trauma

increased stress on bones - stress fractures and fatigue fractures

pathologic fractures - due to disease process that weakens bone such as neoplasms and osteoporosis

visible deformity

sweeling, pain, altered sensation

loss of function

crepitus 

type of incomplete fracture

common in soft bones of children

breaks through cortical bone on one side - not through the entire bone

spontaneous fracture from weakness

occurs with little stress

fracture of distal fibula due to excessive stress on the ankle (tibia may be damaged also)

often due to jumping off from a height

1. rupture of blood vessels

- bleeding, hemostatsis and hematoma formation

- edema causes streching and swelling and pain

- clot forms

2. damage to nerves and surrounding connective tissue structures

3. necrosis at site of fracture

4. damged tissue/debris initiate an inflammatory response

- release of bradykinin and other chemical mediators (more pain)

- systemic signs of inflammation may occur

1. hematoma (clot)

2. granulation tissue

3. Procallus (fibrocartilage callus)

4. bony callus

5. remodeling

(Henry Gram Doesn't Pay Big Raises)

Hematoma (clot) 

What stage of healing and what happens

1st stage of healing

Hematoma develops within medullary cavity at site of fracture, fibrin network is formed within hematoma which serves as a framework for growth of granulation tissue

granulation tissue

what stage of healing and what happens

2nd stage

capillary growth into area, phagocytes invade area and remove necrotic tissue, osteoclasts remove bone fragments, fibroblasts invade area

procallus (fibrocartilage callus)

what stage of healing and what happens

3rd stage 

fibroblasts lay down collagen, chondrocytes migrate in and lay down fibrocartilage, these cells create procallus (unites ends of bones, weak structure, provides framework for bony callus)

bony callus

what stage of healing and what happens

4th stage

osteoblasts from periosteum and endosteum lay down new bone matrix, replace procallus with bony callus

remodeling

what stage of healing and what happens

-amount of local damage (inflammatino and periosteal damage will delay healing)

-proximity of bone ends (better approximation = faster healing)

-presence of foreign material or infection

-blood supply to fracture site

- systemic factores (age, nutrition, anemia, etc.)

1 month in child

2 months in adult

several months in elderly 

muscle spasms

infections (tetanus, osteomyelitis (compound and surgical repair)

ischemia (edema from trauma, tight cast)

fat emboli (large bones like femur/pelvis)

nerve damage

failure to heal or deformity during healing

-malunion = deformity, nonunion = failure to heal (must have reduction to approximate ends of bones)

residual effects such as osteoarthritis

stunted growth

compartment syndrome

-seen more commonly with crush injuries

-edema/bleeding wtihin fascia causes compression of nerves and blood vessels

-accompanied by severe pain

-ischemia develops --> risk of necrosis if pressure not relieved

-may occur with casts that are too tight

closed reduction

open reduction

traction 

separation of two bones at a joint with loss of contact b/t articulating surfaces

usually accompnaied by significant tissue damage

(ligaments and tendons, blood vessels and nerves)

-distortion of joint usually evident

-loss of function

-significant pain

may recure repeatedly, requiring surgery

tear in tendon

think T for Tear and sTrain (no T in sprain)

injuries that develop over a period of time in which the same movement is repeated

- affects muscles, tendons, nerves

-repetivie motion interferes with blood supply

-inflammation

-scar tissue formation

more common in 30-50 yr olds

usually involves upper body

stress is a risk factor

seen with certain occupations/activities such as sports, massage therapists, keyboard/mouse use, running or jogging

-history of joint use and any trauma

-physical exam of joint and ROM

-radiography or MRI

-arthoscopy may be done accompanied by treatment

RICE

NSAIDs

PT

massage of surrounding tissue

Rest

Immobilization

Compression

Elevation

- post-menopausal, senile or idiopathic

- age 50+ years

-decreased sex hormone

-decreased calcium intake

-bone resorption exceeds formation

-results in loss of trabecular bone

-diagnosed with bone density scans (DEXA)

- common sites of fractures = compression fractures of vertebrae, wrist, hip

- loss of height

- kyphosis - "Dowager's hump"

- loss of mobility 

- age 50+ years 

- decreased mobility or sedentary lifestyle

-hormonal factors (excess corticosteroids or PTH, deficiet of estrogen or testoserone)

-deficeits of calcium, vitamin D or protein

-smoking

-lower BMI 

-asian or european ancestry

- excessive caffeine intake

-fair skinned 

occurs in children

inadequate mineralization bones

-results from deficit of vitamin D and phosphates

- leads to weak bones and other skeletal deformities

occurs in adults

- inadequate minerlization of bones

-results from deficit of vitamin D and phosphates

- may lead to soft bones, resulting in compression fractures

-dietary deficits

-malabsorption

-phenobarbitol

-lack of sun exposure

-renal disease

disease characterized by bone destruction and repleacement of bone with fibrous tissue

-results in weakened, enlarged, deformed boones

- occurs in adults older than 40

exact cause unknown

-slow growing virus

-genetic link

-often asymptomatic/mild skeletal pain

-bone deformity (kyphosis, bowlegs, deformed, enlarged skull (compression of cranial nerves, HA, dizziness, deafness))

-CHF, cardiovascular disease

musculoskeletal tumors commonly come from metastic tumors from....

malignant

(known as sarcomas)

-most common primary neoplasm

metaphysic of femur, tibia, fibula is common site of involvement

usually has metastasized to lungs by time of Dx

- common in children, adolescents and young adults

arise from cartilage cells

more common in adults - age 30+

common in pelvis and shoulder girdle bones

excision of tumor if possible

chemo to reduce metastasis

surgical amputation if excision is not feasible (last resort)

-inherited

-destruction of muscle with replacement by fat and fibrous tissue

-s/s are due to loss of muscle tissue

-all are progressive

-s/s as well as severity varies among different types due to selective distribution of muscle damage

4 types of MD

(just the names)

-Ducheene or pseudohypertrophic MD (most common type- affects young boys)

