202 Exam #2 PDF

Breasts and Regional Lymphatics Anatomy of Breasts Landmarks (nipple, areola & Montgomery's [sebaceous] glands) Divided into 4 quadrants plus Tail of Spence ▪ Upper outer quadrant (50% incidence of breast cancer) ▪ Contains Tail of Spence (part...

Breasts and Regional Lymphatics Anatomy of Breasts Landmarks (nipple, areola & Montgomery's [sebaceous] glands) Divided into 4 quadrants plus Tail of Spence ▪ Upper outer quadrant (50% incidence of breast cancer) ▪ Contains Tail of Spence (part of breast tissue extending into axillae) – most common site of malignancy Breast Tissue (determined by age, nutritional status, pregnancy, lactation & genetics) Adipose tissue (most of breast tissue) Glandular tissue (secretes milk) Suspensory ligaments (Cooper's Ligaments) - fibrous bands that attach breast tissue to chest wall muscles o Cancer may cause the ligaments to contract causing pits or dimples in the overlying skin Lymph System Pectoral (behind anterior axillary fold) o drains anterior chest wall & breast Subscapular (located along lateral edge of the scapula just inside posterior axillary fold) o drains posterior chest wall & arm Lateral (along the humerus inside the upper arm) o drains the arm Central axillary (high middle axillae) - receives drainage from all axillary nodes 75% of drainage will go to infraclavicular & supraclavicular nodes on the same side 25% of drainage will go to the opposite breast, abdomen, or deep into breast (a problem for metastatic disease) - increases spread to the other side Developmental Considerations Newborn (estrogen causes white nipple fluid in either sex) - resolves in few days to few weeks Adolescent Estrogen stimulates breast development Breast development (onset 8-8.5 to 13 years; average 10 - 11) - occurs over 3 yrs Note precocious (before 8yo) or delayed (after 13.5) puberty (needs endocrine evaluation) Breasts may normally be asymmetric (teen may need reassurance) Pregnant Female Nipples enlarge, darken Increased venous pattern over skin (superficial vessels) Note elevated Montgomery glands—produce sebum to lubricate nipple for breast feeding Colostrum forms in the 4th month (precursor to milk) – thick yellow fluid Lactation Colostrum changes to milk 3 days postpartum Frequent nursing relieves sensation of tenderness, engorgement Mastitis (inflammation or infection of breast tissue after childbirth) - red, swollen, hot, painful breasts Aging Female Decreased estrogen leads to decrease glandular tissue and increased adipose tissue May have discomfort from sagging breasts- supportive bra may help Axillary hair decreases Implants Implants have a different texture than original breast tissue Male Breast Lifetime risk of breast cancer is 1 in 1,000 Gynecomastia (nub of breast tissue under areola) – feels like a large grape o May normally have enlargement in adolescence (usually unilateral & temporary) -excess testosterone is converted to estrogen o May occur in the aging male (unilateral or bilateral) Left side more common o Estrogen/testosterone imbalance- either estrogen is too high(drugs or tumor) or testosterone is too low. (can be caused by some chronic diseases such as kidney, liver, lung disease) o Unilateral breast mass should be biopsied for cancer Subjective Data Breast Pain Localized or generalized (cancer may cause pain as an initial symptom- although may be a late sign) Character (burning, pulling, vague discomfort) Cyclic pain- pain that comes and goes with menstrual cycle (common with oral contraceptives & fibrocystic changes) Lumps (OLD CART if positive) Fibrocystic (non-cancerous ) lumps May enlarge and become more tender prior to the menstrual period Lumps or thickening Caffeine intake may increase size and tenderness of cystic lumps Changes are bilateral Associated skin changes redness, warmth, dimpling, swelling- can be associated with cancer History of trauma, breast CA, family hx of breast CA Lumps in the underarm area? Nipple Discharge (needs evaluation) Clear discharge – may be due to meds (oral contraceptives ,psychiatric medications, digitalis, diuretics) or a pituitary tumor Galactorrhea (milky discharge while not lactating) associated with a pituitary tumor Bloody discharge or thick yellow with blood (always significant, especially when associated with a lump) – may indicate ductal cancer Other History questions that relate to the breasts: Family history of breast cancer? Menstrual, pregnancy and lactation history Are you taking any hormones, contraceptives, antipsychotic medications, heart medications?  How much coffee, tea do you drink each day? (breast tenderness) Daily alcohol use?- 1 drink/day shown to increases risk of breastCA Do you smoke tobacco? (increased risk of breast CA) Screening Guidelines For Those At Average Risk of Breast Cancer (American Cancer Society) Age 40-44 Woman should have the choice to start annual breast ca screening with mammogram Age 45-54 Women should get mammograms every year Age 55 and older Women can switch to every 2 years, or continue yearly screening. Continue until life expectancy >10 years or more * Women with breast implants and males can get mammograms * Women at high risk for breast cancer because of family history or other reasons may begin screening earlier & more often Breast Cancer 2nd major cause of cancer death in women; lung CA #1 1 in 8 women will develop breast CA in their lifetime Incidence increases with age (80% of breast CA after age 40) Need to identify early & treat early for good results Breast Self Awareness focuses on the importance of women being aware of how their breasts normally look and feel so that that they may report any changes to a healthcare provider. Therefore, women should be taught the basics of SBE so that they may periodically assess for changes. Clinical Breast Exams (exam performed by a healthcare provider) no longer recommended for routine screening of average risk women because they do not provide a clear benefit. indicated when a breast lump is found on Self Breast Exam. Breast Cancer Risk Factors (per American Cancer Society [ACS]) Female (100 x more common in female than males) Age (increases with age) Breast cancer in one breast increases risk 3-4 x in other breast Abnormal breast cells on previous biopsy Family History (especially if occurrence before age 50) in 1st degree relative 20-30% of women with breast cancer will have a family history; 70% will not BRACA 1 or BRACA 2 (these gene mutations are also a risk factor for men) Radiation to chest (especially if before age 30) e.g., treatment for Hodgkin’s lymphoma Current use of oral contraceptives Not having children/not breastfeeding- may have a slight increase Hormone replacement therapy (HRT) – estrogen & progesterone Ashkenazi Jewish heritage Mammograms showing dense tissue (more glandular, less fat)  Overweight or obese after menopause Physical inactivity Alcohol (more than one drink per day increases risk by 7-10% 2 drinks increases to 20% increase) Breast Self-Examination (BSE) and Clinical Breast Evaluation (CBE) BSE No longer recommended by USPSTF or ACOG, however Using the BSE for “breast awareness” is recommended. Key is to “get to know your breasts” and observe for changes. Regular screening CBE is no longer recommended by ACS or USPSTF Tips: A good time to perform a self-breast exam is 4 to 7 days after the 1st day of the menses since this is when