Melanoma
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Develops from benign melanocytic cells (congenital nevi, dysplastic nevi); exact causative factor unknown. UV B radiation may play a role in malginant transformation
Increased number of atypical melanocytes along dermoepidermal junction; cells are not evenly dispersed, but crowd together. Form variable sized nests, extend down follicles and sweat glands. Atypical melanocytes are pleomorphic- differ from one another- larger than normal, and have nuclei of differing size, shape, and staining intensity (cellular atypia) Atypical melanocytes migrate upward within epidermis- buckshot spread. Margins of lesions are not sharply defined, but seem to peter out. Pigmentation varies from one cell to another. Prognosis depends on histologic thickness (breslow level) of tumor Sun exposure important predisposing factor but not as clearly causative as BCC or SCC Most lesions arise de novo, but some arise from precursor lesions such as large congenital nevi. Spread through local extexsion and lymphatic drainage. Highest incidence in men between age 30-49. Most common in people with fair skin, red hair, freckles, blue eyes Increase in number of atypical mal |
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Superficial Spreading Melanoma (SSM)
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Most common form of melanoma
Commonly seen on legs & back in women and on back in men. Usually begins in 50s Exclusively on white people Prolonged HORIZONTAL growth phase of up to 10 years characterized with lesions reaching 1-2 cm before vertical growth phase begins. Characteristics: variegated colors, irregular borders, may have elevated margins |
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Nodular Melanoma (NM)
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Presents are round or irregular, slightly elevated papule of gray-blue color on dark background. No horizontal growth. Tends to grow UP rather than OUT. Worse prognosis.
Lesions ulcerate and bleed frequently Common in Japanese. Early Metastisis with poor prognosis ABCs less helpful- may be symmetrical with uniform black color. |
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Lentigo Maligna Melanoma (LMM)
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Uncommon
Usually occurs on sun-exposed areas, especially face, neck, or extensor forearms. Form of melanoma in situ. Lesions tend to be flat Shows all ABCDs; grows slowly for years. Prognosis excellent before invasion. |
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Acral-Lentiginous Malignant Melanoma (ALM)
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Uncommon
Presents as flat, variably pigmented black-brown macule commonly on tips of fingers and toes or under nail bed, in mouth, genitals, anus. May present as black nail or nail loss. Most common form of melanoma among AA, Asians, Hispanics Tends to invade quickly- poor prognosis. |
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Basal Cell Carcinoma (BCC)
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Most common malignant tumor affecting whites- rare in AA, Latinos, Asians
Highest incidence among fair skinned people with red/blond hair over age 40 Caused by cumulative sun damage to skin over many years Locally invasive tumor that rarely metastisizes |
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Nodule Ulcerative Tumor (Nodular BCC)
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Begins as small, pearly waxy papule that enlarges peripherally with central depression. Border becomes translucent, elevated, shiny.
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Superficial BCC
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Erythematous scaly macular patch with elevated threadlike borders; multiple lesions frequently present.
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Sclerosing, Morpheaform, or Fibrosing BCC
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Lesion begins as slowly enlarging pore, which when fully develops appears as a slightly indurated yellowish white plaque with indistinct border. Blanches with pressure or with stretching; seldom ulcerated
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Squamous Cell Carcinoma (SCC)
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2nd most common skin CA in whites and most common skin CA in AA.
Increased incidence after age 55; earlier in people with sun exposure Smokers: increased lip involvement Response of keratinocytes to any environmental carcinogen (sunlight, burns, chronic ulcers, inflammatory disease). Firm, skin colored to reddish plaque or nodule. Frequently central ulceration. Often found in sunexposed area on face, ears, arms, hands. More likely than BCC to metastisize |
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Bowen's Disease
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SCC in situ
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Actinic Keratosis
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Sun induced damage to epidermal cells, cumulative from birth.
