A Lecture Presentation In Anatomy And Physiology

A LECTURE PRESENTATION IN ANATOMY AND PHYSIOLOGY PRESENTED BY PROFESSOR DENNIS N. MUÑOZ, RN

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The Integumentary System A.k.a., the integument Covers the entire body Accounts for about 7% of total body weight Pliable, yet durable Thickness: 1.5 to 4.0 mm Composed of the epidermis and dermis considered an organ or an organ system body’s largest organ ‡organ of greatest surface area:15-20 sq ft. (1.5-2 m2)

Functions of the Integumentary System •

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Protection o Chemical Barriers (skin secretion and melanin)  Skin secretions (acid mantle) • Low pH and sebum slow bacterial growth on skin surface • Human defensin – natural antibiotic • Cathelicidins – proteins that prevent Strep A infection in wounded skin  Melanin – chemical pigment that prevents UV damage o Physical/Mechanical Barriers – continuity of the skin and hardness of keratinzed cells  Continuity prevents bacterial invasion  Glycolipids prevent diffusion of water and water-soluble substances between cells  Substances that are able to penetrate the skin: • Lipid-soluble substances (i.e., oxygen, carbon dioxide, steroids, and fat-soluble vitamins) • Oleoresins of certain plants (ex. Poison ivy and poison oak) • Organic solvents (ex. Acetone, dry cleaning fluid, and paint thinner) • Salts of heavy metals (ex. Lead, mercury, and nickel) • Penetration enhancers o Biological Barriers – Langerhans’ cells, macrophages, and DNA  Langerhans’ cells in epidermis present antigens to lymphocytes  Dermal macrophages (2nd line of defense) – attack bacteria and viruses that have penetrated the epidermis  DNA structure – the electrons in DNA absorb UV radiation and converts it to heat Body Temperature Regulation o Production of copious amounts of sweat to dissipate heat o Constriction of dermal blood vessels to retain heat  >temp ‡ sweat glands, flushing 
Additional information : Important Definitions • • •

Receptors are the "Transducer" in a sensory system. Receptors respond to a particular stimulus called a "proper stimulus". Their function is to change the form of energy of the proper stimulus into the electrochemical energy of the Nervous system. Name of Receptor

Proper Stimulus

Meissner's Corpuscles

Touch

Merkel's Discs in glabrous skin

Touch

Krause's End-bulbs

Touch

Pacinian Corpuscles

Pressure

Free Nerve Endings

Pain & Temperature

Metabolic Functions Synthesis of Vitamin D – increases calcium absorption in the body Chemical conversion of many substances Blood Reservoir – preferential shunting of blood as needed Excretion o elimination of nitrogen-containing wastes, salt, and water o affects fluid & electrolyte balance o sweat glands release: water, salts, ammonia o oil glands release: lipids, acids nonverbal communication o eg. humans and other primates have much more expressive faces than other animals o o

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Layers of Skin: 1. Epidermis 2. Dermis 3. Hypoderms

1.Epidermis • stratified squamous epithelium • upper layers dead, filled with keratin (waxy protein) • lower layers living cells • replaced every 35-45 days Subdivided Into 5 Identifiable Layers: a. stratum basale • lowermost layer of epidermis • single cell layer thick • only cells that get adequate nutrition and oxygen by diffusion • from tissues below • actively dividing cells • bordered below by basement membrane b. stratum spinosum • several layers thick • less mitosis • flattened, irregular, spinelike projections • [basale + spinosum = stratum germinativum

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‡ growing layers]

c. stratum granulosum • very thin; 2-3 cell layers thick • as cells move up from s. basale they die & get flatter • and thinner • keratinization begins here d. stratum lucidum • thin translucent band • only found in thick areas of epidermis: 1. soles of feet 2. palms of hand e. stratum corneum • thickest of all layers; • 3/4th‘s the thickness of epidermis • 20-30 cell layers thick • dead cells completely filled with keratin • water resistant • main protection against biological and chemical assault • takes keratinocytes 30-40 days from their formation in stratum basale until they flake off of the stratum corneum Cells Of Epidermis: 1. stem cells ‡ undifferentiated cells found only in deepest layer 2. keratinocytes ‡ most cells in epidermis synthesize keratin 3. melanocytes ‡ also in deepest layer synthesize pigment melanin 4. Merkel cells ‡ touch receptors, attached to nerve cell 5. dentritic cells(Langerhans cells) ‡ found in s spinosum and s granulosum • are macrophages that stand guard against toxins, • microbes and other pathogens that penetrate the • skin‡ if detected they alert immune system

2. Dermis (=hide) • strong, flexible, connective tissue • gives skin its strength and resilience • gel-like matrix • contains collagen, elastic and reticular fibers • rich in nerves, receptors, blood vessels, lymph vessels • hair follicles and sweat glands extend into it Two Layers: a. papillary layer • mainly areolar connective tissue • lots of blood vessels • dermal papillae

• capillary loops • sensory cells • produce finger prints b. reticular layer • mainly dense (irregular connective tissue) • lots of collagen fibers • lines of cleavage between collagen bundles • ‡ tension lines • longitudinal in limbs • circular around trunk • incisions parallel to lines heal quicker • dermal tearing = stretch marks (silvery) 3. Subcutaneous Layer • • • • • •

= hypodermis or superficial fascia below skin mainly adipose tissue (ie subcutaneous fat) insulation infants and elderly have less of this than adults and are therefore more sensitive to cold

Skin Color due to combination of three different pigments: 1. melanin • yellow, orange, brown or black pigments • racial shades due mainly to kinds and amount of melanin pigments • mainly in stratum basale • also, amount varies with exposure to sun=suntan 2. carotene • esp in stratum corneum and subcutaneous layers 3. hemoglobin • in blood of skin capillaries Skin Color & Texture in Diagnosis 1. cyanosis = bluish cast ‡poor oxygenation 2. erythema = redness ‡ emotional, hypertension, inflammation 3. pallor = paleness ‡ emotion, anemia, low blood pressure 4. jaundice = yellowing ‡ liver disorder, >bile pigments in blood 5. bronzing = Addison’s disease, adrenal cortex 6. bruising (hematoma)= escaped blood has clotted hematomas ‡ deficiency in Vit C or hemophilia