-Becker MD

- Limb-Girdle Dystrophy

-Facioscapulohumeral Dystrophy

-X-linked

-defect in gene for dystrophin 

muscle cell membrane protein

results in damage/death of muscle cell

-fat and fibrous tissue replaces damaged cells

-usually apparent by 3 years

-early motor weakness

-proximal weakness 

(seen in pelvic girdle initially with results in waddling gait, toe walking, difficultying climbing stairs... Gower maneuver which is pushing up to erect position.... frequent falls)

-tendon reflexes reduced

-deformities develop (kyphoscoliosis, lordosis, flexion contractures)

-weakness sperads to shoulder girdle - resp infections are common

-cardiac myopathy occurs commonly

-impaired mental functioning is possible

-eventually become wheelchair bound 

-prenatal testing

-muscle biopsy (lack of dystrophin, adipose tissue and fibrotic scar tissue)

-electricmyography

-elevated CK enzymes

supportive

no cure

death usually by age 20 often due to resp. complicaitons

group of diseases characterized by generalized pain and stiffness of muscles and soft tissue

- trigger points

- no obvious inflammation or atrophy of tissues

more common in women 20-50 years

stiffness affecting muscles, tendons and soft tissues

(migraine of the muscles, joints are not involved)

sleep disturbance and fatigue

anxiety and/or depression may be present

-cause is unknown

-possible imbalance in serotonin and othe rneurotransmitters or increased production of substance P

-onset often occurs after emotional trauma, infections, steroid use, excessive use of aspartame

-appears to be genetic in predisposition 

-clinical

-trigger points

-labs/imaging studies are negative

-regular physical activity

-avoid stress

-massage therapy

-NSAIDs

-treat anxiety and depression if present

-Lyrica

"wear and tear" joint disease

degenerative joint disease

-most common form of arthritis

-onset of symptoms is usually in 40-50 age range

-by age 80 nearly 100% of people have radiographic evidence, but not all are symptomatic

-incidence is increasing 

DIP

PIP

hip

knee

cervical and lumbar vertebrae

Foot - metatarsal phalangeal joints

related to aging 

genetic component identified

more common in siblings

due to some underlying problem with joints

(trauma, obesity, previous joint infection, metabolic diseases (DM), congenital joint deformities)

-articular cartilage is damaged due to mechanical stress, inflammatory mediators, defects in cartilage metabolism (articular cartilage surface becomes rough and worn)

-tissue damage causes release of enzymes, accelerating disintegration of cartilage

-subchondral bone may be exposed (cysts, osteophytes, or new bone spurs develop)

-osteophytes and cartilage break off into joint space

-joint space narrows

-secondary inflammation of surrounding tissue (tendongs, ligaments)

-loss of normal ROM in joint

-pain with weight bearing and use

-bony enlargement of joint of fingers

Heberden's nodes (DIP)

Bouchard's nodes (PIP)

-aching pain with weight bearing and movement

-decreased ROM of joints

-walking is difficult (risk for falls)

-crepitus

-TMJ (mastication and speaking are difficult)

-no systemic signs/symptoms

-clinical, physical

-no diagnostic lab tests, but can be used to rule out other causes

-imaging studies (sometimes less severe than clincial s/s)

- ancillary services

OT - stress on joints minimized by use of adaptive devices

massage therapy, PT

-exercise

pacing activity, mild exerise program to maintain fitness and joint function

-pharacological

glucosamine - chondroitin supplements

injection of synthetic synovial fluid (hyaluronic acid)

NSAIDs, analgesics

-surgery

drainage fo fluid

arthroscopy (removal of scar tissue)

joint replacement

chronic, inflammatory, autoimmune arthritis with systemic effects

characterized by exacerbations and remissions

affects all age groups

-onset often in 30-50 year range

-tends to be symmetrical

-usually involves small joints of hands, feet, cervical spine but can affect large joints

-exact cause unknown

-genetic factor is present

-some links to viral infections

-autoimmune destruction of synovial lining causes synovitis

-marked inflammation, cell proliferation of synovium due to Rheumatoid factor and immune complexes

-rheumatoid factor is an autoantibody against portion of IgG

-pannus formation follows inflammation (type of granulation tissue that grows over articular cartiage that prevents nutrients from reaching cartilage, relases enzymez that destroy cartilage)

-cartilage erosion ensues creating unstable joint

-fibrosis follows inflammation which calcifies and obliterates joint spaces

-ankylosis (joint fixation and deformity develop if untreated)

-damage to joint initates changes around the joint such as atrophy of muscles, bone alignment shifts, muscle spasms, contractures and deformity)

-can see inflammatory involvemtn of other tissues such as SQ tissue, lungs, heart and eyes.

- joint involvment includes small joints and often symmetrical

(hand involvment - ulnar deviation, swan neck deformity, Boutonniere deformity)

-painful, red, swollen, stiff joints

-decreased ROM

-contractures

-SQ nodules

-systemic effects (marked fatigue, depression, malaise, anorexia, low-grade fever, iron deficiency anemia that is resisteant to iron therapy, generalized lymphadenopathy, generalized aching)

-involvement of other organ systems (eye, heart, kidneys, lungs)

-criteria of American College of Rheumatology

-lab tests (may be RF negative, joint fluid analysis)

-imaging studies

-balance between rest and moderate activity

-heat and cold applications

-physical and occupational therapy

-pharmacological

-NSAIDs

-glucocorticoids for severe inflammation

-analgesia for pain

-disease-modifying anti-rheumatic drugs (DMARD's) e.g., gold salts, methotrexate, hydroxychloroquine

-biologica response-modifying agents - e.g., infliximab, rituximab and anakinra 

-onset more acute than adult form often with more systemic  effects

-large joints frequently affected

-RF is usually not present (other autoantibodies are present (ANA - antinuclear antibody))

-no SQ nodules

-chance for complete remission

3 categories of JRA 

(just the names)

-still disease (systemic form)

-polyarticular JRA

-pauciarticular JRA

systemic form of JRA

fever, rash, lymphadenopathy, hepatomegaly, joint involvement

-involves four or fewer joints

-eye involvement (uveitis) - inflammation of iris, ciliary body, and choroid of eye

