1. Unit 1Pathology for theChapters Physical Therapist1-4AssistantCatherine GoodmanKendra FullerKelly King, PT, MACarrington College

2. OBJECTIVES Explain and differentiate between concepts of health,illness and disability Describe genetic aspects of disease Describe and compare the systemic and local effectsof commonly encoutered pathologic conditions 3. Introduction to Concepts of Pathology Pathology is defined as the branch of medicine that investigates the essential nature of disease Changes in body tissues and organs Cause or caused by disease Why study Pathology? 4. Introduction to Concepts of Pathology Terms: Clinical Pathology Pathology applied to the solution of clinical problems Laboratory methods and clinical diagnosis Pathogenesis The development and progression of each pathologic (disease) condition Cellular changes Manifestation of clinical signs and symptoms 5. Introduction to Concepts of Pathology Pathogenesis Idiopathic disease Arising spontaneously or from an obscure or unknown cause Iatrogenic Induced inadvertently by a physician or surgeon or by medicaltreatment or diagnostic procedures Endogenous Originating within the body or cell (autoimmune or impaired immunesystem) Exogenous Originating outside the body or cell (most infections) 6. Pathology for the PTA Clinical pathology The effects of pathologic processes on the individualsfunctional abilities and limitations or impairments The relationship between impairment and functional limitationis the focus of therapy Most patients have multiple medical pathologies. This requires knowledge of the impact diseases and conditions have on the neuromusculoskeletal system in order to provide safe, effective treatment. 7. Concepts of Health, Illness, andDisability Health no universally accepted definition Absence of illness Physical, mental, and social well-being Either - or (healthy or ill) Health dynamic process dependent oninternal and external environments Homeostasis Biologic, psychologic, spiritual, and sociologic state Wellness incorporates all these aspects 8. Concepts of Health, Illness, andDisability Illness often defined as opposite of health, sickness Disease biologic or psychologic alteration thatresults in malfunction Manifests with specific signs and symptoms (i.e. fever when infection is present) Cause and effect Incidence and Prevalence Natural History 9. Concepts of Health, Illness, andDisability Terms Acute Chronic Disability a physical or mental condition that limitsa persons movements, senses, or activities, specificimpairment(s) 10. Classification Models for Disability Nagi Disablement Model System to classify the impact of disease or trauma Pathology produces pain and impairments Leads to functional limitations and disability Components Disease or pathology Impairment(s) Functional limitations Disability 11. Nagi - Disability Not all disease leads to impairment Not all impairment leads to disability Functional limitations are the result ofimpairments Inability to perform the tasks and roles that constituteusual activities for that individual Disability is patterns of behavior that emergeover long periods of time when functionallimitations cannot be overcome 12. International Classification ofFunctioning, Disability, and Health (ICF) International Classification of Functioning, Disability, and Health The international standard to describe and measure health anddisability Established in 2001 Focus on life vs mortality How people live with illness and disease How to provide increased productivity and quality of life Components: Body functions (b) Body structures (s) Activities and participation (d) Environmental factors (e) Personal factors race, gender, age, education 13. Cognitive Disability Dependent on the location of lesion (local change incells causing abnormal tissue) Lesions have many etiologic factors Head injury Disease Alcohol abuse Anoxia or hypoxia (absence or decrease in oxygen) 14. Cognitive Disability Cognitive deficits are associated with specific areas of the brain 15. Implications for the PTA Physical disability Cognitive disability Treatment must be adapted specifically to eachpatients underlying pathology Treatment areas may need to be modified Learning styles need to be assessed 16. Health Promotion and Disease Prevention Practicing healthy behaviors to decreaseprecipitating factors Health Promotion Self-responsibility Nutritional awareness Vit D and Calcium for bone health Folic Acid and Prenatal vitamins Stress reduction Physical fitness 17. Health Promotion and Disease Prevention Disease Prevention Healthy People 2000 Healthy People 2010 Healthy People 2020 Encompass the entire lifespan Principles: Self-responsibility Nutritional awareness Stress reduction Physical fitness 18. Which Preventive Practices Do YouPractice? 19. Implications for the PTA Screening programs Health Promotion Prescriptive exercise programs to improve health andwellness Understanding how individual variables affect patientoutcomes 20. Genetic Aspects of Disease Most illnesses are caused by acquired gene mutations May be the result of exposure to harmful (toxic) substances Errors in replication are usually repaired by the body When the repair process fails, disease or illness results Acquired gene mutations are not inherited 21. Genetic Aspects of Disease Genes are also chemical messengers of heredity Mutations on the X and Y Chromosomes are passedon to offspring as genetic disorders Genetic disorders are often manifested in neonatalperiod The Human Genome Project allowed completemapping of DNA sequence and increasedunderstanding of susceptibility to disease, prenataldiagnosis 22. Genetic Aspects of Disease Genes are the chemical messengers of heredity Gene therapy Introduction of normal genes into living target cells to return cellactivity to normal Requires a vector that can pass the bodies defenses Genetic engineering Laboratory practices of manipulating genes Goal is to remove defective gene and supply a normal one toeliminate genetic defects Ethical concerns 23. Genetic Engineering 24. Genetic Aspects of Disease Gene doping 25. Genetic Aspects of Disease Gene Testing Identifies people who have inherited a faulty gene The gene may or may not lead to a particular disorder Results in earlier monitoring, preventive treatment, and long-term planning Psychologic implications Ethical issues and privacy concerns 26. Benefits of Genetic Testing 27. Implications for the PTA Important to eliminate factors in disease susceptibility Regular exercise can help control diabetes, bone density, immune function, psychologic function and obesity Understanding of genetic disorders can help therapists understand patient response to interventions and develop individualized plans of care 28. Review of Terms - Acute Illness An illness or disease that has a rapid onset and short duration Often responds to a specific treatment Usually self-limiting Return to previous level of functioning 29. Review of Terms Subacute Illness Between acute and chronic. Present for longer than a few days but less than severalmonths 30. Review of TermsChronic Illness characteristics Permanent impairment or disability Residual physical or cognitive disability Need for special rehabilitation and/or long term