7. leathery skin = overexposure • clumping of elastin fibers • depressed immune system • can alter DNA to cause skin cancer 8. photosensitivity = to antibiotics & antihistamines “Skin Markings” skin is marked by many lines, creases and ridges 1. friction ridges: • ‡ markings on fingertips characteristic of primates • allow us to manipulate objects more easily 2. flexion lines: • on flexor surfaces of digits, palms, wirsts, elbows etc • skin is tightly bound to deep fascia at these points 3. freckles: • flat melanized patches • vary with heredity or exposure to sun 3. moles: • •

elevated patch of melanized skin, of the with hair mostly harmless, beauty marks

“Derivitives of skin” or Skin Accessory •

during embryonic development 1000’s of small groups of epidermal cells from stratum basale push down into dermis to form hair follicles and glands

1. Hair • covers entire body except palms, soles, lips, • nipples, parts of external genitals

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hormones account for the development of “hairy” regions: eg. head, axillary and pubic areas humans are born with as many follicles as they will ever have hairs are among the fastest growing tissues in the body formation similar to epidermis heavily keratinized consists of: 1. shaft: visible part 2. root: 3. follicle: sheath surrounding root 4. papillae: vascularized, growing part of hair 5. Arrector Pili muscles • attached to follicle • causes hair to stand on end (cold, fright) 1. oil glands: ≥2/follicle 2. hair receptor: entwines each follicle, responds to hair movements 3. hair color depends on kinds (yellow, rust, brown, 4. and black) and the amount of melanin cortex of shaft contains 5. hair texture related to differences in cross-sectional shape • eg. straight hair is round • eg. wavy hair is oval • eg. tightly curly hair is relatively flat

2. Nails • scale-like modification of the epidermis • fingernails and toenails are clear,hard derivatives of stratum corneum • very thin, dead, scaly cells, densely packed together • corresponds to hoof or claw of animals • most mammals have claws, flat nails are a primate characteristic • ‡ more fleshy and sensitive fingertips • ‡ still can be used for digging and picking apart food, etc • features: 1. nail matrix: growth zone beneath proximal skin • nail bed composed of stratum basale 2. nail plate: visible portion of nail • fingernails grow 1 mm/wk; toenails more slowly • [adding gelatin to diet has no effect on growth or hardness of nails] • appearance of nails has diagnostic value: • eg. spoonlike, flat, concave ‡ may indicate iron deficiency • eg. clubbed or swollen fingertips ‡ long term hypoxemia • from eg congenital heart defects and emphysema

3. Skin Glands

a. Oil glands (Sebaceous Glands, holocrine) • 2 or more per follicle • keeps hair soft and pliable • esp on face and scalp • not on palms, soles or dorsal side of feet • reduces heat loss • lipids are poor heat conductors • helps prevent water evaporation • become active at puberty ‡ acne

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secrete sebum = breakdown products of dead cells

b.1 Sweat Glands (sudoriferous)(eccrine glands) • 3 Million total on skin • 3000 sweat glands/inch2 • most numerous on palms, soles, forehead, armpits • essentially a tiny coiled tube that opens to skin surface • helps maintain temperature and fluid/electrolyte balance • ‡ heat ‡ sweat ‡ evaporative cooling B.2Scent Glands (apocrine glands) • modified sweat glands ‡ scent, pheromones • much less common • confined to axillary and genital area • their ducts empty into hair follicles • secretions contain fatty acids and proteins in addition to “sweat” • respond especially to stress and sexual stimulation b.3 Mammary Glands

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modified sweat glands produce milk

b.4 Ceruminous Glands • modified sweat glands • in external ear canal • secrete waxy pigmented cerumin • protection ‡ traps dust and particles

Skin Imbalances & Aging • the skin can develop >1000 different ailments • the most common skin disorders result from allergies or infections • less common are burns and skin cancers

A. Allergies 1. Contact Dermatitis allergic response eg. poison ivy, metals, etc

B. Infections 1. viral • eg. cold sores • herpes simplex • especially around lips and oral mucosa 2. Fungal • eg. athletes foot 3. Bacterial

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eg. boils and carbuncles inflammation of hair follicle and sebaceous glands specially on dorsal side of neck eg. impetigo Streptococcus infection

C. Genetic Diseases 1. Psoriasis • chronic, noninfectious skin disease • skin becomes dry and scaly,often with pustules • many varieties • cycle of skin cell production increases by 3-4x’s normal • stratum corneum gets thick as dead cells accumulate • seems to be a genetic component • often triggered by trauma, infection , hormonal changes or stress

2. Hypertrichosis (human werewolves) • patients show dense hair growth on faces and upper bodies • due to malfunction of gene on x chromosome • ‡ a gene silenced during evolution has been reactivated

D. Burns • too much sunlight or heat • categorized by degree of penetration of skin layer

1st • • •

degree burns skin is inflamed, red surface layer of skin is shed

2nd

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degree burns deeper injury blisters form as fluid builds up beneath outer layers of epidermis

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degree burns full thickness of skin is destroyed sometimes even subcutaneous tissues results in ulcerating wounds typically results in catastrophic loss of fluids:  dehydration  electrolyte imbalances  also highly susceptible to infections  slow recovery (from cells of hair follicles if they survive;

3rd

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otherwise must heal from margins of wound) may require: • autografts • cadaver skin • pig skin • prognosis may depend on extent of damage • extend of burn damage estimated by “rule of 9’s” • head, arms 9% of skin surface • front and back of torso, each leg 18% of skin surface • groin 1% of skin surface

ADDITIONAL INPUT ABOUT BURNS Assessing the severity of the burn Morbidity and mortality rise with increasing burned surface area. They also rise with increasing age so that even small burns may be fatal in elderly people. Burns are considered serious if: >15% in an adult >10% in a child The burned patient is very young or elderly. Estimating the burned surface area Adults The ‘Rule of 9’s’ is commonly used to estimate the burned surface area in adults. The body is divided into anatomical regions that represent 9% (or multiples of 9%) of the total body surface The outstretched palm and fingers approximates to 1% of the body surface area. If the burned area is small, assess how many times your hand covers the area. Children The ‘Rule of 9’s’ is too imprecise for estimating the burned surface area in children because the infant or young child’s head and lower extremities represent different proportions of surface area than in an adult. Use the chart shown opposite to calculate the burned surface area in a child.