the breasts are the least engorged and nodular due to cyclic hormonal changes. Pregnant women or postmenopausal women may perform SBE at any time Components of Breast exam Inspect Breasts: size & shape: it is normal to have asymmetry with the left breast being larger than right breast skin characteristics: normally smooth with even color o localized areas of redness, bulging, dimpling, edema o Redness with heat (inflammation) – e.g., seen with mastitis o Peau d' orange (orange peel skin) - e.g., seen with cancer ▪ Caused by blocked lymph ducts ▪ Edema may exaggerate hair follicles causing bumpy texture & large pores appearing like an orange peel surface changes: evaluate by pushing hands on hips with shoulders hunched and observing breasts (underlying lumps may be more notable when pressing hands against hips) Inspect Nipples: stand in front of a mirror and note: Symmetry: normally symmetric and aligned (deviation may indicate CA) Contour: may be everted (protruding outward), flat or inverted (sunken inward) Inverted nipples (suspect malignancy if a recent change & unilateral; tumors may pull on the underlying tissue causing a retraction of the nipple) Abnormalities: scaling, fissures, ulceration, bleeding or discharge (these may indicate disease processes Paget’s disease (advanced ductal CA) - starts as a small crust on the nipple with surrounding erythema Supernumerary nipple (2 nipples along the mammary ridge at MCL); usually of no significance o occurs in 1% of men and women o appears like a nevus Palpate Breasts Women may choose to perform SBE in the shower since soap and water assists with palpation or when lying supine if this is preferred. One effective method is to palpate the breasts with 3 fingers using 3 levels of pressure while palpating in strips (up and down pattern) from the mid axillary line to the sternal border (not to miss the tail of Spence) Palpate Axilla For Lumps Lumps in this region may indicate a metastatic process since breast cancer may metastasize here via the lymphatic drainage system If a breast lump is found on BSE, then a follow-up Clinical Breast Exam is indicated. The healthcare provider will evaluate the characteristics of a breast lump as follows: Location (breast quadrant, distance from nipple, clock position [e.g., 3 o'clock]) Size (length, width, depth): use metric measurements (mm or cm) Shape (round, oval, indistinct) Consistency (soft, hard, firm) Tenderness Borders (defined, irregular) Retraction/dimpling (present or absent) Mobility Mobile = often fibrocystic Fixed = may be CA Note. CA characteristics (painless lump, ulcerated skin, retraction of skin, nipple discharge) Implants: press firmly inward at the edges of the breast implants to feel the ribs beneath, checking for lumps. Be careful not to manipulate or squeeze the valve on the implant (may cause leakage) Skin, Hair and Nails Skin- largest organ in the body Physical barrier that protects tissues from microorganisms, trauma, UV light, and dehydration Temp control (via sweat, and fat insulation) Fluid and electrolyte balance Absorption (medications, Vit d) / excretion (urea in renal failure) Sensation (injured in neuropathy) Immunity Vitamin D synthesis Epidermis (outer layer) – avascular (a superficial epidermal cut won’t bleed) Replaced every 3-4 weeks- aids in wound repair Dermis (inner layer) -contains nerves, sensory receptors, blood vessels, lymphatics, collagen, elastic fibers Eccrine Glands Produces sweat/perspiration (saline) Matures at 2 months of age (infants start to perspire) Apocrine Glands (open into hair follicles) Activated during puberty Secrete fluid in response to emotional stimuli & heat Decomposition of apocrine sweat produces body odor (action of bacteria on fluid) Located in axillae, nipples, areolae, anogenital area, eyelids & external ears Secretion decreases with aging Sebaceous Glands Secretes sebum (oil) that lubricates skin & nails  oil secretion 🡪 leads to soft & supple skin decreased oil secretion 🡪 leads to dry skin & wrinkles Concentrated in scalp & face (absent on palms & soles) Some conditions in adult & child are r/t overproduction of sebum (cradle cap, acne, seborrheic dermatitis) Hair Vellus Fine, soft, non-pigmented (“peach fuzz”) Covers body (except palms & soles, umbilicus, glans penis, inside labia) Terminal Course, thick, pigmented (scalp, eyebrows, eyelashes, axillae, pubic [& face/chest in males]) Subcutaneous Tissue (adipose or hypodermis) - layer below the skin Skin assessment reveals a lot of info regarding overall health status. Nurses have a big responsibility in assessing a patient's skin and protecting from injury. Subjective Data Previous history of skin disease (allergies, psoriasis, atopic (allergic) dermatitis [eczema], acne,etc.) Change in pigmentation Change in a mole (size, color, shape) dysplastic mole (a change which may indicate a precancer or cancerous condition) Xerosis (excessive dryness) – seen in the elderly Seborrhea (AKA dandruff) - oily flakes of skin Pruritus (itching) - common with age (d/t xerosis) or kidney/liver disease (d/t decreased metabolism & excretion of waste) Excessive bruising (abuse, clotting disorder, falls [e.g., arrhythmia, neurologic disorders, ETOH) Rash or lesions Medications: may cause skin eruptions, rashes, pruritus & photosensitivity (sunburn) Alopecia (diffuse, patchy or total hair loss) - chemotherapy, familial, trauma/burns & stress Trichotillomania (pulling out hair) Hirsutism (excess terminal hair growth from increased androgen production by adrenal glands) o most obvious on face in women but can affect entire body Nail changes Sun exposure (increases skin cancer risk) - protect children Self care behaviors (sunscreen, soaps, cosmetics) Objective Data: Integrate skin assessment during physical examination Inspection & Palpation: assess sun exposed areas (increased cancer risk), intertriginous areas (skin folds – e.g., under the breasts for fungus) & feet (particularly in diabetics) identify body piercing and skin condition Describe skin color: pinkish tan, fair (light); light to dark brown; olive, etc. Localized Color Change o Vitiligo: absence of melanin pigment in patchy areas (more common in people with dark skin) o Freckles (ephelides): small, flat, brown macules o Pigmented nevi (moles): inspect for changes o Birthmarks Diffuse Color changes Pallor (white or lighter coloration; ashen gray with brown/black skin ) o Anxiety/fear (vasoconstriction 2o to SNS stimulation)  o Cold/cigarette smoking (peripheral vasoconstriction) o Shock (shunting blood from periphery to major organs) o Arterial insufficiency/anemia (decreased blood supply to PV system) Erythema (red) “flushed appearance” o Hyperemia (excess blood) of superficial capillaries r/t: ▪ fever ▪ local inflammation (also associated with heat) ▪ cellulitis entry point of infection can not always be identified cellulitis of an extremity (e.g., leg) o increased emotions (blushing) o Polycythemia (increased RBCs) o Venous stasis/ DVT o Carbon monoxide poisoning Cyanosis (bluish, grayish): due to decreased perfusion of tissues (tissue hypoxia) o Central cyanosis: 2o to cardio-pulmonary problems (inspect lips, tongue, oral mucosa, and conjunctiva) ▪ Dark skin may appear blue, dull o Peripheral cyanosis: d/t vasoconstriction (e.g., exposure to cold) – inspect nailbeds, extremities) Jaundice (yellow, icteric) o Bilirubin is