medical management 31. Review of Terms Diagnosis Identification of disease through evaluation of signs andsymptoms, laboratory tests (diagnostic tests), or other tools Etiology Causative factors in a particular disease 32. Review of Terms Incidence The number of new cases of a disease in a given population noted within a stated time period Mortality Measurement of the number of deaths related to a disease Epidemic Higher than expected number of cases within a given area 33. Review of Terms Pandemic Higher than expected number of cases within many regions ofthe globe Medical History Personal and family history of current and prior illness essentialfor planning appropriate interventions Predisposing factor Inherent trait may or may not lead to disease or illness(predisposition to blood clots due to inherited trait) 34. Review of Terms Precipitating factor Causes or contributes to the occurrence of a disorder (longflight DVT) Iatrogenic Disease or illness caused inadvertently by a physician or surgeon or by medical treatment Complication New secondary or additional problems that arise after theoriginal disease begins Prognosis The probability or likelihood for recovery, expected outcome 35. Review of Terms Signs Objective indicators (manifestations) of disease (fever, rash orlesions) Symptoms Subjective indicators (pain, nausea, dizziness) Exacerbation Change or increase in severity of chronic condition 36. Application for the PTA CJ is having surgery next week to remove a malignant breast tumor, following discovery of a lump in the breast and a biopsy. Her mother and aunt have had breast cancer. CJ is taking medication for high blood pressure. Match the significant information above to the appropriate term: diagnosis, medical history, etiology, prognosis, neoplasm, signs, complication, treatment, examination of living tissue. Some terms may not be used or may be used more than once. 37. Application for the PTA Malignant breast tumor and high blood pressure:diagnosis High blood pressure and family cancer: medicalhistory Biopsy: examination of living tissue Medication: treatment Surgery: treatment and diagnosis 38. Pair and Sharetime 39. Pathology for the PTAChapter 2Problems Affecting Multiple Systems 40. Problems Affecting Multiple Systems It is important for the PTA to understand systemic, local and functional effects associated with pathological conditions Why? What does it mean if something is Systemic? 41. Inflammation Acute Inflammation systemic effects include fever,tachycardia (rapid heart rate) Can cause changes in blood elevated serum protein Can lead to abscess formation Progressive tissue damage and loss of function 42. Systemic Effects of Inflammation Chronic Inflammation low grade fever, malaise, weight loss, anemia, fatigue, leukocytosis, lymphocytosis, increased erythrocyte sedimentation rates (ESR) Leukocytosis Increased white blood cells Lymphocytosis Increased lymphocytes (type of white blood cell, disease fighting cells) ESR Erythrocyte red blood cell, high sed. rate indicates inflammation somewhere in body 43. Systemic Factors of Chronic Infection Influences on healing Nutrition Psychologic well-being Cardiovascular disease Hematologic disorders Infections Diabetes Corticosteroids Immunosuppressive therapy 44. Other Systemic Factors Consequences of Immunodeficiency Failure of the immune system Predisposed to infection AIDS Effects of Neoplasm Encroaches on healthy tissue May cause pain, swelling Symptoms may include muscular weakness, anorexia, anemia, bruising, bleeding, cachexia (wasting) 45. Implications for the PTA Careful and close monitoring of vital signs, especiallyfor the patient with multiple system involvement Modification of physical therapy to minimize risk Individualized treatment programs Understanding of the disease process, possible risksfor secondary disease, and prognosis 46. Adverse Drug Reactions (ADRs) Most patients are taking multiple prescription or over-the-counter (OTC) medications It is important to know the clinical manifestations ofADRs 47. Adverse Drug Reactions ADRs Unwanted and potentially harmful effects produced bymedications or prescription drugs Mild no treatment needed Moderate may require medication or treatmentchanges Severe potentially life threatening Lethal leads to death Side effects Predictable effects that can occur within therapeutic doseranges 48. Gross Pictures Ahead 49. Adverse Drug Reactions 50. Adverse Drug Reactions 51. Risk Factors for ADRs Age most prevalent Dosages effect Herbals Gender Duration of treatment Ethnicity Noncompliance Alcohol consumption Small stature New drugs Other conditions Number of drugs 52. Signs and Symptoms of ADRs Altered taste Constipation Dry mouth Impaired memory Anxiety Fatigue Dizziness Headache Nasal congestion Vomiting 53. Clinical Manifestation of ADRs Rash Fever Itching Burning Urticaria (hives) Purpura (red or purple discolorations) 54. Other Signs and Symptoms of ADRs 55. Implications for the PTA Exercise can cause sudden changes in the way drugsare metabolized by the body Monitor for signs and symptoms of ADRs Report any suspected ADR to the PT and/or physician Documentation Follow the facilities policies for notification of ADRs May be appropriate to schedule treatment sessionsduring peak pain relief (2 hrs after oral administration) 56. Drug Categories:Nonsteroidal Antinflammatory Drugs NSAIDS Reduce inflammation, decrease pain, reduce fever(ibuprofen, Aspirin, Advil, Naproxen) Tylenol (acetaminophen) NOT an NSAID analgesic and antipyretic only Potential adverse effects of NSAIDs GIcomplications, dyspepsia, bleeding, ulcers, perforation 57. Nonsteroidal Antinflammatory Drugs Interact with high blood pressure medications Anti-coagulant, single dose of aspirin limits clotformation for 5-7 days 58. Implications for the PTA Widespread use both OTC and prescription Post op, fever, musculoskeletal pain, arthritis PTA must observe for any side effects or adversereactions, especially among elderly Easy bruising, bleeding Elevated blood pressure GI symptoms 59. Immunosuppressive Agents Used with organ and bone marrow transplantation May be used with chronic conditions like RA, psoriasis Serious side effects and adverse reactions are common Anaphylactic reactions, renal failure, livertoxicity, neurotoxicity, prone to infection both fungal andbacterial 60. Implications for the PTA Handwashing is essential before contact with immunosuppressed patient Use of Mask may be appropriate Do not work with this patient if you are ill 61. Corticosteroids Naturally occurring hormones in the body Glucocorticoids (cortisol) (hydrocortisone, prednisone, dexamethasone) whichaffect carbohydrate and protein metabolism Mineralocorticoids (aldosterone) Which regulate electrolyte and water metabolism Androgens (testosterone) causes masculinization 62. Glucocorticoids Effective anti-inflammatory agents Side effects: Change in sleep and mood, mild anxiety to psychosis GI irritation Hyperglycemia Fluid retention Susceptibility to infection 63. Glucocorticoids Side effects: Thinning of subcutaneous tissue Delayed wound healing Steroid myopathy: muscle weakness and atrophy Growth retardation Osteoporosis 64. GlucocorticoidsA patient with MS has been on prednisolone for the