Estimating the burned surface area in the adult

Estimating the burned surface area in the child Area

By age in years

0 Head (A/D) 10% Thigh (B/E) 3% Leg (C/F) 2%

1 9% 3% 3%

5 7% 4% 3%

10 6% 5% 3%

Estimating the depth of burn Burns can be divided into three types. It is common to find all three types within the same burn wound and the depth may change with time, especially if infection supervenes. Any full thickness burn is serious. Depth of burn First degree (superficial) burn

Characteristics Cause Erythema Sunburn Pain Absence of blisters Second degree or partial Red or mottled Contact with hot liquids thickness burn Swelling and Flash burns blisters Painful Third degree or full thickness Dark and leathery Fire burn Dry Prolonged exposure to hot Sensation only at liquids/objects edges Electricity or lightning Other factors in assessing the severity of the burn Location/site of burn Burns to the face, neck, hands, feet, perineum and circumferential burns (those encircling a limb, neck, etc.) are classified as serious. Other injuries Inhalation injury, trauma or significant pre-existing illness increase risk. Criteria for hospitalization >15% burns in an adult >10% burns in a child Any burn in the very young, the elderly or the infirm Any full thickness burn Burns of special regions: face, neck, hands, feet, perineum Circumferential burns

Inhalation injury Associated trauma or other pre-existing illness

E. Skin Cancer • caused by excessive or chronic exposure to UV, • xrays or radiation • most forms progress slowly and are easily treated • a few are deadly 1. Basal Cell Carcinoma • least malignant • most common • stratum basale cant form keratin • lose boundary layer between epidermis and dermis • results in tissue erosion and ulceration • 99% of these cancers are fully cured

Treatment of a pigmented basal-cell carcinoma using Mohs micrographic surgery (A) Patient with a pigmented basal-cell carcinoma on the upper lip. (B) Patient with pigmented basal-cell carcinoma after treatment with Mohs micrographic surgery to remove the tumor. (C) The area was repaired using an island pedicle flap on the day of surgery. (D) At 1 year follow-up, the area is well healed without cosmetic or functional deficits. 2. Squamous Cell Carcinoma • cancer of the cells in stratum spinosum • usually induced by sun • cells grow rapidly and grow into the lymphatic tissues

These pictures are examples of what skin cancer might look like. Basal cell carcinoma usually affects the head, neck, back, chest, or shoulders. The nose is the most common site. Signs of basal cell carcinoma can include skin changes such as a: • • • • • • •

Firm, pearly bump with tiny blood vessels in a spiderlike appearance (telangiectasias). Red, tender, flat spot that bleeds easily. Small, fleshy bump with a smooth, pearly appearance, often with a depressed center. Smooth, shiny bump that may look like a mole or cyst. Scarlike patch of skin, especially on the face, that is firm to the touch. Bump that itches, bleeds, crusts over, and then repeats the cycle and has not healed in 3 weeks. Change in the size, shape, or color of a wart or mole.

Squamous cell carcinoma usually affects the face, head, or neck. Signs of squamous cell carcinoma include any: • • • •

Persistent, firm, red bump on sun-exposed skin. Patch of skin that feels scaly, bleeds, or develops a crust. The patch may get bigger over a period of months and form a sore. Skin growth that looks like a wart. Sore that does not heal or an area of thickened skin on the lower lip, especially if you smoke or use chewing tobacco or your lips are often exposed to the sun and wind.

3. Malignant Melanoma • cancer of pigment cells = melanocytes • rare 1% of skin cancers • deadly, poor chance of cure once it develops • often begins with moles

ADDITIONAL INORMATION ABOUT MELANOMA Facts about melanoma you should know Lesions on various skin places used to be a sign of beauty. But until they are benign. As known about 50% of melanoma evolutes from benign lesions(congestion of melanocytes), other appear from unnatural growth of melanocyte cells. So both cases are based on melanocytes where they have invaded an epidermal and dermal layers of skin. There are normally about 10 to 40 lesions on human body. Some of them are native, inborn, some of them appear during 35 – 40 years. Later some of them may disappear. Melanoma is not only a skin disease as it can also appear in eyes, respiratory system, even on cortex of brain. But most of cases (~90%) appears on skin. As mentioned earlier it is hard to detect melanoma in early stages as it may appear as benign lesion. So if there is even a little suspicion about malignant lesions, it is necessary

to attend screening at dermatologic specialist who usually photographs suspicious lesions and then analyses according to ABCD rule. Other non skin cases are even harder to detect. For instance if melanoma appears in lungs patient may have difficulties in breathing – like astma. Melanoma in bones may appear as bone ake. Skin melanomas may be classified as follows: •

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Radial melanoma (about 70% of skin melanoma cases) – appears from displastic lesions. Melanoma progress takes up to 5 years. Can be detected by using ABCD rule. More specific for elder ages. In early phases melanomas spreads in upper layer of skin – epidermis. Later it enters vertical growth phase after then cancer becomes dangerous as it starts to invade inner tissues; Nodular melanoma (about 15% of cases) – This type of melanoma rises very rapidly and is the most aggressive type of skin cancer. From the beginning this type of melanoma grows vertically up and down. So there is a danger from the beginning that melanoma will spread in to inner tissues. This type of melanoma appears to be dark black, blue, grey or red with smooth borders. Lentigoous maligna melanoma – appears usually in head and neck area bigger than 3 centimeters non symmetrical lesion. It takes long time to progress – up to 20 years. Most cases at 70 years old. Acral lentigous melanoma – more common for dar skinned people. It appears on palms of hands and foots – especially under nail of first finger. It takes short time to progress from 3 to 36 moths. Most common among 60 year age. Unclassified – other up to 5% of cases.