a by product of RBC breakdown & is normally excreted through the GI tract. o Jaundice results from rising amounts of bilirubin in the blood with reabsorption into the skin. o Causes of jaundice ▪ Biliary obstruction (prevents excretion of bilirubin via the GI tract) ▪ Ineffective breakdown of bilirubin due to: liver disease immature livers (seen in newborn infants) - the infant is placed under an ultraviolet light (“called a bili light”) which aids in the break down of the bilirubin o Jaundice may be seen in the junction between the hard & soft palate, sclera skin Skin Temperature Hypothermia (d/t to decreased circulation) o generalized [shock] o localized [peripheral arterial insufficiency] Hyperthermia o Generalized (increased metabolic rate) - hyperthyroidism, fever, heavy exercise o Localized (inflammation, infection, dvt) Moisture o Perspiration (normal sweating) o Diaphoresis (profuse sweating) o Dehydration ▪ Dry skin & mucous membranes ▪ Thirst (late sign of dehydration) Texture (smooth versus rough)  Thickness o Thickened areas of dead skin ▪ Calluses and Corns (common on hands/feet) o Thinning of skin ▪ Arterial Insufficiency (thin, shiny, hairless skin) Turgor - pinch skin on anterior chest (below clavicle) o Turgor (how quickly the skin snaps back when pinched) o Poor turgor = tenting (failure of skin to snap back) – indicates dehydration o Note: don't test on hands in elderly (false positive due to loose skin) Hygiene: clean & free of odor Vascularity o Cherry angiomas - genetic bright red papular lesion, 1-5 mm normally increases with age o Telangiectasia (dilated superficial blood vessels) ▪ Spider angioma central arteriole (fiery red) with capillary radiations; blanches (turns white) with pressure o Venous star ▪ bluish spider angioma; non blanching with pressure ▪ associated with increased venous pressure (seen with varicose veins) - ▪ primarily located on legs Petechiae o 1 - 3 mm, deep red, rounded o results from superficial capillary bleeding o caused by bacteremia, bleeding disorders (thrombocytopenia) Ecchymosis (typical bruise) o larger patch of capillary bleeding o r/t trauma, bleeding disorders or liver dysfunction o Purple/purplish-blue fading to green, yellow, brown over time Hematoma: localized collection of blood (raised bruise) Pattern Injuries: suspect abuse (scalding, belt strap/buckle, cigarette burns, etc.) Characteristics of Lesions Color Elevation: flat, raised, pedunculated (stalk; such as skin tag) Configuration (shape or pattern) Size: metric (mm, cm) Number Location (body part) & distribution (localized versus generalized) Discharge or exudate (describe color, odor) Types of Lesions Primary Lesion (initial lesion) Secondary Lesion (results from changes in primary lesion) - scratching, infection, popping a blister, etc. Primary Lesions Flat Lesions o Macule: flat, circumscribed, discolored, 1 cm (vitiligo) Raised lesions o Papule: solid, elevated, circumscribed, < 1 cm (raised nevus, wart [verruca]) o Plaques: coalesced papules, > 1 cm (psoriasis) o Nodule: solid, elevated, 1-2 cm (lipoma = fatty growth) o Tumor: larger than a few centimeters, firm or soft (lipoma) o Wheal: superficial, raised, erythematous, irregular (allergic reaction, PPD, mosquito bite) - causes interstitial edema o Urticaria (hives): wheals coalesce to form extensive reaction; intensely pruritic Fluid Filled (raised) o Vesicle: elevated cavity with clear fluid, 1 cm (blister, burns) o Pustule: contains pus; filled with leukocytes, not necessarily infected (acne) o Cyst: encapsulated fluid filled cavity in dermis or sub-q (sebaceous cyst) If deep, may be hard to differentiate from a nodule or tumor (e.g., breast cyst versus tumor) Secondary Lesions Crust: thickened dried exudate (dried serum/blood/pus) on top of 1o lesion (AKA scab) o rupture of herpes vesicle results in crust with erythematous base impetigo (staph & strep) Scale: compact flakes of skin (psoriasis [white-silvery], seborrheic dermatitis [yellow-greasy], o seborrhea (dandruff) Fissure: linear crack (cheilosis [corners of mouth], callused wwheels, tinea pedis [athletes foot] –between toes,) Erosion: shallow depression, moist, no bleeding (affects epidermis; e.g., varicella after rupture) Ulcer: deep depression into dermis; leaves scar (stasis ulcer, pressure sore) Excoriation: superficial abrasion (dermatitis) – red, open sores Scar: connective tissue replacing normal tissue Atrophic scar: depressed scar - stretch marks (striae) Hypertrophic scar: excess scar tissue 2o to increased collagen formation (keloid) Lichenification: thickening of skin (eczema [atopic dermatitis]; chronic sun exposure) Configurations (Shapes & Patterns) Annular: ring; clear center (tinea corporus [ring worm], pityriasis rosea) Discrete: isolated Confluent: lesions run together (urticaria) Grouped: clusters of lesions Linear: (scratch) Zosteriform: linear vesicles along a nerve route s/p Shingles [herpes zoster] Pressure ulcers Stage 1- non-blanchable erythema of intact skin Stage 2- partial –thickness loss of skin with exposed dermis. Pink bed of skin, top layer of skin may look like it peeled off. Stage 3-full thickness skin loss-adipose is visible Stage 4- full thickness skin and tissue loss with exposed fascia, muscle, tendon, ligament, or bone Unstagable-full thickness skin and tissue loss, obscured by slough or eschar. Skin Cancer (malignant melanoma, basal cell, squamous cell)  Malignant Melanoma o Highly metastatic o Grows deep, not wide o 1/2 arise from pre-existing nevi o High risk (fair skin, sun exposure) o Characteristics ▪ A = Asymmetry (1/2 unlike other) ▪ B = Border (irregular) ▪ C = Color (varied within lesion: tan, brown, black, [red - white - blue = "patriotic lesion"]) ▪ D = Diameter (> 6 mm) Basal Cell CA (BCC) o Most common type of skin CA, grows slowly, seldom metastasizes o Usually starts as skin colored papule/nodule with overlying telangiectasia o May develop a depressed center Squamous Cell CA (SCC) o Usually appears on hands or head (sun exposed areas, usually > 60 yo) o Erythematous scaly patch, 1 cm or more o Develops central ulcer Actinic keratosis (pink, scaly papules) – may be a precursor to SCC Hair Color: graying r/t genetics Texture: fine/coarse, shiny/dull, straight & curly, brittle Distribution: normal male & female pattern Inspect scalp (seborrhea [dandruff], lice or nits on hair shaft) Developmental Considerations Puberty o Increased secretion of apocrine glands - results in body odor o Increased secretion of eccrine sweat glands – increased perspiration o Increased secretion of sebaceous glands (oily skin/acne) ▪ Open comedones (blackheads) ▪ Closed comedones (white heads) o Increased fat deposits (especially females) o Secondary sex characteristic development ▪ Males & females: pubic hair, axillary hair ▪ Males: facial hair ▪ Females: areolae enlarge/darken, breast tissue develops Pregnancy: many changes due to increased estrogen levels o Striae (stretch marks): ABD, breasts, thighs (r/t fragile connective tissue) o Vascular spiders (spider angioma) & palmer erythema (increased estrogen) o Increased pigment in areolae & nipples, vulva & sometimes middle abdomen (linea  o nigra) or face (chloasma - disappears after delivery) o Increased fat deposits (thighs & buttocks) Aged Adult o Sun Related Changes ▪ Solar lentigines: flat, brown macules ▪ Actinic keratosis ▪ Wrinkling (r/t thinning