-usually bacterial

gonococcus

staphylococcus aureus (most common)

lyme disease (migratory arthritis)

-direct introduction of bacteria into joint, e.g., trauma, non-sterile injection, or surgery

-secondary infection due to bacteremia

-develops in single joint

-joint is red, swollen, painful

-decreased movement

-purulent exudates

-great capacity for destruction of joint/cartilage

IV ABX

surgical drainage

also known as gouty arthritis

results from depostis of uric acid crystals in the joint, causing inflammation

-inadequate renal excretion of uric acid

-increased production of uric acid

chemo

metabolic abnormality

genetic factor

-elevated plasma uric acid allows deposition of uric acid crystals in joint and skin

-inflammatory response causes damage to joint

-formation of tophus from deposition in skin - large, hard nodules of urate crystals 

painful, red swollen joints

great toe common affected, Tophi

by reducing uric acid levels by drugs and dietary changes

-colchicine - acute treatment

-allopurinol - preventive treatment

a chronic progressive inflammatory arthritis

(type of spondyloarthopathy)

primarily affects sacroiliac joints, intervertebral spaces and costovertebral joints

more common in men than women (3:1)

onset ages 20-40 years

-cause unknown

-thought to be an autoimmune disorder with genetic basis

strong association with HLA-B27 allele

-vertebral joints inflamed 

-fibrosis and calcification follows inflammation

-fusion of vertebral bodies - loss of mobility, bamboo spine on x-ray

-inflammation in lower back initially, then moves up spine

(ascending)

-kyphosis develops which limits lung expansion 

-lower back pain/morning stiffness, pain when lying down (often nocturnal pain)

-eventual ankylosing of spine (becomes rigid)

-30% of patients have systemic signs such as fatigue, fever, wieght loss, uveitis)

treated by drugs to relieve pain

daily exercise

physiotherapy

occupational therapy

endocrine disorders arise from one of two problems 

1.

2. 

1. excess of hormone

2. deficit of hormone

-resistance to hormone

genetic defect

autoimmune response

excessive demand on target cells

- deficit of hormone or reduced effects

tumor destorys normal glandular tissue (adenomas)

inadequate tissue receptors present (Type II DM)

antagonistic hormone production is increased

malnutrition (body not able to produce enough hormone due to lack of "building blocks")

atrophy or surgical removal of gland

infection: ex: TB infection may result in destruction of adrenal glands

vascular problems (lack of blood supply to endocrine galnd ex: Sheehan's syndrome)

congenital deficit (lack of development of endocrine organ or genetic defect (lack of enzyme))

excess of hormone

(general etiologies)

- tumor prodcues excessive amount of hormone

adenoma (most common cause of endocrine disorders, benign tumor that produces hormone, ex: pituitary adenoma)

-excretion by liver or kidney is impaired (hormone unable to be removed ex: breast development in males with liver failure)

- congenital condition produces excess hormone (hyperplasia of glandular tissue ex: congenital adrenal hyperplasia)

Blood tests

-check serum hormone levels

(releasing hormones from hypothalmus, tropic hormones from pituitary and target hormones from endocrine glands under the influence of the tropic hormone)

*remember hypothalmus has releasing hormones that act on the pituitary, the pituitary has stimulating hormones that act on organ and final hormone from organ, so you can check all three of these in the pathway*

radioimmunoassay

immunochemical methods

urine tests

(24 hour urine collection is more accurate than random single blood level)

stimulation or suppression tests

scans, ultrasounds, MRI, biopsy

deficit may be treated with replacement therapy

excessive secretion may be treated with medications, surgery, radiation 

basic problem is inadequate insulin effects in target tissues

-deficit of insulin secretions

-decreased receptor response to insulin

-production of insulin antagonists

results in abnormal CHO, protein and fat metabolism

-cells are unable to utilize glucose

-use protein and fat instead

some tissues can utilizee glucose in the absence of insulin 

-CNS, kidney, myocardium, Gut, exercising skeletal muscle can partially meet tissue needs w/o insulin

-uptake of glucose by cells 

muscle and fat cells (muscle cells can partially utilize glucose w/o insulin)

does not control glucose uptake by cells in liver, kidney or brain

-uptake of lipids and storage of fat (in adipose tissue)

-uptake of amino acids and protein synthesis (primarily in muscle cells)

-uptake of K+ into cells

oxidation of glucose for ATP production

production of glycogen

conversion of glucose to fat

blood glucose level

-AA - arginine and lysine = increase

-PNS increase = increase

-cholescytokinin = increase

insulin dependent DM

juvenile onset

10% of cases - most severe form

autoimmune destruction of beta cells in pancreas

lack of insulin

genetic/environment interaction

acute onset in children and adolescents (most common)

onset may be in adults but is rare

not linked to obesity 

non-insulin dependent DM

adult onset

onset is slow and insidious usually in middle age

decreased production of insulin and/or increased resistance by body cells to insulin

(oral hypoglycemic meds may be used)

genetic, enviornmental and metabolic interaction

associated with obesity 

-occurs with pregnancy 

-insulin resistance due to hormones associated with pregnancy

-resolves following pregnancy

-increased risk of type 2 DM in next 15 years(~5-10&)

-insulin deficit or lack of response to insulin results in decreased transportation and use of glucose into many cells

polyphagia = lack of nutritients entering cells

fatigue = lack of ATP

catabolism of fats (more common in type I) - ketone production, ketonuira, may progress to ketoacidosis and if untreated develop decompensated metabolic acidosis)

catabolism of proteins (more common in type I) - muscle wasting 

- blood glucose levels rise (hyperglycemia) - cause shift of water from intracellular to extracellular space

- in kidneys high plasma glucose exceeds renal threshold (glucosuira - hyperosmolar filtrate and osmotic dieresis leading to polyuria)