Generally speaking all melanomas growths in two phases: horizontal-radial and vertical. In radial phase lesion spreads in epidermis and papillary dermis without metastases. In this period patient can be easily cured. When growth enters vertical phase lesions spreads in to deeper tissues through dermis and deeper layers of skin. There begins metastases. In meny cases both phases come together. Most common metastases of melanoma are: in Dermis(50 -75%), Lungs(07 – 87%), Liver(54-77%), Brain(36 – 54%), Bones(23 – 49%), Digestive system(26 – 58%), Kidney(35 – 48%), Heart(40 – 45%). How metastases are related to lesion size. • • • •

<0.75mm – regional metastases(2-3%), far metastases(2-3%); 0.76-1.5mm – regional metastases(25%), far metastases(8%); 1.51-4mm – regional metastases(57%), far metastases(15%); >4mm – regional metastases(62%), far metastases(72%);

One of most important criteria is a number of metastases in lymphatic system. Depending on number of metastasis there is a statistics on survival from melanoma. • • •

No metastases in lymph – 73% to survive 5 years; 1 - 3 metastases in lymph - 55% to live 5 more years; 4 metastases in lymph - 26% to live 5 more years;

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macro metastases - 21% to life 5 more years and 12% to live 10 more years.

So number of metastases is proportional to survival. When you should pay more attention to you skin lesions. • • • •

Elder age people have to pay more attention as during age melanoma prognosis become more critical; Gender – man have more chances to get spreaded melanoma; Number of lesions on body – if there are more than average number of lesions on body; Skin color – white skinned people tend to have melanoma more offen than dark skinned people.

Main and only effective cure for melanoma stil is surgery when it is removed. But it is effective if there is no metastases. Otherwise complex treatment is taken without big chances. So it is important to diagnose melanoma in early stages before it has spreaded to other tissues.

F. Aging Skin • effects often become noticeable by late 40’s Hair • thinner and grayer as melanocytes die and mitosis slows Oil glands • sebaceous glands atrophy • skin and hair become drier Skin Layers • mitosis declines, collagen is lost from dermis • skin becomes thinner and translucent • looser and sagging as elastic fibers are lost and dermal • papillae smooth out • fewer blood vessels and those remaining are more fragile • more bruising, slower healing and rosacea‡ tiny dilated • blod vessels esp in nose and cheeks • age spots – accumulation of pigment cells • loss of immune cells and fibroblasts makes skin more susceptible to recurring infections • thermoregulation is less efficient due to loss of blood vessels and glands • ‡ more vulnerable to hypothermia and heatstroke

photoaging = an acceleration of skin aging due to overexposure to sun (UV) • accounts for 90% of the changes that people find medically troubling or cosmetically disagreeable

G. Autoimmune Disease • eg. alopecia areata • causes hair to fall out in small round patches • 2% of population (4.7M in US) have some form of it • hair loss is usually short term and limited to a few patches • in rare cases causes permanent loss of all body hair ADDITIONAL INFORMATION ABOUT ALOPECIA AREATA

Alopecia refers to hair loss in areas of skin that normally have hair. There are two forms of alopecia: •

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Scarring—This is the loss of hair follicles, causing permanent hair loss. Cutaneous lupus erythematous and fungal kerions are the most prevalent forms of scarring alopecia. Nonscarring—In this case, the hair shaft is gone, but the follicles are still present. Because the hair follicles still exist, it often is reversible. It can, however, develop into the scarring type. Alopecia areata is a type of non-scarring alopecia. It is an autoimmune process and the cause is not known. Hair loss lasts approximately six months.

Hair Loss

Causes Many things can cause alopecia, including: •

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Stress that prompts growing hairs to rest and shed o Illness or surgery o Prolonged fever o Childbirth o Emotional/psychological stress o Crash dieting Hormonal problems o Overactive or underactive thyroid gland Medications o Blood thinners o Drugs for gout o Chemotherapy for cancer treatment o Vitamin A o Birth control pills o Antidepressants o Blood pressure and heart medications Allergic reaction to medications Radiation therapy Infections o Fungal infections o Syphilis o HIV o Herpes simplex Autoimmune disorders Systemic and discoid lupus erythematosus Anemia Hair pulled too tightly by: o Hair rollers o Pigtails o Cornrows Hot oil treatments (can inflame the hair follicle and cause scarring) Twisting and pulling hair out due to psychiatric problems Genes o Male-pattern baldness is usually inherited. o Birth defects can include problems with the hair shaft.

Risk Factors A risk factor is something that increases your chance of getting a disease or condition. •

Family history of baldness or hair loss

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Advancing age (for male-pattern baldness only) Pregnancy Stress Poor nutrition

Symptoms Alopecia symptoms depend on the type of hair loss. Some of the more common symptoms include: Male-pattern baldness: • • •

Hair recedes Hair falls out at the top of the head Affects men and women

Female-pattern baldness: • •

Hair thins over the entire head Hair comes out when brushing

Alopecia areata: • • • •

Rapid hair loss Round or oval patches of hair loss Sometimes tiny hairs are visible in the patches Brittle and discolored fingernails and toenails with ridges

Stress-related: • •

Gradual shedding Hairs come out with gentle pulling

Fungal infections: • • • • •

Patches of hair loss Black dots in the patches Itching Scaling Inflammation (such as redness)

Diagnosis The doctor will ask about your symptoms and medical history, and perform a physical exam. The doctor will examine the area(s) of hair loss, noting the pattern of hair loss and condition of the scalp.