past 4years. The medication is now being tapered off. This is thethird time this year that the patient has received this treatmentfor an MS exacerbation. The PTA recognizes that possibleadverse effects of this medication are: 1. weight gain and hyperkinetic behaviors 2. nausea and vomiting 3. muscle wasting, weakness, and osteoporosis 4. spontaneous fractures with prolonged healing 65. Anabolic - Androgenic Steroids Roids Synthetic derivatives of the hormone testosterone Used to enhance sports performance or personal(masculine) appearance Side effects: HTN Left ventricular hypertrophy Liver dysfunction Sudden and premature death 66. Implications for the PTA Harmful side effects of glucocorticoids can be delayedor reduced by exercise Monitor vital signs due to risk of increased bloodpressure both with exercise and with steroid use Increase use of calcium and vit D 67. Implications for the PTA Psychologic considerations Mood change and irritability Notify PT or physician when intense changes are seen Anabolic steroids Frequent or recurrent tendon or muscle strain Male pattern baldness Gynecomastia Personality changes, Roid rage Depression 68. Chemotherapy and Radiation Common treatments for cancer (also other diseases thatare non responsive to treatment) 69. Radiation Increased risk of cancer after medical radiation: X-ray, CTscan Radiation can cause: Causes mutations or alterations in DNA Damages blood vessels Bone marrow depression with decreased leukocytes, platelets, and erythrocytes Epithelial cell damage, erythema, alopecia Mucosal lining of Digestive tract damaged resulting in nausea and vomiting, diarrhea, bleeding Fatigue, lethargy, mental depression 70. Chemotherapy Chemotherapy Anti-neoplastic drugs Interfere with protein synthesis and DNA replication of the tumor cells Specific drugs are designed for specific types of tumor cells 71. Chemotherapy and Radiation Adverse effects of chemotherapy: Bone marrow suppression Alopecia Mucosal inflammation with nausea and vomiting Fibrosis in lungs Damage to heart myocardial cells Neuropathy Chemicals stimulate the emetic centers of the brain causing vomiting 72. Implications for the PTA Patients have a high risk of infection, handwashing is essential Notify PT or physician of any sigh of infection Mood swings Fatigue 73. Implications for the PTA Monitor for complaints of pain, burning, numbness, pins and needles, motor deficits (neuropathy) Possible effects on cardiac and other organs manifests months to years after treatment Closely monitor patient tolerance to exercise and other physical therapy interventions 74. Implications for the PTA Mrs. B.N. is 67 years old and has just completed her recent chemotherapy treatment. She has returned to physical therapy due to her weakness and difficulty walking. 1. Explain why handwashing is essential when treating Mrs. B.N. 2. Describe what clinical signs may be expected with Mrs. B.N. 3. Mrs. B.N. complains of fatigue and requests that her therapy be placed on hold. What is the proper response by the PTA? 75. Implications for the PTA Fatigue is common but should not be discounted (consider dehydration, malnutrition, anorexia, sleep disturbances) Lack of exercise can lead to CRF( cardiac-related fatigue) PT and PTA team must determine the balance of exercise and rest that is effective for the patient 76. Pair and Sharetime 77. Fluid and Electrolyte Imbalances Water composes 45-60% of the adult human body (70%for the infant) Water is the medium in which metabolic reactions andother processes take place Water is the transportation system for the body Carries nutrients into cells Removes wastes from cells Transports enzymes in digestive secretions Moves blood cells around the body 78. Fluid and Electrolyte Imbalances Fluid is distributed between intracellular fluid (ICF) andextracellular fluid (ECF) Cell membranes are water permeable Equal concentrations of dissolved particles on each side of themembrane Maintaining equal volumes of ECF and ICF Homeostasis stable internal environment What causes the shift of water? Shifts of water occur due to changes in concentration of ions likesodium 79. Fluid and Electrolyte Imbalances The amount of water entering the body must equal theamount of water leaving the body. Water enters through the ingestion of fluids in liquids andsolids Water exits the body throughurine, perspiration, feces, exhaled air Too much fluid = hypervolemia Too much fluid loss = dehydration 80. Implications for the PTA Patients with CHF should monitor weight gain/lossfrequently. Any increase in weight should be reported toPT or physician Generally, water should be available and offered topatients during rehab, special considerations should befollowed for CHF or renal diseased patients Educate patient on using urine as a gauge for adequatehydration Dehydration degrades endurance and exerciseperformance 81. Electrolyte Imbalances Sodium Sodium influences blood volume and pressure, fluid loss or gain is the primary cation in extracellular fluid Calcium Calcium is important for neuromuscular activity, skeletal Magnesiummuscle, bones, kidneys, and GI tract Magnesium plays a role 82. Electrolyte Imbalances Sodium and potassium are essential for producing the membrane potential providing the means for transmission of electrochemical impulses Sodium influences blood volume and pressure, fluid loss or gain Potassium is necessary for normal muscle contraction and relaxation (heart, intestines, respiration, neural stimulation of skeletal muscles) 83. What does this have to do with me, thePTA? 84. Implications for the PTA Educate the patient to maintain prescribed sodiumrestrictions Elderly have higher incidence of hypokalemia due tothe use of diuretics resulting in fatigue, cramping,dizziness, etc. Ongoing assessment of fluid and electrolyte balance(subjective and objective findings) Be alert to complaints of headache, thirst, nausea,shortness of breath, muscle strength Ask about fluid intake and output, body weightchanges 85. Implications for the PTA Assessment of Fluid and Electrolyte Imbalance Area Fluid Excess and ElectrolyteFluid Loss and ElectrolyteImbalance Imbalance Head and neckDistended neck veins, facialThirst, dry mucous membranesedema ExtremitiesDependent pitting, edemaMuscle weakness, tingling,tetany Skin Warm, moist, taut, cool feelingwhen edematousDry, decreased turgor RespirationDyspnea, orthopnea,productive cough, moist breathChanges in rate and depth of Circulationbreathing soundsHypertension, atrialarrhythmias Pulse rate irregularities,arrhythmia, posturalhypotension, tachycardia AbdomenIncreased girth, fluid wave Abdominal cramps 86. Acid-Base Imbalances Normal function of the body depends on regulation ofhydrogen ion concentration, pH Three systems act to maintain normal pH Blood buffer systems immediate buffering by excretion of excessacid Lungs excretion of acid (occurs within hours) Kidneys Excretion of acid or reclamation of base (occurs withindays) 87. Acid-Base Imbalances Normal pH level is 7.35 to 7.45 Cell function is impaired when pH falls below 7.2 or rises to 7.55 or higher. Below 7.4, more hydrogen ions are present, considered acidic Above 7.4, fewer hydrogen ions present, considered basic 88. Acid-Base Imbalances Acidosis