Causes proliferation of abnormal, premalignant, dystrophic cells that may eventually transform into SCC May occur on post-irradiation sites Most common in people older than 50; increased incidence in redheads, blondes, and those with freckles Clinical Presentation: rough, erythmatous poorly circumscribed patches with overlaying scales. |
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Actinic Chelitis
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Term used for AK that presents on sunexposed lips (lower lip); loss of vermilion border, milky discoloration, scaling
Treatment: sunscreen, if no resolution in one month, cryotherapy, light electrodisection and curettage, liquid nitrogen, shave, excise |
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Seborrheic Keratosis
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Exact cause unknown
Developmental not dependant on sun exposure and no malignant potential. Most common skin tumor in middle age and elderly; present in 90% of people older than 50. Average age of onset is 30. Clinical Presentation: warty, pigmented, sharply marginated, greasy papule with stuck on quality Most commonly involved: SCALP, BACK, CENTRAL CHEST and FACE |
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Keratosis Pilaris
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Autosomal dominant condition in which keratotic plug forms on each affected hair follice. Presents as firm papule; may or may not be erythematous. Usually appears gray, sandpaper feel. Most present on extensor aspects of upper arms or anterior thighs
Chronic condition; no cure. Lac-Hydrin 12% (or other glycolic acidn), retinoic acid, steroids group V |
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Acrochordon (Skin Tag)
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Derived from ectoderm and mesoderm and represent hyperplastic epidermis. Increased incidence with age
Obesity predisposing factor Also associated with pregnancy, menopause, DM and FH. May be skin colored or brown. Cosmetic disorder Axilla, neck, inguinal region- most common sites May indicate colonic polyps or colon CA if multiple lesions occur rapidly over a few months |
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Hypertorphic Scar
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Remains confined to site of original injury
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Keloid
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Extend beyond wound with clawlike extension.
More common in blacks than whites; most common sites: ear lobes, shoulders, upper back, chest |
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Hair Color
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Color comes from melanin production
Graying begins as early as the 30s due to reduced melanin production in follicles Genetic factors affect onset of graying |
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Hair Texture
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Scalp hair may be fine or thick; may be straight, curly, kinky
Change in texture indicates metabolic or endocrine abnormalities |
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Alopeica Areata
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Well defined, single or multiple patches or asymptomatic nonscarring complete loss of hair. Patches may occur suddenly, frequently overnight.
Familial predisposition Presumed to be autoimmune attack on follicle Most cases between age 5-40; if occurs before age 10, more likely to be permanant loss. Associated with autoimmune conditions Hair pull test |
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Androgenic Alopecia (Male/Female Pattern Baldness)
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Genetically influenced progressive balding that occurs through combined effects of genetic predisposition, action of androgen on hair follicles of scalp
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Telogen Effluvium
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"Flood of resting hairs"
Causes include: acute and chronic illness, emotional stress, physical stress, various meds (beta blockers, allopurinol, warfarin, heparin, retanoids, vit. A, OCPs) Common for loss to continue for 2-5 months |
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Trichotillomania
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Hair loss due to purposeful twisting or pulling of hair. Irregular shaped areas of partial hair loss. Occipital area spared.
Psych referral |
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Beau's Lines
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Transverse grooves, often parallel to lunula. Associated with renal, cardiac, hepatic disease, chemo. Causes nail to grow slowly or cease to grow.
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Mee's Bands
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White transverse line or band instead of groove. Results from acute systemic disease or poisoning. Historically associated with arsenic poisoning.
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Lindsay's Nails
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Half and Half Nails
Proximal portion of nail bed white/ distal portion pink or red. Associated with chronic renal disease, hypoalbuminemai, azotemia. |
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Keloid
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Extend beyond wound with clawlike extension.
More common in blacks than whites; most common sites: ear lobes, shoulders, upper back, chest |
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Hair Color
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Color comes from melanin production
Graying begins as early as the 30s due to reduced melanin production in follicles Genetic factors affect onset of graying |
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Hair Texture
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Scalp hair may be fine or thick; may be straight, curly, kinky
Change in texture indicates metabolic or endocrine abnormalities |
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Alopeica Areata
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Well defined, single or multiple patches or asymptomatic nonscarring complete loss of hair. Patches may occur suddenly, frequently overnight.