dermis) Other Changes o Seborrheic keratosis: raised, crusty, irreg. lesion, "stuck on" appearance, waxy; non cancerous; located on trunk, face, hands (genetic) o Xerosis (r/t to decreased sweat & sebaceous glands) - increased risk of heat stroke o Skin tags: overgrowths of normal skin; not significant o Shearing/tearing injuries (r/t loss of collagen in dermis) o Sagging skin (r/t loss of elasticity) o Increased risk for skin disease & breakdown (r/t thinning skin, decreased vascularity, loss of sub q layer, decreased nutrition, increased sedentary lifestyle Hair Changes o Graying: decreased functioning melanocytes in hair matrix o Changes in distribution ▪ Thinning (male & female) ▪ Men: increased coarse terminal hair (ears, nose, eyebrows) Hormonal changes o Decreased testosterone (males & females): decreased axillary & pubic hair o Decreased estrogen/testosterone unopposed (female): bristly facial hairs Cultural Considerations Fair skin complexions at higher risk for skin cancer Larger amount of melanin in olive and darker skin tones Rashes may appear red in people with light skin In people with darker skin, a rash may appear to just be darker skin. Other signs of infection/irritation would be warm swollen skin in the person with darker skin. Nails: inspect & palpate (note color, shape & lesions) Color: translucent plate (linear bands/streaks may occur in people with darker skin tones) Leukonychia: white hairline markings from trauma or picking at cuticle (normal) Normal nail angle ≤160o o Clubbing: nail angle straightens out to ≥ 180 o & nailbed becomes spongy (r/t chronic hypoxia - COPD, lung CA) Cyanosis (peripheral) Koilonychia (spoon nails/concave) - iron deficiency anemia Paronychia: inflammation/infection of skin around nail bed Onycholysis: loosening of nail plate (fungal infection) Pitting (psoriasis) Subungual hematoma (bleeding under nail plate, painful) Ingrown nail Habit-tic deformity (picking nail with index finger)  Capillary refill: < 2 sec (> 2 sec = altered peripheral circulation) Heart and Neck Vessels Anatomy and Physiology Review Landmarks Precordium -area on anterior chest overlying the heart & great vessels Mediastinum o Midthoracic cavity that contains the heart & great vessels o Location: 2nd to 5th ICS, right sternal border to left MCL Base (Top of heart) Apex (Bottom of heart) o 5th ICS, and the MCL (approximately) - the heart is rotated so that the right side is anterior & the left side is posterior Structures of the Heart Pericardium (fibrous outer sac) o Attached to vessels, esophagus, sternum & pleura; anchored to the diaphragm Epicardium (outer layer) Myocardium (thick muscular pump) Endocardium (lines inside of heart) - contains electrical pathways Valves Unidirectional (prevent backflow of blood) Open & close passively (dependent on pressure changes) Atrioventricular Valves (between atria & ventricles) Left = Mitral [bicuspid] Right= Tricuspid Chordae tendinae attach the AV valves to the papillary muscles & provide stability to valves during systole (rupture of the chordae tendinae may be life threatening) Semilunar Valves (outlet from ventricles) Right = Pulmonic Left = Aortic Conduction & Hemodynamic Systems There are two systems in the heart that work together: Conduction system- the electrical system that initiates and conducts the heartbeat-(the wiring) Hemodynamic system-moves blood through the heart & vessels- (the pump) Conduction (electrical pathway) The SA node is the intrinsic pacemaker. It works like a spark that starts the heart beat & then it is transmitted across atria to the AV node, then to the Bundle of His and finally to the Perkinje fibers in the ventricles. Electrocardiogram (ECG) – reflects the electrical conduction through the heart P wave (depolarization of atria) – spread of stimuli through atria o If the SA node isn’t firing properly or doesn’t fire at all, then the P wave will look abnormal or be absent. o The SA node should fire at a rate of 60-100 bpm o If a lower pacemaker takes over (e.g., AV node), then the rate will be slower PR interval –time from stimulation of atria to stimulation of ventricles QRS complex (depolarization of ventricles) – spread of stimuli through ventricles T wave (repolarization of ventricles) – resting phase U wave (final ventricular repolarization) – not always seen on EKG Mechanics (the pump) Vessels (lie at base of heart) Venous blood (right side- un-oxygenated) Superior and inferior vena cava, pulmonary artery Arterial blood (left side- oxygenated) Pulmonary veins, and aorta Flow of Blood (blood flows from higher to lower pressure gradients) Lower body 🡪 inferior vena cava 🡪 RA Head & Neck 🡪 superior vena cava 🡪 RA ↓ RA 🡪 tricuspid valve 🡪 RV 🡪 pulmonary semilunar valve 🡪 pulmonary arteries🡪 lungs/alveoli 🡪 pulmonary veins 🡪 LA 🡪 mitral valve 🡪 LV 🡪 aortic semilunar valve 🡪 aorta 🡪 body Backward Flow Blood moves by pressure gradients. You can get a backflow of blood when atrial pressures are excessively high. Right heart o No valves between right atrium & vena cava o If pressure in the right atrium is greater than the vena cava, then blood back flows to the veins of the neck & PV system & results in distended neck veins & peripheral edema - r/t valve disease, lung disease, etc. Left Heart No valves between left atrium & pulmonary veins If pressure in the left atrium is greater than the pulmonary veins, then blood back flows to the lungs & results in pulmonary congestion (e.g., crackles/rales hear on auscultation of lungs) o r/t valve disease, HTN, heart failure Systole- When the heart muscle contracts Diastole- When the heart muscle is at rest Cardiac Output CO = HR X SV (SV = volume of blood per beat) Decreased CO can result from: o Decreased HR o Decreased SV (SV= amount of blood ejected with each heartbeat) -dehydration o Increased HR (d/t decreased diastolic filling time) Normal (4 - 6 L/ min) Preload (Left Ventricular End Diastolic Volume) Increased left ventricular volume causes more stretch on the myocardial muscle fibers at the end of diastole Frank Starling Law (the greater the stretch of muscle fibers, the stronger the contraction) The goal is to maximize preload (volume) in order to maximize left ventricular contraction & cardiac output  However, excessive preload leads to decreased C.O and heart failure (compare to an overstretched balloon that loses its ability to snap back) Afterload (also known as SVR or PVR) The opposing pressure the ventricle must generate to open the aortic valve during systole Excessive afterload increases myocardial workload & O2 consumption o may be caused by arteriosclerosis, HTN, sympathetic nervous system stimulation (e.g., stress), excessive alcohol intake Heart Sounds “lup dup, lup dup, lup dup” Heart sounds are produced by closure of the valves Valve Sites (A P E To Man) Aortic valve 2nd ICS, RT sternal border Pulmonic valve 2nd ICS, LT sternal border Erbs point 3rd ICS, LT sternal border (good location for referred sounds) Tricuspid valve 4th ICS, LT sternal border Mitral valve 5th ICS, L MCL Listen to all sites with the diaphragm and bell of the stethoscope Listen for aortic murmurs (sitting and leaning forward is best) - brings heart closure to chest wall Listen for extra heart sounds (left lateral decubitus position is best) AV valves close Semilunar valves close < ---------- [systole] ---------- >< ---------- [diastole] ---------- > S1 