Excess acid in the body Acidemia Excess acid in the blood Alkalosis Excess base in the body Alkalemia Excess base in the blood 89. Acid-Base Imbalances Death occurs if pH level is below 6.8 or above 7.8 90. Acid-Base Imbalances Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis Table 2-7 (pages 44-45) gives an overview of Acid-Base Imbalances 91. Fluid and Electrolyte Balance 92. Implications for the PTA Fruity breath = increased acid levels Hyperventilation re-breathing in bag helpful to preventalkalosis COPD diagnosis may have frequent changes in O2 andCO2 levels with associated symptoms CHF- diuretics cause potassium depletion Notify PT/ MD if signs and symptoms of acid baseimbalance develop 93. Urinary Renal Disorders Urinary Tract Infections (UTI) Very common, men, women, children Bladder infection cystitis Infection of urethra - urethritis Kidney infection pylonephritis 94. Risk Factors of UTI Age Immobility, inactivity (impaired bladder emptying) Catheterization Increased sexual activity Use of diaphragm or condom Uncircumcised penis (first year of life) Female Partner of Viagra User Previous UTI 95. Chronic Kidney Disease (CKD) Alteration in kidney function for greater than 3 months Etiology Diabetes Glomerulonephritis Glomeruli filter waste and fluids from blood Blood and protein lost in urine Excessive aspirin or acetaminophen use 96. End Stage Renal Disease (ESRD) -Renal Failure Final stage of CKD May be due to circulatory disruption to kidneys, toxicsubstances, acute obstruction and trauma SLE Uncontrolled hypertension Uremia end stage toxic condition 97. Renal Failure Red Flags Multi-system abnormalities and failures Dizziness, headaches, anxiety, memory loss, inability toconcentrate, convulsions and coma Hypertension, dyspnea on exertion, heart failure Chronic pain- leg pain and cramps Edema peripheral edema Muscle weakness peripheral neuropathy Osteoporosis Skin pallor, pruritis, dry skin Anemia, bleeding tendencies 98. Dialysis Removal of toxic substances, maintain fluid, electrolyte and acid-base balance Peritoneal or renal (hemodialysis) Signs and symptoms often encountered: Nausea, vomiting, drowsiness, headache, seizures Dementia speech difficulties, confusion Infection at shunt site Multisystem dysfunction 99. Dialysis 100. Implications for the PTA Renal disease may be induced by interactions ofNSAIDS and other analgesics, especially in the elderly Musculoskeletal changes, osteoporosis, atrophy Fluid shifts during dialysis Depression Susceptibility to infection 101. Implications for the PTA Monitor for multisystem dysfunction Vital signs Strength Sensation ROM Function Endurance Locate shunt BP at shunt site contraindicated Locate peritoneal catheters (avoid trauma to these areas) 102. Implications for the PTA Functional mobility training as needed Sit to stand transfers Ambulation Toileting Environmental modifications Toilet rails, raised toilet seat, etc. 103. Implications for the PTA A patient with chronic renal failure is being seen in PT fordeconditioning and decreased gait endurance. The patienthas been scheduled around dialysis. The patient is alsohypertensive and requires careful monitoring. What is thebest approach to take blood pressure? 1. before and after activities, using the nonshunted arm 2. after activity 3. before activity 4. every few minutes during the activity 104. Urinary Incontinence Inability to retain urine Loss of sphincter control Acute - cystitis Persistent stroke, dementia 105. Urinary Incontinence Types: Stress incontinence cough, laugh, sneeze, weakness and laxity of pelvic floor muscles Post partum, menopause, nerve damage Urge incontinence inability to delay voiding after the bladder is full Stroke, hypersensitive bladder Overflow incontinence leaks due to urinary retention Functional incontinence inability or unwillingness to toilet Dementia, stroke, environmental barriers 106. Implications for the PTA Bladder training Prompted voiding, schedule, intermittent catheterization Pelvic floor exercises Kegel exercises incorporate into every day life, withlifting, coughing, changing positions, etc. Behavioral training Record keeping, education on anatomy, muscleweakness, avoiding valsava during activity Adult diapers, pads Psychosocial support 107. Pathology for the PTAChapter 3Injury, Inflammation and Healing 108. Objectives Discuss cell injury and compare/ contrast the factorscausing this injury Differentiate the components of the inflammation reaction Discuss factors that affect tissue healing and phases ofhealing 109. Cell Injury Understanding cell injury, inflammation and tissue healing serves as a solid foundation for clinical decision making 110. Injury Structural and functional changes produced by pathology start with injury to the cells that make up the tissues Injury can occur as a result of Ischemia Infection Immune reactions Genetic factors Nutrition Physical factors Chemical factors 111. Injury Ischemia: limited blood flow Decrease in oxygen and nutrients Decrease in removal of waste products Causes of ischemia Atherosclerosis Clot MI and Stroke are the leading causes of death(lack of blood flow to heard and brain) 112. Injury Infectious agents Bacteria and viral agents most common Sepsis occurs when infectious agents are presentthroughout the body in the blood 113. Injury Immune Reactions Mild allergy to life-threatening anaphylactic reactions Genetic Factors Mutations or alterations in DNA Inherited or acquired 114. Injury Nutritional factors Imbalances can lead to cell injury and death Iron deficiency can lead to anemia Vitamin C deficiency can cause scurvy 115. Injury Physical factors Trauma Incision Excision Excessive heat Excessive cold Pressure Radiation 116. Injury Mechanical factors Soft tissue stress Repetitive or forceful tasks Chemical Factors Chemotherapy and other toxins, topical and metabolic Taken in large amounts most medications can be toxic 117. Cell Injury Reversible Cell injury or stress is short duration and cell is ableto recover Chronic Sub lethal stress remains present over a period oftime causing the cell to adapt but survive (atrophy,hypertrophy, hyperplasia, metaplasia, and dysplasia) Irreversible Results in cell death and necrosis 118. Cell Injury Tissue Calcification Calcium is deposited into the area of damaged tissue,T.B, atherosclerosis, calcific tendinitis can be treatedwith pulsed US 119. Implications for the PTA Signs and symptoms differ depending on the stageof cell injury and the type of organ or tissueinvolved Understanding injury processes and implications 120. Tissue Healing Resolution Minimal tissue damage, cells recover and tissuereturns to normal (sunburn) Regeneration Damaged tissue restored to original form, replaced bysame type of cell (liver) Repair (Replacement)- functional tissue replaced by highlycollagenous scar tissue, loss of function Collagenous scar tissue forms when the injury isextensive, extends beneath the epidermis or cells areunable to undergo mitosis (brain, cardiac cells) 121. Components of Tissue Healing Collagen: most important protein, providesstructural support and tensile strength foralmost all tissues Tendon strength Flexibility of skin Rigidity of bone Elasticity of blood vessels 122. The Healing Process Four