Familial predisposition Presumed to be autoimmune attack on follicle Most cases between age 5-40; if occurs before age 10, more likely to be permanant loss. Associated with autoimmune conditions Hair pull test |
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Androgenic Alopecia (Male/Female Pattern Baldness)
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Genetically influenced progressive balding that occurs through combined effects of genetic predisposition, action of androgen on hair follicles of scalp
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Telogen Effluvium
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"Flood of resting hairs"
Causes include: acute and chronic illness, emotional stress, physical stress, various meds (beta blockers, allopurinol, warfarin, heparin, retanoids, vit. A, OCPs) Common for loss to continue for 2-5 months |
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Trichotillomania
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Hair loss due to purposeful twisting or pulling of hair. Irregular shaped areas of partial hair loss. Occipital area spared.
Psych referral |
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Beau's Lines
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Transverse grooves, often parallel to lunula. Associated with renal, cardiac, hepatic disease, chemo. Causes nail to grow slowly or cease to grow.
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Mee's Bands
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White transverse line or band instead of groove. Results from acute systemic disease or poisoning. Historically associated with arsenic poisoning.
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Lindsay's Nails
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Half and Half Nails
Proximal portion of nail bed white/ distal portion pink or red. Associated with chronic renal disease, hypoalbuminemai, azotemia. |
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Terry's Nails
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White nail beds within 1-2 mm of distal border of nail
Associated with cirrhosis, hypoalbuminemia, HF, DM Type I |
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Internal Carotid
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Supplies cerebrum, basal ganglia, upper 2/3 of diencephalon
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Verterbral Artery
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Supplies Brainstem, lower 2/3 of diencephalon, cerebellum, occipital lobe
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Brain
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2 cerebral hemispheres
4 lobes: frontal, parietal, occipital, temporal Fissures and sulci divide the hemispheres Cerebrum is responsible for motor, sensory, associative and higher mental functions |
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Primary Motor Cortex
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Precentral gyrus
Control voluntary movements to opposite side of the body Cerebrum |
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Primary Sensory Cortex
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Postcentral Gyrus
Paresthesia and cutaneous sensation on opposite side of the body |
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Primary visual Cortex
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Located in occipital lobe
Visual symptoms Homonymous hemianopsia on contralateral side |
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Primary Auditory Cortex
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Temporal lobe along transverse temporal gyrus
Buzzing or ringing in ears |
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Frontal Lobe
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Personality, mood
Moral, ethical, social values Conscious and abstract thought and functions Long term memory Motor strip for opposite side of body which control voluntary skeletal movement and fine repetitive muscle movements |
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Parietal Lobe
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Sensory strip for opposite side of the body
Tactile, visual, gustatory, olfactory, and auditory sensations Comprehension of written word 2-point discrimination Recognition of object by size, shape, weight, texture Body part awareness |
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Temporal Lobe
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Hearing
Speech comprehension Special sense of taste and smell Interpretations Long term memory |
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Occipital Lobe
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Vision, recognition of objects, reading comprehension
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Cerebrum
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Thalamus
Hypothalamus Brain Stem |
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Thalamus
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Large mass located on each side of the 3rd ventricle
Chief sensory and motor integrating mechanism Level of consciousness, alertness, attention Perception of pain and thermal sensation |
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Hypothalmus
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Regulates catchecolamine, TSH, FSH, GH, ACTH, thirst, appetite, water, balance, sex, thermoregulation
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Brainstem
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3 sections:
midbrain pons medulla oblongata |
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Midbrain
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Part of brainstem
Visual system CN III, IV |
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Pons
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Part of brainstem
CN V, VI, VII, VIII, |
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Medulla Oblongata
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Arousal
Assists in controlling respiration, circulation, BP Relays sensory information between the cerebrum and cerebellum Sleep |
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Basal Ganglia
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Deep within the cerebral hemispheres
Fine movements of extremities, tremors, rigid movements |
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Cerebellum
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Keeps individual oriented in space