S2 S1 S3 S4 S1 (loudest at apex) – begins systole- ventricular contraction Mitral/tricuspid valves close 🡪 creates S1 heart sound “(lup”) Aortic/pulmonic valvedes open 🡪ventricles contract and blood is ejected from ventricles S2 (loudest at base)- begins diastole (ventricular relaxation) (“dup”) Aortic/pulmonic valves close 🡪 creates S2 Mitral/tricuspid valves open Rapid filling phase (passive initial filling of ventricles) Atrial kick (atrial contraction ejects last 25% of SV into ventricles in late diastole Extra Heart Sounds (Gallops) - diastolic sounds (best heard at apex with bell) S3 (S1------S2, S3) “Ken------tucky” Indicates ventricular resistance to early passive filling Occurs in early diastole (immediately after S2) Causes -Decreased ventricular compliance (early sign of HF) - High output conditions such as hyperthyroid, pregnancy, etc. S4 (S4, S1------S2) “Tenness------ee”  Indicates ventricular resistance to filling during the atrial kick Occurs in late diastole (immediately before S1) Causes (HTN, elderly) Summation Gallop (S3 & S4) Split Sounds Split S1 (mitral valve closing before the tricuspid valve due to higher pressures on the left) o uncommon since closure of tricuspid is usually too faint to hear Split S2 (aortic valve closes before pulmonic during deep inspiration) o common o changes in intrathoracic pressure with deep inspiration causes asynchronous valve closure Murmurs (blowing/swooshing sound that occurs with turbulent flow through valves or great vessels) Causes increased velocity (exercise) structural valve defects- Valve malfunction- increased backflow through valves or stenosis of valve septal defects (abnormal openings between chambers) Characteristics of Murmurs Timing Systolic versus diastolic Early, mid or late cycle Entire cycle o Holodiastolic (between S2 & S1) o Holosystolic (between S1 & S2) Intensity (graded 1 [soft] through 6 [loud]) Location (valve site)- this will give clue to what valve is causing the murmur. o Murmur at the base of the heart can be from an aortic or pulmonic valve problem o Murmur heard best at the apex of the heart may be a mitral or tricuspid valve problem Innocent Murmur (functional murmur) No valve, cardiac or other pathology Common in childhood (usually due to increased blood flow) Subjective Data (History) Chest Pain Etiology Cardiac (angina, MI, mitral valve prolapse) - r/o ACS (acute coronary syndrome) Severe CP in a young adult with HTN & tachycardia - ask about Cocaine Pulmonary (pneumonia, pleurisy, pulmonary emboli) Pericardial (pericarditis) - common after MI- may auscultate pericardial friction rub Musculoskeletal/chest wall (costochondritis, arthritis) – hurts with palpation Gastrointestinal (may mimic MI) - ulcer, hiatal hernia, esophagitis, indigestion Neurotic- anxiety Describe SXS (OLD CART) Onset (at rest, with activity, after eating, etc.) Location (substernal, localized versus radiating) Duration Character (burning, sharp/stabbing, crushing, pressure, etc.) Angina (myocardial ischemia) - imbalance between O2 supply & demand (thus, more common with exercise) - stop all activity and rest chest discomfort with or without radiation, SOB  Should resolve in a couple of minutes with rest &/or treatment (NTG) 🡪 may progress to an MI if not treated Prolonged symptoms may indicate an MI Myocardial Infarction (heart attack) similar to angina; may also have diaphoresis, N/V, palpitations, sense of impending doom Patients may not realize that chest pressure &/or SOB (rather than severe pain) may be an indication of ischemic heart disease. Be sure to ask them about “chest discomfort” rather than “pain”. Atypical symptoms of CAD (particularly in women or patients with diabetes) SOB sharp chest pain fatigue Risk Factors for CAD Age (male ≥ 45; female ≥ 55, or postmenopausal) HTN or hypertensive treatment Smoking Hyperlipidemia Diabetes (ASSUME THEY HAVE CAD) Family history of premature CAD in 1st degree relative (male < 55; female < 65) Shortness of Breath Dyspnea (shortness of breath) DOE (dyspnea on exertion) PND (dyspnea that awakens from sleep) HF (lying down increases venous return & myocardial workload) Orthopnea (increase HOB to breathe) – how many pillows? Cough (may occur with pulmonary congestion from HF) Fatigue (sudden vs gradual) Syncope (may be related to an arrhythmia and decreased cerebral perfusion) Palpitations (may indicate an arrhythmia) Edema & Nocturia (seen in heart failure) Dependent edema (worse in evening) Nocturia (recumbent position increases venous return to heart 🡪 increases renal blood o flow 🡪 increases U/O) Past HX Cholesterol level, murmurs, congenital heart disease, rheumatic fever, swollen joints,heart surgery, last EKG, stress test (ETT) results, etc. Family HX (HTN, CAD, DM, obesity, congenital heart disease, genetically transmitted disease (e.g., hypertrophic cardiomyopathy is the leading cause of death in young athletes) Personal Habits Diet (high fat, sodium, processed foods) Smoking (vasoconstricts) - increases heart rate, myocardial workload and O2 consumption (watch for angina) ETOH (increases afterload) – cardiac depressant causing sympathetic compensatory response (vasoconstricion & increased B/P) Exercise (increases HDL, myocardial muscle tone) Medications (digitalis, diuretics, beta blockers, calcium channel blockers, NSAIDS etc.) Objective Data (Physical Exam) Assess for cyanosis (with hypoxia) or clubbing-(chronic hypoxia) Neck Vessels (Inspect, palpate & auscultate) Carotid Arteries Visualized at top of neck near mandible Palpate in lower 1/3 of neck between trachea & SCM muscle (avoids carotid sinus which slows HR)  Palpate one artery at a time Pulse strength 2+ (diminished with decreased stroke volume) Auscultate for bruits (narrowing r/t atherosclerosis) Jugular Veins Indirect measure of right atrial pressure Jugular veins reflect changes in right heart filling pressures No valves between jugular veins & RT atrium Increased RIGHT atrial pressure = increased JVD External jugular vein (lies over SCM) Internal jugular vein (IJV) - underneath & medial to SCM Slightly rotate head to LEFT side (look for pulsations at the RIGHT base of the neck (caused by the IJ moving the SCM) Differentiate carotid arteries from internal jugular veins Internal Jugular Veins o Pulsation visible but not palpable o Two undulating waves or fluctuations Carotids o Palpable pulsation (one brisk pulsation wave) Assessing Jugular Venous Distention and Jugular Venous Pressure Raise HOB 30-45 degrees Have patient look to the left Use a tangential light onto the neck Inspect around the suprasternal notch or around the clavicle for pulsation of the IJ. If there is distention of the jugular vein in the mid or upper neck area, note at what degree this is seen (30, 45, 60, 90) o The more upright the patient (ie 90 degrees) the more abnormal the distention is. o There should be no distention, bulging or protruding at 45 degrees or greater Precordium Inspect & palpate Apical impulse (aka PMI) Located at 4th or 5th ICS, left MCL) - palpable in 1/2 of adults decreased with obesity & thick chest walls If shifted farther to the left, this may indicated cardiomegaly (enlarged heart) Heaves (lifts) sustained forceful thrusting of ventricle during systole visualized & palpated at the apex (may indicate myocardial hypertrophy) Thrill (palpable vibrations) Associated with loud harsh murmurs -Palpate across precordium (feels like a purring cat) Auscultate Rate (norm 60 - 100) Rhythm (regular; regular - irregular; irregular) Lub dup, lup dup (s1, s2, s1, s2) Pulse Deficit: (Apical rate is greater than peripheral pulse rate- due to arrhythmia (irregular heartbeat) check for this if the cardiac rhythm is irregular auscultate the apical heart rate & compare this to the radial pulse the apical and radial rates should be the same a pulse deficit occurs when the apical rate is higher than the radial rate Heart sounds – listen to each valve with the diaphragm & bell S1 (loudest at apex) – closure of AV valves Diminished sounds (pericardial effusion, obesity, emphysema) S2 (loudest at base) – closure of semilunar valves (aortic and pulmonic) Split Sounds- (discussed above) Gallops (S3, S4) – turn patient to left side; often more pronounced over apex Rubs and clicks (pericardial friction rub from pericarditis, or clicks from mechanical valve) Murmurs – listen over the valve sites and note any radiation across the precordium Documentation: Normal S1S2, Regular rate and rhythm with no murmurs, rubs or gallops Abnormal findings Dextrocardia Heat on Right side Situs Inversus Organs reversed Heart and stomach on Right Liver on left Murmurs and other problems. Peripheral Vascular System Anatomy/Physiology review ARTERIES - carry oxygenated blood to peripheral tissues Partial arterial occlusion (leads to decreased 02 delivery to distal tissues & tissue ischemia) Untreated total occlusion (may result in tissue death and loss of limb) Exercise (aggravates ischemia due to increased O2 needs) VEINS - consist of superficial & deep veins Return venous blood to the heart Venous return depends on: o skeletal muscle contraction (moves blood proximally) – BR decreases return o functional valves to prevent backflow (valves open towards the heart) o a patent lumen (to keep maximum forward flow) o respirations (help flow by decreasing thoracic pressure & increasing abdominal pressure) Legs (deep veins are responsible for most venous return) o Deep veins (femoral & popliteal veins) o Superficial veins (e.g., great saphenous vein (medial surface) – site for CABG ▪ Removal does not significantly compromise venous return since the deep veins return most blood to the heart o Perforators (connect the veins) SUBJECTIVE DATA (History) General Questions Past history of vascular problems (DVT), inflammatory conditions, heart disease Enlarged lymph nodes (painful, chronic, acute) Smoking Hx (vasoconstriction) Arterial Insufficiency (decreased arterial blood supply to the tissues) Intermittent claudication (muscle ischemia) - usually affects gastrocnemius muscle Classic symptoms (calf pain with exercise; relieved by rest) High occlusive disease may manifest as pain in thigh or buttock Venous Insufficiency (decreased venous return) Swelling /edema Unilateral versus bilateral unilateral (e.g., venous occlusion or DVT) bilateral (e.g., heart failure) Precipitating factors (prolonged standing/sitting, travel (e.g., airplanes) Associated symptoms (SOB, nocturia) – may be HF Nutritional status (hypoalbuminemia may lead to edema) Varicose veins Blood clots (DVT or superficial thrombus) Hormonal contraceptives – increase risk of venous thrombosis Capillaries and Fluid Exchange Capillaries are tiny blood vessels that form connection between arteriole and venules Maintains equilibrium between vascular and interstitial spaces Hydrostatic forces from BP is mechanism by which intravascular fluid seeps out into tissue space Fluid re-enters capillaries by osmotic pressure Lymphatic capillaries remove any excess fluid left behind in the interstitial spaces. If this system is altered, edema occurs OBJECTIVE DATA (Physical exam) Arterial Assessment Assess skin color: should be appropriate for ethnicity and symmetrical. Cyanosis? Pallor? Assess all palpable pulses Head & Neck (temporal, carotid) – covered in other lectures Arms (brachial, radial, ulnar) Legs (femoral, popliteal, posterior tibial, dorsalis pedis) Grade Pulses 0 (absent) 1+ (weak, thready) 2+ (normal) 3+ (full/increased, bounding) ***some institutions use a 4+ scale- We will use 3+ scale Use doppler as needed – if unable to palpate-(detects weak pulses) Auscultatory Sites Assess bruits (temporal, carotid aortic, renal, iliac, femoral) Assess capillary refill (Normal = CRT 1 cm) - due to infection, allergy or neoplasm Malignancy (hard, fixed, unilateral, nontender node) Supraclavicular node (metastatic site) - may indicate a neoplasm in the thorax, breast or abdomen Infection (bilateral, mobile, warm & tender nodes) Nodes receive & drain adjacent tissue (look for source of the problem) Palpation of Lymph Nodes Use systematic approach Touch lightly with fingertips (may compress nodes if pressing too hard) Palpate bilaterally to compare sides Palpate the deep cervical nodes by bending ipsilaterally (same side) - relaxes muscles Assess for supraclavicular nodes (hunch shoulders to relax muscles) Lymph Nodes of the Head & Neck Preauricular Location (anterior to tragus of ear) Drainage (scalp, forehead, lateral eyelids, eyes, upper face & external auditory canal) e.g., adenopathy with eye infection Postauricular Location (behind ear on mastoid process) Drainage (parietal area of scalp & external auditory canal) e.g., adenopathy with otitis externa Occipital Location (base of the skull) Drainage (parietal region of scalp) e.g., adenopathy with scalp lesion Tonsillar (AKA retropharyngeal or jugulodigastric)  Location (at the angle of the jaw [mandible]) Drainage (eyelids, frontotemporal skin, external auditory meatus, tympanic cavity, tonsils, posterior palate, floor of mouth & thyroid) e.g., adenopathy with tonsillitis Submaxillary (submandibular) Location (half way between jaw angle & tip of mandible) Drainage (lips, mouth, tongue & submaxillary glands) e.g., adenopathy with oral cancer Submental Location (midline, behind the tip of the mandible) Drainage (mouth, lips & tongue) e.g., adenopathy with oral cancer Superficial or anterior cervical Location (overlying the SCM muscle) Drainage (skin of ear & neck) Deep cervical chain Location (under the SCM muscle) Drainage (ear, larynx, thyroid, trachea) e.g., adenopathy with laryngeal cancer Posterior cervical chain Location (in the posterior triangle along the edge of the trapezius muscle) Drainage (posterior scalp, posterior skin of neck & thyroid) e.g., adenopathy with thyroid cancer, mononucleosis Supraclavicular Location (above & behind the SCM muscle) Drainage (upper ABD, lungs, breast & arm) r/o neoplasm (adenopathy here is usually bad) Normal Developmental Changes Newborns & Infants Record head circumference (up to age 2) Fetal Skull (separated by sutures & fontanels) - allows for growth Posterior fontanel (triangle shape) - closes at 2 months Anterior fontanell (diamond shape) - closes at 24 months Sunken fontanell = dehydration Bulging fontanels = increased ICP Craniosynostosis (premature closure of one or more cranial sutures while brain growth continues) Children Enlarged nodes are common with minor infection Pregnancy Chloasma (facial discoloration) Palpable thyroid (norm in pregnancy) Aging Adults Change in the curve of the neck to compensate for kyphosis Prominent facial bones due to decreased tissue elasticity Lymphatic System Lymphedema (excessive collection of fluid in the interstitial spaces due to