phases of healing for acute wounds caused by trauma or surgery Hemostasis and degeneration Inflammatory phase Proliferation and migration Remodeling and maturation Phases often overlap and can take months to years to complete 123. The Healing Process - Hemostasis Hemostasis: blood clotting Platelets clump together forming a loose clot Platelets release chemicalmessengers, growth factors that summoninflammatory cells promote cell healing 124. The Healing Process - Hemostasis Degeneration: formation of hematoma, necrosisof dead cells, and start of inflammatory process Repair of tissue occurs after the removal ofdead cells 125. Defense Mechanisms Non-specific: First line of defense: Skin/ mucous membranes Block entry of bacteria or other harmful substances Saliva, tears have enzymes and chemicals that inactivate ordestroy pathogens Second line of defense: Phagocytosis Process by which neutrophils (a leukocyte, WBC) andmacrophages engulf and destroy bacteria, cell debris andforeign matter (pathogens) Inflammation limits the effects of injury 126. Defense Mechanisms Specific Third line of defense Immune system Specific immune cell responses Lymphocytes, macrophages, etc. Provides protection by stimulating the production ofantibodies 127. Inflammation Initial response of vascularized living tissue toinjury After cell injury, the body reacts with theprocess of inflammation Normal defense mechanism in the bodyintended to localize and remove an injuriousagent Not the same as infection, but infection is onecause of inflammation Disorders are named using the ending itis 128. Inflammation is Triggered By Cell InjuryIschemia NutritionInfections Tissue NecrosisImmune Reactions Mechanical FactorsGenetic FactorsExcessive HeatPhysical Factors Excessive coldIncision PressureExcision Irritant and corrosive chemicals 129. The Inflammatory Response http://www.youtube.com/watch?v=_bNN95sA6- 8&feature=fvwrel 130. Wound Pictures Ahead! 131. Inflammation is Triggered By Incision 132. Inflammation is Triggered By Excision 133. Inflammation is Triggered By Tissue Necrosis 134. Inflammation is Triggered By Excessive Heat 135. Inflammation is Triggered By Excessive Cold 136. Inflammation is Triggered By Pressure 137. Inflammation is Triggered By Infection 138. Inflammation is Triggered By Chemical Burn 139. Clinical Manifestations of Inflammation Redness and warmth Due to increased blood flow (vasodilation) to damaged area Swelling (edema) Shift of protein and fluid into the interstitial space Pain Increased pressure of fluid on nerves; release of chemical mediators i.e., bradykinins Loss of function May develop if cells lack nutrients; edema may interferewith movement 140. Acute Inflammation Three major components Dilation of blood vessels and increased blood flow Mast cell changes allowing proteins to leave the cell Migration of proteins to the area of injury 141. Acute Inflammation Events that occur Vascular events blood vessels Cellular events mast cells Chemical events - mediators and complement factors (proteins) 142. Inflammation (Contd) Acute inflammation Self-limiting Essential part of the healing process (not a disease) Lasts 3-7 days Edema and blood clotting usually occur Platelets are activated Platelet plug is formed and stabilized Thrombus (blood clot) formed Increased capillary permeability causes protein and water to escape into compartment or tissue causing edema 143. Inflammation (Contd) Edema Fluid and protein in tissue causes leukocytes (WBC) toaccumulate Lukocytes are attracted to site of inflammation (WBC) Leukocytosis increased WBC count in blood 144. Inflammation (Contd) Acute inflammation Bacteria killed by neutrophils White blood cells that clean up and eliminatepathogens, dead cells and other cellular debris Limited number of Monocytes/macrophages Also provide phagocytosis but with increased role inchronic inflammation 145. Inflammation (Contd) Chronic inflammation Fibrocytes/fibroblasts - play a critical role in wound healing, create collagen and other cellular material Endothelial cells important role in controlling inflammation, release cytokines (Stimulate the release of inflammatory mediators from other cells), line blood vessels and create lymphatic drainage 146. Inflammation (Contd) Page 66 Factors affecting bloodflow Vasodilation + Histamine increased vascular Serotonin permeability = Bradykinins Edema Leukotrienes/prostaglandins Factors leading to inflammation Lack of adequate bloodflow Production of Damaged tissue inflammatory Acute inflammation cellular CancerinfiltratemediatorsPlatelets Infectious biologic organisms Foreign materialNeutrophils Chemicals Monocyte/macrophage Physical agents Fibrocytes/fibroblasts Factors attracting andEndothelial cellsHeat stimulating cellsCold C5aRadiationLipooxygenase products Chronic inflammation cellular Lymphokinesinfiltrate MonokinesMonocyte/macrophageLymphocyteFibrocytes/fibroblastsEndothelial cells 147. Inflammation (Contd) Chronic inflammation Not self-limiting Must be resolved and replaced by acuteinflammation for healing to occur Production of specific antibodies or cell-mediatedimmunity 148. Local Effects of Inflammation Effusion General term referring to the escape of fluid into a compartment or tissue (edema) Exudate Any fluid that filters from the circulatory system into lesions or areas of inflammation Serous exudate Watery, generally clear, contains small amounts of protein and white blood cells (common with allergies, runny nose, etc.) Fibrous exudate Thick and sticky, high cell and fibrin content 149. Local Effects of Inflammation Purulent exudate Thick , yellow-green in color, contain leukocytes, celldebris and microorganisms. (Bacterial infection,referred to as pus) Abscess Localized pocket of purulent exudate in a solid tissue(around a tooth, in the brain) Hemorrhagic exudate Blood, present if blood vessels are damaged 150. Systemic Effects of Inflammation Fever pyrexia Common if inflammation is extensive. If caused by infection, fever can be severe depending on the microorganism. High fever can be beneficial. Impairs the growth and reproduction of pathogenic organisms. Caused by release of pyrogens feverproducing substances Pyrogens circulate in blood, cause hypothalamus to reset temperature control system at higher level Malaise Feeling unwell, fatigue, headache Anorexia Loss of appetite 151. Potential Complications ofInflammation Infection Microorganisms can more easily penetrate edematous tissues. Deep ulcers Result of severe or prolonged inflammation Skeletal muscle spasm Protective response to pain Local complications Depend on site of inflammation but may include obstruction, loss of sensation, and decreased cell function 152. Granulation Tissue 153. Absence of Granulation Tissue 154. Danger Signs Base of wound becomes increasingly moist,changes from healthy red or pink to yellowishor grey tissue Discharge changes from clear to purulent Unpleasant odor is present 155. The Healing Process Epithelial cells are activated, undergo mitosis and extend across the wound from the outside edges inward Fibroblasts enter and produce collagen (basic component of scar tissue) Fibroblasts and macrophages produce growth factors (cytokines), stimulate epithelial cell growth, development of