(loss of electrolytes with glucose espeicaly sodium and potassium)

dehydration from hyperglycemia and polyuria (stimulates thirst center --> polydipsia)

type 1 = thin to normal weight

type 2 = overweight - contributes to onset

the 3 P's (often signal onset)

polyuria - often noticed due to onset of nocturia

polydipsia - due to dehydration (dry mouth, fatigue)

polyphagia - due to lack of glucose availability to cells

-finger stick blood sugar

- urine

glucosuria

ketonuria

diagnostic tests for DM 

(just the names)

fasting blood glucose

oral glucose tolerance test

c peptide

diagnostic test

person fasts for 8 hours

Blood sugar is measured

99 or below = normal

100-125 = pre-diabetes or impaired fasting glucose

126+ = diabetes 

diagnostic test

person fasts for 8 hours

ingests 75 grams of glucose in liquid form

blood sugar is measured before ingestion and 2 hours after ingestion

139 and below = normal

140-199 = prediabetes

200+ = diabetes 

diagnostic test

distinguish between type I and II

used to distinguish endogenous insulin production from exogenously administered insulin

tests for monitoring DM

(just the names)

glycosylated hemoglobin test

fructosamine

hemoglobin A1c

monitor glucose levels over 8-12 weeks

normal is 4-6%

goal for DM is <7%

glucose control over preceding 2-3 weeks

values based on patients age and gender

1. diet and exercise

complex CHO, low glycemic index, adequate protein, low cholesterol, low triglycerides and adequate fiber

exercise improves blood glucose levels, improves cellular insulin response but may lead to hypoglycemia

2. oral medication (type 2) (many categories)

3. insulin replacement (type 1 and some type 2)

SQ injection - protein

Continuous infusion by implantable pumps

oral medication for DM

glyburide (micronase, diabeta)

increases insulin secretion

oral med for DM

reduces blood glucose levels by decreasing hepatic glucose production and increasing insulin sensitivity of cells

-biosynthetic

-produced by recombinant DNA technogly 

-uses human gene in E. coli (most commonly used)

-type of human insulin

-altered to change rate of onset of action

Lispro

regular insulin

Humulin-R

lente

NPH

Humulin -N

variations in diet and alcohol use

change in physical activity

infection

vomiting

surgery

exercise

complications are directly r/t duration adn extent of abnormal blood glucose levels

may be acute or chonic 

acute = hypoglycemia, DKA, HHNKC (hyperosmolar hyperglycemic non-ketotic coma)

chronic = vascular, neuropathies

"insulin shock"

more common with insulin replacement treatment (type 1)

can occur due to excess oral hypoglycemic drugs

excess insulin in circulation 

can be life-threatening or cause brain damage if untreated

(neurons do not use proteins or fats, they need glucose)

(related to low blood glucose)

neurolgic s/s = disorientation and change in behavior, may appear impaired, decreasing LOC

sympathetic nervous system s/s = anxiety, diaphoresis, pallor, tremors, tachcardia

-glucose tablets

-CHO rich food (soda, crackers, candy)

-glucagon (SQ or IM injection, emergency glucagon kits)

-IV dextrose 

diavetic ketoacidosis

more common seen in type 1 

patho:

due to inuffient insulin in blood (may be initiated by infection or stress, may result from error in dosage, change in diet, alcohol intake)

high blood glucose levels result from insuffienient insuin (polyuria results, dehydration)

mobilization and use of lipids to meet celluar needs result in production of ketoacids

metabolic acidosis develops (dehydration and ketoacids)

- dehydration - thirst, dry, rough oral mucosa, warm, dry skin

-rapid, deep respiration - acetone breath, kuss-maul

-lethargy, decreased responsiveness

-metabolic acidosis - fruity breath, may lead to loss of LOC

-electrolyte imbalances - abdominal cramps, N/V, lethargy, weakness, low sodium, high potassium (due to shift of K from intra to extra space, K will be lost in urine)

Hyperosmolar hyperglycemic non-ketotic coma

occurs in type 2 diabetes

insidious in onset and diagnosis may be missed

usually develops with infection, MI, overindulgence in food or acute illness

more common in older clients

results in severe dehydration and electrolyte imbalances

don't see ketosis due to some insulin activity

-marked hyperglycemia >600 mg/dL creates increased serum osmolarity which leads to osmotic dieresis

-severe dehydration develops --> increased Hct, hemoconcentration also worsens hyperglycemia --> increased heart rate and respirations

-electrolyte imbalances result in: neurologic deficits, muscle weakness, difficulties with speech, abnormal reflexes 

altered metabolism of CHO, fats and proteins

hyperglycemia and hyperlipidemia

chronic complication

changes may occur in small and large arteries 

changes in microcirculation

-obstruction or rupture of small capillaries and arteries

-tissue necrosis and loss of function

-retinopathy (leading cause of blindness)

-chronic renal failure (degeneration in glomeruli)

-peripheral neuropathy (common complication due to ischemia in microcirculation to peripheral nerves (impaired sensation, numbness, tingling, weakness, muscle wasting))

-autonomic neuropathy

(bladder incontinence/diarrhea, impotence, orthostatic hypotension)

-complications to both mother and fetus may occur

-increased incidence of spontaneous abortions

-infants born to diabetic mothers (increased size and weight for date, may experience hypoglycemia postnatally)

-lack of parathyroid hormone

-leads to hypocalcemia

-weak cardiac muscle contractions (poorly developed SR)

-increased excitability of nerves (spontaenous contractions of skeletal muscle)

-results in hypercalcemia

"stones, bones, abdominal groans and psychiatric moans"

-osteoporosis 

-predisposition to kidney stones (increased calcium)

-constipation, N/V

-fatigue, lethargy, depression

tumor

secondary to renal failure

paraneoplastic syndrome

adenomas

10% of intracranial tumors

effect of mass

-may cause increased ICP (headaches, seizures, drowsiness)

-may compress individual structures (visual deficits, hemianopsia, compression of optic nerve)

effect on hormone secretion

-dependent on cells and location involved

-may cause excessive or decreased release of hormone

-may have single hormone secretion or multiple hormone secretion affected

untreated frequently leads to panyhypopituitarism

surgery

hormone replacement

hormone antagonists

-dwarfism

-gigantism

-agromegaly

-deficit in growth hormone production/release

-normal proportions

-normal intellect

treatment = GH prior to ephiphyseal plate closure

-excess GH prior to puberty and fusion of epiphysis

-normal proportions and intellect

-excess GH secretion in adults

-often associated with adenoma

-bones become broader and heavier (compression of nerves and vessels)