blocked or infected lymphatic channels) Acquired (2o to lymph duct trauma) - e.g., surgery or metastasis [such as from  mastectomy] Congenital (Milroy disease) – mal-development of the lymph system Acute Lymphangitis - red streaks extending to axilla or groin, fever, chills, etc. Acute Lymphadenitis (inflammation of lymph nodes 2o to systemic neoplastic disease, bacterial infection, or other inflammatory condition) - S/S enlarged, tender, firm nodes with surrounding edema & erythema (e.g., cat scratch disease) Eyes & Visual System Subjective Data (ROS) Vision problems (assess coping methods with vision loss; e.g., psychological impact of losing drivers license) Visual loss o One eye or both eyes o Sudden versus gradual o Total versus partial (part of visual field) o Central versus peripheral ▪ Central – macular degeneration ▪ Peripheral - glaucoma Permanent versus intermittent Blurring Floaters – can be normal after 40 Sudden onset of cobwebs or a shade o may be a retinal detachment or vitreous detachment Halos around lights – r/t acute narrow angle glaucoma; digoxin toxicity Blind spots (Scotoma) - glaucoma, visual pathway disorders (e.g., ocular migraines – may have vision loss rather than HA) Night blindness - r/t optic atrophy [age related], glaucoma, Vitamin A deficiency Strabismus (“crossed eyes” or “lazy eye”) Diplopia (double vision) Eye Pain If pain is sudden with vision changes consider as an EMERGENCY until proven otherwise Quality of Pain (burning, aching, sharp, stabbing, photophobia [light sensitivity]) Redness or Swelling of Eye Infection Allergies (often seasonal symptoms) Dryness Mechanical (e.g., foreign body) Watering or Tearing Epiphora (excessive tearing) - may be due to irritants (allergies), infection or obstruction of lacrimal ducts  Discharge (collection of purulent exudate in eyes in AM?) → bacterial infection Past History Eye injury/trauma Eye infection (vaginal infections at the time of birth may have ocular effects) e.g., gonorrhea, herpes Eye surgery History of allergies Medical history (DM, HTN, hyperthyroidism) – all may effect eyes Diabetic retinopathy o leading cause of blindness o may have eye changes within 10yrs of diagnosis Family History Myopia (near sighted) - distance vision is impaired Hyperopia (far sighted) - near vision is impaired Color blindness Glaucoma Macular degeneration Last Eye Exam Use of contacts or glasses Medications (list all meds taken) Some meds have ocular side effects (e.g., cataracts with prednisone) Eye drops Objective Data Oculus dexter (OD) – right eye Abbreviations OD, OS, and OU not widely used anymore Oculus sinister (OS) – left eye Oculus unites (OU) – both I. Test Visual Acuity (CN 2): Central & Peripheral Vision a) Far Vision Test far vision using a Snellen chart from a 20-foot distance Test each eye individually and then both eyes together Normal = 20/20 vision Legally blind (20/200 after correction) Documentation (e.g., 20/30) can read at 20 ft what normal eyes can see at 30ft Test without glasses if you want to determine level of visual acuity Test with glasses if you want to determine how well the vision is corrected California requires 20/40 vision or better using both eyes to drive b) Near Vision o Test near vision by reading small print ( Jaegar/Rosenbaum cards, newsprint) o Presbyopia (decreased power of accommodation with aging) –decreased ability of the lens to change shape to accommodate for near vision -occurs 42-46 y/o c) Peripheral Vision Test Visual Fields: Confrontation test Face patient (at 2 ft)  Assess when patient can see finger at periphery (test each eye individually for all fields) Documentation (visual fields are full by confrontation, no field cuts, CN 2 intact) II. Test Eye Muscles & Nerves (CN 3, 4, 6) Six muscles are attached to the eyeball for straight & rotary movement Each muscle is coordinated with the same muscle in the other eye so that the eyes move in parallel (or conjugate) movement Cranial Nerves (CN 3, 4, 6 responsible for eye movement) All eye muscles are innervated by CN 3 except superior oblique (CN 4) & lateral rectus (CN 6) o III Oculomotor—all eye movement except… o IV Trochlear---moved eyes down and towards nose o VI Abducens (abduction)- moves eyes temporally a) Extraocular Movements (EOMS) - hold chin to avoid movement Follow a moving object through the 6 cardinal positions of gaze Detect any non-parallel movements (comparing both eyes) Nystagmus (involuntary movement of eyeballs) Normal (initial 1 - 2 beats of nystagmus in extreme lateral gaze) Abnormal (nystagmus at all other positions of gaze) b) Corneal Light Reflex Tests the parallel alignment of the eyes Instruct patient to look straight ahead Direct a light source towards the nasal bridge o Note the position of the light reflection on each cornea-The light should fall on the same spot of each eye Strabismus (deviation of an eye) c) Cover Test Detects eye muscle weakness (strabismus) Ask the patient to focus on a fixed object while covering one eye A weak eye will drift into a relaxed position once the eye is covered Quickly remove the cover from the eye If the covered eye moves to reestablish fixation, then eye muscle weakness is present Repeat procedure for the other eye Document presence/absence of eye drift when eye is covered or “no eye drift with cover test” III. Inspect the External Eye a) Eyebrows Should have symmetrical movement (unequal movement could indicate problem with CN 7 [facial nerve]) Note skin problems (e.g., lesions, seborrhea, etc.) Note eyebrow fullness or loss b) Eyelids Protect from injury, strong light & dust Contain meibomian glands (inside eyelid) -Lubricates lids o Prevents evaporation of tears  o Provides an airtight seal when eyes are closed Note any lesions, rashes, swelling, redness, discharge o Basal cell CA (papule with ulcerated center) o Hordeolum (sty) - localized staph infection of hair follicle at lid margin (painful, red, swollen) o Chalazion - infection or retention cyst of a meibomian gland (swelling with nontender, firm, discrete nodule on lid) Blepharitis (inflammation of eyelids- red, scaley, crusted lid margin Edema (allergies, renal disease, heart disease) Entropion (inward curve of lid & lashes) o Lashes irritate conjunctiva o Occurs with weak muscles & normal aging Ectropion (excessive outward lash & lid curve) o Causes increased tearing, loss of tears & dry eyes o Occurs with muscle loss & normal aging o Can cause conjunctivitis d/t to exposure of palpebral conjunctiva Palpebral fissures (space between eyelids) o Upper lid covers part of the iris (when eyes are open) o Lower lid is at the limbus (border between cornea & sclera) o Findings: ▪ Lid lag (occurs with exophthalmos) ▪ Visible white rim of sclera between the upper lid & iris during downward movement of the eyes hyperthyroidism, facial paralysis ▪ Ptosis (drooping of upper lid) – may involve CN 3, 5, 7 c) Canthus (corner of eye; the angle where lids meet) o Referred to as medial (or inner) & lateral (or outer) d) Lacrimal Apparatus (glands, ducts & lacrimal sac) Forms tears to irrigate conjunctiva & cornea (keeps eye moist & lubricated) Lacrimal glands o Located in upper outer corner or eye o Secretes tears that drain across eye into puncta (located at upper & lower inner canthus) o Tears then drain into the lacrimal sac, through nasolacrimal duct and empty into the inferior meatus in the