new blood vessels (angiogenesis) 156. The HealingProcess 157. Wound Healing 158. The Healing Process Healing by first (primary) intention Clean wound, free of foreign material and necrotictissue, edges are held close together, minimal gapbetween edges Healing by second (secondary) intention Large break in tissue, more inflammation, longerhealing period, formation of more scar tissue 159. Fracture Healing Immediate vascular response with hematomaand inflammation Granulation tissue and fibrocartilage formation soft callus Bony callus replaces soft callus to immobilizethe fracture site Repair bone union occurs when hard callusreplaces soft callus Non-union occurs without proper immobilization Remodeling occurs until the bone returns tonormal Time frame varies minimum 6 weeks 160. Tendon and Ligament Injury Sprain Stretching or tear in a ligament Strain Stretching or tear in a musculotendinous unit Tear inflammation granulation tissue collagen - repair 161. Tendon and Ligament Injury Most tendons and ligaments require surgicalintervention Adhesions are common Aggressive motion and muscle contraction should beavoided after surgical repair for at least 8 weeks High rate of impaired function, re-injury, jointosteoarthritis 162. Tendon and Ligament Injury Not all heal at the same rate ACL does not heal as well as the MCL Tensile strength is only 50-70% of original strength 1year later Torn ligament ends must be in contact with each otherto heal 163. Tendon and Ligament Injury Surgical vs. nonsurgical Depends on degree of injury Involvement of supporting tissues Heal by way of scar tissue proliferation and not ligamentregeneration Untreated ligament tears are biomechanically inferior 164. Tendon and Ligament Injury Progressive, controlled stress must be applied to thehealing tissues during healing However, must be protected against excessive forcesduring remodeling phase 165. Tendon and Ligament Injury Grades of Injury Grade I: microscopic tearing of the ligament without producingjoint laxity Grade II: Tearing of some ligament fibers with moderate laxity Grade III: complete rupture of the ligament with profoundinstability and laxity 166. Tendon and Ligament Injury Grades of Injury Grade I and II are most common Can be treated with protective bracing and rehab withstrengthening to provide dynamic muscular support andproprioception Usually good to excellent results anticipated in 90% of casestreated non-surgically 167. Tendon and Ligament Injury Grades of Injury Grade III 15% of all knee sprains Frequently requires repair of associated tissues Cartilage (meniscus) and MCL, LCL, or PCL injury often seenwith ACL grade III injury 168. Ligament andTendon Injury Phases ofHealing Inflammatory phase 3-5 days Proliferative phase 2-3 weeks Protection, immobilization, irregular collagen formation Maturation phase and remodeling occur around 3 weeks post injury Irregular and immature collagen replaced by mature collagenaligned along lines of stress Final phase - 8-12 weeks Maximum muscle contraction forces should be avoided for atleast 8 weeks 169. Tendon and Ligament Injury -Treatment For a Grade 1-2 sprain, use R.I.C.E (rest, ice,compression and elevation): Rest your ankle with weight bearing astolerated Ice should be immediately applied. It keepsthe swelling down. Compression dressings, bandages or ace-wraps immobilize and support the injuredankle. Elevate your ankle above your heart level for48 hours. 170. Tendon and Ligament Injury -Treatment For a Grade 3 sprain/strain Treatment similar to grade 2 but over alonger period Remodeling can take 8-12 weeks (somereports say 16 weeks) before higher levels ofstress can be applied May require surgical reconstruction Normal strength 40-50 weeks postoperatively 171. Ligament Sprain 172. Ligament Injury 173. Ligament Injury - Dislocation 174. Potential Complications ofInflammation Chronic, long-term inflammation can stop wound healing, damage DNA and promote neoplasm (cancer) 175. Treatment of Inflammation Acetylsalicylic acid (ASA) Aspirin Acetaminophen Tylenol Non-steroidal anti-inflammatory drugs (NSAIDs) Ibuprofen Glucocorticoids Corticosteroids 176. Scar Formation Loss of function Result of loss of normal cells and specializedstructures Hair follicles Nerves Receptors Contractures and obstructions Scar tissue is non-elastic Can restrict range of movement Adhesions Bands of scar tissue joining two surfaces that are normally separated 177. Scar Formation (Contd) Hypertrophic scar tissue Overgrowth of fibrous tissue Leads to hard ridges of scar tissue or keloid formation Ulceration Blood supply may be impaired around scar Results in further tissue breakdown and ulceration at a future time 178. Complications of Scar Tissue 179. Factors Promoting Healing Youth Good nutrition: protein, vitamins A and C Adequate hemoglobin Effective circulation Clean, undisturbed wound No infection or further trauma to the site 180. Factors Delaying Healing Advanced age (reduced cell development,mitosis) Poor nutrition, dehydration Anemia (low hemoglobin) Circulatory problems Presence of other disorders such asdiabetes or cancer Irritation, bleeding, or excessive mobility Infection, foreign material, or exposure toradiation Chemotherapy treatment Prolonged use of glucocorticoids 181. Implications for the PTA Inflammation is necessary for healing butmust be controlled for recovery to proceed Edema causes muscle inhibition so must beeffectively treated Client education needed regarding weightbearing and activity level to promotehealing 182. Implications for the PTA Prevention of re-injury Understanding healing time-lines Immobilization followed by mobilization, DVTassessment Modalities: pain control Physician approved surgical protocols 183. Case Study M.H., age 6, fell while running down stairs and hurt his wrist and elbow. His are was scraped and bleeding slightly, and the elbow became red, swollen, and painful. Normal movement was possible, although painful. 1. Explain why the elbow is red and swollen. 2. Suggest several reasons why movementis painful. 3. State two reasons why healing may beslow in this scraped area on the arm, and twofactors that encourage healing in this boy. 184. Pathology for the PTA Chapter 4 The Immune System 185. Objectives Compare/ contrast the different types of immunity Discuss the effect of physical activity and exercise on theimmune system Compare immunodeficiency diseases 186. Immunology The study of the physiologic mechanisms that allowthe body to recognize materials as foreign and toneutralize or eliminate them. The immune system protects the body from infectionand disease Excessive immune system activity can result inhypersensitivity (i.e. allergies) 187. Immunity Natural (innate) immunity Species specific The viruses that cause leukemia in cats or distemper indogs dont affect humans. Innate immunity works bothways because some viruses that make humans ill such as the virus that causes HIV/AIDS dont makecats or dogs sick 188. Active or Passive Immunity Active innate immunity Natural exposure to pathogenchicken pox Development of antibodies or immunoglobulins Active artificial immunity Pathogen purposefully introduced to body Stimulation of antibody production Immunization----measles Booster immunization 