-cartilage and soft tissue grows (enlarged hands and feet; change in facial features)

-DM develops

-HTN, CVS disease 

-see loss of large volumes of urine (>24 liters in 24 hours)

-adenoma

-head injury or surgery

-possible genetic problem

treatment: replacement of fluid and electrolytes, hormone replacement

may be nephrogenic in origin (tubules don't respond to ADH)

-retention of fluid

-may be temporary, triggered by stress, may be secreted by an ectopic source such as a tumor

treatment: diuretics and sodium supplements 

thyroxine

triiodothyronine

negative feedback involving hypothalamus/pitutary 

(TSH values can be useful in diagnosing thyroid disorders)

-disease of thyroid gland

-disease of pituitary gland

-disease of hypothalamus

** releasing hormone from hypothalamus, stimulating hormone from pituitary, target hormone from thyroid**

interuption in any of the above can result in thyroid dysfunction

enlargement of the thyroid gland

may be due to hypothyroidism or hyperthyroidism

compression of structures in neck (esophagus, trachea)

food that contain elements to block synthesis of T3 and T4 (cabbage and turnips)

see resultant increase in TSH and goiter develops

-results from hyperactivity of thyroid gland

-term refers to the s/s of hyperthyroidism

-may see "nodular goiter"

-toxic goiter, thyroid storm, thyrotoxic crisis 

precipitated by infection, surgery in pt. with hyperthyroidism

sudden onset of uncontrollable s/s of hyperthyroidism

life-threatening event - heart failure, delirium 

many etiologies

most common is Graves disease

autoimmune disorder, auto-antibodies are produced which stimulate TSH receptors in thyroid, results in overproduction of thryoid hormones and goiter

more common in women, onset in 30's

increased body temp, sweating, soft silkly hair and skin, reduced BMI, insomnia, hyperactivity

exophthalmos

-presence of protruding, staring eyes

-decreased blink and eye movement -"lig lag"

-result of increased tissue mass in the orbit and inflmmation of extrinsic muscles by auto-antibodies 

-may result in visual impairment 

hypothyroidism

(most common cause)

-hashimoto thyroiditis 

-myxedema

-cretinism

category of hypothyroidism

also known as chronic lymphocytic thyroiditis 

autoimmune disorder

immune system attacks and destroys thyroid gland

most common cause of hypothyroism in US

more common in middle aged women

hypothyroidism in adults

secondary to tumor, surgical removal or treatment of gland with radioactive iodine 

untreated congenital hypothyroisim

results in short stature, lack of normal physical and sexual matruation and mental retardation 

etiologies: may be r/t iodine deficiency during pregnancy, congenital defect, thyroid aplasia 

(problem with adrenal glands)

change in person's appearance

- round face with ruddy color

-truncal obesity with fat pad between scapulae

-thin limbs

-fragile skin, purple striae

retention of Na and H2O and loss of K+

- due to mineralcorticoid effects

-HTN and edema

-suppresion of the immune response and inflammatory response (increased infections)

stimulation of erythrocyte production

emotional lability and euphoria

increased catabolism of bone and protein (muscle wastin, delayed healing, osteoporosis

increased blood sugar (mimics DM, increased gluconeogenesis, increased insulin resistance)

decreased stress response (with iatrogenic cushing's syndrome - adrenals atrophy with exogenous cortisol, cannot increase cortisol secretion during times of stress)

deficiency of adrenocorticoid secretions

(glucocorticoids, mineralcorticoids, androgens)

-autoimmune reaction is a common cause

-gland may be destroyed by hemorrhage secondary to infections

(TB, meningococcal, histooplasmosis, destruction by tumor)

-decreased blood glucose leveels

-inadequate stress response (can be life-threatening)

-fatigue, weight loss, frequent infections

-low serum sodium concentrations

(decreased blood volume, hypotension, high K levels (cardiac arrhythmias), incrreased pigmentation (seen in creases, buccal mucosa)

addisonian crisis

occurs during times of stress when extra amounts of adrenal hormons are needed

life-threatening 

snellin chart (measures visual acuity)

visual field test (check for central and peripheral vision)

tonometry (assessment of IOP, non-contact tonometry = air puff)

ophthalmoscope (exam of internal structures)

gonioscopy (angel of anterior chamber, Dx. of glaucoma)

testing of extraocular muscle function

coordination tests

cranial nerves

nystagmus

diplopia 

-involuntary, rhythmic oscillations of one or both eyes

(horizontal, vertical, rotary, mixed)

- causes problems with vision/depth perception

-congenital or aquired

-acquired form is seondary to...

CNS damage, drug/ETOH toxicity, inner ear or cerebellar disturbances

double vision

may be due to trauma to cranial nerves resulting in paralysis of extraocular muscles

may occur in stroke

loss of depth perception occurs 

myopia

hyperopia

presbyopia 

astigmatism

strabismus 

-nearsightedness

close up vision is okay

objects in distance are blurred

image is focused in front of the lens

-farsightedness

difficulty focusing on near objects

distant vision is better

eye ball is too short

image is focused behind the retina

age related farsightedness

loss of elasticity of lens and weakness of ciliary muscles reduces accommodation 

-irregular curvature in the cornea or lens (lens common)

normal surface of eye is spherical

cornea may have areas of steeper curvature and flatter curvature (football shape)

light rays are not refracted to specific point of retina

see blurred images

may occur with nearsightedness or farsightedness

-special contacts - conform more closetly to the irregular surface of the cornea, toric contacts, gas permeable contacts

surgery - LASIK

squint or cross-eye

results from diviation of one eye, binocular vision is affected (problems with depth perception), may result in double vision, may be caused by weak or hypertonic muscle, short muscle or neurologic defect

in children must be treated to prevent development of amblyopia

- brain suppresses image from afected eye

-stops sending motor info to eye "lazy eye" develops, visual deficit in affected eye

categories: esotropia, exotropia, hypertropic, hypotropia 

(hordeolum)

infection involvin meibomian or sebaceous glands on the eyelid

staphylococci species

swollen, red mass forms on eyelid, purulent exudates with drainage

infectious agents 

- bacteria - contact lenses are frequent source of infection

-viruses - associated with common cold

inflammatory agents

-allergens or irritating chemicals

bacterial causes = more purulent discharge

- staphylococcus aureus -- frequently occurs in children, sclera and eyelid appear red; spread by fingers, contaminated towels, occurs with contact lens use, contaminated makeup, contaminated medication -- ABX treatment to prevent damage to cornea

other bacterial causes = chlamydia trachomatis and Neisseria gonorrhea -- spread from infant during birth, may be spread by self-inoculation 