nose e) Eyeballs o Inspect for color, moisture, swelling, discharge or lesions o Should be aligned without sunken or protruding appearance ▪ Enophthalmos (sunken eyeballs = dehydration) ▪ Exophthalmos (bulging eyeballs = hyperthyroidism) Three Concentric Coatings 1) Sclera (inspect anterior surface) Tough (fibrous), white, outer covering under transparent bulbar conjunctiva  o Scleral redness (injected) o Scleral icterus (jaundice) Bulbar Conjunctiva (a protective thin mucous membrane covering the sclera [not cornea]) o Conjunctivitis "pink eye" o Mechanical (foreign object), allergic, viral, or bacterial causes o C/O itching, burning, foreign body sensation o Eyes appear red & irritated (red at periphery, clear around iris) o Assess adenopathy (pre-auricular nodes) o Sub-conjunctival hemorrhage (not serious) o Red appearing sclera due to capillary bleeding caused by increased intraocular pressure (IOP) (coughing, sneezing, weight lifting, childbirth, straining with BM) Palpebral Conjunctiva (continuation of mucous membrane that covers inner eyelid) o Normal ▪ Light skin (pink) ▪ Dark skin (gray with brown macules) o Check for palpebral pallor (lower lid) - anemia or cyanosis Limbus (border of sclera & iris) - bulbar conjunctiva merges with the cornea Cornea (transparent; covers & protects the pupil & iris) o Helps refract (bend) light rays to focus on the inner retina (thus, o damaged cornea affects vision) o Shine a light across the cornea from the side ▪ Normal (smooth & clear) ▪ Abnormal (cloudiness in cornea, ant chamber or lens) o Findings ▪ Corneal arcus (grayish around cornea at limbus) - may be normal in pts > 60 yo or indicate lipid abnormality in younger people ▪ Corneal abrasion or corneal ulcer (2o to scratch or foreign object) painful, photophobic ▪ Astigmatism- spherical curve of cornea is asymmetric- light rays spread over diffuse area rather than a focal point on retina. Test corneal reflex (blink reflex) - protects eye o Touch cotton wisp to eye (very sensitive to touch) o Should blink if CN 5 & 7 intact ▪ Trigeminal nerve (CN 5) carries afferent sensation to brain ▪ Facial nerve (CN 7) carries efferent message that stimulates the blink reflex (2) Choroid (middle layer) Iris  o Normally round with even color o Contracts & expands to control pupil size o Color of iris varies (genetic recessive trait) Pupils (should be round & equal in size) Size varies with ANS stimulation o Sympathetic stimulation - pupil dilates- allows for increased light & increased vision in fearful situation- (also stimulant drugs) o Parasympathetic stimulation– pupil constricts (depressant drugs like opioids) o Anisocoria (unequal pupils) - occurs normally in 5% of population Normally constrict with bright light & dilate in dim light o Controlled by afferent (CN 2) & efferent (CN 3) nerves o Test pupillary light reflex ▪ Direct (constriction of same pupil) ▪ Consensual (constriction of other pupil) ▪ Documentation (R 3/1 = 3/1 L) Brisk(B), sluggish(S) or Non reactive(NR) o Test Accommodation (ability to adjust vision from far to near) ▪ Focus on a distant object (pupils dilate) then, look at an object moving towards the nose ▪ Normally the pupils constrict & converge o Documentation = PERRLA Lens Transparent Posterior to the pupil Ciliary body controls lens thickness (changes shape to accommodate for near & far objects) Cataract – clouding of the lens (3)Retina (inner layer) Contains the optic disc, retinal vessels, backgrounds & macula Contains transparent vitreous body Abnormalities include hemorrhages, nicking of vessels, exudates (HTN, DM) IV. Fundoscopic (Ophthalmoscopy) Exam Use the ophthalmoscope for examining the internal eye- Advanced skill Anterior Chamber Between cornea/iris & lens Contains aqueous humor (produced continually by the ciliary body) o Intraocular pressure (norm 13 - 22 mm Hg) o Determined by the amount of aqueous solution produced & the resistance to its outflow at the angle of the anterior chamber o Glaucoma (IOP > 22 mm Hg) - chokes the blood supply to the retina (measured by tonometry) - can cause blindness; affects peripheral vision Fundus-Advanced skill Color Optic disc—abnormal if borders are fuzzy and indistinct- papilledema r/t htn or high ICP Retinal vessels- abnormal = micro hemorrhages or aneurysms. Macula- central vision- (contains rods/cones) V. Visual Pathway & Visual Fields – test peripheral fields to see if a field is out The pathway for light & images in ones visual field (through the cornea, aqueous humor, lens & vitreous body to the retina) The right side of the brain looks at the left visual field The retina changes an image (stimulus) into nerve impulses that are conducted by the optic nerve and optic tract to the visual cortex of the occipital lobe Left Optic Tract (has fibers from the Lt half of each retina) Right Optic Tract (contains fibers from the right half of each retina) Optic Chiasm (location where fibers from both temporal visual fields cross over) Astigmatism –curve of the cornea is asymmetric, thus light rays are spread over a diffuse area rather than on a focal point on the retina (causes blurred vision; may be corrected with glasses) Developmental Considerations Infant & Child Test light perception (by observing the blink reflex) – present at birth Test pupillary light reflex - present at 3 wks By 1 month (should fixate on yellow, bright object) By 4 months (should fixate on an object with both eyes) - vision approx 20/200 Screen vision (use picture cards) - around age 2 or when child is cooperative (vision approximately 20/40) Check visual fields - by age 3 or preschool Check color vision (X linked) - between age 4 - 8 o Ishirara's test (series of polychromatic cards that have numbers imbedded in different colors) Extra Ocular Muscle Function DO NOT MISS STRABISMUS (asymmetric eye axes) If diagnosed after age 6→ poor prognosis Strabismus (results in disuse of the deviated eye) Amblyopia (loss of vision or blindness d/t disuse) Setting sun sign (eyes deviate downward with rim of sclera showing above iris) – may indicate hydrocephalus Iris color (permanently differentiates by 6 to 9 months) Check for bilateral red reflex Aging Adult May normally have decrease in eyebrow cover on temporal side Xanthelasma (lipid deposits at inner canthus) Pseudoptosis (lids may droop & cover eyes 2o to loss of elasticity, fat & muscle atrophy, thus loose skin) Ectropion (outward turn of lid) Entropion (inward turn of lid) Dry eyes & burning (decreased function of lacrimal gland and entropion) Arcus senilis (collection of broken down lipids forming a gray - white circle around the limbus) – seen in hyperlipidemia Decreased pupil size (creates problems with night vision & night driving) Senile cataract (lens opacifies by age 70) - everyone will develop cataracts if they live long enough Floaters (occurs in the vitreous due to condensed vitreous fibers or exudates)  Visual acuity may gradually diminish, but central visual acuity generally (85%) remains intact Presbyopia (decreased ability of lens to change shape to accommodate for near vision) 3 primary causes of vision problems: o Cataracts (lens opacity) - pupil may appear cloudy o Glaucoma (loss of peripheral vision) o Age-related macular degeneration (AMD) ▪ loss of central vision; leading cause of blindness ▪ test changes with Amsler grid Note. Emphasize regular eye exams and glaucoma testing