This physical exam may include: • • • •

Gentle pulling on the hair Taking samples of scalp areas with inflammation and examining them under a microscope Analyzing samples of hair Checking for hair loss on other parts of the body

The doctor will ask questions about: • • • • •

Diet Hair care Medication use Your personal and family medical history Pregnancies, menopause, and monthly menstrual cycles

Other tests may include: • •

Blood tests to help identify underlying conditions that may be causing the hair loss Biopsy of the scalp—removal of a small tissue sample to be analyzed under the microscope

Treatment Alopecia treatment depends on the cause of the condition. Treatments include: Medications • • • •

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Drugs to correct a hormonal imbalance or deficiency Switching to a different medication if a drug you are taking is contributing to the hair loss Antifungal shampoos and pills to treat fungal infections For baldness in men, a prescription drug taken in pill form (finasteride) Note: Pregnant women should not even handle this medication. Even a small amount absorbed through the skin of the hands can cause birth defects in baby boys. Over-the-counter medication (minoxidil) that is applied to the scalp daily (must be used on a regular basis) Note: If you have heart problems, discuss this drug with the doctor before using it. To help speed-up hair re-growth in alopecia areata, your doctor may inject a steroid preparation into your scalp. For some patients, not responding to other therapies, topical immunotherapy (usually administered by a dermatologist) may be helpful. It involves applying an allergen to scalp that causes local reaction like redness, itching and also induces hair growth.

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Phototherapy is another potential treatment for patients with alopecia areata. Therapy is usually administered for 4 to 6 months.

Lifestyle Changes Be gentle with your hair. Avoid pulling it tightly. If pulled over a long period of time, scarring can occur resulting in permanent hair loss. If treatment does not correct the hair loss, you may opt for a wig, hairpiece, or hair weaving. If emotional stress is the cause, learn and practice stress-management techniques. Surgery This can involve: •

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Hair transplant—taking hair from the back and sides of the head and transplanting it in bald areas. As many as 300 grafts may be needed. You must return multiple times for the grafts. Scalp reduction with flaps—cutting the scalp and pulling the areas with hair closer together.

Chemotherapy Induced • • •

It could be minimal, moderate or severe. It is transient and completely reversible after discontinuation of chemotherapy. Currently, there are no medications available that were shown to reduce the risk of alopecia associated with cancer treatments.

Prevention There are no prevention guidelines for the most common type of hair loss, male-pattern baldness. However, the following tips may help you avoid other types of hair loss: • • • •

Do not pull your hair tightly into a ponytail, cornrows, or curlers. Learn and practice stress-management techniques. Obtain medical care for acute illnesses and to manage chronic conditions. Eat healthy, well-balanced meals.

Clinical Terms: • Necrosis – cellular or tissue death, gangrene • Biopsy – tissue analysis

ORGAN LEVEL OF ORGANIZATION LECTURE 1 “INTEGUMENT”

ORGAN & SYSTEM LEVEL OF ORGANIZATION

All living things share basic characteristics Dependent on functional interdependence of organ systems & all body cells LEVEL OF ORGANIZATION 1.

CHEMICAL LEVEL

2.

CELLULAR LEVEL ~ MICROSCOPIC

3.

TISSUE LEVEL

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ORGAN LEVEL - Skin

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ORGAN SYSTEM LEVEL - Skin

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ORGANISMAL LEVEL ~ HUMAN BODY

Organ systems cannot work in isolation “Spider Web” ~ Form Follows Function

INTEGUMENTARY SYSTEM “Dermatology” ~ study & treatment of skin Accounts for 16% of body weight Connects body to outside world ~ first line of defense -------------------------------------------------Cutaneous Membrane ~ “The Skin” Epidermis ~ stratified squamous epithelium ~ TOP Dermis ~ connective tissue layer ~ DEEP

Accessory Structures Mostly in dermis but protrude into epidermis Hair & Nails Exocrine Glands ~ sweat & sebaceous glands -------------------------------------------------“Hypodermis” ~ Subcutaneous Layer (S.Q.) “Superficial Fascia” ~ NOT part of skin . . . it’s below Below Dermis ~ interwoven with Dermis “loose” connective tissue ~ mostly adipose tissue Connects skin to “deep fascia” Contains ~ blood vessels . . . lymph vessels . . . nerves Functions of the Skin Protection Protects underlying tissue & organs against Shock . . . Trauma . . . Chemicals . . . Radiation Excretion Salts, water, & waste ~ excreted by glands Temperature Maintenance ~ Thermoregulation Insulates ~ outside temperature & elements Evaporative cooling ~ perspiration cools body Nutrient Storage Lipids in dermis & subcutaneous ~ energy Vitamin D3 Synthesis ~ steroid Steroid converted to calcitrol hormone

Required for calcium metabolism Sensory Detection ~ many corpuscles ~ nerve ends “Sensory” for touch, pressure, pain & temperature Relays information to nervous system EPIDERMIS Top layer of skin Stratified squamous epithelium ~ 30 to 50 layers “Keratinocytes” ~ body’s MOST abundant cells Avascular ~ NO blood vessels Obtains nutrients by diffusion Superficial epidermis cells ~ inert or dead Deep epidermis cells ~ MOST metabolically active Germinative Cells ~ Basal Cells ~ stem cells “Basal Lamina” ~ junction of epidermis & dermis THIN Skin Covers MOST of body Epidermis is thin ~ Four layers of “keratinocytes” Thin Stratum Corneum ~ NOT much keratin THICK Skin ~ soles of feet & hands ~ calluses Epidermis is thick ~ Five layers of “keratinocytes” Thick Stratum Corneum ~ LOTS of keratin EPIDERMAL LAYERS 30 – 50 layers

1.