Coordination of: voluntary motor movements, equilibrium, posture, muscle tone |
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Spinal Cord
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31 pairs of spinal nerves
Each has a ventral (motor) and dorsal (sensory) root. 8 Cervical 12 Thoraicic 5 Lumbar 5 Sacral 1 coccygeal |
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Anterior Root
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Consists of efferent fibers
Originate in anterior and lateral gray matter Travels from the spinal cord to the peripheral nerve and muscle MOTOR ROOT |
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Ventral Root
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Consists of afferent fibers
Cell bodies in the dorsal root ganglion Carries impulses from the sesnory receptors to the body of the spinal cord and brain SENSORY ROOT |
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Glasglow Coma Scale
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International method for grading neuro responses
Scores from 3-15 (less than 8 is bad) Evaluates: Eye opening Verbal Motor |
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Mental Status
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Total expression of a person's emotional response, mood, cognitive functioning, and personality
Assessment is done thorughout the examination Cerebrum is responsible for mental state |
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Mini Mental Status Exam
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Does not test mood or thought disorders
Brief test Global assessment of many domains: orientation, registration of 3 words, attention/calculation, recall of 3 words, language, visual construction Score above 27 considered normal Scores 23-26 are borderline Scores below 22 are abnormal With dx of Alzheimers: Scores of 20-26 are mild Alzheimers 10-19 are mod. Alzheimers Below 10 is Severe Without tx, a person loses 2-4 points per year. |
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Mini-Cog
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3 minute instrument
Screen for cognitive impairment in older adults Screens for executive dysfunction and memory Say 3 unrelated words to patient. Have the patient repeat them Perform clock drawing test Have patient recall the words after 3 minutes Scoring: Recall 1-2 and clock is normal; nondemented Recall 1-2 and clock is abnormal- demented |
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Apraxia
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Inability to perform a task.
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Ideational Apraxia
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Unable to initiate, but understands
Bilateral lesions or disease |
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Ideomotor Apraxia
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Performs but makes errors
Unilateral lesion |
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Agnosia
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Inability to recognize
Generally associated with parietal lobe lesions |
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Prosopanosia
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Does not recognize faces
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Asomatoagnosia
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Does not recognize own hand
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Astereognosia
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Inability to recognize object in hand
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Agraphesthesia
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Unable to recognize number or letter on hand
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CN III
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Oculomotor
Consensual light response Elevation of eyelids Eye movement Double vision when looking at a near object and causes trouble when reading |
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CN IV
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Trochlear
Internal rotation Has trouble walking down the stairs |
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CN VI
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Abducens
PERRLA Lateral and Vertical Gaze Double vision when looking at distant objections |
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Doll's Eyes
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CN III Oculocephalic Reflex
Tests intactness of oculomotor and vestibular pathways Should not be tested with neck injuries Normal: eyes deviate towards opposite side of head turn Head turned right; eyes deviate left |
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CN V
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Trigeminal
3 different divisions: Opthalamic Maxillary Mandibular Test sensation to face, nasal and buccal mucosa, and teeth Motor branches: Palpate the temporal and masseter muscle and inspect face for fasciculations Sensory branches: test for pain/sensation, test corneal reflex, test temporalis and massester muscle against resistance |
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CN XII
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Hypoglossal
Supplies motor fibers to muscles of tongue Ask patient to open mouth and assess tongue- tongue protrusion, tongue side to side movement, lingual speech sounds |
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CN IX
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Glossopharyngeal
Pharynx, posterior 1/3 of tongue, TM, parotid gland Test gag reflex and ability to swallow Ability to identify sour and bitter tastes |
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CN X
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Vagus
Gag reflex Uvula and palate for symmetry |
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CN XI
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Spinal Accessory
Shoulder shrug and face turn against resistance |
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Primary Sensory Functions
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Superficial Touch: Cotton swab; have patient point to area touched
Superficial Pain: broken stick; ask patient to identify Vibration: tuning fork on joint Proprioception: eyes closed; hold great toe and move up and down Temperature and Deep Pressure |