189. Immunity (Contd) Passive innate immunity Transferred from mother to fetus Across placenta Through breast milk Protection of infant for the first few months of life or untilweaned Passive artificial immunity Injection of antibodies----antiserum Short-term protection 190. Immunity (Contd) Primary immune response First exposure to antigen 1 to 2 weeks for antibody titer to be effective Secondary immune response Repeat exposure to the same antigen More rapid response with effectiveness in 1 to 3 days 191. Components of the Immune System Lymphoid structures Lymph nodes Spleen Tonsils Intestinal lymphoid tissue Lymphatic circulation Immune cells Lymphocytes Macrophages 192. Componentsofthe ImmuneSystem 193. Components of the Immune System(contd) Tissues involved in immune cell development Bone marrow Origination of immune cells Thymus Maturation of immune cells 194. Components of the Immune System (Contd) Spleen large lymphatic organ Generates response to bloodborne antigens Removes foreign matter and old or defective blood cells Lymph vessels filters fluids to lymph nodes 195. Components of the Immune System(Contd) Lymph nodes Help body recognize and fight germs, infections, and other foreign substances, dependent on type of problem and body parts involved. Contain lymphocytes Tonsils Part of the immune system to filter germs, bacteria and viruses when they enter the body through the nose and mouth 196. Components of the Immune System(Contd) Thymus Responsible for development of T lymphocytes (T cells) Bone Marrow Source of stem cells, leukocytes, and the maturation of Blymphocytes (B cells) Lymphocyte WBC, determine the immune response to foreign substances (B and T cells) 197. Pathogen Infectious organism that causes disease Recognized as being foreign by the body Single celled microorganisms Virus Bacteria Yeast unicellular fungus Multicellular parasites Fungi Worms 198. Pathogen Antigen Protein on the surface of a cell Pathogens have antigens on their surface Antigens trigger the immune response and the production of antibodies 199. Pathogenesis How pathogens (infectious organisms) causedisease Secretion of toxins Endotoxins Direct killing of host cells Physical blockage 200. Pathogenesis Secretion of toxins Bacteria produce toxins which cause pathology anddisease Neurotoxin from Clostridum bacteria causes tetanus Shigalla dysenteria bacteria causes dysentery 201. Pathogenesis Endotoxins Located in cell wall of pathogens Cause fever, lower blood pressure, inflammation Direct killing of host cells Replication within the cell by pathogens can kill the cell,causes release of replicated pathogens to infect othercells Physical blockage Size of pathogen can block tissues 202. Pathogenesis Pathogenesis of Rheumatoid Arthritis 203. How Does the Body Fight Pathogens? 204. ImmunoglobulinsY shaped proteins IgG most common antibody in the blood,crosses placenta producing passive immunity innewborn IgM bound to B lymphocytes, forms naturalantibodies, first antibody secreted by B cells IgA found in tears, saliva, colostrum, providesprotection for newborn IgE Binds to mast cells, causes release ofhistamine resulting in inflammation IgD attached to B cells, activates B cells(Humoral Immunity) 205. Cells - Macrophage Macrophage mature from monocytes Means large eaters Essential first step in immune system is engulfment of pathogen by macrophage Pathogen is introduced to lymphocytes by macrophage 206. Cells - Lymphocytes Primary cells of the immune system are Lymphocytes B Lymphocytes Responsible for production of antibodies - humoral immunity(immunoglobulins) Mature in bone marrow Become plasma cells producing specific antibodies B-memory cells are also formed and provide repeatedproduction of antibodies 207. Cells - Lymphocytes (Contd) T-Lymphocytes From bone marrow stem cells Further differentiation in thymus CMI cell mediated immunity T-killer cells cytotoxic, release enzymes or chemicals to destroy foreign cells Helper T cells activate B and T cells, control or limit specific immune response Memory cells remember antigen and quickly stimulate immune response on re-exposure 208. Development of Cellular and Humoral Immunity 209. The Immune Systemhttp://www.youtube.com/watch?v=IWMJIMzsEMg 210. Factors That Alter Immunity Aging Sex and hormonal influences Nutrition and malnutrition Environmental pollution Exposure to toxic chemicals Trauma Sleep disturbances 211. Factors That Alter Immunity Presence of concurrent illness and diseases: Malignancy Diabetes mellitus Chronic renal failure Human immunodeficiency virus (HIV) infection Medications, immunosuppressive drugs Hospitalization, surgery, general anesthesia Splenectomy Stress, psycho spiritual well-being, socioeconomic status 212. What does this have to do with PTA? 213. Implications for the PTA Intense or strenuous exercise may be detrimental to the immune system in young subjects It takes 6 to 24 hours for the immune system to recover from the acute effects of severe exercise A lifetime of moderate exercise and physical activity enhances immune function 214. Implications for the PTA Intense or strenuous exercise has no detrimental effect on immune function or rate of infections in older adults. Relatively intense exercise programs may be prescribed to maximize cardiopulmonary and musculoskeletal function without impairing immune function in frail elderly people. Intense exercise during anyinfections episode should be avoided 215. Immunodeficiency Partial or total loss of one or more immune systemcomponents Increased risk of infection and cancer 216. Immunodeficiency (Contd) Primary deficiencies Basic developmental failure somewhere in the system Secondary or acquired immune deficiencies Loss of the immune response due to specific causes Can occur at any time during the lifespan Infections, splenectomy, malnutrition, liverdisease, immunosuppressantdrugs, radiation, chemotherapy (cancer) 217. Immunodeficiency (Contd) Predisposition to the development of opportunisticinfections Caused by normal flora Usually difficult to treat due to immunodeficiency Prophylactic antimicrobial drugs may be used prior toinvasive procedures 218. Acquired Immunodeficiency Syndrome(AIDS) AIDS chronic infectious disease caused by thehuman immunodeficiency virus (HIV) HIV destroys helper T-cells - lymphocytes Loss of immune response Increased susceptibility to secondary infectionsand cancer Development may be suppressed by antivirals 219. AIDS (Contd) HIV positive Virus is known to be in the body. No evidence of immune suppression AIDS Marked clinical symptoms, multiple complications Individual is often identified as HIV positive before the development of AIDS. Current therapies start if HIV infection is diagnosed in the early stages. 