Stratum Basale ~ inner most layer “Stratum Germanitivum” ~ base layer 1-2 cell layers thick ~ “keratinocytes” High metabolic & mitotic activity Replaces most superficial cells ~ VERY FAST Basal cells ~ germinative “stem” cells Attached to Dermis by Hemi-desmosomes “Epidermal Ridges” ~ project into dermis Interlock with “dermal papillae” Improves gripping ability “Fingerprints” ~ individual specific Increases skins sensitivity “Merkel Cells” ~ Tactile Cells Sensory Receptors ~nerve endings Pain . . . touch . . . pressure . . . temperature “Melanocytes” ~ produce melanin ~ skin color

EPIDERMAL LAYERS

2.

Stratum Spinosium 8-10 cell layers thick ~ keratinocytes “Langerhans Cell” ~ Dendritic Cells Part of Immune System ~ macrophages Stimulate first response to skin penetration

3.

Stratum Granulosum 2-5 cell layers thick Flattened Keratinocytes Produce “Keratin” Tough “fibrous” protein Main component of Hair, Nails & corneum

4.

Stratum Lucidum Only found in THICK skin 1-2 layers in THIN skin ~ MANY layers in THICK skin Densely packed Keratinocytes

Filled with keratin EPIDERMAL LAYERS 5.

Stratum Corneum ~ free or exposed surface 15-30 layers of keratinized cells ~ “cornification” Cells filled with Keratin ~ fibrous protein Thickest portion of skin Cells connected with Desmosomes ~ very tight Peel off in large groups or sheets ~ sunburn Inert or Dead ~ NOT metabolic activity Cells remain for 2 weeks before shedding “Dander” ~ shed dead cells

“Dandruff” ~ dander plus scalp oils Surface is dry ~ unsuitable for bacteria growth Coated by lipid secretions from underlying sebaceous glands “Acid Mantle” ~ pH 4-6

5.

Stratum Corneum ~ Water Resistant but NOT water proof Sensible Perspiration ~ planned ~ 1 Gallon/hr Water leaves body via sweat glands in skin Controls body temperature Insensible Perspiration ~ NOT planned Water leaves body through skin via diffusion NOT through sweat pores Water moves from underlying interstitial fluids & cells 500 ml per day lost ~ 1 pint Caused by Damage to epithelium or “tonicity” Blisters or Burns Separation of epidermal layers Separation between epidermis & dermis Water loss can be severe Hypertonic Solutions ~ slow dehydration ~ sea (salt) H2O Hypotonic Solutions ~ Water moves into epidermis

Bath tub soaking → cells swell Fresh H2O (not salt) is hypotonic relative to body fluid ORGAN LEVEL OF ORGANIZATION LECTURE 2 “INTEGUMENT” DERMIS Between Epidermis & S.Q. Dermal Layers 1.

Papillary Layer ~ superficial dermis ~ top 20% Areolar CT ~ loose ~ fragile Dermal Papilla’s extend into epidermis

2.

Reticular Layer ~ deeper dermis ~ bottom 80%

Dense, irregular CT ~ very tough

Collagen & elastic fibers Resists tension & twisting in the skin Dermal Layers Supply Epidermis with nutrients via: Blood vessels Lymphatic vessels Sensory nerves Organs of Dermis ~ extend through epidermis

Hair Follicles Sweat Glands ~ sudoriferous glands Sebaceous Glands ~ oil producing glands Dermal Blood Supply ~ highly vascular Cutaneous Plexus ~ “subcutaneous plexus” Larger arteries to skin form “network” in subcutaneous layer at junction of SQ &reticular layers of the dermis Papillary Plexus ~ papillary layer of dermis Smaller arteries & capillaries branch toward epidermis BOTH Plexuses supply accessory structures Sweat Glands Hair Follicles Sebaceous Glands Contusion = Damage to skin → broken vessels in dermis → “black & blue marks Decubitus Ulcers ~ bed sores or pressure sores Erosion of epidermis - - - > Exposure of Dermis Distension of Dermis → “stretch marks” Loss of Elasticity ~ Elastin - - - > causes wrinkles Pregnancy . . . Obesity . . . Aging . . . Weight loss Hematoma ~ clotted blood under the skin Caused By:

Broken Blood Vessel . . . Anticoagulants

(Covered in Detail in Chapter 16) Dermal Nerve Supply ~ Innervation Sensory Receptors ~ MANY IN SKIN

Pain Pressure Temperature Touch ~ tactile Corpuscles ~ sensory cells ~ NERE ENDINGS Detect light pain, pressure, touch & temperature Very Sensitive ~ mosquito on skin, bug on hair Merkel Cells Merkel Discs Merkel Corpuscles Tactile Corpuscles

SUBCUTANEOUS LAYER ~ SQ or SC Hypodermis ~ Superficial Fascia layer Areolar & Adipose CT ~ interwoven with dermis Boundary indistinct ~ between dermis & SQ SQ stabilizes skin against underlying organs & tissues Limited blood supply . . . supplies large vessels to dermis NO vital organs in Sub-Q Ideal for “subcutaneous injection” ~ “hypodermic needle”

Subcutaneous Fat ~ energy storage Distribution differences Male: 12 - 18% Female:

Neck, arms, lower back, butt

18 - 24%

Breast, butt, hips, thighs

Aging: increases in abdominal area “pot belly” DEEP FASCIA Below S.Q Deepest layer of connective tissue Skin Color ~ Dermal Blood Supply & Epidermal Pigment Dermal Blood Supply ~ reddish due to “Hemoglobin” Erythema ~ Vasodilation →Reddness ~ inflammation ~ warm Palor ~ Vasoconstriction → Pale ~shock or scare ~ cold Cyanosis ~ poor blood supply (NO O2) ~ Lips or nails Epidermal Pigmentation Carotene ~ Orange-yellow pigment Accumulates in fat of dermis Carotene converted to Vitamin A Normal maintenance of epithelia Melanin ~ brown, yellow-brown, black pigment Melanocytes in Stratum Germinativum Protects from UV radiation ~ sunburn