-caused by chlamydia trachomatis

infection of conjunctive

follicles develop on inner surface of eyelids

eyelids sell and eyelashes turn inward

eyelashes cause painful abrading cornea every time pt. blinks ("scratchy eye")

cornea becomes scarred --> loss of transparency

globally most common cause of vision loss where water is scarce and inadequate hygeine occurs

can occur in any age group

ABX treatment is curative if given before scarring occurs

-inflammation of cornea (severe pain and photophobia, risk of ulceration of cornea with scar tissue formation and resultant loss of vision)

may be due to trauma

may be due to chemical irritation - damage from chemicals, splashes, fumes

may be due to infection

bacteria - pseudomonas seruginosa - contact lenses (bacteria produces enzymes that degrade cornea

fungi

viruses such as herpes simplex

-result of increased IOP caused by excessive accumulation of aqueous humor

due to increased production or decreased drainage

most common and preventable loss of vision in developed countries

may be acute or chronic

-increased pressure in anterior cavity is transmitted back to posterior cavity 

-pressure on retina and optic nerve causes atrophy of structures

-irreversible and eventally can cause blindness

-halos around lights at night

-loss of peripheral vision

-pain may occur if IOP is greatly increased as in acute form

acute or narrow-angle glaucoma

10% of cases

angle between cornea and iris is decreased

-iris pushed forward and to side

-block the outflow of aqueous humor

-sudden marked increase in IOP

may be caused by aging, developmental abnormalities or scar tissue from trauma/infection

may be triggered by pupil dilation 

sudden ocular pain (develop high ocular pressure acutely)

halos around lights

red eye

decreased vision

fixed, mild-dilated pupils

N/V

medical emergency 

-medications

decrease aqueous humor production

pupil constriction - increases angle

-surgery

iridotomy

laser trabculoplasty 

open-angle glaucoma

higher incidence post age 50

90% of cases

thickening of trabecular network and blockage of canal of Schlemm

interferes with resorption of aqueous humor

insidious onset - no acute attacks

painless

gradual visual field loss - peripheral vision is lost

-age related or caused by metabolic abnormalities (DM)

-excessive exposure to sunlight

-congenital (maternal toxoplasmosis or rubella)

-traumatic (sports injuries to eye)

size, site and density of clouding vary among individuals

- may be different in indviduals two eyes

rate or progression varies

blurred vision

vision loss over time

ghost images

night driving especially difficult (halos around lights)

outpatient surgery for lens replacement

phacoemulsification - damaged lens is broken up using sound waves, suctioned out of lens capsule, monofocal or multifocal lens is inserted

monofocal - provides fixed degree of focusing - distant vision

need glasses for close vision 

retina tears away from the underlying choroid

tear allows vitreous humor to flow behind retina

increasing protion of the retina is lifted away from choroid

retinal ischemia develops

can lead to irreversible loss of receptors

acute emergency

http://www.youtube.com/watch?v=VQWT3Gn0ihA

no pain or discomfort

visual field contains area of blackness (scotomas)

as if a curtain has fallen over eye

severe myopia

trauma

age

-evaluation by opthalmologist

bed rest if small

surgery 

age related macular degeneration 

common cause of visual loss in older adults

-unknown

-combination of genetic factors and environmental factors

caucasian, female, smoker, diet poor in vegetables

dry or atrophic (90%)

more common - deposits form in retainl pigment cells

wet or exudative (10%)

neovascularization 

no pain

central vision becomes blurred, then lost

-irreversible changes

-laser surgery to destroy new blood vessles (wet)

-antioxidants - lutein and zeaxanthin (investigational), zinc 

conduction deafness

sensorineural impairment

-sound is blocked in the external ear or middle ear

-accumulation of wax, foriegn object, scar tissue

-scarring of tympanic membrane (tears in tympanic membrane)

-osteosclerosis of the ossicles 

-damage to the organ or corti (receptors) or auditory nerve (CN VIII)

-infection

-head trauma

-neurologic disorders

-ototoxic drugs - aminoglycosides

-sudden very loud sounds or prolonged exposure to loud noise

-presbycusis - age related loss of hair cells

-congenital defects 

used if appropriate for individual hearing deficit

some damage to sensory receptors - some functional receptors

-used successfully in some cases of sensorineural loss

-device provides direct electrical stimulation to the auditory nerve

bypasses the hair cells in cochlea

must have functional auditory nerve fibers

best results if inserted by age 2-3 years 

-swelling/inflmmatino of eustachian tube following URI causes blockage of eustachian tube

-air in middle ear cavity is reabsorbed into surrounding tissues

-negative pressure in middle ear cavity creates vacuum and fluid is pulled into cavity

-creates breeding ground for bacteria and infection results

-fluid creates pressure on tympanic membrane (pain, may cause rupture of membrane)

bacteria

- may spread along nasopharynx and resp. structures

-Haemophilus influenza (particularly in young children)