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Practice Pearls- Sensory Functions
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Look for side to side asymmetry
Look for distal graded sensory loss Allow at least 2 seconds between stimulus |
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Cortical Sensory Functioning
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Stereognosis: have patient close eyes and identify object placed in hands
Graphesthesia: have patient close eyes and draw letter or # on hand 2 Point Discrimination: use paper clip; alternate touching with 1 or 2 points. Find point at which patient can no longer distinguish 2. Tongue: 1 mm Fingertips, Toes: 2-8mm Chest: 40 mm Back: 40-70 mm UE and thighs: 75 mm 2 Point Extinction:Pt sits with eyes closed; touch patient and have them point to location. Repeat touching 2 points on opposite sides simultaneously Test IMPAIRED SIDE first |
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Reflexes
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Examine for symmetry, hyper, hyporeflexia
2 types of reflexes: Superfical and Stretch (Deep) 0-no response 1+ Dimished 2+ Normal 3+ Increased 4+ Hyperactive Reflexes check intactness of reflex arc in the peripheral nervous system Sensory afferent fibers- dorsal root- spinal cord Synapse occurs with the motor neuron in the anterior horn Leaves spinal cord through ventral horn-motor efferent fibers- muscle |
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Superficial Reflexes
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Upper Abdominal: Assessment of T7-9
Lower Abdominal: T10-12 Cremasteric: L1-2 Plantar: Negative Babinski- no fanning Positive Babinski indicates an upper motor neuron lesion of the pyramidal tract Lesions of the pyramidal tract will cause decrease or absence of superficial reflexes and will be lost in deep sleep or coma |
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Deep Tendon Reflexes
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Biceps and Brachioradialis: C5-6
Triceps: C7-8 Patellar: L2-4 Achilles: S1-2 |
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Jendrassik's Manuever
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Used to augment DTR response
Pt clasps hands together and isometrically pulls while reflex is tested Also can clench teeth or grasp thigh with opposite hand |
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Grasp Reflex
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Pathological Reflex
Involuntary grasp of finger Unilateral: frontal lesion of contralateral side Bilateral: diffuse bifrontal dysfunction |
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Glabellar tap
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Pathological Reflex
Also called Meyerson's sign Gentle tapping of nasal area with finger out of view Normal: patient adapts to stimulus without further blinking Abnormal: compulsive or irresistable blinking Parkinsons |
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Clonus
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Rhythmic jerking
Test on wrist and foot Preeclampsia |
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Hyperreflexia
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Indicates an upper motor neuron lesion
Hyperthyroidism, electrolyte (Ca) imbalance, muscles spasms associated with polio |
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Hyporreflexia
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Indicates a lower motor neuron lesion
Decreased muscle bulk, flacid paralysis, hypothyroidism |
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Rigidity of muscles
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Increased muscle tone
Common in degenerative muscle conditions Parkinsons Disease |
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Spasticity
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Increased muscle tone which becomes greater with progressive muscle stretch
Initial resistance is low but will increase gradually as muscle progressessively stretches Common in patients with pyramidal (corticospinal)tract damage |
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Flaccidity
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Decreased muscle tone, floppy
Common in damage to peripheral nervous system, nerves supplying muscles themselves |
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Pronator Drift
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May indicate hemiparesis, CVA
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Chorea
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involuntary writhing and twisting motion
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Tremor
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Rhythmic muscular oscillation around a joint in a to and fro or up and down fashion
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Myoclonus
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Sudden, shock-like, jerking or twitching motion of a joint
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Dystonia
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Persistent, flexed contraction of a muscle.
Ex. Torticollis |
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Atrophy
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Muscle wasting caused by damage of the muscle supplying nerves
May be caused by disease or muscle disuse |
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Decerebrate
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Rigid and sustained contraction of the exstensor muscles, back and neck may be arched, teeth clenched
Due to midbrain or pontine damage, severe metabolic disorders that depress diencephalic function |
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Decorticate
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Hyperflexion of the arms, hyperextension and internal rotation of the legs and plantar flexion.
Found in unconscious patients with cerebral hemisphere lesions |
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Monofilament Test
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Used to test for peripheral neuropathy in diabetes
Use the 5.07 monofilament Apply the monofilament for 1.5 seconds until it bends Should feel a sensation at each site |
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Neck and Spine
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Examine for s/s of increased tone, paraspinal tenderness.
Pt flat; passively life chin to chest |