Repeated UV Exposure damages melanocytes DNA damaged → Mutation → Melanoma Albinism ~ lack of melanin Jaundice ~ yellowing due to TOO much bilirubin Liver Disease or Gall Bladder Blockage Skin Tumors ~ Skin Cancer Produced by abnormal cell growth Rapid Cell Division >>> Anaplasia (cancer) Tumor ~ “neoplasm” ~ benign or malignant Benign ~ Tumor is encapsulated in CT (non-cancerous) NOT invasive or NON spreading Size could cause functional disturbance Malignant ~ Cells SPREAD locally by invasion (cancerous) Cells SPREAD to distant tissues by “metastasis” Mutant Cells “out of control” NOT encapsulated ~ NOT contained Cancerous Skin Tumors Basal Cell Carcinoma ~ local invasive ~ treatable Squamous Cell Carcinoma ~ local invasive ~ treatable Melanoma ~ highly metastatic ~ poor prognosis A ~ asymetrical irregular shape B ~ irregular raised border C ~ mottled with many colors D ~ more than 6mm (.2”) diameter ACCESSORY STRUCTURES ~ Hair & Nails

HAIR & NAILS NOT covered in lecture ~ read in text) Hair ~ NOT covered in lecture ~ read in text 4 million hairs in body Non-living structure ~ contains “hard keratin” Grows by addition of new cells in “hair matrix” that push hair shaft toward surface Growth cycles alternate between production & shedding Hair Follicle ~ complex organ ~ hair origin Hair Structure Long, cylindrical ~ extends beyond epidermis Root Anchors hair to dermis at “Hair Base” ~ “Hair Bulb” Hair Bulb surrounds “Papilla” at base of root Papilla ~ contains capillaries and nerves ~ living Shaft ~ extension of root ~ projects beyond epidermis Root Hair Plexus ~ sensory nerves located in hair bulb Medulla ~ center of hair ~ contains soft keratin Cortex ~ surrounds medulla ~ contains hard keratin Cuticle ~ Superficial layer of dead cells ~ protects hair

Types of Hair ~ NOT covered in lecture ~ read in text 1.

Vellus Hairs ~ very thin hairs ~ “peach fuz” Located all over body surfaces

Lightly pigmented Genital and armpit hair ~ before puberty 2.

Terminal Hairs ~ heavy or “regular” hair More heavily pigmented Head, eyebrows, eyelashes Genital and armpit hair ~ after puberty “hormonal related” ~ testosterone

Hair Color ~ NOT covered in lecture~ read in text From pigment produced by melanocytes in hair papilla Genetically Determined Impacted by hormonal and environmental conditions Pigment production decreases with age ~ graying Hair Functions ~ NOT covered in lecture~ read in text Protect scalp from UV radiation & environment Insulate & protect skull from blow Help prevent entry of foreign particles into body Nose, Ears & Eyelashes Early sensory warnings ~ can feel single shaft moving Hair Growth Cycle ~ NOT covered in lecture~ read in text Determines hair growth and shedding patterns Epithelial cells in “Hair Matrix” divide and push shaft toward surface Typical hair grows for 2-5 years then is shed Hair samples ~ tool for diagnosing conditions & ID ~DNA

Club Hair ~ no longer growing Pushed to surface & shed ~ 50 hairs /day Pubic Hairs Eyelash hairs Eyebrow hairs Head Hairs “Alopecia” ~ thinning or loss of hair

NAILS ~ NOT covered in lecture~ read in text Location:

Dorsal side of Fingers and Toes

Function:

Protection

Nail Body Covers nail bed ~ visible part Dead, tightly compacted keratinized cells Nail Bed ~ “epidermal” tissue

Lateral Nail Grooves Depression between nail body and Stratum Corneum Bound by “lateral nail folds” Free Edge Extends over “hyponychium” Thickened Stratum Corneum Nail

Root ~ epithelial tissue Growth occurs at “Nail Root” ~ in Nail Matrix Nail Root covered by “cuticle” ~ “eponychium” Thickened Stratum Corneum

Lunule ~ Near Root ~ vessels obscure ~ white crescent area Underlying blood vessels in dermis give nail its color

ACCESSORY STRUCTURES ~ Hair & Nails Arrector Pili Muscles ~ “Piloerector” Muscle Erection of hairs Smooth muscle surrounds hair follicle ~ 4 - 5 million Associated with sebaceous glands Autonomic Nervous System Control ~ involuntary control Sympathetic nervous system ~ adrenaline Reflex standing of hairs ~ several situations

Cold ~ goose bumps Fear ~ hair stands up Animals ~ increases thickness of coat

Exocrine Skin Glands ~ Cutaneous “Oil” Glands Sebum ~ waxy . . . oily . . . odorus lipid ~ coats skin Triglycerides, cholesterol, proteins, & electrolytes Inhibits bacteria growth Lubricates & protects hair shaft Conditions surrounding skin Holocrine ~ cell burst releasing secretory material Sebaceous Glands ~ Associated with hair follicles Sebum released into “lumen” of gland Arrector pili muscle contracts → Sebum moves into hair follicle via duct Contraction pushes sebum to skin surface Inflammation → seborrhea dermatitis ~ dandruff Oil secretion plus dead dry epithelial cells Sebaceous Follicles ~ NOT associated with hair follicles Large sebaceous glands ~ secrete “sebum” directly

onto epidermal surface Face, back, neck, chest, nipples, & genital area Pimples & Zits ~ white heads, black heads Activity increases at puberty ~ “Acne” Sweat Glands ~ Sudoriferous Glands Produce 99% watery + 1% NaCl secretion Direct water loss ~ through sweat pores in skin Eccrine Sweat Glands ~ traditional sweat glands Merocrine gland ~ pure, watery secretion, no odor Numerous & widely distributed ~ millions Location: throughout body ~ hands & feet Secretes pure “watery” material through ducts directly to “sweat pore” on to skin MOST of Sensible Perspiration ~ 1 Gallon/hr Apocrine Sweat Glands ~ apocrine secretion Coiled, tubular glands ~ associated with hair follicle Sticky, slight odorous secretion ~ scent glands Secretes material thru duct onto hair follicle in dermis Location:

Arm pits . . . groin area

Begin secreting at puberty ~ sex hormones Functions of Sudoriferous “Sweat” Glands Cool surface of skin to lower body temperature Protects against External Exposure ~ Antibacterial Functions of Sudoriferous Sweat Glands (NOT covered, read text) Cool surface of skin to lower body temperature

Could loose 1 gallon of H2O per hour Severe electrolyte loss can occur Maintains thermoregulation homeostasis “Negative Feedback Mechanism” EG:

High body temp → vasodilation & activation of sweat glands → profuse sweating → lower body temperature → system shut off → stop sweating

Protects against External Environment Hazards Sweat dilutes chemicals on skin Sweat discourages growth of micro-organsims antibiotic properties

OTHER ASSOCIATED CUTANEOUS GLANDS May NOT covered in lecture . . . Read in text Mammary Glands ~ breasts Specialized gland in relation to skin Structurally ~ similar to apocrine sweat glands Controlled by sex & pituitary hormones Prolactin & Oxytocin ~ positive feedback

Ceruminous Glands ~ ear Located in ear canal ~ holocrine secretion Produce “cerumen” ~ waxy secretion ~ ear wax Cerumen traps foreign particles in canal Prevents debris from reaching ear drum ~ lubricates drum Control of Glandular Secretion (Discussed with Nervous System) Sebaceous Glands & Apocrine Sweat Glands Controlled by Autonomic Nervous System Sympathetic Stimulation ~ Adrenalin BURNS & GRAFTS Causes:

Heat . . . chemicals . . . radiation . . . electric shock

Affect:Severe destruction of skin & underlying tissue Severity dependent on depth of damage 1st Degree Burns ~ only epidermis affected Pain, . . . redness only ~ erythema EG:

Sunburn

2nd Degree Burns ~ entire epidermis & some dermis damaged ~ “partial thickness burn” Accessory Structures NOT damaged Pain . . . redness . . . swelling . . . blistering occur 3rd Degree Burns ~ epidermis, dermis & subcutaneous destroyed ~ “full thickness burn”

Accessory Structures & nerves destroyed Less painful (nerves destroyed), severe swelling, fluid loss (electrolytes), severe infection, body heat loss CANNOT repair itself ~ NO epithelial cells Burns covering > 20% of skin ~ life threatening New Therapies & skin grafts can save those with burns over 80% of body (50% survival) ~ EGF HEALING Auto-regulation ~ independent of other systems Local Control ~ NO central control involved Skin regenerates very effectively after considerable damage Stem Cells ~ in epithelium & connective tissue Basal Cells ~ Mesenchymal Cells ~ Fibroblasts Differentiate into different types of epithelial & CT cells “Which heals faster. . . a long incision or short incision? “Which heals better. . . a perpendicular or parallel incisions? Dermal Cleavage ~ elastic fiber pattern lines of dermis Surgical significance for incision lines & scaring LESS scaring if incision is parallel to cleavage lines MORE scaring if incision is perpendicular Healing is delayed or inhibited if interfering factors present Sharpe . . . clean cut heals MOST RAPIDLY Scrape . . . jagged abraison ~ heals more SLOWLY Dirty . . . infected wound ~ heals more SLOWLY Must clear infection first . . . before healing can occur

TISSUE INJURIES & HEALING

(Read Pages 184-186 in text)

Irritation . . . Infection . . . Injury causes damaged or killed cells Involves Overlapping:

Inflammation & Regeneration

INFLAMMATION ~ immediate clean up process after injury Occurs first ~ causes pain . . . swelling . . . reddenss Infection must be removed ~ Pathogens: bacteria, parasites Damaged cells respond Bleeding Occurs Cells release chemicals, ions, proteins, & waste Mast Cells release Histamine ~ potent vasodilator Heparin ~ anti-coagulant Both result in increased blood supply to damaged area Phagocytes & white blood cells move in ~ clean up Epithelial cells migrate to area Fibroblasts activate & new capillaries form Temporary sealing & filling in ~ Clot & Scab Results: necrosis (death), pus, abscess, or a clean scab REGENERATION Occurs at end of Inflammatory Process Migrating epithelium & fibroblasts form a mesh Phagocytic activity ends ~ now a clean site Fibroblasts produce Collagen Fibers

“Fibrosis” ~ making of scar tissue Epidermis regeneration is now complete Scab shed Collagen fibers fill in space ~ fibrosis Hair follicles, sweat glands, muscle cells, nerves, blood vessels replaced by fibrous tissue “Scar tissue” results Granulation Tissue ~ visible scar Forms in larger wounds where scar or fibrous scar tissue fills in to surface of skin Underlying structures in dermis replaced by scar tissue Surface epithelial tissue replaced by scar tissue

Tissues vary in regeneration capability Rapid ~ Epithelial Tissue Good ~ Connective Tissue (except cartilage) Smooth Muscle Poor ~ Cardiac Muscle (no centrioles) Neural Tissue Aging Affects on Tissue Repair Cell activity declines ~ slow healing ~ dry & scaly skin Fewer melanocytes ~ susceptible to sun Epithelia get thinner ~ easier bruising ~ wrinkles Bones become more brittle & CT becomes less elastic

Blood flow decreases ~ always feeling cold Abnormal Tissue Development ~ Smoking Dysplagia ~ change in normal shape, size, numbers of cells & loss of cilia & goblet cells ~ reversible Metaplagia ~ change in structure or type of cells ~ reversible Columnar Epithelium - - -> Stratified Squamous Anaplagia ~ tissue cells become tumor cells ~ CANCER IRREVERSIBLE