-Pneumococci, beta-hemolytic streptococci, staphylococci

viral infections also common

-frequently complicated by secondary bacterial infections

ear pain

fever

nausea might be present

tympanic membrane red and bulging

mild hearing loss or feeling of fullness

may be asymptomatic in chronic stages 

-prolonged infection is likely to produce scar tissue and adhesion

can lead to permanent conductive hearing loss or speech probems

-chronic infection may lead to mastoiditis

infection involving mastoid cells of temporal bone

-cholesteotoma

epidermoid cyst filled with keratin

expanding lesion destroys middle ear structures, labyrinth, mastoid hair cells

-ibuprofen or acetaminophen to reduce discomfort in first 48 hours

- use of antibacterials if bacterial infection

-decongestant may be useful in draining auditory tube

-surgery may be done to insert temporary tubes in tympanic membrane to allow for drainage 

also referred to as "swimmers ear"

infection of the external auditory canal and pinna

usually bacterial but may be fungal

pain usually increased with movement of pinna

purulent discharge and hearing deficit

treatment: ABX drops, ear wick

imbalance in bone formation and resorption

development of excess bone in middle ear cavity (stapes becomes fixed to oval window)

blocakge of conduction sounds to cochlea (causes conductive deafness)

may be due to genetic or environmental factors ( more common in young adult females)

surgical removal of stapes and replacement prosthesis to restore hearing 

onset ages 30-50 years

affects one ear

stress may precipitate attacks

changes in barometric pressure

vertigo

nausea, vomiting, sweating

attack may last minutes or hours - change in barometric pressure may precipitate attack

intermittent with remissions and exacerbations 

treatment with drugs to reduce production of endolymph

antihistamines

home exercise programs to reduce sensitivity to motion 

-systemic disorders - liver disease

-systemic infections - chickenpox

-allergies to ingested food or drugs

-localized factors - infection, irritation, allergies

-location

-appearance

may change over time

primary lesions

secondary lesions - change in appearance due to the application of topical medications, external forces and secondary trauma (scratching), progression of the disease

-length of time the lesion has been present

-physical appearance - color, elevation, texture, type of exudates

-presence of pain

-presence of pruitus (itching)

associated with allergic response, chemical irritaiton due to insect bites, infestations by parasites e.g., scabies

mechanism not totally understood - histamine release (if type 1 hypersensivity reaction), can be due to stimulation of pain receptors 

small, flat circumscribed area, different color

example: freckles, nevi

small, elevated, firm, circumscribed lesion

example: moles, warts

solid, elevated circumscribed lesion, varies in size

example: neurofibromas

elevated, erythematous lesion with purulent exudates

example: acne

elevated, circumscribed lesion with serous fluid 

example: blister, chicken pox

elevated lesion with flat top - often with scales

example: psoriasis

cavity with loss of tissue from epidermis and dermis, often bleeding or weeping

example: stasis ulcers

small, deep, linear cracks - extend into dermis, may be wet or dry

example: athlete's foot

dried serum, blood or purulent exudates

example: impetigo

thickened, rough - leather like skin

example: chronic dermatitis

shallow, moist cavity in epidermis

example: ruptured blisters

-culture and staining of specimens (bacterial infections, viral culture)

-wood's lamp (blacklight used in diagnosing some fungal infections)

-scraping of lesions (scabies, fungal infections)

-biopsy (detection of malignant changes) (safeguard prior to or following removal of lesions)

-blood tests - helpful in diagnosis of conditions due to allergy or abnormal immune reaction

skin testing using patch or scratch method - allergy testing

allergic contact dermatitis

direct chemical or mechanical irritation

exposure to allergen

metals, cosmetics, soaps, chemicals, plants, hair dyes, rubber, latex

type IV hypersensitivity reaction - cell mediated

-sensitization occurs on 1st exposure

-pruitic rash develops at site a few hours after second exposure (vesicular rash, erythema, pruritis/pain, edema)

does not involve immune response

inflammatory response due to direct exposure to irritant

- urine, harsh soaps, detergents, removal or irritant, reduction of inflammatino with topical glucocorticoids

-erythema

-pruritis/pain

-vesicular rash

-edema

(hives)

result of type 1 hypersensitivity

-ingestion of substances

(shell fish, drugs, certain fruits, peanuts)

-insect bites

-red, raised wheals

-may see central clearning with erythematous border

-lesions are highly pruitic

hives are often part of anaphylaxis!!!

-check for swelling around mouth and check airway

-administer EpiPen or other first aid as required 

(eczema)

common problem in infancy

-rash is erythematous with serous exudates

-occurs on face, spreads to scalp, chest, extremities and abdomen

in adults

-rash is dry, scaly and pruitic

-often on flexor surfaces

-lichenification 

-genetic component - assoicated wtih FH of atopy - asthma, eczema, allergic rhinitis

-defect in epidermal barrier

chronic inflammation results from response to allergens

see eosinophilia and increased serum IgE levels

topical glucocorticoids

antihistamines 

chronic inflammatory skin disorder

-onset usually in teen years

abnormal T-cell activation 

-excessive cytokine production

-inflammation

-excessive proliferation of keratinocytes leads to thickening of skin

-small red papules initally which enlarge

-silvery plaque forms over erythematous base (pinpoint bleeds if plaque is removed)

-itching or burning sensations

-lesions found on face, scalp, elbows, kneeds

-fingernails may show pitting

-may be associated with arthritis (psoriatic arthritis)

several forms

-may occur as skin disorder

-may be systemic and affect viscera

primary cause unknown

-increased collagen deposition is observed in all cases

-collagen deposits in arterioles and capillaries

inflammation and fibrosis develops in response

decreased capillary networks

-hard, shiny, tight, immovable areas of the skin

-impaired movement of mouth and eyes

systemic form may cause renal failure, intestinal obstruction, resp. failure due to distortion of tissues

infection of the connective tissue within the dermis and SQ layers

causative organism

-staphylococcus aureus most common

-sometimes streptococcus

-more superficial infection of dermis and upper SQ layer

-well demarcated border

-may be iatrogenic

-causative organism is usually streptococcus

-both present with erythema, pain, and warmth

-red streaks may develop running along lymph vessels proximal to infected area

-frequently in lower trunks and legs

-usually secondary to damage in skin

abraisions, spider bites, cuts

-infection of hair follicles (follicultitis) that has spread to surrounding dermis

-common on face, neck, back

- frequently drains large amounts of purulent exudates

-usually caused by S. aureus

sometimes caused by autoinoculation

squeezing boils can result in spread of infection to other areas of the skin

http://www.youtube.com/watch?v=PnG0QlMeXIs

(skip to 0:43)