220. Clinical Manifestations of AIDS Musculoskeletal Myalgia and arthralgia Musculoskeletal pain and wasting Pelvic pain Tuberculosis Delayed healing 221. Clinical Manifestations of AIDS Cardiopulmonary SOB Cough Frequent infections of respiratory system Cardiomyopathy Integumentary Alopecia Basal cell carcinoma Mucocutaneous ulcers Rash Delayed wound healing 222. Clinical Manifestations of AIDS Neurologic and Neuromuscular HIV encephalitis: Gait disturbance Intention tremor Dementia Behavioral: Apathy, lethargy, social withdrawal, irritability,depression Cognitive: Memory impairment, confusion, disorientation Motor: Ataxia, leg weakness, los of fine motor,incontinence, paraplegia Radiculopathy 223. Treatment of AIDS No cure Antiviral drugs reduce the replication of viruses but donot kill the virus (AZT) Frequent mutations require cocktails of additionaldrugs HAART therapy (highly active antiretrovirus therapy) With treatment, the prognosis is muchimproved, decades Without treatment, death occurs within several years 224. AIDS 225. Implications for the PTA Primary role of Physical Therapy is assisting the patient with the management of physical dysfunctions common with this chronic disease Strength training ADL and energy conservation Treatment of neuropathy or radiculopathy Balance and gait training Body mechanics and posture Breathing exercises Individualized exercise based on stage of disease 226. Implications for the PTA Hand washing, standard precautions, disinfectionimportant for all patients Critical for the immuno-deficient patient Pulmonary complications common Susceptibility to infection Often debilitated and easily fatigued Frequent mobility and body positioning enhancegas respiration and promote comfort whilemaintaining strength Individualized programs 227. Chronic Fatigue Syndrome (CFS) Result of a combination of factors Unexplained fatigue of greater than 6 months Thought to be result of neuroendocrine systemabnormality No known cure 228. Implications for the PTA Monitor vital signs Because blood pressure and pulse remain low Avoid overexertion, reduce stress, gentle stretching Borg Scale of Perceived Exertion can be helpful in grading exercises at the sub-maximal level 229. Borg Rate Perceived Exertion Scale 6 No exertion at all 7 Extremely light (7.5)8 9 Very light 10 11 Light 12 13 Somewhat hard 14 15 Hard (heavy) 16 17 Very hard 18 19 Extremely hard 20 Maximal exertion 9 corresponds to "very light" exercise. For a healthy person, it is likewalking slowly at his or her own pace for some minutes13 on the scale is "somewhat hard" exercise, but it still feels OK to continue.17 "very hard" is very strenuous. A healthy person can still go on, but he orshe really has to push him- or herself. It feels very heavy, and the person isvery tired.19 on the scale is an extremely strenuous exercise level. For most peoplethis is the most strenuous exercise they have ever experienced. 230. Hypersensitivity Reactions (Contd) Type I hypersensitivity allergic reactions (Contd) Hay fever/allergic rhinitis Nasal mucosa Food allergies Digestive tract mucosa Atopic dermatitis/eczema Skin Asthma Bronchial mucosa 231. Type I Hypersensitivity (Allergy) 232. Anaphylaxis/Anaphylactic Shock Severe, life-threatening Systemic hypersensitivity reaction Decreased blood pressure due to release ofhistamine Airway obstruction Severe hypoxia Can be caused by: Latex materials Insect stings Nuts or shellfish; various drugs 233. Anaphylaxis (Contd) Signs and symptoms Generalized itching (pruritus)or tingling especially in oral cavity Coughing Difficulty breathing Feeling of weakness Dizziness or fainting Sense of fear and panic Edema around eyes, lips, tongue, hands, feet Hives Collapse with loss of consciousness 234. Signs and Symptoms of Anaphylaxis 235. Treatment for Anaphylaxis Requires first aid response: Administer EpiPen if available Call 911 (many paramedics can start drug treatment and oxygen) Treatment in Emergency Department: Epinephrine Glucocorticoids Antihistamines Oxygen Stabilize BP 236. Type II Cytotoxic Antibody-DependentHypersensitivity Blood typing depends on the particular glycoprotein 3 variants A, B and O Individual can be O, A, B, or AB Will have antibodies to the type of glycoprotein they do not have 237. Type IV Cell-Mediated or DelayedHypersensitivity Occurs only after exposure to antigen Delayed response by sensitized T-lymphocytes Release of lymphokines - help regulate the immunesystem and activate macrophages Inflammatory response Destruction of the antigen Examples: Tuberculin test Contact dermatitis Allergic skin rash 238. Autoimmune Disorders Development of antibodies against own cells/tissues Auto-antibodies are antibodies formed against self-antigens loss of self-tolerance Disorder can affect single organs or tissues or can begeneralized 239. Autoimmune DisordersOrgan Specific Disorders Systemic DisordersAddisons disease AmyloidoisisCrohns disease Ankylosing spondylitisChronic active hepatitisMultiple sclerosisDiabetes mellitus Myasthenia gravisHemolytic anemiaPolymyalgia rheumaticaThrombocytopeniaSclerodermaPolymyositis, Psoriasisdermatomyositis Reiters syndromePostviral Rheumatoid arthritisencephalomyelitis SarcoidosisPrimary biliary cirrhosis Systemic lupusThyroiditis erythematosus (SLE)Graves diseaseHashimotos diseaseUlcerative colitis 240. Systemic Lupus Erythematosus (SLE) Chronic inflammatory disease Affects a number of organ systems Characteristic facial rash butterfly rash Affects primarily young women Incidence is higher in African Americans, Asians, Hispanics, Native Americans 241. Butterfly Rash Associated with SLE 242. Butterfly Rash Associatedwith SLERash can vary from arosy blush to thickenedepidermis with scalypatches 243. SLE (Contd) Signs and symptoms vary due to organ involvement but commonly include: Arthralgia, fatigue, and malaise Cardiovascular problems Polyuria increased production of urine Diagnostic test Serum antibodies; other blood work Treatment Usually treated by a rheumatologist Prednisone (glucocorticoid) Non-steroidal anti-inflammatory drugs 244. Implications for the PTA Functional limitations of patients with SLE vary according to severity of the disease Exercise may be limited during exacerbation of disease Gradual resumption of activities must be balanced with rest periods Energy conservation, pacing of activities Joint protection Prevention of skin breakdown Observe for complications of high dose corticosteroids avascular necrosis of hip, knee 245. Fibromyalgia Disorder characterized by pain andstiffness affectingmuscles, tendons, and surroundingsoft tissues Eighteen specific tender or triggerpoints No obvious signs of inflammation ortissue degeneration 246. Fibromyalgia 247. Fibromyalgia Diagnosis made after elimination andreview of medical history Patients often told their pain is all intheir head Chronic and complex condition oftenrecognized in physical therapy aftermultiple prior interventions 248. Implications for the PTA Primary treatment for fibromyalgia is exercise (to tolerance) Increased cardiovascular fitness has been shown to decrease pain and improve function Stretching exercises reduce fatigue Aquatic therapy often very helpful May initially require short exercise sessions with the goal of 30 minutes daily Avoid pushing through the pain 249. Autoimmune disorders http://www.youtube.com/watch?v=0mz33fLJGwQ 250. Autoimmune Disorders (contd) RAJoint Protection 251. Challenge Question Explain three reasons why the immune system might not respond correctly to foreign material in the body.The immune system does not recognize the foreign material: Deficit of lymphocytes, stem cells or macrophages Antibody is not produced Lymphoid tissue is damaged Genetic immune deficiency is present