-collection of furuncles that coalesce to form a large infected mass

- usually have several points of opening to skin with drainage

-higher risk of scarring

http://www.youtube.com/watch?v=PnG0QlMeXIs

(skip to 1:09)

surgical drainage is significant collection of pus

antibiotics 

impetigo

and etiology

common infection in infants and children

- strains of staphyloccous aureus (main cause)

in neonates staphy may cause staphylococcus scaled skin syndrome - may been seen as outbreaks in nurseries/NICU

streptococcus pyogenes

bacteria produce exotoxins and coagulase which damage skin

may arise in intact skin or on broken skin

highly contagious !!! - autoinoculation

-erythematous vesicles - usually starting around the nose or mouth (lesions coalesce, may appear anywhere on the body)

-vesicles filled with yellow/golden fluid

-rupture of vesicles leads to crusting (honey colored crust)

-painless

-pruitus common (leading to scratching and further spread of infection

-topical AVBX if few lesions

- oral ABX

-good hygiene 

flesh eating bacteria

infection of the dermis and SQ tissue that rapidly spreads along fascial planes

two types:

mixture of aerobic and anaerobic bacteria

streptococcus pyogenes or MRSA

bacteria secrete toxins that break down fascia and connective tissues (proteases)

t-cell activation causing massive production of cytokins that results in severe inflammation and tissue necrosis

systemic signs = shock - toxic shock syndrome

necorsis and gangrene of tissue

often preceding history of minor trauma or infection in the skin and SQ tissue of an extremity 

majority of cases occur in individuals who are immunocompromised but can occur in healthy individual

surgical debridement, amputation, hyperbaric oxygen, aggressive ABX (vacomycin)

25% mortality rate

herpes simplex "fever blisters"

HSV - 1

most common cause of cold sores or fever blisters

HSV -2 

genital herpes

both types cause similar effects

primary infection may be asymptomatic

in young children will often present as herpetic stomatitis

after initial infection virus remains in latent in sensory nerve ganglia

recurrence may be triggered by common cold, sun exposure, stress, hormonal changes

spread by direct contact with fluid from lesion

spread of infection to others possivel prior to appearance of lesions

potential complication of herpes simplex HSV-1

spread of virus to eye - keratitis

herpetic whitlow - painful infection of the fingers

(warts)

viral infection of the epithelium caused by HPV

over 130 types

HPVs type 1-4 - plantar warts

genital warts - HPV types 6 and 11

frequently develop in children and young adults

virus enters skin through small breaks

viral replication and viral shedding of the skin surface - contagious

see thickening of layers

thrombosis of small capillaries - "seeds"

may resolve spontaneously within time

liquid nitrogen

caustic agents - destroys virus and with resulting inflammation get activation of immune response 

fungal infections are usually superficial

fungus lives in dead keratinized epithelial cells

- may spread systemically in immunocompromised

many types of fungi

-candida is associated with DM, also seen in infants

-transmitted by direct contact, damp surfaces - shower floors, pets

infection of the scalp, common in kids, bald spots with scale

treatment: griseofulvin

-infection of the body, particularly non-hair parts

-circular lesions

-periphery - erythematous, may have vesicles/papules

-central area - clear and scaly

treatment: topical anti-fungals

typically involves toes

maceration of skin between toes

pruritic and painful

foul odor to feet

common in areas where people are barefoot - showers, pools, gyms

treatmetn: topical anti-fungals

infections of the nails - in particular the toenails

nail becomes discolored - white, yellow, brown

nail thickens and cracks, becomes friable

infection is spread to other nails

treatment: requries 4-6 months of oral medication 

invasion by mite sarcoptes scaviei

-requires living host

can exist for short time off of human host

-female burrows into epidermis

-lays eggs over a period of several weeks

-larvae migrate to skin surface

-burrow into skin in search for nutrients

-larvae mature and cycle is repeated

-can occur almost anywhere on the body

spares face/scalp except in infants/elderly

commonly seen in body creases - axillae, wrist, elbows, web space of fingers, along belt line, external genetalia

popular rash

burrows appear on skin as tiny, light brown lines

intensly pruiritic - allergic reaction, due to presence of mites/fecal material, can take weeks to resolve pruitis after mites have been eradicated

topical permethrin

lindane is the second line drug (toxicity)

(lice)

infestations can occur in any area of the body covered by hair

female lice lay eggs on hair shafts - after hatching, louse bites human host, sucking blood for production of ova

nits - egg sacks attached to hair

bites are visible as macules or papules

intensely pruritic - excoriations result from scratching

adult lice are difficult to see

lice spread by close contact

inseticides - permethrin, pyrethrin

(resistance has developed)

fine toothed comb

clean bedding, pillows etc.

r/t aging (not really UV light exposure)

proliferation of basal cells

-waxy, "pasted on skin" appearance

-leasions are oval, elevated

-may be smooth or rough

-color varies from white to black

-may appear anywhere on the body

"solar keratoses"

-pre-cancerous lesion

20% untreated lesions progress to squamous cell carcinoma

-occur on skin exposed to ultravilet radiation

sunlight, tanning beds

-commonly in fair-skinned person

-lesions appears as pigmented, scaly patch 

-painless, malignant tumor of the epidermis

second most common form of skin cancer

most commonly found on exposed areas of the skin

-face and neck, ears, lips, arms, hands, legs

associated with long term sun exposure

higher incidence in smokers

higher incidence in fair skinned, blue/green eyed blondes, red-heads

may occur in oral cavity

-base of tongue, lesions are red, scaly, may crust or bleed

excellent prognosis when lesion is removed early

-poorer prognosis once metastasized

invavsive type arises from premalignant conditions

-leukoplakia 

most common form of skin cancer

seen in sun exposed areas

slow growing

-rarely metastasizes

-good prognosis usually

lesions

-appear white, pearly, tan or flesh colored

-usually raised papules with rolled edges and slightly depressed central area

-may be flat or wart-like

-may appear as a sore that does not heal